Cardiovascular System
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| Pathophysiologic manifestations | |
| Aneurysm | |
| Cardiac shunts | |
| Embolus | |
| Release of cardiac enzymes and proteins | |
| Stenosis | |
| Thrombus | |
| Valve incompetence | |
| Disorders | |
| Atrial septal defect | |
| Cardiac arrhythmias | |
| Cardiac tamponade | |
| Cardiomyopathy | |
| Coarctation of the aorta | |
| Coronary artery disease | |
| Heart failure | |
| Hypertension | |
| Myocardial infarction | |
| Myocarditis | |
| Patent ductus arteriosus | |
| Pericarditis | |
| Raynaud's disease | |
| Rheumatic fever and rheumatic heart disease | |
| Shock | |
| Tetralogy of Fallot | |
| Transposition of the great arteries | |
| Valvular heart disease | |
| Varicose veins | |
| Ventricular septal defect |
T he cardiovascular system begins its activity when the fetus is barely 4 weeks old and is the last system to cease activity at the end of life. This body system is so vital that its activity helps define the presence of life.
The heart, arteries, veins, and lymphatics form the cardiovascular network that serves the body's transport system. This system brings life-supporting oxygen and nutrients to cells, removes metabolic waste products, and carries hormones from one part of the body to another.
The cardiovascular system, often called the circulatory system, may be divided into two branches: pulmonary and systemic circulations. In pulmonary circulation , blood picks up oxygen and liberates the waste product carbon dioxide. In systemic circulation (which includes coronary circulation), blood carries oxygen and nutrients to all active cells and transports waste products to the kidneys, liver, and skin for excretion.
Circulation requires normal heart function, which propels blood through the system by continuous rhythmic contractions. Blood circulates through three types of vessels: arteries, veins, and capillaries. The sturdy, pliable walls of the arteries adjust to the volume of blood leaving the heart. The aorta is the major artery arching out of the left ventricle; its segments and sub-branches ultimately divide into minute, thin-walled (one cell thick) capillaries. Capillaries pass the blood to the veins, which return it to the heart. In the veins, valves prevent blood backflow.
PATHOPHYSIOLOGIC MANIFESTATIONS
Pathophysiologic manifestations of cardiovascular disease may stem from aneurysm, cardiac shunts, embolus, release of cardiac enzymes, stenosis, thrombus, and valve incompetence.
Aneurysm
An aneurysm is a localized outpouching or dilation of a weakened arterial wall. This weakness can be the result of either atherosclerotic plaque formation that erodes the vessel wall, or the loss of elastin and collagen in the vessel wall. Congenital abnormalities in the media of the arterial wall, trauma, and infections such as syphilis may lead to aneurysm formation. A ruptured aneurysm may cause massive hemorrhage and death.
Several types of aneurysms can occur:
- A saccular aneurysm occurs when increased pressure in the artery pushes out a pouch on one side of the artery, creating a bulge. (See Types of aortic aneurysms .)
- A fusiform aneurysm develops when the arterial wall weakens around its circumference, creating a spindle-shaped aneurysm.
- A dissecting aneurysm occurs when blood is forced between the layers of the arterial wall, causing them to separate and creating a false lumen.
- A false aneurysm develops when there is a break in all layers of the arterial wall and blood leaks out but is contained by surrounding structures, creating a pulsatile hematoma.
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TYPES OF AORTIC ANEURYSMS
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Cardiac shunts
A cardiac shunt provides communication between the pulmonary and systemic circulations. Before birth, shunts between the right and left sides of the heart and between the aorta and pulmonary artery are a normal part of fetal circulation. Following birth, however, the mixing of pulmonary and systemic blood or the movement of blood between the left and right sides of the heart is abnormal. Blood flows through a shunt from an area of high pressure to an area of low pressure or from an area of high resistance to an area of low resistance.
Left-to-right shunts
In a left-to-right shunt, blood flows from the left side of the heart to the right side through an atrial or ventricular defect, or from the aorta to the pulmonary circulation through a patent ductus arteriosus. Because the blood in the left side of the heart is rich in oxygen, a left-to-right shunt delivers oxygenated blood back to the right side of the heart or to the lungs. Consequently, a left-to-right shunt that occurs as a result of a congenital heart defect is called an acyanotic defect .
In a left-to-right shunt, pulmonary blood flow increases as blood is continually recirculated to the lungs, leading to hypertrophy of the pulmonary vessels. The increased amounts of blood circulated from the left side of the heart to the right side can result in right-sided heart failure. Eventually, left-sided heart failure may also occur.
Right-to-left shunts
A right-to-left shunt occurs when blood flows from the right side of the heart to the left side such as occurs in tetralogy of Fallot, or from the pulmonary artery directly into the systemic circulation through a patent ductus arteriosus. Because blood returning to the right side of the heart and the pulmonary artery is low in oxygen, a right-to-left shunt adds deoxygenated blood to the systemic circulation, causing hypoxia and cyanosis. Congenital defects that involve right-to-left shunts are therefore called cyanotic defects . Common manifestations of a right-to-left shunt related to poor tissue and organ perfusion include fatigue, increased respiratory rate, and clubbing of the fingers.
Embolus
An embolus is a substance that circulates from one location in the body to another, through the bloodstream. Although most emboli are blood clots from a thrombus, they may also consist of pieces of tissue, an air bubble, amniotic fluid, fat, bacteria, tumor cells, or a foreign substance.
Emboli that originate in the venous circulation, such as from deep vein thrombosis, travel to the right side of the heart to the pulmonary circulation and eventually lodge in a capillary, causing pulmonary infarction and even death. Most emboli in the arterial system originate from the left side of the heart from conditions such as arrhythmias, valvular heart disease, myocardial infarction, heart failure, or endocarditis. Arterial emboli may lodge in organs, such as the brain, kidneys, or extremities, causing ischemia or infarction.
Release of cardiac enzymes and proteins
When the heart muscle is damaged, the integrity of the cell membrane is impaired, and intracellular contents ― including cardiac enzymes and proteins ― are released and can be measured in the bloodstream. The release follows a characteristic rising and falling of values. The released enzymes include creatine kinase, lactate dehydrogenase, and aspartate aminotransferase; the proteins released include troponin T, troponin I, and myoglobin. (See Release of cardiac enzymes and proteins .)
Stenosis
Stenosis is the narrowing of any tubular structure such as a blood vessel or heart valve. When an artery is stenosed, the tissues and organs perfused by that blood vessel may become ischemic, function abnormally, or die. An occluded vein may result in venous congestion and chronic venous insufficiency.
When a heart valve is stenosed, blood flow through that valve is reduced, causing blood to accumulate in the chamber behind the valve. Pressure in that chamber rises in order to pump against the resistance of the stenosed valve. Consequently, the heart has to work harder, resulting in hypertrophy. Hypertrophy and an increase in workload raise the oxygen demands of the heart. A heart with diseased coronary arteries may not be able to sufficiently increase oxygen supply to meet the increased demand.
When stenosis occurs in a valve on the left side of the heart, the increased pressure leads to greater pulmonary venous pressure and pulmonary congestion. As pulmonary vascular resistance rises, right-sided heart failure may occur. Stenosis in a valve on the right side of the heart causes an increase in pressures on the right side of the heart, leading to systemic venous congestion.
Thrombus
A thrombus is a blood clot, consisting of platelets, fibrin, and red and white blood cells, that forms anywhere within the vascular system, such as the arteries, veins, heart chambers, or heart valves.
Three conditions, known as Virchow's triad, promote thrombus formation: endothelial injury, sluggish blood flow, and increased coagulability. When a blood vessel wall is injured, the endothelial lining attracts platelets and other inflammatory mediators, which may stimulate clot formation. Sluggish or abnormal blood flow also promotes thrombus formation by allowing platelets and clotting factors to accumulate and adhere to the blood vessel walls. Conditions that increase the coagulability of blood also promote clot formation.
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RELEASE OF CARDIAC ENZYMES AND PROTEINS
Because they're released by damaged tissue, serum enzymes and isoenzymes ― catalytic proteins that vary in concentration in specific organs ― can help identify the compromised organ and assess the extent of damage. After acute myocardial infarction (MI), cardiac enzymes and proteins rise and fall in a characteristic pattern, as shown in the graph below. <center></center> |
The consequences of thrombus formation include occlusion of the blood vessel or the formation of an embolus (if a portion of a thrombus breaks loose and travels through the circulatory system until it lodges in a smaller vessel).
Valve incompetence
Valve incompetence, also called insufficiency or regurgitation, occurs when valve leaflets do not completely close. Incompetence may affect valves of the veins or the heart.
In the veins, valves keep the blood flowing in one direction, toward the heart. When valve leaflets close improperly, blood flows backward and pools above, causing that valve to weaken and become incompetent. Eventually, the veins become distended, which may result in varicose veins, chronic venous insufficiency, and venous ulcers. Blood clots may form as blood flow becomes sluggish.
In the heart, incompetent valves allow blood to flow in both directions through the valve, increasing the volume of blood that must be pumped (as well as the heart's workload) and resulting in hypertrophy. As blood volume in the heart increases, the involved heart chambers dilate to accommodate the increased volume. Although incompetence may occur in any of the valves of the heart, it's more common in the mitral and aortic valves.
DISORDERS
Atrial septal defect
In this acyanotic congenital heart defect, an opening between the left and right atria allows the blood to flow from left to right, resulting in ineffective pumping of the heart, thus increasing the risk of heart failure.
The three types of atrial septal defects (ASDs) are:
- an ostium secundum defect , the most common type, which occurs in the region of the fossa ovalis and, occasionally, extends inferiorly, close to the vena cava
- a sinus venosus defect that occurs in the superior-posterior portion of the atrial septum, sometimes extending into the vena cava, and is almost always associated with abnormal drainage of pulmonary veins into the right atrium
- an ostium primum defect that occurs in the inferior portion of the septum primum and is usually associated with atrioventricular valve abnormalities (cleft mitral valve) and conduction defects.
ASD accounts for about 10% of congenital heart defects and appears almost twice as often in females as in males, with a strong familial tendency. Although an ASD is usually a benign defect during infancy and childhood, delayed development of symptoms and complications makes it one of the most common congenital heart defects diagnosed in adults.
The prognosis is excellent in asymptomatic patients and in those with uncomplicated surgical repair, but poor in patients with cyanosis caused by large, untreated defects.
Causes
The cause of an ASD is unknown. Ostium primum defects commonly occur in patients with Down syndrome.
Pathophysiology
In an ASD, blood shunts from the left atrium to the right atrium because the left atrial pressure is normally slightly higher than the right atrial pressure. This shunt results in right heart volume overload, affecting the right atrium, right ventricle, and pulmonary arteries. Eventually, the right atrium enlarges, and the right ventricle dilates to accommodate the increased blood volume. If pulmonary artery hypertension develops, increased pulmonary vascular resistance and right ventricular hypertrophy follow. In some adults, irreversible pulmonary artery hypertension causes reversal of the shunt direction, which results in unoxygenated blood entering the systemic circulation, causing cyanosis.
Signs and symptoms
The following are signs and symptoms of an ASD:
- fatigue after exertion due to decreased cardiac output from the left ventricle
- early to midsystolic murmur at the second or third left intercostal space, caused by extra blood passing through the pulmonic valve
- low-pitched diastolic murmur at the lower left sternal border, more pronounced on inspiration, resulting from increased tricuspid valve flow in patients with large shunts
- fixed, widely split S 2 due to delayed closure of the pulmonic valve, resulting from an increased volume of blood
- systolic click or late systolic murmur at the apex, resulting from mitral valve prolapse in older children with ASD
- clubbing and cyanosis, if right-to-left shunt develops.
| AGE ALERT An infant may be cyanotic because he has a cardiac or pulmonary disorder. Cyanosis that worsens with crying is most likely associated with cardiac causes because crying increases pulmonary resistance to blood flow, resulting in an increased right-to-left shunt. Cyanosis that improves with crying is most likely due to pulmonary causes as deep breathing improves tidal volume. |
Complications
Complications of an ASD may include:
- physical underdevelopment
- respiratory infections
- heart failure
- atrial arrhythmias
- mitral valve prolapse.
Diagnosis
The following tests help diagnose atrial septal defect:
- Chest X-rays show an enlarged right atrium and right ventricle, a prominent pulmonary artery, and increased pulmonary vascular markings.
- Electrocardiography results may be normal but often show right axis deviation, prolonged PR interval, varying degrees of right bundle branch block, right ventricular hypertrophy, atrial fibrillation (particularly in severe cases after age 30) and, in ostium primum defect, left axis deviation.
- Echocardiography measures right ventricular enlargement, may locate the defect, and shows volume overload in the right side of the heart. It may reveal right ventricular and pulmonary artery dilation.
- Cardiac catheterization may confirm an ASD. Right atrial blood is more oxygenated than superior vena caval blood, indicating a left-to-right shunt, and determines the degree of shunting and pulmonary vascular disease. Dye injection shows the defect's size and location, the location of pulmonary venous drainage, and the competence of the atrioventricular valves.
Treatment
Correcting an ASD typically involves:
- surgery to repair the defect by age 3 to 6, using a patch of pericardium or prosthetic material. A small defect may be sutured closed. Monitor for arrhythmias postoperatively because edema of the atria may interfere with sinoatrial node function.
- valve repair if heart valves are involved
- antibiotic prophylaxis to prevent infective endocarditis
- antiarrhythmic medication to treat arrhythmias.
Cardiac arrhythmias
In arrhythmias, abnormal electrical conduction or automaticity changes heart rate and rhythm. Arrhythmias vary in severity, from those that are mild, asymptomatic, and require no treatment (such as sinus arrhythmia, in which heart rate increases and decreases with respiration) to catastrophic ventricular fibrillation, which requires immediate resuscitation. Arrhythmias are generally classified according to their origin (ventricular or supraventricular). Their effect on cardiac output and blood pressure, partially influenced by the site of origin, determines their clinical significance.
Causes
Common causes of arrhythmias include:
- congenital defects
- myocardial ischemia or infarction
- organic heart disease
- drug toxicity
- degeneration of the conductive tissue
- connective tissue disorders
- electrolyte imbalances
- cellular hypoxia
- hypertrophy of the heart muscle
- acid-base imbalances
- emotional stress.
However, each arrhythmia may have its own specific causes. (See Types of cardiac arrhythmias .)
Pathophysiology
Arrhythmias may result from enhanced automaticity, reentry, escape beats, or abnormal electrical conduction. (See Comparing normal and abnormal conduction .)
Signs and symptoms
Signs and symptoms of arrhythmias result from reduced cardiac output and altered perfusion to the organs, and may include:
- dyspnea
- hypotension
- dizziness, syncope, and weakness
- chest pain
- cool, clammy skin
- altered level of consciousness
- reduced urinary output.
Complications
Possible complications of arrhythmias include:
- sudden cardiac death
- myocardial infarction
- heart failure
- thromboembolism.
Diagnosis
- Electrocardiography detects arrhythmias as well as ischemia and infarction that may result in arrhythmias.
- Laboratory testing may reveal electrolyte abnormalities, acid-base abnormalities, or drug toxicities that may cause arrhythmias.
- Holter monitoring detects arrhythmias and effectiveness of drug therapy during a patient's daily activities.
- Exercise testing may detect exercise-induced arrhythmias.
- Electrophysiologic testing identifies the mechanism of an arrhythmia and the location of accessory pathways; it also assesses the effectiveness of antiarrhythmic drugs.
Treatment
Follow the specific treatment guidelines for each arrhythmia. (See Types of cardiac arrhythmias .)
Cardiac tamponade
Cardiac tamponade is a rapid, unchecked rise in pressure in the pericardial sac that compresses the heart, impairs diastolic filling, and reduces cardiac output. The rise in pressure usually results from blood or fluid accumulation in the pericardial sac. Even a small amount of fluid (50 to 100 ml) can cause a serious tamponade if it accumulates rapidly.
Prognosis depends on the rate of fluid accumulation. If fluid accumulates rapidly, cardiac tamponade requires emergency lifesaving measures to prevent death. A slow accumulation and rise in pressure may not produce immediate symptoms because the fibrous wall of the pericardial sac can gradually stretch to accommodate as much as 1 to 2 L of fluid.
Causes
Cause of cardiac tamponade may include:
- idiopathic causes (e.g., Dressler's syndrome)
- effusion (from cancer, bacterial infections, tuberculosis and, rarely, acute rheumatic fever)
- hemorrhage from trauma (such as gunshot or stab wounds of the chest)
- hemorrhage from nontraumatic causes (such as anticoagulant therapy in patients with pericarditis or rupture of the heart or great vessels)
- viral or postirradiation pericarditis
- chronic renal failure requiring dialysis
- drug reaction from procainamide, hydralazine, minoxidil, isoniazid, penicillin, methysergide maleate, or daunorubicin
- connective tissue disorders (such as rheumatoid arthritis, systemic lupus erythematosus, rheumatic fever, vasculitis, and scleroderma)
- acute myocardial infarction.
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TYPES OF CARDIAC ARRHYTHMIAS
This chart reviews many common cardiac arrhythmias and outlines their features, causes, and treatments. Use a normal electrocardiogram strip, if available, to compare normal cardiac rhythm configurations with the rhythm strips below. Characteristics of normal sinus rhythm include:
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Pathophysiology
In cardiac tamponade, the progressive accumulation of fluid in the pericardial sac causes compression of the heart chambers. This compression obstructs blood flow into the ventricles and reduces the amount of blood that can be pumped out of the heart with each contraction. (See Understanding cardiac tamponade .)
Each time the ventricles contract, more fluid accumulates in the pericardial sac. This further limits the amount of blood that can fill the ventricular chambers, especially the left ventricle, during the next cardiac cycle.
The amount of fluid necessary to cause cardiac tamponade varies greatly; it may be as little as 200 ml when the fluid accumulates rapidly or more than 2,000 ml if the fluid accumulates slowly and the pericardium stretches to adapt.
Signs and symptoms
The following signs and symptoms may occur:
- elevated central venous pressure (CVP) with neck vein distention due to increased jugular venous pressure
- muffled heart sounds caused by fluid in the pericardial sac
- pulsus paradoxus (an inspiratory drop in systemic blood pressure greater than 15 mm Hg) due to impaired diastolic filling
- diaphoresis and cool clammy skin caused by a drop in cardiac output
- anxiety, restlessness, and syncope due to a drop in cardiac output
- cyanosis due to reduced oxygenation of the tissues
- weak, rapid pulse in response to a drop in cardiac output
- cough, dyspnea, orthopnea, and tachypnea because the lungs are compressed by an expanding pericardial sac.
Complications
Reduced cardiac output may be fatal without prompt treatment.
Diagnosis
- Chest X-rays show slightly widened mediastinum and possible cardiomegaly. The cardiac silhouette may have a goblet-shaped appearance.
- Electrocardiography (ECG) may show low-amplitude QRS complex and electrical alternans, an alternating beat-to-beat change in amplitude of the P wave, QRS complex, and T wave. Generalized ST-segment elevation is noted in all leads. An ECG is used to rule out other cardiac disorders; it may reveal changes produced by acute pericarditis.
- Pulmonary artery catheterization detects increased right atrial pressure, right ventricular diastolic pressure, and CVP.
- Echocardiography may reveal pericardial effusion with signs of right ventricular and atrial compression.
Treatment
Correcting cardiac tamponade typically involves:
- supplemental oxygen to improve oxygenation
- continuous ECG and hemodynamic monitoring in an intensive care unit to detect complications and monitor effects of therapy
- pericardiocentesis (needle aspiration of the pericardial cavity) to reduce fluid in the pericardial sac and improve systemic arterial pressure and cardiac output. A catheter may be left in the pericardial space attached to a drainage bag to allow for continuous drainage of fluid
- pericardectomy ― the surgical creation of an opening to remove accumulated fluid from the pericardial sac
- resection of a portion or all of the pericardium to allow full communication with the pleura, if repeated pericardiocentesis fails to prevent recurrence
- trial volume loading with crystalloids such as intravenous 0.9% normal saline to maintain systolic blood pressure
- inotropic drugs, such as isoproterenol or dopamine, to improve myocardial contractility until fluid in the pericardial sac can be removed
- in traumatic injury, a blood transfusion or a thoracotomy to drain reaccumulating fluid or to repair bleeding sites may be necessary
- heparin-induced tamponade requires administration of heparin antagonist protamine sulfate to stop bleeding
- warfarin-induced tamponade may necessitate use of vitamin K to stop bleeding.
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COMPARING NORMAL AND ABNORMAL CONDUCTION
NORMAL CARDIAC CONDUCTION
ABNORMAL CARDIAC CONDUCTION
Altered automaticity
Automaticity may be enhanced by drugs such as epinephrine, atropine, and digoxin and conditions such as acidosis, alkalosis, hypoxia, myocardial infarction, hypokalemia, and hypocalcemia. Examples of arrhythmias caused by enhanced automaticity include atrial fibrillation and flutter; supraventricular tachycardia; premature atrial, junctional, and ventricular complexes; ventricular tachycardia and fibrillation; and accelerated idioventricular and junctional rhythms.
Reentry
Conditions that increase the likelihood of reentry include hyperkalemia, myocardial ischemia, and the use of certain antiarrhythmic drugs. Reentry may be responsible for dysrhythmias such as paroxysmal supraventricular tachycardia; premature atrial, junctional, and ventricular complexes; and ventricular tachycardia. An alternative reentry mechanism depends on the presence of a congenital accessory pathway linking the atria and the ventricles outside the AV junction, for example, Wolff-Parkinson-White syndrome.
Conduction disturbances
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Cardiomyopathy
Cardiomyopathy generally applies to disease of the heart muscle fibers, and it occurs in three main forms: dilated, hypertrophic, and restrictive (extremely rare). Cardiomyopathy is the second most common direct cause of sudden death; coronary artery disease is first. Approximately 5 to 8 per 100,000 Americans have dilated congestive cardiomyopathy , the most common type. At greatest risk of cardiomyopathy are males and blacks; other risk factors include hypertension, pregnancy, viral infections, and alcohol use. Because dilated cardiomyopathy is usually not diagnosed until its advanced stages, the prognosis is generally poor. The course of hypertrophic cardiomyopathy is variable. Some patients progressively deteriorate, whereas others remain stable for years. It is estimated that almost 50% of all sudden deaths in competitive athletes age 35 or younger are due to hypertrophic cardiomyopathy. If severe, restrictive cardiomyopathy is irreversible.
Causes
Most patients with cardiomyopathy have idiopathic, or primary, disease, but some are secondary to identifiable causes. (See Comparing the cardiomyopathies .) Hypertrophic cardiomyopathy is almost always inherited as a non�sex-linked autosomal dominant trait.
Pathophysiology
Dilated cardiomyopathy results from extensively damaged myocardial muscle fibers. Consequently, there is reduced contractility in the left ventricle. As systolic function declines, stroke volume, ejection fraction, and cardiac output fall. As end-diastolic volumes rise, pulmonary congestion may occur. The elevated end-diastolic volume is a compensatory response to preserve stroke volume despite a reduced ejection fraction. The sympathetic nervous system is also stimulated to increase heart rate and contractility. The kidneys are stimulated to retain sodium and water to maintain cardiac output, and vasoconstriction also occurs as the renin-angiotensin system is stimulated. When these compensatory mechanisms can no longer maintain cardiac output, the heart begins to fail. Left ventricular dilation occurs as venous return and systemic vascular resistance rise. Eventually, the atria also dilate as more work is required to pump blood into the full ventricles. Cardiomegaly occurs as a consequence of dilation of the atria and ventricles. Blood pooling in the ventricles increases the risk of emboli.
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UNDERSTANDING CARDIAC TAMPONADE
<center> <br /> </center> The pericardial sac, which surrounds and protects the heart, is composed of several layers. The fibrous pericardium is the tough outermost membrane; the inner membrane, called the serous membrane, consists of the visceral and parietal layers. The visceral layer clings to the heart and is also known as the epicardial layer of the heart. The parietal layer lies between the visceral layer and the fibrous pericardium. The pericardial space ― between the visceral and parietal layers ― contains 10 to 30 ml of pericardial fluid. This fluid lubricates the layers and minimizes friction when the heart contracts. <center></center>In cardiac tamponade, blood or fluid fills the pericardial space, compressing the heart chambers, increasing intracardiac pressure, and obstructing venous return. As blood flow into the ventricles falls, so does cardiac output. Without prompt treatment, low cardiac output can be fatal. |
| AGE ALERT Barth syndrome is a rare genetic disorder that can cause dilated cardiomyopathy in boys. This syndrome may be associated with skeletal muscle changes, short stature, neutropenia, and increased susceptibility to bacterial infections. Evidence of dilated cardiomyopathy may appear as early as the first few days or months of life. |
Unlike dilated cardiomyopathy, which affects systolic function, hypertrophic cardiomyopathy primarily affects diastolic function. The features of hypertrophic cardiomyopathy include asymmetrical left ventricular hypertrophy; hypertrophy of the intraventricular septum; rapid, forceful contractions of the left ventricle; impaired relaxation; and obstruction to left ventricular outflow. The hypertrophied ventricle becomes stiff, noncompliant, and unable to relax during ventricular filling. Consequently, ventricular filling is reduced and left ventricular filling pressure rises, causing a rise in left atrial and pulmonary venous pressures and leading to venous congestion and dyspnea. Ventricular filling time is further reduced as a compensatory response to tachycardia. Reduced ventricular filling during diastole and obstruction to ventricular outflow lead to low cardiac output. If papillary muscles become hypertrophied and do not close completely during contraction, mitral regurgitation occurs. Moreover, intramural coronary arteries are abnormally small and may not be sufficient to supply the hypertrophied muscle with enough blood and oxygen to meet the increased needs of the hyperdynamic muscle.
Restrictive cardiomyopathy is characterized by stiffness of the ventricle caused by left ventricular hypertrophy and endocardial fibrosis and thickening, thus reducing the ability of the ventricle to relax and fill during diastole. Moreover, the rigid myocardium fails to contract completely during systole. As a result, cardiac output falls.
Signs and symptoms
Clinical manifestations of dilated cardiomyopathy may include:
- shortness of breath, orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, fatigue, and a dry cough at night due to left-sided heart failure
- peripheral edema, hepatomegaly, jugular venous distention, and weight gain caused by right-sided heart failure
- peripheral cyanosis associated with a low cardiac output
- tachycardia as a compensatory response to low cardiac output
- pansystolic murmur associated with mitral and tricuspid insufficiency secondary to cardiomegaly and weak papillary muscles
- S 3 and S 4 gallop rhythms associated with heart failure
- irregular pulse if atrial fibrillation exists.
Clinical manifestations of hypertrophic cardiomyopathy may include:
- angina caused by the inability of the intramural coronary arteries to supply enough blood to meet the increased oxygen demands of the hypertrophied heart
- syncope resulting from arrhythmias or reduced ventricular filling leading to a reduced cardiac output
- dyspnea due to elevated left ventricular filling pressure
- fatigue associated with a reduced cardiac output
- systolic ejection murmur along the left sternal border and at the apex caused by mitral regurgitation
- peripheral pulse with a characteristic double impulse (pulsus biferiens) caused by powerful left ventricular contractions and rapid ejection of blood during systole
- abrupt arterial pulse secondary to vigorous left ventricular contractions
- irregular pulse if an enlarged atrium causes atrial fibrillation.
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COMPARING THE CARDIOMYOPATHIES
Cardiomyopathies include a variety of structural or functional abnormalities of the ventricles. They are grouped into three main pathophysiologic types ― dilated, hypertrophic, and restrictive. These conditions may lead to heart failure by impairing myocardial structure and function.
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COMPARING DIAGNOSTIC TESTS IN CARDIOMYOPATHY
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Clinical manifestations of restrictive cardiomyopathy may include:
- fatigue, dyspnea, orthopnea, chest pain, edema, liver engorgement, peripheral cyanosis, pallor, and S 3 or S 4 gallop rhythms due to heart failure
- systolic murmurs caused by mitral and tricuspid insufficiency.
Possible complications of cardiomyopathy include:
The following tests help diagnose cardiomyopathy:
- Echocardiography confirms dilated cardiomyopathy.
- Chest X-ray may reveal cardiomegaly associated with any of the cardiomyopathies.
- Cardiac catheterization with possible heart biopsy can be definitive with hypertrophic cardiomyopathy.
- Diagnosis requires elimination of other possible causes of heart failure and arrhythmias. (See Comparing diagnostic tests in cardiomyopathy .)
Correction of dilated cardiomyopathy may involve:
- treatment of the underlying cause, if identifiable
- angiotensin-converting enzyme (ACE) inhibitors, as first-line therapy, to reduce afterload through vasodilation
- diuretics, taken with ACE inhibitors, to reduce fluid retention
- digoxin, for patients not responding to ACE inhibitor and diuretic therapy, to improve myocardial contractility
- hydralazine and isosorbide dinitrate, in combination, to produce vasodilation
- beta-adrenergic blockers for patients with New York Heart Association class II or III heart failure. (See Classifying heart failure .)
- antiarrythmics such as amiodarone, used cautiously, to control arrhythmias
- cardioversion to convert atrial fibrillation to sinus rhythm
- pacemaker insertion to correct arrhythmias
- anticoagulants (controversial) to reduce the risk of emboli
- revascularization, such as coronary artery bypass graft surgery, if dilated cardiomyopathy is due to ischemia
- valvular repair or replacement, if dilated cardiomyopathy is due to valve dysfunction
- heart transplantation in patients refractory to medical therapy
- lifestyle modifications, such as smoking cessation; low-fat, low-sodium diet; physical activity; and abstinence from alcohol.
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CLASSIFYING HEART FAILURE
The New York Heart Association (NYHA) classification is a universal gauge of heart failure severity based on physical limitations. CLASS I: MINIMAL
CLASS II: MILD
CLASS III: MODERATE
CLASS IV: SEVERE
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Correction of hypertrophic cardiomyopathy may involve:
- beta-adrenergic blockers to slow the heart rate, reduce myocardial oxygen demands, and increase ventricular filling by relaxing the obstructing muscle, thereby increasing cardiac output
- antiarrhythmic drugs, such as amiodarone, to reduce arrhythmias
- cardioversion to treat atrial fibrillation
- anticoagulation to reduce risk of systemic embolism with atrial fibrillation
- verapamil and diltiazem to reduce ventricular stiffness and elevated diastolic pressures
- ablation of the atrioventricular node and implantation of a dual-chamber pacemaker (controversial), in patients with obstructive hypertrophic cardiomyopathy and ventricular tachycardias, to reduce the outflow gradient by altering the pattern of ventricular contraction
- implantable cardioverter-defibrillator to treat ventricular arrhythmias
- ventricular myotomy or myectomy (resection of the hypertrophied septum) to ease outflow tract obstruction and relieve symptoms
- mitral valve replacement to treat mitral regurgitation
- cardiac transplantation for intractable symptoms.
Correction of restrictive cardiomyopathy may involve:
- treatment of the underlying cause, such as administering deferoxamine to bind iron in restrictive cardiomyopathy due to hemochromatosis
- although no therapy exists for restricted ventricular filling, digoxin, diuretics, and a restricted sodium diet may ease the symptoms of heart failure
- oral vasodilators may control intractable heart failure.
Coarctation of the aorta
Although the cause of this defect is unknown, it may be associated with Turner's syndrome.
The following signs and symptoms may occur:
- during the first year of life, an infant may display tachypnea, dyspnea, pulmonary edema, pallor, tachycardia, failure to thrive, cardiomegaly, and hepatomegaly due to heart failure
- claudication due to reduced blood flow to the legs
- hypertension in the upper body due to increased pressure in the arteries proximal to the coarctation
- headache, vertigo, and epistaxis secondary to hypertension
- upper extremity blood pressure greater than lower extremity blood pressure because blood flow through the coarctation is greater to the upper body than to the lower body
- pink upper extremities and cyanotic lower extremities due to reduced oxygenated blood reaching the legs
- absent or diminished femoral pulses due to restricted blood flow to the lower extremities through the constricted aorta
- continuous midsystolic murmur due to left-to-right shunting of the blood; the murmur is best heard at the base of the heart
- chest and arms may be more developed than the legs because circulation to legs is restricted.
Possible complications of this defect include:
- heart failure
- severe hypertension
- cerebral aneurysms and hemorrhage
- rupture of the aorta
- aortic aneurysm
- infective endocarditis.
The following tests help diagnose coarctation of the aorta:
- Physical examination reveals the cardinal signs ― resting systolic hypertension in the upper body, absent or diminished femoral pulses, and a wide pulse pressure.
- Chest X-rays may demonstrate left ventricular hypertrophy, heart failure, a wide ascending and descending aorta, and notching of the undersurfaces of the ribs due to erosion by collateral circulation.
- Electrocardiography may reveal left ventricular hypertrophy.
- Echocardiography may show increased left ventricular muscle thickness, coexisting aortic valve abnormalities, and the coarctation site.
- Cardiac catheterization evaluates collateral circulation and measures pressure in the right and left ventricles and in the ascending and descending aortas (on both sides of the obstruction). Aortography locates the site and extent of coarctation.
Correction of coarctation of the aorta may involve:
- digoxin, diuretics, oxygen, and sedatives in infants with heart failure
- prostaglandin infusion to keep the ductus open
- antibiotic prophylaxis against infective endocarditis before and after surgery
- antihypertensive therapy for children with previous undetected coarctation until surgery is performed
- preparation of the infant with heart failure or hypertension for early surgery, or else surgery is delayed until the preschool years. A flap of the left subclavian artery may be used to reconstruct the aorta. Balloon angioplasty or resection with end-to-end anastomosis or use of a tubular graft may also be performed.
Coronary artery disease
ATHEROSCLEROTIC PLAQUE DEVELOPMENT
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The following signs and symptoms may occur:
- angina, the classic sign of CAD, results from a reduced supply of oxygen to the myocardium. It may be described as burning, squeezing, or tightness in the chest that may radiate to the left arm, neck, jaw, or shoulder blade (See Types of angina .)
- nausea and vomiting as a result of reflex stimulation of the vomiting centers by pain
- cool extremities and pallor caused by sympathetic stimulation
- diaphoresis due to sympathetic stimulation
- xanthelasma (fat deposits on the eyelids) occurs secondary to hyperlipidemia and atherosclerosis.
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TYPES OF ANGINA
There are four types of angina:
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| AGE ALERT CAD may be asymptomatic in the older adult because of a decrease in sympathetic response. Dyspnea and fatigue are two key signals of ischemia in an active, older adult. |
The following tests help diagnose coronary artery disease:
- Electrocardiography may be normal between anginal episodes. During angina, it may show ischemic changes, such as T-wave inversion, ST-segment depression and, possibly, arrhythmias. ST-segment elevation suggests Prinzmetal's angina.
- Exercise testing may be performed to detect ST-segment changes during exercise, indicating ischemia, and to determine a safe exercise prescription.
- Coronary angiography reveals location and degree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery beyond the narrowing.
- Myocardial perfusion imaging with thallium-201 may be performed during treadmill exercise to detect ischemic areas of the myocardium; they appear as “cold spots.”
- Stress echocardiography may show abnormal wall motion.
- nitrates, such as nitroglycerin (given sublingually, orally, transdermally, or topically in ointment form) or isosorbide dinitrate (given sublingually or orally) to reduce myocardial oxygen consumption
- beta-adrenergic blockers to reduce the workload and oxygen demands of the heart by reducing heart rate and peripheral resistance to blood flow
- calcium channel blockers to prevent coronary artery spasm
- antiplatelet drugs to minimize platelet aggregation and the risk of coronary occlusion
- antilipemic drugs to reduce serum cholesterol or triglyceride levels
- antihypertensive drugs to control hypertension
- estrogen replacement therapy to reduce the risk for CAD in postmenopausal women
- coronary artery bypass graft (CABG) surgery to restore blood flow by bypassing an occluded artery using another vessel
- “key hole” or minimally invasive surgery, an alternative to traditional CABG using fiber-optic cameras inserted through small cuts in the chest, to correct blockages in one or two accessible arteries
- angioplasty, to relieve occlusion in patients without calcification and partial occlusion
- laser angioplasty to correct occlusion by vaporizing fatty deposits
- rotational atherectomy to remove arterial plaque with a high-speed burr
- stent placement in a reopened artery to hold the artery open
- lifestyle modifications to reduce further progression of CAD; these include smoking cessation, regular exercise, maintaining an ideal body weight, and following a low-fat, low-sodium diet.
Heart failure
Causes of heart failure may be divided into four general categories. (See Causes of heart failure .)
CAUSES OF HEART FAILURE
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Early clinical manifestations of left-sided heart failure include:
- dyspnea caused by pulmonary congestion
- orthopnea as blood is redistributed from the legs to the central circulation when the patient lies down at night
- paroxysmal nocturnal dyspnea due to the reabsorption of interstitial fluid when lying down and reduced sympathetic stimulation while sleeping
- fatigue associated with reduced oxygenation and a lack of activity
- nonproductive cough associated with pulmonary congestion.
Later clinical manifestations of left-sided heart failure may include:
- crackles due to pulmonary congestion
- hemoptysis resulting from bleeding veins in the bronchial system caused by venous distention
- point of maximal impulse displaced toward the left anterior axillary line caused by left ventricular hypertrophy
- tachycardia due to sympathetic stimulation
- S 3 heart sound caused by rapid ventricular filling
- S 4 heart sound resulting from atrial contraction against a noncompliant ventricle
- cool, pale skin resulting from peripheral vasoconstriction
- restlessness and confusion due to reduced cardiac output.
Clinical manifestations of right-sided heart failure include:
- elevated jugular venous distention due to venous congestion
- positive hepatojugular reflux and hepatomegaly secondary to venous congestion
- right upper quadrant pain caused by liver engorgement
- anorexia, fullness, and nausea may be caused by congestion of the liver and intestines
- nocturia as fluid is redistributed at night and reabsorbed
- weight gain due to the retention of sodium and water
- edema associated with fluid volume excess
- ascites or anasarca caused by fluid retention.
| CULTURAL DIVERSITY In the Chinese culture, disagreement or discomfort isn't typically displayed openly. Direct questioning and vigilant assessment skills are necessary to ensure that a patient's quiet nature doesn't mask signs and symptoms that may be life-threatening. |
Acute complications of heart failure include:
Chronic complications include:
The following tests help diagnose heart failure:
- Chest X-rays show increased pulmonary vascular markings, interstitial edema, or pleural effusion and cardiomegaly.
- Electrocardiography may indicate hypertrophy, ischemic changes, or infarction, and may also reveal tachycardia and extrasystoles.
- Laboratory testing may reveal abnormal liver function tests and elevated blood urea nitrogen and creatinine levels.
- Echocardiography may reveal left ventricular hypertrophy, dilation, and abnormal contractility.
- Pulmonary artery monitoring typically demonstrates elevated pulmonary artery and pulmonary artery wedge pressures, left ventricular end-diastolic pressure in left-sided heart failure, and elevated right atrial pressure or central venous pressure in right-sided heart failure.
- Radionuclide ventriculography may reveal an ejection fraction less than 40%; in diastolic dysfunction, the ejection fraction may be normal.
Correction of heart failure may involve:
- treatment of the underlying cause, if known
- angiotensin-converting enzyme (ACE) inhibitors to patients with left ventricle dysfunction to reduce production of angiotensin II, resulting in preload and afterload reduction
| AGE ALERT Older adults may require lower doses of ACE inhibitors because of impaired renal clearance. Monitor for severe hypotension, signifying a toxic effect. |
- digoxin for patients with heart failure due to left ventricular systolic dysfunction to increase myocardial contractility, improve cardiac output, reduce the volume of the ventricle, and decrease ventricular stretch
- diuretics to reduce fluid volume overload and venous return
- beta-adrenergic blockers in patients with New York Heart Association class II or class III heart failure caused by left ventricular systolic dysfunction to prevent remodeling (See Classifying heart failure .)
- diuretics, nitrates, morphine, and oxygen to treat pulmonary edema
- lifestyle modifications (to reduce symptoms of heart failure) such as weight loss (if obese); limited sodium (to 3 g/day) and alcohol intake; reduced fat intake; smoking cessation; reduced stress; and development of an exercise program. Heart failure is no longer a contraindication to exercise and cardiac rehabilitation.
| CULTURAL DIVERSITY Asian Americans consume large amounts of sodium. Encourage an Asian patient to substitute fresh vegetables, herbs, and spices for canned foods, monosodium glutamate, and soy sauce. |
- coronary artery bypass surgery or angioplasty for heart failure due to coronary artery disease
- cardiac transplantation in patients receiving aggressive medical treatment but still experiencing limitations or repeated hospitalizations
- other surgery or invasive procedures may be recommended in patients with severe limitations or repeated hospitalizations, despite maximal medical therapy. Some are controversial and may include cardiomyoplasty, insertion of an intra-aortic balloon pump, partial left ventriculectomy, use of a mechanical ventricular assist device, and implanting an internal cardioverter-defibrillator.
| AGE ALERT Heart failure in children occurs mainly as a result of congenital heart defects. Therefore, treatment guidelines are directed toward the specific cause. |
Hypertension
Risk factors for primary hypertension include:
| AGE ALERT Older adults may have isolated systolic hypertension (ISH), in which just the systolic blood pressure is elevated, as atherosclerosis causes a loss of elasticity in large arteries. Previously, it was believed that ISH was a normal part of the aging process and should not be treated. Results of the Systolic Hypertension in the Elderly Program (SHEP), however, found that treating ISH with antihypertensive drugs lowered the incidence of stroke, coronary artery disease (CAD), and left ventricular heart failure. |
| CULTURAL DIVERSITY Blacks are at increased risk for primary hypertension when predisposition to low plasma renin levels diminishes ability to excrete excess sodium. Hypertension develops at an earlier age and, at any age, it is more severe than in whites. |
- obesity
- tobacco use
- high intake of sodium
- high intake of saturated fat
- excessive alcohol consumption
- sedentary lifestyle
- stress
- excess renin
- mineral deficiencies (calcium, potassium, and magnesium)
- diabetes mellitus.
Causes of secondary hypertension include:
- coarctation of the aorta
- renal artery stenosis and parenchymal disease
- brain tumor, quadriplegia, and head injury
- pheochromocytoma, Cushing's syndrome, hyperaldosteronism, and thyroid, pituitary, or parathyroid dysfunction
- oral contraceptives, cocaine, epoetin alfa, sympathetic stimulants, monoamine oxidase inhibitors taken with tyramine, estrogen replacement therapy, and nonsteroidal anti-inflammatory drugs
- pregnancy-induced hypertension
- excessive alcohol consumption.
Several theories help to explain the development of hypertension, including:
- changes in the arteriolar bed causing increased peripheral vascular resistance
- abnormally increased tone in the sympathetic nervous system that originates in the vasomotor system centers, causing increased peripheral vascular resistance
- increased blood volume resulting from renal or hormonal dysfunction
- an increase in arteriolar thickening caused by genetic factors, leading to increased peripheral vascular resistance
- abnormal renin release, resulting in the formation of angiotensin II, which constricts the arteriole and increases blood volume. (See Understanding blood pressure regulation .)
The pathophysiology of secondary hypertension is related to the underlying disease. For example:
- The most common cause of secondary hypertension is chronic renal disease. Insult to the kidney from chronic glomerulonephritis or renal artery stenosis interferes with sodium excretion, the renin-angiotensin-aldosterone system, or renal perfusion, causing blood pressure to rise.
- In Cushing's syndrome, increased cortisol levels raise blood pressure by increasing renal sodium retention, angiotensin II levels, and vascular response to norepinephrine.
- In primary aldosteronism, increased intravascular volume, altered sodium concentrations in vessel walls, or very high aldosterone levels cause vasoconstriction and increased resistance.
- Pheochromocytoma is a chromaffin cell tumor of the adrenal medulla that secretes epinephrine and norepinephrine. Epinephrine increases cardiac contractility and rate, whereas norepinephrine increases peripheral vascular resistance.
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UNDERSTANDING BLOOD PRESSURE REGULATION
Hypertension may result from a disturbance in one of the following intrinsic mechanisms.
RENIN-ANGIOTENSIN SYSTEM
AUTOREGULATION
SYMPATHETIC NERVOUS SYSTEM
ANTIDIURETIC HORMONE
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Although hypertension is frequently asymptomatic, the following signs and symptoms may occur:
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WHAT HAPPENS IN HYPERTENSIVE CRISIS
Hypertensive crisis is a severe rise in arterial blood pressure caused by a disturbance in one or more of the regulating mechanisms. If untreated, hypertensive crisis may result in renal, cardiac, or cerebral complications and, possibly, death. <center></center> |
| AGE ALERT Because many older adults have a wide auscultatory gap ― the hiatus between the first Korotkoff sound and the next sound ― failure to pump the blood pressure cuff up high enough can lead to missing the first beat and underestimating the systolic blood pressure. To avoid missing the first Korotkoff sound, palpate the radial artery and inflate the cuff to a point approximately 20 mm beyond which the pulse beat disappears. |
- occipital headache (may worsen on rising in the morning as a result of increased intracranial pressure); nausea and vomiting may also occur
- epistaxis possibly due to vascular involvement
- bruits (which may be heard over the abdominal aorta or carotid, renal, and femoral arteries) caused by stenosis or aneurysm
- dizziness, confusion, and fatigue caused by decreased tissue perfusion due to vasoconstriction of blood vessels
- blurry vision as a result of damage to the retina
- nocturia caused by an increase in blood flow to the kidneys and an increase in glomerular filtration
- edema caused by increased capillary pressure.
Complications of hypertension include:
- hypertensive crisis, peripheral arterial disease, dissecting aortic aneurysm, CAD, angina, MI, heart failure, arrhythmias, and sudden death (See What happens in hypertensive crisis .)
- transient ischemic attacks, cerebrovascular accident, retinopathy, and hypertensive encephalopathy
- renal failure.
The following tests help diagnose hypertension:
- Serial blood pressure measurements may be useful.
- Urinalysis may show protein, casts, red blood cells, or white blood cells, suggesting renal disease; presence of catecholamines associated with pheochromocytoma; or glucose, suggesting diabetes.
- Laboratory testing may reveal elevated blood urea nitrogen and serum creatinine levels suggestive of renal disease, or hypokalemia indicating adrenal dysfunction (primary hyperaldosteronism).
- Complete blood count may reveal other causes of hypertension, such as polycythemia or anemia.
- Excretory urography may reveal renal atrophy, indicating chronic renal disease. One kidney smaller than the other suggests unilateral renal disease.
- Electrocardiography may show left ventricular hypertrophy or ischemia.
- Chest X-rays may show cardiomegaly.
- Echocardiography may reveal left ventricular hypertrophy.
- diuretics (thiazide diuretics such as hydrochlorothiazide, loop diuretics such as furosemide, and combination diuretics such as hydrochlorothiazide-spironolactone) to reduce excess fluid volume
RISK STRATIFICATION AND TREATMENT
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| CULTURAL DIVERSITY According to the treatment guidelines issued by the National Institutes of Health in 1997, drug therapy for blacks should consist of calcium channel blockers and diuretics. |
- beta blockers (such as metoprolol) to reduce heart rate and contractility, and to dilate the blood vessels
| CULTURAL DIVERSITY Asians are twice as sensitive as whites to propranolol and are able to metabolize and clear this drug more rapidly. Hypertensive whites are more responsive to beta blockers than are hypertensive blacks. |
- calcium channel blockers such as diltiazem to reduce heart rate and contractility; these agents are also effective against vasospasm
- angiotensin-converting enzyme (ACE) inhibitors such as captopril or angiotensin II receptor blockers such as valsartan to produce vasodilation
- alpha-receptor blockers such as doxazosin to produce vasodilation
- alpha-receptor agonists such as clonidine to lower peripheral vascular resistance
| AGE ALERT Older adults are at an increased risk for adverse effects of antihypertensives, especially orthostatic hypotension. Lower doses may be needed. |
- treatment of underlying cause of secondary hypertension and controlling hypertensive effects
- treatment of hypertensive emergencies with a parenteral vasodilator such as nitroprusside or an adrenergic inhibitor, or oral administration of a selected drug, such as nifedipine, captopril, clonidine, or labetalol, to rapidly reduce blood pressure
- lifestyle modifications, including weight control; limited alcohol, saturated fat, and sodium (2.4 g/day) intake; regular exercise; and smoking cessation
- inclusion of adequate amounts of calcium, magnesium, and potassium in the diet.
Myocardial infarction
Predisposing risk factors include:
- positive family history
- gender (men and postmenopausal women are more susceptible to MI than premenopausal women, although the incidence is rising among women, especially those who smoke and take oral contraceptives)
- hypertension
- smoking
- elevated serum triglyceride, total cholesterol, and low-density lipoprotein levels
- obesity
- excessive intake of saturated fats
- sedentary lifestyle
- aging
- stress or type A personality
- drug use, especially cocaine and amphetamines.
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ZONES OF MYOCARDIAL INFARCTION
Myocardial infarction has a central area of necrosis surrounded by a zone of injury that may recover if revascularization occurs. This zone of injury is surrounded by an outer ring of reversible ischemia. Characteristic electrocardiographic changes are associated with each zone. <center></center> |
The following signs and symptoms may occur:
- persistent, crushing substernal chest pain that may radiate to the left arm, jaw, neck, or shoulder blades caused by reduced oxygen supply to the myocardial cells; it may be described as heavy, squeezing, or crushing
| AGE ALERT Many older adults do not have chest pain with MI, but experience atypical symptoms such as fatigue, dyspnea, falls, tingling of the extremities, nausea, vomiting, weakness, syncope, and confusion. |
- cool extremities, perspiration, anxiety, and restlessness due to the release of catecholamines
- blood pressure and pulse initially elevated as a result of sympathetic nervous system activation. If cardiac output is reduced, blood pressure may fall. Bradycardia may be associated with conduction disturbances
- fatigue and weakness caused by reduced perfusion to skeletal muscles
- nausea and vomiting as a result of reflex stimulation of vomiting centers by pain fibers or from vasovagal reflexes
- shortness of breath and crackles reflecting heart failure
- low-grade temperature in the days following acute MI due to the inflammatory response
- jugular venous distention reflecting right ventricular dysfunction and pulmonary congestion
- S 3 and S 4 heart sounds reflecting ventricular dysfunction
- loud holosystolic murmur in apex possibly caused by papillary muscle rupture
- reduced urine output secondary to reduced renal perfusion and increased aldosterone and antidiuretic hormone.
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PINPOINTING MYOCARDIAL INFARCTION
Depending on location, ischemia or infarction causes changes in the following electrocardiographic leads.
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- arrhythmias
- cardiogenic shock
- heart failure causing pulmonary edema
- pericarditis
- rupture of the atrial or ventricular septum, ventricular wall, or valves
- mural thrombi causing cerebral or pulmonary emboli
- ventricular aneurysms
- myocardial rupture
- extensions of the original infarction.
The following tests help diagnose MI:
- Serial 12-lead electrocardiography (ECG) may reveal characteristic changes, such as serial ST-segment depression in non�Q-wave MI (subendocardial MI that affects the innermost myocardial layer) and ST-segment elevation in Q-wave MI (transmural MI with damage extending through all myocardial layers). An ECG can also identify the location of MI, arrhythmias, hypertrophy, and pericarditis. (See Pinpointing myocardial infarction .)
- Serial cardiac enzymes and proteins may show a characteristic rise and fall of cardiac enzymes, specifically CK-MB, and the proteins troponin T and I, and myoglobin to confirm the diagnosis of MI. (See Release of cardiac enzymes and proteins .)
- Laboratory testing may reveal elevated white blood cell count and erythrocyte sedimentation rate due to inflammation, and increased glucose levels following the release of catecholamines.
- Echocardiography may show ventricular wall motion abnormalities and may detect septal or papillary muscle rupture.
- Chest X-rays may show left-sided heart failure or cardiomegaly.
- Nuclear imaging scanning using thallium-201 and technetium 99m can be used to identify areas of infarction and areas of viable muscle cells.
- Cardiac catheterization may be used to identify the involved coronary artery as well as to provide information on ventricular function and pressures and volumes within the heart.
Treatment of an MI typically involves following the treatment guidelines recommended by the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines. These include:
- assessment of patients with chest pain in the Emergency Department within 10 minutes of an MI because at least 50% of deaths take place within 1 hour of the onset of symptoms. Moreover, thrombolytic therapy is most effective when started within the first 6 hours after the onset of symptoms
- oxygen by nasal cannula for 2 to 3 hours to increase oxygenation of the blood (See Blocking myocardial infarction .)
- nitroglycerin sublingually to relieve chest pain, unless systolic blood pressure is less than 90 mm Hg or heart rate is less than 50 or greater than 100 beats per minute
- morphine or meperidine (Demerol) for analgesia because pain stimulates the sympathetic nervous system, leading to an increase in heart rate and vasoconstriction
- aspirin 160 to 325 mg/day indefinitely, to inhibit platelet aggregation
- continuous cardiac monitoring to detect arrhythmias and ischemia
- intravenous thrombolytic therapy to patients with chest pain of at least 30 minutes' duration who reach the hospital within 12 hours of the onset of symptoms (unless contraindications exist) and whose ECG shows new left bundle branch block or ST-segment elevation of at least 1 to 2 mm in two or more ECG leads. The greatest benefit of reperfusion therapy, however, occurs when reperfusion takes place within 6 hours of the onset of chest pain
- intravenous heparin for patients who have received tissue plasminogen activator (tPA) to increase the chances of patency in the affected coronary artery. Limited evidence exists that intravenous or subcutaneous heparin is beneficial in patients with acute MI treated with nonspecific thrombolytic drugs, such as streptokinase or anistreplase
- percutaneous transluminal coronary angioplasty (PTCA) may be an alternative to thrombolytic therapy if it can be performed in a timely manner in an institution with personnel skilled in the procedure
- limitation of physical activity for the first 12 hours to reduce cardiac workload, thereby limiting the area of necrosis
- keeping atropine, lidocaine, transcutaneous pacing patches or a transvenous pacemaker, a defibrillator, and epinephrine readily available to treat arrhythmias. The ACC/AHA doesn't recommend the prophylactic use of antiarrhythmic drugs during the first 24 hours
- intravenous nitroglycerin for 24 to 48 hours in patients without hypotension, bradycardia, or excessive tachycardia to reduce afterload and preload and relieve chest pain
- early intravenous beta blockers to patients with an evolving acute MI followed by oral therapy, as long as there are no contraindications, to reduce heart rate and myocardial contractile force, thereby reducing myocardial oxygen requirements
- angiotensin-converting enzyme inhibitors in patients with an evolving MI with ST-segment elevation or left bundle branch block, but without hypotension or other contraindications, to reduce afterload and preload and prevent remodeling
- if needed, magnesium sulfate for 24 hours to correct hypomagnesemia
- angiography and possible percutaneous or surgical revascularization for patients with spontaneous or provoked myocardial ischemia following an acute MI
- exercise testing before discharge to determine adequacy of medical therapy and to obtain baseline information for an appropriate exercise prescription; it can also determine functional capacity and stratify the patient's risk of a subsequent cardiac event
- cardiac risk modification program of weight control; a low-fat, low-cholesterol diet; smoking cessation; and regular exercise to reduce cardiac risk.
Myocarditis
Common causes of myocarditis include:
- viral infections (most common cause in the United States and western Europe), such as Coxsackie virus A and B strains and, possibly, poliomyelitis, influenza, Epstein-Barr virus, human immunodeficiency virus, cytomegalovirus, measles, mumps, rubeola, rubella, and adenoviruses and echoviruses
- bacterial infections, such as diphtheria, tuberculosis, typhoid fever, tetanus, and staphylococcal, pneumococcal, and gonococcal infections
- hypersensitive immune reactions, including acute rheumatic fever and post-cardiotomy syndrome
- radiation therapy ― large doses of radiation to the chest in treating lung or breast cancer
- toxins such as lead, chemicals, cocaine, and chronic alcoholism
- parasitic infections, especially South American trypanosomiasis (Chagas' disease) in infants and immunosuppressed adults; also, toxoplasmosis
- fungal infections, including candidiasis and aspergillosis
- helminthic infections such as trichinosis.
The following signs and symptoms may occur:
- nonspecific symptoms such as fatigue, dyspnea, palpitations, and fever caused by systemic infection
- mild, continuous pressure or soreness in the chest (occasionally) related to inflammation
- tachycardia due to a compensatory sympathetic response
- S 3 and S 4 gallops as a result of heart failure
- murmur of mitral insufficiency may be heard, if papillary muscles involved
- pericardial friction rub, if pericarditis exists
- if myofibril degeneration occurs, it may lead to right-sided and left-sided heart failure, with cardiomegaly, neck vein distention, dyspnea, edema, pulmonary congestion, persistent fever with resting or exertional tachycardia disproportionate to the degree of fever, and supraventricular and ventricular arrhythmias.
Complications of myocarditis include:
- recurrence of myocarditis
- chronic valvulitis (when it results from rheumatic fever)
- dilated cardiomyopathy
- arrhythmias and sudden death
- heart failure
- pericarditis
- ruptured myocardial aneurysm
- thromboembolism.
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BLOCKING MYOCARDIAL INFARCTION
This chart shows how treatments can be applied to myocardial infarction at various stages of its development. <center></center> |
- History reveals recent febrile upper respiratory infection.
- Laboratory testing may reveal elevated levels of creatine kinase (CK), CK-MB, aspartate aminotransferase, and lactate dehydrogenase. Also, inflammation and infection can cause elevated white blood cell count and erythrocyte sedimentation rate.
- Antibody titers may be elevated, such as antistreptolysin-O titer in rheumatic fever.
- Electrocardiography may reveal diffuse ST-segment and T-wave abnormalities, conduction defects (prolonged PR interval, bundle branch block, or complete heart block), supraventricular arrhythmias, and ventricular extrasystoles.
- Chest X-rays may show an enlarged heart and pulmonary vascular congestion.
- Echocardiography may demonstrate some degree of left ventricular dysfunction.
- Radionuclide scanning may identify inflammatory and necrotic changes characteristic of myocarditis.
- Laboratory cultures of stool, throat, and other body fluids may identify bacterial or viral causes of infection.
- Endomyocardial biopsy may confirm diagnosis. A negative biopsy does not exclude the diagnosis.
Correction of myocarditis may involve:
- antibiotics to treat bacterial infections
- antipyretics to reduce fever and decrease stress on the heart
- bed rest to reduce oxygen demands and the workload on the heart
- restricted activity to minimize myocardial oxygen consumption; supplemental oxygen therapy; sodium restriction and diuretics to decrease fluid retention; angiotensin-converting enzyme inhibitors; and digoxin to increase myocardial contractility for patients with heart failure. Administer digoxin cautiously because some patients may show a paradoxical sensitivity even to small doses
- antiarrhythmic drugs, such as quinidine or procainamide, to treat arrhythmias; use cautiously because these drugs may depress myocardial contractility. A temporary pacemaker may be inserted if complete atrioventricular block occurs
- anticoagulation to prevent thromboembolism
- corticosteroids and immunosuppressants, although controversial, may be used to combat life-threatening complications such as intractable heart failure
- nonsteroidal anti-inflammatory drugs are contraindicated during the acute phase (first 2 weeks) because they increase myocardial damage
- cardiac assist devices or transplantation as a last resort in severe cases resistant to treatment.
Patent ductus arteriosus
- premature birth, probably as a result of abnormalities in oxygenation or the relaxant action of prostaglandin E, which prevents ductal spasm and contracture necessary for closure
- rubella syndrome
- coarctation of the aorta
- ventricular septal defect
- pulmonary and aortic stenosis
- living at high altitudes.
The following signs and symptoms may occur:
- respiratory distress with signs of heart failure in infants, especially those who are premature, due to the tremendous volume of blood shunted to the lungs through a patent ductus and the increased workload on the left side of the heart
- classic machinery murmur (Gibson murmur), a continuous murmur heard throughout systole and diastole in older children and adults due to shunting of blood from the aorta to the pulmonary artery throughout systole and diastole. It is best heard at the base of the heart, at the second left intercostal space under the left clavicle. The murmur may obscure S 2 . However, in a right-to-left shunt, this murmur may be absent
- thrill palpated at the left sternal border caused by the shunting of blood from the aorta to the pulmonary artery
- prominent left ventricular impulse due to left ventricular hypertrophy
- bounding peripheral pulses (Corrigan's pulse) due to the high-flow state
- widened pulse pressure because of an elevated systolic blood pressure and, primarily, a drop in diastolic blood pressure as blood is shunted through the PDA, thus reducing peripheral resistance
- slow motor development caused by heart failure
- failure to thrive as a result of heart failure
- fatigue and dyspnea on exertion may develop in adults with undetected PDA.
Possible complications of PDA may include:
The following tests help diagnose patent ductus arteriosus:
- Chest X-rays may show increased pulmonary vascular markings, prominent pulmonary arteries, and enlargement of the left ventricle and aorta.
- Electrocardiography may be normal or may indicate left atrial or ventricular hypertrophy and, in pulmonary vascular disease, biventricular hypertrophy.
- Echocardiography detects and estimates the size of a PDA. It also reveals an enlarged left atrium and left ventricle, or right ventricular hypertrophy from pulmonary vascular disease.
- Cardiac catheterization shows higher pulmonary arterial oxygen content than right ventricular content because of the influx of aortic blood. Increased pulmonary artery pressure indicates a large shunt or, if it exceeds systemic arterial pressure, severe pulmonary vascular disease. Cardiac catheterization allows for the calculation of blood volume crossing the ductus, and can rule out associated cardiac defects. Injection of contrast agent can conclusively demonstrate PDA.
Correction of PDA may involve the following:
- surgery to ligate the ductus if medical management can't control heart failure. Asymptomatic infants with PDA don't require immediate treatment. If symptoms are mild, surgical ligation of the PDA is usually delayed until age 1
- indomethacin (a prostaglandin inhibitor) to induce ductus spasm and closure in premature infants
- prophylactic antibiotics to protect against infective endocarditis
- treatment of heart failure with fluid restriction, diuretics, and digoxin
- other therapy, including cardiac catheterization, to deposit a plug or umbrella in the ductus to stop shunting.
Pericarditis
Common causes of pericarditis include:
- bacterial, fungal, or viral infection (infectious pericarditis)
- neoplasms (primary, or metastases from lungs, breasts, or other organs)
- high-dose radiation to the chest
- uremia
- hypersensitivity or autoimmune disease, such as acute rheumatic fever (most common cause of pericarditis in children), systemic lupus erythematosus, and rheumatoid arthritis
- previous cardiac injury, such as myocardial infarction (Dressler's syndrome), trauma, or surgery (post-cardiotomy syndrome), that leaves the pericardium intact but causes blood to leak into the pericardial cavity
- drugs such as hydralazine or procainamide
- idiopathic factors (most common in acute pericarditis)
- aortic aneurysm with pericardial leakage (less common)
- myxedema with cholesterol deposits in the pericardium (less common).
The following signs and symptoms of pericarditis may occur:
- pericardial friction rub caused by the roughened pericardial membranes rubbing against one another; although rub may be heard intermittently, it's best heard when the patient leans forward and exhales
- sharp and often sudden pain, usually starting over the sternum and radiating to the neck (especially the left trapezius ridge), shoulders, back, and arms due to inflammation and irritation of the pericardial membranes. The pain is often pleuritic, increasing with deep inspiration and decreasing when the patient sits up and leans forward, pulling the heart away from the diaphragmatic pleurae of the lungs.
- shallow, rapid respirations to reduce pleuritic pain
- mild fever caused by the inflammatory process
- dyspnea, orthopnea, and tachycardia as well as other signs of heart failure may occur as fluid builds up in the pericardial space causing pericardial effusion, a major complication of acute pericarditis
- muffled and distant heart sounds due to the buildup of fluid
- pallor, clammy skin, hypotension, pulsus paradoxus, neck vein distention and, eventually, cardiovascular collapse may occur with the rapid fluid accumulation of cardiac tamponade
- fluid retention, ascites, hepatomegaly, jugular venous distention, and other signs of chronic right-sided heart failure may occur with chronic constrictive pericarditis as the systemic venous pressure gradually rises
- pericardial knock in early diastole along the left sternal border produced by restricted ventricular filling
- Kussmaul's sign, increased jugular venous distention on inspiration, occurs due to restricted right-sided filling.
The following tests help diagnose pericarditis:
- Electrocardiography may reveal diffuse ST-segment elevation in the limb leads and most precordial leads that reflects the inflammatory process. Upright T waves are present in most leads. QRS segments may be diminished when pericardial effusion exists. Arrhythmias, such as atrial fibrillation and sinus arrhythmias, may occur. In chronic constrictive pericarditis, there may be low-voltage QRS complexes, T-wave inversion or flattening, and P mitrale (wide P waves) in leads I, II, and V 6 .
- Laboratory testing may reveal an elevated erythrocyte sedimentation rate as a result of the inflammatory process or a normal or elevated white blood cell count, especially in infectious pericarditis; blood urea nitrogen may detect uremia as a cause of pericarditis.
- Blood cultures may identify an infectious cause.
- Antistreptolysin-O titers may be positive if pericarditis is due to rheumatic fever.
- Purified protein derivative skin test may be positive if pericarditis is due to tuberculosis.
- Echocardiography may show an echo-free space between the ventricular wall and the pericardium, and reduced pumping action of the heart.
- Chest X-rays may be normal with acute pericarditis. The cardiac silhouette may be enlarged with a water bottle shape caused by fluid accumulation, if pleural effusion is present.
Correcting pericarditis typically involves:
- bed rest as long as fever and pain persist, to reduce metabolic needs
- treatment of the underlying cause, if it can be identified
- nonsteroidal anti-inflammatory drugs, such as aspirin and indomethacin, to relieve pain and reduce inflammation
- corticosteroids if nonsteroidal anti-inflammatory drugs are ineffective and no infection exists; corticosteroids must be administered cautiously because episodes may recur when therapy is discontinued
- antibacterial, antifungal, or antiviral therapy if an infectious cause is suspected
- partial pericardectomy, for recurrent pericarditis, to create a window that allows fluid to drain into the pleural space
- total pericardectomy may be necessary in constrictive pericarditis to permit adequate filling and contraction of the heart
- pericardiocentesis to remove excess fluid from the pericardial space
- idiopathic pericarditis may be benign and self-limiting.
Raynaud's disease
Although family history is a risk factor, the cause of this disorder is unknown.
Raynaud's phenomenon may develop secondary to:
- connective tissue disorders, such as scleroderma, rheumatoid arthritis, systemic lupus erythematosus, or polymyositis
- pulmonary hypertension
- thoracic outlet syndrome
- arterioocclusive disease
- myxedema
- trauma
- serum sickness
- exposure to heavy metals
- previous damage from cold exposure
- long-term exposure to cold, vibrating machinery (such as operating a jackhammer), or pressure to the fingertips (such as occurs in typists and pianists).
- intrinsic vascular wall hyperactivity to cold
- increased vasomotor tone due to sympathetic stimulation
- antigen-antibody immune response (the most likely theory because abnormal immunologic test results accompany Raynaud's phenomenon).
The following signs and symptoms may occur:
- blanching of the fingers bilaterally after exposure to cold or stress as vasoconstriction or vasospasm reduces blood flow. This is followed by cyanosis due to increased oxygen extraction resulting from sluggish blood flow. As the spasm resolves, the fingers turn red as blood rushes back into the arterioles
- cold and numbness may occur during the vasoconstrictive phase due to ischemia
- throbbing, aching pain, swelling, and tingling may occur during the hyperemic phase
- trophic changes, such as sclerodactyly, ulcerations, or chronic paronychia may occur as a result of ischemia in longstanding disease.
The following tests help diagnose Raynaud's disease:
- Clinical criteria include skin color changes induced by cold or stress; bilateral involvement; absence of gangrene or, if present, minimal cutaneous gangrene; normal arterial pulses; and patient history of symptoms for at least 2 years.
- Antinuclear antibody (ANA) titer to identify autoimmune disease as an underlying cause of Raynaud's phenomenon; further tests must be performed if ANA titer is positive.
- Arteriography to rule out arterial occlusive disease.
- Doppler ultrasonography may show reduced blood flow if symptoms result from arterial occlusive disease.
Treatment of this disorder typically involves:
- teaching the patient to avoid triggers such as cold, mechanical, or chemical injury
- encouraging the patient to cease smoking and avoid decongestants and caffeine to reduce vasoconstriction
- keeping fingers and toes warm to reduce vasoconstriction
- calcium channel blockers, such as nifedipine, diltiazem, and nicardipine, to produce vasodilation and prevent vasospasm
- adrenergic blockers, such as phenoxybenzamine or reserpine, which may improve blood flow to fingers or toes
- biofeedback and relaxation exercises to reduce stress and improve circulation
- sympathectomy to prevent ischemic ulcers by promoting vasodilation (necessary in less than 25% of patients)
- amputation if ischemia causes ulceration and gangrene.
Rheumatic fever and rheumatic heart disease
Rheumatic fever is caused by group A beta-hemolytic streptococcal pharyngitis.
The classic symptoms of rheumatic fever and rheumatic heart disease include:
- polyarthritis or migratory joint pain, caused by inflammation, occurs in most patients. Swelling, redness, and signs of effusion usually accompany such pain, which most often affects the knees, ankles, elbows, and hips
- erythema marginatum, a nonpruritic, macular, transient rash on the trunk or inner aspects of the upper arms or thighs, that gives rise to red lesions with blanched centers
- subcutaneous nodules ― firm, movable, and nontender, about 3 mm to 2 cm in diameter, usually near tendons or bony prominences of joints, especially the elbows, knuckles, wrists, and knees. They often accompany carditis and may last a few days to several weeks
- chorea ― rapid jerky movements ― may develop up to 6 months after the original streptococcal infection. Mild chorea may produce hyperirritability, a deterioration in handwriting, or inability to concentrate. Severe chorea causes purposeless, nonrepetitive, involuntary muscle spasms; poor muscle coordination; and weakness.
Other signs and symptoms include:
- report of a streptococcal infection a few days to 6 weeks earlier; it occurs in 95% of those with rheumatic fever
- temperature of at least 100.4° F (38° C) due to infection and inflammation
- a new mitral or aortic heart murmur or a worsening murmur in a person with a preexisting murmur
- pericardial friction rub caused by inflamed pericardial membranes rubbing against one another, if pericarditis exists
- chest pain, often pleuritic, due to inflammation and irritation of the pericardial membranes. Pain may increase with deep inspiration and decrease when the patient sits up and leans forward, pulling the heart away from the diaphragmatic pleurae of the lungs
- dyspnea, tachypnea, nonproductive cough, bibasilar crackles, and edema due to heart failure in severe rheumatic carditis.
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JONES CRITERIA FOR DIAGNOSING RHEUMATIC FEVER
The Jones criteria are used to standardize the diagnosis of rheumatic fever. Diagnosis requires that the patient have either two major criteria, or one major criterion and two minor criteria, plus evidence of a previous streptococcal infection.
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Possible complications of rheumatic fever and rheumatic heart disease include:
- destruction of the mitral and aortic valves
- pancarditis (pericarditis, myocarditis, and endocarditis)
- heart failure.
The following tests help diagnose rheumatic fever:
- Jones criteria revealing either two major criteria, or one major criterion and two minor criteria, plus evidence of a previous group A streptococcal infection, are necessary for diagnosis. (See Jones Criteria for diagnosing rheumatic fever .)
- Laboratory testing may reveal an elevated white blood cell count and erythrocyte sedimentation rate during the acute phase.
- Hemoglobin and hematocrit may show slight anemia due to suppressed erythropoiesis during inflammation.
- C-reactive protein may be positive, especially during the acute phase.
- Cardiac enzyme levels may be increased in severe carditis.
- Antistreptolysin-O titer may be elevated in 95% of patients within 2 months of onset.
- Throat cultures may continue to show the presence of group A beta-hemolytic streptococci; however, they usually occur in small numbers.
- Electrocardiography may show changes that are not diagnostic, but PR interval is prolonged in 20% of patients.
- Chest X-rays may show normal heart size or cardiomegaly, pericardial effusion, or heart failure.
- Echocardiography can detect valvular damage and pericardial effusion, and can measure chamber size and provide information on ventricular function.
- Cardiac catheterization provides information on valvular damage and left ventricular function.
Typically, treatment of these disorders involves:
- prompt treatment of all group A beta-hemolytic streptococcal pharyngitis with oral penicillin V or intramuscular benzathine penicillin G; erythromycin is given for patients with penicillin hypersensitivity
- salicylates to relieve fever and pain and minimize joint swelling
- corticosteroids if the patient has carditis or if salicylates fail to relieve pain and inflammation
- strict bed rest for about 5 weeks for the patient with active carditis to reduce cardiac demands
- bed rest, sodium restriction, angiotensin-converting enzyme inhibitors, digoxin, and diuretics to treat heart failure
- corrective surgery, such as commissurotomy (separation of adherent, thickened valve leaflets of the mitral valve), valvuloplasty (inflation of a balloon within a valve), or valve replacement (with a prosthetic valve) for severe mitral or aortic valvular dysfunction that causes persistent heart failure
- secondary prevention of rheumatic fever, which begins after the acute phase subsides with monthly intramuscular injections of penicillin G benzathine or daily doses of oral penicillin V or sulfadiazine; treatment usually continues for at least 5 years or until age 21, whichever is longer
- prophylactic antibiotics for dental work and other invasive or surgical procedures to prevent endocarditis.
Shock
Causes of neurogenic shock may include:
- spinal cord injury
- spinal anesthesia
- vasomotor center depression
- severe pain
- medications
- hypoglycemia.
Causes of septic shock may include:
- gram-negative bacteria (most common cause)
- gram-positive bacteria
- viruses, fungi, Rickettsiae , parasites, yeast, protozoa, or mycobacteria.
| AGE ALERT The immature immune system of newborns and infants and the weakened immune system of older adults, often accompanied by chronic illness, make these populations more susceptible to septic shock. |
Causes of anaphylactic shock may include:
Causes of cardiogenic shock may include:
- myocardial infarction (most common cause)
- heart failure
- cardiomyopathy
- arrhythmias
- obstruction
- pericardial tamponade
- tension pneumothorax
- pulmonary embolism.
Causes of hypovolemic shock may include:
- blood loss (most common cause)
- gastrointestinal fluid loss
- burns
- renal loss (diabetic ketoacidosis, diabetes insipidus, adrenal insufficiency)
- fluid shifts
- ascites
- peritonitis
- hemothorax.
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TYPES OF SHOCK
DISTRIBUTIVE SHOCK
CARDIOGENIC SHOCK
HYPOVOLEMIC SHOCK
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In the compensatory stage of shock, signs and symptoms may include:
- tachycardia and bounding pulse due to sympathetic stimulation
- restlessness and irritability related to cerebral hypoxia
- tachypnea to compensate for hypoxia
- reduced urinary output secondary to vasoconstriction
- cool, pale skin associated with vasoconstriction; warm, dry skin in septic shock due to vasodilation.
In the progressive stage of shock, signs and symptoms may include:
- hypotension as compensatory mechanisms begin to fail
- narrowed pulse pressure associated with reduced stroke volume
- weak, rapid, thready pulse caused by decreased cardiac output
- shallow respirations as the patient weakens
- reduced urinary output as poor renal perfusion continues
- cold, clammy skin caused by vasoconstriction
- cyanosis related to hypoxia.
| AGE ALERT Hypotension, altered level of consciousness, and hyperventilation may be the only signs of septic shock in infants and the elderly. |
In the irreversible stage , clinical findings may include:
- unconsciousness and absent reflexes caused by reduced cerebral perfusion, acid-base imbalance, or electrolyte abnormalities
- rapidly falling blood pressure as decompensation occurs
- weak pulse caused by reduced cardiac output
- slow, shallow or Cheyne-Stokes respirations secondary to respiratory center depression
- anuria related to renal failure.
Possible complications of shock include:
- acute respiratory distress syndrome
- acute tubular necrosis
- disseminated intravascular coagulation (DIC)
- cerebral hypoxia
- death.
The following tests help diagnose shock:
- Hematocrit may be reduced in hemorrhage or elevated in other types of shock due to hypovolemia.
- Blood, urine, and sputum cultures may identify the organism responsible for septic shock.
- Coagulation studies may detect coagulopathy from DIC.
- Laboratory testing may reveal increased white blood cell count and erythrocyte sedimentation rate due to injury and inflammation; elevated blood urea nitrogen and creatinine levels due to reduced renal perfusion; serum lactate may be increased secondary to anaerobic metabolism; and serum glucose may be elevated in early stages of shock as liver releases glycogen stores in response to sympathetic stimulation.
- Cardiac enzymes and proteins may be elevated, indicating myocardial infarction as a cause of cardiogenic shock.
- Arterial blood gas analysis may reveal respiratory alkalosis in early shock associated with tachypnea, respiratory acidosis in later stages associated with respiratory depression, and metabolic acidosis in later stages secondary to anaerobic metabolism.
- Urine specific gravity may be high in response to effects of antidiuretic hormone.
- Chest X-rays may be normal in early stages; pulmonary congestion may be seen in later stages.
- Hemodynamic monitoring may reveal characteristic patterns of intracardiac pressures and cardiac output, which are used to guide fluid and drug management. (See Putting hemodynamic monitoring to use .)
- Electrocardiography determines the heart rate and detects arrhythmias, ischemic changes, and myocardial infarction.
- Echocardiography determines left ventricular function and reveals valvular abnormalities.
Correction of shock typically involves the following measures:
- identification and treatment of the underlying cause, if possible
- maintaining a patent airway; preparing for intubation and mechanical ventilation if the patient develops respiratory distress
- supplemental oxygen to increase oxygenation
- continuous cardiac monitoring to detect changes in heart rate and rhythm; administration of antiarrhythmics, as necessary
- initiating and maintaining at least two intravenous lines with large-gauge needles for fluid and drug administration
- intravenous fluids, crystalloids, colloids, or blood products, as necessary, to maintain intravascular volume.
Additional therapy for hypovolemic shock may include:
- pneumatic antishock garment, although controversial, which may be applied to control both internal and external hemorrhage by direct pressure
- fluids such as normal saline or lactated Ringer's solution, initially, to restore filling pressures
- packed red blood cells in hemorrhagic shock to restore blood loss and improve oxygen-carrying capacity of the blood.
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PUTTING HEMODYNAMIC MONITORING TO USE
Hemodynamic monitoring provides information on intracardiac pressures and cardiac output. To understand intracardiac pressures, picture the cardiovascular system as a continuous loop with constantly changing pressure gradients that keep the blood moving.
RIGHT ATRIAL PRESSURE (RAP), OR CENTRAL VENOUS PRESSURE (CVP)
RIGHT VENTRICULAR PRESSURE (RVP)
PULMONARY ARTERY PRESSURE
PULMONARY CAPILLARY WEDGE PRESSURE (PCWP)
LEFT ATRIAL PRESSURE
CARDIAC OUTPUT
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Additional measures for cardiogenic shock may include:
- inotropic drugs such as dopamine, dobutamine, amrinone, and epinephrine, to increase contractility of the heart and increase cardiac output
- vasodilators, such as nitroglycerin or nitroprusside, given with a vasopressor to reduce the workload of the left ventricle
- diuretics to reduce preload, if patient has fluid volume overload
- intra-aortic balloon pump therapy to reduce the work of the left ventricle by decreasing systemic vascular resistance. Diastolic pressure is increased, resulting in improved coronary artery perfusion
- thrombolytic therapy or coronary artery revascularization to restore coronary artery blood flow, if cardiogenic shock is due to acute myocardial infarction
- emergency surgery to repair papillary muscle rupture or ventricular septal defect, if either is the cause of cardiogenic shock
- ventricular assist device to assist the pumping action of the heart when intra-aortic balloon pump and drug therapy fail
- cardiac transplantation, which may be considered when other medical and surgical therapeutic measures fail.
Correction of septic shock may also include:
- antibiotic therapy to eradicate the causative organism
- inotropic and vasopressor drugs, such as dopamine, dobutamine, and norepinephrine, to improve perfusion and maintain blood pressure
- although still investigational, monoclonal antibodies to tumor necrosis factor, endotoxin, and interleukin-1, to counteract mediators of septic shock.
Additional therapy for neurogenic shock may include:
- vasopressor drugs to raise blood pressure by vasoconstriction
- fluid replacement to maintain blood pressure and cardiac output.
Tetralogy of Fallot
The cause of tetralogy of Fallot is unknown. It may be associated with:
The following signs and symptoms may occur:
- cyanosis, the hallmark of tetralogy of Fallot, is caused by a right-to-left shunt
- cyanotic or “blue” spells (Tet spells), characterized by dyspnea; deep, sighing respirations; bradycardia; fainting; seizures; and loss of consciousness following exercise, crying, straining, infection, or fever. It may result from reduced oxygen to the brain because of increased right-to-left shunting, possibly caused by spasm of the right ventricular outflow tract, increased systemic venous return, or decreased systemic arterial resistance
- clubbing, diminished exercise tolerance, increasing dyspnea on exertion, growth retardation, and eating difficulties in older children due to poor oxygenation
- squatting with shortness of breath to reduce venous return of unoxygenated blood from the legs and to increase systemic arterial resistance
- loud systolic murmur best heard along the left sternal border, which may diminish or obscure the pulmonic component of S 2
- continuous murmur of the ductus in a patient with a large patent ductus, which may obscure systolic murmur
- thrill at the left sternal border caused by abnormal blood flow through the heart
- obvious right ventricular impulse and prominent inferior sternum associated with right ventricular hypertrophy.
Possible complications of tetralogy of Fallot include:
- pulmonary thrombosis
- venous thrombosis
- cerebral embolism
- infective endocarditis
- risk of spontaneous abortion, premature birth, and low-birth-weight infants born to women with tetralogy of Fallot.
The following tests help diagnose tetralogy of Fallot:
- Chest X-rays may demonstrate decreased pulmonary vascular marking (depending on the severity of the pulmonary obstruction), an enlarged right ventricle, and a boot-shaped cardiac silhouette.
- Electrocardiography shows right ventricular hypertrophy, right axis deviation and, possibly, right atrial hypertrophy.
- Echocardiography identifies septal overriding of the aorta, the VSD, and pulmonary stenosis, and detects the hypertrophied walls of the right ventricle.
- Laboratory testing reveals diminished oxygen saturation and polycythemia (hematocrit may be more than 60%) if the cyanosis is severe and longstanding, predisposing the patient to thrombosis.
- Cardiac catheterization confirms the diagnosis by providing visualization of pulmonary stenosis, the VSD, and the overriding aorta and ruling out other cyanotic heart defects. This test also measures the degree of oxygen saturation in aortic blood.
Tetralogy of Fallot may be managed by:
- a knee-chest position, and administration of oxygen and morphine to improve oxygenation
- palliative surgery with a Blalock-Taussig procedure, which joins the subclavian artery to the pulmonary artery to enhance blood flow to the lungs to reduce hypoxia
- prophylactic antibiotics to prevent infective endocarditis or cerebral abscesses
- phlebotomy to reduce polycythemia
- corrective surgery to relieve pulmonary stenosis and close the VSD, directing left ventricular outflow to the aorta.
Transposition of the great arteries
The cause of this disorder is unknown.
The following signs and symptoms may occur:
- cyanosis and tachypnea that worsens with crying within the first few hours after birth, when no other heart defects exist that allow mixing of systemic and pulmonary blood. Cyanosis may be minimized with associated defects such as ASD, VSD, or PDA
- gallop rhythm, tachycardia, dyspnea, hepatomegaly, and cardiomegaly within days to weeks due to heart failure
- loud S 2 because the anteriorly transposed aorta is directly behind the sternum
- murmurs of ASD, VSD, or PDA
- diminished exercise tolerance, fatigability, and clubbing due to reduced oxygenation.
Transposition of the great arteries may be complicated by:
The following tests help diagnose transposition of the great arteries:
- Chest X-rays are normal in the first days after birth. Within days to weeks, right atrial and right ventricular enlargement characteristically cause the heart to appear oblong. X-ray may also show increased pulmonary vascular markings, except when pulmonary stenosis exists.
- Electrocardiography typically reveals right axis deviation and right ventricular hypertrophy but may be normal in a neonate.
- Echocardiography demonstrates the reversed position of the aorta and pulmonary artery, and records echoes from both semilunar valves simultaneously, due to aortic valve displacement. It also detects other cardiac defects.
- Cardiac catheterization reveals decreased oxygen saturation in left ventricular blood and aortic blood; increased right atrial, right ventricular, and pulmonary artery oxygen saturation; and right ventricular systolic pressure equal to systemic pressure. Dye injection reveals the transposed vessels and the presence of any other cardiac defects.
- Arterial blood gas analysis indicates hypoxia and secondary metabolic acidosis.
Treatment of this disorder may involve:
- prostaglandin infusion to keep the ductus arteriosus patent until surgical correction
- atrial balloon septostomy (Rashkind procedure) during cardiac catheterization if needed as a palliative measure until surgery can be performed; enlarges the patent foramen ovale and thereby improves oxygenation and alleviates hypoxia by allowing greater mixing of blood from the pulmonary and systemic circulations
- digoxin and diuretics after atrial balloon septostomy to lessen heart failure until the infant is ready to withstand corrective surgery (usually between birth and age 1)
- surgery to correct transposition, although the procedure depends on the physiology of the defect.
Valvular heart disease
Pathophysiology of valvular heart disease varies according to the valve and the disorder.
Possible complications of valvular heart disease include:
Correcting this disorder typically involves:
- digoxin, a low-sodium diet, diuretics, vasodilators, and especially angiotensin-converting enzyme inhibitors to treat left ventricular failure
- oxygen in acute situations, to increase oxygenation
- anticoagulants to prevent thrombus formation around diseased or replaced valves
- prophylactic antibiotics before and after surgery or dental care to prevent endocarditis
- nitroglycerin to relieve angina in conditions such as aortic stenosis
- beta-adrenergic blockers or digoxin to slow the ventricular rate in atrial fibrillation or atrial flutter
- cardioversion to convert atrial fibrillation to sinus rhythm
- open or closed commissurotomy to separate thick or adherent mitral valve leaflets
- balloon valvuloplasty to enlarge the orifice of a stenotic mitral, aortic, or pulmonic valve
- annuloplasty or valvuloplasty to reconstruct or repair the valve in mitral regurgitation
- valve replacement with a prosthetic valve for mitral and aortic valve disease.
Varicose veins
Primary varicose veins can result from:
- congenital weakness of the valves or venous wall
- conditions that produce prolonged venous stasis or increased intra-abdominal pressure such as pregnancy, obesity, constipation, or wearing tight clothes
- occupations that necessitate standing for an extended period of time
- family history of varicose veins.
Secondary varicose veins can result from:
- deep vein thrombosis
- venous malformation
- arteriovenous fistulas
- trauma to the venous system
- occlusion.
TYPES OF VALVULAR HEART DISEASE
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The following signs and symptoms may occur:
- dilated, tortuous, purplish, ropelike veins, particularly in the calves, due to venous pooling
- edema of the calves and ankles due to deep vein incompetence
- leg heaviness that worsens in the evening and in warm weather; caused by venous pooling
- dull aching in the legs after prolonged standing or walking, which may be due to tissue breakdown
- aching during menses as a result of increased fluid retention.
Possible complications of varicose veins include:
| AGE ALERT As a person ages, veins dilate and stretch, increasing susceptibility to varicose veins and chronic venous insufficiency. Because the skin is very friable and can easily break down, ulcers in the elderly caused by chronic venous insufficiency may take longer to heal. |
The following tests help diagnose varicose veins:
- Manual compression test detects a palpable impulse when the vein is firmly occluded at least 8” above the point of palpation, indicating incompetent valves in the vein.
- Trendelenburg's test (retrograde filling test) detects incompetent deep and superficial vein valves.
- Photoplethysmography characterizes venous blood flow by noting changes in the skin's circulation.
- Doppler ultrasonography detects the presence or absence of venous backflow in deep or superficial veins.
- Venous outflow and reflux plethysmography detects deep venous occlusion; this test is invasive and not routinely used.
- Ascending and descending venography demonstrates venous occlusion and patterns of collateral flow.
Correction of this disorder typically involves:
- if possible, treatment of the underlying cause, such as an abdominal tumor or obesity
- antiembolism stockings or elastic bandages to counteract swelling by supporting the veins and improving circulation
- a regular exercise program to promote muscular contraction to force blood through the veins and reduce venous pooling
- injection of a sclerosing agent into small to medium-sized varicosities
- surgical stripping and ligation of severe varicose veins
- phlebectomy, removing the varicose vein through small incisions in the skin, may be performed in an outpatient setting.
Additional treatment measures include the following:
- Discourage the patient from wearing constrictive clothing that interferes with venous return.
- Encourage the obese patient to lose weight, to reduce increased intra-abdominal pressure.
- Elevate the legs above the heart whenever possible to promote venous return.
- Instruct the patient to avoid prolonged standing or sitting because these actions enhance venous pooling.
Ventricular septal defect
A VSD may be associated with the following conditions:
- fetal alcohol syndrome
- Down syndrome and other autosomal trisomies
- renal anomalies
- patent ductus arteriosus and coarctation of the aorta
- prematurity.
Signs and symptoms of a VSD may include:
- thin, small infants who gain weight slowly when a large VSD is present secondary to heart failure
- loud, harsh systolic murmur heard best along the left sternal border at the third or fourth intercostal space, caused by abnormal blood flow through the VSD; murmur is widely transmitted
- palpable thrill caused by turbulent blood flow between the ventricles through a small VSD
- loud, widely split pulmonic component of S 2 caused by increased pressure gradient across the VSD
- displacement of point of maximal impulse to the left due to hypertrophy of the heart
| AGE ALERT Typically, in infants the apical impulse is palpated over the fourth intercostal space, just to the left of the midclavicular line. In children older than age 7, it's palpated over the fifth intercostal space. When the heart is enlarged, the apical beat is displaced to the left or downward. |
- prominent anterior chest secondary to cardiac hypertrophy
- liver, heart, and spleen enlargement because of systemic congestion
- feeding difficulties associated with heart failure
- diaphoresis, tachycardia, and rapid, grunting respirations secondary to heart failure
- cyanosis and clubbing if right-to-left shunting occurs later in life secondary to pulmonary hypertension.
Complications of a VSD may include:
- pulmonary hypertension
- infective endocarditis
- pneumonia
- heart failure
- Eisenmenger's syndrome
- aortic regurgitation (if the aortic valve is involved).
The following tests help diagnose ventricular septal defect:
- Chest X-rays appear normal in small defects. In large VSDs, the X-ray may show cardiomegaly, left atrial and left ventricular enlargement, and prominent vascular markings.
- Electrocardiography may be normal with small VSDs, whereas in large VSDs it may show left and right ventricular hypertrophy, suggestive of pulmonary hypertension.
- Echocardiography can detect VSD in the septum, estimate the size of the left-to-right shunt, suggest pulmonary hypertension, and identify associated lesions and complications.
- Cardiac catheterization determines the size and exact location of the VSD and the extent of pulmonary hypertension; it also detects associated defects. It calculates the degree of shunting by comparing the blood oxygen saturation in each ventricle. The oxygen saturation of the right ventricle is greater than normal because oxygenated blood is shunted from the left ventricle to the right.
Typically, correction of a VSD may involve:
- early surgical correction for a large VSD, usually performed using a patch graft, before heart failure and irreversible pulmonary vascular disease develop
- placement of a permanent pacemaker, which may be necessary after VSD repair if complete heart block develops from interference with the bundle of His during surgery
- surgical closure of small defects using sutures. They may not be surgically repaired if the patient has normal pulmonary artery pressure and a small shunt
- pulmonary artery banding to normalize pressures and flow distal to the band and to prevent pulmonary vascular disease if the child has other defects and will benefit from delaying surgery
- digoxin, sodium restriction, and diuretics before surgery to prevent heart failure
- prophylactic antibiotics before and after surgery to prevent infective endocarditis.
