Cardiovascular Conditions PDF

19 Cardiovascular Conditions OBJECTIVES Upon completion of this chapter, the reader should be able to describe: 1. The definition, etiology, pathophysiology, presentation and medical management of cardiac cond...

19 Cardiovascular Conditions OBJECTIVES Upon completion of this chapter, the reader should be able to describe: 1. The definition, etiology, pathophysiology, presentation and medical management of cardiac conditions including: congestive heart failure, hypertension, angina, acute coronary syndrome, atrial fibrillation, car- diomyopathy, cardiac effusion, cardiac tamponade, peripheral vascular disease, and pulmonary embolism 2. Common physical therapy managements in these cardiac conditions including: Congestive heart failure, hypertension, angina, acute coronary syndrome, atrial fibrillation, cardiomy- opathy, cardiac effusion, cardiac tamponade, peripheral vascular disease, and pulmonary embolism 3. Medications frequently prescribed in these cardiac conditions including: Congestive heart failure, hypertension, angina, acute coronary syndrome, atrial fibrillation, cardiomy- opathy, peripheral vascular disease, and pulmonary embolism This chapter describes common cardiac conditions, clinical information, and medications that pertain to physical therapy management. CONGESTIVE HEART FAILURE Definition Congestive heart failure (CHF) is defined as the inability of the heart to pump sufficient amounts of oxy- genated blood to meet the metabolic demands of the body both at rest and during activity. Etiology and Pathophysiology Right-sided heart failure is characterized by blood backing up in the systemic circulation resulting in systemic venous hypertension and edema. Chronic left heart failure is a common cause of right heart failure. Other caus- es are: increased left atrial pressure, right ventricular infarct, pulmonary hypertension, pulmonary emboli, COPD, tricuspid valve regurgitation (Table 19-1), and pulmonary regurgitation. Another term for right-sided heart failure is cor pulmonale. Left heart failure is characterized by blood backing up in the pulmonary circulation leading to pulmonary congestion. It can be classified as: Diastolic dysfunction—inability of the ventricle to relax completely resulting in high left ventricular end diastolic pressure and pulmonary edema. Left ventricular hypertrophy is also a frequent finding. Examples of causes include: restrictive cardiomyopathy, ischemic heart disease, pericardial tamponade, mitral valve regurgitation (see Table 19-1), and stenosis. 150 Chapter 19 Table 19-1 Overview of Congenital Heart and Valve Diseases Definition Prevalence/ Etiology and Clinical Presentation and Incidence Pathophysiology Course Congenital Heart The incidence is Many congenital Heart murmurs due to turbu- Disease: Anatomic 1/120 live births. cardiac defects do lent flow are common. Signs of defects of the heart Some common not produce signif- heart failure, cyanosis, and and great vessels causes are: chromo- icant hemodynamic hepatomegaly may be present present at birth somal defects (eg, alteration. Others in the newborn. Long-standing trisomy 13 or 18), cause abnormal hypoxemia can lead to club- maternal illness ventricular volume bing, polycythemia, and other (eg, diabetes mell- load, ventricular signs of inadequate systemic itus, fetal alcohol pressure load, and perfusion. Dilation and hyper- syndrome, rubella), atrial emptying; trophy of cardiac chambers medication (eg, venous admixture; or may result from the increased thalidomide). inadequate systemic cardiac workload. cardiac output. Mitral Valve Disease: Between 1% and 6% Complete myxom- In mild cases, patients are A bulging of one or in otherwise normal atous degeneration asymptomatic. Patients might both mitral valve populations. It is of the valve can lead have a crisp systolic sound or leaflets into the left higher in persons to severe mitral reg- click and a delayed or late atrium during systole with Duchenne mus- urgitation, or floppy systolic mitral regurgitation cular dystrophy, my- valve syndrome. murmur. In more severe cases, otonic dystrophy, can present with arrhythmias, sickle cell disease, palpitations, syncope, fatigue, atrial septal defect, lightheadedness, transient and rheumatic heart ischemic attacks, dyspnea, and disease. About 25% hemoptysis and abnormal EKG of patients have joint findings despite normal coro- laxity, a high-arched nary angiograms. palate, or other skel- etal abnormalities. Aortic Valve Incidences of aortic LV volume and Dyspnea on exertion, orthop- Disease: Retrograde regurgitation usually LV stroke volume nea, and paroxysmal nocturnal flow from the aorta increases with age. are increased because dyspnea develop. Palpitations into the left ventricle Common causes are: the LV receives may occur because of the through incompetent idiopathic degenera- blood regurgitated awareness of the heart due to aortic cusps tion of the aortic in diastole in ad- LV enlargement. Angina is valves or root, rheu- dition to the normal especially common at night. matic heart disease, blood flow from the infective endocarditis, pulmonary veins. LV and trauma. Less hypertrophy occurs common causes are: proportionally with severe hypertension dilation in order to and some auto- maintain pressure. immune diseases. Cardiovascular Conditions 151 Table 19-1 continued Overview of Congenital Heart and Valve Diseases Definition Prevalence/ Etiology and Clinical Presentation and Incidence Pathophysiology Course Tricuspid Valve Due to a cleft tri- Severe pulmonary Fatigue, cold skin, dyspnea, Disease: Retrograde cuspid valve (eg, hypertension or RV edema, and the sensation of flow of blood from in endocardial cush- outflow obstruction pulsations in the neck due to right ventricle to ion defects), blunt leads to RV dilation the high jugular regurgitant right atrium due to trauma, or carci- that frequently re- are common. Right upper inadequate app- noid disease, in sults in tricuspid quadrant abdominal discom- osition of the tri- which the valve may valve regurgitation. fort due to hepatic congestion cuspid valves be fixed in a semi- may occur. Atrial fibrillation open position. Less or flutter, which usually common causes are: occurs when the right atrium infective endocard- enlarges, further decreases the itis, papillary mus- cardiac output and may pre- cle dysfunction, cipitate sudden, severe heart RV infarction, or failure. the use of fenflur- amine. Abbreviation: LV: left ventricle; RV: right ventricle Systolic dysfunction o Reduced inotrophy (myocardial contractility) results in decreased ejection fraction, cardiac output, and oxygen transport. Examples of causes are: CAD and dilated cardiomyopathies. o Increased afterload —increased resistance to flow down stream. Examples of causes are: aortic stenosis or regurgitation, systemic hypertension, coarctation of the aorta, and left-to-right shunt. Clinical Presentation and Course CHF classically manifests itself with shortness of breath and frothy pinkish sputum. Clinical signs of left heart failure and associated pulmonary edema are: Dyspnea—related to pulmonary edema. Initially happens during activity and can progress to occur at rest. Orthopnea—dyspnea when lying down flat because of an increase in venous return. Sometimes it is accompanied by a dry hacking cough, which is relieved by sitting up. Adventitious breath sounds—cardiac asthma (which consists of wheezes) and moist crackles. Frothy sputum (white/pink) Abnormal heart sound—murmurs, S3 (decompensatory heart failure), S4 (cardiac hypertrophy results in a stiff ventricle) Decreased exercise capacity Radiographic changes—see Case 10 for example Additional clinical signs commonly associated with systolic dysfunction: Tachycardia, decreased pulse pressure Syncope, lightheadedness, lethargy Skin can be cold and clammy 152 Chapter 19 Table 19-2 Classification of Blood Pressure for Adults Age 18 Years and Older Category Systolic BP (mmHg) Diastolic BP (mmHg) Normal 100 Adapted from: www.nhlbi.nih.gov/guidelines/hypertension; Chobanian AV, Bakris GL, Black HR, et al. The seventh report of the joint national committee on prevention, detection, evaluation, and treat- ment of high blood pressure: the JNC 7 report. JAMA. 2003; 289:2560-2571.1 Medical and Surgical Intervention Medical treatments involve reversing or optimizing the underlying problem, using of diuretics, pneumovax (pneumococcal vaccination), properly balancing fluids, controlling hypertension, and improving cardiac func- tion.2 HYPERTENSION Definition Arterial hypertension is the elevation of systolic and/or diastolic BP that can be termed either primary (unknown etiology) or secondary (associated with a known underlying cause) hypertension. Table 19-2 provides the classification of hypertensive and normal BP for adults aged 18 years or older.1 Prevalence It is estimated that nearly 50 million Americans and about 1 billion worldwide are hypertensive (systolic BP >140 mmHg and/or diastolic >90 mmHg, or taking antihypertensive medication). The prevalence of hyperten- sion increases with age (Figure 19-1).3 Etiology and Pathophysiology In primary or essential hypertension, the etiology is unknown. The cause is likely multifactoral, leading to diverse hemodynamic and pathophysiologic dysfunctions.1 The condition may be hereditary and lifestyle factors such as increased salt intake, obesity, and stress can further aggravate the condition. Secondary hypertension is associated with conditions such as renal parenchymal disease, Cushing's syndrome, primary aldosteronism, hyperthyroidism, or coarctation of the aorta. It is also associated with the use of excessive alcohol,4 sympath- omimetics, corticosteroids, cocaine, or licorice. Clinical Presentations and Course No early pathologic changes occur in primary hypertension. Hypertension is also called a silent killer. Patients are usually asymptomatic until complications develop in target organs. Over time, generalized arterio- lar sclerosis develops and is characterized by medial hypertrophy and hyalinization. Patients often develop left ventricular hypertrophy in order to overcome increased peripheral vascular resistance. This can eventually progress to dilation of the left ventricle. Coronary, cerebral, aortic, renal, and peripheral atherosclerosis are more common in hypertensive patients. Hypertension is a more important risk factor for stroke than for atheroscle- rotic heart disease. Cardiovascular Conditions 153 Figure 19-1. Prevalence of hypertension in the United States based on studies from 1988 to 1994. (Reprinted from McArdle WD, Katch KI, Katch VL. Exercise Physiology. Energy, Nutrition, and Human Performance. 5th ed. Philadelphia: Lipincott, Williams & Wilkins. 2001;316, with permission.)3 Medical and Surgical Intervention Antihypertensive Drug Therapy1,5 For prehypertension, antihypertensive drugs are usually prescribed if lifestyle modificaitons do not normalize BP. For stage 1 and 2 hypertension, drug therapy should be initiated promptly when target organ damage or other risk factors are present. In patients with heart failure, symptomatic coronary atherosclerosis, cerebrovascular dis- ease, and renal failure, immediate and judicious antihypertensive therapy is required. For more details see the consensus recommendations for the management of hypertension.1,5 Lifestyle Modifications6-9 Lifestyle modifications include weight reduction in obese individuals; increase in physical activities; dietary changes—selecting foods that are rich in potassium and calcium but low in sodium, and saturated and total fat content; increase in intake of fruit and vegetables; and moderation of alcohol consumption. Patients with uncomplicated hypertension are not required to restrict their activities so long as their BP is controlled. Dietary restrictions can help control coexisting diabetes mellitus, obesity, and blood lipid abnormalities in addition to facilitating the control of hypertension in some individuals. 154 Chapter 19 Table 19-3 Differentiating Characteristics of Chest Pain Characteristics Angina Pericarditis Musculoskeletal Location Sternal, substernal Left sided, substernal Variable over chest wall Radiation Jaw, left arm, neck Neck, trapezius ridge None Quality Heavy pressure, Sharp, stabbing, deep Sharp tightness, squeezing feeling Alleviating factors Rest, nitroglycerin Lean forward sitting, Rest, anti-inflammatory or shallow breathing analgesia medications Aggravating factors Exercise, stress, Inspiration, supine Muscle movement and cold weather lying, laughter, cough contraction, palpation Duration 5 to 10 minutes Hours Variable ANGINA Definition Angina is pain in the chest arising from myocardial ischemia that is initially precipitated by myocardial oxy- gen supply not meeting demand. It is a common cardiac symptom. Resting EKG is unchanged and troponin I levels are normal; however, reversible ischemia EKG changes can be seen during a spontaneous attack. Not all chest pain is angina. Table 19-3 shows differentiating characteristics of chest pain. Etiology and Pathophysiology Stable angina is caused by myocardial oxygen supply not meeting demand. The imbalance is reversible and is relieved with rest and nitroglycerin. Coronary spasm is frequently associated with stable angina with no inti- mal disruption or thrombus. Atherosclerotic segments in coronary arteries tend to have a decreased response to vasodilators, an increased response to vasoconstrictors, and sometimes paradoxical vasoconstriction when exposed to vasodilators. Increased platelet reactivity and platelet aggregates further contribute to vessel lumen narrowing and release chemicals that can trigger vasoconstriction. An episode of angina is not a heart attack although it is an indication of underlying CHD. The pain is caused by the transient ischemia, which is reversible. Thus, episodes of angina seldom cause permanent damage to the heart muscle. When patients have repeating but stable patterns of angina, an episode of angina does not mean that a heart attack is imminent. However, they are at an increased risk of heart attack compared to those who have no symptoms of CAD. Patients with angina and who subsequently developed coronary events are likely to have many vulnerable lesions throughout the coronary tree. In contrast, when the pattern of angina changes— if episodes become more frequent, last longer, or occur without exercise—the risk of heart attack in subsequent days or weeks is much higher. Specifically, the levels of markers of acute inflammation10,11 such as C-reactive protein and fibrinogen are higher in patients with unstable coronary disease than in those with stable coronary disease. Moreover, persistent elevation of C-reactive protein in patients with unstable angina is predictive of future myocardial ischemia and infarction. The New York Heart Association Angina Classification is a scale used to indicate the severity of angina according to symptoms. New York Heart Association Angina Classification Class I—No limitation of physical activity (ordinary physical activity does not cause symptoms). Class II—Slight limitation of physical activity (ordinary physical activity does cause symptoms). Class III—Moderate limitation of physical activity (comfort at rest but less than ordinary physical activ- ity cause symptoms). Class IV—Unable to perform any physical activity without discomfort (may be symptomatic even at rest). Cardiovascular Conditions 155 Medical and Surgical Intervention The use of medication to relieve symptoms, lifestyle modification, and risk reduction is frequently used to slow the progression of disease and to reduce future adverse events.12,13 Exercise can increase the level of pain- free activity, relieve stress, improve the heart's blood supply, and help control weight. Sedentary patients should build up their activity level gradually. For example, they should start with a short walk to tolerance and increase by 1 minute per day over days or weeks. The idea is to gradually increase fitness level by working at a steady pace and avoiding sudden bursts of effort. ACUTE CORONARY SYNDROME Definition Acute coronary syndrome (ACS) consists of a spectrum of clinical presentations of acute myocardial ischemia and infarct.14 ACS is suspected when chest pain is accompanied with ischemic changes in the EKG or elevated troponin I from a blood sample. Etiology and Pathophysiology ACS is caused by the myocardial oxygen supply not meeting the demand. The imbalance is reversible or could progress to a nontransmural or transmural myocardial infarct. Common examples of supply ischemia are from functional or structural disruption of the coronary artery circulation such as vasospasm, nonocclusive thrombus, and significant coronary artery stenosis. Common examples of demand ischemia are associated with increased work of the heart such as during exercise and stress. Cardiovascular Disease Risk Factors With Coronary Artery Disease15-23 Risk factors that cannot be changed: Age—cardiovascular risk increases with age Gender—cardiovascular risk is higher in males Family history—cardiovascular risk increases with a family history Risk factors that can be changed: Smoking—is extremely harmful Diabetes—should be aggressively managed Elevated serum cholesterol—proper diet is important Hypertension—should be closely regulated. Exercise has a slightly beneficial effect in lowering the sys- tolic BP by about 4 mmHg and diastolic BP by about 3 mmHg Obesity—weight loss is beneficial Left ventricular hypertrophy Protective factors: Elevated HDL cholesterol Active lifestyle Estrogen replacement therapy Moderate alcohol use Having multiple risk factors can drastically increase the cardiovascular disease (CVD) risk. There are many models using CVD risk factors to predict the probability of cardiovascular disease. One study20 reported that the use of antihypertensive medication or diabetes can double the CVD risk over 5 years while cigarette smoking may increase the risk by 50%. A more practical way to see the effects of combinations of CVD risk factors on the risk score (level of risk of having CVD in the future) is to use a CVD risk calculator. Below are some car- diovascular risk calculators located on different Web sites: http://hin.nhlbi.nih.gov/atpiii/calculator.asp http://livingheart.com/main/riskmain.asp http://www.americanheart.org/presenter.jhtml?identifier=3003499 156 Chapter 19 Table 19-4 Differentiating Characteristics Between Q-Wave and Non Q-Wave Myocardial Infarcts Characteristics Q-Wave Non-Q Wave Prevalence 47% 53% Incidence of coronary occlusion 80% to 90% 15% to 25% In-hospital mortality High Low 1-month mortality 10% to 15% 3% to 5% 2-year mortality 30% 30% Infarct size Big Small Acute complications Frequent Infrequent Adapted from Fus RV, Alexander RW, O’Rourke RA. Hurst’s the Heart. New York: McGraw Hill; 2001. Clinical Presentations and Course ACS consists of 3 levels: 1. Unstable angina, which is caused by the myocardial oxygen supply not meeting the demand. The imbal- ance is reversible or could progress to the next 2 levels. The pain is usually longer, variable, and not com- pletely relieved by nitroglycerin. Nausea, sweating, and dyspnea are other commonly associated symp- toms. In progressing to unstable angina, patients who formerly had stable angina usually recognize new symptoms or a change in symptoms. The EKG taken, while pain-free, is usually normal. The EKG taken while having angina shows signs of ischemia (ST segment depression, peaked or inverted T waves). 2. Non-ST elevation MI or non Q-wave MI. This is also termed a non-transmural infarct. Early spontaneous reperfusion may occur (Table 19-4). Troponin I is elevated.12,24 3. ST elevation MI or Q-wave MI. This is also termed a transmural infarct. The Q-wave might appear as early as 10 hours post infarct or take as long as 1 to 2 days. It is a sign of myocardial death (see Table 19-4). The EKG findings and clinical presentations depend on the site or sites of coronary artery blockage (Table 19-5). Troponin I is elevated.24,25 Sometimes EKG findings are not conclusive, especially in patients with an old infarct or bundle branch block. Variations between EKG findings and site of infarct also exist. Additional laboratory tests are used: Echocardiogram is used to evaluate wall motion abnormalities and overall ventricular function. This also can identify complications of an acute MI (eg, valvular insufficiency, ventricular dysfunction, pericardial effusion). Technetium-99m sestamibi scan (MIBI). The radioisotope is taken up by the myocardium in proportion to the blood flow and is redistributed minimally after injection. Thallium scanning: thallium accumulates in the viable myocardium. Coronary angiography is usually done prior to percutaneous transluminal coronary angioplasty (PTCA) especially in patients who have failed to respond to previous thrombolytics. Common Complications With an Acute Myocardial Infarction Arrhythmias—Most common complication but tends to be self-limiting. Ventricular ectopy may lead to more serious arrhythmias; supraventricular ectopy is more benign. Sinus bradycardia and sinus tachycar- dia, especially the former, can be medication related. Infarct expansion—Frequently occurs a week after a large transmural anterior MI Heart failure—Common with elderly or patients with a large infarct of the left ventricle Angina—Usually associated with ongoing ischemia or infarct extension Infarct extension—Associated with increased CK-MB beyond the normal time frame Cardiogenic shock—Frequently occurs with a large left ventricular infarct or patients with a previous MI Cardiovascular Conditions 157 Table 19-5 Site of Myocardial Infarct, Diagnosis and Clinical Significance Site of infarction Vessel Involved Hyperacute EKG Clinical Presentations Findings Anterior Left anterior des- ST-segment elevation Heart failure, AV block, cending coronary in V1 to V4 sinus tachycardia, mural artery thrombi, BBB, septal rup- ture Inferior 80% right coronary ST-segment elevation Sinus block, atrial arrhyth- artery (posterior des- in II, III, aVF mia, 2-degree AV block, cending branch). Reciprocal changes hiccup, nausea, vomit- 20% left circumflex in I, aVL, V2, V3 ing indigestion, sinus artery bradycardia, hypotension, papillary muscle rupture Posterior Posterior intervent- ST-segment depression Usually associated with a ricular artery or post- in V1 to V4 lateral or inferior MI. erior descending artery Serious rhythm distur- bances, left ventricular failure Lateral Left circumflex artery ST-segment elevation Conduction abnormality, in I, aVL, V5, V 6 arrhythmia, heart failure, Reciprocal changes ventricular aneurysm in V1 to V4 Right ventricle Right coronary artery ST-segment elevation Usually associated with in III more than II inferior-posterior infarct. with ST-segment de- Right heart failure, throm- pression in lead I. bus/emboli, atrial fibrilla- Right-sided EKG to be tion, indigestion done when associated with inferior MI Pericarditis—Usually associated with a transmural MI. In rare occasions, this can lead to cardiac tam- ponade. Medical and Surgical Intervention Management involves treating the underlying cause of the ischemia and restoring perfusion to the myocardi- um with treatments such as thrombolytic therapy, angioplasty, or coronary artery bypass grafts (CABG).26,27 Cardiac medications are used to optimize the cardiac function and to reduce future adverse events.15 Pneumovax (pneumococcal vaccination) is recommended as the condition becomes more chronic. Lifestyle modifications to minimize cardiac risk factors are important.6-9,28-34 Primary and secondary risk factor reduction accounted for more than the 70% decline in mortality in patients with coronary disease in the United States between 1980 and 1990. Some examples of lifestyle modification included reduced intake of red meat, diet that included nuts, weight loss in overweight patients, low to moderate alcohol intake, regular exercise, and smoking cessation. The use of vitamin (vitamin E, vitamin C, and multivitamin) supplements, however, have not been shown to be effective in lowering cardiovascular disease risk.35 Coronary Artery Bypass Graft When cardiac patients have unrelenting chest pain, unstable angina, or other serious cardiac symptoms that are refractive to medical management and angioplasty, invasive surgery such as CABG is considered.36 Under 158 Chapter 19 Figure 19-2. Coronary art- eries. Aorta Left main coronary artery Left circumflex Right coronary Left artery anterior descending general anesthesia, the chest is opened through the midline of the sternum (sternotomy). In order to maintain blood flow to the heart muscle beyond blockages, blood is bypassed onto the same artery beyond the blockage with a graft (Figure 19-2). In order to attach the grafts, the heart is cooled with iced physiologic salt solution, while a preservative solution is injected into the heart arteries. This process minimizes damage caused by reduc- ing blood flow during surgery. The heart is stopped and placed on a bypass pump to allow attachment of the graft to the artery. The blockage is left in place, and blood is simply shunted around it. After the grafts are connect- ed, the heart is disconnected from the bypass machine and restarted. Once the cardiac circulation has resumed, the chest wall layers are wired and sutured. The whole procedure lasts several hours depending on the number of vessels involved. Graft vessels are usually obtained from: The internal mammary arteries Saphenous vein graft with an associated leg incision Physical therapy intervention during the postoperative period: Patients will be transferred to the intensive care unit. Ventilator, chest drainage tubes, and other invasive lines (eg, arterial line, pulmonary catheter) are usually removed the next morning. Postoperative physi- cal therapy routine usually involves thoracic expansion exercises, coughing, and mobilization. By the second day, patients are usually transferred to the step down cardiac unit. The patient may attend exercise class if stable and continue with breathing exercises and ambulation. Up to 25% of patients develop atrial fibrillation within the first 3 or 4 days after CABG surgery. It is relat- ed to the trauma during surgery and responds well to medication.37-38 Cardiovascular Conditions 159 By day 3 or 4, patients may start walking 1 to 2 flights of stairs. Patients are usually ready for discharge home on day 5 postoperatively. Recovering at Home At this stage, it is important for the patient to get sufficient rest and gradually increase his or her activity level. Patients are encouraged to participate in stage 2 cardiac rehabilitation. The patients are instructed to con- tinue to follow sternal precautions (see Answer Guide for Case 12) for 6 to 8 weeks. It is normal for patients to be emotional after heart surgery or any health crisis. Feelings of depression, anger, and fear are rather common. This is a normal part of the healing process and will resolve with time. The patient should be encouraged to try to resume regular nonexertional activities that he or she enjoys. ATRIAL FIBRILLATION Definition Atrial fibrillation (AF) is when the atria quiver instead of beating in a coordinated rhythm. This results in a very fast, uncontrolled heart rhythm of the ventricles. During AF, the atrial rate could be as high as 600 beats per minute. Etiology and Pathophysiology Common causes of AF are: Medical related conditions such as: aging, post MI (especially right ventricle infarction, or diseases that result in atrial wall distension), heart failure, open heart surgery, hyperthyroidism, alcoholism, hyperten- sion, and diabetes Drug related problems such as: illicit drug abuse or digoxin toxicity. The use of calcium channel blockers might increase the level of digoxin in the blood. The use of calcium channel blockers with amiodarone can cause bradycardia and decrease cardiac output. When used concurrently with beta-blockers, they can increase cardiac depression During AF, the pumping action of the atria is fast and not synchronized with the ventricles such that the blood is not completely emptied from the atrial chambers. Blood clots are frequently formed. In about 5 percent of patients with AF, clotted blood dislodges from the atria and results in a stroke. AF with a concurrent diagno- sis of hypertension, cardiac valve problems, or MI can increase the risk of stroke or heart failure. The American Heart Association estimates that in the United States, AF is responsible for over 70,000 strokes each year. Clinical Presentations and Course Palpitations, arrhythmias, dyspnea, chest discomfort, and dizziness Feelings of weakness caused by decreased cardiac output Anxiety from the awareness of a rapid and/or irregular heart beat Patients with underlying heart disease are generally less able to tolerate AF without complications Symptomatic AF implies poor overall cardiac function resulting in conditions such as angina, CHF, hemodynamic dysfunction, and embolism Types of Atrial Fibrillation 1. Paroxysmal AF is characterized by brief episodes of the arrhythmia, which can resolve on its own 2. Persistent AF—the episodes require some form of intervention to return the heart rhythm back to normal 3 Permanent AF—intervention (if successful at all) only restores normal heart rhythm for a brief time Medical and Surgical Intervention Management involves treating the underlying cause of the fibrillation, cardioverting (converting using med- ications or electric shocks) back to normal sinus rhythm, rate control with medication, and the use of antico- agulation. Ablations (surgical removal) of the focal triggers of AF are sometimes used on selected patients. 160 Chapter 19 Table 19-6 Functional Classification and Clinical Signs of Cardiomyopathies Dilated Congested Hypertrophic Restrictive Name Cardiomyopathy Cardiomyopathy Cardiomyopathy Common Idiopathic, hypertension, Genetic disorders and hypertension. Idiopathic, amyloido- causes viral infection, immuno- sis, and endomyocar- logic disorders and toxic dial fibrosis. effects from chemical agents. Heart char- Dilatation of both vent- Massive ventricular hypertrophy Decreased compliance acteristics ricles frequently with with small ventricular cavities. and size of the ventric- systolic dysfunction and There are obstructive and non- ular cavities. increased myocardial obstructive types. The obstructive mass. type is caused by the hypertrophic ventricular septum restricting mitral valve motions leading to the obstr- uction of blood flow during systole. Heart function The grossly enlarged The most important feature is diast- The most important ventricles resulted in olic dysfunction. The massive vent- feature is decreased myocardial contractile ricular wall results in a small vent- myocardial compli- dysfunction. ricular space with a reduced end ance leading to dias- diastolic volume. The ejection vol- tolic dysfunction. ume is above normal (sometimes Systolic function and approaching 90%) and end systolic ejection fraction is usu- ventricular volume is markedly de- ally normal. creased. Clinical Similar to that of left Dyspnea, chest pain, and ventri- Dyspnea with exertion manifestation and right heart failure. cular arrhythmia are common. and may progress to Dyspnea, nocturnal dry Sudden death in young athletes is nocturnal dyspnea. cough, pulmonary and frequently associated with hyper- The decrease in ven- peripheral edema might trophic cardiomyopathy. tricular compliance occur. usually leads to pul- monary and systematic congestion. Diagnostic tests Coronary angiography Echocardiography, radionuclide Radionuclide imaging, and left heart catheter- imaging, and angiography. angiography and ization. myocardial biopsy. CARDIOMYOPATHY Definition Cardiomyopathy is a disease of the heart muscle. The contractile function of the heart is affected resulting in decreased cardiac output. Etiology and Pathophysiology This can be one of many varieties (Table 19-6). It can arise because of genetic causes, a viral infection, or consumption of toxins (lead, alcohol, etc.). In many cases, the condition is idiopathic. Ventricular remodeling occurs when the myocardium undergoes structural reorganization, usually resulting in a loss of wall motion and decreased contractile function. Ventricular remodeling is a common adverse effect of ACS. Cardiovascular Conditions 161 Clinical Presentation and Course The disorder is usually chronic and common clinical features are: Dyspnea with exertion Fatigue Normal or low blood pressure Sinus tachycardia Basal crackles on lung auscultation Jugular venous distension Peripheral pitting edema In severe cases, hepatomegaly, ascites, and skeletal muscle wasting occur Medical and Surgical Intervention Management involves treating the underlying cause, improving cardiac output, controlling heart failure, pneumovax (pneumococcal vaccination), and minimizing complications and future adverse events. Appropriate rest and stress avoidance are important. Physical exercise within the limits imposed by symptoms improves over- all well being. Surgical procedures involving removal of strips of myocardium to remodel the dilated ventricle can be useful in selected patients.2 CARDIAC EFFUSION AND CARDIAC TAMPONADE Definition Cardiac effusion is an abnormal fluid accumulation in the pericardial space between the myocardium and pericardium. Cardiac tamponade occurs when fluid accumulation in pericardial space compresses the heart.39-40 Etiology and Pathophysiology The pericardium has an outer fibrous layer and an inner serous layer. The fibrous layer is a flask-shaped with a tough outer sac. It is attached to the diaphragm, sternum, and costal cartilages. The thin serous layer lies next to the surface of the heart. The pericardium protects the heart from the spread of infection or inflammation from other areas. Inflammation of the pericardium, known as pericarditis, may occur in conditions such as malignant disease, cardiac surgery, post MI and tuberculosis. Fluid accumulates in the pericardial space resulting in a cardiac effu- sion. The pericardial space normally contains approximately 20 ml of fluid but can accommodate an extra 120 ml of fluid without deleterious effects. Cardiac tamponade is caused by further increases in fluid in pericar- dial space that compresses the heart. Hemodynamic effects such as a decreased venous return and decreased dias- tolic filling leads to decreased cardiac output and shock. Clinical Presentation and Course Clinical Presentation of Pericarditis Chest pain but it differs from angina (see Table 19-3) Dyspnea and pericardial friction rub (heard on auscultation) Low-grade fever is common Premature atrial and ventricular contractions occasionally are present Clinical Presentation of Cardiac Tamponade Jugular venous distension, hypotension, and muffled heart sounds Pulsus paradoxus. The first sphygmomanometer reading is recorded at the point when beats are audible during expiration and disappear during inspiration. The second reading is taken when each beat is audi- ble during the respiratory cycle. A difference of more than 10 mmHg defines pulsus paradoxus. Cyanosis, decreased level of consciousness, shock. 162 Chapter 19 In patients with slow fluid accumulation > 200 mL, the chest x-ray can show an enlarged cardiac silhou- ette. However, with rapid fluid accumulation, the cardiac silhouette may be normal. Medical and Surgical Intervention EKG, echocardiography, and CT scan are useful in the diagnosis of pericardial effusion and tamponade. Management involves treating the underlying cause, providing adequate pain control, and drainage of the fluid with a chest tube or creating a pericardial window with surgery.2,38,39 PERIPHERAL VASCULAR DISEASE Definition The arterial system can be affected by processes such as atherosclerosis and/or the venous system can be affected by processes such as thrombo-embolism, which can result in impeded blood supply to the muscles or venous return to the heart. Etiology and Pathophysiology Common causes of arterial insufficiency are atherosclerosis, thrombo-embolism, and trauma (eg, compart- ment syndrome). Common causes of chronic venous insufficiency are obesity, ascites, lymphatic obstruction or destruction, malignant disease, surgery and radiation therapy. Deep vein thrombosis (DVT) is common after limb surgery (eg, total knee replacement) and immobilization (eg, bed rest, casted limb, paralysis). It can progress to chronic insufficiency with a large clot or repeated episodes (see Answer Guide for Case 17). Clinical Presentations and Course Arterial Occlusive Disease Peripheral arterial diseases usually are present in patients with atherosclerosis and coronary artery disease. Both of the conditions share similar risk factors. Common clinical signs and symptoms are pain, minimal swelling, and a cold dusky appearance. A decrease or absence of pulses in the affected limb is the main distin- guishing factor from venous insufficiency. In chronic cases, symptoms of claudication—a pain, ache, cramp, or tired feeling that occurs when walking—are most common in the lower leg. Claudication is aggravated by walk- ing rapidly or uphill but is usually alleviated by rest. Delayed wound healing, skin ulcers, and gangrene are com- mon in more severe cases. Doppler ultrasound is frequently used to check for peripheral pulses. An arteriogram is diagnostic. Venous Insufficiency The condition is usually chronic except in the case of DVT. Common clinical presentations are redness, warmth, and a swollen calf muscle with pain and tenderness on palpation. Passive dorsiflexion of ankle (Homan's sign) also increases the pain. Doppler ultrasound or venogram is used for the diagnosis of DVT. Medical and Surgical Intervention Medications, proper foot care and fitting shoes, and smoking cessation are essential for patients with arteri- al insufficiency. Complete arterial occlusion requires immediate medical or surgical attention to limit cell dam- age or death. DVT requires anticoagulation therapy (eg, heparin and warfarin) while chronic venous insuffi- ciency management involves treating the cause and supportive treatment such as medication to decrease edema and the use of compression stockings. Ambulation has been shown to be beneficial in patients with claudica- tion from peripheral vascular disease. Table 19-7 provides a brief description of an outpatient exercise program.41 COMMON MEDICATIONS PRESCRIBED IN CARDIAC PATIENTS A brief summary of some common medications for management of hypertension, congestive heart failure, angina, myocardial infarct, and blood clots is presented (Table 19-8). However, a comprehensive list is beyond the scope of this book. The Web sites in the references at the end of this chapter provide detailed up-to-date information about medical conditions and medical treatment. Cardiovascular Conditions 163 Table 19-7 Ambulation Program for Patients With Claudication From Peripheral Vascular Disease How to Do Warm-up and cool-down periods of 5 to 10 minutes each Intensity Treadmill walking or track walking with initial workload set to a speed and grade that elicits clau- dication symptoms within 3 to 5 minutes Patients may rest briefly in standing or sitting to permit symptoms to decrease Resume ambulation when able Duration Cycles of ambulation with rest periods in between Exercise to tolerance initially Increase the time by 5 minutes per session until 50 minutes of intermittent ambulation is reached Frequency 3 to 5 times per week Adapted from Stewart KJ, Hiatt WR, Regensteiner JG, et al. Exercise training for with claudication from peripheral vascular disease. N Eng J Med. 2002:347;1941-1951.41 Table 19-8 Examples of Common Medication Prescribed to Cardiovascular Patients Medication Trade name (Drug name) Medication Effect Physical Therapy Considerations Diuretics "Water pill," which Patients may complain of feeling dizzy, and light- Spironolactone, reduces plasma volume. headed with postural change, light sensitive and fre- (Aldatone), Lasix Antihypertensive effect. quent voiding. Bedside commode or urinal is useful in (Furosemide). mobility-impaired individuals especially at night. Beta-blocker Decreases the work of Not suitable for asthmatics and restricts heart rate Inderal (propra- the heart. Has anti- response to exercise. nolol), Lopressor anginal, anti-hyper- (metoprolol), tensive, anti-arrhythmic, Sotacor (sotalol), antiadrenergic effects, Atenolol (ten- and prevents additional ormin). heart attacks. Calcium channel Has anti-anginal, anti- Patients may complain of dizziness, coughing, wheez- blocker Cardi- hypertensive, anti-arrhy- ing, and swelling of the lower limbs. zem, (diltiazem), thmic effects. It affects the Isoptin (vera- movement of calcium into pamil), Plendil the cells of the heart and (felodipine), blood vessels, relaxes blood Procardia (ni- vessels, and increases the fedipine). supply of blood and oxy- gen to the heart while re- ducing its workload. 164 Chapter 19 Table 19-8 continued Common Medication Prescribed to Cardiovascular Patients Medication Trade name (Drug name) Medication Effect Physical Therapy Considerations ACE-inhibitor Antihypertensive, vaso- Light headedness and dizziness especially with exer- Accupril (quina- dilator and used in pat- cise or hot weather. Frequent dry irritating cough. pril), Altace ients with congestive (ramipril),Capo- heart failure or with an MI. ten (captopril), Monopril (fosin- opril),Vasotec (enalapril). Angiotensin II Similar to ACE-inhibitor Receptor blocker but more specific action Lorsartan (coz- with fewer side effects. aar), Valsartan (diovan). Nitrol (nitro- Lowers systolic BP and Ensure patients carry their nitro with them if they have glycerin), Isordil dilates systemic veins, frequent angina. (isosorbide) thus reducing myocardial wall tension, a major de- terminant of myocardial oxygen need. Used for treatment of angina. Streptokinase, Thrombolytic frequently Increased risk of bleeding. Follow specific protocol in anistreplase, used in MI patients. coronary care unit. alteplase, and reteplase. Aspirin Prevents thrombus form- Bleeding. Plavix (clopid- ation by inhibition of ogrel) platelet aggregation. Heparin Anticoagulation therapy Patient is prone to bruising and bleeding. Coumadin (clot-preventing medication) (warfarin). consists of intravenous infusion of heparin initially, follow by oral warfarin. Abbreviations: ACE: angiotensin-converting enzyme EXERCISES Photocopy Table 18-3, Problems and Associated Outcome Measures, and complete a table for cardiac con- ditions by identifying outcome measures that could be used by a physical therapist to evaluate whether improve- ment has occurred after treatment for a specific problem. The problems are grouped because often outcome measures do not distinctly reflect 1 problem but may reflect similar or related problems.