Chapter 13: Heart Disease

Surface Anatomy

The heart lies within the left thoracic cavity. The base of the heart is located superiorly, approximately between the second and third rib; the apex is located inferiorly, approximately at the level of the fifth rib (Fig. 13.1). In this position, the heart is rotated in the sagittal plane so that the right ventricle (RV) is positioned anterior to the left ventricle (LV) and tipped anteriorly, bringing the apex closer to the chest wall. In the posterior–anterior view of a chest x-ray, the RV occupies a significant portion of the frontal plane. The right atrium (RA) is generally located in the area of the second intercostal spaces and the angle of Louis. When one palpates the sternum, the angle of Louis is the "bump" that demarcates the manubrium from the body of the sternum. The second intercostal spaces are lateral and slightly below the angle of Louis. The second intercostal spaces are an important auscultatory landmark; the right space is known as the aortic area, the left as the pulmonic area. The apex of the normal heart is in the fifth intercostal space at the midclavicular line. In a healthy heart, this area, known as the point of maximal impulse (PMI), is where the contraction of the LV is most pronounced.

Figure 13.1

Surface anatomy of the heart.

Heart Tissue

The heart wall is made up of three tissue layers (Fig. 13.2). The outermost layer of the heart is a double-walled sac termed the pericardium. The two layers of the pericardium include an outer tough fibrous layer of dense irregular connective tissue termed the parietal pericardium and an inner thin visceral pericardium.⁵ Between these two layers is a closed space filled with pericardial fluid, which serves as a lubricant allowing the two surfaces to slide past one another. Clinically, patients may develop an infection with resultant inflammation of the pericardium termed pericarditis. The clinical signs that accompany this pathology and used to differentially diagnose pericarditis include a pericardial friction rub (an audible grating sound suggesting irritation of the pericardium) that can be auscultated with each heartbeat accompanied by constant chest pain.⁶ In some patients excessive fluid accumulation within the closed pericardial space may lead to a secondary condition known as cardiac tamponade. Tamponade involves compression of the heart caused by fluid buildup in the space between the myocardium and pericardium. In this state, patients will demonstrate compromised cardiac function and contractility due to the excess fluid within the closed space pushing against the heart.^7,8

Figure 13.2

Layers of the heart.

The muscular middle layer of the heart is termed the myocardium. It is the layer that facilitates the pumping action of the heart to move blood to the entire body. Alterations in the muscular wall of the heart are termed cardiomyopathies. There are three common classifications of cardiomyopathies: dilated, hypertrophic, and restrictive.⁹ Dilated cardiomyopathy is evidenced by ventricular dilation and altered cardiac muscle contractile function. CAD is the prime cause of dilated cardiomyopathy, causing mitochondrial dysfunction and resultant myocardial damage. Myocarditis (inflammation of the heart muscle) and alcohol abuse are additional causes of dilated cardiomyopathy. Hypertrophic cardiomyopathy presents as diastolic dysfunction with an increased ventricular mass. Chronic HTN and aortic stenosis are examples of hypertrophic cardiomyopathy. Restrictive cardiomyopathy also presents as diastolic dysfunction owing to the presence of excessively rigid ventricular walls, resulting in a decrease in compliance. The connective tissue changes of the heart associated with diabetes are an example of a restrictive cardiomyopathy. Damage to myocardial cells from cardiomyopathies and various other etiologies lead to cardiac muscle dysfunction and resultant heart failure, which will be comprehensively discussed later in this chapter.

The innermost layer of the heart is termed the endocardium. The tissue of the endocardium forms the inner lining of the chambers of the heart and is continuous with the tissue of the valves and the endothelium of the blood vessel. Because the endocardium and valves share similar tissue, patients with infections of the endocardium are at risk for developing valvular dysfunction. Endocardial infections can spread into valvular tissue developing vegetations (a mixture of bacteria and blood clots) on the valve.⁹ In patients with newly developed vegetations, bronchopulmonary hygiene procedures including percussions and vibrations are contraindicated because they may dislodge, move as emboli, and cause an embolic stroke.⁹

Coronary Arteries

The coronary arteries originate in the sinus of Valsalva located in the wall of the aorta near the aortic valve.⁵ The right coronary originates from the area near the right aortic leaflet, the left coronary from the area near the left aortic leaflet. When the aortic valve is open during systole, the origins of the coronary arteries are located behind the aortic leaflets within the wall; when the aortic valve is closed during diastole, the openings of the coronaries are clearly exposed, allowing them to be easily perfused.⁵ The coronary arteries therefore receive the majority of their blood flow during diastole, unlike the other arteries of the body that are perfused during systole. The left coronary artery begins as the left main (LM) and then branches into the left anterior descending (LAD) and the circumflex (CX) (Fig. 13.3). The LAD may have further divisions, known as diagonal branches, that come off of the primary LAD. The LAD and its diagonal branches primarily supply the anterior and apical surfaces of the LV, as well as portions of the interventricular septum. The circumflex may also have branches, known as marginal branches. The circumflex and its marginal branches supply the lateral and part of the inferior surfaces of the LV and portions of the left atrium (LA). The right coronary artery (RCA) supplies the RA, most of the RV, part of the inferior wall of the LV, portions of the interventricular septum, and the conduction system. The posterior descending artery (PDA) is most commonly a branch of the RCA and perfuses the posterior heart. If the RCA does not perfuse the posterior heart, the CX will supply this area. When the PDA comes from the RCA, the anatomy is referred to as being right dominant; if the PDA comes from the circumflex, the anatomy is referred to as being left dominant. For physical therapists, there is no clinical importance to whether the anatomy of the myocardium is either left or right dominant.

Figure 13.3

Coronary circulation. (A) left main (LM); (B) left anterior descending (LAD); (C) left circumflex (CX); (D) right coronary (RCA); (E) posterior descending (PDA). The branches of the LAD are known as diagonals; the branches of the CX are known as marginals.

The inner diameter (i.e., the opening) of the arteries through which the blood flows is the lumen. The size of the lumen is critical for adequate blood flow. A significant narrowing of the lumen, such as that which occurs with a fixed atherosclerotic lesion of CAD, will decrease the available blood supply to the myocardium. Lumen size may also be altered by the smooth muscle within the walls of the arteries, because smooth muscle regulates vasomotor tone of the coronary arteries. Vasodilation will increase lumen diameter as a result of relaxation of smooth muscle, and vasoconstriction will decrease lumenal diameter as a result of smooth muscle contraction. The responsiveness of arterial smooth muscle is also influenced by the integrity of the endothelium, the lining of the coronary artery that is in direct contact with the lumen. The endothelium has a number of normal functions and "plays the central role in controlling the biology of the vessel wall."^{10, p. 1,265} Some of these important functions are anti-inflammatory actions, antithrombotic activity, and its influence on vasodilation. Endothelial cells release endothelial-derived relaxing factor (EDRF), which facilitates vascular smooth muscle relaxation. Nitric oxide (NO) is the most prevalent EDRF. An injury to endothelium can result in impaired NO release and a decrease in vasodilation.¹¹ NO release is influenced by many factors, including acetylcholine, norepinephrine, serotonin, adenosine diphosphate, bradykinin, and histamine.¹¹

The etiology of the clinical condition known as coronary spasm, in which smooth muscle contraction within the walls of the artery results in narrowing of the coronary artery, is not clearly understood. Coronary spasm occurs in arteries that have endothelial injury (e.g., atherosclerosis), as well as in those arteries that appear to be normal but exhibit hyperreactivity to a variety of vasoconstrictor stimuli, such as serotonin and ergonovine, and loss of EDRF.¹²

Heart Valves

Four heart valves ensure one-way blood flow through the heart. Two atrioventricular valves are located between the atria and ventricle. The atrioventricular valve, positioned between the RA and RV, is termed the tricuspid valve; the left atrioventricular valve is the mitral valve (also known as the bicuspid valve), located between the left atrium and ventricle. The semilunar valves lie between the ventricles and arteries and are named based on their corresponding vessels (i.e., pulmonic valve on the right in association with the pulmonary artery, and aortic valve on the left relating to the aorta).

Flaps of tissue called leaflets or cusps guard the heart valve openings. The right atrioventricular valve has three cusps and is therefore termed tricuspid, whereas the left atrioventricular valve has only two cusps and hence is termed bicuspid. These leaflets are attached to the papillary muscles of the myocardium by chordae tendineae. The primary function of the atrioventricular valves is to prevent backflow of blood into the atria during ventricular contraction or systole, while the semilunar valves prevent backflow of blood from the aorta and pulmonary artery into the ventricles during diastole. Opening and closing of each valve depends on pressure gradient changes within the heart created during each cardiac cycle.

Cardiac Cycle

The cardiac cycle consists of two interrelated phases: systole, the contraction phase, and diastole, the filling phase. During diastole, the ventricles fill with blood from the atria via open atrioventricular valves. The atrioventricular valves lie between the atria and the ventricles and include the tricuspid valve on the right and mitral valve on the left. The first two-thirds of ventricular filling is passive; during the last one-third the atria contract and push the blood into the ventricles. This contraction is known as the atrial kick. After the atrial kick, diastole ends and the atrioventricular valves close. Systole begins with both the atrioventricular and semilunar valves closed. An initial isovolumetric contraction, similar to an isometric contraction of striated muscle, increases the pressure within the ventricles, and the semilunar valve opens. The LV then undergoes a concentric contraction, causing a volume to be ejected, termed the stroke volume (SV). After the SV is ejected, the aortic valve closes and systole is complete. The cardiac cycle is defined by the presence of normal heart sounds, S₁ and S₂. Heart sounds are associated with valvular closings; S₁ is associated with atrioventricular valve closure, and S₂ is associated with semilunar valve closure. Systole occurs between S₁ and S₂, and diastole occurs between S₂ and S₁ (Fig. 13.4).

Figure 13.4

Heart sounds of the cardiac cycle.

Blood Flow and Hemodynamic Values

Blood enters the heart via the superior and inferior vena cava into the RA. Blood moves forward from the RA through the tricuspid valve to the RV, and through the pulmonic valve to the pulmonary artery (PA) and pulmonary capillaries. The capillaries perfuse the alveoli, and the alveolar capillary membrane is the site of gas exchange. Newly oxygenated blood within the pulmonary veins (PVs) travels to the left atrium (LA) and passes through the mitral valve into the LV. Blood within the LV travels down to the apex, where it is squeezed in a wringing motion during systole and moved from the apex to the LV outflow tract and finally out through the aortic valve to the aorta.

Blood volume in any chamber or vessel generates a pressure. The normal pressure recordings for the cardiovascular system are presented in Table 13.1. Owing to the relationship between blood volumes and pressures, a direct measure of blood volumes within the heart is accomplished by invasive monitoring of the intravascular or chamber pressures. In a right-sided heart catheterization, an invasive catheter known as a Swan-Ganz catheter or PA catheter, with pressure-sensitive recording ability, is inserted into the internal jugular or subclavian vein and progressed antegrade through the right side of the heart. Common measurements taken with a right-sided heart catheterization are RA pressure, PA pressure, and pulmonary capillary wedge pressure (PCWP). The PCWP is an indirect measure of the left ventricular end-diastolic pressure (LVEDP), one of the most sensitive measures of LV function. An advantage of right-sided heart catheterization is the ability to monitor filling pressures not only on the right side, but also left-side heart pressures, by estimation, without the need for the more difficult and risky LV catheterization. Invasive monitoring through left-sided heart catheterization is accomplished by placing a catheter into the femoral or radial artery and advancing it retrograde to the flow of blood through the aorta, across the aortic valve, and into the LV where LVEDP can be directly monitored. The LV catheter lies within a high-pressure system (the left side of the heart and the aorta), and therefore can stay in place for only a short period of time (e.g., 1 hour) because of the difficulties associated with cannulation (catheter insertion) of a high-pressure system. In contrast, the right-sided heart catheter, which lies within a relatively low-pressure system (the right side of the heart), provides continuous monitoring of pressures and can be kept in place for several days.

Table 13.1Hemodynamic Variables

Table 13.1 Hemodynamic Variables

Right-Sided Heart Catheterization

Normal Ranges

Central venous pressure (CVP)

0–8 mm Hg

Right atrial (mean)

0–8 mm Hg

Pulmonary artery (PA)

Systolic 20–25 mm Hg

Diastolic 6–12 mm Hg

Mean 9–19 mm Hg

Pulmonary capillary wedge pressure (PCWP)

6–12 mm Hg

Left-Sided Heart Catheterization

Normal Ranges

Left ventricular end-diastolic pressure

5–12 mm Hg

Left ventricular peak systolic pressure

90–140 mm Hg

Systemic arterial pressure

Systolic 110–120 mm Hg

Diastolic 70–80 mm Hg

Mean 82–102 mm Hg

Cardiac output (CO)

4–5 L/min

Cardiac index

(CO ÷ body surface area)

2.5–3.5 L/min

Stroke volume

55–100 mL/beat

Systemic vascular resistance

800–1200 dynes/sec/cm^–5

Adapted from Braunwald, E, Zipes, D, and Libby, R (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. Saunders, Philadelphia 1997, p 188; and Parrillo, JE: Current Therapy in Critical Care Medicine. BC Decker Inc., 1987, p 36.

Neurohormonal Influences on the Cardiovascular System

The autonomic nervous system (ANS) influences the heart and blood vessels through direct neural and indirect neurohormonal mechanisms. The heart has dual direct innervation from the sympathetic and parasympathetic nervous systems.¹³ The sympathetic receptors of the heart are primarily beta-adrenergic receptors¹⁴ and are located on the sinus node and within the myocardium. Stimulation of the receptors by the neurotransmitter norepinephrine (noradrenaline) increases the overall activity of the heart by increasing the heart rate (HR) (chronotropy) and force of contraction (inotropy), and also results in coronary artery dilation.¹³ Sympathetic stimulation of the alpha-adrenergic receptors on peripheral blood vessels causes vasoconstriction and an increase in peripheral vascular resistance (PVR).

The sympathetic nervous system may also stimulate the adrenal cortex to secrete the catecholamine epinephrine. This blood-borne hormone has sympathetic effects that at times may even be more long lasting and potent than direct sympathetic activation. Epinephrine is released as part of the normal exercise response, especially when exercise is continued beyond a few minutes. The increase in HR and contractility noted with exercise is in part due to this hormonal influence. Many cardiovascular drugs either enhance or suppress sympathetic functioning. Those that mimic the action of the sympathetic nervous system are known as sympathomimetics; those that suppress sympathetic functioning are known as sympatholytics. Frequently used sympathomimetics are dopamine, epinephrine, and atropine, which are commonly used in critical care settings. Dopamine and epinephrine increase cardiac output (CO), and atropine increases HR in the presence of critical bradycardia. Frequently used sympatholytics are the category of drugs known as beta-blockers (beta-adrenergic antagonists) that suppress beta-adrenergic activity. They are commonly used as part of an anti-ischemic drug regimen and for the medical management of HTN.

The normal parasympathetic influence via the vagus nerve has a primary impact on the resting heart, influencing resting HR substantially more than the sympathetic nervous system. Parasympathetic stimulation results in a depression of HR, decreased force of atrial contraction, and decreased speed of conduction through the atrioventricular (AV) node. Vagal fiber innervation to ventricular myocardium is relatively small; therefore the effect on LV function is minimal.¹⁴ During exercise, the effects of the sympathetic nervous system and catecholamine release significantly override any effect from the parasympathetic system. The impact of direct parasympathetic influence on peripheral blood vessels is limited to a vasodilatory effect on the bowel, bladder, and genitals.¹⁴

The catecholamine role in myocardial functioning during exercise is especially crucial for the patient who has lost direct sympathetic activation to the heart. For a patient who has undergone a heart transplant, the heart is essentially denervated; the sympathetic and parasympathetic fibers to the heart are excised. Sympathetic influence on the denervated heart is therefore solely dependent on catecholamine stimulation of the beta-adrenergic myocardial receptors to increase HR and contractility. Clinically, the patient with a denervated heart following transplantation will present with elevated resting HRs to achieve normal cardiac output, delayed elevation in HRs with exercise due to circulating catecholamines, decreased maximum HR responses, and slower decreases in HR values during the recovery phase of exercise.¹⁵

Cardiac Output

The goal of the heart is to provide adequate CO to generate aerobic energy to meet the metabolic demands of the body. Because the energy demands of the body are constantly changing, the heart's CO must also be able to adapt to the changing systemic energy demands, as well as to its own myocardial oxygen needs. CO is defined as the amount of blood that leaves the ventricles per minute, expressed in L/min. Normal CO at rest is approximately 4 to 6 L/min. It is influenced by HR (expressed as beats per minute [bpm]) and stroke volume (expressed as milliliters per minute [mL/min]).

Stroke volume (SV) is the volume of blood ejected with each myocardial contraction and is influenced by three factors: (1) preload, the amount of blood in the ventricle at the end of diastole (also known as left ventricular-end diastolic volume [LVEDV]); (2) contractility, the ability of the ventricle to contract; and (3) afterload, the force the LV must generate during systole to overcome aortic pressure and open the aortic valve.⁸ Afterload may also be described as the "load…against which the LV contracts during left ventricular ejection."¹⁶

Throughout the cardiac cycle, diastole and systole place different demands on the ventricles. During diastole, the ventricles must be compliant, able to stretch to accommodate the blood entering the ventricles (preload). During systole, the ventricles must be able to contract adequately to eject the SV. The principle of Starling's length–tension relationship is applicable to the myocardium and the relationship between the properties of diastole and systole. During diastole as muscle length increases (e.g., the ventricular chamber size increases) the ability of the myocardium to develop force is increased, up to a point. Beyond a certain length, however, force development is impaired owing to the inadequate alignment of the actin and myosin filaments (Fig. 13.5).

Figure 13.5

Left ventricular (LV) function curves. (A) With normal LV function, as the left ventricular volume increases, stroke volume will also increase. (B) With LV function impairment, the curve will shift to the right, and for any given length, stroke volume is decreased compared to normal (point b has a deceased SV compared to point a). (C) When normal LV function experiences an increase in sympathetic activity, the curve will shift to the left and SV will increase (note that point c is greater than point aa).

In general, SV will increase with an increase in preload or contractility and will decrease with an increase in afterload. Normally about 55% to 75% of the preload is ejected as the SV. The ejection fraction (EF) demonstrates this relationship between SV and LVEDV such that EF = SV ÷ LVEDV. This value represents the ratio of the volume of blood ejected by the LV per contraction relative to the volume of blood received by the LV following diastole. Normal EF is approximately 55% to 75% (67% ± 8%) and is widely used clinically as an index of contractility.¹⁷

Clinically, especially in critical care settings, the concept of cardiac index (CI) is often preferred to CO. CI expresses the CO in relationship to the body surface area (BSA) expressed in meters such that CI = CO/BSA. Normal CO range at rest is 4 to 5 L/min; normal CI range is 2.5 to 3.5 L/min/m². CI provides a more complete determination of the adequacy of an individual's CO than CO alone. For example, in comparing a 6-ft tall individual and a 5-ft tall individual each with a CO of 3 L/min, the 5-ft tall person will have a higher CI and therefore better tissue perfusion because there is less BSA requiring the 3 L of CO. Determination of BSA and CI is often done using nomograms (two-dimensional diagrams) based on the Geigy scientific tables.¹⁸

Electrical Conduction of the Heart

It is important to note that mechanical contraction of the ventricles only occurs with appropriate electrical conduction through the heart. Effective contraction depends on an intact electrical conduction system that results in depolarization of the myocardium and timely repolarization. In normal sinus rhythm (NSR) the impulse begins in the sinus node and travels through the atria, the A–V node, bundle of His, Purkinje fibers, septum, and ventricles.

Electrical conduction can be viewed via the electrocardiogram (ECG) complex (Fig. 13.6). Each component of the complex reflects a certain phase of conduction pathway.¹⁹

Figure 13.6

Schematic representation of the heart and normal cardiac electrical activity. The ECG is the body surface manifestation of the depolarization and repolarization waves of the heart. The P wave is generated by atrial depolarization, the QRS by ventricular muscle depolarization, and the T wave by ventricular repolarization. The PR interval is a measure of conduction time from atrium to ventricle, and the QRS duration indicates the time required for all of the ventricular cells to be activated. The QT interval reflects the duration of the ventricular action potential. (Adapted from Taber's Cyclopedic Medical Dictionary, ed 21. FA Davis, Philadelphia, PA, 2005, p 1,022, with permission.)

The P wave depicts sinus node and atrial depolarization.
The PR segment demonstrates conduction through AV node.
The QRS complex denotes electrical flow through the ventricles causing ventricular depolarization.
The ST segment describes the initiation of ventricular repolarization.
The T wave illustrates the completion of ventricular repolarization.

Each ECG complex represents one cardiac cycle or one heartbeat. In a series of ECG complexes representing sinus rhythm, each QRS complex should be preceded by a P wave and the QRS complexes should be equally spaced apart, indicating a regular rhythm. ECG interpretation enables the clinician to differentially diagnose the cause of reduced CO that may occur from a true mechanical problem versus that occurring from an electrical problem disrupting mechanical activity of the heart.

Myocardial Oxygen Supply and Demand

Myocardial oxygen supply and myocardial oxygen demand must be in balance. Myocardial oxygen supply depends on the delivery of oxygenated blood through the coronary arteries, the oxygen-carrying capacity of arterial blood, and the ability of the myocardial cells to extract oxygen from the arterial blood. Myocardial oxygen demand (MVO₂), the energy cost to the myocardium, is dependent on many factors. Clinically, MVO₂ is calculated as the product of HR and systolic blood pressure (SBP), known as the rate pressure product (RPP) or double product.⁹ Any activity that increases HR and/or BP will increase MVO₂. Therefore, any increase in systemic oxygen demand (e.g., exercise) will increase the energy cost of the heart and increase MVO₂.

The myocardium is routinely very efficient at extracting oxygen from its blood supply. Therefore, during times of increased energy demand, very little increase in extraction can occur. The primary mechanism for increasing myocardial oxygen supply during times of increased demand is by increased coronary blood flow (CBF).¹¹ In general, there is a linear relationship between CBF and MVO₂. During exercise, CBF may increase five times above resting level in response to the increased demand. Unlike skeletal muscle, which has the capability of both aerobic and anaerobic metabolism, the heart muscle (myocardium) is essentially dependent on aerobic metabolism and has very limited anaerobic capacity.

Laboratory Values

When managing patients with heart disease, certain laboratory values are particularly important. Table 13.2 provides reference values for various laboratory tests. The hemoglobin and hematocrit levels depict the oxygen-carrying capacity within the system. Each gram of hemoglobin carries approximately 1.34 mL of oxygen within arterial blood. A normal hemoglobin level is approximately 12 to 14 g/100 mL of blood in adult males and 14 to 16 g/100 mL of blood in adult women. For example, for a hemoglobin level of 15 g/100 mL of blood, the oxygen-carrying capacity is approximately 20 mL O₂/100 mL of blood (15 × 1.34 = 20). Now, if we consider a patient with a hemoglobin level reduced to 7.5 g/100 mL of blood, the oxygen-carrying capacity is reduced by half and is approximately 10 mL of O₂/100 mL of blood. With reduced oxygen-carrying capacity, the heart must work harder to compensate for low oxygen levels to provide sufficient oxygen to the peripheral tissue. During heart failure, increased workload placed on a failing heart will exacerbate the failure. A general rule of thumb is to use caution and lower the intensity when exercising patients with hemoglobin levels less than 8 g/100 mL of blood.

Table 13.2Laboratory Tests and Reference Values

Table 13.2 Laboratory Tests and Reference Values

Test

Reference Value

Sodium

135–145 mEq/L

Potassium

3.5–5.0 mEq/L

Chloride

95–105 mEq/L

Calcium

9–11 mg/dL

BUN

10–20

Creatinine

0.5–1.2 mg/dL

Glucose

70–110 mg/dL

Carbon dioxide

20–29 mEq/L

Magnesium

1.5–2.5 mEq/L

Hgb (g/dL)

Adult female: 12-16

Adult male: 13–18

HCT (%)

Adult female: 36-46

Adult male: 37–49

Electrolyte levels are also important to consider before treating patients with heart disease. Appropriate levels of potassium, calcium, and magnesium allow for normal electrical conduction through the heart. Hypokalemia, low potassium (usually less than 3.5 mEq/L), produces arrhythmias with flattened T waves and depressed ST segments, as well as bilateral lower extremity muscle cramping. Hypocalcemia (low blood serum calcium levels) and hypomagnesemia (low magnesium in blood) have the potential of increasing ventricular ectopy within the heart. In addition, calcium enhances contractile function of muscle cells. Patients with hypocalcemia have reduced cardiac contractility whereas those with hypocalcaemia present with erratic heart beats.

Renal function tests are done to determine kidney function and examine blood urea nitrogen (BUN) and creatinine levels. These levels are especially important to review in patients with heart failure and patients prescribed with diuretics. Finally, a large number of patients with heart disease also have diabetes and therefore it is important to review blood glucose levels before exercise.

CARDIOVASCULAR RESPONSES TO AEROBIC EXERCISE

Normal Responses

An increase in oxygen uptake occurs with an increase in external workload. There is a direct, almost linear relationship between HR and external workload (Fig. 13.7). Therefore, if the physical therapy intervention requires an increase in systemic oxygen consumption expressed as either an increase in MET levels, kcal, L/O₂, or ml of O₂ per kg of body weight per minute, then HR should also increase. Although some cardiac medications, particularly the beta-blockers, which suppress the sympathetic nervous system's effect on the heart, will limit the actual amount of increase, HR should rise nonetheless. Failure of the HR to increase with increasing workloads (chronotropic incompetence) should be immediately evaluated. Other physiological parameters should be quickly examined, such as BP, respiratory rate, skin color, and temperature, as well as the patient's level of cognition and perceived exertion. An adverse response in any of these parameters is an indication of the patient's inability to hemodynamically respond to the given amount of work.

Blood pressure (BP) should be taken before and immediately after exercise with the patient in the same position (i.e., supine, sitting, standing) and from the same arm each time. Ideally, BP should be taken during exercise to determine the actual hemodynamic response to the increased workload. However, depending on the type of exercise modality, this may be technically difficult. In these cases HR and BP must be taken immediately after exercise. As with HR, a linear increase in systolic pressure is expected with increasing levels of work (see Fig. 13.7). Hellerstein et al²⁰ reported that for each 10% increment of maximal HR, systolic BP increased 12 to 15 mm Hg. Naughton and Haider²¹ interpreted an increase in systolic BP in excess of 12 mm Hg/MET as a hypertensive exercise response and an increase below 5 mm Hg as a hypotensive exercise response. Diastolic pressure exhibits limited changes with exercise; it may not change, or may either increase or decrease by 10 mm Hg.

Figure 13.7

Cardiopulmonary response to acute aerobic exercise. (Adapted from Berne, RM, and Levy, MN: Cardiovascular Physiology, ed 5. CV Mosby, St. Louis, 1986, p 237; Zadai, CC: Clinics in Physical Therapy, Pulmonary Management in Physical Therapy. Churchill Livingstone, New York, 1992, p 27; and McArdle, WD, et al: Essentials of Exercise Physiology. Lea & Febiger, Philadelphia, 1994, p 230.)

In addition, as systemic oxygen requirements increase, the depth and rate of respirations will normally increase from rest. Therefore, tidal volume depicting the depth of respiration and respiration rate indicating the number of breaths per minute will change to meet the metabolic needs of the tissue.

Abnormal Responses

Signs and symptoms of exercise intolerance are presented in Box 13.1. If a patient experiences any of these symptoms, the activity should be stopped and the patient stabilized. It is also important to inform patients that some responses may be delayed for as long as several hours after exercise (e.g. prolonged fatigue, insomnia, sudden weight gain due to fluid retention). Observation of the patient throughout the physical therapy intervention provides a mechanism for ongoing examination. The therapist must be alert to subtle changes in the patient's facial expression, skin color, tone of voice, or thought processing because these may indicate activity intolerance and may require immediate patient examination and modification of the intervention. In addition to the patient's subjective complaint of fatigue or discomfort, there are other responses that warrant termination of an exercise session.¹⁵ These abnormal responses are included in Box 13.1.

Box 13.1 Indications of Exercise Intolerance That Warrant Modification or Termination of an Exercise Session

Signs and Symptoms

Moderately severe or increasing angina
Marked dyspnea
Dizziness, light-headedness, or ataxia
Cyanosis or pallor
Excessive fatigue
Leg cramps or claudication

Other Abnormal Responses

Failure of the systolic pressure to rise as exercise continues
A hypertensive BP response, including a systolic pressure of greater than 200 mm Hg and/or a diastolic pressure greater than 110 mm Hg
A progressive fall in systolic pressure of 10–15 mm Hg
A significant change in cardiac rhythm detected either by palpation or by ECG monitoring (e.g., arrhythmias, ST-T wave changes).

Adapted from ACSM's Guidelines for Exercise Testing and Prescription, ed 8. Lippincott Williams & Wilkins, Philadelphia, 2010.

CARDIAC PATHOLOGIES AND PHYSICAL THERAPY IMPLICATIONS

The pathophysiological conditions that underlie heart disease are HTN, atherosclerosis within the coronary arteries, altered myocardial muscle mechanics, valvular dysfunction, and arrhythmias. The clinical presentations of CVD are diverse and depend on the source of the impairment: perfusion of coronary arteries, contractility of LV myocardium, or alteration of electrical activity. Common signs and symptoms associated with heart disease are chest pressure, dyspnea, fatigue, syncope, and palpitations. However, although these clinical manifestations are strongly associated with heart disease, they are not exclusive for heart disease. Therefore, taking a thorough patient history and performing an appropriate examination and evaluation are crucial to establishing the physical therapy diagnosis, anticipated goals, expected outcomes, and plan of care (POC).

An important consideration is that there is no direct objective measurement of activity limitations based solely on the cardiac diagnosis and pathology. Individuals with seemingly similar cardiac pathology may experience different activity limitations. Activity limitations experienced by the patient with CAD or heart failure may vary widely and are influenced by many factors other than the amount of intact, perfused myocardium or LV function. In response to cardiac impairments, neurohormonal and cardiovascular compensatory mechanisms are activated that allow cardiac functioning to continue for a period of time before the patient becomes symptomatic or there is a significant change in function. Activity limitations are therefore influenced by the amount of compensation as well as the pharmacological management. The following section will delineate the major pathologies affecting heart function, medical management of these conditions, and pertinent implications for physical therapist practice.

Hypertension

HTN is "the most prevalent cardiovascular disease in the United States and one of the most powerful contributors to cardiovascular morbidity and mortality."²² It is estimated that 76 million Americans have HTN.¹ In addition, the prevalence of HTN in blacks in the United States is highest in the world with prevalence increasing from 35.8% to 41.4% from 1994 to 2002.²³

HTN is defined as a persistent elevation of the systolic arterial blood pressure above 140 mm Hg or diastolic blood pressure above 90 mm Hg. In some patients, the blood pressure is not consistently elevated and fluctuates between hypertensive and normal values. This is termed labile HTN and is diagnosed following the evaluation of elevated blood pressure values over a prolonged period of time.

The Joint National Committee (JNC VII) that evaluates and makes recommendations for HTN management defines the following stages of HTN: prehypertension, stage 1, stage 2, and stage 3 (Table 13.3).²⁴ Hypertensive individuals may have elevations in both systolic and diastolic values; however, in the elderly, isolated systolic hypertension (ISH) is commonly noted with elevations in the systolic blood pressure above 140 mm Hg with diastolic blood pressures in the normal range.²⁴

Table 13.3Stages of Hypertension as Defined by JNC VII²⁴

Table 13.3 Stages of Hypertension as Defined by JNC VII²⁴

Hypertension is defined by either systolic or diastolic elevation. A BP of 110/90 is Stage 1 diastolic hypertension; a BP of 160/60 is Stage 3 systolic hypertension.

Stages of Hypertension

Systolic Blood Pressure (mm Hg)

Diastolic Blood Pressure (mm Hg)

Prehypertension

120–130

80–89

Stage 1

130–140

90–100

Stage 2

140–160

100–110

Stage 3

>160

>110

Normal: 119/79 or below.

Broadly, HTN may be divided into two major categories: primary (or essential) HTN and secondary (or nonessential) HTN. Primary or essential HTN is diagnosed when there is no known cause for the elevation in BP values and exists in approximately 90% to 95% of all patients with HTN. Genetic factors, environmental influences (including dietary sodium intake), stress, obesity, alcohol consumption, and other risk factors (including age, lack of exercise, and glucose intolerance) have implications on the occurrence of essential HTN. Regardless of the underlying cause, HTN results secondary to failure of control mechanisms responsible for lowering BP. Secondary or nonessential HTN occurs in approximately 5% to 10% of the hypertensive population and is caused by an identifiable medical problem such as renal, endocrine, vascular, or neurological complications.

Uncontrolled elevated BP levels produce a variety of additional complications, including heart failure, renal failure, dissecting aneurysms, PVD, retinopathy, and stroke. These negative consequences are directly related to the level of BP. Prior research indicates that higher systolic blood pressure at any given level of diastolic blood pressure increases morbidity in both genders.²⁵

Medical Management of Hypertension

Pharmacological intervention is the most common form of medical management of HTN. Six classes of medications currently exist: beta-adrenergic blockers, alpha-adrenergic blockers, angiotensin-converting enzyme (ACE) inhibitors, diuretics, vasodilators, and calcium channel blockers.⁹ In addition to pharmacology, it is important for clinicians to recommend lifestyle modifications, including weight reduction, sodium restriction, moderation of alcohol intake, and regular aerobic exercise, for patients diagnosed with HTN. The benefits of these lifestyle changes include lowering the dosage of medications and reduced occurrence of adverse side effects.

Implications for the Therapist

HTN is generally asymptomatic until complications develop in various organs throughout the body. It has therefore been called the "silent killer." When HTN affects heart function, the individual develops hypertensive heart disease and presents with exertional dyspnea, fatigue, impaired exercise tolerance, tachycardia, chest discomfort, and possible signs of heart failure. The Guide to Physical Therapist Practice indicates that BP monitoring is crucial for all adults over age 35 and in younger patients who are obese or have a history of glucose intolerance, diabetes, or renal dysfunction.²⁶ In addition, clinical monitoring of BP values must be done both at rest and during exercise. According to the American College of Sports Medicine, if resting BP is elevated (above 200 mm Hg systolic or above 100 mm Hg diastolic), physician clearance must be obtained before exercising the patient.¹⁵ Also, if SBP rises to more than 250 mm Hg or if DBP exceeds 115 mm Hg, exercise must be terminated.¹⁵

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is the new terminology for ischemic heart disease or CAD. It involves a spectrum of entities ranging from the least involved condition on the spectrum (unstable angina) to the worst involved condition (sudden cardiac death). Additional entities on the spectrum include non-Q myocardial infarction (NQMI) or non–ST-elevation myocardial infarction (NSTEMI) and Q myocardial infarction (QMI), also referred to as ST-segment elevation myocardial infarction (STEMI). The hallmark sign for any patient presenting with any condition on the spectrum is ischemic chest pain because of a dyssynchrony between the myocardial oxygen supply and demand.

The primary impairment in acute coronary syndrome is an imbalance of myocardial oxygen supply to meet the myocardial oxygen demand (MVO₂). The decrease in supply results from a narrowing of the lumen of the coronary artery, usually due to a fixed atherosclerotic lesion. Atherosclerosis is a disease in which lipid-laden plaque (lesions) is formed within the intimal layer of the blood vessel wall of moderate and large size arteries; over time the plaque may extend into the lumen causing a decreased lumenal diameter. The lesion results from an initial endothelial injury that causes changes within the intima of the blood vessel and progresses to lumenal narrowing. The cause of the initial injury is not well understood, but risk factors have been identified that are associated with an increased risk for the formation of an atherosclerotic lesion. The earliest identified risk factors by epidemiological studies such as the classic Framingham Heart Study included smoking, high cholesterol, HTN, diabetes, emotional stress, and family history.^27,28,29 Obesity, sedentary lifestyle, and elevated blood homocysteine and fibrinogen levels have also been identified as possible contributors.³⁰

Clinical Manifestations

Occlusions may occur in coronary arteries and not produce symptoms. In general, symptoms of CAD are not experienced until the lumen is at least 70% occluded. There are, therefore, many patients who are unaware of their subacute occlusions. It is imperative that an individual's risk factors are known and interventions and monitoring adjusted accordingly.

The clinical conditions resulting from atherosclerosis of the coronary arteries are due to inadequate myocardial oxygen supply to meet the MVO₂. The three common clinical presentations of ACS are angina, injury, and infarction.

Angina

Angina, or cardiac-related chest pain, is due to ischemia. Ischemia is characterized by reduced blood flow to the myocardium. Ischemia is a temporary condition due to the imbalance between the myocardial oxygen supply and demand. On restoring the balance between oxygen supply and demand, ischemia will be reversed and the angina will disappear.

There are three major types of angina: unstable, stable, and variant angina. Unstable angina, sometimes referred to as preinfarction angina or crescendo angina, typically occurs at rest without any obvious precipitating factors or with minimal exertion. It is chest pain that increases in severity, frequency, and duration and is refractory to treatment. Unstable angina usually warrants immediate medical intervention, because the patient is at impending risk for further complications such as an MI or a lethal arrhythmia (V-tach or V-fib).

The term stable angina is used when angina occurs during exercise or activity. Chest pain is experienced at a certain intensity of exercise when the myocardial oxygen demand exceeds the blood supply to the myocardium and is alleviated by decreasing the MVO₂. As mentioned earlier, the MVO₂ is calculated as the product of HR and SBP, known as the rate pressure product (RPP). When patients experience episodes of stable angina, exercise must be terminated and HR and BP need to be taken to determine the RPP (RPP = HR × SBP). In addition to terminating exercise and resting, MVO₂ can also be reduced through the use of nitroglycerin (NTG). In stable angina, the patient often describes the sensation as an intensity less than 5/10, which improves to 0/10 when the oxygen supply is able to balance the demand. It is important to remember that any report of angina requires intervention; the clinician cannot ignore the symptoms even when the patient describes the sensation as light (1 to 2/10).

The third type of angina is variant or Prinzmetal angina and is caused by a vasospasm of coronary arteries in the absence of occlusive disease. Patients with this type of angina respond to NTG for short-term management of their chest pain. However, the preferred long-term pharmacological choice is a calcium channel blocker to reduce the influx of calcium into the smooth muscle cells of the coronary arteries and reduce vasospasm.

Injury and Infarction

Injury represents the presence of a new acute MI.³¹ The term injury is used because the myocardial tissue is being acutely injured during a sudden heart attack. Acute injury to the myocardial tissue then progresses to irreversible, dead infarcted tissue. The tissue, once dead, is irreversible and dead forever. Thus the term injury illustrates the presence of a new MI, whereas the term infarction depicts an old heart attack with dead tissue that cannot be reversed.

Individual myocardial cells may differ in their tolerance for ischemia; however, irreversible changes start to appear 20 minutes to 2 hours from the onset of myocardial ischemia.³² The actual process of injury and infarction evolves over a period of hours. Angina commonly precedes an MI, but the intensity of the symptoms is dramatically increased. Patients frequently describe their discomfort as 10 out of 10 on a pain scale during an acute MI. Infarction is irreversible. Whereas ischemia is due to a partial blockage of the coronary artery, an infarction results from complete occlusion of the vessel. This occlusion commonly results from a rupture of a vulnerable plaque with resultant formation of a thrombus. The type of plaque, more so than the size, will influence the risk of rupture. Lipid-rich and soft plaques are more vulnerable to rupture than collagen-rich and hard plaques. Angiographically large plaque lesions are not necessarily more susceptible to rupture than smaller lesions. Because atherosclerosis begins within the walls of the artery, many vulnerable plaques are invisible via angiogram or appear smaller than their actual size. Although not as common as plaque rupture, coronary occlusion can occur as a result of coronary spasm, coronary emboli, congenital anomalies, and a wide variety of inflammatory diseases.³³ The actual cause of plaque rupture is not clearly understood; however, as a result of the rupture, a thrombus is formed. There may be several mechanisms for thrombosis formation, such as mechanical obstruction of the lumen, release of tissue thromboplastin and the initiation of the clotting cascade, and platelet plug formation from the contact of platelets and exposed collagen.³⁴ Only lesions that occlude the lumen by 70% or more can cause ischemia, but smaller lesions can and do cause MIs. It is important to remember that the size of the initial lesions does not determine whether or not an MI can occur; a small plaque lesion of 30% as well as a larger lesion of 80% may rupture and subsequently form a thrombus that occludes the remainder of the lumen. The majority of MIs occur as a result of initial plaque lesions that occlude less than 60% of the lumen and are not hemodynamically significant to cause ischemia.³⁵ The effects on the ventricle as a result of the infarction often extend beyond the acute infarction period; these long-term effects occur primarily in ventricles that have sustained a moderate to large MI. As the ventricle heals, a process of remodeling occurs as a result of the presence of the infarcted tissue and subsequent dilation. Over time, this reengineering process produces an alteration in ventricular size, shape, and function. Thus, the resultant ventricle often operates at an increased myocardial energy cost due to its inefficient muscle mechanics. Often pictured as three concentric circles (although not absolutely histologically correct), the area of infarction would be at the center of the circle surrounded first by an area of injury and then an outside area of ischemia (Fig. 13.8).

Figure 13.8

ECG following an MI. (A) Zone of infarction: when infarction occurs through the full thickness of the myocardium (transmural) an abnormal Q wave usually appears. (B) Zone of injury: ST elevation occurs in the area of injury. (C) Zone of ischemia: ST depression and/or T-wave inversion occurs in an area of decreased perfusion (ischemia).

Although most MIs heal initially without incident, complications may occur. The major complications following an MI are recurrence of ischemia, LV failure, and ventricular arrhythmias. Therefore, when a patient is said to have had a complicated MI, it is indicative that ischemia, LV failure, or significant ventricular arrhythmias have developed in the acute post-MI period. Ischemia after MI is particularly important because it indicates that there may be vulnerable myocardium with a reduced oxygen supply that may go on to infarct and thereby potentially enlarge the MI. The ultimate complication would be cardiogenic shock with inadequate CO and insufficient arterial BP to perfuse the major organs as a result of severe LV failure. This may necessitate extraordinary medical interventions such as the intra-aortic balloon pump (IABP). The IABP facilitates CO, decreases MVO₂, and increases coronary artery perfusion. The IABP is a balloon catheter placed within the aorta that inflates during diastole, thereby increasing coronary artery perfusion, and deflates during systole, thereby decreasing afterload. The IABP may be used in other conditions besides post-MI cardiogenic instability, for example, patients with hemodynamic decompensation who are awaiting heart transplantation, patients with unstable angina and malignant arrhythmias (such as V-tach or V-fib), or post–cardiac surgical patients with severe hemodynamic instability.¹⁶

Evaluation of Acute Coronary Syndrome (the Evaluation Triad)

In addition to the history taking and review of systems, the evaluation of patients with ACS places emphasis on three major components: evaluating patient complaints, ECG changes, and cardiac enzyme levels (Fig. 13.9). Below is a review of each component.

Figure 13.9

Evaluation triad for patients with acute coronary syndrome.

Patient Complaints

Chest pain from ischemic origin is diffuse and retrosternal. The patient usually reports an intense pressure like "an elephant sitting on the chest." It may radiate to anywhere in the upper extremities and thorax, most specifically to the left arm and left jaw. Figure 13.10 delineates common areas for referred patterns of chest pain. The hallmark approach to differentially diagnosing ischemic chest pain from nonischemic chest pain is to observe for accompanying signs and symptoms of compromised cardiac output. These signs include dizziness, lightheadedness, weakness, diaphoresis (sweating), fatigue, and weakness. Thus, cardiac chest pain during ischemia or an infraction will be accompanied by signs of compromised CO, but chest pain from other etiologies, including pulmonary chest pain, pleural pain, or musculoskeletal pain will not.

Figure 13.10

Referral pattern for chest pain.

ECG Changes

MIs are identified by 12-lead ECG findings. The ECG (also referred to as EKG) is used to examine HR, rhythm, conduction delays, and coronary perfusion. Two of the most common types of ECG are the single-lead and the 12-lead ECG (Fig. 13.11). In the single-lead ECG, only one area of the heart (e.g., anterior, lateral, or inferior) may be viewed at a time. This area may be changed, however, by altering the location of the electrodes. In the 12-lead ECG, 12 areas may be viewed.

Figure 13.11

Normal 12-lead ECG from 50-year-old woman; slight ST elevation is insignificant. Twelve leads are presented; at the bottom of the page is a rhythm strip from lead II. Heart rate from the rhythm strip is approximately 52 (there are 5.8 large boxes between complex 3 and 4; therefore 300/5.8 = 52).

The single-lead ECG is sensitive to rate and rhythm changes and is commonly used for monitoring patients during ambulation and activity. Continuous monitoring is accomplished either via telemetry (radio transmission), allowing the patient freedom to move around when wearing this portable device, or by hardwire, where the patient is attached to the monitor by a cable approximately 15 ft long, therefore limiting mobility. A variation of the single-lead ECG is the 3-lead ECG, which is usually hardwire and is used for monitoring in an inpatient setting. It can be worn continuously throughout an entire treatment session or throughout the entire hospitalization. Unlike the single-lead or 3-lead system, the 12-lead ECG does not provide continuous monitoring, except during an exercise tolerance test (ETT). Two common uses for the 12-lead ECG are the resting ECG taken with the patient quietly supine and the ETT. Twelve-lead ECGs are invaluable in identifying perfusion impairments in the coronary arteries and in assisting with arrhythmia detection. During the ETT, the ECG is continuously monitored to determine the presence of ischemia or arrhythmias with each increase in workload. The 12-lead ECG is sensitive to changes in perfusion as well as rate, rhythm, and conduction. Each coronary artery is represented by a cluster of leads that, although not absolutely correlated with each individual's anatomy, gives a general schema for myocardial perfusion.

During the examination of a 12-lead ECG, the ST segment is clinically useful in identifying the presence of impaired coronary perfusion, either ischemia or injury. The J point, the point where the S wave turns into the ST segment, is the point of reference for interpreting the ST segment. If ischemia is present, the ST segment will be depressed (one or two small boxes) at two small boxes beyond the J point, and the T wave may also be inverted (flipped). Ischemic changes will be present only while the ischemia is present; when the ischemia has resolved, the ECG will return to normal. Conversely, a large acute MI, with subsequent injury to the myocardial tissue, will produce ST-segment elevations on the 12-lead ECG. Large ST elevation myocardial infarction (STEMI) will produce pathological Q waves hours to days following the acute process. Therefore a QMI represents a large MI (formerly known as a transmural MI because it was believed to involve the full thickness of the ventricular wall). Conversely, an acute MI may be relatively smaller and not cause acute injury to the myocardial tissue. In this case, ST segments are not seen on the ECG and the MI is termed an NSTEMI or an NQMI. An NQMI was formerly known as a nontransmural or subendocardial MI because it usually involved the endocardium. An MI that initially presents as an STEMI may be an indication for emergent thrombolytic therapy or revascularization.¹⁶

Anatomical classifications for MIs are based on the surfaces of the LV and not the anatomical heart. An anterior MI involves the anterior surface of the LV, an inferior MI involves the inferior surface of the LV (the diaphragmatic region), a lateral MI involves the lateral surface of the LV (also may be referred to the free wall of the LV for the lateral wall is not adjacent to another structure), a septal MI involves the septum, and a posterior MI involves the LV posterior wall. MIs to different aspects of the ventricle result from compromised levels of blood flow within specific vessels. The RCA supplies blood to the inferior and posterior aspects of the LV and therefore is responsible for producing an inferior- or posterior-wall MI. The anterior and septal aspects of the LV are perfused by the LAD and therefore LAD occlusions are likely to produce anterior or septal MIs. The CX artery supplies blood to the lateral wall of the LV and thereby produces a lateral infarction when it is occluded. The involvement of specific vessels can be determined by a 12-lead ECG. RCA involvement is most likely depicted on leads II, III, and aVF (augmented unipolar limb lead). LAD pathology will be illustrated in chest leads V1, V2, V3, and V4, whereas CX pathology will most likely be demonstrated in leads I, aVL, V5, and V6 (Fig. 13.12).

Figure 13.12

Anatomic pathology and ECG interpretation. Leads I, aVL, V5, and V6 depict problems in the lateral aspect of the left ventricle due to occlusion of blood flow within the circumflex artery. Leads II, III, and aVF depict problems in the inferior aspect of the left ventricle due to occlusion of blood flow within the right coronary artery. Leads V1 to V4 depict problems in the anterior aspect of the left ventricle due to occlusion of blood flow within the left anterior descending artery.

Enzyme Levels

Blood work also helps determine the presence of an MI. Creatine kinase MB subunit (CK-MB), an isoenzyme, is released into blood and elevates with intracellular myocardial damage. Creatine kinase (CK) is found in many tissues besides the myocardium, especially striated muscle, brain, and liver. Injury to these areas will elevate total CK. To differentiate the type of tissue injured, use of CK-MB will isolate the source to the myocardium. Troponin levels should not be elevated in the setting of striated muscle trauma. Other markers that may be used to diagnose an acute MI are the proteins troponin I, troponin T, and myoglobin. Total CK-MB, troponin I, and troponin T have a high sensitivity for the diagnosis of an MI.^10,11 CK-MB and myoglobin may be the most sensitive biomarkers for patients presenting for emergent medical intervention within 6 to 10 hours of the onset of an MI.¹⁰ For patients presenting after 10 hours, troponin biomarkers are preferred over CK-MB because of their increased sensitivity.¹¹ Table 13.4 provides a summary of enzyme levels that are elevated with a myocardial infarction.

Table 13.4Cardiac Enzymes Associated with Myocardial Injury and Infarction

Table 13.4 Cardiac Enzymes Associated with Myocardial Injury and Infarction

Enzyme

Normal Level

Minor Cardiac Dysfunction

Major Cardiac Dysfunction

Peak Levels

Creatine kinase-myocardial band CK-MB

0%–3%

10%

14–36 hours

Lactic dehydrogenase LDH

100–225 mU/mL or 127 IU

300–750 mU/mL

≥1000 mU/mL

Troponin

0–0.2 μg/mL

5 μg/mL

≥10 μg/mL

24–36 hours

Myoglobin

<100 ng/mL

200 ng/mL

≥500 ng/mL

Medical Management of Acute Coronary Syndrome

Once the diagnosis of an MI has been reached (i.e., the patient is "ruled in" for an MI), the goal of medical management is to keep the patient hemodynamically stable and optimize the wound healing of the myocardium. Revascularization procedures and pharmacological interventions are addressed in the following sections.

Revascularization Procedures

Percutaneous Transluminal Coronary Angioplasty

Percutaneous transluminal coronary angioplasty (PTCA) uses a balloon and collapsed stents (stainless steel "cagelike" tube with multiple slots) on the tip of a catheter inserted into the radial or femoral artery and advanced retrograde along the aorta to the openings of the coronary arteries. The catheter is inserted into the coronary artery until the site of the lesion is reached. The balloon is then inflated and the stent expands, compressing the plaque against the interior artery walls, thereby increasing the lumenal area. The balloon is deflated and removed and the stent holds the lumen open. The stent is commonly coated with a drug (e.g., paclitaxel [Abraxane]). Drug-coated stents (collectively referred to as drug-eluting stents) are used to prevent endothelial cell proliferation, which may occur in response to endothelial trauma and the presence of a foreign object placed within the coronary artery and result in restenosis (recurrence of stenosis).

Clinical Implications for the Therapist

The surgical and catheterization reports identify which vessels were revascularized and which vessels have less than 70% lesions and were therefore not revascularized. Because a vessel is not currently a candidate for revascularization does not guarantee that it will not be problematic at a later date, either by rupturing or continuing to demonstrate progressive atherosclerosis. It would be short sighted to assume that a patient who has had a revascularization procedure cannot become ischemic.

There are at present no strict guidelines for when a patient may resume aerobic training following an angioplasty. Conventional wisdom, however, favors waiting approximately 2 weeks to allow the inflammatory process resulting from the intervention an appropriate time to subside. The new exercise prescription should be based on the results of the post-angioplasty ETT, not the pre-angioplasty ETT, which was more than likely positive. Patients may continue to ambulate at a low intensity and comfortable pace during the first 1 to 2 weeks following the PTCA, but should avoid the moderate to higher intensities associated with aerobic training.

Coronary Artery Bypass Graft

Coronary artery bypass graft (CABG) uses a donor vessel to bypass the lesion (narrowed lumen) and establish an alternate improved blood supply. The donor vessel may be the radial artery of the nondominant upper extremity (UE), the saphenous vein, or the internal mammary artery. The patient's harvested saphenous vein or radial artery must be completely detached from both its proximal and distal insertions; the graph is sutured proximally into the aorta and distally into the involved artery beyond the occlusion. When the internal mammary artery is used, it maintains its native proximal attachment while the distal segment is reattached below (bypass) the area of occlusion. Bypass surgery techniques are constantly evolving; traditionally, the full sternum was cut and retracted, but newer minimally invasive techniques termed minimally invasive direct coronary artery bypass (MIDCAB) have emerged that involve less sternal cutting, and some techniques involve no sternal cutting at all, but access the heart via the intercostal space.

Most CABG procedures involve placing the patient on an artificial heart–lung machine (bypass pump), which maintains the oxygenation and circulation of the blood while the heart is stopped during the surgical procedure. As a result of the bypass pump, patients may have additional fluid weight gain following surgery, may feel fatigued, and some patients may have transient A-fib and cognitive changes. Newer techniques have facilitated the use of off-pump procedures to limit the time on the bypass pump. Thus the surgeon operates on a beating heart for the entire or part of the procedure to limit time on the heart–lung machine and reduce the negative sequelae that result from excessive pump time.

Clinical Implications for the Therapist

For patients who have had bypass surgery (e.g., CABG), recovery is somewhat slower than that for PTCA owing to the complexity of the surgical procedure and the incisional healing. Prolonged time in the crucifix position during surgery may predispose individuals to developing an ulnar nerve palsy after surgery. Examination of sensation and manual muscle testing is indicated to rule out the potential for brachial plexus injuries.

The number and location of incisions depend on the surgeon's technique (i.e., either a full sternal cut, partial sternal cut, or intercostal approach). The donor graph site may require additional incisions: a leg incision if saphenous vein is used, a nondominant arm incision if radial artery is used, or no additional incision if grafted with the internal mammary artery. Physical therapy intervention will address any soft tissue impairments associated with the incision to maintain appropriate tissue extensibility and range of motion (ROM), with awareness that patients often indicate soreness and/or discomfort around the donor site. If a sternal wound is present, appropriate posture, scapula retraction, and functional shoulder movements should be encouraged. Proprioceptive neuromuscular facilitation (PNF) UE diagonal patterns often work well, as do the traditional cardinal plane ROM exercises. Patients should be reminded that only a few repetitions at a time throughout the day are better tolerated than more intensive repetitions 1 to 2 times per day; the latter regimen often results in incisional soreness. Some surgeons choose to limit UE ROM exercises during the 4 to 6 weeks following surgery while the sternum is healing; however, it is unclear as to the rationale for the limitation.

Sternal precautions are commonly applied to reduce dehiscence of the incision. Cited risk factors for dehiscence include diabetes, pendulous breasts, obesity, and COPD.³⁶ Interestingly, there is no direct evidence that links the use of arm movements or activity to an increased risk of sternal complications after surgery.³⁶ Prior research has indicated that patients with chronic sternal instability demonstrate greatest sternal separation when pushing up from a chair with sit-to-stand transfers and least sternal separation when elevating both arm overhead.³⁷ In addition, in normal health individuals, the greatest amount of sternal skin movement was seen with sit-to-stand and supine–to–long sitting transfers and the least movement was noted when raising a unilateral weighted UE (less than 8 lb) above shoulder height.³⁸ Patients with chronic sternal instability tend to experience pain that is greater when raising a unilateral loaded UE compared to raising bilateral loaded UEs.³⁹

Sternal precautions vary greatly by physician, institution, and type of surgery performed. Instructions may include limiting lifting of objects between 5 and 10 pounds for up to 8 weeks after surgery. It is important to develop a professional collegial relationship with the surgical team to discuss surgical techniques and mobility concerns to ensure the best outcome for the patient.

To avoid sternal discomfort, all patients will benefit from splinting the incision with a hand or pillow when laughing, coughing, or sneezing. Patients will also appreciate information regarding energy conservation and rest periods. Even though the heart function is perhaps the best it has been in quite some time, the effects of major surgery on energy level and mobility must be emphasized. The impact of fatigue on the patient's sense of well-being may be profound, and it is important that patients understand the need for rest as well as ambulation. Early ambulation and mobility beginning the first day after surgery will assist in the patient's physical and emotional recovery.

During the initial weeks following cardiac surgery, the early in-hospital limitations following cardiac surgery have perhaps more to do with the surgical procedure and altered mobility and less to do with the heart itself, which is theoretically healthier than it was before surgery. Postoperative fatigue may be due to a combination of factors, including anesthesia, blood loss, initial weight gain due to cardiopulmonary bypass machine, common arrhythmias such as A-fib, and the energy cost of healing. As with the post-MI recovery period, when the patient returns home following surgery it is a good idea to break the day into many subunits including rest, leisure activity, and perhaps visiting with friends by phone or in person. Developing a schedule but keeping it flexible helps the patient exert some control over the day and energy level.

The patient is encouraged to gradually increase walking, with a goal of 30 minutes of ambulation 1 to 2 times per day at 4 to 6 weeks after surgery. If the patient is walking in the neighborhood, suggest that the initial walks be back and forth in front of the house rather than around the block. In this way, if the patient overestimates his or her energy level, the close proximity of home will provide a welcomed rest and prevent overexertion. Many patients ambitiously begin their walk only to find themselves suddenly fatigued and further from home than they would like. Continuing exercises for posture, UE and trunk mobility, and sternal protection are also important components of the home exercise program (HEP).

Once a patient's incisions have healed (approximately 6 weeks) and his or her blood counts including hematocrit and hemoglobin are in acceptable ranges, cardiac rehabilitation may begin. The patient may have a maximal ETT and begin aerobic and strength training.

Pharmacological Management

Cardiovascular pharmacological agents are critical in the medical management of patients with CAD. There are a variety of drugs designed to reestablish the balance of myocardial supply and demand, with new drugs being added all the time. The major anti-ischemic categories are beta-blockers, calcium channel blockers, and nitrates. Beta-blockers decrease beta-sympathetic activity on the heart, resulting in a decrease in HR and contractility and therefore energy demand. Calcium channel blockers reduce BP and therefore decrease the work of the heart. Calcium channel blockers are also somewhat unique in preventing coronary smooth muscle spasm and thereby may increase myocardial blood supply. Nitrates, one of the oldest categories of drugs, are potent vasodilators that decrease preload and afterload, and therefore decrease myocardial work, as well as dilate coronary arteries. Afterload reducers, particularly those that affect the renin–angiotensin–aldosterone system such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), are frequently used to normalize BP and reduce workload on the heart. The effect of some of the more widely used cardiac drugs on HR, BP, and ECG findings are presented in Table 13.5.

Table 13.5Effects of Medications on Heart Rate, Blood Pressure, ECG, and Exercise Capacity

Table 13.5 Effects of Medications on Heart Rate, Blood Pressure, ECG, and Exercise Capacity

Medications

Heart Rate

Blood Pressure

ECG

Exercise Capacity

I. Beta-blockers (including carvedilol and labetalol)

↓^∗ (R and E)

↓ (R and E)

↓ HR^∗ (R)

↓ ischemia^† (E)

↑ in patients with angina; ↓ or ↔ in patients without angina

II. Nitrates

↑ (R)

↑ or ↔ (E)

↓ (R)

↓ or ↔ (E)

↑ HR (R)

↑ or ↔ HR (E)

↓ ischemia^† (E)

↑ in patients with angina; ↔ in patients without angina; or ↔ in patients with congestive heart failure (CHF)

III. Calcium channel blockers Amlodipine Isradipine Nicardipine Nifedipine Nimodipine Diltiazem Verapamil

↓ or ↔ (R and E)

↓ (R and E)

↑ or ↔ HR (R and E)

↓ ischemia (E)

↓ HR (R and E)

↓ ischemia^† (E)

↑ in patients with angina; ↔ in patients without angina

IV. Digitalis

↓ in patients w/atrial fibrillation and possibly CHF Not significantly altered in patients w/sinus rhythm

↔ (R and E)

May produce nonspecific ST-T wave changes (R) May produce ST segment depression (E)

Improved only in patients with atrial fibrillation or in patients with CHF

V. Diuretics

↔ (R and E)

↔ or ↓ (R and E)

↔ or PVCs (R) May cause PVCs and "false-positive" test results if hypokalemia occurs May cause PVCs if hypomagnesemia occurs (E)

↔ except possibly in patients with CHF

VI. Vasodilators, ACE inhibitors and angiotensin II blockers Alpha-adrenergic blockers Antiadrenegic agents without selective blockade

↑ or ↔ (R and E) ↔ (R and E)

↔ (R and E)

↓ or ↔ (R and E)

↓ (R and E)

↑ or ↔ HR (R and E) ↔ (R and E)

↔ (R and E)

↓ or ↔ HR (R and E)

↔ except ↑ or ↔ in patients with CHF

↔

VII. Nicotine

↑ or ↔ (R and E)

↑ (R and E)

↑ or ↔ HR May provoke ischemia, arrhythmias (R and E)

↔ except ↓ or ↔ in patients with angina

Adapted from American College of Sports Medicine: Guidelines for Exercise Testing and Prescription, ed 8. Lippincott, Williams & Wilkins, Baltimore, 2010, pp 286, 287, and 289, with permission.

Key: ↑ = increase; ↔ = no effect; ↓ = decrease; E = exercise; R = rest.

^∗Beta-blockers with intrinsic sympathomimetic action (ISA) lower resting HR only slightly.

^†May prevent or delay myocardial ischemia.

Heart Failure

Heart failure is a syndrome characterized by impaired cardiac pump function, resulting in inadequate systemic perfusion and an inability to meet the body's metabolic demands. Being a syndrome, patients in heart failure present with an array of signs and symptoms. This section presents the epidemiology, causes and types of heart failure, pathophysiological and clinical presentation of heart failure, and medical management and evaluation for this patient population. A discussion of physical therapy interventions for managing patients with heart failure will be delineated later in this chapter.

Epidemiology of Heart Failure

With the marked improvement in anti-ischemic medications, increased knowledge and management of CAD risk factors, availability of sophisticated monitoring, and revascularization techniques, more patients are living longer with coronary disease than similar patients 20 or 30 years ago. New technology and medications continually improve the understanding and management of CAD; however, an undesired effect of long-term CAD may be the increased prevalence of heart failure, also known as congestive heart failure (CHF). Technology and other advances in medicine are reducing mortality with a concomitant increase in morbidity. Therefore, patients with heart failure are less likely to die and more likely to live longer with the worldwide prevalence and incidence of heart failure approaching epidemic proportions. In the United States, heart failure affects 5.7 million individuals with approximately 670,000 incident cases of heart failure diagnosed annually.⁴⁰ Estimates of the prevalence of heart failure in the general European population are similar to the Unites States and range from 0.4% to 2%.⁴¹ In North America and Europe the lifetime risk of developing heart failure in both sexes at age 40 is approximately 1 in 5. In addition, 6% to 10% of people older than 65 have heart failure, indicating an exponential rise in the prevalence of heart failure with increasing age.⁴² In looking at gender differences, although the relative incidence of heart failure is lower in women compared to men, women constitute half of all cases with heart failure because of their longer life expectancy.⁴³ Heart failure has surpassed MI as the leading cause of cardiac deaths in the United States and is the most frequent cardiac diagnosis for hospital admissions and readmissions.

Causes of Heart Failure

The most common cause of heart failure is cardiac muscle dysfunction. Cardiac muscle dysfunction is a general term describing altered systolic and/or diastolic activity of the myocardium that usually develops as a result of an underlying abnormality within the cardiac structure or function.⁹ Several reasons exist for the development of cardiac muscle dysfunction. Box 13.2 presents potential precursors and risk factors for the development of cardiac muscle dysfunction.

Box 13.2 Causes of Cardiac Muscle Dysfunction

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Precursors

Description

Hypertension

Increased peripheral arterial pressure contributes to increased afterload and pathological hypertrophy of the left ventricle.

Coronary artery disease

Acute injury to myocardial tissue damages ventricular contractility causing systolic dysfunction. Scar formation seen in infracted tissue alters relaxation and may lead to diastolic dysfunction.

Cardiac dysrhythmias

Normal electrical conduction through the heart allows for normal mechanical contraction of the ventricles. Altered electrical conduction alters the mechanical activity of the ventricles exacerbating heart failure.

Valve abnormalities

Cardiac valve pathology (stenosis or regurgitation) causes structural changes to the chamber behind the valve resulting in cardiac muscle dysfunction and failure.

Pericardial pathology

Pericarditis (fluid in the pericardial space) with resultant cardiac tamponade compresses the ventricles leading to cardiac muscle dysfunction and heart failure.

Cardiomyopathies

Damage to the myocardial cells from various pathological processes alters the systolic and/or diastolic function of the ventricles.

Types of Heart Failure

Heart failure may be categorized based on a structural perspective and a functional perspective. From a structural perspective, heart failure is described as being left-sided heart failure or right-sided heart failure.⁴⁴ Left-sided heart failure occurs with LV insult. Pathology of the LV reduces the CO leading to a backup of fluid into the LA and lungs. The increased fluid in the lungs produces the two hallmark pulmonary signs of left-sided heart failure: shortness of breath (SOB) and cough. Primary right-sided heart failure occurs from direct insult to the RV caused by conditions that increase PA pressure. Increased pressure within the PA subsequently increases the afterload, thereby placing greater demands on the RV and causing it to go into failure. With RV failure, blood is not effectively ejected from the RV and backs up into the RA and venous vasculature, producing two hallmark peripheral signs: jugular venous distention and peripheral edema. Often, left-sided heart failure may be severe as seen in patients experiencing a heart failure exacerbation. With severe LV pathology, fluid from the LV backs up into the lungs, increasing PA pressure and causing fluid to back up into the right side of the heart and the systemic venous vasculature. This is termed biventricular failure. Therefore, patients with biventricular failure will present with both pulmonary and systemic signs of heart failure. Table 13.6 provides hemodynamic pressures noted with left, right, and biventricular failure.

Table 13.6Example of Hemodynamic Pressures Associated with Heart Failure

Table 13.6 Example of Hemodynamic Pressures Associated with Heart Failure

An increase in PAP and/or PCWP is associated with LV failure; an increase in CVP is associated with RV failure; and an increase in CVP, PAP, and PCWP is associated with biventricular failure.

Pressure (Norms)

LV Failure

RV Failure

Biventricular Failure

CVP (0–8 mm Hg)

6 mm Hg

12 mm Hg

PAP (9–19) mm Hg

22 mm Hg

16 mm Hg

22 mm Hg

PCWP (6–12) mm Hg

18 mm Hg

10 mm Hg

18 mm Hg

CVP = central venous pressure; LV = left ventricle; PAP = pulmonary artery pressure; PCWP = pulmonary capillary wedge pressure; RV = right ventricle;

From a functional perspective, heart failure is described as systolic or diastolic dysfunction.^44,45 Systolic dysfunction is characterized by compromised contractile function of the ventricles causing reductions in the SV, CO, and EF. Patients with systolic dysfunction will usually present with compromised ejection fractions (EFs) less than 40%. Diastolic dysfunction is characterized by compromised diastolic function of the ventricles. With this condition, the ventricles cannot relax and fill appropriately during the relaxation (diastolic) phase of the cardiac cycle. The impaired ability to fill the ventricles with blood reduces the volume of blood ejected with each contraction (the SV) and the overall volume of blood ejected per minute (the CO). EF is unaltered and remains normal between 55% and 75%. No reduction in the ratio is noted because there is no change in the contractile ability of the ventricles. However, there is a low volume of blood being ejected with each contraction as less blood entered into the ventricle before the contraction phase.

Pathophysiology of Heart Failure

Heart failure involves a complex series of events involving pathophysiological and compensatory factors in response to cardiac muscle dysfunction.^{46,47,48,49,50,51} When the myocardium is dysfunctional, compensatory mechanisms are activated with the goal of maintaining adequate cardiac output. Neurohormonal mechanisms including activation of the sympathetic nervous system are triggered to increase HR and maintain CO at rest. Thus patients experiencing an acute bout of heart failure are very likely to be tachycardic at rest.

When patients are in heart failure and the ventricle is ejecting low blood volumes, blood begins to accumulate within the ventricles, causing congestion. This congestion increases the LVEDV and contributes to an elevation in LV pressure. The increased pressure is transmitted retrograde toward the LA and the pulmonary veins. This increase in hydrostatic pressure in the pulmonary veins causes fluid to move from the veins into the interstitial space of the lung, resulting in pulmonary edema.⁴⁵

It is also important to consider kidney function for patients with heart failure. Low blood volume pumped out of the heart causes less blood to perfuse the kidney and is likely to put the kidney in failure. Patients experiencing an acute heart failure exacerbation often go into renal failure. It is therefore crucial for therapists to monitor BUN and plasma creatinine levels. An increase in urea production, elevated BUN and creatinine levels, and decreased urine output indicate renal dysfunction.⁴⁵

From a musculoskeletal standpoint, patients with heart failure often present with skeletal muscle wasting, myopathies, and osteoporosis. These negative sequelae are associated with inactivity and prolonged bedrest. Several studies have investigated the effects of CHF on skeletal muscle abnormalities and found reductions in the size and number of Type I and Type II muscle fibers.^52,53,54 It is therefore imperative that the physical therapy POC place emphasis on interventions to improve overall endurance and functional mobility in this patient population.

Clinical Manifestations of Heart Failure

The clinical presentation of the patient with CHF depends not only on the amount of LV failure, but also on the status of compensatory mechanisms and the impact of drug therapy. Over time, the energy cost of the compensatory mechanisms proves to be too much for the impaired myocardium. The patient then begins to present with signs and symptoms of CHF, and now moves from being asymptomatic to symptomatic. Although the terminology may be somewhat confusing, it is important to note that when a patient is referred to as being in compensated heart failure, the patient's congestive symptoms can be relieved by medical intervention. A patient who is non-compensated is showing signs and symptoms of congestion and requires medical and pharmacological readjustment.

Common signs and symptoms of CHF include fatigue, dyspnea, edema (pulmonary and peripheral), fluid weight gain, presence of an S₃ heart sound, and renal dysfunction. Pulmonary edema may be evident by chest x-ray and auscultation of adventitious sounds. Peripheral edema may be evident in gravity-dependent LEs by the presence of indentations in the skin when pressure is applied, that is, pitting edema. Pitting edema associated with CHF is usually bilateral and may extend from the foot to the pretibial area.^55,56 Documentation should include a numerical grade based on the duration of indentation after fingertip pressure. See Chapter 14, Vascular, Lymphatic, and Integumentary Disorders, for pitting edema grading scale. Weight gain and peripheral edema are among the signs of systemic volume overload.

On auscultation of the heart and lungs characteristic sounds are heard with CHF. The usual abnormal heart sound associated with CHF is the presence of an S₃ heart sound. This is a low-frequency heart sound heard in early diastole and occurs due to poor ventricular compliance and subsequent turbulence of blood within the ventricle.⁷ Heart murmurs (extra heart sounds), especially those of mitral regurgitation, may also be present owing to the effect of the enlarged LV pulling on the mitral valve. Lung auscultation for patients with heart failure reveals the presence of crackles or rales. These are crackling/bubbling sounds suggesting fluid in the lung. The sounds are usually heard during inspiration and represent the movement of fluid in the alveoli and subsequent opening of the alveoli that were previously closed because of the excess fluid.⁴⁴

Dyspnea is one of the most common symptoms experienced with left-sided CHF. The SOB is associated with pulmonary edema. When fluid accumulates in the lungs, gas exchange is altered at the alveolar capillary interface. Gas exchange (respiration) will occur at the alveolar capillary interface only when ventilation within the alveoli is matched with perfusion within the pulmonary capillary (V/Q matching). Excessive amounts of fluid within the pulmonary parenchyma cause a ventilation/perfusion mismatch, thereby reducing the amount of oxygen delivered to blood and causing dyspnea.

Two other symptoms reported by patients in CHF are paroxysmal nocturnal dyspnea and orthopnea. Paroxysmal nocturnal dyspnea (PND) is characterized by sudden episodes of SOB occurring in the night. Orthopnea is increased SOB in the recumbent position. The severity of orthopnea is often crudely documented by observing the number of pillows a patient needs to keep the upper body in an upright or semirecumbent position. Therefore, a patient with three- or four-pillow orthopnea suggests a greater severity of heart failure when compared to a patient with one-pillow orthopnea. Physiologically, as patients assume a recumbent position from an upright position, with their legs elevated to the same horizontal level as their trunk, fluid moves back to the heart causing an increase in preload. A failing heart cannot keep up with the additional preload and excess fluid returning to the heart and therefore causes a backup into the lungs producing increased symptoms of SOB.

Increased arterial resistance is also seen in patients with CHF and results in an increase in afterload and therefore in MVO₂. The increased resistance may result from a combination of factors, including (1) increased sympathetic adrenergic stimulation; (2) decreased vasodilation of vascular smooth muscle as a result of a decrease in the availability of the endothelium-derived relaxant factor, nitric oxide; (3) an increase in the endothelial-derived smooth muscle vasoconstrictor, endothelin-1; (4) an increase in vascular stiffness as a result of salt and water retention; and (5) the presence of the powerful peripheral vasoconstrictors angiotensin II and vasopressin.⁵⁷

One of the common complaints of patients with CHF is early onset of muscle fatigue. The cause of the muscle fatigue may be multifactorial, including a decrease in peripheral blood flow, changes within the peripheral vascular beds, peripheral vasoconstriction, atrophy of muscle fibers, and increased utilization of anaerobic metabolism for energy production.^58,59 The contribution of intracellular mechanisms to muscle fatigue has been studied. Examples of these intracellular mechanisms include an alteration in the control of calcium release and reuptake⁶⁰ and myocyte apoptosis.⁶¹ In addition to peripheral muscle functioning in patients with heart failure, exercise studies have also investigated various other factors, including oxygen uptake kinetics, neurohormonal parameters, and endothelial function, that may influence the exercise response.^62,63,64 Although there are many potential reasons for the fatigue associated with CHF (especially Class III and IV), a recently identified contributor is obstructive sleep apnea. Sleep apnea may be treated in this patient population with the use of continuous positive airway pressure worn while sleeping.^65,66

Patients with heart failure will present with decreased exercise tolerance owing to a culmination of the pathophysiological and compensatory events associated with heart failure. It is difficult for patients to exercise when they have gained weight, have SOB, and have a rapid HR. There are a variety of methods to measure exercise tolerance in patients with heart failure. Physicians utilize the New York Heart Association (NYHA) and Functional Classification Scale (Table 13.7). Classification is based on the development of symptoms and the amount of energy required to provoke them. Patients in Class I have mild heart failure and relatively better exercise tolerance compared to patients in Class IV with severe CHF and poor exercise tolerance.

Table 13.7Functional Classifications of Patients with Diseases of the Heart

Table 13.7 Functional Classifications of Patients with Diseases of the Heart

Functional

Continuous-Intermittent Permissible Workloads

Maximum

Class I

4.0–6.0 cal/min

Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.

6.5 METs

Class II

3.0–4.0 cal/min

Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.

4.5 METs

Class III

2.0–3.0 cal/min

Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain.

3.0 METs

Class IV

1.0–2.0 cal/min

Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.

1.5 METs

Four-level classification system based on functional limitations. Reprinted by permission of the American Heart Association, New York.

Medical Examination and Evaluation of Heart Failure

Medical interventions include a variety of tests to identify the etiology and evaluate the severity of heart failure. Following an examination of signs and symptoms of heart failure in a given patient, several key tests are typically performed. These include a chest x-ray, laboratory tests, echocardiography, and nuclear imaging studies.

Radiological Findings in CHF

Three hallmark characteristics of the chest x-ray help confirm the diagnosis of CHF⁹ (Fig. 13.13):

Figure 13.13

Radiographic examination to confirm CHF.

An enlarged cardiac silhouette: The enlargement of the heart in patients with CHF occurs secondary to congestion of fluid in the lungs and possible pathological hypertrophy of the ventricles.
Opacities (white areas) in the lung field with interstitial and parenchymal edema. This occurs when excessive fluid collects in the lung when LV end-diastolic pressures exceed 25 mm Hg.⁴⁴
Blunting of the costophrenic angle. The lower ribs meeting the diaphragm creates this sharp image observed on the chest x-ray. In patients with CHF, fluid settles to the lower, dependent aspect of the lung, producing an opaque appearance, and blunts the costophrenic angle.

Laboratory Findings in CHF

Natriuretic peptides including atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP) are released from atrial and ventricular myocytes in response to volume overload within the respective chambers.⁶⁷ ANP and BNP are cardiac neurohormones that target the kidney when released to increase diuresis and decrease the overall volume of fluid within the vasculature and chambers of the heart.⁴⁴ Circulating levels of BNP are elevated in plasma in patients with heart failure. There is no level of BNP that perfectly separates patients with and without heart failure. Normal levels of BNP are less than 100 pg/mL. Values above 500 are generally considered to be positive for heart failure. The BNP level provides an indication of the extent of heart failure where higher BNP levels without renal failure indicate worsening failure of the ventricles. Therefore a patient with a BNP of 1,000 pg/mL has more significant heart failure than a patient with a BNP of 500 pg/mL. BNP has been found to be a statistically significant (p < 0.05) prognostic indicator of heart failure,^68,69 and studies have discovered moderate to strong (from r = −0.38 to −0.64) correlations between BNP and peak oxygen uptake (VO_2max).^68,69

Echocardiogram and Nuclear Imaging

With ultrasound technology, the echocardiogram is used to examine wall motion integrity, valvular status, wall thickness, chamber size, and LV function. The EF may also be calculated using the data obtained from the echocardiogram. An echocardiogram may accompany a stress test and is known as a stress echo. The purpose of a stress echo is to compare LV function and wall motion between rest and exercise when an increased VO₂ results in an increased MVO₂. A positive stress echo indicates a worsening of LV function as activity increases; a negative stress echo indicates that the LV has adequately adapted to the increase in energy demand. Nuclear imaging (e.g., thallium sestamibi) compares coronary perfusion between rest and exercise. If there is no decrease in perfusion with increasing workloads, the test is negative; if there is a decrease, the test is considered positive.

Pharmacological Management of CHF

With the advent of new medications such as combined alpha- and beta-blockers, ACE inhibitors, and vasodilators, the symptoms of volume overload are more effectively managed.^70,71 The principles of drug management with CHF are twofold: (1) to increase the contractility or pumping ability of the heart to relieve congestion and (2) to decrease the workload on the heart by reducing either the total volume of fluid in the system (the preload) or the vascular resistance (the afterload). Drugs that increase contractility are known as positive inotropes; the common oral drug in this category is digoxin. Diuretics decrease preload, thereby decreasing LVEDV. Patients are often on a sliding scale dosage of diuretics depending on the amount of fluid weight gain; they are instructed to weigh themselves daily and adjust diuretics accordingly. Afterload reducers, particularly those that block the effects of the renin–angiotensin system (e.g., ACE inhibitors or ARBs), are often a critical component of drug management in this population. By blocking salt and water retention through aldosterone suppression, preload is decreased; by blocking vasoconstriction through angiotensin II suppression, afterload is reduced. The increase in sympathetic activity that accompanies heart failure causes an increase in MVO₂ (from beta-receptor stimulation), peripheral vasoconstriction, and resultant reduction in peripheral blood flow (from alpha-receptor stimulation). Drugs that combine both beta-receptor blockade and alpha-receptor blockade minimize these affects. Beta-blockade will result in a decrease in MVO₂ and alpha-blockade will result in decreased afterload due to suppression of peripheral vasoconstriction.

Mechanical and Surgical Support

For the symptomatic patient in NYHA Class III/IV, there are dramatic surgical options that may improve function, such as heart transplant, left ventricular assist devices (LVADs), myoplasty, and biventricular pacing. It is beyond the scope of this chapter to discuss in detail the complexity of each of these procedures. Heart transplantation involves replacing the patient's heart with a donor heart. The donor heart will be denervated; therefore, it will not have any direct sympathetic or parasympathetic connection and will be dependent on the intrinsic pacemaker of the SA node and hormonal stimulation to increase HR. The patient with a heart transplant requires careful pharmacological management. Immune-suppressing drugs are used to prevent the body from rejecting the organ, as well as for careful control of infection.

The LVAD is a temporary pump inserted into the patient to perform the work of the LV or to augment the function of the failing heart. The patient is connected to an external energy source but also has the option of wearing a battery pack that allows freedom of movement for hours, in which the patient can go shopping, go to the movies, and so forth. It is important for the therapist to consider the effects of a 6-lb mass (created by the external energy source) resting below the diaphragm that is likely to alter ventilator performance. Finally, gentle progression of exercise intensity must be utilized. Therapists must be vigilant to check for flow limitations (10 to 12 L/min) or changes in cardiovascular function that may occur secondary to use of a mechanically driven pump.

Myoplasty is a surgical procedure in which an enlarged LV undergoes a size reduction by removing dilated, scarred myocardium that is ineffective in contributing to contractility.

A new class of pacemaker, the biventricular pacer, includes an intraventricular conduction delay (e.g., left bundle branch block on the ECG) for patients with severe CHF. This pacer coordinates the contraction of the right and left ventricles and in doing so provides a more effective LV contraction and increased CO.⁷³

Valvular Heart Disease

Broadly, three major disorders encompass valvular dysfunction of one or more of the four heart valves.⁷⁴ These are stenosis, prolapse, and regurgitation.

Stenosis involves narrowing of a heart valve limiting the flow of blood through the valve. As the pathological condition progresses, the chamber behind the valve pathologically hypertrophies to pump against the obstruction.
Prolapse involves enlarged valve cusps that become floppy and bulge backward. When the cusps and support mechanisms of the valve are destroyed, the valve droops down. As the disease progresses, prolapse may progress to regurgitation.⁷⁵
Regurgitation refers to the forward and backward movement of blood resulting from incomplete valve closure. During certain phases of the cardiac cycle valves must close appropriately to prevent blood from flowing in a retrograde fashion. In a regurgitant valve, the valve does not close properly leading to regurgitation of blood into the chamber behind the pathological valve.

Valve replacements are often used for treating valvular disease. Patients with stenosis or regurgitation of the aortic or mitral valves are prime candidates for valve replacement surgeries. A median sternotomy is the route to access the heart. Two major types of valves are used for valve replacement procedures: (1) mechanical valves and (2) biological valves derived from cadavers, porcine tissue, or bovine tissue.^74,76 Mechanical valves are preferred in patients younger than 65 because of their durability and long life. However, the major disadvantage is that they tend to be thrombogenic. Patients who receive a mechanical valve must be on lifelong anticoagulation therapy. For this reason, patients who have a history of a prior bleed, wish to become pregnant, or have poor medication adherence may not be candidates for a mechanical valve. For these patients, biological valves may be more appropriate. The postoperative care for patients with a valve replacement is similar to that for patients who have had a CABG. In addition, neurological monitoring must be continuous postoperatively owing to the potential for an embolic stroke that may occur during or after the procedure.

Electrical Conduction Abnormalities

Arrhythmias are any alteration in the electric conduction of the heart from the normal beat. They are caused by a disturbance in the electrical activity of the heart, resulting in impaired electrical impulse formation or conduction.⁷⁶ Arrhythmias may present as benign or malignant (i.e., life threatening). Examples of malignant arrhythmias are sustained ventricular tachycardia (V-tach) and ventricular fibrillation (V-fib). An example of a common benign arrhythmia in the elderly population would be atrial fibrillation (A-fib) with a controlled ventricular response. This section will review a few conduction abnormalities and relevant implications for the physical therapist.

Ectopic Beats

A beat that originates from a site other than the sinus node is known as an ectopic beat. The common ectopic beats are atrial (premature atrial contractions [PACs]) and ventricular (premature ventricular contractions [PVCs]). PVCs may occur either by themselves or in groups such as couplets (two PVCs) or triplets (three PVCs), or alternating with sinus beats such as bigeminy (every other beat a PVC) or trigeminy (every third beat a PVC).^77,78

A PAC is an ectopic beat that originates in the atria and may present as an irregular rhythm (Fig. 13.14B). It may be difficult to distinguish a PAC from a premature junctional contraction (PJC), an ectopic beat that originates within the area around the A-V node. Usually, PACs or PJCs will not compromise CO, and physical therapy intervention may be appropriate if accompanied by adequate hemodynamic responses.

Figure 13.14

Examples of ectopy and arrhythmias. (A) Atrial fibrillation. (B) Atrial premature beat, also known as premature atrial contraction (PAC) (note third complex). (C) Supraventricular tachycardia (SVT). (D) Premature ventricular contraction (PVC) (note third complex). (E) Bigeminy (note second, fourth, and sixth complexes are PVCs). (F) Trigeminy (note second, fifth, and eighth complexes are PVCs). (G) Couplets (note fourth and fifth complexes are PVCs). (H) Ventricular tachycardia (V-tach). (I) Ventricular fibrillation (V-fib) (V-tach deteriorates into V-fib). (From Brown, K, and Jacobson, S: Mastering Dysrhythmias: A Problem-Solving Guide. FA Davis, Philadelphia, 1988, p 30, with permission.)

The presence of ectopic beats results in an irregular rhythm. Usually, ectopic beats are transient, and their severity depends on their impact on CO. It is certainly common to have a few PVCs even in a normal heart. Many people may have ectopic beats during times of stress or with stimulants such as nicotine and caffeine. Even though this may be a common response in a normal heart, it is important to educate patients with myocardial impairments who may have ectopic beats or irregular rhythms to avoid these aggravators. An increase in ectopy is undesired. It is unwise for any patient with cardiac disease to engage in exercise following recent cigarette smoking. Although the specific time frame that a patient may be at risk for increased ectopy is not clearly known, a good rule of thumb may be abstinence of smoking for at last 2 hours either before or after exercise. Patient education on wellness strategies and smoking cessation is always useful for any patient identified as a smoker.

Supraventricular Ectopy

Supraventricular ectopy involves the rapid firing of an ectopic focus that originates in any location above the ventricles (atrial or junctional area). Examples of supraventricular ectopy include (1) paroxysmal atrial tachycardia and (2) supraventricular tachycardia. A sudden run of PACs occurring at a fast rate (100 to 200 bpm) is known as paroxysmal atrial tachycardia (PAT). A run of either PACs or PJCs at a rate of 150 to 250 bpm is known as supraventricular tachycardia (SV-tach) (Fig. 13.14C). Patients with SV-tach usually respond to a carotid massage where stimulation of the baroreceptors within the carotid bodies of the carotid artery produce a parasympathetic response. Other treatment interventions to reduce heart rate for patients with SV-tach include coughing and breath-holding techniques achieved through the Valsalva maneuver.

Ventricular Ectopy

PVCs are ectopic beats that originate in the ventricle and may present as irregular rhythms. Two hallmark characteristics identify PVCs on the ECG: (1) A P wave is absent as the impulse originates in the ventricle and (2) a wide and bizarre QRS complex signifying abnormal electrical conduction through the ventricle (Fig. 13.14D). Single PVCs will not compromise CO if less than 7 per minute. Therefore, physical activity may be appropriate if accompanied by an adequate hemodynamic response. If the PVCs increase with activity, the activity should be stopped and the patient examined for possible signs of compromised cardiac output. PVCs may come from the same irritable site and are termed unifocal PVCs. If they originate from different ectopic sites within the ventricle they are known as multifocal PVCs (Fig. 13.15A). Multifocal PVCs suggest a more irritable ventricle and are therefore more serious than unifocal PVCs. It is appropriate for the therapist to have the patient medically evaluated before beginning or continuing an activity. Finally, a rare type of PVC known as an R-on-T PVC occurs when PVC fires very prematurely, on the T wave of the preceding cardiac cycle (Fig. 13.15B). These patients must be monitored closely because they are at an increased risk for developing a life-threatening dysrhythmia such as ventricular tachycardia.⁷⁷

Figure 13.15

(A) Multifocal or multiform PVCs; (B) R-on-T PVC; (C) first-degree AV block; (D) Wenckebach rhythm; (E) second-degree type II; (F) third-degree AV block; (G) bundle branch block. (From Jones, S: ECG Success: Exercises in ECG Interpretation. FA Davis, Philadelphia, 2008.)

In ventricular bigeminy (Fig. 13.14E), every other beat is a PVC; in trigeminy, every third beat is a PVC (Fig. 13.14F).⁷⁷ These rhythms occur transiently or episodically, and many patients have frequent bursts of these rhythms. If ectopy increases with activity, the activity should be immediately stopped. When two PVCs occur together, it is known as a couplet (Fig. 13.14G); when three PVCs occur together, it is known as a triplet. Couplets and triplets are important in that they suggest a high level of ventricular irritability. Altered LV function and ischemia are two of the more common causes for ventricular ectopy; therefore, medical management is directed toward improved LV function and perfusion whenever possible, as well as arrhythmia control. Physical therapy intervention is conservative at best and depends on the hemodynamic stability of the patient.

Ventricular Tachycardia

A run of four or more PVCs in a row is known as V-tach (Fig. 13.14H). V-tach may be either sustained or nonsustained. Sustained V-tach, by definition, occurs at an HR of at least 100 bpm and lasts for at least 30 seconds.⁷⁹ The patient may or may not have a palpable pulse and, if present, the pulse will be weak. Because of the severe decrease in CO and rapid hemodynamic deterioration associated with this rhythm, the presence of sustained V-tach is considered an emergency situation. Medical intervention must be initiated as soon as possible. No physical therapy intervention is appropriate, except assisting the patient in stabilization, initiating cardiopulmonary resuscitation (CPR) when indicated, and activating the advanced cardiac life support (ACLS) system. V-tach may deteriorate quickly into V-fib.

Nonsustained V-tach occurs either in groups of three to five PVCs known as salvos, or a run of six or more PVCs lasting for up to 30 seconds.⁷⁹ Nonsustained V-tach is considered a high-risk indicator for potentially lethal arrhythmias. Because the rhythm is nonsustained, the decrease in CO may not be sufficient to cause symptoms. However, until the etiology of the arrhythmia is identified and the rhythm controlled, physical therapy intervention is generally inappropriate.

Ventricular Fibrillation

V-fib is characterized by quivering of the ventricles resulting from inadequate electrical stimulation. The ECG demonstrates a sustained run of different-looking PVCs coming from different ectopic foci (Fig. 13.14I). When the ventricles do not contract but rather quiver, there is ineffective CO. The patient will arrest and expire if this rhythm is not altered immediately. The treatment of choice is activation of ACLS, including electrical defibrillation and medication. Patients who survive fibrillation through defibrillation become candidates for an indwelling defibrillator placement known as an automatic implantable cardiac defibrillator (AICD).

Automatic Implantable Cardiac Defibrillator

The AICD is implanted in patients who have life-threatening ventricular arrhythmias (V-tach, V-fib). The AICD is programmed to deliver an electrical shock if it detects an HR higher than its programmed HR limit. Therefore, it is important for the physical therapist to know this limit and avoid an exercise intensity that may inadvertently activate the device.⁸⁰ In addition to knowing the HR settings for the patient with an AICD, there are other considerations. ST-segment changes on the ECG may be common and are not specific for ischemia; therefore, other diagnostic studies must be done. In addition, UE aerobic or strengthening exercises should be avoided initially after placement of the pacer to avoid inadvertently dislodging the device or the lead wires.⁸⁰ Checking with the physician when these exercises may be included is prudent. There may be a danger for patients with AICDs or pacemakers from electromagnetic signals such as anti-theft devices, either causing the AICD to discharge or causing pacers to slow down or speed up. It may be no problem for patients to walk through these devices but lingering within a few feet could be dangerous.⁸¹

Atrial Fibrillation

A-fib is characterized by quivering of the atria due to inadequate electrical stimulation. A varied number of non–sinus originating P waves (known as fibrillatory waves) exist for each QRS complex (Fig. 13.14A). The ventricular rhythm is said to be "irregularly irregular" because there is no regularity to the irregularity of the ventricular rhythm. It is important to note that effective contraction of the atria accounts for approximately 15% to 20% of CO—the atrial kick.^9,74 In patients with abnormal electrical conduction causing a quivering of the atria (A-fib), the mechanical contractile ability of the atria is reduced, resulting in a low atrial kick and compromised CO.^9,74

Patients may exhibit A-fib continuously as their baseline rhythm or go in and out of this rhythm at rest or with activity. Physical therapy intervention may be appropriate for patients in A-fib who have a good ventricular rate at rest, with appropriate hemodynamic and HR increase with exercise. In patients with A-fib and rapid ventricular rates (greater than 100 bpm) at rest, exercise intensity must be lowered and hemodynamic responses monitored carefully. This is because a rapid ventricular rate in addition to the loss of atrial kick further compromises the CO and results in altered hemodynamic responses. A good rule of thumb is to avoid physical activity and seek medical consultation if the patient's resting HR is greater than 115 bpm, if the patient appears uncomfortable, or if there is an inadequate hemodynamic response. Because this rhythm is irregular, it is important to monitor the HR for a full minute rather than 15 to 30 seconds to obtain an accurate pulse rate.

Conduction Delays and Blocks

Changes in the length of the PR interval, the width of the QRS complex, and the length of the QT interval are some of the ECG measurements indicative of conduction abnormalities.

Conduction delays through the A-V node are classified as first-, second-, or third-degree heart blocks. First-degree heart block occurs when the conduction time through the A-V node is prolonged; therefore, the ECG will have an increased length of the PR interval (Fig. 13.15C). There are two categories of second-degree heart block: Mobitz type I and Mobitz type II; each is hallmarked by the presence of dropped beats. Mobitz I, also known as Wenckebach, presents with a gradual increase in PR interval length in the preceding beats and then an eventual dropped beat (Fig. 13.15D); Mobitz II has normal PR intervals in all the beats preceding the dropped beat (Fig. 13.15E). In third-degree heart block, a mismatch of atrial and ventricular conduction exists, so there is no consistency between the atrial contraction and the ventricular contraction (i.e., no relationship between P waves and QRS complex on the ECG) (Fig. 13.15F). Patients in first-degree block have no limitations to exercise. Whether or not exercise is permitted with second- and third-degree blocks depends on the etiology and subsequent hemodynamic responses. Medical clearance is warranted before beginning any exercise.

Conduction delays through the bundle of His are known as either right bundle branch block (RBBB) or left bundle branch block (LBBB). Bundle branch blocks are not true arrhythmias because there is no change in the actual rhythm, just in the timing of conduction through the bundle of His. The heart is still depolarized from the same pacemaker; only the route of activation is changed. Bundle branch blocks present on the ECG as a distortion of the QRS complex with an increased duration (i.e., widening) (Fig. 13.15G). The presence of an LBBB on the ECG is usually permanent and indicates a pathological condition. RBBB may occur from a variety of reasons; it may be a permanent change due to underlying disease, or it may be benign. RBBB can also occur transiently. LBBB usually indicates the presence of more significant disease than RBBB.

The presence of a new bundle branch block should be medically evaluated before beginning or progressing an exercise program. Following medical clearance, there is usually no contraindication to exercise in either the RBBB or LBBB population. Because of the alteration of the QRS complex and as a result the ST segment, the sensitivity of the ECG in detecting ischemia via ST depression is lost in the patient with LBBB.

Pacemakers

The use of pacemakers has increased considerably, with the most common indications for placement of a permanent pacemaker being (1) an HR that is too slow (symptomatic bradycardia); (2) an HR that fails to increase appropriately with exercise (chronotropic incompetence); or (3) an electric pathway that it blocked resulting in atrioventricular delays or bundle branch blocks.⁸²

A pacemaker is a device that is placed subdermally near the heart and consists of an implantable pulse generator and lead wires that connect the pacemaker to the myocardium. The pulse generator contains a long-life battery and circuitry for timing, sensing, and output functions. The life of the battery usually dictates the life of the pacemaker and varies depending on the type of battery and the extent to which the pacemaker is being used. In some cases, the patient is dependent on the pacemaker for every cardiac contraction and is likely to utilize the life of the battery in a shorter period of time.⁸³ The average pacemaker battery life is between 5 and 10 years. Replacement of pacemaker batteries is done after serial assessments have confirmed a reduction in battery life. Battery life may be consumed more rapidly when the patient is more reliant on the pacemaker for maintaining an appropriate HR.

Patients are reliant on pacemakers at different levels. Some patients have normal electric conduction at most times and do not need to be reliant on the pacemaker at all times. Other patients have altered electrical conduction through the heart and may be very reliant on the pacemaker to keep them alive. Therefore, it is important for therapists to determine how reliant the patient may be on his or her pacemaker. When pacemakers trigger a pace due to altered electrical conduction through the heart, the ECG reveals a pacer spike. Thus, if the patient has a pacemaker and no pacer spikes are evident on the ECG, the therapist can infer that the heart is conducting normally, and the pacemaker is there for emergency needs only. Conversely, if the ECG demonstrates a pacer spike in every cardiac cycle, the therapist must understand that this patient is 100% reliant on the pacemaker and thus ensure that the pacemaker is adequately rate responsive during activity.

The basic functions of the pacemaker lead wires are to provide the pacemaker with information on intrinsic myocardial activity and pace the myocardium when intrinsic activity fails. There are four primary functions of pacemakers: (1) the ability to sense intrinsic cardiac function, (2) the ability to stimulate cardiac depolarization in response to failed intrinsic activity, (3) the ability to respond to increased metabolic demand by providing rate-responsive pacing, and (4) the ability provide diagnostic information stored within the pacemaker.⁸⁴

Pacemakers have rate and rhythm sensitivity as well as the ability to override certain arrhythmias. Pacemakers may also be combined with AICD capabilities. Pacemakers are coded by either a three- or five-category system according to which chamber (atria or ventricle) is sensed, what chamber is paced (atria or ventricle), and whether the electrical stimulus will trigger a response or be inhibited⁸⁵ (Table 13.8). Because pacemakers may fail to work properly, ECG monitoring is helpful to determine if the pacer is working properly.

Table 13.8Pacemaker Classification System

Table 13.8 Pacemaker Classification System

Chamber Paced

Chamber Sensed

Response

Rate Responsive Pacing

O = none

R = rate responsive

A = atria

I = inhibit

V = ventricle

T = trigger

D = dual chamber

D = capacity to both inhibit and trigger

Pacemakers are commonly identified by a three-letter code as displayed in the first three columns. Pacemakers may also have the capacity to respond to physiological stimuli to increase rate (column 4) and to override atrial tachycardia. A fifth column, for antitachycardiac function, is rarely used due to the increased sophistication of the newer implantable defibrillators/pacemakers, which renders this function unnecessary. Example: VVI pacer will provide an electrical impulse to the ventricle if it senses that there is no ventricular activity within an appropriate time frame. If there is intrinsic ventricular electrical activity, the pacemaker will be inhibited.

As stated previously, patients with Class III CHF and LBBB may be candidates for a specialized pacemaker known as a biventricular pacemaker, the purpose of which is to synchronize LV contractility to provide a more effective CO. The biventricular pacer does not influence HR or heart rhythm.⁸⁶

Heart Transplant

Patients who have undergone a heart transplant may present with the following: (1) calf cramps (occurring in approximately 15% of patients) owing to the immunosuppressive drug cyclosporine; (2) decreased LE strength; (3) obesity owing to long-term corticosteroid use; (4) increased risk of fracture owing to osteoporosis associated with long-term, high-dose corticosteroids; and (5) an increased probability of developing atherosclerosis in the coronary arteries of the donor heart after the first postsurgical year.⁸⁷ Because the heart is denervated, HR alone provides a limited measure of exercise intensity. Therefore, BP and perceived exertion should be included in the routine data collection.

CARDIOVASCULAR EXAMINATION

Owing to the increasing incidence and prevalence of heart disease on our society, many patients referred to physical therapy will have cardiovascular dysfunction or may be at risk for developing CVD. The history taking, review of systems, and data from specific tests and measures will guide and inform development of the physical therapy diagnosis, anticipated goals and expected outcomes, prognosis, and POC. This section addresses tests and measures specific to the cardiovascular system.

Medical Record Review

The medical record of a patient with a history of cardiovascular impairments may at times be overwhelming. The patient interview is typically helpful if clarification of the medical record is needed. Depending on the type of setting (inpatient, outpatient, acute rehabilitation, home care), the specific contents of the medical record may vary. Important items to note within the medical record include the following:

Medical problems, past medical history, physician's examination
Medications, including type, dosage, and schedule
Laboratory tests
- Blood tests for specific cardiac enzymes that may indicate an MI has occurred, such as a positive CK-MB or troponin level
- Electrolytes, including potassium, and magnesium and calcium if ventricular arrhythmias are present
- Complete blood count (CBC), which may indicate the presence of anemia via the hemoglobin and hematocrit values
- Status of the kidney (BUN and creatinine) and liver function (liver function tests)
- Presence of CAD risk factors, such as elevated lipid values (e.g., total cholesterol, low-density lipoproteins [LDLs], triglyceride), and elevated blood sugars (glucose)
- Arterial blood gases (ABGs)
Results of any diagnostic studies or interventions: chest x-ray, ECGs, ETT, cardiac catheterization, surgical reports, hemodynamic monitors (e.g., pressure readings from central line and/or arterial line)
Nursing and other health care provider notes

The medical record contains information regarding what has happened to the patient, as well as the status of the patient within the last 24 hours or since the last health care provider intervention. Flow charts, which record vital signs, temperature, oxygenation requirements, and volume status over time, provide up-to-date patient data, especially when working with the more medically challenged patient.

Patient Interview

The formal patient interview should follow the medical record review. A determination of overall cognition (e.g., orientation, memory, learning needs, comprehension) should be made. Information regarding the patient's lifestyle, previous level of functioning, recreational interests, work requirements, and goals is important in establishing the intervention. Data should also be obtained about the patient's response to health and illness, coping status, support systems, and knowledge of heart disease. It is important to note that not all the information from the interview needs to be obtained on the first session. During subsequent sessions, the patient may begin to feel better and less anxious and may therefore be able to communicate more easily. Patient education can often be woven into the interview process, either subtly or overtly. The patient should describe, in his or her own words, the quality and location of the symptom for which medical attention is being sought. It is common for physical therapists to ask a patient about pain; for patients with cardiac disease, one should be cautious about assuming that the patient's symptom is pain. Many patients will not use pain as their qualifier, but instead describe their symptoms as pressure, heaviness, SOB (dyspnea), aching, heartburn, or general malaise, to identify a few. Knowing the symptom presentation for each individual will make patient education and activity progression easier. It is also important to identify any consistent precipitating factors and alleviators, as well as duration and frequency of symptoms.

The interview also helps to establish rapport and trust between therapist and patient, creating an environment for mutual goal setting. This in turn facilitates patient adherence to the rehabilitation program. Patients who are recovering from an MI or from surgery need to have an understanding of time frames for healing and convalescence. Education for family members and significant others is also crucial for patient adherence and understanding.

Physical Examination

The physical therapist carefully monitors vital signs (see Chapter 2, Examination of Vital Signs) at rest and with activity, auscultates the heart and lungs, and performs a general observation of the patient's appearance. An overview of the pertinent components is presented.

Heart Rate and Rhythm

In taking an initial HR, either by palpation or auscultation, it is important to count for a full minute. When examining the patient's response to an activity and no arrhythmia is present, an immediate postexercise HR can be taken for 10 to 15 seconds. Always note if the rhythm is regular or irregular and report it as such. Unless there is ECG monitoring, it is impossible to identify a specific rhythm by palpation or auscultation alone. Note that there is a normal respiratory variation in HR; inspiration results in an increase in HR, exhalation in a slowing down of HR.

HR can also be determined from an ECG strip. The ECG graph paper consists of a series of small boxes (represented by light black lines) and large boxes (represented by heavy black lines). Each large box is made up of five small boxes. The horizontal axis represents time; when the ECG paper is moving at the usual speed of 25 mm/sec, five large boxes constitutes one second. Knowing that time is on the x-axis, there are many ways to calculate HR from the ECG graph paper. An easy way to calculate a minute rate is to count the number of complexes in 6 seconds (i.e., 30 large boxes) and multiply by 10. Often the ECG paper will have 3-second intervals premarked. An alternative approach is to identify an R wave from one ECG complex that is close to or on a heavy black line (i.e., a large box), and then assign each of the following heavy black lines (large boxes) a number in the following order: 300, 150, 100, 75, 60, 50, 40. The heavy line closest to the next R wave will provide an approximation of HR (Fig. 13.16). Finally, dividing 300 by the number of large boxes between two R waves will also indicate the HR. If the rate is regular, any of the preceding strategies will work. If the rate is irregular, however, the complexes will need to be counted over a long time frame, and a minimum of a 6-second strip should be used.

Figure 13.16

Calculation of a heart rate from a rhythm strip. Begin with the fifth complex (which falls on a large black line) and count each large black line to the right of this complex in the order of 300, 150, 100, 75, 60, 50. The sixth complex falls between two large lines (i.e., 50 and 60). There are five small lines between each large line. Between 50 and 60 there are 10 beats, therefore each small line in this case would be two beats. The heart rate would be 60 – 4 = 56. An alternate method would be to count the number of complexes in a 6-second strip and multiply by 10.

Respiratory Rate, Rhythm, and Dyspnea

As with the heart, both rate and rhythm of respirations should be noted, as well as the breathing pattern and use of accessory muscles. Patients with cardiac impairments frequently complain of dyspnea. Patients with LV dysfunction from CAD, CHF, cardiomyopathies, valvular dysfunction, hypertensive heart disease, pericarditis with tamponade, and arrhythmias may all present with dyspnea. Sometimes, dyspnea begins with activity and is termed dyspnea on exertion (DOE) and progresses to occurring at rest. It is important to document and understand the amount and types of activity that provoke DOE. Dyspnea associated with a cardiovascular etiology is usually accompanied by signs and symptoms of compromised CO, including lightheadedness, dizziness, fatigue/weakness, and hypotension; symptoms may worsen in the supine position (orthopnea).⁸⁸ Some patients may experience dyspnea as their anginal equivalent; that is, they do not have the typical chest discomfort often associated with ischemia but instead experience SOB. For these patients, treatment should be immediate and follow the guidelines for ischemia. A commonly used tool to objectively identify subjective feelings of dyspnea is the Dyspnea Scale (Box 13.3).

Box 13.3 Dyspnea Scale

0 = No dyspnea

1 = Mild, noticeable

2 = Mild, some difficulty

3 = Moderate difficulty, but can continue

4 = Severe difficulty, cannot continue

Angina

The classical presentation of angina is substernal chest pressure accompanied by the Levine sign (the patient clenching his or her fist over the sternum). The Levine sign has a high diagnostic accuracy for ischemia.⁸⁹ For some patients, angina does not present in the classic way but rather may present as a pain or heaviness in the shoulder, jaw, arm, elbow, or upper back between scapulae. Angina may radiate from the chest to the arm or up to the throat, or it may present as indigestion or even SOB. The patient is often asked to rank his or her discomfort on the Angina Scale (Box 13.4).

Box 13.4 Angina Scale

0 = No angina

1 = Light, barely noticeable

2 = Moderate, bothersome

3 = Severe, very uncomfortable: preinfarction pain

4 = Most pain ever experienced: infarction pain

Blood Pressure

Arterial BP is a product of CO and total peripheral resistance (TPR) where BP = CO × TPR. An increase in either of these factors will increase BP, and a decrease in either may decrease BP. Clinically, therefore, aerobic exercise of increasing intensity increases CO and concomitantly increases BP. Conversely, a drop in BP during aerobic exercise indicates a drop in CO, or signifies the inability of the heart to meet the metabolic needs of the peripheral tissue.⁹⁰ This drop in BP is usually accompanied by signs of compromised CO, including fatigue, weakness, tiredness, dizziness, and so forth, that occur during the activity. Therefore, BP values of a patient with heart disease who demonstrates signs of compromised CO during ambulation should be closely monitored to determine if CO is being maintained. Lower exercise BP values when compared to resting values denote that CO is not being met during exercise.

Accurate measurement of BP is a vital process within the examination process. Using inappropriate cuff sizes when measuring BP is the most frequent error in BP measurement.⁹¹ Proper cuffs must have a bladder length of 80% and a width of 40% of arm circumference. In addition, maintaining the arm at the level of the heart promotes accurate measurement of BP to negate the effects of hydrostatic pressure. For every 2.5 cm above or below the level of the heart, BP readings can change by 1 to 2 mm Hg. An arm maintained above the level of the heart lowers BP readings and if placed at a level below the heart falsely increases BP measurements.⁹¹ For more information on measurement of BP, see Chapter 2, Examination of Vital Signs.

Observation and Inspection

The patient's skin color should be inspected. Cyanosis, a bluish color of the skin, nail beds, and possibly lips and tongue, may be present when arterial oxygen saturation is 85% or less.⁷⁴ Pallor, the absence of a pink, rosy color, may indicate a decrease in CO. Diaphoresis (excess sweating, cool clammy skin) should also be noted because it may indicate excessive effort or inadequate cardiovascular response. Cold fingertips may be due to compensatory vasoconstriction in response to a decreased CO or from the suppressed beta-sympathetic response of some beta-blockers.

The extremities are inspected for the presence of edema; patients with LV failure may have an increase in peripheral edema owing to the increase in hydrostatic intravascular pressure associated with increased pressure from the LV transmitted retrograde through the heart to the venous system. Bilateral peripheral edema may be a result of CHF. Edema of one leg, however, is usually associated with local factors within the same leg such as varicose veins, lymphedema, or thrombophlebitis.⁹⁰ The patient with chronic CHF who has a weight gain owing to sodium and water retention may notice edema of the ankles and lower legs during the day (due to an increase in hydrostatic pressure) that diminishes during the night.

Heart Auscultation

Invaluable information as to the status of the heart is obtained from auscultation (listening) of the heart and lungs. Normal heart sounds are identified as S₁ (lub), which occurs at the time of the closure of the mitral (and tricuspid) valve and marks the beginning of systole and S₂ (dub), which occurs at the time of aortic (and pulmonic) valve closure and marks the end of systole. Figure 13.17 depicts locations on the chest for appropriate auscultation of each valve. The aortic valve is best auscultated at the second intercostal space, right sternal border. The pulmonic valve is heard at the second intercostal space, left sternal border. The tricuspid valve is auscultated at the fourth intercostal space, left sternal border, and the mitral valve is best heard at the fifth intercostal space, along the midclavicular line.

Figure 13.17

Anterior view of the chest wall of a man showing skeletal structures, heart, location of the heart-valves, and auscultation points.

Murmurs are abnormal heart sounds commonly the result of valvular disorders due to the changes in blood flow around and through the altered valve. A systolic murmur will present as audible turbulence between S₁ and S₂, and a diastolic murmur as turbulence between S₂ and S₁. A stenotic valve has impaired opening, and a regurgitant valve has impaired closing. A valve may be both stenotic and regurgitant.

Other abnormal sounds are S₃ and S₄. S₃, also known as a ventricular gallop, occurs after S₂ and is clinically associated with LV failure. S₄, also known as an atrial gallop, occurs before S₁ and is clinically associated with an MI or chronic HTN.

Another type of auscultatory finding is the pericardial friction rub. These friction sounds are high pitched with a leathery and scratchy quality, although they may vary in intensity from hour-to-hour or day-to-day, or may even transiently disappear.⁹² The pericardial rub has been described as similar to the squeaking sound of rubbed leather.⁹³ This rub results from an inflammation of the pericardial sac, either with or without excessive fluid. Pericardial disease may result from many causes such as trauma, infections, tumors, collagen diseases, anticoagulants, and MI. Post-MI pericarditis is known as Dressler's syndrome.⁹⁴ An example of documentation for heart sounds would be Cor: RRR ⊘ m, g, r, which would be interpreted as Heart: regular rate and rhythm without murmurs, gallops, or rubs.

Auscultation of the heart borders is also done to examine size. The location of the apex and point of maximal impulse (PMI) is noted. The PMI is usually present at the fifth intercostal space along the midclavicular line. If the LV has increased in size, as frequently occurs with patients in LV failure, the PMI will be displaced laterally toward the axilla.

Lung Auscultation

Auscultating the lungs is an important component of the cardiac physical examination. Normal lung tissue produces vesicular (soft, low-pitched) sounds in the peripheral aspect of the lungs and bronchial breath (loud, high-pitched) sounds centrally along the manubrium of the sternum.⁷ Vesicular sounds are longer and louder with inspiration, whereas bronchial breath sounds are longer and louder with expiration. Figure 13.18 demonstrates appropriate sites for the auscultation of lung fields.

Figure 13.18

Auscultation of lungs.

Patients with LV failure often have the adventitious sounds of crackles. Crackles may also appear as a result of atelectasis; in that case, deep breathing with an inspiratory hold and coughing may correct this impairment. A patient with decreased breath sounds or consolidations may have a decrease in the oxygen content of his or her blood; a decrease in oxygenation may result in an increase in myocardial work and aggravate a preexisting cardiac impairment.

Jugular Venous Distention

Patients with CHF with backup of fluid into the venous vasculature should be examined for the presence of jugular venous distention. To examine for this sign, the patient is placed at a 45-degree semirecumbent position.⁷⁴ The patient's head is turned away from the side to be evaluated and the clinician observes for a distention or pulsations of the jugular vein 3 to 5 cm above the sternum.⁴⁴ The highest point of visible pulsation is determined and the vertical distance between this level and the level of the sternal angle of Louis is recorded (Fig. 13.19).

Figure 13.19

Examination of jugular venous distention.

Pitting Edema

In patients with congestive heart failure, low SV causes a reduced blood volume perfused to the periphery. This stimulates the pressoreceptors as they sense a decrease in volume. These pressoreceptors subsequently relay a message to the kidney to retain fluid. This retention of fluid increases the hydrostatic pressure within the peripheral vasculature, thereby pushing fluid into the interstitial space resulting in peripheral edema and weight gain. Edema can be assessed through girth measurements or by using the pitting edema scale. See Chapter 14, Vascular, Lymphatic, and Integumentary Disorders, for the pitting edema grading scale. The severity of peripheral edema is categorized into four stages based on the time taken for the skin to rebound to its original contour after pitting. It is also important to note that edema can accumulate in the abdominal area (ascites) or sacral areas of the body.

Exercise Tolerance Tests

To examine the ability of the cardiovascular system to accommodate to increasing metabolic demand, an ETT, stress test, or graded exercise test is performed. The patient exercises through stages of increasing workloads, expressed in units of oxygen. Oxygen cost may be expressed in L/min, mL O₂/kg/min, kcal, or metabolic equivalents (METs); the MET represents the basic systemic oxygen requirement at rest, roughly 3.5 mL O₂/kg/min. The clinical usefulness of METs is that an activity can be expressed in comparison to resting energy cost. For example, the first stage of the Bruce protocol requires roughly 5 METs of energy (i.e., it requires five times the energy expended at rest). The most common modalities used in exercise testing of patients with cardiac impairments are the treadmill, bicycle, and arm ergometer (Fig. 13.20). In the earlier years of exercise testing for examination of CAD, the step test was routinely used; however, it has for the most part been replaced by the other modalities. The step test is useful for fitness screening in the relatively healthy population and in exercise training for both the cardiac and noncardiac populations.

Figure 13.20

Estimated oxygen requirements for step, bicycle, and treadmill. The standard Bruce protocol begins at 1.7 mph and 10 percent grade (roughly 5 METs). Oxygen requirements increase with progressive increases in workload for all modalities. (Adapted from Fletcher et al,¹¹² p. 156.)

Knowledge of systemic energy requirements is important in prescribing exercise and activity guidelines, as well as in exercise testing for patients with cardiac impairments. Many charts are available that express systemic energy requirements using a variety of oxygen equivalents (Table 13.9).

Table 13.9Metabolic Equivalent (MET) Chart

Table 13.9 Metabolic Equivalent (MET) Chart

Intensity (70-kg Person)

Endurance Promoting

Occupational

Recreational

1½–2 METs

4–7 mL/kg/min

2–2½ kcal/min

Too low in energy level

Desk work, driving auto, electric calculating machine operation, light housework, polishing furniture, washing clothes

Standing, strolling (1 mph), flying, motorcycling, playing cards, sewing, knitting

2–3 METs

7–11 mL/kg/min

2½–4 kcal/min

Too low in energy level unless capacity is very low

Auto repair, radio and television repair, janitorial work, bartending, riding lawn mower, light wood-working

Level walking (2 mph), level bicycling (5 mph), billiards, bowling, skeet shooting, shuffleboard, powerboat driving, golfing with power cart, canoeing, horseback riding at a walk

3–4 METs

11–14 mL/kg/min

4–5 kcal/min

Yes, if continuous and if target heart rate is reached

Brick laying, plastering, wheelbarrow (100-lb load), machine assembly, welding (moderate load), cleaning windows, mopping floors, vacuuming, pushing light power mower

Walking (3 mph), bicycling (6 mph), horseshoe pitching, volleyball (6-person, noncompetitive), golfing (pulling bag cart), archery, sailing (handling small boat), fly fishing (standing in waders), horseback riding (trotting), badminton (social doubles)

4–5 METs

14–18 mL/kg/min

Recreational activities promote endurance; occupational activities must be continuous, lasting longer than 2 min

Painting, masonry, paper-hanging, light carpentry, scrubbing floors, raking leaves, hoeing

Walking (3½ mph), bicycling (8 mph), table tennis, golfing (carrying clubs), dancing (foxtrot), badminton (singles), tennis (doubles), many calisthenics, ballet

5–6 METs

18–21 mL/kg/min

Yes

Digging garden, shoveling light earth

Walking (4 mph), bicycling (10 mph), canoeing (4 mph), horseback riding (posting to trotting), stream fishing (walking in light current in waders), ice or roller skating (9 mph)

6–7 METs

21–25 mL/kg/min

7–8 kcal/min

Yes

Shoveling 10 times/min (4½ kg or 10 lb), splitting wood, snow shoveling, hand lawn mowing

Walking (5 mph), bicycling (11 mph), competitive badminton, tennis (singles), folk and square dancing, light downhill skiing, ski touring (21/2 mph), water skiing, swimming (20 yards/min)

7–8 METs

25–28 mL/kg/min

8–10 kcal/min

Yes

Digging ditches, carrying 36 kg or 80 lb, sawing hardwood

Jogging (5 mph), bicycling (12 mph), horseback riding (gallop), vigorous downhill skiing, basket-ball, mountain climbing, ice hockey, canoeing (5 mph), touch football, paddleball

8–9 METs

28–32 mL/kg/min

10–11 kcal/min

Yes

Shoveling 10 times/min (5½ kg or 14 lb)

Running (5½ mph), bicycling (13 mph), ski touring (4 mph), squash (social), handball (social), fencing, basketball (vigorous), swimming (30 yards/min), rope skipping

10+ METs

32+ mL/kg/min

11+ kcal/min

Yes

Shoveling 10 times/min (7½ kg or 16 lb)

Running (6 mph = 10 METs, 7 mph = 11½ METs, 8 mph = 13½ METs, 9 mph = 15 METs, 10 mph = 17 METs), ski touring (5+ mph), handball (competitive), squash (competitive), swimming (greater than 40 yards/min)

From Fox, SM, et al: Physical activity and cardiovascular health: 3. The exercise prescription: Frequency and type of activity. Mod Con Cardiovasc Dis 41:26, 1972, with permission.

The two major goals of exercise testing are to detect the presence of ischemia and to determine the functional aerobic capacity of the individual. The patient is monitored with a 12-lead ECG throughout the test and recovery; information regarding perfusion, rhythm, or conduction changes is therefore immediately available. In addition to the ECG, other diagnostic tools may be used, most commonly the echocardiogram and nuclear imaging. The stress echo examines wall motion abnormalities that may or may not be present at rest, but may become more pronounced with increasing workloads. Nuclear imaging (e.g., thallium sestamibi) compares coronary perfusion between rest and exercise. If there is no decrease in perfusion with increasing workloads, the test is negative; if there is a decrease, the test is considered positive.

Stress tests are interpreted as either positive (+) or negative (–). A positive ETT indicates that there is a point at which the myocardial oxygen supply is inadequate to meet the myocardial oxygen demand, and the test is therefore positive for ischemia. A negative ETT indicates that at every tested physiological workload there is a balanced oxygen supply and demand. Patients are often confused regarding this grading system. It is helpful to reassure them that in this case, a negative test is in fact good. Stress tests are not unlike other diagnostic tools; however, they are not 100% specific and sensitive in identifying the presence of ischemia. A false-negative ETT is one that is interpreted as negative but the patient in fact has ischemia. Conversely, a false-positive ETT is one that is interpreted as positive but the patient does not have ischemia.

When a patient is unable to perform an exercise test because of limitations such as musculoskeletal or neurological impairments, a pharmacological stress test such as a persantine thallium test is often recommended. Persantine, when given intravenously, decreases coronary vascular resistance by causing arterioles to vasodilate, and therefore increases the blood flow through the capillary beds. If an artery is atherosclerotic, its arteriole may have gradually dilated over time in an attempt to increase capillary blood flow by means of pressure autoregulation. Therefore, when persantine is given, the diseased arteries may have a limitation in the amount of further arteriolar dilation that can occur. In comparison to the nondiseased arteries, there will be a relative decrease in blood flow through the capillary beds of the diseased arteries. Imaging studies will thus detect a relative decrease in blood flow to the area of the myocardium that is perfused by the diseased artery compared to that perfused by a nondiseased artery. Adenosine, which is a coronary and peripheral vasodilator (as well as an antiarrhythmic), has similar effects as persantine and may be used instead.⁹⁵

Assessment of Aerobic Capacity and Endurance

The best indicator of an individual's aerobic capacity is through examination of the peak oxygen uptake or VO₂ maximum and anaerobic threshold. However, to obtain these numbers, sophisticated and expensive equipment such as a metabolic cart is required. Most physical therapists do not have access to this equipment to determine these numbers. Therefore, the physical therapist can continually monitor the patient's responses during exercise to better understand the individual's tolerance and level of endurance. HR, BP, pulse oximetry, and respiratory rate and rhythm at every given level of intensity will provide clinicians with a good picture of the patient's aerobic capacity and endurance.

Another useful test to determine an individual's functional status, exercise tolerance and oxygen consumption is the 6-Minute Walk Test (6-MWT). Patients are asked to walk as far as they can in 6 minutes, taking as many rests as needed during this time.^96,97,98 The 6-MWT, although considered submaximal, closely approximates the maximal exercise of persons with CHF and can be correlated to peak oxygen consumption.^98,99 In addition to prediction of the peak oxygen uptake, a distance of 300 m is an important indicator of short-term and long-term survival in patients with CHF. Coats¹⁰⁰ found that patients unable to ambulate greater than 300 m during the 6-MWT had poorer short-term survival, and Bittner et al¹⁰¹ reported that patients who were unable to ambulate distances over 300 m had poorer long-term survival.

PHYSICAL THERAPY INTERVENTION FOR PATIENTS WITH HEART DISEASE

Intervention for Patients with Coronary Artery Disease

According to the APTA Guide to Physical Therapist Practice, the preferred practice pattern for management of patients with CVD is Pattern 6-D. The development of specific anticipated goals and expected outcomes for the individual with CAD is based on the general goals of physical therapy intervention presented in Box 13.5.

Box 13.5 Coronary Artery Disease—Anticipated Goals and Expected Outcomes

Aerobic capacity is increased.
Ability to perform physical tasks related to self-care, home management, community and work integration or reintegration, and leisure activities is increased.
Physiological response to increased oxygen demand is improved.
Strength, power, and endurance are increased.
Symptoms associated with increased oxygen demand are decreased.
Ability to recognize a recurrence is increased, and intervention is sought in a timely manner.
Risk of recurrence is reduced.
Behaviors that foster healthy habits, wellness, and prevention are acquired.
Decision making is enhanced regarding health of patient and the use of health care resources by patient/client, family, significant others, and caregivers.

Physical therapists treat not only patients who have a primary diagnosis of heart disease, but also, and perhaps more commonly, patients with multiple medical diagnoses, only one of which is cardiac. Physical therapy intervention during the traditional acute cardiac rehabilitation phase involves following the patient while recovering from his or her cardiac event, such as an MI, providing hemodynamic monitoring of progressive activity, discharge guidelines, education, and information regarding outpatient referral. It may include outpatient management as well, ideally in a multidisciplinary setting including nursing and nutrition. Patients with cardiac histories commonly have physical therapy needs at other points throughout their lives. For example, the patient with a previous MI might require ambulation training as a result of a fractured hip, an outpatient knee rehabilitation program following a skiing injury, tennis elbow intervention, prosthetic ambulation training, or intervention following a CVA. If the physical therapist understands the pathophysiology of the cardiac condition and the energy demands being placed on the patient, the therapist will be able to adjust the POC accordingly.

It is important to remember that a patient with known CAD may not have symptomatic ischemia, either because the lesions are not of significant size to interfere with blood flow, or the anti-ischemic medications are able to keep the patient's physiological response to activity below his or her ischemic threshold. Following a noncomplicated MI, ischemia should not occur in the area perfused by the involved artery because infarcted tissue cannot become ischemic. However, if there is disease in other arteries, ischemia can occur in any noninfarcted tissue that has a compromised blood supply. A physical therapist working with patients with significant CAD must be aware that their basic cardiac impairment is an imbalance of myocardial oxygen supply and demand, and any increase in systemic oxygen consumption will increase myocardial oxygen consumption. A past medical history of CAD does not mean that the disease occurred in the past and is no longer present; once a person has been diagnosed with CAD, he or she has the potential for atherosclerosis progression at any later point in time. Although the precipitating factors for plaque rupture are not clearly understood, the plaque with increased levels of oxidized LDLs is thought to be unstable with a greater potential for rupture.¹⁰² It is important to note that plaque rupture may occur with lesions of any size, not just those that are greater than 70%.¹⁰² Therefore, it is prudent for the physical therapist to know the status of all the coronary arteries, not just those that were revascularized or have a greater than 70% lesion.

The degree of a patient's risk for increased morbidity and mortality is based on a number of factors. The American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR) and the American College of Physicians provide a framework for stratifying patients with cardiac impairments (Table 13.10).

Table 13.10Risk Stratification Criteria for Cardiac Patients by the American College of Physicians (ACP) and American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR)

Table 13.10 Risk Stratification Criteria for Cardiac Patients by the American College of Physicians (ACP) and American Association of Cardiovascular and Pulmonary Rehabilitation (AACVPR)

ACP

AACVPR

Low Risk

Uncomplicated MI or CABG

Uncomplicated MI, CABG, angioplasty, or atherectomy

Functional capacity ≥8 METs 3 weeks after clinical event

Functional capacity ≥6 METs 3 or more weeks after clinical event

No ischemia, left ventricular dysfunction, or complex arrhythmias

No resting or exercise-induced myocardial ischemia manifested as angina and/or ST-segment displacement No resting or exercise-induced complex arrhythmias

Asymptomatic at rest with exercise capacity adequate for most vocational and recreational activities

No significant left ventricular dysfunction (EF ≥50%)

Intermediate (Moderate) Risk

Functional capacity <8 METs 3 weeks after clinical event

Functional capacity <5–6 METs 3 or more weeks after clinical event

Shock or CHF during recent MI (<6 months) (EF 31%–49%) Inability to self-monitor heart rate

Mild to moderately depressed left ventricular function

Failure to comply with exercise prescription

Exercise-induced ST-segment depression <2 mm

Exercise-induced ST-segment depression of 1-2 mm or reversible ischemic defects (echocardiography or nuclear radiography)

High Risk

Severely depressed LV function (EF <30%)

Severely depressed LV function (EF ≤30%)

Resting complex ventricular arrhythmias (low grade IV or V)

Complex ventricular arrythmias at rest or appearing or increasing with exercise

PVCs appearing or increasing with exercise

Exertional hypotension (≥15 mm Hg decrease in systolic pressure during exercise)

Decrease in systolic blood pressure of >15 mm Hg during exercise or failure to rise consistent with exercise workloads

Recent MI (<6 months) complicated by serious ventricular arrhythmias

MI complicated by CHF, cardiogenic shock, and/or complex-ventricular arrhythmias

Exercise-induced ST-segment depression >2 mm

Patients with severe CAD and marked (>2 mm) exercise-induced ST-segment depression

Survivor of cardiac arrest

From American College Sports Medicine: Guidelines for Exercise Testing, ed 5. Williams & Wilkins, Baltimore, 1995, pp 20, 21, with permission.

CABG = coronary artery bypass graft; CHF = congestive heart failure; EF = ejection fraction; LV = left ventricular; MET = metabolic equivalent; PVC = premature ventricular contraction.

Exercise Prescription

The Clinical Practice Guidelines for Cardiac Rehabilitation were established after extensive and critical review of published scientific literature.¹⁰³ These guidelines support the beneficial effect of exercise training on exercise tolerance for patients with heart disease. The most consistent benefit appeared to occur with exercise training at least three times per week for 12 or more weeks' duration. The duration of aerobic exercise training sessions varied from 20 to 40 minutes at an intensity approximating 70% to 85% of the baseline maximal exercise test HR. Exercise prescriptions are based on frequency, intensity, time (duration), and type (mode), the FITT equation. Activity should be gradually progressive in a logical stepwise fashion of increasing energy costs (i.e., METs, kilocalories) with appropriate HR and BP monitoring.

Although exercise is highly recommended for the patient with heart disease, there are conditions in which exercise is unwise. The AACVPR established guidelines for evaluating a patient's appropriateness for exercise participation. Contraindications for exercise training include unstable angina, symptomatic and uncompensated heart failure, uncontrolled arrhythmias, moderate to severe aortic stenosis, uncontrolled diabetes, resting blood pressure values in excess of 200/110, and uncontrolled resting tachycardia.¹⁰⁴

The patient should be evaluated once these conditions have been corrected and, when appropriate, begin (or resume) the exercise program. Recognizing that cardiac disease is a dynamic process, and that the patient who was stable and able to participate in physical therapy last week may not be stable this week, is a critical concept. The importance of a patient-specific examination and evaluation before each session will allow the physical therapist to critically plan the appropriate intervention.

Exercise Intensity

Intensity may be prescribed by either HR or by subjective report, a rating of perceived exertion (RPE). Subjective ratings of intensity of exertion have been used to quantify effort during exercise. The original Rating of Perceived Exertion Scale (The Borg RPE Scale), developed by Borg, has been used extensively (Table 13.11). It consists of numbers ranging from 6 to 20, which patients use to rate their perceptions of how hard they are working. Descriptive words accompany the numbers, such as hard or very hard. Commonly, patients are asked to limit their exertion to between fairly light and somewhat hard. Borg also developed a category-ratio scale of 0 to 10. Both local symptoms, such as muscle aches, cramps, pain, or fatigue, and central symptoms, such as feelings of fatigue or breathlessness, contribute to the overall feelings of work performance. High correlation of RPE ratings with HR and aerobic power has been found in normal individuals and in patients with cardiac disease.

A common aerobic exercise prescription based on HR is 70% to 85% of HR_max. However, the more deconditioned patient may be aerobically trained at as low as 50% to 60% of HR_max. Any patient who has documented CAD should have a medically supervised ETT before beginning an aerobic exercise program. Without an ETT, it is impossible to assume what the maximum HR would be for a patient with cardiac disease. The ECG monitoring during the ETT is useful in the detection of exercise-induced ischemia. If no ETT data are available, it is unwise to prescribe an exercise based on HRs. Cautious progression of activity is warranted, along with use of RPE and knowledge of adverse signs and symptoms for exercise intolerance. An easy tool for self-monitoring is for the patient to be able to talk without becoming breathless while exercising. This is termed the Talk Test and provides a fair indication that the patient is appropriately exercising below his or her anaerobic threshold, which usually occurs at approximately 55% to 70% of the maximal oxygen uptake.

Exercise Frequency

Exercise is commonly prescribed three to five times per week. The patient should not experience increased fatigue as a result of exercise. If fatigue does occur, the frequency and/or intensity of exercise should be decreased. Patients who choose to exercise daily must watch for signs and symptoms of fatigue and overexertion, recognizing that fatigue may not just occur during the activity, but be delayed until later in the day or the next day.

Exercise Duration (Time)

The goal of 30 to 40 minutes of aerobic exercise with an additional 5 to 10 minutes of warm-up and an adequate cool-down is appropriate. If this amount of activity is uncomfortable for the patient, whatever amount he or she can do comfortably without adverse symptoms is appropriate. Patients who are deconditioned may require interval work, brief rests every 5 minutes during their early training. Adequate warm-up is crucial for all patients but especially for patients with CAD. By gradually increasing the MVO₂ and allowing the coronary arteries time to vasodilate, a balanced myocardial supply and demand may be possible with subsequent activity.

Mode of Exercise (Type)

The variety of exercise equipment has expanded in the last 20 years. The good news is that the patient has the opportunity to experience a variety of equipment including treadmills, stair climbers, bicycles, rowers, cross-country ski simulators, reclining bicycles, steppers, arm ergometers, and others. Patients frequently ask which is the best equipment; the one that they enjoy and the one that they will use is by far the best for them.

If a patient becomes symptomatic with angina during a physical therapy intervention, the immediate goal is to decrease MVO₂; the activity should be immediately stopped. The patient should sit or, if possible, lie down on a bed or plinth. The physical therapist should take the patient's HR and BP and calculate the rate pressure product (RPP = HR (SBP) as soon as possible to determine the MVO₂ at which the patient became ischemic, termed the ischemic threshold. If the patient is in an inpatient facility, help may be sought immediately to ensure that facility guidelines are quickly initiated. Such guidelines may include supplemental oxygen, a 12-lead ECG, administration of NTG, and other anti-ischemic medications. If the patient is in an outpatient setting and has his or her own NTG (which the patient should be carrying at all times), the patient should take it and follow the prescribed guidelines. NTG usually produces a tingling or burning sensation if it is effective. Failure of the NTG to produce these sensations may indicate that the NTG is outdated. Patients are generally instructed to take one NTG pill sublingually (under the tongue), although some patients use an NTG spray. They can then wait 5 minutes and repeat administration if the symptoms are not completely gone. A third NTG may also be taken after waiting another 5 minutes. Patients are frequently told that if the symptoms have not resolved completely after three doses of NTG they should come to the emergency department for further management. If the patient is in an outpatient setting without his or her own NTG and has symptoms that do not re-solve after a few minutes of rest, the facility guidelines to activate advanced care for the patient should begin quickly. If the patient's symptoms escalate, even after the first NTG, emergency care needs to be initiated immediately. If the patient is climbing stairs, the patient should stop, take a few easy deep breaths, and then descend when the symptoms have abated and walk slowly to the first available support. However, if the patient's symptoms are quickly accelerating despite stopping the activity and taking deep breaths, the patient should be assisted to a position of comfort and further medical assistance sought immediately. It is important that therapists maintain a calm demeanor, reassuring the patient that the situation can be handled efficiently and easily.

Cardiac Rehabilitation: Myocardial Infarction

Although it is common today to take cardiac rehabilitation for granted, it was not so long ago that treatment for patients with MI included weeks of prolonged bedrest. In the pivotal 1952 study by Levine and Lown,¹⁰⁵ chair rest and low-level activity was found to be more beneficial than the traditional 8 weeks of bedrest. Today, the patient with a noncomplicated MI may be hospitalized for as few as 3 to 5 days.

Cardiac rehabilitation (cardiac rehab) is multidisciplinary and may include the physician, nurse, physical and occupational therapists, exercise physiologist, nutritionist, and social service caseworker. Cardiac rehab begins in the hospital and extends indefinitely into the maintenance phase. The inpatient component is referred to as Phase I. Outpatient phases include Phase II, the exercise-training period, and Phase III, the maintenance period. Phase II is usually described as occurring immediately after discharge, requiring intensive monitoring and supervision including ECG monitoring and intensive risk factor interventions.¹⁰⁶ Aerobic and strength training may begin based on the results of the ETT, which is usually done at approximately 4 weeks. In Phase III, the patient has stabilized and requires ECG monitoring only if signs and symptoms necessitate; endurance training and risk factor modification continue. Ideally, Phase II is initiated within 2 weeks of hospital discharge. It is important to note that these phases are not absolutes and the timelines and activities of these phases may vary according to managed care models, contracts with reimbursement plans, and treatment protocol designs. Owing to insurance coverage, some patients do not enter into a formal cardiac rehab program until after their symptom-limited maximum ETT at 4 to 6 weeks post-MI.

Inpatient/Phase 1

The length of hospital stay for a patient with an MI has changed dramatically in the last decade and is commonly 3 to 5 days for an uncomplicated MI (no post-MI angina, malignant arrhythmias, or heart failure), compared to at least three to four times that duration in the early 1980s. Inpatient cardiac rehab uses a team approach based on activity progression, patient education, and hemodynamic and ECG monitoring, together with medical and pharmacological management. The role of the physical therapist is to monitor activity tolerance, prepare for discharge, educate the patient to recognize adverse symptoms with activity, support risk factor modification techniques, provide emotional support, and collaborate with other team members.

Vital sign monitoring occurs before and after and, if possible, during activity. The intensity of the activity is considered to be low level, and perceived exertion for the patient should be comparable to the "fairly light range" of the Borg RPE Scale (see Table 13.11). For an increase of 1 to 2 METs, an HR increase of 10 to 20 bpm is appropriate, if beta-blockers or other HR suppressers are not used; however, the absence of beta blockade in Phase I is uncommon. If a beta-blocker is used, there is no standardization as to the degree of HR suppression; subjective ratings of perceived exertion and objective observation of patient effort become increasingly important. A patient on beta-blockers who has an HR increase of 20 bpm during low-level inpatient activity would be considered inadequately medicated, unless the activity level was considerably higher than appropriate. A decrease in HR or BP during activity for any patient, regardless of medications, should be evaluated for the presence of an arrhythmia. Following the physical therapy intervention, the patient's tolerance of activity and hemodynamic stability should be documented.

There are a variety of inpatient cardiac rehab programs, frequently progressive based on levels of increasing energy costs (e.g., MET levels). Each facility will establish its own levels and criteria for activity progression and education; an example of an inpatient program is shown in Table 13.12. Following are some general comments and recommendations about the various levels. It is important to note that activity progression occurs along a continuum and is not done in a rigid format. Although a patient must demonstrate the ability to sit at the bedside with appropriate hemodynamic response before ambulating in the hallway, the patient's individual response and medical history will dictate how quickly he or she is able to progress. A patient may progress through more than one level within any treatment session.

Table 13.12Inpatient Cardiac Rehabilitation Program

Table 13.12 Inpatient Cardiac Rehabilitation Program

CCU-Essentially Bedrest

Progressive Hall Ambulation

Level 1

1–1.5 METs

Evaluation and patient education
Arms supported for meals and activities of daily living (ADL)
Bed exercises and dangle with feet supported (if CK levels have peaked and patient has no complications)

Education

Introduction to inpatient cardiac rehab and role of physical therapy
- Education
- Monitored progression of activity
- Home exercise/activity guidelines/outpatient cardiac rehab

Sitting—Limited Room Ambulation

Level 2

1.5–2 METs

Sitting 15-30 min, 2-4 times/day
Leg exercises
Commode privileges
Reclining upright chair
Limited ADL
Electric razor
Limited supervised room ambulation for small uncomplicated MI

Education

Identification of CAD risk factors
Concept of "healing interval" and need to pace activities

Room—Limited Hall Ambulation

Level 3

2–2.5 METs

Room or hall ambulation up to 5 min as tolerated 3-4 times/day
Standing leg exercises optional^∗
Sit on side of bed or in bathroom to wash (per discretion nurse/physical therapist [PT])
Manual shave
Bathroom privileges
Independent or assisted ambulation in room or hall as advised by PT

Education

Size of infarct and how it relates to the need for gradual resumption of activities
Impact of exercise on reducing the patient's risk factors
Teach use of Borg's Scale for Rating of Perceived Exertion and appropriate parameters with activity

Level 4

2.5–3 METs

Hall ambulation 5-7 min as tolerated 3-4 times/day
Standing trunk exercises optional^∗
Independent or assisted ambulation in hall as advised by PT

Education

Teach pulse taking and appropriate parameters with activity
Reinforce benefits of outpatient cardiac rehabilitation

Progressive Hall Ambulation

Level 5

3–4 METs

Hall ambulation 8-10 min as tolerated
Arm exercises optional^∗
Standing shower
Independent hall ambulation as advised by PT

Education

Written home exercise/activity guidelines reviewed
Patient given written information on outpatient cardiac rehab

Stair Climbing

Level 6

4–5 METs

Progressive hall ambulation as tolerated
Full flight of stairs (or as required at home) up and down one step at a time†

Education

Answer patient's questions
Check for understanding of activity guidelines

Patient Outcome—No Evidence of Hemodynamic Compromise with Activity Progression (All Levels)

No systolic drop in BP >10 mm Hg or increase >30 mm Hg

No HR increase >12 if beta blocked, or no HR increase >20 if not beta blocked

No complaints of dizziness, lightheadedness, or angina Perceived exertion <13/20

Hemodynamic Monitoring

Level 1

HR and BP before and after supine bed exercises
Orthostatic signs supine and dangling at bedside

Level 2

Orthostatic signs (supine, sit, and stand) before exercises and transfer
HR and BP after leg exercises/transfer to chair
HR and BP after return to bed

Levels 3–6

HR and BP in sitting and standing prior to activity
HR and BP immediately following activity
HR and BP 5 min after activity

From Rehabilitation Services Department, Newton Wellesley Hospital, Newton, MA, with permission.

^∗Optional exercises are at the discretion of the PT and may be used to establish the patient's CV response in the room, prior to moving on to more challenging hallway ambulation; or in those patients who require general strengthening exercises.

Stair climbing activities should take place after the ETT if the scheduling of the ETT permits. Otherwise patients may, at the discretion and supervision of the PT, climb stairs on the day prior to the ETT.

Level 1. The patient is in the intensive care unit (ICU) and is stable; generally physical therapy intervention does not begin until after the first 24 hours from admission or until the patient has been stable for 24 hours. Physical therapy intervention should begin after the blood work has indicated the MI is completed. CK and troponin (both I and T) levels are monitored. For both CK and troponin levels, reliable diagnostic sensitivity (greater than 90%) is reached within 12 to 16 hours of the onset of symptoms.¹⁰⁶ CK peak levels occur between 14 and 36 hours, with a return to normal level after 48 to 72 hours; troponin peaks at 24 to 36 hours, with a return to normal levels within 10 to 12 days.¹⁰⁷ Commonly, three sets of CK levels collected 8 hours apart are collected. Because CK is released very quickly into the bloodstream with cellular damage, it is typical for the first and second CK levels to show a progressive increase and the third set to be less than the second (i.e., the CK peak has occurred, and the values are now trending downward). Because CK may be released with cellular damage to areas other than to the myocardium, specific myocardial isoenzymes known as CK-MB are monitored. Appropriate activity for the patient in the ICU during the first 24 hours is to move comfortably within the bed, perform ankle pumps, perform deep-breathing exercises, use the commode (if hemodynamically stable), and perform limited personal care.

Level 2. Once the patient has been hemodynamically stable for 24 hours he or she may progress out of bed (OOB). The therapist should also be alert to signs of orthostatic hypotension when the patient changes position from supine to sitting on the side of the bed. The patient's feet should be supported on a stool to assist venous return if they are not able to touch the floor. The patient walks to a bedside chair. The patient sits in an upright chair for up to 30 minutes a few times a day. There is a real temptation for many health care providers to have the patient "do" something while seated, such as washing, eating, or visiting with family. It is probably wise to just let the patient sit for the first time, without being encumbered with other tasks. The therapist is thus better able to evaluate the patient's response to being upright. If the patient has had a large MI or requires a slow progression to upright posture, the use of a reclining chair is a way to gradually assume the upright position. The patient performs LE exercises such as ankle pumps, knee extensions, or marching in place. Vital signs are monitored for hemodynamic stability and appropriate activity response. Ensuring sufficient healing time, pacing activities, and creating a healthful environment are components of a comprehensive patient education program.

Level 3. Patients are instructed to gradually increase their ambulation. One approach is to educate patients to judge their ambulation in terms of time instead of distance. Time is a more reproducible measurement, whereas distance may be difficult to judge (e.g., "I want you to walk for 2 minutes" vs. "I want you to walk 200 ft"). It also allows for an easier transition to the HEP, which is commonly based on length of time. For documentation purposes, it is most effective to document the distance covered in the time period whenever possible (e.g., "Patient ambulated 500 ft in 6 minutes with an RPE of 10/20"). Information regarding CAD risk factors allows patients to begin to take responsibility for their choices about activity and lifestyle. However, for some patients this may be too early in their recovery, and they are unable to focus on what is being said. Giving patients written information is a good way to provide education and yet give patients the choice when to read it. Use of the Borg RPE Scale assists the patient in monitoring of activity intensity.

Levels 4 through 6. Patients gradually increase the frequency and time of their walks at a comfortable and leisurely pace. The goal is to progress walks from 2 minutes, to 5 minutes, to 10 minutes with appropriate hemodynamic response. Stairs may be climbed foot over foot with a planned rest halfway or so, or one foot at a time, depending on the status of the patient. Patients are often hesitant to move, especially in stretching their arms overhead; therefore performing a variety of trunk, arm, and standing leg exercises for a few repetitions each often allays the fear and helps the patient feel more comfortable moving.

Patients need to be made aware of the fatigue that often accompanies seemingly innocuous activities (e.g., showering) and plan their rests accordingly. Visitors are often a hidden energy cost; patients are often very excited and reassured to have visitors, but the fatigue that follows is sometimes very disconcerting. Helping the patient understand the concept of energy and the cost of not just physical but emotional and mental activities is invaluable. Comparing energy costs to money may help the patient to pace activity. Patients are told that they have a dollar's worth of energy and everything they do is going to cost them some part of that dollar; however, they can never spend more than 50 or 60 cents at one time. Every time they rest, it is like going to the ATM for a quick refill. In this way, patients become knowledgeable about the expendability of energy and yet are given the responsibility to spend (and save) as they choose.

Documentation

There are many ways to document physical therapy examination and intervention. In this patient population, appropriate documentation would include the following:

Objective activity data, including time period and distance ambulated, type of sitting and standing exercises, and stair climbing (number of steps); number and duration of rests.
Patient's vital sign response to each activity, including a statement that addresses patient performance with respect to vital signs (e.g., "Patient ambulated 6 minutes covering 500 ft and climbed 10 steps foot over foot using handrail with adaptive VS response without signs or symptoms of hemodynamic compromise").
Education provided and response of patient, family, and caregivers.

Home Exercise Program

Two of the more important concepts for a patient to understand at the time of discharge are symptom recognition and appropriate activity guidelines. It is crucial that the patient recognizes cardiac symptoms and understands the action to take if they occur.

Physical therapists establish activity guidelines during the first 4 to 6 weeks after MI while the myocardium is healing. During this healing phase, physical activity involves a gradual increase in ambulation time, with a goal of 20 to 30 minutes of ambulation one to two times per day at 4 to 6 weeks after MI. Patients are encouraged to walk comfortably, dress appropriately, and to try to exercise in ambient temperature at indoor malls if weather is not appropriate (i.e., below 40°F including wind chill factor, over 80°F, or excessive humidity and poor air quality). Some patients are very sensitive to environmental factors and should exercise only in ambient conditions or indoors. For some patients, home exercise equipment is affordable and may be a reasonable alternative to outdoor exercise. For safety reasons, the patient should be monitored on similar equipment before independently beginning to exercise at home. This is not the time for a patient to try a new type of exercise modality but to stay with what is familiar. Walking appears to be the exercise of choice owing to its ease and familiarity.

The patient's days will be a combination of rest and low-level activity including ambulation and LE and UE mobility. The patient should be encouraged to try to change positions or activity every 1 to 2 hours. For example, it is generally not a good idea for the patient to be up all morning and then rest all afternoon. It is invaluable to have patients verbally outline what their days will include once they are discharged. This affords an opportunity to better understand the interests of the patient and make specific suggestions, as well as provide an opportunity to determine the patient's understanding of activity guidelines and energy conservation techniques.

Outpatient Phase II

Patients commonly undergo a symptom-limited maximal stress test (ETT) at 4 to 6 weeks after MI. Based on the results of the tests, either positive (+) for ischemia or negative (–) for ischemia, an exercise prescription is prescribed. For a (–) ETT, a common exercise prescription would be 70% to 85% of the peak achieved on the test (i.e., HR_max); however, an equally effective alternative would be 65% to 80% of HR_max. Understanding that a negative test does not mean the patient is disease free and that vulnerable plaques may exist, a conservative prescription may be a wiser choice.

If a patient has had a positive ETT, the exercise prescription becomes relatively simple: during aerobic training, it is important to keep MVO₂ below the patient's ischemic MVO₂. Remember that a clinical measure of MVO₂ is the product of HR and SBP, known as the rate pressure product (RPP = HR × SBP). The importance of considering the ischemic threshold is the recognition that BP will vary during use of different pieces of exercise equipment owing in part to the differences in muscle recruitment. If there is a difference in BP for a given HR, then there will be a difference in the MVO₂ to the patient. For example, if a patient has an HR of 100 bpm and a BP of 140/80 mm Hg while exercising on the treadmill, and an HR of 100 bpm and a BP of 160/80 mm Hg while exercising on the stationary bicycle, the bicycle is costing the myocardium more energy than the treadmill, even though HR is the same. Depending on the patient's ischemic threshold, it is possible that angina may occur on the bicycle but not on the treadmill. A good safety tip is to not exceed 90% of the ischemic RPP. The remainder of the exercise prescription may follow the common guidelines for aerobic training in regard to frequency, intensity, and duration for patients with cardiac involvement.

Strength Training

The inclusion of strength training in a cardiac rehab program is a relatively recent addition to the traditional cardiac rehabilitation program. Initial concern was that resistance work would inordinately increase MVO₂ and ventricular arrhythmias and therefore be detrimental.¹⁰⁸ A publication by Beniamini et al¹⁰⁹ gives excellent insight into this area. The AACVPR's thorough review of the literature on this topic concluded that "resistance exercise has been shown to be a safe and effective method for improving strength and cardiovascular endurance, modifying risk factors and enhancing self efficacy in low-risk cardiac patients."¹⁰⁶ Resistance training may begin with the use of elastic bands and light hand weights (1 to 3 lb) and progress to a load that allows 12 to 15 repetitions comfortably.¹¹⁰AACVPR guidelines further state that resistance training should not begin until the patient has been in a cardiac rehab program for at least 3 weeks and is at least 5 weeks post-MI or 8 weeks post-CABG.¹¹⁰ Some guidelines for resistance training include the following: (1) exercising large muscle groups before small; (2) stressing exhalation with exertion; (3) avoiding a sustained, tight grip; (4) focusing on RPE 11 to 13; (5) using slow, controlled movements; and (6) stopping exercise with any warning of concerning or uncomfortable signs or symptoms.¹¹⁰ The American Heart Association (AHA), American College of Sports Medicine (ACSM), and AACVPR all advocate the importance of muscular fitness for the patient with cardiac impairment and support the inclusion of resistance training into the patient's exercise program.^{106,110,111,112}

Intervention for Patients with Congestive Heart Failure

The APTA Guide to Physical Therapist Practice includes management of patients with CHF under the category of Impaired Aerobic Capacity and Endurance Associated with Cardiovascular Pump Dysfunction or Failure, Pattern 6-D.²⁶ The development of specific anticipated goals and expected outcomes for the patient with CHF is based on the general goals of physical therapy intervention presented in Box 13.6.

Box 13.6 Congestive Heart Failure—Anticipated Goals and Expected Outcomes

Physiological response to increased oxygen demand is improved.
Self-management of symptoms is improved.
Ability to perform physical tasks is increased.
Behaviors that foster healthy habits, wellness, and prevention are acquired.
Disability associated with acute or chronic illness is reduced.
Risk of secondary impairments is reduced.
Awareness and use of community resources is improved.
Performance of and independence in ADL is increased.

ADL = activities of daily living.

Exercise Prescription

Exercise programs for patients with CHF are relatively recent. Patients whose cardiac status was once thought to be too fragile to participate in organized exercise are now not only participating, but exercise is recommended as an integral component of their medical management.^{113,114,115,116} Studies have shown that patients with heart failure can exercise safely, and regular exercise may improve functional status, quality of life, and exercise capacity, and decrease symptoms.^{117,118,119,120,121,122,123}

The safety and importance of strength training and peripheral adaptations have also been studied.^124,125 Using a multidisciplinary approach that includes a thorough physical examination before each exercise session with a review of symptoms and medications, low-level exercise may begin if the patient is hemodynamically stable. CHF is a multisystem disease that affects not just the heart but peripheral muscle and arteries as well. Studies have demonstrated muscle fiber atrophy of skeletal and respiratory muscle, as well as an alteration in arterial vasodilation capacity. Exercise has been shown to limit some of these adverse changes; therefore, an exercise program should consider not only systemic conditioning, but also peripheral endurance training, low-level resistance training, and respiratory muscle training.^126,127,128 Exercise training can be initiated when the patient is in compensated CHF. Box 13.7 provides the relative criteria for initiation and relative criteria for modification and termination of exercise in patients with heart failure.

Box 13.7 Criteria for Modification or Termination of Exercise in Patients with Heart Failure

Marked dyspnea or fatigue
RR > 40 breaths/min
Development of S₃ heart sound
Increase in pulmonary crackles
Decrease in HR or BP of > 10 bpm or mm Hg respectively during steady state or progressive exercise
Increase in the CVP by 10 mm of Hg
Diaphoresis, pallor, or confusion

Criteria for Initiation of Exercise

Compensated CHF
Able to speak comfortably without signs of dyspnea with RR < 30 breaths/min
Less than moderate fatigue
CI > 2.0 L/min
CVP < 10 mm Hg
Crackles in less than one half of the lungs
Resting heart rate < 120 bpm

Aerobic Exercise

There is no paucity of research indicating that aerobic exercise is beneficial for patients with CHF. Exercise prescription must keep intensity low and gradually increase duration as the patient tolerates. In general, aerobic exercise training may include low-impact exercise with gradual progression of intensity, frequency, and duration. Intensity should be monitored through the use of the dyspnea or perceived exertion scales and should be kept to a rating of fairly light. HR cannot be relied on for evaluating intensity due to the effects of various medications, including beta-blockers. It is also important to note that in the normal heart, an increase in HR is accompanied by an increase in inotropy. In the failing heart, an increase in HR may actually result in a decrease in force; this is known as the negative treppe effect.¹²⁹

Monitoring BP response is crucial to determine if CO is being maintained during aerobic exercise. A drop in BP during aerobic exercise signifies the inability of the heart to maintain CO during exercise. For these patients, therapists may chose to reduce the aerobic component and focus more on strength training to achieve peripheral adaptations as opposed to central adaptations. By strength training the peripheral muscles, therapists can increase the number of mitochondria and utilization of blood and oxygen at the level of the muscle, thereby enabling the muscle to make more energy to sustain activity without putting excessive stress on the heart.

Two important studies depict the benefits of exercise training in patients with heart failure. A meta-analysis conducted by van Tol et al¹³⁰ in 2006 investigated 35 original randomized crossover trials of patients with systolic heart failure.¹³⁰ The average exercise within these studies included aerobic exercise 3 times/week for 60 minutes/session for 12 weeks. The investigators found an increase in 6-minute walk distance with an effect size of 46.2 m, within 15 studies including 599 patients. In 31 studies with approximately 1,240 patients, maximum oxygen uptake was found to increase after exercise with an effect size of 2.06 mL/kg/min. The researchers also found improvements in the resting diastolic BP, resting CO, and resting HR values following exercise. Finally, patients were able to demonstrate an increase in the LVEF and tolerate greater intensity following the 12 weeks of exercise. A systematic review published by Smart and Marwick¹³¹ investigated 81 studies involving 2,387 exercising subjects with 1,197 patients enrolled in controlled studies and included 60,000 patient hours of exercise training. Mean number of subjects was 30 ± 25; mean age was 59 ± 7 years, and mean EF was 27% ± 7%. The investigators reported that studies utilizing aerobic exercise training (n = 40) demonstrated VO_{2 max} increase of 16.5%. In addition, studies utilizing strength training alone (n = 3) demonstrated VO_{2 max} increase of 9.3%, and studies that combined aerobic and strength programs (n = 30) demonstrated VO_{2 max} increase of 15%. Clinically, this could mean that an individual with a VO_{2 max} of 15 mL/kg/min could increase to 17.4 mL/kg/min, which is an approximately .68 MET increase and could lead to sustained walking on a level surface. Box 13.8 Evidence Summary presents related research investigating the effects of exercise in patients with heart failure.^{132,133,134,135,136,137,138,139,140,141}

Box 13.8 Evidence Summary Studies Investigating the Effects of Exercise on Patients with Congestive Heart Failure

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First Author (Reference)

Design

Controls (n)

Exercise

Training Time, Frequency, Duration

Intensity and of Training

Change in Oxygen Consumption

Adamopoulos¹³²

Crossover

30 min, 5 sessions/wk, 12 wk

60%–80% maximum heart rate; aerobic

15%

Barlow¹³³

Longitudinal

60 min, 3 sessions/wk, 16 wk

50% of 1 repetition max; 90% anaerobic threshold; aerobic + strength

Delagardelle¹³⁴

Longitudinal

40 min, 3 sessions/wk, 12 wk

50%–75% max oxygen consumption; 60% of 1 repetition max

0% strength; 8% aerobic

Harris¹³⁵

Longitudinal

30 min, 5 sessions/wk, 6 wk

70% maximum heart rate; aerobic

Kemppainen¹³⁶

Controlled nonrandomized

45 min, 3 sessions/wk, 20 wk

70% max oxygen consumption; aerobic + strength

27%

Stolen¹³⁷

Controlled nonrandomized

45 min, 3 sessions/wk, 20 wk

50%–70% max oxygen consumption; aerobic + strength

27%

Malfatto¹³⁸

Controlled nonrandomized

60 min, 5 sessions/wk, 12 wk

40%–50% max oxygen consumption; aerobic

18%

Radzewitz¹³⁹

Longitudinal

25 min, 3 sessions/wk, 4 wk

60%–80% max oxygen consumption; aerobic + strength

11%

Santoro¹⁴⁰

Longitudinal

90 min, 3 sessions/wk, 16 wk

50%–60% max oxygen consumption; 50% of 1 repetition max; aerobic + strength

18%

Vibarel¹⁴¹

Longitudinal

46 min, 3 sessions/wk, 8 wk

70%–80% max oxygen consumption; aerobic

22%

Strength Training

Strength training is a crucial component of the exercise plan for patients with heart failure to help improve peripheral muscle strength and endurance. Inclusion of light resistance work has been shown to be safe in this population.¹⁴² Modalities for resistance training may include elastic bands for mild UE and LE resistance work or light weights. A review by Braith and Beck¹⁴³ provides clinicians with the benefits of resistance training in helping to improve skeletal muscle morphology and provides clinical guidelines for prescription of resistance exercise. Box 13.9 delineates recommendations for resistance exercise in patients with heart failure.

Box 13.9 Resistance Training Recommendations for Patients with CHF

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NYHA Class I

NYHA Class II–II

Frequency

2–3 days/wk

1–2 days/wk

Duration

15–30 min

12–15 min

Intensity

50%–60%, 1 RM^∗

40%–50%, 1 RM^∗

Sets

2–3

1–2

Reps

6–15

4–10

^∗1 RM = 1 repetition maximum.

Ventilatory Muscle Training

Breathing exercises^144,145 and inspiratory muscle training^146,147 have been shown to be beneficial in patients with heart failure. Diaphragmatic breathing may help reduce excessive accessory muscle use and reduce the work of breathing. Pursed-lip breathing has been shown to promote the positive end-expiratory pressure not only in patients with COPD but also in patients with CHF.¹⁴⁴ Pursed-lip breathing is also beneficial in helping slow down the respiratory rate in patients with heart failure.¹⁴⁵

Patients with heart failure are known to have poor ventilatory muscle strength.¹⁴⁸ Strength of the ventilator muscles can be enhanced through use of a device known as a threshold inspiratory muscle trainer. Improvements in the maximal inspiratory pressure are achieved by having the patient breathe with this device, which resists inspiration, thereby strengthening the inspiratory muscles. A general protocol is to use the threshold inspiratory muscle trainer at 20% of the maximal inspiratory pressure, to be used 3 times per day for 5 to 15 minutes at each session.⁹

Activity Pacing and Energy Conservation Techniques

Patients with heart failure require activity pacing and energy conservation techniques to decrease the workload on the heart. A few techniques that may be beneficial for patients include the following:

Recommending frequent rest intervals before they get tired.
Participate in activities that require greater energy costs at times of the day when they have the most energy.
Plan ahead to decide activities that possibly may be avoided and delegated to others.
Alternate easy and difficult tasks with rest intervals.
Adjust the environment to make tasks easier and sit when feasible while doing strenuous activity.

EDUCATION FOR PATIENTS WITH HEART DISEASE

For patients with heart disease, patient and family education develops along a continuum, depending on the patient's baseline status and readiness to attend to the information. The physical therapist, along with other members of the health care team, must determine the patient's and family's ability to understand and adhere to the information. Appropriate discharge or ongoing outpatient topics to be addressed include the following.

Activity Guidelines. Patients (and family) need to be able to understand specific activity guidelines, which include planned exercise sessions as well as leisure time and rests.
Self-Monitoring. Patients may monitor the intensity of their activity in a variety of ways; two of the more common ways are palpating a pulse and RPE. Because many older patients have decreased sensitivity in their palpation skills, the use of RPE may be easier and more reliable. Those patients who are able to take a pulse or choose to invest in an HR monitor may prefer to use those methods. Self-monitoring not only involves HR or RPE, but awareness of other symptoms or signs that may suggest exercise intolerance, such as lightheadedness, mental confusion, dyspnea, and inability to carry on a brief conversation while performing an activity. Patients with CHF commonly use the dyspnea scale and the Borg RPE Scale.
Symptom Recognition and Response. Being able to recognize their specific cardiac symptoms and to know how to respond is a key component in patient education. Patients should have written information regarding the action they should take when symptoms occur, for example, when to call their physician or go to the hospital. Angina is the most common symptom associated with coronary heart disease, whereas weight gain (2 lb over 1 to 2 days), dyspnea, LE edema, and increased pillows for sleep are common signs and symptoms for CHF.
Nutrition. Patients commonly meet with a nutritionist to discuss their usual dietary habits and to make recommendations when needed for a more heart-healthy diet. Most commonly, patients with heart disease are instructed to reduce fat intake; patients with CHF are instructed to monitor salt and fluid intake.
Medications. Patients receive written information regarding the desired action of their medications, potential side effects, dosage, and timing of medications. Patients should also know which nonprescription drugs such as cold, sinus, allergy, or anti-inflammatory medications they should avoid because of possible interactions with prescription drugs. Patients should also be encouraged to disclose all herbal remedies and supplements that they may be taking.
Lifestyle Issues. Many factors influence whether a patient will return to work after a cardiac event. Many patients with CAD return to work if they were employed before their event; patients with CHF are, in general, an older population when compared to patients with CAD and therefore may have already retired.

Resumption of sexual activity may be an uncomfortable discussion for some patients. There may be many issues of concern for the patient (e.g., fear, anxiety, performance concerns, lack of libido). Patients and their partners are encouraged to verbalize their concerns to each other and to seek appropriate information from their health care team. Some medications (e.g., beta-blockers) may blunt the sexual response, and it is important that patients communicate this with their physician. Often, another medication or category of medication may be better tolerated. When patients feel ready for sex, their energy level throughout the day is satisfying for them, and they are able to walk outdoors and climb stairs comfortably, they are probably ready for sexual activity. It may be helpful for patients to remember that sexual activity is not unlike other physical activity with respect to energy cost, and therefore planning, pacing, and warm-up are powerful contributors for a more comfortable outcome. In some cases, the physician may recommend taking prophylactic NTG before sexual activity.
See Box 13.10 Suggested Topics for Patient, Family, and Caregiver Education and Counseling from the U.S.

Department of Health and Human Services Clinical Practice Guidelines for Patients with CHF.¹⁴⁹

Box 13.10 Suggested Topics for Patient, Family, and Caregiver Education and Counseling

General Counseling

Explanation of heart failure and the reason for symptoms
Cause or probable cause of heart failure
Expected symptoms
Symptoms of worsening heart failure
What to do if symptoms worsen
Self-monitoring with daily weights
Explanation of treatment/care plan
Clarification of patient's responsibilities
Importance of cessation of tobacco use
Role of family members or other caregivers in the treatment/care plan
Availability and value of qualified local support group
Importance of obtaining vaccinations against influenza and pneumococcal disease

Prognosis

Life expectancy
Advance directives
Advice for family members in the event of sudden death

Activity Recommendations

Recreation, leisure, and work activity
Exercise
Sex, sexual difficulties, and coping strategies

Dietary Recommendations

Sodium restriction
Avoidance of excessive fluid intake
Fluid restriction (if required)
Alcohol restriction

Medications

Effects of medications on quality of life and survival
Dosing
Likely side effects and what to do if they occur
Coping mechanisms for complicated medical regimens
Availability of lower-cost medications or financial assistance

Importance of Compliance with the Treatment Care Plan

From Clinical Practice Guidelines, Number 11, Heart Failure: Evaluation and Care of Patients with Left-Ventricular Systolic Dysfunction, AHCPR Publication No. 94-0612, p 42, with permission.

PSYCHOLOGICAL/SOCIAL ISSUES

Cardiac disease may not only create new emotional issues but also enhance some that might have existed before the cardiac event. Reassure patients that many of these issues are normal sequelae of their event. Encourage them to seek guidance and counseling in whatever arena they feel appropriate (e.g., health care, counseling, religion).

Many studies have addressed the relationship of emotional depression following CABG.^150,151,152 Although depression is reported to exist, there is difficulty in objectively measuring the direct impact of CABG on subsequent depression. Some of the difficulty arises in the use of depression scales (Beck or CES-D), grading criteria, the presurgical emotional status, and gender. Burg et al^150,151 reported two studies in 2003 in which 89 men were followed preoperatively and up to 2 years following surgery. They found that presurgical depression was an independent predictor of postoperative prolonged surgical pain and failure to return to previous activity. In a study by Blumenthal et al,¹⁵² 817 patients were studied preoperatively, up to a mean of 5.2 years postoperatively. They reported that patients with moderate to severe depression at baseline (preoperatively) that persisted postoperatively had an increased death rate compared to the nondepressed patients.¹⁵² Ai et al¹⁵³ reported that the presence of preoperative co-morbidities strongly influenced whether depression existed. McKhann et al,¹⁵⁴ in their study of 124 patients, concluded that the majority of patients depressed after surgery were in fact depressed before surgery. Pirraglia et al¹⁵⁵ reported on 237 patients and noted that 43% were classified as depressed preoperatively and only 23% postoperatively. Factors that influenced postsurgical scores were length of ICU stay and the amount of reported social support.¹⁵⁵ The decrease in postoperative depression compared to preoperatively was supported by Lindquist et al¹⁵⁶ in 2003; they studied more than 650 men and women and found less anxiety and depression following surgery than preoperatively. Of interest, they also noted that women's report of quality of life (QOL) was lower than men's up to 1 year following surgery. Westin et al¹⁵⁷ also reported a gender difference in CABG outcomes in regard to depression and QOL measures. In their study of more than 300 patients, women scored lower on the QOL and higher on depression scale than men at 1 month and 1 year following CABG, compared to men.¹⁵⁷ Phillips et al¹⁵⁸ reported women to be at greater risk for both cognitive difficulties and anxiety than men at 1-year postoperative CABG than men. The physical therapist, therefore, needs to be aware that depression may exist following surgery and, as a member of the health care team, assist in directing appropriate care and support for the patient.

PRIMARY PREVENTION OF CORONARY ARTERY DISEASE

Patients who do not have documented CAD but who have identifiable risk factors should be encouraged to adopt lifestyle behaviors that can modify their risk factors. Health education and primary prevention programs through individualized education and exercise guidelines attempt to modify an individual's risk factors and thereby prevent CAD.

Patients are instructed in appropriate dietary guidelines, including low fat, adequate fiber, minerals and vitamins, and decreased salt, particularly if the patient has high BP. Besides lowering total dietary fat, patients are instructed to decrease their percentage of saturated fats and avoid trans fatty acids. Elevated levels of the amino acid homocysteine appear to increase the risk of arterial endothelial disease. Folic acid, a B vitamin, lowers homocysteine levels. If weight loss is needed, patients are encouraged to see a nutritionist to design a sensible eating plan. Patients are encouraged to gradually increase their endurance activity, such as walking toward a goal of 30 to 40 minutes (not including warm-up and cool-down) four times a week. The American College of Sports Medicine and the American Heart Association recommend that anyone over age 40 with two or more risk factors should have an ETT before beginning an aerobic or strengthening exercise program. The purpose of the ETT is to identify the presence of any latent ischemia.

If no ischemia is present, a typical aerobic exercise prescription might be as follows:

Intensity: 70% to 85% of HR_max as the aerobic training zone
Duration: 30 to 40 minutes in the aerobic training zone; appropriate warm-up of 5 to 10 minutes, and cool-down
Frequency: three to four times per week

Maximum HR may be estimated by subtracting the person's age from 220; this, however, is not an exact science for any individual and cannot be accurate if the person is on any cardiac medications, such as beta-blockers, that may decrease the maximum HR. Supplemental resistance work is also encouraged at moderate intensities, with initial monitoring of HR and BP.

Modification of the other CAD risk factors is also key to the success of any primary prevention intervention. Patients are encouraged to identify risk factors and to seek resources to assist in modifying them. There are many community-based smoking cessation programs or medically supervised programs that a patient might explore. Stress management programs are also varied and can be adapted to the individual's needs. Proper and consistent use of any medications that might be used in controlling risk factors, such as antihypertensives, antihypercholesterolemias, blood glucose–lowering agents (hypoglycemics), and antianxiety agents or antidepressants, is crucial to the success of any program.

HTN, as the most prevalent CVD in the United States, is one of the most powerful contributors to cardiovascular morbidity and mortality. The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommends a multifactorial approach and suggests that lifestyle modifications, including weight reduction, physical activity, and moderation of dietary sodium, are recommended as either definitive or adjunctive therapy for HTN.²⁴

SUMMARY

Physical activity is important for all individuals and is especially beneficial for those individuals already diagnosed with CAD and CHF. Individuals with heart disease should understand that a consistent exercise program is part of the management for their disease and is as necessary as their medications. Having heart disease means that the person needs to understand the parameters in which he or she may safely participate in activity either recreationally or as a prescribed exercise. The role of the physical therapist is to provide a safe exercise prescription for all patients.

During the time of illness, the effects of decreased activity can be devastating. A paradox exists, however, in that the less activity that is done, the less activity can be done as a result of a decreased work capacity. Therefore, the relative energy cost of all activity increases, and the heart actually works harder for any given task. Not encouraging the patient to resume activity when he or she is medically stable is a disservice. As physical therapists, our role is clear: to understand the pathophysiology of the disease process, to accurately examine the patient, and to establish a safe POC. The ultimate goal is to improve the patient's physiological response to activity and, in doing so, decrease the work of the cardiovascular system.

Questions for Review

Discuss key differences between an NSTEMI and an STEMI.
Discuss three different types of angina. How would you instruct your patient in symptom recognition? Delineate the physical therapy management if a patient has angina during a treatment session.
Discuss sternal precautions that you would instruct your patient to use following a median sternotomy procedure.
Discuss differences between compensated and uncompensated CHF.
Discuss the physical therapy implications when managing patients with pacemakers.
Discuss appropriate goals, education, and treatment interventions for patients with acute coronary syndrome in Phase I cardiac rehabilitation.
Discuss appropriate goals and treatment guidelines for patients with CHF.
Delineate the adaptation that may be noted following an aerobic training exercise program in patients with heart failure.

CASE STUDY

A 58-year-old man presents to the local emergency department (ER) with chief complaint of SOB and difficulty sleeping last night; patient had to sit up all night to make symptoms even a little better. Patient came to the ER because he was unable to get ready for work owing to increased SOB. Patient reports that he has felt SOB off and on for a couple of months, usually associated with physical activity; symptoms, however, usually resolved with rest. Today's episode was the first related to sleeping.

PAST MEDICAL HISTORY

Coronary artery disease: anterior MI 4 years ago
Hypercholesterolemia
Peripheral vascular disease

MEDICATIONS

Digoxin, captopril, furosemide (Lasix), diltiazem, simvastatin (Zocor)

FAMILY/SOCIAL

Patient works full-time as an engineer; travels 3 to 4 days per month.
Married, lives with his wife in a two-story home on a 2-acre lot; three college-aged children.
Patient is an avid golfer; enjoys gardening and landscaping.

PHYSICAL EXAMINATION

Heart sounds: S₁, S₂ normal; S₃ present, no S₄; 2/6 systolic murmur
Lung sounds: crackles 1/3 way
Rhythm/rate: irregular, 140 bpm
Blood pressure: 100/60 mm Hg
Respiratory rate: 26 breaths/min
SaO₂:90%
Jugular venous distention: 5 cm
Echocardiogram: akinetic apex, akinetic distal septum and anterior wall; dilated atria and LV
Chest x-ray: unavailable

LABORATORY DATA

Enzyme pending; CBC WNL except BUN and creatinine slightly elevated.
BNP: 900 pg/mL.
Patient remained in the hospital for 2 days while medications were adjusted. During this time patient underwent further testing, including an ETT.

RESULTS OF ETT

Bruce protocol: 4 minutes; estimated VO₂ max; 20 mL O₂/kg/min (approximately 6 METs); max VS: 130 bpm HR; 120/60 mm Hg BP
ECG: (–) negative for ischemia, chest pain
Reason for stopping: absolute exhaustion
Examination immediately post-ETT: (+) S₃
Physical and occupational therapy were requested to assist with exercise guidelines and discharge planning

PATIENT'S GOALS

Return to work.
Resume hiking.
Begin to prepare his garden for spring planting within the next 5 weeks.

PHYSICAL THERAPY INTERVENTION

Exercise tolerance via low-level exercises sitting and standing, as well as 5-minute walk.

Vital Signs

Sitting (rest): HR 90 bpm; BP 110/60 mm Hg
Sitting exercises: HR 108 bpm; BP 110/60 mm Hg
Standing (rest): HR 110 bpm; BP 108/60 mm Hg
Standing exercise: HR 116 bpm: BP 110/60 mm Hg
5-minute walk: 1000 ft; HR 120 bpm; BP 116/60 mm Hg

HOME INSTRUCTIONS

Meetings planned with patient and his family to discuss discharge guidelines over the next 4 to 8 weeks.

FOLLOW-UP

Patient returns to his primary care provider 3 months after discharge. Echocardiogram is unchanged with EF 30%. Patient states that he has been following discharge guidelines.

Vital Signs

HR 100 bpm; BP 116/70 mm Hg (resting).
Patient states that he feels great and just wants to get on with his life.

QUESTIONS

What is a reasonable presenting diagnosis? Identify each piece of information (and how you interpreted it) that you used to make this diagnosis.
Explain the pathophysiology of the patient's presenting symptoms. Discuss the significance of his HR and heart rhythm in relation to his symptoms.
If the patient's symptoms and signs worsened, and he was admitted to the coronary care unit (CCU)
1. What do you think his Swan-Ganz reading could reasonably look like?
2. What would you expect these signs/symptoms would be that would bring the patient to the CCU?
3. What might be a reasonable cause of his signs/symptoms worsening?
4. What other drugs/interventions might be given in the CCU?
What rhythm do you think the patient is in and why? What do you think might be a reason that he is in this rhythm?
What do you think the chest x-ray would look like and why?
What is your interpretation of the patient's vital sign response to PT intervention? What is your plan for your next session?
What exercise prescription would you recommend for the patient at home (modality, intensity, duration, frequency)?

REFERENCES