Cardiovascular and Pulmonary Pathophysiology

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Cardiovascular and Pulmonary Pathophysiology

Elizabeth Dean

Key Terms

Because cardiovascular and pulmonary conditions are among the leading causes of morbidity and premature mortality, they often present clinically to the physical therapist as secondary as well as primary diagnoses. In addition, patients commonly have one or more risk factors for one or both of these broad categories of conditions. Thus physical therapists need a thorough understanding of these conditions, their prevention, their presentation, and their management. Lifestyle and environmental factors are primary causes and contributors (see Chapter 1); thus prevention and reversal of symptoms are aimed at modifying these factors wherever possible.

Smoking is a principal contributor to cardiovascular disease and the primary cause of chronic obstructive pulmonary disease (COPD). Abstinence from smoking is the only intervention that can prevent the majority of cases of COPD, and smoking cessation is the only intervention to retard its progression. Thus cessation of smoking is a primary health care goal at the community, societal, and individual levels,1,2 and it should be a primary intervention by the physical therapist in any patient who smokes (see Chapter 1).

Risk factors for cardiovascular and pulmonary conditions should be assessed in every patient, irrespective of the reason for physical therapy referral or management. An individual with an overt history of cardiovascular or pulmonary conditions is managed based on the related signs and symptoms. However, if a patient comes to the physical therapist with dysfunction of the musculoskeletal, neuromuscular, or other system and happens to have a secondary diagnosis of a cardiovascular or pulmonary condition, this diagnosis must be considered in overall management and the interventions modified accordingly. Because it is life-threatening, a secondary diagnosis of a cardiovascular or pulmonary condition may be more clinically important for the physical therapist to manage than the primary diagnosis (e.g., low back pain, osteoarthritis, or Parkinson syndrome).

Recent advances in understanding the pathophysiology of cardiovascular and pulmonary conditions have highlighted a common denominator: inflammation of the endothelium of the blood vessels and the epithelium of the airways. With increasing severity of the condition, proteins alter their structure, and repair is required to maintain their essential structure and function with the upregulation of reparative proteins.3 Activation of this defense system is triggered by ischemia, hypoxemia, and inflammation.

Myopathic changes have been observed in the peripheral muscles of people with chronic cardiovascular conditions and lung conditions (see Chapters 24 and 31). People with COPD, for example, have increased muscle fibrosis compared with age-matched people without the disease, and the cross-sectional area of type IIX muscle fibers is smaller.4

Some common causes underlying COPD have been proposed. The Dutch hypothesis explaining the development of both asthma and chronic obstructive lung disease proposes that environmental factors (e.g., smoking and air pollutants) are superimposed upon and interact with allergic and airway hyperresponsiveness components (genetic components). Smoking and airway hyperresponsiveness are the major risk factors for these conditions.5

It has been reported that gender plays a role in susceptibility to cardiovascular and pulmonary dysfunction, as well as in the severity of the dysfunction and the response to its management. This is reflected in the finding that women with COPD have an almost three-fold greater death rate than men. Specifically, women are more susceptible to the long-term adverse effects of smoking. Compared with men, they develop pathological changes more readily and have more severe symptomatology for a given long-term exposure to tobacco.6

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has proposed universal guidelines for the classification of COPD7 on the basis of both spirometry and clinical symptoms to define stage of disease (Table 5-1). Serum or tissue markers are being sought to provide a basis for an objective diagnosis and refine intervention strategies.8

Table 5-1

Universal Guidelines for the Classification of COPD

  Predicted FEV1/FVC FEV1
Mild COPD <70% ≥80%
Moderate COPD <70% <50% to 80%
Severe COPD <70% <30%

From Crapo RO, Morris AH, Gardner RM: Reference spirometric values using techniques and equipment that meet ATS recommendations, Am Rev Respir Dis 123:659-664, 1981.

Objective measures of limitations of structure and function or impairments associated with cardiovascular and pulmonary conditions are not necessarily closely associated with health-related quality of life. Outcome measures of health-related quality of life and life satisfaction are supplemental to structure and function outcomes and are now being included in the overall clinical assessment of people with these conditions.9 Thus management programs focus on interprofessional rehabilitation consisting of multiple components to address the complexity of the limitations associated with these conditions rather than traditional primary focus on limitations of functions and structures (see Chapters 1 and 17).10

This chapter describes common pathophysiology of the cardiovascular and pulmonary systems and some common conditions that affect these systems secondarily.

The first part of this chapter describes the pathophysiology of common cardiovascular conditions. CAD is manifested in various clinical syndromes and most commonly results from atherosclerosis in the coronary arteries, which ultimately affects heart performance (i.e., stroke volume and heart rate, hence, cardiac output). The causes of clinical syndromes associated with CAD and the medical management and prognoses are briefly reviewed.

The two classic types of lung pathophysiology (obstructive and restrictive) are then presented. Interdependent pathophysiology of these lung pathologies, which invariably affects the heart as well as the lung, is described in Chapters 6 and 31 (also in Chapters 16, 34, and 36, which are related to critical care). The structure and function of the cardiovascular and pulmonary systems are interdependent (see Chapters 2, 3, 4, 5 and 6).11 Dysfunction in one system can affect the function of the other.

Obstructive pulmonary conditions are characterized by a reduced expiratory airflow rate due to increased airway resistance. Restrictive pulmonary conditions are marked by the reduced inspiratory capacity of the lungs. Often, however, overlap exists between the two categories.

Coronary Artery Disease

Hypercholesterolemia

Although hypercholesterolemia is a primary risk factor for the development of atherosclerosis, increased cholesterol affects cardiac function independently in the absence of atherosclerosis and primary ischemic heart disease.12 Elevated cholesterol levels change the structure and function of cell membranes, which in turn, affects myocardial contractility, excitability, and conduction properties. In addition, smooth muscle and endothelial dysfunction occurs, and enzyme activity and cation transporters are disrupted throughout the cardiovascular system. Thus the consequences of hypercholesterolemia are pervasive and warrant assessment even in the absence of overt atherosclerosis and ischemic heart disease.

Atherosclerosis

Pathophysiology

Atherosclerosis is triggered by trauma to the intima of the arterial wall. The trauma may be related to various primary cardiac risk factors, such as high blood pressure and cigarette smoking. Oxidative stress has been identified as the common denominator for atherogenesis, acute myocardial infarction (MI), and heart failure.13 Healthy endothelium is central to optimal vascular control. High blood pressure has been identified as a trauma inducer because increased pressure and turbulence can damage the endothelial cells of the intima of the blood vessel wall, thus exposing the media to the circulation. The media, which consists primarily of smooth muscle, is thought to be the origin of the atherosclerotic lesion.

Cigarette smoking has also been identified as a potential inducer of trauma in the blood vessel wall. The hypothesized mode of injury appears to be different from that observed with increased blood pressure. Cigarette smoke is high in carbon monoxide and hydrocarbons that are carried by the red blood cells and the plasma. The hydrocarbons and carbon monoxide are thought to bind to the endothelial cells, causing damage to and possibly death of these cells.

Diabetes is another risk factor for cardiovascular disease of the myocardium and of the peripheral arteries.14 The reduced contractility of the heart in people with diabetes is attributed to reduced calcium handling in the sarcoplasmic reticulum of muscle.

Once the media is exposed to the circulation, the process of atherosclerosis is initiated and this predisposes an individual to thromboembolic events, in even mild cases. Platelets aggregate at the injury site and release substances that induce endothelial and smooth muscle cell replication. It is at this site that fatty streaks and fibrous plaques develop. The cause of fatty-streak development is the deposition of low-density lipoproteins (LDLs) into the smooth muscle of the media. Why this occurs is unknown, but it appears to be related to smooth muscle cell proliferation and perhaps to increased energy demands. The initial fatty streaks are generally raised only slightly and do not impede circulation. When a fibrous plaque develops, however, impingement on the vessel lumen occurs. The plaque is relatively hard and consists of connective scar-like tissue, smooth muscle, and fat. Finally, the plaque may undergo calcification or may lead to hemorrhaging if the vessel wall necroses. The result is decreased blood flow (ischemia) and oxygenation (hypoxia) or complete lack of blood flow and oxygen (anoxia) to the target organ.

Atherothrombosis is a generalized and diffuse progressive process affecting multiple vascular beds.15,16 The clinical consequences include the acute coronary syndromes, ischemic stroke, and peripheral arterial disease. Thus these conditions can be viewed as diverse manifestations of a common underlying pathology. The time course of these conditions is unpredictable; yet they can be life-threatening.

Thyroid is an important regulator of cardiac function and cardiovascular hemodynamics.17 The effects of the physiologically active form of thyroid hormone triiodothyronine (T3) on the systemic vasculature include relaxation of the vascular smooth muscle, hence reduced resistance and diastolic blood pressure. In hypothyroidism, cardiac contractility and cardiac output are decreased and systemic vascular resistance is increased, whereas the opposite occurs in hyperthyroidism. Cardiac dysfunction is associated with low levels of T3.

Because of the current appreciation and understanding of the involvement of inflammation and endothelial injury in cardiovascular dysfunction, endothelial function biomarkers have been proposed as a sensitive means of evaluating cardiovascular disease.18,19

Risk Factors

As described earlier, high blood pressure, cigarette smoking, and hyperlipidemia are direct or primary risk factors for atherosclerosis. Secondary risk factors include age, gender, race, obesity, stress, and activity level. Modifiable risk factors include hypertension, hyperlipidemia, smoking, obesity, abnormal glucose tolerance and diabetes, stress level, and activity level. Homocysteine levels have a strong relationship with atherothrombotic disease and venous thromboembolism, and elevated levels may indicate thrombotic tendencies in individuals, particularly those who are younger, in the absence of other established risk factors.20 Homocysteine levels can be reduced and regulated through diet by increasing fruit and vegetable intake. Recently, the tendency to panic has been implicated as a risk factor for cardiovascular disease,21 and depression can result in a worse outcome.22

Vascular calcification is an established marker of atherosclerosis, which leads to increased arterial stiffness and reduced compliance and increased pulse pressure. Vascular calcification is highly correlated with mortality resulting from cardiovascular disease, particularly if diabetes or renal disease complicates the clinical presentation.23,24 The three primary risk factors—diet, hypertension, and smoking—are modifiable by the individual, and altering the diet alone can reduce the probability of CAD five- to ten-fold.25,26,27

A proposed and potentially underestimated risk factor for cardiovascular disease is related to circadian rhythms.28 It has been well established that people with heart failure have a higher rate of mortality in the early morning hours. This probably reflects diurnal variations in neurohumoral factors, including the activity of the sympathetic nervous system. The cardiac circadian clock synchronizes the response of the heart to the diurnal variations in the environment. Impairment of this mechanism could contribute to the pathogenesis of cardiovascular disease.

Aging has been implicated in lowering the threshold for the manifestation of cardiovascular disease.29 Stiffening of the arteries increases afterload and alters left ventricular architecture. Left ventricular diastolic function changes, whereas systolic function remains unchanged.

Angina Pectoris

Angina pectoris is defined as chest pain that is related to ischemia of the myocardium. Ischemic pain, however, may be referred to the left shoulder, neck, jaw, or between the shoulder blades. In fact, pain anywhere above the umbilicus could be related to coronary ischemia. Angina can be classified as stable, unstable, or variant. People with chest pain but normal coronary arteries on angiography tend to be women, and this presentation is not as benign as previously believed.30 With the advent of the ability to assess endothelial function, those at risk may be more readily identified and managed.

Prognosis of Angina

Individuals do not die of angina per se. The progression of atherosclerosis of the coronary arteries is reflected in the clinical changes that occur between the experience of angina and an MI. Even though there is no risk of mortality as a result of angina, an individual’s lifestyle can change drastically. People with angina may be fearful of being active and may deny that they are having exertional chest pain. Denial, depression, anger, and hostility are common psychosocial correlates.31 Depression and further reduction in physical activity can be associated with angina (diagnosed or undiagnosed and denied). Although restricted activity is an important component of initial treatment, low levels of activity can modify several risk factors and arrest the progression of atherosclerosis.32 In addition, diet and exercise have been documented to reverse atherosclerosis.25,26,33

Obstructive Sleep Apnea Syndrome

Obstructive sleep apnea (OSA) has a greater incidence in individuals with atherosclerosis, cardiac dysrhythmias, and hypertension than in those without.34 This has been explained in part by the presence of proinflammatory and prothrombotic factors.35 OSA is characterized by the repetitive closing and opening of the posterior pharynx that are synchronized with breathing while sleeping, usually when recumbent. Apneic periods and arterial desaturation are also common to the syndrome. Additional pathologies common to OSA and atherosclerosis include endothelial dysfunction, increased C-reactive protein, fibrinogen, reduced fibrinolytic activities, and increased platelet activity and aggregation. OSA is now considered a risk factor for cardiovascular disease. The complications of sleep apnea syndrome are exacerbated by autonomic dysfunction as well. Sleep apnea often coexists undiagnosed in people with cardiovascular disease, activates mechanisms known to aggravate and advance cardiovascular injury, and contributes to resistance to therapeutic interventions.34

Myocardial Infarction

MI is defined as necrosis of a portion of the myocardium. The death of the myocardium occurs as a result of ischemia and anoxia. The vessels affected by occlusion are the right and left coronary arteries and their anterior and posterior descending branches. The right coronary artery supplies the posterior section and portions of the inferior section of the left ventricle. The left coronary artery branches and forms the circumflex and anterior descending arteries. The circumflex supplies the lateral portion of the left ventricle, and the anterior descending artery supplies the anterior portion. In addition, the right coronary artery supplies the right atrium atrioventricular bundle and the right ventricle. The left coronary artery supplies the left atrium and the primary portion of the conduction pathway. Generally, the clinical symptoms are similar to those of angina, with emphasis on extreme pressure as well as tightness over the sternal region. In addition, pain can radiate to the jaw, upper back, and shoulders (on the left more often than on the right).

MIs are categorized by location, size, and degree of involvement of the myocardial wall. The terms small and large are often used to describe MIs. Degrees of complication are also used in conjunction with size. MIs can be described as uncomplicated and complicated, based on the size of the MI and the patient’s recovery. Location indicates the area of the heart involved and the coronary artery or branches that are involved. The anatomic areas of the heart are differentiated as anterior, posterior, lateral, and inferior. Finally, MIs are classified by the extent of damage to the wall. A transmural (or full-wall) infarct extends from the endocardium to the epicardium, whereas only some involvement of the ventricle wall may occur, for example, just beneath the epicardium (subepicardial) or just beneath the endocardium (subendocardial).

Silent ischemia is particularly prevalent in patients with high cardiac risk and is associated with a poor outcome.36 Silent MIs can be detected when a patient has undergone ECG investigation or imaging for other problems.

Uncomplicated Myocardial Infarction

An uncomplicated MI is described as a small infarction with no complications during recovery. Usually the result is full recovery without a significant decrease in cardiac performance at rest and during minimal to moderate activity.37 Location and the extent of the MI are critical with respect to outcome. MIs located in the inferior portion of the heart are considered the least clinically significant, and partial-wall-thickness MIs are less significant than transmural MIs.

Treatment

Initially, the treatment of a patient with an uncomplicated MI is comparable to that of a patient with a complicated MI, so the patient is cared for in a coronary care unit. The medical treatment is designed to decrease myocardial work and oxygen demand. Patients receive supplemental oxygen and are administered coronary vasodilators (nitroglycerin) to increase myocardial blood flow and analgesics to reduce ischemic pain. In addition, calcium channel blockers or beta blockers are administered to reduce the contractility and work of the myocardium. Antidysrhythmia medication may be prescribed if an aberrant cardiac rhythm is present or likely to occur.

Because the clinical course is uncomplicated, a patient’s stay in the coronary care unit may be only a couple of days, with a total hospital stay of 3 to 5 days. Once the patient’s condition is stabilized, management is oriented toward increasing physical activity and educating the patient and family with respect to risk factor reduction (see Chapters 29, 30, and 31).38 This process is described as cardiac rehabilitation, phase I (see Chapter 30).

Complicated Myocardial Infarction

A complicated MI is distinct from an uncomplicated case because the patient may have one, a combination, or all four of the following complications: dysrhythmia, heart failure, thrombosis, and damage to heart structures.

Dysrhythmias

Dysrhythmias occur in 95% of patients with MIs. The type and severity of the dysrhythmia is dependent on the location and extent of the myocardial damage. Imbalance in autonomic regulation has been implicated in dysrhythmogenesis and sudden cardiac death.39 Blunted heart rate variability has been established as a marker of sympathovagal imbalance and can serve as an indicator of cardiac risk.

The risk for serious or frequent dysrhythmias is lower in a patient with an uncomplicated MI because a small area of the myocardium is involved. Dysrhythmias that are life-threatening include complete AV heart block, ventricular-paced dysrhythmia, and ventricular tachycardia including ventricular flutter and fibrillation. In these conditions, either heart rate (comprising stroke volume, ejection fraction, and overall cardiac output) is too slow and cardiac output is impaired, or heart rate is too fast. Treatment of these conditions is immediate and requires drugs. If refractory to conservative management, cardioversion or electric shock (for flutter and fibrillation) is indicated. If a normal rhythm cannot be restored and maintained by the patient’s own inherent pacemaker, an artificial pacemaker may have to be implanted.

Dysrhythmias may be present in the absence of overt myocardial ischemia or heart damage. Common dysrhythmias are presented in Chapter 4, and their clinical implications are presented in Chapter 12. One conduction abnormality that is receiving increasing attention is atrial fibrillation.40 This dysrhythmia warrants management, given its association with thromboemboli and stroke (see Chapters 6 and 32). Furthermore, atrial fibrillation is the most common dysrhythmia associated with cardiac surgery (25% to 60%), and it leads to increased postoperative morbidity and mortality and to associated health care costs.41,42 Atrial fibrillation has been reported to be more common in men—and also to be better tolerated by them than by women.43

Heart Failure

Another complication after MI is cardiac insufficiency and failure. Heart failure is a condition in which the heart is weakened by myocardial damage and is unable to provide cardiac output to meet the body’s metabolic needs for oxygen, nutrition, and removal of waste products. When the heart experiences ischemia, the myocardium contracts with less force and conduction abnormalities may alter the mechanics of the contraction. If an area of the heart is infarcted, the affected myocardium does not contract, thus affecting overall cardiac output. Another type of heart failure not directly related to ischemia and infarction is congestive heart failure (described in the next section).

Recent terminology regarding the classification of heart failure differentiates diastolic and systolic heart failure.44–47 Diastolic heart failure refers to the presence of the symptoms of heart failure in the absence of left ventricular dysfunction, the hallmark of systolic heart failure. Diastolic heart failure in which the left ventricle is stiff (reduced compliance and impaired relaxation resulting in increased end diastolic pressure) has been estimated to account for 40% to 50% of all cases of heart failure.48 Diastolic dysfunction has been of increasing interest in nonprimary heart disease such as systemic sclerosis, and it appears to be more common than previously thought.49 The two types of heart failure must be distinguished on the basis of Doppler echocardiography because their signs and symptoms are comparable. Both types are associated with marked morbidity and mortality.

Immediately post-MI, cardiac output is markedly reduced. The compensatory response of the body is to increase sympathetic and renin-angiotensin-aldosterone stimulation, resulting in increased heart rate and myocardial contractility. The result of this compensation is to normalize cardiac output to normal resting values. If myocardial damage is extensive, the kidneys compensate by retaining sodium and water to improve circulatory volume and venous return. Depending on the amount of myocardial tissue death, the individual may survive, but with resulting chronic congestive heart failure through persistent fluid retention and hypotension. If more than 40% of the left ventricle is infarcted, the result is usually cardiogenic shock followed by the death of the individual. Renin-angiotensin-aldosterone activation contributes to left ventricular remodeling, which is further augmented by vascular endothelial dysfunction, resulting in decreased nitric oxide bioavailability.50

Diabetic cardiomyopathy leads to heart failure independent of underlying coronary artery disease.51 Both structural and functional abnormalities associated with diabetic cardiomyopathy have been linked to an underlying metabolic disorder. Other factors include myocardial fibrosis due to an inflammatory process, small blood vessel pathology, cardiac autonomic neuropathy, and insulin resistance.52

Thrombosis

Deep vein thrombosis (DVT) and related pulmonary emboli are largely preventable clinical complications, and when they do occur, their diagnosis may be missed in hospitalized patients.53,54 These life-threatening complications are serious and warrant early detection. Mortality resulting from thrombi that migrate to the lungs (pulmonary emboli) is greatest initially after an acute MI. DVTs can be challenging to detect because of the lack of specificity of their clinical presentation. Another complication is increased incidence of thrombosis originating in deep leg veins and in the damaged heart itself. Thrombosis that starts in deep leg veins occurs because of lower limb inactivity and circulatory stasis. This is a complication that can be observed in patients after surgery. Emboli from a deep leg vein thrombus usually cause pulmonary complications. If the emboli are large or numerous, the result can be pulmonary tissue infarction and death. The incidence of pulmonary emboli has been reduced because patients now are usually ambulated soon after a medical event or surgery. Nonetheless, a pulmonary embolus must be considered a distinct possibility in all patients after an MI, surgery, or major trauma.

Heart, or mural wall, thrombosis can lead to an embolus lodging in the brain, intestine, kidney, artery to the extremities, or any location in the systemic arterial circulation. Usually, mural thrombi do not affect the pulmonary system because the small fragments become lodged in the capillaries and fail to access the venous system.

Structural Damage

Structural damage to the myocardium is another serious complication of MI. If the neural conduction pathway (bundle branch) located primarily within the septum is damaged, dysrhythmias result. In addition, papillary muscles that regulate heart valve closure can be infarcted. Valve incompetence leads to regurgitation and retrograde flow of blood from the ventricles, thus impeding the forward movement of blood through the heart and decreasing cardiac output. Full-thickness damage to the myocardial wall from atherosclerotic plaques significantly compromises normal cardiac function. Heart wall damage can result in ventricular aneurysms or ventricular wall rupture. Ventricular aneurysm, or the bulging of the weakened ventricular wall, occurs in transmural (full-wall-thickness) infarcts. Ventricular wall rupture, which can occur acutely after transmural infarction but is more common in the first to second week post-MI after an aneurysm, is usually fatal. Therefore, after an MI, it is critical to determine whether an aneurysm has occurred within the myocardium so that appropriate surgical intervention can be performed.

Risk factors for cardiac rupture include being female, being older, having hypertension, and experiencing the first cardiac event.55 Clinical signs of rupture include syncope, chest pain, and jugular venous distention. In addition, defective ventricular remodeling may predispose the heart to rupturing.

Treatment

The treatment of a complicated MI is initially like that of an uncomplicated MI, where the patient is cared for in the coronary care unit. Similarly, medical treatment is designed to decrease myocardial work and oxygen demand. Patients receive supplemental oxygen and coronary vasodilators (nitroglycerin) to increase myocardial blood flow and analgesics to help further reduce ischemic pain. Myocardium calcium channel blockers or beta blockers are administered to reduce contractility. Finally, antidysrhythmia medication is prescribed to stabilize the electrical conduction system of the heart or if an aberrant cardiac rhythm is present.

Patients with complicated MIs require longer stays in the coronary care unit, and their total hospital stay times are longer than those of patients with uncomplicated MIs. The time in coronary care and total hospital stay are dependent on the complications that occur after the MI. Individuals with heart failure, thrombolytic events, or structural damage requiring surgery may be in the coronary care unit for a couple of weeks. Total hospital-stay times for patients with complicated MIs may exceed this length of time. Treatment after discharge from the intensive care unit, however, is similar to that of the patient with an uncomplicated MI; the goal is to increase physical activity and educate the patient and family in risk-factor reduction. The major difference in phase I cardiac rehabilitation for patients with complicated rather than uncomplicated MIs is the intensity, duration, and frequency of the initial exercise workload (i.e., a much lighter workload is prescribed for patients with complicated MI).56 These patients also require closer monitoring. Progression is more conservative because patients are at higher risk after a complicated MI than after an uncomplicated MI.56

Prognosis after a Myocardial Infarction

After an MI, the prognosis depends on many factors. Compared with the patient’s premorbid status, cardiovascular performance is reduced, unless the structural damage to the ventricle is minor (as in the case of many patients with uncomplicated MIs). The most important factor is the extent of ventricular damage. With early detection of transmural infarction and improvement in surgical intervention and coronary care, however, the number of acute post-MI deaths has been reduced.38 Other critical factors include remaining cardiac capacity and cardiac status and risk factors. Even though CAD mortality has declined in the United States, the disease remains the leading cause of death in adults.

Severe infarction can necessitate emergency or elective revascularization surgery. Emergency surgery for an acute MI complicated by cardiogenic shock is associated with satisfactory long-term survival; however, perioperative risk is high.57

Congestive Heart Failure

Congestive heart failure (CHF) is a leading cause of hospitalization and death. It is characterized by the inability of the heart to maintain adequate cardiac output. The incidence of congestive heart failure appears to be increasing because of the prevalence of injurious lifestyle behaviors, aging, and improved survival after acute cardiac episodes.58

Almost half of all patients with congestive heart failure are women.59 Smoking, diabetes, and high blood pressure are stronger risk factors for CHF in women than in men. Peripartum cardiomyopathy, which is unique to women in their childbearing years, occurs either in the late stages of pregnancy or within several months after giving birth.

The causative factors of heart failure are usually ischemia and MI secondary to ischemic heart disease. For the heart to maintain optimal blood flow to the pulmonary and systemic circulations, heart rate and stroke volume must be adequate. If heart rate is regular and within an acceptable range, stroke volume is the critical factor for maintaining adequate cardiac output. Stroke volume is a function of the amount of blood in the left ventricle at the end of diastole (preload); the amount of pressure and resistance the heart must overcome to eject blood into the systemic circulation (afterload); and myocardial contractility, which is the amount of force the left ventricle can apply to the blood within the chamber. If any one of these three variables is adversely affected, cardiac output is reduced. Progressive deterioration of myocardial contractility and dilation and fluid overload precipitate heart failure.

Dyspnea is the primary complaint of people with congestive heart failure. It can be challenging to distinguish between dyspnea resulting from CHF and dyspnea resulting from pulmonary causes. B-type natriuretic peptide (BNP) is synthesized, stored, and released in the ventricular myocardium, and it is stimulated by changes in ventricular wall tension and stretch.60 The use of BNP holds some promise as a marker for congestive heart failure and a guide to clinical management.

Congestive heart failure is a major contributor to progressive renal dysfunction and anemia.61 Anemia is observed in one-third of all patients with CHF. Conversely, chronic renal dysfunction can cause severe cardiac injury and is often associated with anemia. Thus congestive heart failure, chronic renal insufficiency, and anemia create a vicious circle that warrants aggressive medical management to attenuate the progression of the three conditions.

Acute Heart Failure

If an individual has a significant MI, the contractility and pumping ability of the heart is immediately reduced. The initial result is decreased cardiac output and the damming of blood in the veins. (The damming of blood in the pulmonary circulation leads to congestive heart failure, as discussed earlier.) The result is increased systemic venous pressure. This acute phase, which may reduce cardiac output to 40% of normal resting values, is short-lived, lasting only a few seconds before the sympathetic nervous system is stimulated, and the parasympathetics become reciprocally inhibited. Sympathetic innervation causes an increase in the contractility of viable myocardial tissue, and the increase in cardiac output may be 100%. In addition, sympathetic innervation increases venous return because the tone of blood vessels is increased. The result is increased systemic filling pressure and, thus, increased preload. The sympathetic reflex after MI becomes maximally operational within 30 seconds; therefore, except for some pain and fainting, individuals experiencing mild MIs may not know they have suffered a heart attack. The sympathetic response can continue if cardiac output is maintained at an adequate level at rest. Ischemic pain, however, may persist and warrants treatment.

Chronic Heart Failure

After an MI, several physiological responses occur along with sympathetic reflex compensation. The kidneys retain fluid almost immediately after an MI. A decrease in glomerular pressure secondary to decreased cardiac output is implicated. In addition, there is an increase in renin output and therefore an increase in angiotensin production. Angiotensin promotes reabsorption of water and salt from the renal tubules. The effect of moderate fluid retention is an increase in blood volume and venous return. This increases preload, hence cardiac output. If the MI was severe, however, the result can be excessive fluid retention. This results in systemic edema and overstretching of the heart due to excessive blood volume and venous return. In the chronic state, this condition is termed chronic heart failure.

Recovery of the damaged myocardium occurs after MI. New collateral arteries are formed to supply the peripheral portions of the infarcted region. This revascularization can assist marginally active cells to become fully functional again. In addition, the unaffected myocardial cells hypertrophy. In a mild to moderate MI, such recovery can result in major improvement in cardiac function and can take 6 weeks to several months, depending on extent of injury.

Gas transfer across the alveolar-capillary membrane is impeded in CHF. This may be explained by the pressure and volume overloading, which injures the alveolar blood-gas barrier, hence impairing the diffusion of blood across it.62 In the short term these changes may be reversible. If the membrane is chronically challenged, however, the anatomic and physiological integrity of the membrane is remodeled. These changes have been associated with worsened symptoms and exercise tolerance. Further, these changes may be prognostic of patient outcome.

Cardiac remodeling is a central feature of heart-failure progression.63 Remodeling refers to the alteration of the structure and geometry of the heart in response to myocardial insult or pressure or volume overload. Such remodeling reflects the adaptation that is needed to maintain adequate heart function with changing conditions. Increased muscle mass is one of the primary adaptations, and it usually involves left ventricular hypertrophy.64 Adaptive hypertrophy of the left ventricle is clinically important in that it is associated with increased morbidity and mortality rates.65 A further consequence of adaptive cardiac hypertrophy is the potential for reduced responsiveness to the metabolic and functional effects of insulin, which further contributes to the heart’s hypoeffectiveness.66 Pharmacological studies have been conducted to examine the role of drugs on the remodeling process in individuals with heart failure. Studies of the role of nonpharmacological interventions, including exercise, in cardiac remodeling have not been made.

A reciprocal relationship between CHF and diabetes has been well established.67 People with CHF may be at increased risk for diabetes due to reduced physical activity, cellular metabolic defects, reduced muscle perfusion, and poor nutrition. The increased sympathetic stimulation associated with CHF increases insulin resistance and decreases insulin release from the beta cells of the pancreas. Both factors contribute to glucose intolerance and diabetes, which in turn lead to hyperglycemia and increased risk for cardiovascular and metabolic complications.

Even in patients with chronic heart failure, regular exercise may be associated with a protective metabolic phenotype.68 This effect of exercise could explain why fit people have less severe MIs than nonfit people.

Compensated and Decompensated Heart Failure

Compensated heart failure is the final stage after the acute, then chronic, physiological compensation for cardiac dysfunction. In this state the heart can pump blood effectively but at a reduced cardiac output compared with the pre-MI condition. The individual’s cardiac reserve, that is, the difference between maximum and resting cardiac output, is greatly reduced. With even small increases in metabolic demand through exercise, symptoms of acute failure reappear because the limits of compensation are exceeded. These symptoms include rapid heart rate, pallor, and diaphoresis.

Decompensated heart failure affects 5 million Americans and is associated with a 5-year mortality rate of almost 50%.69 Decompensated failure occurs when the heart is so severely damaged or weakened that normal cardiac output cannot be attained. This type of failure is defined as a sustained deterioration of at least one New York Heart Association functional class, usually with evidence of sodium retention.70 Cardiac output is insufficient to maintain normal renal function. Fluid continues to accumulate so the heart is stretched and weakened further, permitting only moderate to low quantities of blood to be pumped. In unilateral heart failure, the left ventricle may fail while the right ventricle continues to pump vigorously. Blood volume and pulmonary capillary pressure increase. If this occurs, fluid filters into the interstitial spaces of the alveoli, resulting in pulmonary edema, impaired gas exchange, and suffocation. As the heart weakens, not only is systemic blood flow compromised, so is the coronary system. The area most affected is the subendocardial region. As these cells become infarcted, the heart weakens further until other regions of the heart also become ischemic and infarcted.

Prognosis

End-stage cardiac disease without effective pharmaceutical or surgical intervention, including revascularization or heart transplantation, results in death. Intermediate measures to avert deterioration have emerged, including cardiac resynchronization therapy through biventricular pacing.71 The addition of implantable cardioverter defibrillators may help to minimize the occurrence of sudden death in people with CHF. Left-ventricle assistance devices may be used to support the function of the failing heart until it responds to conservative management or until surgery is scheduled.72 Surgical ventricular restoration holds some promise for reversing inappropriate remodeling of the myocardium after infarction and restoring its normal elliptical shape.73 The primary pharmaceutical interventions used to mitigate heart failure include diuretics to reduce fluid overload and cardiac glycosides such as digitalis to improve myocardial contractility. These interventions are combined with modification of salt and fluid intake. Other factors can predict a poor outcome. Sleep apnea syndrome, for example, is common in people with CHF and is associated with a poor prognosis. As ejection fraction is decreased, the risk for thrombus formation and stroke increases.74

In cases where the heart has compensated poorly and remains weak and the cardiac output is minimal, heart transplant is the only recourse. Because organ donors are not readily available, the number of individuals who need new hearts far exceeds the available donor organs. Posttransplant prognosis is related to the recipient’s surgical suitability and the health of the donor organ. The prognosis will also reflect the amount of cardiac reserve.

Valvular Heart Disease

Heart valve incompetence is classified as being either congenital or acquired (i.e., after a bacterial or viral infection of the heart valves) and can affect any one of the four heart valves. Surgical repair or replacement of defective mitral valves, tricuspid valves, and aortic valves constitutes a significant proportion of cardiac surgeries. Mitral and aortic valve disease is particularly common in people over 65 years of age.75,76 In this age group, symptoms can be masked by such comorbidities as cardiovascular disease, pulmonary disease, and hypertension. Surgical repair is associated with favorable short- and long-term outcomes. Some valve defects are benign and treatment is not indicated. Some people can tolerate heart valve defects as children, but they become symptomatic with age. Currently, these types of valve defects are often corrected at birth or early in life.

One common valve defect is prolapse of the mitral valve, which is more common in women than in men and may warrant repair.

Cardiac defects may be present as secondary diagnoses in an individual being managed by a physical therapist. Such defects need to be considered in terms of an individual’s capacity to respond to exercise, as well as the condition’s overall effect on the individual’s life. Exercise limitation secondary to heart valve disease may mask limitations due to other causes, or vice versa.

Athletic Heart Syndrome

Although physical fitness is associated with innumerable health benefits (see Chapters 1 and 18), cardiovascular adaptation to intense exercise in athletes (athletic heart syndrome) can mimic disease processes associated with cardiovascular disease.77 Sudden cardiac death in athletes is often associated with cardiac hypertrophy, dysrhythmias, or both. In addition, cardiac episodes in athletes may reflect the manifestation of congenital abnormalities in electrical activity or mechanical function of the heart. Thus screening athletes for cardiovascular adaptation is warranted. Physical therapists involved with sports teams need to be vigilant regarding risk factors associated with the athletic heart syndrome to detect and avoid untoward events.

Systemic Hypertension

Systemic hypertension, or wide pulse pressure hypertension, has become increasingly prevalent and is implicated in multiorgan dysfunction, not only in cardiac dysfunction and failure (see Chapter 1). Systolic hypertension syndrome refers to a complex of hemodynamic maladaptations, including stiff central arteries, normal peripheral arteries, arteriolar constriction, metabolic abnormalities, cardiac hypertrophy, and increased blood pressure variability.78 In addition to the conventional measures of hemodynamic status, measures of arterial mechanics, including arterial compliance, elastic modulus, impedance, pulse wave velocity, and pulse pressure amplification, are used for diagnosis and management.

Hypertension is strongly implicated in cardiovascular disease and stroke.79 When systemic hypertension syndrome advances to heart disease, the prognosis is poor.80

Obesity is considered a primary risk factor for hypertension, as well as for heart disease, stroke, and renal dysfunction. Mechanisms that have been proposed for obesity-related hypertension include insulin resistance, hyperinsulinemia, dyslipidemia, increased sympathetic activity, sodium and water retention, cardiac dysfunction, and endothelial dysfunction.81 To adapt to an increasing workload, the heart enlarges. When it can no longer adequately compensate, the heart begins to fail, and that is usually coupled with respiratory failure. Myocardial hypertrophy is considered an independent risk factor for cardiovascular disease in people who are obese and is a strong predictor of heart failure.

The occurrence and clinical implications of myocardial fibrosis in people with hypertension are well established.82 The rennin-angiotensin-aldosterone system and contributions of mineralocorticoids and endothelin have been implicated in the development of myocardial fibrosis.

Thyroid hormone has well-documented effects on cardiovascular function, including blood pressure.17 In hyperthyroidism, pulse pressure is increased, whereas in hypothyroidism, pulse pressure is narrowed. Adaptations of the cardiovascular system alter blood pressure to accommodate new demands on the system. The effects of thyroid hormone on blood pressure, therefore, are mediated both directly and indirectly.

Pulmonary Hypertension

Pulmonary hypertension is increasingly recognized as a pathology that can occur secondary to some other pulmonary condition or with no apparent cause (idiopathic pulmonary hypertension). By definition, pulmonary hypertension exists when the mean pulmonary pressure is greater than 25 mm Hg at rest and greater than 30 mm Hg during exercise.83 Pulmonary blood pressure can increase in response to increased pulmonary vascular resistance, blood flow, and pulmonary artery wedge pressure. The cause of pulmonary hypertension has shifted from being attributed to vasoconstrictive dysfunction to being attributed to angioproliferative dysfunction.84 Endothelial dysfunction has been implicated.85 Although the prognosis is variable, with some people surviving months and others decades, guidelines have been recommended to assess the prognosis for individuals with pulmonary artery hypertension and to institute appropriate intervention expeditiously.86

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