Internal Medicine EOR: Cardiology Practice Exam
A 46-year-old man comes to the office because of a four-month history of intermittent episodes of chest discomfort and tightness. His symptoms typically occur only on exertion, such as when gardening or playing with his children, and are relieved by rest. He says the episodes last less than 20 minutes. He has otherwise been healthy and his personal medical history is noncontributory. His father has coronary artery disease but is alive and well. Physical exam, laboratory studies and ECG are normal. The medication most appropriate for treating his acute episodes acts by which of the following mechanisms?
Blocking calcium channels
Controlling coronary artery vasospasm
Decreasing heart rate
Question 1 Explanation:
Stable angina pectoris results when myocardial oxygen demand exceeds oxygen supply. Nitrates, the first-line therapy for acute episodes and they act principally through smooth muscle relaxation and venodilation which causes blood pooling in the peripheral vasculature with a concomitant reduction in preload. Decreased preload decreases cardiac contractility and oxygen demand. View topic
A 65-year-old patient comes to the office because of increased shortness of breath for 3 months. His symptoms are particularly bad at night. Medical history includes long-standing hypertension and alcoholism. Examination shows a displaced apex beat and normal breath sounds. Cardiac auscultation shows an S3 gallop and a pan-systolic murmur radiating to the axilla. The chest X-ray is shown here. Which of the following is the most likely diagnosis?
Deep venous thrombosis
Question 2 Explanation:
The correct answer is dilated cardiomyopathy. Left ventricular dilation (as seen in the radiograph) and systolic dysfunction (shortness of breath, murmur) must be present for diagnosis. Most causes are idiopathic. The two most common causes of secondary dilated cardiomyopathy are ischemia and long-standing hypertension. An S3 gallop signifies the end of rapid ventricular filling in the setting of fluid overload and is often associated with dilated cardiomyopathy. View topic
A 65-year-old man comes to the emergency department because of a sudden onset of chest pain and dizziness. He has a history of uncontrolled hypertension, hyperlipidemia, alcohol abuse, and a family history of coronary artery disease. He currently takes enalapril, simvastatin, and low-dose aspirin. His temperature is 35.3°C (95.5°F), the pulse is 110/min, respirations are 30/min, blood pressure is 80/60 mm Hg, and pulse oximetry on room air shows an oxygen saturation of 90%. He looks pale and diaphoretic and when his head is positioned at 45°, the filling level of the external jugular vein is 9 cm vertical height above the sternal angle. His heart sounds are clear and he has no extra cardiac sounds on examination, nor rales on pulmonary examination. There is no change in blood pressure on inspiration. An electrocardiogram reveals ST-elevation in the right precordial leads. This clinical presentation is most consistent with which of the following conditions?
Anterior cardiac wall rupture
Anterior cardiac wall rupture commonly occurs 3-7 days after a myocardial infarction and can cause cardiac tamponade. It's most commonly associated with thrombosis of the left anterior descending artery. This patient has ECG findings consistent with a right ventricular infarction which is supplied by the right coronary artery.
Cardiac tamponade is a condition where there is a fluid buildup in the pericardial sac which results in compression of the heart. Signs of classical cardiac tamponade is known as Beck's triad. Low blood pressure occurs because of decreased stroke volume, jugular-venous distension due to impaired venous return to the heart, and muffled heart sounds due to fluid buildup inside the pericardium. Other signs of tamponade include pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration), and diffuse ST segment changes on the electrocardiogram which may also show low voltage QRS complexes. Although this patient has low blood pressure and elevated jugular-venous distension, his heart sounds are clear and the ECG findings are not indicative of classic cardiac tamponade.
Pulmonary edema is caused by increased hydrostatic pressure in the left ventricle that is transmitted back into the pulmonary capillaries, leading to accumulation of water in the pulmonary interstitial space and the alveoli. Patients with pulmonary edema typically present with shortness of breath, rust-colored sputum, and bi-basilar inspiratory crackles.
Right-sided heart failure
Diastolic heart failure
Diastolic heart failure is characterized by elevated left ventricular pressure, despite a normal end diastolic volume (EDV). Patients with diastolic heart failure typically present with a normal ejection fraction and an S4 atrial gallop due to increased stiffness of the ventricle during filling in late diastole.
Question 3 Explanation:
This patient has a right ventricular myocardial infarction leading to right-sided heart failure, which explains the increase in the jugular venous pressure. The external jugular vein pulsation should normally be <3 cm vertical height above the sternal angle.
A 75-year-old woman comes to the office because of a 3-month history of chest pain and shortness of breath on exertion. Physical examination shows bilateral pitting edema of the lower extremities. Diffuse crackles are heard over the lower lung fields on auscultation. Cardiac examination shows jugular venous distention and an S3 gallop. Serum studies show undetectable troponin levels. Chest X-ray shows cardiomegaly and pulmonary edema. Which of the following medications would be effective in lowering her mortality risk?
Digoxin, an inotropic agent that increases myocardial contractility by inhibiting the Na+/K+-ATPase pump, can be useful in treating the symptoms of heart failure but has not been proven to reduce mortality.
Furosemide, a loop diuretic that inhibits the Na+-K+-2Cl- cotransporter in the thick ascending limb of the loop of Henle, can provide symptomatic relief and reduce volume overload in patients with acute decompensation of heart failure. However, loop diuretics have not been shown to reduce mortality.
β-blockers can improve symptoms and reduce mortality by modulating neurohormonal pathways. However, only bisoprolol, carvedilol, and metoprolol succinate have been shown to reduce morbidity and mortality in clinical trials.
Nondihydropyridine calcium channel blockers like verapamil may be harmful in patients with low left ventricular ejection fraction due to their negative inotropic effects and should be avoided.
Question 4 Explanation:
Heart failure with reduced ejection fraction is typically characterized by dyspnea, orthopnea, and peripheral edema. Medications that have been demonstrated to reduce mortality are angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), β-blockers, spironolactone, and hydralazine (in African American patients).
A 48-year-old man comes to the emergency department because of severe substernal chest pain radiating to his left arm that began 1.5 hours prior to arrival. The pain is accompanied by diaphoresis and shortness of breath. His blood pressure is 165/94 mm Hg, pulse is 82/min, and respiratory rate is 18/min. An acute myocardial infarction is suspected. Which of the following tests is the most important tool in the initial evaluation of this patient?
Aspartate aminotransferase is a nonspeciﬁc protein that is found in cardiac, liver, and skeletal muscle cells. Levels peak around 2 days post-myocardial infarction and are negative at 3 days post-myocardial infarction.
Creatine kinase-myocardial bound
Serial measurements of creatine kinase-myocardial bound fraction along with troponin-I are made in every patient with suspected myocardial infarction. However, these enzymes take 4–6 hours to accumulate in the blood. Creatine kinase-myocardial bound levels peak around 24 hours and are negative at 3 days post-myocardial infarction.
Echocardiography would not be the most cost and time efﬁcient means of diagnosis. Echocardiograms can deﬁne the extent of infarction and assess the overall left ventricle and right ventricle function. Echocardiograms can identify complications of myocardial infarction such as acute mitral regurgitation, left ventricular rupture, or pericardial effusion.
Lactate dehydrogenase was once the test of the choice for diagnosing myocardial infarction. Lactate dehydrogenase levels are elevated 2–7 days post-myocardial infarction and peak around 3 days post-myocardial infarction.
Question 5 Explanation:
Electrocardiogram is the gold standard for diagnosing myocardial infarction within the ﬁrst 6 hours of symptom onset. Electrocardiogram changes will include ST-segment elevation (signifying transmural infarct), ST-segment depression (signifying subendocardial infarct), and Q waves (signifying transmural infarct).
A 71-year-old woman comes to the emergency department because of severe central chest pain for 30 minutes this morning. She says the pain was cramping in nature and radiated down her left arm. She has a history of atrial fibrillation and type 2 diabetes mellitus. Her temperature is 36.8°C (98°F), pulse is 97/min, respirations are 18/min, and blood pressure is 163/91 mm Hg. Cardiovascular examination shows no abnormalities. ECG is obtained and is shown below. Which of the following biochemical measures would most likely be elevated and remain elevated for a week after this acute event?
Alanine aminotransferase (ALT) is found predominantly in the liver, with clinically negligible quantities found in the kidneys, heart, and skeletal muscle. It is a specific marker of liver damage, but is not elevated in myocardial infarction.
Aspartate transaminase (AST) is found in the liver, heart (cardiac muscle), skeletal muscle, kidneys, brain, and red blood cells. It was the first used cardiac biomarker, but is not specific for heart damage, and it is also one of the liver function tests.
The creatinine kinase-MB (CK-MB) isoform of creatine kinase is expressed in heart muscle. It cannot be used for late diagnosis of acute myocardial infarction but can be used to suggest infarct extension if levels rise again. Levels peak between 10-24 hours and are usually back to normal within 2–3 days.
Lactate dehydrogenase (LDH)
Lactate dehydrogenase catalyzes the conversion of pyruvate to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found predominantly in blood serum. A high ratio of LDH-1 concentration to LDH-2 concentration suggests myocardial infarction. LDH concentrations are also high in tissue breakdown or hemolysis. Concentrations peak at 72 hours post myocardial infarction.
Question 6 Explanation:
Troponin I is an enzyme that's useful in evaluating a myocardial infarction (MI). Troponin I levels begin to rise within 2-3 hours post-MI, peak at about 2 days, and continue to stay elevated for about 7 days.
A 55-year-old woman is admitted to the hospital because she has shortness of breath and pain on both sides of her chest with deep breathing which has worsened over the past 5 days. In recent weeks, she has been feeling fatigued and has had low grade fevers and night sweats, and was found to have a new cardiac murmur on examination. Her temperature is 38.1°C (100.6°F), pulse is 106/min, respirations are 26/min, and blood pressure is 136/88 mm Hg. She appears diaphoretic and is in mild respiratory distress. Cardiac auscultation reveals a faint systolic murmur heard over the lower left sternal border. Her neck veins are distended and abdominal examination shows hepatomegaly. Which of the following is the most likely cause of her clinical presentation?
Fat embolism to the pulmonary circulation almost always occurs with major trauma, including surgical procedures like intramedullary nailing of long bones. Fat emboli can occlude the microvasculature, triggering a systemic inflammatory response. The woman did not have recent trauma, and a fat embolism would not explain her cardiac murmur.
Clinical presentation of myocardial infarction most often includes substernal crushing chest pain, radiation of pain to the arms, left shoulder, back, neck, and jaw, as well as shortness of breath, anxiety, and fatigue. A myocardial infarction would not explain her developing a new cardiac murmur in recent weeks.
Rheumatic fever is an autoimmune inflammatory process that develops as a sequela of streptococcal infection. Clinical manifestations include polyarthritis, carditis, erythema marginatum, chorea, and subcutaneous nodules. Rheumatic fever can cause some of the symptoms seen in this case, but the acute onset makes this option less likely.
Small cell lung cancer
Although small cell lung cancer can present with pulmonary symptoms and low grade fevers, it wouldn't easily explain her new cardiac murmur or the signs of right-sided heart failure.
Question 7 Explanation:
Infective endocarditis (IE) is an infection of the endocardial surfaces of the heart, most commonly the heart valves. IE occurs when a microorganism begins to invade the heart valves causing an inflammatory reaction that damages the valve - sometimes leading to stenosis and sometimes leading to regurgitation. This patient developed a new cardiac murmur in recent weeks that is described as a faint systolic murmur heard over the lower left sternal border. This is most consistent with tricuspid regurgitation. She also has distended neck veins and hepatomegaly, both of which suggest right-sided heart failure which can result from tricuspid regurgitation. Small infectious emboli can break away from the primary lesion on the tricuspid valve and go into the pulmonary vasculature causing shortness of breath and pleuritic chest pain. Most cases of IE are caused by Staphylococcus aureus and Viridans streptococci, and diagnosis is confirmed by obtaining multiple blood cultures that show that there is continuous bacteremia.
A 54-year-old man comes to the emergency department following a four-day history of left-sided chest pain and shortness of breath. One week ago, he experienced upper respiratory symptoms along with myalgias and general fatigue. He has no known past medical history. He has not traveled outside the US. His temperature is 38.1°C (100.6°F), pulse is 104/min, respirations are 17/min, oxygen saturation is 94% on room air, and blood pressure is 100/72 mm Hg. Physical examination shows an ill-appearing man with bibasilar rales, jugular venous distention of 11 cm with no murmurs, rubs, or gallops, and 1+ bilateral pitting edema of the lower extremities. His labs are within normal limits and his blood cultures are negative. An echocardiogram shows an ejection fraction of 35%. Which of the following is the most likely cause of this patient's condition?
Chagas disease, caused by Trypanosoma cruzi, is one of the most common causes of myocarditis worldwide. However, this patient has no history of travel outside the United States.
Coxsackie A virus
Though coxsackie B virus is one of the most common causal pathogens of acute myocarditis, Coxsackie A causes herpangina, aseptic meningitis, and hand, foot, and mouth disease.
Staphylococcus aureus is a common cause of bacterial endocarditis, not myocarditis. Endocarditis is more likely to present with a new murmur and signs of distant emboli such as nail-bed hemorrhage and Janeway lesions.
Corynebacterium diphtheriae is the causal agent of diphtheria, which may involve myocarditis. However, the patient would then most likely have other symptoms of the disease, including pseudomembranous pharyngitis, lymphadenopathy, or an arrhythmia.
Question 8 Explanation:
Myocarditis in the United States is most commonly caused by a viral infection, typically adenovirus, coxsackie B, parvovirus B19, or others. It often presents with systemic symptoms such as fatigue and chest pain, but may cause sudden death.
A 42-year-old woman comes to the emergency department because of chest pain, dyspnea, and lightheadedness. She recently recovered from a presumed viral upper respiratory infection and has a 10-year history of systemic lupus erythematosus. Physical examination shows a decrease in systolic blood pressure by 20 mm Hg during inspiration. An ECG is shown here. Which of the following is the most likely diagnosis?
Patients with aortic dissection classically present with a tearing or ripping pain in the chest or back and may have a significant variation in systolic blood pressure between arms (not across respirations).
The severity of tricuspid regurgitation varies widely, ranging from asymptomatic disease to symptoms of right-sided heart failure (hepatosplenomegaly, ascites, peripheral edema).
Patients with aortic stenosis, the most common cause of left ventricular outflow obstruction, typically present with exertional dizziness or angina. In end-stage disease, symptoms may progress to heart failure.
Mitral stenosis obstructs the flow of blood from the left atrium to the left ventricle and typically manifests as exertional dyspnea and decreased exercise tolerance.
Question 9 Explanation:
Pericardial effusions are associated with a variety of causes, including autoimmune disorders and infectious pericarditis. If pericardial effusion leads to cardiac tamponade, patients may have pulsus paradoxus, or a decrease in systolic blood pressure during inspiration of more than 10 mm Hg. Certain ECG findings are characteristic for pericardial effusion. In particular, electrical alternans (shown by arrows) is highly specific for pericardial effusion (usually in association with cardiac tamponade) but not particularly sensitive. This pattern, characterized by beat-to-beat changes in the QRS axis in the limb and precordial leads, is caused by swinging of the heart within the accumulated pericardial fluid. Other common findings on ECG include sinus tachycardia and low QRS voltage.
A 57-year-old man comes to the emergency department because of intermittent, severe leg pain in both his calves for 2 weeks. He has a history of untreated high blood pressure, diabetes, and high cholesterol. For the past 3 years, the pain started after walking three blocks and only going away upon resting. In the past 2 weeks, he has had the same pain at rest. His temperature is 36.5°C (97.7°F), pulse is 78/min, respirations are 17/min, and blood pressure is 160/89 mm Hg. Examination shows both calves are atrophied and there is a paucity of hair, but no swelling or discoloration. Additionally, his lower calves are cool to the touch and dusky in appearance. Doppler ultrasound shows perfusion to both feet, and with its assistance blood pressures of 35/20 mm Hg in the posterior tibial artery are obtained bilaterally. Which of the following is most appropriate next step in management?
Immediate high-dose statin therapy
Statin therapy has shown to be effective in treating intermittent claudication. However, this intervention is appropriate only when the patient is deemed to be stable, and the risk of limb ischemia has been addressed.
Immediately consult vascular surgery
Alteplase (tPa) has been used to treat intermittent claudication, but its use is outside the scope of the emergency physician. Treatments initiated in the emergency department are unfractionated heparin, aspirin, pain control, and positioning of the leg to maintain perfusion.
Pain control and discharge; refer to vascular surgery as an outpatient
The patient has significant impairment of perfusion to his legs. Discharge and vascular surgery follow-up as an outpatient would be inappropriate and likely to result in morbidity or mortality.
Rest, elevate, and compress the affected leg
While this leg should be rested, compression and elevation are the opposite of what is needed. These therapies will further decrease the blood flow to the leg and put the patient at increased risk of complications.
Question 10 Explanation:
Peripheral vascular disease with intermittent claudication and signs of decreased perfusion should be examined using Doppler ultrasound and the ankle-brachial index (ABI). An ABI of <0.41 is grounds for the immediate surgical consultation.
A 6-year-old boy comes to the pediatric clinic because of 4 weeks of fatigue and shortness of breath. His medical history is notable for poor follow-up with yearly check-ups, but his mother notes that he has been fairly healthy for the duration of his life, except for a "bad sore throat that needed antibiotics" about 6 months ago. On examination, the boy appears fatigued, but is appropriately oriented and responsive, and is generally non-toxic appearing. He is afebrile. Cardiac examination is notable for a widely split S2, a quiet S1, and point of maximum impulse displaced to the left. Which of the following is the next best step in the management of this patient?
Digoxin is a purified cardiac glycoside that is typically used in the treatment of various heart conditions, such as atrial fibrillation, atrial flutter, and heart failure that cannot be controlled by other medication. It is not recommended for use in rheumatic fever.
Short-term course of clindamycin
Clindamycin is an antibiotic used to treat middle ear infections, bone or joint infections, pelvic inflammatory disease, strep throat, pneumonia, and endocarditis. Clindamycin is typically used as endocarditis prophylaxis for patients that are already receiving penicillin for secondary rheumatic fever prophylaxis.
Reassurance & routine care
This patient is suffering from rheumatic fever, which can lead to rheumatic heart disease. This can cause significant carditis which manifests as congestive heart failure.
Ceftriaxone is an antibiotic used to treat numerous bacterial infections, such as pneumonia, ear infections, skin infections, urinary tract infection, and meningitis. It is not used in the treatment of rheumatic fever.
Question 11 Explanation:
Rheumatic heart disease is caused by autoimmune cross-reactivity following a Streptococcal infection. Development of antibody-mediated mitral valve damage is common. Long-term penicillin is suitable for acute treatment and prophylaxis from complications.
A 35-year-old woman, gravida 2, para 1, comes to the office because of her first prenatal visit at 12 weeks' gestation. She has no current concerns, and her first child was born without complications. She has a history of long-standing untreated hypertension. Her temperature is 36.5°C (97.7°F), pulse is 78/min, respirations are 17/min, and blood pressure is 150/89 mm Hg. Which of the following medications would most likely be appropriate as initial treatment?
Atenolol is a β-blocker medication, which decreases blood pressure by decreasing heart rate and stroke volume. It is contraindicated in pregnancy because it has been associated with fetal growth restriction. β-blockers considered safe in pregnancy are metoprolol and labetalol.
Hydrochlorothiazide is a thiazide diuretic which decreases blood pressure via volume depletion. Diuretics do not cause fetal malformations but are generally avoided in pregnancy, as they prevent the physiologic volume expansion seen in normal pregnancy. They may be used in states of volume-dependent hypertension, such as renal or cardiac disease.
Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor which decreases blood pressure through inhibition of the renin-angiotensin-aldosterone system. ACE inhibitors and the closely related angiotensin-receptor blockers are contraindicated in pregnancy because of the risk of birth defects including renal dysgenesis and oligohydramnios.
Losartan is an angiotensin II receptor blocker (ARB) which decreases blood pressure through inhibition of the renin-angiotensin-aldosterone system. ARBs and the closely related angiotensin converting enzyme (ACE) inhibitors are contraindicated in pregnancy because of the risk of birth defects including renal dysgenesis and oligohydramnios.
Question 12 Explanation:
Chronic hypertension in pregnancy can be treated with some medications and labetalol is recommended as a first-line therapy for treatment of hypertension during pregnancy. Angiotensin-converting enzymes (ACE) inhibitors and angiotensin II receptor blockers (ARBs) should be avoided.
A 42-year-old man comes to the office for a routine check-up. Medical history includes diabetes mellitus and a long history of smoking. Family history includes coronary artery disease. Temperature is 36.5°C (97.7°F), pulse is 78/min, respirations are 17/min, and blood pressure is 160/89 mm Hg. A repeat blood pressure taken 2 days later shows 143/88 mm Hg. Which of the following is most likely the best initial therapy?
Furosemide is a loop diuretic that can be used to treat hypertension but it is not a first line agent. Unlike ACE inhibitors, loop diuretics have no renoprotective qualities and therefore are a worse initial choice in a hypertensive diabetic patient.
Hydrochlorothiazide is a thiazide diuretic and a first-line agent for the treatment of hypertension in non-diabetic patients. It is relatively contraindicated in diabetes because it has the potential adverse effect of hyperglycemia. It may also precipitate attacks of gout by increasing uric acid concentrations.
Metoprolol is a β-blocker that is used for the treatment of hypertension but is not a first line treatment. Also, β-blocker are contraindicated in asthma, as well as in diabetic patients due to its potential to mask signs of low blood sugar.
Nifedipine is a calcium channel blocker that is used in the treatment of hypertension but it is not a first line therapy. It has no renoprotective effects, and commonly causes peripheral edema as an unwanted adverse effect.
Question 13 Explanation:
Hypertension in the setting of diabetes should be treated, with a goal systolic blood pressure of <130 mm Hg. The best first choice of medication is an angiotensin-converting enzyme inhibitor (ACEi).
A 45-year-old obese Caucasian gentleman arrives at your clinic for a routine check-up after having some blood work done during a workplace health screening. He is found to have an LDL cholesterol level of 550 mg/dL. He states that his father and brother had high cholesterol and both died at a young age from a heart attack. He has a follow-up appointment with his cardiologist because of some occasional chest pain and abnormalities seen on his EKG. Additionally, you notice that he has well-demarcated yellow deposits around his eyes. He is started on high dose statin and his LDL at 12 weeks is 350 mg/dL. What is the next best step in this patient's management?
Continue high dose statin, the patient's LDL is at goal
Add niacin 100 mg three times daily
Add ezetimibe (Zetia) 10 mg daily
Add a PCSK9 inhibitor
Refer to a lipid specialist
Question 14 Explanation:
If LDL-C is not at goal after 6-12 weeks the next best step for the treatment of familial hypercholesterolemia is to add ezetimibe 10 mg daily and check again in 6-12 weeks. If at that time the patient’s LDL is still not at goal (ideally < 150) refer to lipid specialist to consider adding a PCSK9 inhibitor.
A 65-year-old man comes to the emergency department because of progressive dyspnea, coughing, and orthopnea. The patient says that over the past 2 months he has been feeling fatigued with ordinary physical activity. His medical history is relevant for dyslipidemia, type II diabetes mellitus, and a posterior myocardial infarction 4 months ago. Auscultatory findings reveal a pansystolic murmur over the mitral area. His temperature is 37.5°C (99.5°F), pulse is 90/min, respirations are 17/min, blood pressure is 120/90 mm Hg, and pulse oximetry on room air shows an oxygen saturation of 95%. This patient most likely has which of the following conditions?
Aortic stenosis is the reduction of the valvular orifice (<2 cm) with left ventricular outflow obstruction. Patients with aortic stenosis present with chest pain, syncopal episodes, and dyspnea. Here, the patient has progressive dyspnea (NYHA II), and a pansystolic murmur (mitral area), which relates to mitral valve regurgitation
Aortic valve regurgitation
Aortic valve regurgitation (AOR) is described as an inefficient closure of the aortic valve leading to a retrograde blood flow into the left ventricle during diastole. Patients will present with a wide pulse pressure (Corrigan hammer pulse) or an Austin-Flint murmur (severe), none of which are present in this case.
Mitral valve regurgitation
Mitral valve stenosis
Mitral valve stenosis (MVS) is the reduction of the mitral valve orifice (<2.5cm). The left atrium becomes dilated and hypertrophied because of increased work of the left atrium. Patients with MVS present with dyspnea, rust-colored sputum, atrial fibrillation, and a diastolic heart murmur (diastolic rumble and opening snap).
Pulmonary stenosis is an uncommon valvular lesion. It is commonly associated with congenital heart disease and carcinoid heart disease. Patients present a systolic ejection murmur in the left second intercostal space.
Question 15 Explanation:
Mitral valve regurgitation is defined as an incompetent closure of the mitral valve. Classically patients will present with a pansystolic heart murmur over the mitral area. Posterior myocardial infarction is the second most common cause of mitral valve regurgitation. Mitral valve regurgitation is characterized by an incompetent closure of the mitral valve. This condition causes retrograde blood flow into the left atrium during systole. The most common cause of mitral regurgitation is mitral valve prolapse, followed by a dysfunction of the posteromedial papillary muscle due to posterior myocardial infarction. Other causes may include, endocarditis or stretching of the mitral valve ring.
A 43-year-old man with a history of rheumatic fever comes to the primary care clinic for a check up. Cardiac examination reveals a late systolic crescendo murmur with midsystolic click best heard over the apex and loudest just before S2. Which of the following maneuvers will cause an earlier onset of the click/murmur? A. Inspiration B. Rapid squatting C. Standing D. Hand grip E. Left lateral cubital position
The click of mitral valve prolapse is heard closer to S2 in the event of increased preload. Preload is increased by hand grip, squatting and inspiration.
The click of mitral valve prolapse is heard closer to S2 in the event of increased preload. Preload is increased by hand grip, squatting and inspiration.
The click of mitral valve prolapse is heard closer to S2 in the event of increased preload. Preload is increased by hand grip, squatting and inspiration.
Left lateral cubital position
Placing the patient in the left lateral cubitus position will not affect preload and will have no effect on the timing of the click in mitral valve prolapse.
Question 16 Explanation:
The ‘click' of mitral valve prolapse, caused by the tightening of the chordae tendinae, moves closer to S2 with increased preload. Increased preload causes the left ventricle to stretch, as a result, the chordae tendinae are stretched as well. This makes it harder for the mitral valve to prolapse until the ventricles shrink enough to allow the chordae tendinae to let the mitral valve prolapse. Since there is more blood in the ventricles, it takes them longer to pump it out and shrink to a point at which MVP can occur, hence it occurs later in systole. Thus, the click will get closer to S2 with increased preload. Hand grip, rapid squatting, and inspiration all increase preload. Standing decreases preload and will cause an earlier onset of the click.
There are 16 questions to complete.