Cardiovascular System PDF

Cardiovascular System Maryann Z. Skrabal and Robyn M. Teply This chapter includes material written for the second edition by Rhonda M. Jones. GLOSSARY TERMS ◗ Afterload ◗ Angina pectoris ANATOMY AND PHYSIO...

Cardiovascular System Maryann Z. Skrabal and Robyn M. Teply This chapter includes material written for the second edition by Rhonda M. Jones. GLOSSARY TERMS ◗ Afterload ◗ Angina pectoris ANATOMY AND PHYSIOLOGY OVERVIEW ◗ Angioplasty Circulatory System ◗ Arrhythmia The circulatory system consists of two types of blood vessels: the ◗ Arteriosclerosis arteries and the veins. Arteries carry blood away from the heart, and ◗ Atherosclerotic Cardiovascular Disease veins carry blood back to the heart. The blood vessels are arranged (ASCVD) in two continuous loops, the pulmonary circulation and the systemic circulation, which are connected by the heart on one end and the vari- ◗ Blood pressure ous organ systems on the other. The rhythmic pumping of the heart ◗ Bradycardia delivers nutrients to and removes waste products from all the organ ◗ Bruit systems within the body (Fig. 12.1). ◗ Cardiac output ◗ Circus senilis Heart ◗ Contractility The heart is a combination of cardiac muscles that maintain the cir- ◗ Corneal arcus culation of the blood. The heart wall is composed of several layers ◗ Coronary heart disease (Fig. 12.2). The pericardium is a tough, double-walled, fibrous sac that encases and protects the heart. It has two layers that contain a ◗ Diastole small amount of visceral fl uid, which allows friction-free movement ◗ First heart sound of the heart muscle. The myocardium is the muscular wall of the heart ◗ Heart failure and is responsible for most of the ventricular pumping. The endocar- ◗ Hepatojugular reflex dium is the thin layer of endothelial tissue that lines the inner surface of the heart chambers and valves. ◗ Hypertension The heart itself is divided into four chambers: the left and right ◗ Murmur atria and the left and right ventricles (Fig. 12.3). The left heart is com- ◗ Myocardial infarction posed of the left atrium and ventricle; the right heart is composed of the right atrium and ventricle. The atria are thin-walled reservoirs for ◗ Orthopnea holding blood, and the ventricles are muscular pumping chambers. ◗ Paroxysmal nocturnal dyspnea The left and right heart are separated by a blood-tight partition called ◗ Preload the cardiac septum. ◗ Prinzmetal angina The four chambers are separated by two sets of valves, the main purpose of which is to prevent backfl ow of blood. The valves open ◗ Pulse pressure and close passively in response to pressure gradients in the moving ◗ Second heart sound blood, and they permit blood flow in only one direction. The two ◗ Stable angina atrioventricular (AV) valves separate the atria and the ventricles. The ◗ Stroke volume tricuspid is the right AV valve, and the bicuspid (or mitral) is the left AV valve. The AV valves open during diastole (the heart’s filling phase) ◗ Systole to allow the ventricles to fill with blood. The semilunar (SL) valves ◗ Tachycardia are between the ventricles and the arteries. The SL valves are the pul- ◗ Unstable angina monic in the right side of the heart and the aortic in the left side of the heart. The SL valves open during systole (the heart’s pumping phase) to allow blood to be ejected from the heart. 213 214 PART II ASSESSMENT OF BODY SYSTEMS Parietal pericardium Pericardial cavity Capillary bed head, neck, upper limbs Visceral Pulmonary circulation pericardium Myocardium (cardiac muscle tissue) TO PULMONARY Endocardium CIRCULATION Left atrium FIGU R E 12.2 The cardiac muscle. TO SYSTEMIC Right atrium CIRCULATION The circulation of blood through the body occurs in one Right ventricle continuous loop. Deoxygenated red blood cells (venous blood) Left are transported from the body’s periphery to the right atrium ventricle (RA) through the inferior and superior vena cava. From the Hepatic circulation RA, the venous blood passes through the tricuspid valve into the right ventricle (RV). From the RV, the blood passes through the pulmonic valve into the lungs via the pulmonary Arteries artery. The lungs then oxygenate the blood, and the pulmo- Veins nary veins carry the oxygenated blood back to the left atrium (LA). From the LA, the blood passes through the mitral valve to the left ventricle (LV). The LV ejects the blood through the aortic valve to the aorta, and the aorta then delivers the oxy- genated blood to the body. Portal vein Conduction System Capillary bed spleen, digestive tract The heart functions autonomously within the body. An intrinsic electrical conduction system allows it to stimu- late and coordinate the sequence of muscular contractions within the cardiac cycle (Fig. 12.4). An electrical current or impulse stimulates each myocardial contraction. This im- pulse is both generated and paced by the sinoatrial node, which is located at the juncture of the superior vena cava Renal circulation and the RA. From the sinoatrial node, the impulse travels through both atria to the AV node, which is located in the atrial septum. While at the AV node, the impulse is delayed for approximately one-tenth of a second before it passes into the AV bundle (or bundle of His) and then down its left and right branches. The Purkinje fi bers spread the impulse Capillary bed throughout the ventricular myocardium, where it stimulates trunk, lower limbs ventricular contraction. A small amount of electrical current spreads to the heart’s surface, where it can be measured and recorded on an electrocardiogram (ECG). Each electrical impulse produces a series of waves that is recorded on the ECG. The peaks and troughs of these waves are arbitrarily la- beled PQRST (Fig. 12.5). Their clinical significance is as FI GU R E 1 2.1 The circulatory system. follows: P wave: atrial depolarization (the spread of a stimulus through the atria) PR interval: the time between initial stimulation of the atria and initial stimulation of the ventricles  Chap te r 12 Cardi ovascular System 215 Left common carotid artery Left subclavian artery Brachiocephalic artery Aortic arch Superior Ligamentum arteriosum vena cava (ductus arteriosus in fetus) Right Pulmonary trunk pulmonary arteries Left pulmonary arteries Fossa ovalis (foramen ovalis Left pulmonary in fetus) veins Left atrium Right atrium Aortic semilunar valve Interatrial septum Pulmonary semilunar valve Cusp of left AV (mitral valve) Cusp of right AV (tricuspid valve) Left ventricle Inferior vena cava Interventricular septum Right ventricle Apex Descending (thoracic) aorta F I GU R E 12.3 Anatomy of the heart. Atrioventricular node Sinoatrial node Left bundle branch Bundle of His (posterior-superior division) Left bundle branch Right bundle branch (anterior-superior division) Purkinje fibers F I GU R E 12.4 Cardiac conduction. 216 PART II ASSESSMENT OF BODY SYSTEMS R PR interval T Electrocardiogram P Q Atrial Ventricular depolarization repolarization S QRS complex Heart sounds S3 S4 S1 S2 “lub” “dub” DIASTOLE SYSTOLE DIASTOLE... (Cycle repeats) Rapid Slow Presystole Isometric Ejection Isometric Rapid filling filling contraction relaxation filling (protodiastolic) FI GU R E 1 2.5 The cardiac cycle and ECG. QRS complex: ventricular depolarization (the spread of a is complete, the pressure in the ventricles drops below that in stimulus through the ventricles) the aorta and the pulmonary artery, and the SL valves snap T wave: ventricular repolarization (the return of stimulated shut, causing the second heart sound (S2) and the end of sys- ventricular muscle to a resting state) tole. Once again, the ventricles relax and the atria fill with blood delivered from the lungs and the systemic circulation, The electrical impulse slightly precedes the corresponding which is the start of diastole. myocardial contraction that it stimulates within the heart. Heart Sounds Cardiac Cycle As mentioned, events during the cardiac cycle generate The cardiac cycle defines the events that are involved in each sounds that can be heard through a stethoscope placed over full heartbeat. It occurs in two phases: diastole and systole the chest wall. These sounds include both normal sounds (see Fig. 12.5). During diastole, the ventricles relax, the AV (S1 and S2) and, occasionally, extra heart sounds (S3 and S4) valves open, and blood flows passively from the pressure- (see Fig. 12.5). filled atria into the low-pressure ventricles. As the ventricles fill with blood, the pressure within them rises. In turn, this rise Normal Heart Sounds The first heart sound (S 1) is produced in pressure causes the AV valves to close, preventing regurgi- by closure of the AV valves and signals the beginning of sys- tation of blood into the atria and producing the first heart tole. The characteristic description of the first heart sound is sound (S1). Occurrence of the first heart sound signals the “lub,” and it is usually loudest over the apex area of the heart. beginning of systole. Once the pressure in the ventricles ex- The second heart sound (S 2) is produced by closure of the SL ceeds the pressure in the aorta and the pulmonary artery, the valves and signals the ending of systole. The characteristic ventricles contract, the SL valves open, and blood is ejected description of the second heart sound is “dub,” and it is usu- into the pulmonary and systemic arteries. When the ejection ally loudest over the base of the heart.  Chap te r 12 Cardi ovascular System 217 Extra Heart Sounds With the opening of the AV valves, rapid cardiovascular disease (ASCVD), so an understanding of filling of the ventricles (diastole) begins. This is normally a these components is essential. The key components include passive and quiet interval until ventricular filling is almost cholesterol, triglycerides, lipoproteins, and apolipoproteins. complete. Occasionally, however, a third heart sound (S3) Cholesterol is a cell membrane component and precursor may be heard at the end of the rapid filling interval. An S3 for the formation of steroid hormones and bile acids. Most is normal in children and young adults, but when present in cholesterol synthesis occurs in the liver and intestinal mucosa, individuals older than 30 years of age, it represents a volume and synthesis is greater during the night than during the day. overload to the ventricle. Conditions that may be responsible Total cholesterol is equal to the sum of low-density lipopro- for this volume overload include regurgitant valvular lesions tein (LDL) plus high-density lipoprotein (HDL) plus approxi- and congestive heart failure (CHF). mately one fifth of the triglycerides (i.e., very low-density At the end of diastole, a fourth heart sound (S4) may be lipoprotein [VLDL]). heard. Again, this is normal in children and young adults, but Triglycerides consist of free fatty acids and glycerol, and when present in those older than 30 years of age, it typically in- they are an important source of stored energy. Their role dicates an increased resistance to filling secondary to a noncom- in atherosclerosis is controversial, but extremely high levels pliant ventricle or an increase in volume. Conditions that may ( 500 to 1,000 mg/dL) can cause pancreatitis. Triglycerides be associated with S4 include hypertension, coronary artery dis- are dependent on dietary fat. When elevated, they tend to be ease (CAD), aortic stenosis, severe anemia, or hyperthyroidism. associated with low HDL, which is important in the athero- The presence of an S3 or S4 creates a beat or rhythm similar sclerotic process. to the gallop of a horse. Therefore, these sounds are com- Lipoproteins are water-soluble particles that are respon- monly called an S3 or S4 gallop. sible for the transport of water-insoluble cholesterol and tri- Blood flowing through normal cardiac chambers and glycerides in the plasma. The density of the lipoproteins is valves usually makes no noise. Some conditions, however, determined by the relative content of protein and lipid. Lipo- cause turbulent blood flow, and a subsequent heart murmur proteins include chylomicrons, VLDL, intermediate-density can be heard. A heart murmur is a gentle, blowing, swishing lipoproteins, LDL, HDL, and lipoprotein (a). The LDL is sound that can be heard on the chest wall. Often, heart mur- considered to be the “bad cholesterol,” and it is the subfrac- murs have no pathological significance, but they may indicate tion of cholesterol that lodges into the arterial wall, becomes serious heart disease. Conditions resulting in a heart mur- oxidized, and stimulates development of the atherosclerotic mur include structural defects in the valves, unusual open- plaque. The HDL is considered to be the “good cholesterol” ings in the chambers, or increases (e.g., exercise) or decreases and is responsible for removal of cholesterol from the arte- (e.g., anemia) in the blood velocity. rial wall and peripheral tissues and its transport back to the liver for disposal. Lipoprotein (a) is genetically determined Pumping Action of the Heart and highly inheritable. It is similar to LDL but, in addition, contains a protein that has an increased tendency to clot. On contraction of the left and right ventricles, blood is pumped Apolipoproteins play a major role in the binding, solubiliza- into the systemic and the pulmonary circulation, respectively. tion, and transport of lipids. They are responsible for provid- Stroke volume is the amount of blood that is ejected in one full ing structure to the lipoprotein, activating enzyme systems, and heartbeat. It depends on preload, afterload, and myocardial binding with cell receptors. Lipoprotein metabolism includes contractility. Preload refers to the passive stretching of the ven- an exogenous and an endogenous pathway (Fig. 12.6). The tricular muscle as the volume of blood in the ventricle at the end exogenous pathway involves the metabolism of dietary fat. of diastole increases. Afterload refers to the vascular resistance Dietary fat is absorbed into the intestinal wall to become chy- against which the ventricle must contract. Myocardial contractil- lomicrons, which empty into the peripheral venous system and ity refers to the ability of the cardiac muscle, when given a load, then travel through the circulation into the arterial system and, to shorten and contract. The volume of blood that is pumped eventually, into muscle or adipose tissues. Lipoprotein lipase from each ventricle in 1 minute is the cardiac output; this is the hydrolyzes the triglycerides to produce fatty acids for energy product of the heart rate and the stroke volume. To adapt to the or storage. The endogenous pathway involves the synthesis body’s metabolic needs, the heart can alter its cardiac output. of cholesterol in the liver and begins with the production of Blood pressure is the force of the blood as it pushes against VLDL. After lipoprotein lipase metabolizes VLDL in the circu- the vessel walls. Systolic blood pressure is the maximum pres- lation, intermediate-density lipoprotein is produced and, even- sure felt on the artery during left ventricular contraction or tually, is used for production of LDL in the liver. Production systole. It is regulated by the stroke volume and the compli- of LDL is regulated by increasing or decreasing LDL receptors ance of the blood vessels. Diastolic blood pressure is the rest- on the liver. Reverse cholesterol transport refers to the activity ing pressure that the blood exerts in between each ventricular of HDL, which acts as a cholesterol scavenger by removing contraction. It is dependent on peripheral vascular resistance. cholesterol from peripheral tissues and returning it to the liver. The pulse pressure is the difference between the systolic and the diastolic pressure, and it reflects the stroke volume. (For a full discussion of blood pressure, see Chapter 5). Special Considerations Pediatric Patients Lipid Metabolism Development of the heart and the circulatory system occurs Regulation of serum lipid levels by lipoproteins and apoli- very early in life. By the third week of fetal development, a poproteins plays an important role in the development of tubular heart is pumping and circulating blood. The lungs are coronary heart disease (CHD), also known as atherosclerotic nonfunctional, however, so the blood is oxygenated through 218 PART II ASSESSMENT OF BODY SYSTEMS EXOGENOUS PATHWAY ENDOGENOUS PATHWAY Key Dietary fat C Chylomicrons V VLDL Bile acids C C and cholesterol C Liver I IDL C L L LDL C H HDL F Free fatty acids C Intestine L I V L I L I I Chylomicron I I V L remnants I C V L H H I Lipoprotein V C C V lipase C C Lipoprotein REVERSE I lipase Cholesterol CHOLESTEROL I I acyltransferase TRANSPORT H H F H F F F Extrahepatic F F F tissue F F F F F F F F FI GU R E 1 2.6 Lipoprotein metabolism: exogenous and endogenous pathways and reverse transport. the umbilical vessels of the placenta. Because there is no need Geriatric Patients for blood to be circulated to the lungs for oxygenation, fetal Functioning of the cardiovascular system gradually declines circulation has two major differences. First, a gap between with age. The maximum cardiac output is reduced, and cal- the two atria, the foramen ovale, allows blood to fl ow from cification of weakened vessel walls, or arteriosclerosis, di- the RA to the LA (see Fig. 12.3). Second, the ductus arteriosus minishes their elasticity and vasomotor tone, reducing their provides an external short circuit between the pulmonary and ability to adjust to changing body needs. This stiffening of aortic blood vessels (see Fig. 12.3). Through these mecha- nisms, only a small amount of blood enters the pulmonary circulation, and both the right and left ventricles pump blood into the systemic circulation. At birth, major changes occur. As the baby takes his or her first breath, the lungs and pulmonary blood vessels expand. The foramen ovale closes, separating the left and right atria, and the ductus arteriosus also closes, isolating the pulmonary and systemic blood vessels. The RV now pumps blood to the pulmonary circulation, and the LV pumps blood to the sys- temic circulation, just as in the adult heart. The position of the heart, however, is more horizontal in the chest of infants and children than in adults (Fig. 12.7). The adult heart posi- tion is usually reached by 7 years of age. Hyperlipidemia in children is often related to a genetic process. Early detection is important because the risk for Fourth interspace cardiovascular events is greatly increased at a much younger age in this population. All children should be tested early if Fifth interspace a family history exists. Dietary therapy is generally recom- mended after age 2 years, and drug therapy may be used after FIGU R E 12.7 Location of the heart in pediatric and adult age 10 years to bring the cholesterol down to desirable levels. patients.  Chap te r 12 Cardi ovascular System 219 the blood vessels may lead to an aneurysm, which can cause stroke, infarct, or massive hemorrhage depending on the ves- 12.1 Risk Factors for Coronary sel involved. Coronary circulation can also be restricted by Heart Disease the progression of atherosclerosis. Formation of these athero- sclerotic plaques can increase the risk of thrombi formation CAUSATIVE and, thus, the risk of developing CAD. Cigarette smoking Changes in the ECG occur secondary to histological Hypertension changes within the conduction and neurological systems. Low high-density lipoprotein cholesterol ( 40 mg/dL) Common ECG changes in older adults include PR interval High total and low-density lipoprotein cholesterol prolongation (i.e., fi rst-degree AV block), QT interval prolon- Type 1 and type 2 diabetes mellitus gation, left-axis deviation, and bundle-branch block. PREDISPOSING Hyperlipidemia in elderly patients carries a higher risk for CHD than in younger patients. Many studies have found Obesity/overweight that increases in body weight associated with aging (espe- Physical inactivity Family history of premature coronary heart disease (in cially central obesity) contribute to abnormal lipid concen- male, first-degree relative 55 years; in female, first- trations in elderly people. Central obesity is more strongly degree relative 65 years) associated than lower body obesity with diabetes, hyperten- Age (men 45 years; women 55 years) sion, altered lipid profiles, and gallbladder disease. Excess Insulin resistance upper body fat associated with insulin resistance leads to increased hepatic production of triglycerides and choles- Information from National Cholesterol Education Program. Summary of the Third Report of the National Cholesterol Education Program Expert terol-rich lipoproteins. Levels of HDL cholesterol are higher Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in women than in men until menopause, but then they are in Adults (Adult Treatment Panel III). Bethesda, MD: National Heart, Lung, equal. In men, triglycerides increase until age 50 years and and Blood Institute, 2001. NIH publication 01-3670; Trujillo TC, Nolan PE. then decline. Ischemic heart disease: anginal syndromes. In: Koda-Kimble MA, Young LY, Kradjan WA, et al, eds. Applied Therapeutics: The Clinical Use of Drugs, 8th ed. Baltimore:, Lippincott Williams & Wilkins, 2005:17.1–17.33. Pregnant Patients Pregnancy causes several cardiovascular changes. Total blood volume increases by 30% to 40%, with the cellular compo- Angina Pectoris nents increasing approximately 20% and the fluid compo- Angina pectoris refers to intermittent chest pain caused by nent increasing approximately 40% to 50%. The heart rate increases by approximately 10 to 15 bpm. The stroke vol- temporary oxygen insufficiency and myocardial ischemia. It can be classified into three major variants: (1) stable angina, ume also increases, so the total cardiac output increases by (2) unstable angina, and (3) Prinzmetal or variant angina. approximately 32%. Blood pressure remains constant, how- ever, throughout most normal pregnancies. Cholesterol levels increase by approximately 30 to 40 mg/dL, Stable Angina Stable angina occurs most commonly when and triglyceride levels increase by approximately 150 mg/dL in the workload of the heart increases through exertion or pregnancy. Dietary therapy is preferred over drug therapy in stress. It is usually associated with a significant amount of these patients. atherosclerotic narrowing in one or more coronary arteries. Because of the large amount of obstruction, the myocardial oxygen supply cannot be increased suffi ciently to meet the PATHOLOGY OVERVIEW higher oxygen demands that are required by exercise or other conditions that stress the heart. Anginal or cardiac chest pain Cardiac dysfunction is a common cause of morbidity and mor- is typically described as a diffuse, heavy pressure or a deep tality. Major cardiac diseases include CHD, angina pectoris, squeezing, crushing, and aching feeling over the sternum area myocardial infarction, CHF, hypertension, and arrhythmias. within the chest. The pain may (or may not) radiate to the shoulder, jaw, back, neck, left arm, and, occasionally, the Coronary Heart Disease right arm. Differentiating characteristics of common types of chest pain are listed in Table 12.1. Coronary heart disease, which is also termed coronary artery Factors that may precipitate angina include: disease, ischemic heart disease, and atherosclerotic cardiovas- cular disease (ASCVD), refers to degenerative changes in the Exercise or strenuous activity coronary circulation resulting from an imbalance between Activity involving use of the arms above the head myocardial oxygen demand and the blood supply. The most Cold environment common cause of CHD is a progressive atherosclerosis of the coronary arteries. This buildup of atherosclerotic plaques Emotional stress (fatty deposits) narrows the vessel lumen, reducing coronary Extreme fear or anger arterial blood supply and causing myocardial ischemia. Risk Coitus factors are either directly associated with development of CHD (i.e., causative) or directly affect development of caus- Anginal pain is usually relieved with rest, which decreases ative risk factors (i.e., predisposing). Causative and predis- the workload of the heart, or with nitroglycerin. Stable angina posing risk factors are listed in Box 12.1, but one of the most can often be controlled with a combination of lifestyle changes common symptoms of CHD is angina pectoris. and pharmacological therapy. Lifestyle changes include