Cardiovascular and Pulmonary Phy-PDF

CHAPTER 4 44 Cardiopulmonary Pathology 99 LV Diastolic Dysfunction 3 Possible Dyspnea,...

CHAPTER 4 44 Cardiopulmonary Pathology 99 LV Diastolic Dysfunction 3 Possible Dyspnea, pulmonary cough, edema Exercise tolerance 3 Pulmonary vascular Dyspnea volume and pressure on exertion 4 Pressure Arterial Lightheadedness, Venous load on RV system JVD dizziness system Liver, RVH Exercise ascites 2 tolerance 6 Impaired RV pump function LE edema, Muscle weight gain LA volume weakness, 2 RV failure and pressure fatigue 2 5 5 RA volume 1 6 Systemic EDP at any 2 CO even though and pressure 4 venous pressure volume nL EF 1 Prolonged relaxation and ventricular Coronary compliance driving pressure Angina or its Myocardial LV filling rate equivalents ischemia LV passive filling volume and EDV Dependence on active if HR or atrial contraction arrhythmias 1 = Primary cardiac problem # = Resulting forward problems = Increased Clinical manifestations are encircled # = Resulting backward problems = Decreased Figure 4-12: The pathophysiology of ventricular diastolic dysfunction, which develops early in the process of hypertensive heart disease and also occurs during myocardial ischemia and in other causes of ventricular hypertrophy. The initial pathophysiological effect is prolongation of ventricular relaxation, which results in a less compliant (stiffer) ventricle. As LV dysfunction progresses, its effects on the lungs and RV, as well as on cardiac output, become more apparent. The clinical manifestations associated with various events are encircled. CO, Cardiac output; EDP, end-diastolic pressure; EDV, end-diastolic volume; ESV, end-systolic volume; HR, heart rate; JVD, jugular venous distension; LA, left atrial; LE, lower extremity; LV, left ventricular; RA, right atrial; RV, right ventricular; RVH, right ventricular hypertrophy. between SBP and diastolic blood pressure [DBP]) if 60 mm Hg Atherosclerotic heart disease are strong predictors of CVD risk.49,80 Renal insufficiency or failure, nephrosclerosis Aortic aneurysm, simple or dissecting Clinical Manifestations Peripheral vascular disease HTN is generally asymptomatic until complications develop in Retinopathy target organs, resulting in: The clinical manifestations of hypertensive heart disease An accelerated, malignant course include the following: Cerebral vascular accident Exertional dyspnea Hypertensive heart disease Fatigue 100 CARDIOVASCULAR AND PULMONARY PHYSICAL THERAPY LV Systolic Dysfunction Dyspnea, 3 Possible cough, pulmonary Exercise edema tolerance 3 Pulmonary vascular volume and pressure Dyspnea on exertion 4 Pressure Arterial Lightheadedness, JVD Venous load on RV system dizziness system Liver, RVH Exercise ascites 2 tolerance 6 Impaired RV pump function Weakness, LE edema, 2 LA volume weight gain fatigue and pressure RV failure 2 5 1 EDV and EDP 6 Systemic 5 RA volume 4 2 CO venous pressure and pressure ESV 1 Impaired LV pump function SV EF 1 = Primary cardiac problem # = Resulting forward problems = Increased Clinical manifestations are encircled # = Resulting backward problems = Decreased Figure 4-13: The pathophysiology of ventricular systolic dysfunction, which is induced by many pathologies that eventually lead to impairment of pump function. The results include reductions in ejection fraction (EF) and stroke volume (SV) with consequently increased end-systolic volume (ESV), as well as increases in end-diatolic volume and pressure (EDV and EDP, respectively). The elevated filling pressures are transmitted back to the pulmonary vasculature. As LV dysfunction progresses, its effects on the pulmonary vessels and RV, as well as on cardiac output, become important. CO, Cardiac output; JVD, jugular venous pressure; LA, left atrial; LE, lower extremity; LV, left ventricular; RA, right atrial; RV, right ventricular; RVH, right ventricular hypertrophy. Impaired exercise tolerance Pharmacologic therapy (see Chapter 5, page 168): Increased symptoms with tachycardia and loss of active atrial 4 Diuretics contraction 4 b-Blockers Exertional chest discomfort 4 a-Blockers Possible signs and symptoms of heart failure (see page 109) 4 Calcium channel blockers (CCBs) 4 Angiotensin-converting enzyme (ACE) inhibitors 4 Angiotensin receptor blockers (ARBs) Specific Treatment 4 Vasopeptidase inhibitors (VPIs) Successful treatment of HTN usually requires two or more medica- Lifestyle modifications: tions along with lifestyle modifications. For most patients the goal 4 Weight reduction (SBP and DBP decrease
1 mm Hg for is to achieve a BP less than 140/90 mm Hg; however, lower levels every kilogram of weight loss)167 (35 in. (88 cm) for females{ Sedentary lifestyle Persons not participating in a regular exercise program or not accumulating 30 minutes of moderate physical activity on most days of the week CV disease History of angina, MI, peripheral arterial disease, TIA, ischemic stroke Other Factors " Triglycerides 150 mg/dL Thrombogenic/hemostatic " Levels of fibrinogen, plasminogen activator inhibitor-1, tissue factor, tissue plasminogen activator factors antigen Infection/inflammation High-sensitivity CRP >3 Ethnicity, socioeconomic African Americans, non-Hispanic whites, Hispanic Americans, lower socioeconomic class class Psychosocial factors Depression, mental stress, chronic hostility, social isolation, perceived lack of social support Exogenous estrogens Hormone replacement therapy started >10 yr after onset of menopause{ Alcohol consumption No consumption or >1 drink per day for females, >2 drinks per day for males Other medical conditions Examples: rheumatoid arthritis, systemic lupus ", Increased; BMI, body mass index; CRP, C-reactive protein; CV, cardiovascular; DBP, diastolic blood pressure; DM, diabetes mellitus; HDL, high-density lipoprotein; LDL, low-density lipoprotein; MI, myocardial infarction; SBP, systolic blood pressure; TIA, transient ischemic attack. *Unless otherwise noted, all data is compiled from American College of Sports Medicine: ASCM’s Resource Manual for Guidelines for Exercise Testing and Prescription. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2001; and Zipes DP, Libby P, Bonow PO, Braunwald E, editors. Braunwald’s Heart Disease. 7th ed. Philadelphia: Saunders; 2005. { Refer to Table 6-31 on page 287. { Based on data from references 149a,149b,164, and 198a. mass index (BMI) or abdominal obesity, is a leading risk factor for of women with chest pain.182 Newer techniques using magnetic major cardiovascular morbidity and death in women. In addition, resonance spectroscopy appear to be more useful.141 clustering of traditional and novel risk factors (e.g., metabolic syn- The majority of women (and some men) who undergo coro- drome plus inflammation, as indicated by high levels of high-sensi- nary angiography for evaluation of chest pain do not show sig- tivity C-reactive protein) further intensifies the risk in women.141 nificant obstructive coronary disease, but are more likely to The role of hormone replacement therapy (HRT) in relation to exhibit abnormal microvascular coronary flow reserve and risk for CAD has been controversial. For years HRT was pre- macrovascular endothelial dysfunction.123,190 scribed to protect against the increase in CVD that occurs after Women with persistent chest pain despite normal coronary menopause. However, major research studies have failed to doc- angiograms and those who demonstrate endothelial dysfun- ument CV benefits despite desirable changes in lipid levels, and in ction experience significantly more adverse cardiovascular fact, one study found an increased risk of CVD in some women events, including acute myocardial infarction, CHF, stroke, taking HRT, mainly during the first year of treatment.149b,163c Fur- and death.32,123 ther analyses of the data reveal that HRT, when started early in After suffering a cardiac event, women tend to play down the menopause, does offer cardioprotective effects and is associated impact of their health situation, avoid burdening their social with a reduction in all-cause mortality.149a,198a contacts, and have greater psychosocial distress and lower Despite equivalent risk profiles, women are much more likely self-efficacy and self-esteem.23 to be classified as lower risk and less likely to receive appropri- ate evidence-based care. Myocardial Ischemia Standard stress testing evaluating inducible electrocardiographic Myocardial ischemia is a relative condition that results from (ECG) changes, myocardial perfusion defects, and regional wall insufficient oxygen supply to meet the metabolic demands of motion abnormalities is of limited value in the assessment a region of myocardium, which can be induced by excessive 104 CARDIOVASCULAR AND PULMONARY PHYSICAL THERAPY myocardial demand, reduced level of oxygenation of the blood, In addition, higher LV EDP due to either diastolic or systolic or insufficient blood supply. It is usually caused by reduced dysfunction further reduces coronary driving pressure and thus blood supply due to fixed atherosclerotic stenoses in the epicar- blood flow (which occurs during diastole only), thereby induc- dial coronary arteries or occasionally by coronary vasospasm or ing more ischemia. small-vessel disease superimposed on increasing demand pro- Myocardial irritability producing arrhythmias voked by activity. The various factors that affect the balance Myocardial stunning: When the balance between myocardial between myocardial oxygen supply and demand are illustrated oxygen supply and demand is restored, myocardial function in Figure 4-14, as are the clinical consequences. Because the usually returns to normal; however, reperfusion injury (flow myocardium relies almost entirely on aerobic metabolism to compromise with impairment of coronary vasodilation) some- provide its energy, ventricular dysfunction develops quickly times delays recovery of contractile function, producing myo- when there is insufficient coronary blood flow. Notably, many cardial stunning, until blood flow is restored and glycogen patients experience symptoms of myocardial ischemia immedi- stores are replenished. ately after activity because of the postexercise rise in plasma Myocardial hibernation: Repeated episodes of ischemia–reper- catecholamine levels.9 fusion can induce a state of depressed function, or myocardial hibernation, with noncontractile but viable myocardium that Pathophysiology may regain function after revascularization. An imbalance between myocardial oxygen supply relative to demand, which typically occurs during exertion or emotional Clinical Manifestations stress with luminal narrowing of more than 65% to 70% in an Angina pectoris (ischemic chest discomfort): classic characteris- epicardial coronary artery, leads to: tics include the following: Impaired diastolic function (i.e., impaired relaxation), as 4 Pain type: Pressure, heaviness, squeezing, tightness, burning detailed in Figure 4-12, resulting in increased LV EDP 4 Location: Substernal, jaw, shoulder, epigastrium, back or arm Impaired systolic ventricular function (i.e., diminished force of 4 Precipitated by: Exertion, stress, emotions, meals contraction) leading to reduced SV, as described in Figure 4-13 4 Duration: 3 to 15 minutes MAJOR DETERMINANTS OF MYOCARDIAL OXYGEN DEMAND AND SUPPLY Normal Coronary blood flow: nonischemic state - Perfusion pressure - Vascular resistance Heart rate Balanced Contractility demand/supply Systolic wall Myocardial Myocardial stress: oxygen demand oxygen supply - pressure - volume Demand/supply Oxygen content of imbalance blood: - Hemoglobin level - Oxygen saturation Myocardial ischemia Metabolic changes Diastolic and contractile Electrophysiologic Symptoms (angina) dysfunction abnormalities Figure 4-14: Major determinants of myocardial oxygen supply and demand and the consequences of an imbalance between them (i.e., ischemia). (From Shah PK, Falk E. Pathophysiology of myocardial ischemia. In Crawford MH, DiMarco JP, Paulus WJ, editors. Cardiology, 2nd ed. St. Louis: Mosby; 2004.)  CHAPTER 4 44 Cardiopulmonary Pathology 105 4 Relieved by: Rest or mitigation of stress, nitroglycerin Myocardial Infarction 4 Pain free: Between bouts Myocardial infarction (MI) occurs as a result of interruption of Anginal equivalents: Other symptoms (e.g., dyspnea, fatigue, blood supply to an area of myocardium for 20 minutes or more, lightheadedness, or belching) that are brought on by exertion causing tissue necrosis. In more than 80% of cases, MI is precipi- or stress and relieved by rest or nitroglycerin tated by thrombosis due to disruption of the fibrous cap (see Arrhythmias resulting from myocardial irritability the previous section) or superficial erosion of the endothelium of Characteristic ECG changes: ST-segment depression with possi- a atheromatous plaque; less often it is produced by coronary ble T-wave inversion (see Figure 6-4, page 233), although sig- spasm, embolism, and thrombosis in a normal coronary artery.33 nificant transmural ischemia may produce transient ST- Acute MI is usually classified according to the presence or absence segment elevation of ST-segment elevation. Hypotension caused by reduced cardiac output STelevation MI (STEMI) is the most lethal form of ACS and results Note: Most patients with known myocardial ischemia have at from total occlusion of a coronary artery, leading to cessation of least some episodes of silent ischemia (i.e., without any symp- blood flow to a zone of myocardium. They are usually associated toms), up to one third of patients experience the vast majority of with Q-wave formation and full or nearly full-thickness myocardial episodes as silent, and some patients have only silent ischemia necrosis and thus produce marked increases in specific serum car- (particularly those with diabetes and elderly males). Only 18% of diac markers (e.g., troponins, creatine kinase MB; see page 407). heart attacks are preceded by long-standing angina.11 Non-ST elevation MI (NSTEMI) is diagnosed in patients with Stable or chronic stable angina describes the presence of episodic ST depression or other ST- or T-wave changes accompanied chest discomfort that is generally predictable, as described previously. by a rise and fall in serum cardiac markers. Unstable angina is defined as chest pain or other anginal equiv- Other diagnostic criteria include the clinical history and pre- alent that occurs at rest or with minimal exertion and usually lasts senting signs and symptoms, evolution of the ECG changes at least 20 minutes (unless interrupted by nitroglycerin), or severe over time, and cardiac imaging showing reduced or absent tis- chest pain of new onset, or anginal discomfort occurring with sue perfusion or wall motion abnormalities. increasing frequency, duration, and/or severity. It is usually a warning sign of impending MI. Pathophysiology Prinzmetal’s or variant angina (also called atypical angina) is Acute MI creates three concentric pathological zones: the cen- chest pain, often severe, that typically occurs at rest or at night tral area of myocardial necrosis and the surrounding areas of rather than with exertion or emotional stress and is associated injury and ischemia (Figure 4-15), which can give rise to: with ST elevation and often arrhythmias. It is caused by coronary 4 Diastolic and systolic dysfunction, which may lead to ventric- vasospasm, which usually occurs adjacent to or at the site of at ular dilation and CHF or cardiogenic shock, depending on least minimal atherosclerotic changes, if not severe atherosclerosis, the size of the infarct (see Figures 4-10 and 4-11) and can be intense enough to cause acute MI. 4 Increased myocardial irritability, causing arrhythmias and Chest pain with normal coronary arteries (sometimes called possible sudden death cardiac syndrome X ) is a clinical entity that describe patients with 4 Rupture of infarcted tissue producing a ventricular septal many of the common features of angina-like chest pain, normal defect, cardiac rupture, or acute mitral regurgitation epicardial coronary arteries, and no evidence of large-vessel spasm. 4 Extension of infarction with expanded area of necrosis The etiology of this syndrome is likely heterogeneous, including 4 Pericarditis; pulmonary or systemic emboli microvascular dysfunction with an exaggerated response of the Hyperkinesis of the remaining noninfarcted myocardium small coronary arteries to vasoconstrictor stimuli, myocardial met- occurs during the first 2 weeks after acute MI, although there abolic abnormalities, and enhanced pain perception or sensitivity may also be some areas of hypokinesis. (sensitive heart syndrome). Some patients demonstrate evidence b-Adrenergic antagonists (b-blockers) are known to limit the of myocardial ischemia, particularly of the subendocardium. extent of myocardial damage and increase survival after acute MI, apparently by reducing myocardial oxygen demand. Acute Coronary Syndromes Over time, ventricular remodeling occurs, leading to changes The term acute coronary syndrome (ACS) is used to describe in ventricular size, shape, and thickness of both the infarcted patients who present to the emergency room with either acute MI and noninfarcted areas. or unstable angina. This diagnostic term is designed to expedite 4 Myocardial wall motion may appear normal, as in a small MI the triage and management of these patients in hopes of reducing or a subendocardial MI with scarring of only the innermost myocardial damage and associated morbidity and mortality. layer of the heart; or The most common cause of ACS is rupture of a noncalcified 4 It may be abnormal, as in a transmural MI with full-thickness atheromatous plaque that is less than 50% occlusive, followed scar, as shown in Figure 4-16: by formation of a superimposed thrombus. 8 Hypokinesis occurs when an area of the myocardium con- Current research is investigating the role of various biomar- tracts less than normal kers, including troponin, B-type natriuretic peptide (BNP), 8 Akinesis is depicted by lack of motion of an area of and a number of inflammatory biomarkers, as a means of stra- myocardium tifying risk and guiding management of patients with ACS, par- 8 Dyskinesis is characterized by paradoxical systolic expan- ticularly those without ST elevation.90 sion of an area of myocardium 106 CARDIOVASCULAR AND PULMONARY PHYSICAL THERAPY 3. Zone of ischemia 2. Zone of injury 1. Zone of infarction R P Reciprocal changes T shown on opposite side Q LEFT VENTRICLE Figure 4-15: The zones of infarction and the electrocardiographic changes that correspond to them. 1, The innermost zone of infarction causes permanent Q waves along with acute ST elevation. 2, The surrounding zone of injury causes acute ST-segment elevation and some T-wave inversion. 3, The outermost zone of ischemia causes acute inversion of the T wave. (From Aehlert B. ECGs Made Easy. 3rd ed. St. Louis: Mosby; 2005.) End diastole Clinical Manifestations End systole Classic symptoms of acute MI: 4 Severe crushing chest pain, with or without radiation to the arm(s), neck, jaw, teeth, or back 4 Diaphoresis 4 Dyspnea 4 Nausea, vomiting 4 Lightheadedness, dizziness, syncope 4 Apprehension or sense of impending doom Normal Hypokinesis 4 Weakness 4 Denial Sudden death Note: 20% to 25% of MIs occur without any symptoms (“silent” MIs).9 ECG changes (ST elevation or depression), which evolve over time, as illustrated in Figure 4-17. Elevation of specific serum enzymes or isoenzymes: troponins and creatine kinase or phosphokinase (CK or CPK, particularly Akinesis Dyskinesis the myocardial band isoenzyme, MB) (see page 407) Figure 4-16: Regional wall motion abnormalities observed after myocardial infarction (MI): Reduced motion of a myocardial wall Ischemic Cardiomyopathy segment is called hypokinesis, lack of motion of a segment of Some patients with severe coronary artery disease develop diffuse myocardium is termed akinesis, and paradoxic motion of a segment myocardial dilation with reduced contractility, even without any is known as dyskinesis, which produces a ventricular aneurysm. evidence of previous myocardial infarction. This ischemic cardio- (Redrawn from Kennedy JW. Cardiovasc. Nurs. 1976;12:23–27.) myopathy can be induced by frequent recurrent episodes of  CHAPTER 4 44 Cardiopulmonary Pathology 107 Normal Early Hours−days Days−weeks Months−years Figure 4-17: Sequential electrocardiogram (ECG) changes following acute MI. Initially, there is a Q wave with marked ST elevation. Over the next few days the Q wave becomes deeper and wider, the ST segment moves toward the baseline, and the T wave becomes inverted. Within weeks of an acute MI, the ST segment is near the baseline and the T wave is deeply inverted. Finally, within months the T wave returns to a less inverted or somewhat upright position. myocardial ischemia–reperfusion, especially if the patient has myo- 4 Transmyocardial revascularization cardial stunning or large segments of hibernating myocardium 4 Pacemaker insertion or diffuse fibrosis, or by multiple infarctions, or by a combination 4 Automatic implantable cardiac defibrillator (AICD) of these. Other 4 Lifestyle modifications for risk factor reduction (see page 59) Congestive Heart Failure 4 Cardiac rehabilitation (see pages 59 and 309) CHF can develop as an acute or chronic manifestation of CAD. Acute onset of CHF is most commonly precipitated by MI, partic- Clinical Implications for Physical Therapy ularly with a large, transmural anterior infarction or papillary mus- Because of the deleterious effects of bedrest, early mobiliza- cle dysfunction. On occasion, CAD is first diagnosed when a tion, including therapeutic exercise and ambulation, is benefi- patient exhibits the signs and symptoms of acute CHF (see page cial for patients after acute MI and cardiac surgery. 110) resulting from LV systolic dysfunction. Chronic CHF due to Individuals with cardiac disease are at increased risk of having CHD is usually related to loss of at least 20% of the myocardium a cardiac event during exercise and rehabilitation activities, or ventricular septal defect or severe mitral regurgitation caused which can be stratified according to several clinical factors by acute MI. With improved disease management, patients with (see page 238). The risk is greatest in patients with poor LV CAD are living longer, and the prevalence of associated CHF is function (EF