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.
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 ||Download (.pdf) 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 |
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 (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
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, 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 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).
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.
Evaluation triad for patients with acute coronary syndrome.
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.
Referral pattern for chest pain.
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.
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).
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.
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 ||Download (.pdf) 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% ||5% ||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.
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.
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 ||Download (.pdf) 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 || |
↑ or ↔ (E)
↓ 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)
|↓ (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)
↓ (R and E)
↓ (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
↔ 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 |
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.
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
|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. |
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 ||Download (.pdf) 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 ||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 |
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 ||Download (.pdf) Table 13.7 Functional Classifications of Patients with Diseases of the Heart
|Functional ||Continuous-Intermittent Permissible Workloads ||Maximum |
|Class I || |
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 || |
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 || |
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 || |
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 |
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):
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 (VO2max).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
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.
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.
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 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.
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
(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.
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.
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
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.
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 ||Download (.pdf) Table 13.8 Pacemaker Classification System
|Chamber Paced ||Chamber Sensed ||Response ||Rate Responsive Pacing |
|O = none ||O = none ||O = none ||R = rate responsive |
|A = atria ||A = atria ||I = inhibit || |
|V = ventricle ||V = ventricle ||T = trigger || |
|D = dual chamber ||D = dual chamber ||D = capacity to both inhibit and trigger || |
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
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.