1. C. The left anterior descending artery is the primary source of blood for the anterior wall of the heart. The circumflex artery supplies the lateral wall, the internal mammary artery supplies the mammary, and the right coronary artery supplies the inferior wall of the heart.
2. B. Although the coronary arteries may receive a minute portion of blood during systole, most of the blood flow to coronary arteries is supplied during diastole. Breathing patterns are irrelevant to blood flow
3. B. Coronary artery disease accounts for over 50% of all deaths in the US. Cancer accounts for approximately 20%. Liver failure and renal failure account for less than 10% of all deaths in the US.
4. A. Atherosclerosis, or plaque formation, is the leading cause of CAD. DM is a risk factor for CAD but isn’t the most common cause. Renal failure doesn’t cause CAD, but the two conditions are related. Myocardial infarction is commonly a result of CAD.
5. B. Arteries, not veins, supply the coronary arteries with oxygen and other nutrients. Atherosclerosis is a direct result of plaque formation in the artery. Hardened vessels can’t dilate properly and, therefore, constrict blood flow.
6. C. Because “heredity” refers to our genetic makeup, it can’t be changed. Cigarette smoking cessation is a lifestyle change that involves behavior modification. Diabetes mellitus is a risk factor that can be controlled with diet, exercise, and medication. Altering one’s diet, exercise, and medication can correct hypertension.
7. D. Cholesterol levels above 200 mg/dl are considered excessive. They require dietary restriction and perhaps medication. Exercise also helps reduce cholesterol levels. The other levels listed are all below the nationally accepted levels for cholesterol and carry a lesser risk for CAD.
8. B. Enhancing myocardial oxygenation is always the first priority when a client exhibits signs and symptoms of cardiac compromise. Without adequate oxygen, the myocardium suffers damage. Sublingual nitorglycerin is administered to treat acute angina, but its administration isn’t the first priority. Although educating the client and decreasing anxiety are important in care delivery, nether are priorities when a client is compromised.
9. C. Oral medication administration is a noninvasive, medical treatment for coronary artery disease. Cardiac catheterization isn’t a treatment but a diagnostic tool. Coronary artery bypass surgery and percutaneous transluminal coronary angioplasty are invasive, surgical treatments.
10. C. The right coronary artery supplies the right ventricle, or the inferior portion of the heart. Therefore, prolonged occlusion could produce an infarction in that area. The right coronary artery doesn’t supply the anterior portion (left ventricle), lateral portion (some of the left ventricle and the left atrium), or the apical portion (left ventricle) of the heart.
11. A. The most common symptom of an MI is chest pain, resulting from deprivation of oxygen to the heart. Dyspnea is the second most common symptom, related to an increase in the metabolic needs of the body during an MI. Edema is a later sign of heart failure, often seen after an MI. Palpitations may result from reduced cardiac output, producing arrhythmias.
12. B. The correct landmark for obtaining an apical pulse is the left intercostal space in the midclavicular line. This is the point of maximum impulse and the location of the left ventricular apex. The left second intercostal space in the midclavicular line is where the pulmonic sounds are auscultated. Normally, heart sounds aren’t heard in the midaxillary line or the seventh intercostal space in the midclavicular line.
13. D. Pulmonary pain is generally described by these symptoms. Musculoskeletal pain only increase with movement. Cardiac and GI pains don’t change with respiration.
14. C. Abnormalities of the pulmonic valve are auscultated at the second left intercostal space along the left sternal border. Aortic valve abnormalities are heard at the second intercostal space, to the right of the sternum. Mitral valve abnormalities are heard at the fifth intercostal space in the midclavicular line. Tricuspid valve abnormalities are heard at the third and fourth intercostal spaces along the sternal border.
15. C. Troponin I levels rise rapidly and are detectable within 1 hour of myocardial injury. Troponin I levels aren’t detectable in people without cardiac injury. Lactate dehydrogenase is present in almost all body tissues and not specific to heart muscle. LDH isoenzymes are useful in diagnosing cardiac injury. CBC is obtained to review blood counts, and a complete chemistry is obtained to review electrolytes. Because CK levles may rise with skeletal muscle injury, CK isoenzymes are required to detect cardiac injury.
16. D. Morphine is administered because it decreases myocardial oxygen demand. Morphine will also decrease pain and anxiety while causing sedation, but isn’t primarily given for those reasons.
17. C. Coronary artery thrombosis causes occlusion of the artery, leading to myocardial death. An aneurysm is an outpouching of a vessel and doesn’t cause an MI. Renal failure can be associated with MI but isn’t a direct cause. Heart failure is usually the result of an MI.
18. C. Supplemental potassium is given with furosemide because of the potassium loss that occurs as a result of this diuretic. Chloride and sodium aren’t loss during diuresis. Digoxin acts to increase contractility but isn’t given routinely with furosemide.
19. D. Both glucose and fatty acids are metabolites whose levels increase after a myocardial infarction. Mechanical changes are those that affect the pumping action of the heart, and electro physiologic changes affect conduction. Hematologic changes would affect the blood. 20. A. Rapid filling of the ventricles causes vasodilation that is auscultated as S3. Increased atrial contraction or systemic hypertension can result is a fourth heart sound. Aortic valve malfunction is heard as a murmur.
21. A. The left ventricle is responsible for the most of the cardiac output. An anterior wall MI may result in a decrease in left ventricular function. When the left ventricle doesn’t function properly, resulting in left-sided heart failure, fluid accumulates in the interstitial and alveolar spaces in the lungs and causes crackles. Pulmonic and tricuspid valve malfunction causes right-sided heart failure.
22. D. The ECG is the quickest, most accurate, and most widely used tool to determine the location of myocardial infarction. Cardiac enzymes are used to diagnose MI but can’t determine the location. An echocardiogram is used most widely to view myocardial wall function after an MI has been diagnosed. Cardiac catheterization is an invasive study for determining coronary artery disease and may also indicate the location of myocardial damage, but the study may not be performed immediately.
23. B. Administering supplemental oxygen to the client is the first priority of care. The myocardium is deprived of oxygen during an infarction, so additional oxygen is administered to assist in oxygenation and prevent further damage. Morphine and sublingual nitroglycerin are also used to treat MI, but they’re more commonly administered after the oxygen. An ECG is the most common diagnostic tool used to evaluate MI.
24. A. Validation of the client’s feelings is the most appropriate response. It gives the client a feeling of comfort and safety. The other three responses give the client false hope. No one can determine if a client experiencing MI will feel or get better and therefore, these responses are inappropriate.
25. A. Beta-adrenergic blockers work by blocking beta receptors in the myocardium, reducing the response to catecholamines and sympathetic nerve stimulation. They protect the myocardium, helping to reduce the risk of another infarction by decreasing the workload of the heart and decreasing myocardial oxygen demand. Calcium channel blockers reduce the workload of the heart by decreasing the heart rate. Narcotics reduce myocardial oxygen demand, promote vasodilation, and decreased anxiety. Nitrates reduce myocardial oxygen consumption by decreasing left ventricular end-diastolic pressure (preload) and systemic vascular resistance (afterload).
26. C. Arrhythmias, caused by oxygen deprivation to the myocardium, are the most common complication of an MI. cardiogenic shock, another complication of MI, is defined as the end stage of left ventricular dysfunction. The condition occurs in approximately 15% of clients with MI. Because the pumping function of the heart is compromised by an MI, heart failure is the second most common complication. Pericarditis most commonly results from a bacterial of viral infection but may occur after MI. 27. B. Elevated venous pressure, exhibited as jugular vein distention, indicates a failure of the heart to pump. Jugular vein distention isn’t a symptom of abdominal aortic aneurysm or pneumothorax. An MI, if severe enough, can progress to heart failure; however, in and of itself, an MI doesn’t cause jugular vein distention.
28. C. Jugular venous pressure is measured with a centimeter ruler to obtain the vertical distance between the sternal angle and the point of highest pulsation with the head of the bed inclined between 15 and 30 degrees. Inclined pressure can’t be seen when the client is supine or when the head of the bed is raised 10 degrees because the point that marks the pressure level is above the jaw (therefore, not visible). In high Fowler’s position, the veins would be barely discernible above the clavicle.
29. A. An apical pulse is essential or accurately assessing the client’s heart rate before administering digoxin. The apical pulse is the most accurate point in the body. Blood pressure is usually only affected if the heart rate is too low, in which case the nurse would withhold digoxin. The radial pulse can be affected by cardiac and vascular disease and therefore, won’t always accurately depict the heart rate. Digoxin has no effect on respiratory function.
30. A. One of the most common signs of digoxin toxicity is the visual disturbance known as the green halo sign. The other medications aren’t associated with such an effect.
31. A. Crackles in the lungs are a classic sign of left-sided heart failure. These sounds are caused by fluid backing up into the pulmonary system. Arrhythmias can be associated with both right and left-sided heart failure. Left-sided heart failure causes hypertension secondary to an increased workload on the system.
32. D. The most accurate area on the body to assed dependent edema in a bedridden client is the sacral area. Sacral, or dependent, edema is secondary to right-sided heart failure. Diabetes mellitus, pulmonary emboli, and renal disease aren’t directly linked to sacral edema.
33. C. Inadequate deactivation of aldosterone by the liver after right-sided heart failure leads to fluid retention, which causes oliguria. Adequate urine output, polyuria, and polydipsia aren’t associated with right-sided heart failure.
34. D. Inotropic agents are administered to increase the force of the heart’s contractions, thereby increasing ventricular contractility and ultimately increasing cardiac output. Beta-adrenergic blockers and calcium channel blockers decrease the heart rate and ultimately decrease the workload of the heart. Diuretics are administered to decrease the overall vascular volume, also decreasing the workload of the heart.
35. B. Stimulation of the sympathetic nervous system causes tachycardia and increased contractility. The other symptoms listed are related to the parasympathetic nervous system, which is responsible for slowing the heart rate.
36. D. Weight gain, nausea, and a decrease in urine output are secondary effects of right-sided heart failure. Cardiomyopathy is usually identified as a symptom of left-sided heart failure. Left-sided heart failure causes primarily pulmonary symptoms rather than systemic ones. Angina pectoris doesn’t cause weight gain, nausea, or a decrease in urine output.
37. A. Atherosclerosis accounts for 75% of all abdominal aortic aneurysms. Plaques build up on the wall of the vessel and weaken it, causing an aneurysm. Although the other conditions are related to the development of an aneurysm, none is a direct cause. 38. B. The portion of the aorta distal to the renal arteries is more prone to an aneurysm because the vessel isn’t surrounded by stable structures, unlike the proximal portion of the aorta. Distal to the iliac arteries, the vessel is again surrounded by stable vasculature, making this an uncommon site for an aneurysm. There is no area adjacent to the aortic arch, which bends into the thoracic (descending) aorta.
39. A. The presence of a pulsating mass in the abdomen is an abnormal finding, usually indicating an outpouching in a weakened vessel, as in abdominal aortic aneurysm. The finding, however, can be normal on a thin person. Neither an enlarged spleen, gastritis, nor gastic distention cause pulsation.
40. A. Abdominal pain in a client with an abdominal aortic aneurysm results from the disruption of normal circulation in the abdominal region. Lower back pain, not upper, is a common symptom, usually signifying expansion and impending rupture of the aneurysm. Headache and diaphoresis aren’t associated with abdominal aortic aneurysm.
41. D. Lower back pain results from expansion of the aneurysm. The expansion applies pressure in the abdominal cavity, and the pain is referred to the lower back. Abdominal pain is most common symptom resulting from impaired circulation. Absent pedal pulses are a sign of no circulation and would occur after a ruptured aneurysm or in peripheral vascular disease. Angina is associated with atherosclerosis of the coronary arteries.
42. B. An arteriogram accurately and directly depicts the vasculature; therefore, it clearly delineates the vessels and any abnormalities. An abdominal aneurysm would only be visible on an X-ray if it were calcified. CT scan and ultrasound don’t give a direct view of the vessels and don’t yield as accurate a diagnosis as the arteriogram.
43. B. Rupture of the aneurysm is a life-threatening emergency and is of the greatest concern for the nurse caring for this type of client. Hypertension should be avoided and controlled because it can cause the weakened vessel to rupture. Diminished pedal pulses, a sign of poor circulation to the lower extremities, are associated with an aneurysm but isn’t life threatening. Cardiac arrhythmias aren’t directly linked to an aneurysm.
44. C. The factor common to all types of aneurysms is a damaged media. The media has more smooth muscle and less elastic fibers, so it’s more capable of vasoconstriction and vasodilation. The interna and externa are generally no damaged in an aneurysm.
45. C. The aorta lies directly left of the umbilicus; therefore, any other region is inappropriate for palpation.
46. B. Continuous pressure on the vessel walls from hypertension causes the walls to weaken and an aneurysm to occur. Atherosclerotic changes can occur with peripheral vascular diseases and are linked to aneurysms, but the link isn’t as strong as it is with hypertension. Only 1% of clients with syphilis experience an aneurysm. Diabetes mellitus doesn’t have direct link to aneurysm.
47. A. A bruit, a vascular sound resembling heart murmur, suggests partial arterial occlusion. Crackles are indicative of fluid in the lungs. Dullness is heard over solid organs, such as the liver. Friction rubs indicate inflammation of the peritoneal surface.
48. B. Severe lower back pain indicates an aneurysm rupture, secondary to pressure being applied within the abdominal cavity. When rupture occurs, the pain is constant because it can’t be alleviated until the aneurysm is repaired. Blood pressure decreases due to the loss of blood. After the aneurysm ruptures, the vasculature is interrupted and blood volume is lost, so blood pressure wouldn’t increase. For the same reason, the RBC count is decreased – not increase. The WBC count increases as cells migrate to the site of injury.
49. C. Blood collects in the retroperitoneal space and is exhibited as a hematoma in the perineal area. This rupture is most commonly caused by leakage at the repair site. A hernia doesn’t cause vascular disturbances, nor does a pressure ulcer. Because no bleeding occurs with rapid expansion of the aneurysm, a hematoma won’t form.
50. C. Marfan’s syndrome results in the degeneration of the elastic fibers of the aortic media. Therefore, clients with the syndrome are more likely to develop an aortic aneurysm. Although cystic fibrosis is hereditary, it hasn’t been linked to aneurysms. Lupus erythematosus isn’t hereditary. Myocardial infarction is neither hereditary nor a disease.
51. D. When the vessel ruptures, surgery is the only intervention that can repair it. Administration of antihypertensive medications and beta-adrenergic blockers can help control hypertension, reducing the risk of rupture. An aortogram is a diagnostic tool used to detect an aneurysm.
52. A. Cardiomyopathy isn’t usually related to an underlying heart disease such as atherosclerosis. The etiology in most cases is unknown. Coronary artery disease and myocardial infarction are directly related to atherosclerosis. Pericardial effusion is the escape of fluid into the pericardial sac, a condition associated with pericarditis and advanced heart failure.
53. A. Although the cause isn’t entirely known, cardiac dilation and heart failure may develop during the last month of pregnancy of the first few months after birth. The condition may result from a preexisting cardiomyopathy not apparent prior to pregnancy. Hypertrophic cardiomyopathy is an abnormal symmetry of the ventricles that has an unknown etiology but a strong familial tendency. Myocarditis isn’t specifically associated with childbirth. Restrictive cardiomyopathy indicates constrictive pericarditis; the underlying cause is usually myocardial.
54. C. In hypertrophic cardiomyopathy, hypertrophy of the ventricular septum – not the ventricle chambers – is apparent. This abnormality isn’t seen in other types of cardiomyopathy.
55. A. Because the structure and function of the heart muscle is affected, heart failure most commonly occurs in clients with cardiomyopathy. Myocardial infarction results from prolonged myocardial ischemia due to reduced blood flow through one of the coronary arteries. Pericardial effusion is most predominant in clients with percarditis. Diabetes mellitus is unrelated to cardiomyopathy.
56. A. Cardiomegaly denotes an enlarged heart muscle. Cardiomyopathy is a heart muscle disease of unknown origin. Myocarditis refers to inflammation of heart muscle. Pericarditis is an inflammation of the pericardium, the sac surrounding the heart.
57. D. These are the classic symptoms of heart failure. Pericarditis is exhibited by a feeling of fullness in the chest and auscultation of a pericardial friction rub. Hypertension is usually exhibited by headaches, visual disturbances and a flushed face. Myocardial infarction causes heart failure but isn’t related to these symptoms. 58. B. Cardiac output isn’t affected by hypertrophic cardiomyopathy because the size of the ventricle remains relatively unchanged. Dilated cardiomyopathy, and restrictive cardomyopathy all decrease cardiac output. 59. D. An S4 occurs as a result of increased resistance to ventricular filling adterl atrial contraction. This increased resistance is related to decrease compliance of the ventricle. A dilated aorta doesn’t cause an extra heart sound, though it does cause a murmur. Decreased myocardial contractility is heard as a third heart sound. An s4 isn’t heard in a normally functioning heart.
60. B. By decreasing the heart rate and contractility, beta-adrenergic blockers improve myocardial filling and cardiac output, which are primary goals in the treatment of cardiomyopathy. Antihypertensives aren’t usually indicated because they would decrease cardiac output in clients who are often already hypotensive. Calcium channel blockers are sometimes used for the same reasons as beta-adrenergic blockers; however, they aren’t as effective as beta-adrenergic blockers and cause increase hypotension. Nitrates aren’t’ used because of their dilating effects, which would further compromise the myocardium.