Cardiovascular System

佚名

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.

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.

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.

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.