Introduction: Cardiovascular Disorders

Introduction: Cardiovascular Disorders: Excerpt from Professional Guide to Diseases (Eighth Edition)

The cardiovascular system begins its activity when the fetus is barely a month old and is the last body system to cease activity at the end of life. This system is so vital that its activity defines the presence of life.

Life-giving transport system

The heart, arteries, veins, and lymphatics form the cardiovascular network that serves as the body’s transport system, bringing life-supporting oxygen and nutrients to cells, removing metabolic waste products, and carrying hormones from one part of the body to another. Often called the circulatory system, it may be divided into two branches: pulmonary circulation, in which blood picks up new oxygen and liberates the waste product carbon dioxide; and systemic circulation (including coronary circulation), in which blood carries oxygen and nutrients to all active cells while transporting waste products to the kidneys, liver, and skin for excretion.

Circulation requires normal functioning of the heart, which propels blood through the system by continuous rhythmic contractions. Located behind the sternum, the heart is a muscular organ the size of a man’s fist. It has three layers: the endocardium — the smooth inner layer; the myocardium — the thick, muscular middle layer that contracts in rhythmic beats; and the epicardium — the thin, serous membrane, or outer surface of the heart. Covering the entire heart is a saclike membrane called the pericardium, which has two layers: a visceral layer that’s in contact with the heart and a parietal, or outer, layer. To prevent irritation when the heart moves against this layer during contraction, fluid lubricates the parietal pericardium.

The heart has four chambers: two thin-walled chambers called atria and two thick-walled chambers called ventricles. The atria serve as reservoirs during ventricular contraction (systole) and as booster pumps during ventricular relaxation (diastole). The left ventricle propels blood through the systemic circulation. The right ventricle, which forces blood through the pulmonary circulation, is much thinner than the left because it meets only one-sixth the resistance.

ELDER TIP As a person’s body ages, the ventricular and aortic walls stiffen, decreasing the heart’s pumping action.

Heart valves

Two kinds of valves work inside the heart: atrioventricular and semilunar. The atrioventricular valve between the right atrium and ventricle has three leaflets, or cusps, and three papillary muscles; hence, it’s called the tricuspid valve. The atrioventricular valve between the left atrium and ventricle consists of two cusps shaped like a bishop’s miter and two papillary muscles and is called the mitral valve. The tricuspid and mitral valves prevent blood backflow from the ventricles to the atria during ventricular contraction. The leaflets of both valves are attached to the ventricle’s papillary muscles by thin, fibrous bands called chordae tendineae; the leaflets separate and descend funnellike into the ventricles during diastole and are pushed upward and together during systole to occlude the mitral and tricuspid orifices. The valves’action isn’t entirely passive, because papillary muscles contract during systole and prevent the leaflets from prolapsing into the atria during ventricular contraction.

The two semilunar valves, which resemble half moons, prevent blood backflow from the aorta and pulmonary arteries into the ventricles when those chambers relax and fill with blood from the atria. They’re referred to as the aortic valve and pulmonic valve for their respective arteries.

ELDER TIP In elderly people, fibrotic and sclerotic changes thicken heart valves and reduce their flexibility. These changes lead to rigidity and incomplete closure of the valves, which may result in systolic or diastolic murmurs.

The cardiac cycle

Diastole is the phase of ventricular relaxation and filling. As diastole begins, ventricular pressure falls below arterial pressure, and the aortic and pulmonic valves close. As ventricular pressure continues to fall below atrial pressure, the mitral and tricuspid valves open, and blood flows rapidly into the ventricle. Atrial contraction then increases the volume of ventricular filling by pumping 15% to 25% more blood into the ventricle. When systole begins, the ventricular muscle contracts, raising ventricular pressure above atrial pressure and closing the mitral and tricuspid valves. When ventricular pressure finally becomes greater than that in the aorta and pulmonary artery, the aortic and pulmonic valves open, and the ventricles eject blood. Ventricular pressure continues to rise as blood is expelled from the heart. As systole ends, the ventricles relax and stop ejecting blood, and ventricular pressure falls, closing both valves.

S₁ (the first heart sound) is heard as the ventricles contract and the atrioventricular valves close. S₁ is loudest at the heart’s apex, over the mitral area. S₂ (the second heart sound), which is normally rapid and sharp, occurs when the aortic and pulmonic valves close. S₂ is loudest at the heart’s base (second intercostal space on both sides of the sternum).

Normally, with inspiration, a split S₂ will be auscultated. With expiration, the splitting becomes closer or may become single. However, a fixed split S₂ will be heard if the patient has a right bundle-branch block.

Ventricular distention during diastole, which can occur in heart failure, creates low-frequency vibrations that may be heard as a third heart sound (S₃), or ventricular gallop. An atrial gallop (S₄) may appear at the end of diastole, just before S₁, if atrial filling is forced into a ventricle that has become less compliant or overdistended or has a decreased ability to contract. A pressure rise and ventricular vibrations cause this sound.

Cardiac conduction

The heart’s conduction system is composed of specialized cells capable of generating and conducting rhythmic electrical impulses to stimulate heart contraction. This system includes the sinoatrial (SA) node, the atrioventricular (AV) junction, the bundle of His and its bundle branches, and the ventricular conduction tissue and Purkinje fibers.

Normally, the SA node controls the heart rate and rhythm at 60 to 100 beats/minute. Because the SA node has the lowest resting potential, it’s the heart’s pacemaker. If it defaults, another part of the system takes over. The AV junction may emerge at 40 to 60 beats/minute; the bundle of His and bundle branches at 30 to 40 beats/minute; and ventricular conduction tissue at 20 to 30 beats/minute.

ELDER TIP As the myocardium of the aging heart becomes more irritable, extra systoles may occur along with sinus arrhythmias and sinus bradycardias. In addition, increased fibrous tissue infiltrates the SA nodes and internodal atrial tracts, which may cause atrial fibrillation and flutter.

Cardiac output

Cardiac output — the amount of blood pumped by the left ventricle into the aorta each minute — is calculated by multiplying the stroke volume (the amount of blood the left ventricle ejects during each contraction) by the heart rate (number of beats/minute). When cellular demands increase, stroke volume or heart rate must increase.

Many factors affect the heart rate, including exercise, pregnancy, and stress. When the sympathetic nervous system releases norepinephrine, the heart rate increases; when the parasympathetic system releases acetylcholine, it slows. As a person ages, the heart rate takes longer to normalize after exercise.

Stroke volume depends on the ventricle’s blood volume and pressure at the end of diastole (preload), resistance to ejection (afterload), and the myocardium’s contractile strength (inotropy). Changes in preload, afterload, or inotropic state can alter the stroke volume.

ELDER TIP Exercise cardiac output declines slightly with age. A decrease in maximum heart rate and contractility may cause this change.

Circulation and pulses

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 major artery branching out of the left ventricle is the aorta. Its segments and subbranches 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.

ELDER TIP Aging contributes to arterial and venous insufficiency as the strength and elasticity of blood vessels decrease.

Pulses are felt best wherever an artery runs near the skin and over a hard structure. (See Pulse points.) Easily found pulses are:

❑ radial artery — anterolateral aspect of the wrist

❑ temporal artery — in front of the ear, above and lateral to the eye

❑ common carotid artery — neck (side)

❑ femoral artery — groin.

The lymphatic system also plays a role in the cardiovascular network. Originating in tissue spaces, the lymphatic system drains fluid and other plasma components that build up in extravascular spaces and reroutes them back to the circulatory system as lymph, a plasmalike fluid. Lymphatics also extract bacteria and foreign bodies.

Cardiovascular assessment

Physical assessment provides vital information about cardiovascular status.

❑ Check for underlying cardiovascular disorders, such as central cyanosis (impaired gas exchange), edema (heart failure or valvular disease), and clubbing (congenital cardiovascular disease).

❑ Palpate the peripheral pulses bilaterally and evaluate their rate, equality, and quality on a scale of 0 (absent) to +4 (bounding). (See Pulse amplitude scale.)

❑ Inspect the carotid arteries for equal appearance. Auscultate for bruits; then palpate the arteries individually, one side at a time, for thrills (fine vibrations due to irregular blood flow).

❑ Check for pulsations in the jugular veins (more easily seen than felt). Watch for jugular vein distention — a possible sign of right-sided heart failure, valvular stenosis, cardiac tamponade, or pulmonary embolism. Take blood pressure readings in both arms while the patient is lying, sitting, and standing.

❑ Palpate the precordium for any abnormal pulsations, such as lifts, heaves, or thrills. Use the palms (at the base of the fingertips) or the fingertips. The normal apex will be felt as a light tap and extends over 1" (2.5 cm) or less.

❑ Systematically auscultate the anterior chest wall for each of the four heart sounds in the aortic area (second intercostal space at the right sternal border), pulmonic area (second intercostal space at the left sternal border), right ventricular area (lower half of the left sternal border), and mitral area (fifth intercostal space at the midclavicular line). However, don’t limit your auscultation to these four areas. Valvular sounds may be heard all over the precordium. Therefore, inch your stethoscope in a Z pattern, from the base of the heart across and down and then over to the apex, or start at the apex and work your way up. For low-pitched sounds, use the bell of the stethoscope; for high-pitched sounds, the diaphragm. Carefully inspect each area for pulsations, and palpate for thrills. Check the location of apical pulsation for deviations in normal size ( ⅜" to ¾" [1 to 2 cm]) and position (in the mitral area) — possible signs of left ventricular hypertrophy, left-sided valvular disease, or right ventricular disease.

❑ Listen for the vibrating sound of turbulent blood flow through a stenotic or incompetent valve. Time the murmur to determine where it occurs in the cardiac cycle — between S₁ and S₂ (systolic), between S₂ and the following S₁ (diastolic), or throughout systole (holosystolic). Finally, listen for the scratching or squeaking of a pericardial friction rub.

Special cardiovascular tests

Electrocardiography (ECG) measures electrical activity by recording currents transmitted by the heart. It can detect ischemia, injury, necrosis, bundle-branch blocks, fascicular blocks, conduction delay, chamber enlargement, and arrhythmias. In Holter monitoring, a tape recording tracks as many as 100,000 cardiac cycles over a 12- or 24-hour period. This test may be used to assess the effectiveness of antiarrhythmic drugs or to evaluate arrhythmia symptoms. A signal-averaged ECG will identify after potentials, which are associated with a risk of ventricular arrhythmias. (See Positioning chest electrodes.)

Chest X-rays may reveal cardiac enlargement and aortic dilation. They also assess pulmonary circulation. When pulmonary venous and arterial pressures rise, characteristic changes appear, such as dilation of the pulmonary venous shadows. When pulmonary venous pressure exceeds oncotic pressure of the blood, capillary fluid leaks into lung tissues, causing pulmonary edema. This fluid may settle in the alveoli, producing a butterfly pattern, or the lungs may appear cloudy or hazy; in the interlobular septa, sharp linear densities (Kerley’s lines) may appear.

Exercise testing using a bicycle ergometer or treadmill determines the heart’s response to physical stress. This test measures blood pressure and ECG changes during increasingly rigorous exercises. Myocardial ischemia, abnormal blood pressure response, or arrhythmias indicate the circulatory system’s failure to adapt to exercise.

Cardiac catheterization evaluates chest pain, the need for coronary artery surgery or angioplasty, congenital heart defects, and valvular heart disease and determines the extent of heart failure. Right-sided catheterization involves threading a pulmonary artery thermodilution catheter, which can measure cardiac output, through a vein into the right side of the heart, pulmonary artery, and its branches in the lungs to measure right atrial, right ventricular, pulmonary artery, and pulmonary artery wedge pressures. Left-sided catheterization entails retrograde catheterization of the left ventricle or transseptal catheterization of the left atrium. Ventriculography during left-sided catheterization involves injecting radiopaque dye into the left ventricle to measure ejection fraction and to disclose abnormal heart wall motion or mitral valve incompetence.

In coronary arteriography, radiopaque material injected into coronary arteries allows cineangiographic visualization of coronary arterial narrowing or occlusion.

Digital subtraction angiography evaluates the coronary arteries through the use of X-ray images that are digitally subtracted by computer. Time-based color enhancement shows blood flow in nearby areas.

Echocardiography uses echoes from pulsed high-frequency sound waves (ultrasound) to evaluate cardiac structures. M-mode echocardiography, in which a single, stationary ultrasound beam strikes the heart, produces a vertical view of cardiac structures. Two-dimensional echocardiography (most common), in which an ultrasound beam rapidly sweeps through an arc, produces a cross-sectional or fan-shaped view of cardiac structures. Both M-mode and two-dimensional echocardiography may use contrast agents for enhancement. Doppler echocardiography records blood flow within the cardiovascular system. Color Doppler echocardiography shows the direction of blood flow, which provides information about the degree of valvular insufficiency. Transesophageal echocardiography combines ultrasound with endoscopy to better view the heart’s structures. This procedure allows images to be taken from the heart’s posterior aspect.

Echocardiography provides information about valve leaflets, size and dimensions of heart chambers, and thickness and motion of the septum and the ventricular walls. It can also reveal intracardiac masses, detect pericardial effusion, diagnose hypertrophic cardiomyopathy, and estimate cardiac output and ejection fraction. This test can also evaluate possible aortic dissection when it involves the ascending aorta.

In multiple-gated acquisition scanning, a radioactive isotope in the intravascular compartment allows measurement of stroke volume, wall motion, and ventricular ejection fraction. Myocardial imaging usually uses the radioactive agent thallium-201 or Tc-99m sestamibi (Cardiolite) to detect abnormalities in myocardial perfusion. This agent concentrates in normally perfused areas of the myocardium but not in ischemic areas (“cold spots”), which may be permanent (scar tissue) or temporary (from transient ischemia). These tests can be done as exercise studies or can be combined with drugs, such as adenosine or Persantine, in patients unable to exercise.

Acute infarct imaging documents muscle viability (not perfusion) through the use of technetium-labeled pyrophosphate. Unlike thallium, technetium accumulates only in irreversibly damaged myocardial tissue. Areas of necrosis appear as “hot spots” and can be detected only during an acute myocardial infarction (MI). This test determines the size and location of an infarction but can produce false results.

Cardiac enzymes (cellular proteins released into the blood as a result of cell membrane injury) in the blood confirm acute MI or severe cardiac trauma. All cardiac enzymes — creatine kinase (CK), lactate dehydrogenase, and aspartate aminotransferase, for example — are also found in other cells. Fractionation of enzymes can determine the source of damaged cells. For example, three fractions of CK are isolated, one of which (an isoenzyme called CK-MB) is found only in cardiac cells. CK-MB in the blood indicates injury to myocardial cells.

Measurement of a cardiac protein called troponin is the most precise way to determine if a patient has experienced an MI. Some 6 hours after an MI, a blood test can detect two forms of troponin: T and I. Troponin T levels peak about 2 days after an MI and return to normal about 16 days later. Troponin I levels reach their peak in less than 1 day after an MI and return to normal in about 7 days.

Peripheral arteriography consists of a fluoroscopic X-ray after arterial injection of a contrast medium. Similarly, phlebography defines the venous system after injection of a contrast medium into a vein. Impedance plethysmography evaluates the venous system to detect pressure changes transmitted to lower leg veins.

Doppler ultrasonography evaluates the peripheral vascular system and assesses arterial occlusive disease.

Endomyocardial biopsy can detect cardiomyopathy, infiltrative myocardial diseases, and transplant rejection.

Electrophysiologic studies help diagnose conduction system disease and serious arrhythmias. Electronic induction and termination of arrhythmias aid drug selection. Endocardial mapping detects an arrhythmia’s focus using a finger electrode. Epicardial mapping uses a computer and a fabric sock with electrodes that’s slipped over the heart to detect arrhythmias.

Magnetic resonance imaging can investigate cardiac structure and function. Positron emission tomography and magnetic resonance spectroscopy are used to assess myocardial metabolism.

Electron beam computed tomography, also known as ultrafast computed tomography, is used to detect micro-calcifications in the coronary arteries. This test is useful for identifying early coronary artery disease.

Managing cardiovascular disease

Patients with cardiovascular disease pose a tremendous challenge. Their sheer numbers alone compel a thorough understanding of cardiovascular anatomy, physiology, and pathophysiology. Anticipate a high anxiety level in cardiac patients, and provide support and reassurance, especially during procedures such as cardiac catheterization.

Cardiac rehabilitation programs are widely prescribed and offer education and support along with exercise instruction. Rehabilitation programs begin in health care facilities and continue on an outpatient basis. Helping the patient resume a satisfying lifestyle requires planning and comprehensive teaching. Inform the patient about health care facilities and organizations that offer cardiac rehabilitation programs.

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Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

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More About This Book: Title: Professional Guide to Diseases (Eighth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2005 ISBN: 1-58255-370-X

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