MS CH 21 Cardiovascular System Function Assessment and Therapeutic Measures PDF
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Lincoln University
Linda S. Williams and Janice L. Bradford
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This document details the anatomy and functions of the human cardiovascular system. It also includes assessment and therapeutic measures for related conditions. The author is Linda S. Williams and Janice L. Bradford, both likely associated with a university or college textbook.
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4068_Ch21_387-416 15/11/14 1:38 PM Page 388 21 Cardiovascular System Function, Assessment, and Therapeutic Measures KEY TERMS atherosclerosis (ATH-er-oh-skleh-ROH-siss) bruit (brew-EE) claudication (KLAW-dih-KAY-shun) clubbing (KLUH-bing) dysrhythmias (dis-RITH-mee-yahs) Homans’ sign (HOH-manz SY...
4068_Ch21_387-416 15/11/14 1:38 PM Page 388 21 Cardiovascular System Function, Assessment, and Therapeutic Measures KEY TERMS atherosclerosis (ATH-er-oh-skleh-ROH-siss) bruit (brew-EE) claudication (KLAW-dih-KAY-shun) clubbing (KLUH-bing) dysrhythmias (dis-RITH-mee-yahs) Homans’ sign (HOH-manz SYNE) hypomagnesemia (HYE-poh-MAG-neh-SEE-mee-ah) ischemic (iss-KEY-mick) murmur (MUR-mur) pericardial friction rub (PEAR-ih-KAR-dee-uhl FRIKshun RUB) poikilothermy (POY-kih-loh-THER-mee) point of maximum impulse (POYNT OF MAKSih-muhm IM-puls) preload (PREE-lohd) pulse deficit (PULS DEF-ih-sit) sternotomy (stir-NAW-tuh-mee) thrill (THRILL) 388 LINDA S. WILLIAMS AND JANICE L. BRADFORD LEARNING OUTCOMES 1. Identify the normal anatomy of the cardiovascular system. 2. Explain the normal function of the cardiovascular system. 3. List data to collect when caring for a patient with a disorder of the cardiovascular system. 4. Identify diagnostic tests commonly performed to diagnose disorders of the cardiovascular system. 5. Plan nursing care for patients undergoing diagnostic tests for cardiovascular disorders. 6. Describe current therapeutic measures for disorders of the cardiovascular system. 7. Describe preoperative and postoperative care for patients undergoing cardiac surgery. 4068_Ch21_387-416 15/11/14 1:38 PM Page 389 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures NORMAL CARDIOVASCULAR SYSTEM ANATOMY AND PHYSIOLOGY The cardiovascular system consists of the heart, blood, and vessels (including arteries, capillaries, and veins). Its function is to distribute the blood throughout the body. Heart 389 the first branches of the ascending aorta, just outside the left ventricle (Fig. 21.1). The superior chambers of the heart are the thin-w alled right and left atria, which are separated by the interatrial septum. The lower chambers are the thicker walled right and left ventricles, which are separated by the interventricular septum. Each septum is made of myocardium that forms a common wall between the two chambers. CORONARY BLOOD FLOW. The right atrium receives deoxy- Cardiac Structure and Function LOCATION OF THE HEART. The heart is located in the medi- astinum within the thoracic ca vity. It is enclosed by three membranes. The outermost is the fibrous pericardium, which forms a loose-fitting pericardial sac around the heart. The second, or middle, layer is the parietal pericardium, a serous membrane that lines the f ibrous layer. The third and inner most layer, the visceral pericardium or epicardium, is a serous membrane on the surf ace of the heart muscle. Between the parietal and visceral layers is serous fluid, which pre vents friction as the heart beats. STRUCTURE OF THE HEART AND CORONARY BLOOD VESSELS. The walls of the four chambers of the heart are made of cardiac muscle (myocardium) and are lined with endocardium, which is smooth epithelial tissue that prevents abnormal clotting. The epithelium also covers the valves of the heart and continues into blood v essels as the endothelium. Coronary circulation provides oxygenated blood throughout the myocardium and returns deoxygenated blood to the right atrium via the coronary sinus. The two main coronary arteries are genated blood from the coronary sinus, the upper body by way of the superior v ena cava, and from the lo wer body by way of the inferior vena cava (see Fig. 21.1). This blood flows from the right atrium through the tricuspid valve into the right ventricle. Backflow during ventricular systole (contraction and emptying) is prevented by the tricuspid, or right, atrioventricular (AV) valve (Fig. 21.2). The right ventricle pumps blood through the pulmonary semilunar valve to the lungs by way of the pulmonary artery. The pulmonary semilunar valve prevents backflow of blood into the right v entricle during ventricular diastole (relaxation and filling). The left atrium receives oxygenated blood from the lungs by way of the four pulmonary v eins. This blood flo ws through the mitral, or left, AV valve (also called the bicuspid valve) into the left ventricle. The mitral valve prevents backflow of blood into the left atrium during v entricular systole. The left ventricle pumps blood through the aortic semilunar valve to the body by w ay of the aorta. The aortic valve prevents backflow of blood into the left ventricle during ventricular diastole. Left subclavian artery Left internal jugular vein Left common carotid artery Brachiocephalic (trunk) artery Aortic arch Superior vena cava Left pulmonary artery (to lungs) Right pulmonary artery Left atrium Left pulmonary veins (from lungs) Right pulmonary veins Circumflex artery Left coronary artery Left coronary vein Left anterior descending artery Left ventricle Right atrium Right coronary artery Inferior vena cava Right ventricle Aorta FIGURE 21.1 Anterior view of the heart and major blood vessels. From Scanlon, V., & Sanders, T. (2015). Essentials of anatomy and physiology, 7th ed. Philadelphia: F.A. Davis, with permission. 4068_Ch21_387-416 15/11/14 1:38 PM Page 390 390 UNIT FIVE Understanding the Cardiovascular System Left common carotid artery Brachiocephalic artery Left subclavian artery Aortic arch Superior vena cava Left pulmonary artery Right pulmonary artery Left atrium Left pulmonary veins Mitral valve Right pulmonary veins Pulmonary semilunar valve Left ventricle Right atrium Aortic semilunar valve Tricuspid valve Interventricular septum Inferior vena cava Chordae tendineae Apex Right ventricle Papillary muscles FIGURE 21.2 Frontal section of the heart showing internal structures and cardiac blood flow. From Scanlon, V., & Sanders, T. (2015). Essentials of anatomy and physiology, 7th ed. Philadelphia: F.A. Davis, with permission. The tricuspid and mitral valves consist of three and tw o cusps, respectively. These cusps, or flaps, are connective tissue covered by endocardium and are anchored to the floor of the ventricle by the chordae tendineae and papillary muscles. The papillary muscles are columns of myocardium that contract along with the rest of the v entricular myocardium. This contraction pulls on the chordae tendineae and prevents hyperextension of the AV valves during ventricular systole (see Fig. 21.2). Although each ventricle pumps the same amount of blood, the much thicker walls of the left v entricle pump with approximately five times the force of the right ventricle to distribute the blood throughout the body. This difference in force is reflected in the great difference between systemic and pulmonary blood pressure. capable of generating the beat of the v entricles, but at the much slower rate of about 20 to 35 beats per minute. A cardiac cycle is the sequence of mechanical events that occurs during each heartbeat. Simply stated, the tw o atria contract simultaneously, followed by the simultaneous contraction of the tw o ventricles (a fraction of a second later). The contraction (emptying), or systole, of each set of chambers is followed by relaxation (f illing), or diastole, of the same set of chambers. The events of the cardiac c ycle create the normal heart sounds. The first of the tw o major sounds (the “lubb” of “lubb-dupp”) is caused by the closure of theAV valves during ventricular systole. The second sound is created by the closure of the aortic and pulmonary semilunar valves. Cardiac Conduction Pathway and Cardiac Cycle Cardiac output is the amount of blood ejected from the left ventricle in 1 minute (the right v entricle pumps a similar amount). It is determined by multiplying strok e volume by heart rate. Stroke volume is the amount of blood ejected by a ventricle in one contraction and a verages 60 to 80 mL/beat. With an average resting heart rate of 75 beats per minute, average resting cardiac output is 5 to 6 L (approximately the total blood volume of an individual that is pumped within 1 minute). Ejection fraction is a measure of v entricular efficiency and is normally 55% to 70% of the total amount of blood within the left v entricle that is ejected with e very heartbeat. The cardiac conduction pathway is the pathway of electrical impulses that generates a heartbeat. The sinoatrial (SA) node in the wall of the right atrium is autorhythmic and depolarizes about 100 times per minute, initiating each heartbeat. (While at rest, parasympathetic f ibers dominate and slo w the SA node to about 75 beats per minute.) F or this reason, the SA node is called the pacemaker, and a normal heartbeat is called a normal sinus rhythm. From the SA node, impulses tra vel on a specific path (Fig. 21.3). If the SA node becomes nonfunctional, the AV node can initiate each heartbeat, b ut at a slower rate of 40 to 60 beats per minute.The bundle of His is Cardiac Output 4068_Ch21_387-416 15/11/14 1:38 PM Page 391 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures 1 Normal cardiac impulses arise in the sinoatrial (SA) node from its spot in the wall of the right atrium just below the opening of the superior vena cava. 391 2 An interatrial bundle of conducting fibers rapidly conducts the impulses to the left atrium, and both atria begin to contract 3 The impulse travels along three internodal bundles to the atrioventricular (AV) node (located near the right AV valve at the lower end of the interatrial septum). There, the impulse slows considerably to allow the atria time to contract completely and the ventricles to fill with blood. The heart’s skeleton insulates the ventricles, ensuring that only impulses passing through the AV node can enter. 4 After passing through the AV node, the impulse picks up speed. It then travels down the bundle of His, also called the atrioventricular (AV) bundle. AV node 5 The AV bundle soon branches into right and left bundle branches. 6 Punkinje fibers conduct the impulses throughout the muscle of both ventricles, causing them to contract almost simultaneously. FIGURE 21.3 Conduction pathway. From Thompson, G. S. (2013). Understanding anatomy and physiology. Philadelphia: F.A. Davis, p. 274. During exercise, venous return increases and stretches the ventricular myocardium, which in response contracts more forcefully. This is known as Starling’s law of the heart, and the result is an increase in strok e volume. More blood is pumped with each beat, and at the same time, the heart rate increases, causing cardiac output to increase by as much as four times the resting level, or more for fit athletes. Regulation of Heart Rate The heart generates its own electrical impulse, which begins at the SA node. The nervous system, however, can change the heart rate in response to environmental circumstances. In the brain, the medulla oblongata receives sensory input and alters heart function (Fig. 21.4). Hormones and the Heart The hormone epinephrine, secreted by the adrenal medulla in stressful situations, is sympathomimetic in that it increases the heart rate and force of contraction and dilates the coronary vessels. This in turn increases cardiac output and systolic blood pressure. Aldosterone, a hormone produced by the adrenal cortex, is important for cardiac function because it helps regulate blood levels of sodium and potassium, both of which are needed for the electrical activity of the myocardium. The blood level of potassium is especially critical because even a small deviation impairs the rhythmic contractions of the heart. The atria of the heart secrete a hormone of their o wn called atrial natriuretic peptide or atrial natriuretic hormone. As its name suggests, atrial natriuretic peptide increases the excretion of sodium by the kidneys by inhibiting secretion of aldosterone by the adrenal cortex. Atrial natriuretic peptide is secreted when a higher blood pressure or greater blood volume stretches the w alls of the atria. The loss of sodium is accompanied by the increase loss of w ater in urine, which decreases blood v olume and therefore blood pressure as well. Blood Vessels Arteries and Veins Arteries and arterioles carry blood from the heart to capil laries. Their walls are relatively thick and consist of three 4068_Ch21_387-416 15/11/14 1:38 PM Page 392 392 UNIT FIVE Understanding the Cardiovascular System The medulla in the brain contains a CARDIAC CENTER. In turn, the cardiac center contains an: Factors such as exercise and stress stimulate the acceleratory center. ACCELERATORY and CENTER INHIBITORY CENTER The acceleratory center sends out impulses via the SYMPATHETIC NERVOUS SYSTEM The sympathetic nervous system sends impulses through cardiac nerves (which secrete norepinephrine) to the SA node, the AV node, and the myocardium. This accelerates the heart rate and increases the force of contractions. Factors such as a rise in blood pressure stimulate the inhibitory center The inhibitory center sends signals via the PARASYMPATHETIC NERVOUS SYSTEM HR HR The parasympathetic nervous system sends signals via vagus nerves (which secrete acetylcholine) to the SA and AV nodes, which slows the heart rate. FIGURE 21.4 Factors affecting heart rate. From Thompson, G. S. (2013). Understanding anatomy and physiology. Philadelphia: F.A. Davis, p. 278. layers. Arteries carry blood under high pressure, and the outer layer of fibrous connective tissue prevents rupture of the artery. The middle layer of smooth muscle and elastic connective tissue contributes to the maintenance of normal blood pressure, especially diastolic blood pressure, by changing the diameter of the artery. The diameter of arteries is regulated primarily by the sympathetic division of the autonomic nervous system. By use of the smooth muscle, the arteries can also alter where the greatest volume of blood is directed. The inner layer or lining of the artery is simple squamous epithelium, called endothelium, which is v ery smooth to prevent abnormal clotting. Veins and venules carry blood from capillaries to the heart. Their walls are relatively thin because they have less smooth muscle than arteries. Sympathetic impulses can bring about extensive constriction of v eins, however, and this becomes important in situations such as severe hemorrhage. The lining of veins is, like arteries, endothelium that prevents abnormal clotting; at intervals it is folded into valves to prevent backflow of blood. Valves are most numerous in the veins of the extremities, especially the legs, where blood must return to the heart against the force of gravity. Capillaries Capillaries carry blood from arterioles to v enules and form extensive networks in most tissues. The exceptions are cartilage, covering/lining epithelia, and the lens and cornea of the eye. Capillary walls, a continuation of the lining of arteries and veins, are one cell thick to permit the exchanges of gases, nutrients, and waste products between the blood and tissues (Fig. 21.5). Blood flow through a capillary network is regulated by a precapillary sphincter, a smooth muscle fiber ring 4068_Ch21_387-416 15/11/14 1:38 PM Page 393 Chapter 21 Tunica externa Cardiovascular System Function, Assessment, and Therapeutic Measures External elastic lamina Tunica media 393 Internal elastic Endothelium (lining) lamina Artery Arteriole Endothelial cells Smooth muscle Precapillary sphincter Capillary Blood flow Tunica intima Venule Vein Tunica externa Tunica media Valve FIGURE 21.5 Structure of an artery, arteriole, capillary network, venule, and vein. From Scanlon, V., & Sanders, T. (2015). Essentials of anatomy and physiology, 7th ed. Philadelphia: F.A. Davis, with permission. that contracts or relaxes in response to tissue needs. In an active tissue such as e xercising skeletal muscle, for e xample, the rapid oxygen uptake and carbon dioxide production cause dilation of the precapillary sphincters to increase blood flow. At the same time, precapillary sphincters in less active tissues constrict to reduce blood flow. This is important because the body does not have enough blood to fill all of the capillaries at once; the fixed volume must constantly be shunted or redirected to where it is needed most. Exchange between blood and tissue fluids occurs primarily due to diffusion and/or filtration at the capillaries. Diffusion is important to gas exchange. Filtration is a vital mechanism for homeostasis of extracellular fluids. Some of this tissue fluid returns to the capillaries, and some is collected in lymph capillaries. Lymph is returned to the blood by lymph v essels. Should blood pressure within the capillaries increase, more tissue fluid than usual is formed, too much for the lymph vessels to collect. This may result in tissue swelling, called edema. Blood Pressure Blood pressure is the force of the blood against the walls of the blood vessels and is measured in millimeters of mercury (mm Hg), systolic o ver diastolic. The normal average of systemic arterial pressure is 120/80 mm Hg. Blood pressure decreases in the arterioles and capillaries, and the systolic and diastolic pressures mer ge into one pressure. As blood enters the veins, blood pressure decreases further and approaches zero as it flo ws into the right v entricle. As mentioned previously, the blood pressure in the capillaries is of great importance, and normal blood pressure is high enough to permit f iltration for nourishment of tissues b ut low enough to prevent rupture. The arterioles (and v eins during increased sympathetic stimulation) are usually in a state of slight constriction that helps to maintain normal blood pressure, especially diastolic pressure. This is called peripheral resistance; it is re gulated 4068_Ch21_387-416 15/11/14 1:38 PM Page 394 394 UNIT FIVE Understanding the Cardiovascular System by the vasomotor center in the medulla, which receives input via the glossopharyngeal and vagus nerves. Blood pressure is also af fected by many other factors. If heart rate and force increase, blood pressure increases within limits. If the heart is beating very fast, the ventricles are not filled before the y contract, cardiac output decreases, and blood pressure drops. The strength of the heart’s contractions depends on adequate venous return, which is the amount of blood that flows into the atria. Decreased v enous return results in weaker contractions. Venous return depends on several factors: constriction of the veins to reduce pooling, the sk eletal muscle pumping to squeeze the deep v eins of the le gs, and the diaphragm’ s downward pressure during inhalation to compress the abdominal veins as the thoracic veins are decompressed. The valves in the veins prevent backflow of blood and thus contribute to the return of blood to the heart. The elasticity of the large arteries also contributes to normal blood pressure. When the left ventricle contracts, the blood stretches the elastic w alls of the large arteries, which absorb some of the force. When the left ventricle relaxes, the arterial walls recoil, exerting pressure on the blood. Normal elasticity, therefore, lowers systolic pressure, raises diastolic pressure, and maintains normal pulse pressure. Pulse pressure is the difference between the systolic and diastolic pressures.The usual ratio of systolic to diastolic to pulse pressure is 3:2:1. Renin-Angiotensin-Aldosterone Mechanism The kidneys are of great importance in the regulation of blood pressure. If blood flow through the kidneys decreases, renal filtration decreases and urinary output decreases to preserve blood volume. Decreased blood pressure stimulates the kidneys to secrete renin, which initiates the renin-angiotensinaldosterone mechanism, raising blood pressure (Fig. 21.6). Other hormones that affect blood pressure include those of the adrenal medulla, norepinephrine and epinephrine, which increase cardiac output and cause vasoconstriction in skin and viscera. Antidiuretic hormone, released from the posterior pituitary, directly increases w ater reabsorption by the kidneys, thus increasing blood v olume and blood pressure. Atrial natriuretic peptide, secreted by the atria of the heart, inhibits aldosterone secretion and thereby increases renal excretion of sodium ions and w ater, which decreases blood volume and subsequently blood pressure. Circuits of Circulation The two circuits of circulation are pulmonary and systemic (see Fig. 21.2). Pulmonary circulation begins at the right ventricle, which pumps deoxygenated blood toward the lungs for gas exchange at the alveoli. Oxygenated blood returns to the left atrium by way of the pulmonary v eins. Low pressure in the pulmonary capillaries prevents filtration in pulmonary capillaries, keeping tissue fluid from accumulating in the alveoli of the lungs, which can otherwise result in pulmonary edema. Systemic circulation begins in the left v entricle, pumping oxygenated blood into the aorta, the many branches of which eventually give rise to capillaries within the tissues. Deoxygenated blood returns to the right atrium by way of the superior Low blood pressure Extracellular fluid deficit Renal ischemia Elevated urine sodium Renin released in kidney and splits angiotensinogen to angiotensin I Angiotensinogen Angiotensin I Angiotensin-converting enzyme Liver Angiotensin II Releases aldosterone Lungs Causes peripheral vasoconstriction Causes sodium reabsorption Increases blood volume Blood pressure increases FIGURE 21.6 The renin-angiotensin-aldosterone mechanism. and inferior vena cava and the coronary sinus. The hepatic portal circulation is a special part of the systemic circulation in which blood from the capillaries of the digesti ve organs and spleen flows through the portal vein and into the sinusoids in the liver before returning to the heart. This pathway permits the liver to regulate the blood levels of nutrients such as glucose, amino acids, and iron and to remove potential toxins such as alcohol or medications from circulation. Aging and the Cardiovascular System The aging of blood v essels, especially arteries, is belie ved to begin in childhood, although the ef fects are not apparent until later in life (Fig. 21.7). Atherosclerosis is the deposition of lipids in the walls of arteries over a period of years. The deposited lipids can narrow the arteries’ lumens and form rough surfaces that may stimulate intra vascular clot formation. Atherosclerosis decreases blood flow to the affected organ. With age, the heart muscle becomes less efficient, and maximum cardiac output and heart rate both decrease, although resting levels may be more than sufficient (“Gerontological Issues”). Valves may become thickened by fibrosis, leading to heart murmur. • WORD • BUILDING • atherosclerosis: athere—porridge + sklerosis—hardness 4068_Ch21_387-416 15/11/14 1:38 PM Page 395 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures health by not smoking, e xercising, following a healthy diet, and maintaining normal blood pressure, blood glucose, total cholesterol levels, and weight. Exercise is essential for everyone, especially children, because Americans continue to be sedentary and eat excess calories. The Aging Cardiovascular System Conduction cells less effective Vein valves incompetent Atherosclerosis Resting blood pressure increases Decreased heart rate NURSING ASSESSMENT OF THE CARDIOVASCULAR SYSTEM Venous stasis; ulceration Dysrhythmias Fatigue Narrowed vessel lumens; rough surfaces Clot formation 395 Decreased blood flow to heart and other organs Left ventricle workload increases Stroke Leftsided heart failure FIGURE 21.7 Aging and the cardiovascular system concept map. Gerontological Issues The older adult is at increased risk for developing orthostatic hypotension, which could precipitate a fall. This is often due to a combination of age-related changes, immobility, chronic illnesses, and medications. CARDIOVASCULAR DISEASE In 2010, according to U.S. statistics of theAmerican Heart Association (AHA, 2014), about one in six deaths were due to coronary heart disease; about 33% of United States adults over 19 years of age have hypertension per data from 2007 to 2010, and hypertension occurrence in African American adults is the highest in the w orld. For more information on cardiovascular disease statistics, visit www .americanheart.org. In women, the greatest cause of death is cardiovascular disease. A movement called Go Red for Women gives women encouragement and tools to pre vent cardiovascular disease and live healthy. For more information on Go Red forWomen, visit www.goredforwomen.org. Lifestyle plays a major role in risk factors for cardiovascular disease. The AHA recommends impro ving cardiovascular Nursing assessment of the cardio vascular system includes a patient health history and physical examination (“Gerontological Issues”). If the patient is experiencing an acute problem, focus on the most serious signs and symptoms and physical data until he or she is stabilized (T able 21.1). In-depth data collection can be completed when the patient is stable. TABLE 21.1 ACUTE CARDIOVASCULAR DATA COLLECTION History Allergies Significance For medication administration, diagnostic dyes Smoking history Risk factor for cardiovascular disorders Medications Toxic levels; influencing symptoms Pain: location, radiation, description Possible angina, myocardial infarction, thrombus, embolism Dyspnea Left-sided heart failure; pulmonary edema or embolism Fatigue Decreased cardiac output Palpitations Dysrhythmias Dizziness Dysrhythmias Weight gain Right-sided heart failure Physical Examination Vital signs Possible Abnormal Findings Bradycardia, tachycardia, hypotension, hypertension, tachypnea, apnea, shock Heart rhythm Dysrhythmias Edema Right-sided heart failure Jugular venous distention Right-sided heart failure Breath sounds Crackles, wheezes with left-sided heart failure Cough, sputum Acute heart failure—dry cough, pink frothy sputum 4068_Ch21_387-416 15/11/14 1:38 PM Page 396 396 UNIT FIVE Understanding the Cardiovascular System Gerontological Issues Older adults commonly ha ve signs and symptoms that are not typical of a disorder, such as fatigue and nausea. The only symptom of myocardial inf arction (MI) in an older patient may be dyspnea. Chest pain, a typical symptom, may not be present. Health History To understand a patient’s cardiovascular problems, ask about past and current symptoms, medications, use of recreational drugs, surgeries, treatments, and risk factors such as diet, activity, tobacco use, and recent stressors. Data collection includes asking questions in the WHAT’S UP? format: where it is, how it feels, aggravating and alleviating factors, timing, severity, useful data for associated symptoms, and perception by the patient of the problem. The health history helps determine the cause of the symptom. For example, shortness of breath can be the result of heart failure or chronic obstructi ve pulmonary disease (COPD). With cardiovascular problems, data collection focuses on the areas listed in Table 21.2. Medical History Previous medical records can pro vide objective patient data that can be supplemented with patient responses. Childhood illnesses that can lead to heart disease, such as rheumatic fever or scarlet fever, are noted. Other conditions noted include pulmonary disease, hypertension, kidney disease, cerebral vascular accident or brain attack, transient ischemic (restricted blood flow) attack, renal disease, anemia, streptococcal sore throat, • WORD • BUILDING • ischemic: ischein—hold back + haima—blood TABLE 21.2 CARDIOVASCULAR HEALTH HISTORY Question Pain: WHAT’S UP? Format Where is pain? Does it radiate? Rationale Cardiac pain may radiate to shoulders, neck, jaw, arms, or back. Vascular disorders cause extremity pain. How does it feel? Discomfort, burning, aching, indigestion, squeezing, pressure, tightness, heaviness, numbness in chest area? Fullness, heaviness, sharpness, throbbing in legs? Pain can be associated with angina or myocardial infarction. The quality of pain varies. Venous pain is a fullness or heaviness. Arterial pain is sharp or throbbing. Aggravating/alleviating factors that increase/relieve the pain? Activity may cause or increase angina. Rest or medications may relieve angina. Leg activity pain, intermittent claudication, results from decreased perfusion that is aggravated by activity. Rest pain, from severe arterial occlusion, increases when lying. Dangling reduces the pain because blood flow is increased by gravity. Timing of pain: onset, duration, frequency? Pain may be continuous, intermittent, acute, or chronic. Arterial occlusion causes acute pain. Severity of pain? Rate pain on a scale of 0 to 10. Useful data for associated symptoms? Accompanying symptoms and their characteristics guide diagnosis and treatment. Perception of patient about problem? Patient’s insight to problem is helpful in planning care. Level of Consciousness (LOC) What is your name? What is the month? Year? Where are you now? A lack of oxygen caused by cardiac disease can decrease LOC. Dyspnea Are you short of breath? What increases your shortness of breath? What relieves your shortness of breath? Dyspnea can be present with heart failure that reduces cardiac output, on exertion in angina pectoris or from a pulmonary embolus resulting from thrombophlebitis, heart failure, or dysrhythmias. 4068_Ch21_387-416 15/11/14 1:38 PM Page 397 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures 397 TABLE 21.2 CARDIOVASCULAR HEALTH HISTORY—cont’d Question Palpitations Are you having palpitations or irregular heartbeat? Does your heart ever race, skip beats, or pound? Fatigue Have you noticed a change in your energy level? Are you able to perform activities that you would like to? Edema Have you had any swelling in your feet, legs, or hands? Rationale Palpitations can occur from dysrhythmias resulting from ischemia, electrolyte imbalance, or stress. Dizziness can be associated with dysrhythmias. Fatigue occurs from reduced cardiac output resulting from heart failure. Functional abilities can be limited from fatigue. Right-sided heart failure can cause fluid accumulation in the tissues. Have you gained weight? Fluid retention causes weight gain. Paresthesia/Paralysis Any numbness, tingling, or other abnormal sensations in extremities? Numbness and tingling, pins and needles, and crawling sensations are paresthesia. Can you move your extremity? congenital heart disease, thrombophlebitis, and alcoholism. Patient allergies, previous hospitalizations, and surgeries are documented. Baseline diagnostic tests are helpful for comparison with current tests. Functional limitations that are related to cardiovascular problems, such as difficulty performing activities of daily li ving (ADLs), walking, climbing stairs, or completing household tasks, are also assessed. Medication Use of prescription drugs, over-the-counter medications such as aspirin that can prolong clotting time, and recreational drugs is noted. Patient’s understanding of medications (name, dosage, reason for taking, last dose, and length of use) is documented. Paralysis is inability to move extremity. Reduced nerve conduction from decreased oxygen supply causes paresthesia and paralysis. of the brain, is noted. Height, weight, and vital signs are recorded. Blood Pressure Normal blood pressure is considered less than 120/80 (see Chapter 22). Readings in both arms are done for comparison (Box 21-1). A difference in the readings is reported to the HCP. The arm with the higher reading is used for ongoing measurements. If necessary, blood pressure may be measured in the leg using a larger blood pressure cuff. The reading in the leg is normally 10 mm Hg higher than in the arm (see “Evidence-Based Practice”). Family History A family history (parents, siblings, and grandparents) of cardiovascular conditions is noted because man y cardiac problems are hereditary. For example, those who ha ve had a parent die of sudden cardiac death before age 60 are at increased risk for sudden cardiac death. Health Promotion Risk factors such as diet, acti vity, tobacco use, and recent stressors for the patient are noted. The patient’s health promotion activities are explored, especially for risk factors that are modifiable with changes in lifestyle. Physical Examination The patient’s general appearance is observ ed. The patient’s level of consciousness, which is an indicator of oxygenation EVIDENCE-BASED PRACTICE Clinical Question Is blood pressure self-measurement at home more accurate for hypertension control and predictive of the risk of cardiovascular events than office blood pressure measurement? Evidence In a meta-analysis of studies conducted across a variety of populations, it was shown that home blood pressure recordings were a stronger predictor of long-term cardiovascular events than office blood pressure measurements. Home blood pressure monitoring overcomes the “white Continued 4068_Ch21_387-416 15/11/14 1:38 PM Page 398 398 UNIT FIVE Understanding the Cardiovascular System coat effect” (increase in blood pressure during an office visit) of traditional office blood pressure measurement, increases accuracy, and is cost-effective. Implications for Nursing Practice Patients can effectively be taught to take blood pressure at home. Teaching guidelines include using an oscillometric monitor that measures blood pressure on the upper arm with proper cuff size; return demonstration of blood pressure measurement; resting for 5 minutes in the seated position; then taking three consecutive readings in the morning and at night, over a period of 1 week. Monitors should be validated periodically. REFERENCE Sheikh, S., Sinha, A., & Agarwal, R. (2011). Home blood pressure monitoring: How good a predictor of long-term risk? Current Hypertension Report, 13, 192–199. Box 21-1 Taking Accurate Blood Pressure Measurements • Instruct patient to avoid exercise, caffeine, and smoking for 30 minutes before the blood pressure measurement and to void before the reading. • Use auscultatory method with properly calibrated and validated blood pressure instrument. • Seat patient quietly for at least 5 minutes in a chair (not on examination table) with feet on the floor and arm supported at heart level before the blood pressure measurement. • Use appropriate-sized cuff in which cuff bladder encircles at least 80% of arm. • Ask patient to remain still and do not talk during measurement as motion alters reading. • Determine the patient’s baseline blood pressure by inflating the cuff and noting the reading when the radial pulse is no longer felt. When taking blood pressure, inflate the cuff to 20 numbers above the obtained baseline reading. (Overinflation may cause inaccurate reading.) • During measurement, deflate the cuff slowly at rate of 2 mm Hg/seconds. • Take at least two blood pressure measurements and average. • Systolic blood pressure = first of two or more sounds heard. • Diastolic blood pressure = disappearance of sounds. • Provide patients, verbally and in writing, their specific blood pressure reading. Note. Adapted from National Heart, Lung, and Blood Institute. Retrieved January 26, 2014, from www.nhlbi.nih.gov/hbp/detect/tips.htm ORTHOSTATIC BLOOD PRESSURE. Measurements are taken with the patient lying, sitting, and standing to detect abnormal variations with postural changes. When the patient sits or stands, a drop in the systolic pressure of up to 15 mm Hg and either a drop or slight increase in the diastolic pressure of 3 to 10 mm Hg is normal. In response to the drop in blood pressure, the pulse increases 15 to 20 beats per minute to maintain cardiac output. Orthostatic hypotension (postural hypotension), is a drop in systolic blood pressure greater than 15 mm Hg, a drop or slight increase in the diastolic blood pressure greater than 10 mm Hg, and an increase in heart rate greater than 20 beats per minute in response to the drop in blood pressure. It indicates a problem that should be investigated by the health care provider (HCP) (Box 21-2). The patient often reports lightheadedness or syncope because the drop in blood pressure decreases the amount of oxygen-rich blood traveling to the brain. Factors that may cause orthostatic hypotension include def icient fluid volume, diuretics, analgesics, and pain. Pulses The apical pulse is auscultated for 1 minute to assess rate and rhythm. Normal heart rate is 60 to 100 beats per minute. In athletic people, the heart rate is often slower, around 50 beats per minute, because the well-conditioned heart pumps more efficiently. Apical pulse rhythm is documented as re gular or irregular. The apical rate can be compared with the radial rate to assess equality. If there are fe wer radial beats than apical beats, a pulse deficit exists and should be reported to the HCP. Arterial pulses are palpated for v olume and pressure quality. They are palpated bilaterally and compared for equality. A normal vessel feels soft and springy. A sclerotic vessel feels stiff. The quality of the pulses is described on a four-point scale as follows: 0 is absent; 1+ is weak, thready; 2+ is normal; and 3+ is bounding. An absent pulse is not palpable. A thready pulse is one that disappears when slight pressure is applied and returns when the pressure is removed. The normal pulse is easily palpable. The bounding pulse is strong and present even when slight pressure is applied. When the normal vessel is palpated, a tapping is felt. In the abnormal vessel that has a bulging or narrowed wall, a vibration is felt, which is called a thrill. When auscultating an abnormal vessel, a humming is heard that is caused by the turb ulent blood flo w through the vessel. This is referred to as a bruit. BE SAFE! Anticipate potential drops in blood pressure with position changes. Orthostatic hypotension can be found in patients of any age but is most commonly found in the older patient. The blood pressure drop increases the risk of fainting and falling. Use fall precautions such as a walking belt or two-person assist for patients at risk of or with orthostatic hypotension. 4068_Ch21_387-416 15/11/14 1:38 PM Page 399 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures 399 Inspection Box 21-2 Orthostatic Hypotension Assessment To assess orthostatic hypotension: 1. Explain procedure to patient; determine if patient can safely stand. 2. Patient should not exercise, eat, or smoke 30 minutes before readings. 3. Have patient lie flat in bed at least 5 minutes before readings. 4. Use correct size blood pressure cuff. 5. Patient should not talk during readings and should sit up with legs uncrossed while sitting. 6. Take patient’s lying blood pressure and heart rate. 7. Assist patient to sitting position. Ask if dizzy or lightheaded with each position change. If yes, ensure safety from fainting or falling. A gait or walking belt can be used. With any position change, if patient experiences additional symptoms with the dizziness and decreased blood pressure and increased heart rate, assist the patient to lie down, take blood pressure, and notify the HCP. Consider the possible cause of the orthostatic hypotension (hemorrhaging, dehydration, diuretics) to plan patient care. 8. Wait 3 minutes, and then take patient’s sitting blood pressure and heart rate. If patient is dizzy or lightheaded, continue sitting position for 5 minutes if tolerated. Do not attempt to bring the patient to standing. Repeat sitting blood pressure. If blood pressure has increased and patient is no longer dizzy, assist patient to stand. 9. Assist patient to stand and take blood pressure and pulse immediately. Then take again in 3 minutes. If blood pressure drops and patient is dizzy or lightheaded, do not attempt to ambulate patient. 10. Document all heart rate and blood pressure measurements, including extremity used and patient position when reading was obtained (e.g., right arm: lying 132/78 mm Hg, sitting 118/68 mm Hg, standing 110/60 mm Hg). Also document patient tolerance, symptoms, and nursing interventions if symptomatic. 11. Report abnormal findings to HCP. During the health history , inspection be gins by noting shortness of breath when the patient speaks or moves. The patient’s skin is noted for oxygenation status through the color of skin, mucous membranes, lips, earlobes, and nailbeds. Pallor may indicate anemia or lack of arterial blood flow. Cyanosis shows an oxygen distrib ution deficiency. A reddish brown discoloration (rubor) found in the lower extremities occurs from decreased arterial blood flow. A brown discoloration and cyanosis when the extremity is dependent may be seen in the presence of v enous blood flow problems. Hair distribution on the e xtremities is observed. Decreased hair distribution, thick, brittle nails, and shiny, taut, dry skin occur from reduced arterial blood flow. Venous blood return is assessed by inspecting extremities for varicose veins, stasis ulcers, or scars around the ankles and signs of thrombophlebitis such as swelling, redness, or a hard, tender vein. The patient’s internal and external jugular neck veins are observed for distention in a 45- to 90-degree upright position. Normally, the veins are not visible in this position. Distention indicates an increase in the venous volume, often caused by right-sided heart failure. Capillary refill time is 3 seconds or less and indicates arterial blood flow to the extremities. The patient’s nailbed is briefly squeezed, causing blanching, and then released. The time that it tak es for the color to return to the nailbed after release of the squeezing pressure is the capillary ref ill time. Longer times indicate anemia or a decrease in blood flow to the extremity. Clubbing of the nailbeds occurs from oxygen def iciency over time. It is often caused by congenital heart defects or the long-term use of tobacco. The distal ends of the fingers and toes swell and appear clublike. With clubbing, the normal 160-degree angle formed between the base of the nail and the skin is lost, causing the nail to be flat (Fig. 21.8). Later, the nail base elevates, the angle exceeds 180 degrees, and the nail feels spongy when squeezed. To check for this, touch your inde x fingers together at the nailbeds and first joint. Look through the space created at the nailbeds. Do you see a diamond? If so, that is normal. If there is not a diamond, this indicates the nailbeds are clubbed and therefore f illing that space. This should be reported to an HCP for follow-up. LEARNING TIP Six Ps characterize peripheral vascular disease: Respirations The rate and ease of respirations are observ ed. Breath sounds are auscultated. Sputum characteristics such as amount, color, and consistency are noted. Pink, frothy sputum is an indicator of acute heart f ailure. A dry cough can occur from the irritation caused by the lung congestion resulting from heart failure. • Pain • Poikilothermia • Pulselessness • Pallor • Paralysis • Paresthesia (decreased sensation) 4068_Ch21_387-416 15/11/14 1:38 PM Page 400 UNIT FIVE 400 Understanding the Cardiovascular System Clubbing—early 160° Clubbing—severe Greater than 180° of the edema by pressing with a finger for 5 seconds over a bone, the medial malleolus or tibia, in the area of edema. If the finger imprint or indentation remains, the edema is pitting. Measuring the leg circumference is an accurate method for monitoring the edema. Homans’ sign is an assessment for v enous thrombosis; however, in less than 50% of patients with thrombosis, the test is not positive. A positive Homans’ sign is pain in the patient’s calf or behind the knee when the foot is quickly dorsiflexed with the knee in a slightly fle xed position (Fig. 21.10). Homans’ sign should not be performed if a positive diagnosis of thrombosis has been made because a clot could be dislodged with the movement. Auscultation FIGURE 21.8 Clubbing of the fingers. Palpation In addition to palpating the arteries, the thorax can be palpated at the point of maximum impulse . The point of maximum impulse is palpated by placing the right hand over the apex of the heart. If palpable, a thrust is felt when the v entricle contracts. An enlarged heart may shift the pulse of maximum impulse to the left of the midclavicular line. The temperature of the extremities is palpated bilaterally for comparison. Palpation begins proximally and moves distally along the extremity. In areas of decreased arterial blood flow, the ischemic area feels cooler than the rest of the body because it is blood that w arms the body. In the absence of sufficient arterial blood flow, the area becomes the temperature of the environment (poikilothermy). A warm or hot extremity indicates a venous blood flow problem. Edema is palpated in the lower extremities or dependent areas such as the sacrum for the supine patient (Fig. 21.9). Edema can occur from right-sided heart f ailure, gravity, or altered venous blood return. The nurse assesses the severity FIGURE 21.9 Pitting edema. Application of pressure over a bony area displaces the excess fluid, leaving an indentation or pit. Normal heart sounds are produced by the closing of the heart valves. Sound in blood-flowing vessels is transmitted in the direction of the blood flow. The first heart sound (S1) is heard at the beginning of systole as “lubb” when the tricuspid and mitral (AV) valves close (Fig. 21.11). The second heart sound (S 2) is heard at the start of diastole as “dupp” when the aortic and pulmonic semilunar v alves close. The diaphragm of the stethoscope is used to hear the high-pitched sounds of S 1 and S2. Normally, no other sounds are heard between S 1 and S2. With the bell of the stethoscope placed at the apex, a third heart sound (S 3) or a fourth heart sound (S 4) may be heard. Ha ving patients lean forward or lie on their left side can mak e the heart • WORD • BUILDING • poikilothermy: poikilos—varied + therme—heat FIGURE 21.10 Assessment of Homans’ sign for venous thrombosis. The foot is quickly dorsiflexed with the knee flexed. Calf or knee pain is noted. This assessment should not be performed if a positive diagnosis of thrombosis has been made. 4068_Ch21_387-416 15/11/14 1:38 PM Page 401 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures QRS Murmurs are caused by a narro wed valve opening or a valve that does not close tightly . A murmur is a prolonged, swishing sound that ranges in intensity from faint to very loud. A pericardial friction rub occurs from inflammation of the pericardium. The intensity of a rub can range from f aint to loud enough to be audible without a stethoscope.A rub has a grating sound like sandpaper being rubbed together that occurs when the pericardial surfaces rub together during a heartbeat. (See the Learning Tip on pericardial friction rub in Chapter 23.) Having the patient sit and lean forward allows a rub to be heard more clearly. The rub is best heard to the left of the sternum using the diaphragm of the stethoscope. A pericardial friction rub may occur after a MI or chest trauma. QRS P T S1 P S2 T S1 401 S2 Aortic valve Pulmonic valve CRITICAL THINKING S1 S2 Mitral valve S2 S1 Tricuspid valve FIGURE 21.11 Heart sounds shown on electrocardiogram: S1 is heard at the beginning of systole, and S2 is heard at the beginning of diastole. sounds easier to hear by bringing the area of the heart where the sound may be heard closer to the chest wall. The S3 heart sound is normal for children and younger adults. It sounds like a gallop and is a lo w-pitched sound heard early in diastole. In older adults, S3 may be heard with leftsided heart failure, fluid volume overload, and mitral valve regurgitation. The S4 heart sound is also a lo w-pitched sound, similar to a gallop b ut heard late in diastole. It occurs with hypertension, coronary artery disease, and pulmonary stenosis. LEARNING TIP This sentence can help you remember the heart’s auscultation points: All (aortic) People (pulmonic) Eat (Erb’s point) Three (tricuspid) Meals (mitral) Mrs. Smith ■ Mrs. Smith, age 78, baseline weight 162 pounds, is admitted to the hospital with shortness of breath. Initial assessment findings are BP 152/88 mm Hg, pulse 104 beats per minute, respirations 26 per minute, temperature 99.4°F (37.2°C), shortness of breath at rest that increases with activity, ankles sw ollen, heart tones distant, nailbeds pale, no pain, has not eaten well for 2 weeks, 6-pound weight gain in 1 week, sleeps on three pillows, neck veins visible bilaterally. A diagnosis of acute MI with heart failure is made by her HCP. 1. Why might Mrs. Smith not be having chest pain with a diagnosis of acute MI? 2. How should swollen ankles be assessed to provide complete and measurable data? 3. What should be documented for the assessment performed on the swollen ankles and how should the assessment findings be documented? 4. How should the assessment findings be documented for the additional symptoms Mrs. Smith has? 5. What is Mrs. Smith’s weight in kilograms? 6. What health care team members might provide collaborative care for Mrs. Smith? Suggested answers are at the end of the chapter. DIAGNOSTIC TESTS FOR THE CARDIOVASCULAR SYSTEM Diagnostic test results are combined with the health history and physical assessment to plan care for the patient (Table 21.3). Noninvasive Studies Chest X-Ray Examination A chest x-ray e xamination shows the size, position, contour, and structures of the heart (Fig. 21.12). It can re veal (Text continued on page 406) 4068_Ch21_387-416 15/11/14 1:39 PM Page 402 402 UNIT FIVE Understanding the Cardiovascular System TABLE 21.3 DIAGNOSTIC PROCEDURES AND LABORATORY TESTS FOR THE CARDIOVASCULAR SYSTEM Definition Significance of Abnormal Findings Nursing Management Anterior-posterior and left lateral views of chest. Heart enlargement, calcifications, fluid around heart Ask females if pregnant. Remove metal items. Teaching: no discomfort. Computed tomography scan Evaluates heart, structures. Plaque or calcification indicates atherosclerosis. Kidney function checked if contrast used. If renal insufficiency, prophylaxis such as N-acetylcysteine (Mucomyst) and IV hydration with 0.45% sodium chloride hydration or a bicarbonate infusion can be given to protect kidneys. Cardiac magnetic resonance imaging (MRI)/angiography (MRA) Provides threedimensional image of heart. Contrast agent given for MRA to visualize arteries. Cardiac abnormalities Ask if implants, non-MRI safe pacemaker, metallic items, and claustrophobia. Give antianxiety medication as ordered before MRI. Assess allergies for contrast agent. Teaching: must lie still in cylinder with loud, pounding sounds. Can talk to technician, listen to music. Electrocardiogram (ECG) Electrodes on skin carry electrical activity of heart from different views. Dysrhythmias, enlarged heart chamber size, myocardial ischemia or infarction, electrolyte imbalances Teaching: no discomfort. Explain procedure. Holter monitor Recording of ECG for up to 24 hours to match abnormalities with symptoms recorded in patient’s diary. Dysrhythmias, infrequent myocardial ischemia Apply electrodes and leads. Teaching: keep accurate diary; push event button for symptoms. No showers or baths. Return visit. Event Recorder Worn longer time periods and can record 3 cardiac events. Infrequent cardiac events. Teaching: push event button for symptomatic event. Can bathe. Echocardiogram Sound waves bounce off heart to produce heart images and show blood flow. Heart enlargement, coronary artery disease, valvular abnormalities, thickened cardiac walls or septum, pericardial effusion Useful in heart failure, cardiomyopathy, to guide treatment, May be done at bedside. Patient lies on left side. Teaching: no discomfort, gel applied. Procedure Noninvasive Chest x-ray film Strain echocardiogram Comprehensive assessment of the function of the heart muscle. Can eat before test. Teaching: no discomfort, gel applied. 4068_Ch21_387-416 15/11/14 1:39 PM Page 403 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures 403 TABLE 21.3 DIAGNOSTIC PROCEDURES AND LABORATORY TESTS FOR THE CARDIOVASCULAR SYSTEM—cont’d Procedure Definition Significance of Abnormal Findings evaluate cardiac surgery or transplant See Echocardiogram. Nursing Management Transesophageal echocardiogram Probe with transducer on end inserted into esophagus. Exercise stress echocardiogram Evaluates effects of exercise on heart and vascular circulation. Dysrhythmias, ischemia Sound waves bounce off moving blood producing recordings. Decreased blood flow in peripheral vascular disease Teaching: explain procedure. IV injection of thallium-201 to evaluate cardiac blood flow. With exercise, thallium given 1 minute before end of test to circulate thallium. Scan done within 10 minutes and repeated in 2 to 4 hours for comparison. If thallium not delivered to cardiac cells by good blood flow then see “cold spots” that show ischemia initially or infarcted areas later. Teaching: explain procedure, inform that radioactivity is small and gone within a few hours. Light meal only between scans. Dipyridamole thallium imaging Dipyridamole (Persantine) IV is a vasodilator given to increase blood flow to coronary arteries; test is same as thallium imaging. If thallium not delivered to cardiac cells by good blood flow then see “cold spots” that show ischemia initially or infarcted areas later. Teaching: explain procedure, instruct no caffeine or aminophylline 12 hours before. Same as thallium imaging. Technetium pyrophosphate or technetium-99m sestamibi imaging Radioisotope given IV. Scanned 1.5 to 2 hours later. Areas of myocardial cell damage take up the radioisotope, which appears as hot spots. Teaching: explain procedure, inform that radioactivity is small and gone within a few hours. Multiple-gated acquisition (MUGA) scan Technetium-99m pertechnetate is given IV. Studies effects of drugs, recent myocardial infarction Teaching: explain procedure. Doppler ultrasound Radioisotopes Thallium imaging Monitor vital signs and oxygen saturation. Check gag reflex before NPO status is discontinued. Suction continually during procedure. Teaching: NPO 6 hours before test. Sedation and local throat anesthetic given. Monitor vital signs and ECG before, during, and after test until stable. Teaching: explain procedure, wear walking shoes and comfortable clothes. Continued 4068_Ch21_387-416 15/11/14 1:39 PM Page 404 404 UNIT FIVE Understanding the Cardiovascular System TABLE 21.3 DIAGNOSTIC PROCEDURES AND LABORATORY TESTS FOR THE CARDIOVASCULAR SYSTEM—cont’d Significance of Abnormal Findings (MI), and congestive heart failure. Procedure Definition Serial studies are done over several hours. May be done at bedside. Positron emission tomography (PET) Nitrogen-13 ammonia IV given and scanned for cardiac perfusion. Then fluoro-18deoxyglucose IV given and scanned for cardiac metabolic function. Exercise may also be used. In normal heart, scans match; in injured heart, they differ. Patient’s blood glucose must be 60 to 140 mg/dL for accuracy. Teaching: explain procedure. Must lie still during scan. If exercise used, NPO and no tobacco use. CRP level can indicate low-grade inflammation in coronary vessels. CV disease risk: Low = <1 mg/L Average = 1–3 mg/L High = >3 mg/L Elevated levels indicate MI risk. No special care. Homocysteine Amino acid in the blood. Normal: 7– 8 micromol/L Elevated levels linked with higher risk of coronary artery disease (CAD) and PVD. Encourage high-risk patients to have adequate intake of folic acid and vitamin B. Creatine kinase (CK) Heart, brain, skeletal muscle contain CK enzymes. Normal male: 5– 55 units/mL Normal female: 5– 25 units/mL Damaged cells release CK. With MI, CK elevates in 6 hours and returns to baseline in 48–72 hours. Avoid IM injections, and take baseline CK before inserting IVs to avoid elevating CK from muscle cell damage. Serial sampling done. CK-MB Heart muscle contains MB isoenzyme. Normal: 0– 7 international units/L Rises with MI in 6 hours and returns to baseline in 72 hours. Same as CK. Cardiac troponin I or T Cardiac cell protein. Normal: Varies by lab; very low levels Elevated levels sensitive indicator of MI. Levels elevated up to 7 days. No special care. Myoglobin Protein found in cardiac cells; 99% indicative of MI. Normal: 0–85 ng/mL Rises in 1 hour after MI and peaks in 4 to 12 hours, so must be drawn within No special care. Serum Tests Highly sensitive Creactive protein (hs-CRP) Nursing Management 4068_Ch21_387-416 15/11/14 1:39 PM Page 405 Chapter 21 Cardiovascular System Function, Assessment, and Therapeutic Measures 405 TABLE 21.3 DIAGNOSTIC PROCEDURES AND LABORATORY TESTS FOR THE CARDIOVASCULAR SYSTEM—cont’d Significance of Abnormal Findings 18 hours of chest pain onset. Procedure Definition Magnesium Electrolyte necessary to regulate heartbeat and blood pressure. Normal: 1.6 to 2.6 mg/dL Hypomagnesemia may cause cardiac arrhythmias, hypertension, tachycardia. No special care. Phospholipids May elevate in cardiovascular disease. Normal: 125– 380 mg/dL CAD risk Same as triglycerides. Lipoproteins Electrophoresis done to separate lipoproteins: VLDL, LDL, HDL. HDL protects against CAD Normal lipoproteins: 400–800 mg/dL Desirable: LDL less than HDL (values vary with age) Elevated LDL increases CAD risk. LDL <100 desirable HDL >60 Same as triglycerides. Contrast agent injected into vessels to make them visible on x-rays. Coronary: coronary arteries via cardiac catheter. Peripheral: peripheral arteries or veins. Assesses vessel patency, injury, or aneurysm. Precare: Informed consent. NPO 4 to 18 hours before test. Assess allergies. Teaching: sedative and local anesthesia may be used; burning sensation from dye; monitored continuously. Postcare: Monitor vital signs, hemorrhage at the injection site, pulses. Catheter inserted into heart for data on oxygen saturation and chamber pressures. Contrast may be injected to visualize structures. Cardiac disease Precare: Same as angiography. Sensory teaching: table is hard; cool cleansing solution used; sting felt from local anesthetic; hear monitor beeping; feel pressure of catheter insertion; dye warm, burning feeling; headache; brief chest pain; hear camera; feel table move. Postcare: Monitor vital signs, circulation, mobility, sensation, catheter insertion site, for hemorrhage or hematoma every 15 minutes for 1 hour, then every 30 minutes to 1 hour. Apply insertion site pressure as needed. Invasive Angiography Cardiac catheterization Nursing Management Continued 4068_Ch21_387-416 15/11/14 1:39 PM Page 406 406 UNIT FIVE Understanding the Cardiovascular System TABLE 21.3 DIAGNOSTIC PROCEDURES AND LABORATORY TESTS FOR THE CARDIOVASCULAR SYSTEM—cont’d Significance of Abnormal Findings Procedure Definition Nursing Management Immobilize extremity for several hours as ordered. Hemodynamic monitoring Diagnoses and guides treatment with continuous readings compared to normal for: Right atrial pressure: 2–6 mm Hg Pulmonary artery systolic/diastolic: 20–30/0–10 Pulmonary artery wedge pressure: 4– 12 mm Hg Cardiac output: 4– 8 L/min SvO2: 60%–80% Blood pressure, cardiac and pulmonary pressure abnormalities. Informed consent signed. Continuous mo