A 62-year-old woman comes to the physician because of a 2-month history of exertional shortness of breath and fatigue. She sometimes wakes up at night coughing and gasping for air. Cardiac examination shows a grade 3/6 holosystolic murmur best heard at the apex. Which of the following physical exam findings would be consistent with an exacerbation of this patient's condition?
Q12
A 50-year-old man comes to the physician for the evaluation of recurrent palpitations and a feeling of pressure in the chest for the past 6 months. He also reports shortness of breath when walking several blocks or while going upstairs. There is no personal or family history of serious illness. He does not smoke. He has a 30-year history of drinking 7–10 beers daily. His temperature is 37°C (98.6°F), pulse is 110/min, respirations are 18/min, and blood pressure 130/80 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 92%. There are jugular venous pulsations 9 cm above the sternal angle. Crackles are heard at both lung bases. Cardiac examination shows an S3 gallop and a displaced point of maximum impulse. There is pitting edema below the knees. Which of the following is the most appropriate step in the management of the underlying cause of this patient's current condition?
Q13
A 59-year-old male presents to the emergency room with shortness of breath. Ten days ago, he was in the cardiac critical care unit after receiving a balloon angioplasty and a bare metal stent for an ST-elevation myocardial infarction (STEMI). On physical examination, a holosystolic murmur is heard at the cardiac apex radiating to the axilla. You also detect an S3 and bilateral crackles in the lung bases. What is the most likely etiology of this patient's acute decompensated heart failure?
Q14
A 64-year-old man presents to the emergency department because he has been experiencing increased shortness of breath for the last 2 weeks. Specifically, he says that he can barely walk up the stairs to his apartment before he feels winded. In addition, he has been waking up at night gasping for breath and has only been able to sleep propped up on 2 more pillows than usual. Physical exam reveals jugular venous distention as well as pitting lower extremity edema. Which of the following abnormal sounds will most likely be heard in this patient?
Q15
A 67-year-old woman presents with progressive shortness of breath, lower extremity swelling, and early satiety. These symptoms started 4 months ago and have been progressively worsening. She has had type 2 diabetes mellitus for 25 years and hypertension for 15 years; for these, she takes metformin and captopril. She had an anterolateral ST-segment elevation myocardial infarction 6 years ago. Her blood pressure is 110/60 mm Hg, the temperature is 36.3°C (97.3°F), and the pulse is 95/min and regular. On examination, she has a laterally displaced apical impulse with a loud 4/6 holosystolic murmur at the apex, which increases in intensity with breath-holding for 3–5 seconds. Jugular veins are distended to the angle of the jaw. Some basilar crackles are present on both sides. There is a history of increased abdominal girth, and the patient presents with shifting dullness on percussion. There is 2–3+ pitting edema in both lower extremities. Echocardiography shows a left ventricular ejection fraction of 40% and moderate mitral and tricuspid regurgitation. Which of the following is the mechanism that applies to this patient’s illness?
Q16
A 53-year-old woman visits her physician with complaints of shortness of breath and fatigue over the last few weeks. Her past medical history includes hypertension diagnosed 20 years ago. She takes hydrochlorothiazide and losartan daily. Her mother died at the age of 54 from a stroke, and both of her grandparents suffered from cardiovascular disease. She has a 13 pack-year history of smoking and drinks alcohol occasionally. Her blood pressure is 150/120 mm Hg, pulse is 95/min, respiratory rate is 22/min, and temperature is 36.7°C (98.1°F). On physical examination, she has bibasilar rales, distended jugular veins, and pitting edema in both lower extremities. Her pulse is irregularly irregular and her apical pulse is displaced laterally. Fundoscopy reveals ‘copper wiring’ and ‘cotton wool spots’. Which of the following echocardiographic findings will most likely be found in this patient?
Q17
A 63-year-old man presents to the emergency room because of worsening breathlessness that began overnight. He was diagnosed with asthma 3 years ago and has been using albuterol and steroid inhalers. He does not have a prior history of cardiac disease or other respiratory diseases. The man is a retired insurance agent and has lived his entire life in the United States. His vital signs include: respiratory rate 40/min, blood pressure 130/90 mm Hg, pulse rate 110/min, and temperature 37.0°C (98.6°F). Physical examination shows severe respiratory distress, with the patient unable to lie down on the examination table. Auscultation of the chest reveals widespread wheezes in the lungs and the presence of S3 gallop rhythm. The man is admitted to hospital and laboratory investigations and imaging studies are ordered. Test results include the following:
WBC count 18.6 × 109/L
Eosinophil cell count 7.6 × 109/L (40% eosinophils)
Troponin T 0.5 ng/mL
Anti-MPO (P-ANCA) antibodies positive
Anti-PR3-C-ANCA negative
Immunoglobulin E 1,000 IU/mL
Serological tests for HIV, echovirus, adenovirus, Epstein-Barr virus, and parvovirus B19 are negative. ECG shows regular sinus tachycardia with an absence of strain pattern or any evidence of ischemia. Transthoracic echocardiography reveals a dilated left ventricle with an ejection fraction of 30% (normal is 55% or greater). Which of the following diagnoses best explains the clinical presentation and laboratory findings in this patient?
Q18
A 60-year-old man presents to the emergency department with progressive dyspnea for the last 3 weeks. He complains of shortness of breath while lying flat and reports nighttime awakenings due to shortness of breath for the same duration. The patient has been a smoker for the last 30 years. Past medical history is significant for myocardial infarction 7 months ago. Current medications include metoprolol, aspirin, and rosuvastatin, but the patient is noncompliant with his medications. His temperature is 37.2°C (98.9°F), the blood pressure is 150/115 mm Hg, the pulse is 110/min, and the respiratory rate is 24/min. Oxygen saturation on room air is 88%. Chest auscultation reveals bilateral crackles and an S3 gallop. On physical examination, the cardiac apex is palpated in left 6th intercostal space. Bilateral pitting edema is present, and the patient is in moderate distress. Which of the following is the best next step in the management of the patient?
Q19
A 59-year-old African-American man presents with dyspnea on exertion and bilateral lower leg edema. The patient had a myocardial infarction 2 years ago, in which he developed chronic heart failure. Also, he has type 2 diabetes mellitus. His medications include bisoprolol 20 mg, lisinopril 40 mg, and metformin 2000 mg daily. The vital signs at presentation include: blood pressure is 135/70 mm Hg, heart rate is 81/min, respiratory rate is 13/min, and temperature is 36.6℃ (97.9℉). The physical examination is significant for bilateral lower leg pitting edema. The cardiac auscultation demonstrated an S3 and a systolic murmur best heard at the apex. Which of the following adjustments should be made to the patient’s treatment plan?
Q20
A 76-year-old woman seeks evaluation at a medical office for chest pain and shortness of breath on exertion of 3 months' duration. Physical examination shows bilateral pitting edema on the legs. On auscultation, diffuse crackles are heard over the lower lung fields. Cardiac examination shows jugular venous distention and an S3 gallop. Troponin is undetectable. A chest film shows cardiomegaly and pulmonary edema. Which of the following medications would be effective in lowering her risk of mortality?
Heart failure US Medical PG Practice Questions and MCQs
Question 11: A 62-year-old woman comes to the physician because of a 2-month history of exertional shortness of breath and fatigue. She sometimes wakes up at night coughing and gasping for air. Cardiac examination shows a grade 3/6 holosystolic murmur best heard at the apex. Which of the following physical exam findings would be consistent with an exacerbation of this patient's condition?
A. Head bobbing
B. Early diastolic extra heart sound (Correct Answer)
C. Prominent V wave
D. Radiation of the murmur to the axilla
E. Absence of A2 heart sound
Explanation: ***Early diastolic extra heart sound***
- The patient's symptoms (dyspnea, orthopnea, paroxysmal nocturnal dyspnea) and holosystolic murmur at the apex are consistent with **mitral regurgitation**, leading to **left ventricular dysfunction** and elevated left atrial pressures.
- An early diastolic extra heart sound, or an **S3 gallop**, indicates increased left ventricular end-diastolic pressure and volume overload, a classic finding in **decompensated heart failure**.
- This is a key sign of **acute exacerbation** when heart failure worsens.
*Head bobbing*
- **Head bobbing** (De Musset's sign) is a peripheral sign of **severe aortic regurgitation**, not mitral regurgitation.
- This sign represents the rhythmic bobbing of the head with each heartbeat due to the large pulse pressure from AR.
*Prominent V wave*
- A prominent V wave in the jugular venous pressure waveform is associated with **tricuspid regurgitation**, reflecting increased right atrial pressure during ventricular systole.
- While jugular venous distention can occur in severe biventricular failure, this specific finding is characteristic of TR, not MR exacerbation.
*Radiation of the murmur to the axilla*
- **Radiation of the murmur to the axilla** is a characteristic finding of the **mitral regurgitation murmur itself**, present at baseline in this patient.
- This describes the location and transmission of the existing murmur, not a new finding indicating acute exacerbation or decompensation.
- The question asks for a sign of exacerbation, requiring evidence of worsening heart failure.
*Absence of A2 heart sound*
- **Absence of the A2 heart sound** suggests severe **aortic stenosis**, where the aortic valve leaflets are so rigid and immobile they do not produce an audible closing sound.
- This finding is unrelated to mitral regurgitation or its exacerbation.
Question 12: A 50-year-old man comes to the physician for the evaluation of recurrent palpitations and a feeling of pressure in the chest for the past 6 months. He also reports shortness of breath when walking several blocks or while going upstairs. There is no personal or family history of serious illness. He does not smoke. He has a 30-year history of drinking 7–10 beers daily. His temperature is 37°C (98.6°F), pulse is 110/min, respirations are 18/min, and blood pressure 130/80 mm Hg. Pulse oximetry on room air shows an oxygen saturation of 92%. There are jugular venous pulsations 9 cm above the sternal angle. Crackles are heard at both lung bases. Cardiac examination shows an S3 gallop and a displaced point of maximum impulse. There is pitting edema below the knees. Which of the following is the most appropriate step in the management of the underlying cause of this patient's current condition?
A. Salt and fluid restriction
B. Thiamine substitution
C. Levothyroxine substitution
D. Dietary iron restriction
E. Abstinence from alcohol (Correct Answer)
Explanation: ***Abstinence from alcohol***
- This patient presents with signs and symptoms consistent with **dilated cardiomyopathy** and **heart failure**, including dyspnea, palpitations, S3 gallop, displaced PMI, JVD, crackles, and pitting edema. His 30-year history of heavy daily alcohol consumption strongly suggests **alcoholic cardiomyopathy** as the underlying cause.
- **Abstinence from alcohol** is the most crucial and effective measure to prevent further progression of myocardial damage and often leads to significant improvement or even reversal of alcoholic cardiomyopathy.
*Salt and fluid restriction*
- While salt and fluid restriction are essential components of heart failure management to reduce fluid overload and its symptomatic effects, they address the **manifestations of heart failure** rather than the underlying cause of this patient's cardiomyopathy.
- This step would be appropriate as adjunctive therapy, but not the most appropriate initial step for managing the **underlying etiology**.
*Thiamine substitution*
- **Thiamine deficiency** can lead to **wet beriberi**, which presents as high-output cardiac failure. However, this patient's presentation with an S3 gallop and displaced PMI is more indicative of dilated cardiomyopathy and low-output heart failure exacerbated by alcohol.
- While chronic alcoholics are at risk for thiamine deficiency and it might be considered to rule out beriberi, it's not the primary underlying cause for the described dilated cardiomyopathy, and **alcohol abstinence** directly targets the most likely etiology.
*Levothyroxine substitution*
- **Hypothyroidism** can lead to symptoms like fatigue, bradycardia, and sometimes pericardial effusions or impaired myocardial contractility, but it rarely presents with the prominent dilated cardiomyopathy and overt heart failure signs described here.
- This patient's symptoms are not typical for hypothyroidism, and there's nothing in the history to suggest thyroid dysfunction.
*Dietary iron restriction*
- **Hemochromatosis** is a genetic disorder leading to iron overload, which can cause **restrictive cardiomyopathy** or dilated cardiomyopathy. However, there is no mention of other typical symptoms of hemochromatosis like skin bronzing, diabetes, or liver dysfunction.
- In the absence of evidence for iron overload, and given the strong history of chronic heavy alcohol use, dietary iron restriction is not the most appropriate intervention for this patient's symptoms.
Question 13: A 59-year-old male presents to the emergency room with shortness of breath. Ten days ago, he was in the cardiac critical care unit after receiving a balloon angioplasty and a bare metal stent for an ST-elevation myocardial infarction (STEMI). On physical examination, a holosystolic murmur is heard at the cardiac apex radiating to the axilla. You also detect an S3 and bilateral crackles in the lung bases. What is the most likely etiology of this patient's acute decompensated heart failure?
A. Rupture of the septal papillary muscle on the right ventricle
B. Rupture of the posteromedial papillary muscle of the left ventricle (Correct Answer)
C. Rupture of the posterior papillary muscle on the right ventricle
D. Rupture of the anterolateral papillary muscle of the left ventricle
E. Rupture of the anterior papillary muscle of the right ventricle
Explanation: ***Rupture of the posteromedial papillary muscle of the left ventricle***
- The patient's presentation with acute decompensated heart failure following a STEMI, new holosystolic murmur radiating to the axilla, S3, and bilateral crackles is highly suggestive of acute **mitral regurgitation**.
- The posteromedial papillary muscle is particularly susceptible to ischemic injury and rupture after an **inferior or posterior STEMI** because it has a **single blood supply** from the posterior descending artery (PDA), making it a common complication within days to weeks post-MI.
*Rupture of the septal papillary muscle on the right ventricle*
- The right ventricle does not have "septal" papillary muscles; it has anterior, posterior, and septal papillary muscles, but a distinct "septal papillary muscle on the right ventricle" causing systemic symptoms like those described is anatomically incorrect in this context.
- Right ventricular papillary muscle rupture would primarily affect the **tricuspid valve**, leading to **tricuspid regurgitation**, which typically presents with signs of **right-sided heart failure** (e.g., jugular venous distention, hepatomegaly) rather than a murmur radiating to the axilla.
*Rupture of the posterior papillary muscle on the right ventricle*
- Rupture of a posterior papillary muscle of the right ventricle would primarily cause **tricuspid regurgitation**, not mitral regurgitation.
- This would lead to signs of **right heart failure**, and the murmur would typically be heard loudest at the **lower left sternal border**, intensifying with inspiration, not radiating to the axilla.
*Rupture of the anterolateral papillary muscle of the left ventricle*
- While rupture of the anterolateral papillary muscle can cause acute mitral regurgitation, it is **less common** than posteromedial rupture.
- This is because the anterolateral papillary muscle has a **dual blood supply** from both the left anterior descending (LAD) and circumflex arteries, making it more resistant to ischemia.
*Rupture of the anterior papillary muscle of the right ventricle*
- This would result in **tricuspid regurgitation**, not mitral regurgitation.
- Symptoms would be consistent with **right heart failure**, and the murmur's characteristics would differ from those described (e.g., location, radiation).
Question 14: A 64-year-old man presents to the emergency department because he has been experiencing increased shortness of breath for the last 2 weeks. Specifically, he says that he can barely walk up the stairs to his apartment before he feels winded. In addition, he has been waking up at night gasping for breath and has only been able to sleep propped up on 2 more pillows than usual. Physical exam reveals jugular venous distention as well as pitting lower extremity edema. Which of the following abnormal sounds will most likely be heard in this patient?
A. Opening snap
B. Extra heart sound in early diastole (Correct Answer)
C. Extra heart sound in late diastole
D. Fixed splitting
E. Parasternal holosystolic murmur
Explanation: ***Extra heart sound in early diastole***
- The patient's symptoms (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, jugular venous distention, edema) are classic for **congestive heart failure (CHF)**.
- An **S3 gallop** is an extra heart sound occurring in **early diastole** and is pathognomonic for **volume overload** and **ventricular dysfunction** in CHF.
*Opening snap*
- An **opening snap** is typically heard in **mitral stenosis**, which is not directly indicated by the patient's symptoms of volume overload from heart failure.
- This sound occurs shortly after S2 as the stenotic mitral valve opens.
*Extra heart sound in late diastole*
- An extra heart sound in **late diastole** is often an **S4 gallop**, which indicates **poor ventricular compliance** (e.g., in hypertension or aortic stenosis) rather than the pronounced volume overload suggested by the current presentation.
- An S4 is heard just before S1, as the atria contract to push blood into a stiff ventricle.
*Fixed splitting*
- **Fixed splitting of S2** is characteristic of an **atrial septal defect (ASD)**, where there is a constant delay in pulmonic valve closure, independent of respiration.
- This is not a typical finding in the context of acute decompensated heart failure as described.
*Parasternal holosystolic murmur*
- A **parasternal holosystolic murmur** is typically associated with **ventricular septal defect (VSD)** or **tricuspid regurgitation**.
- While tricuspid regurgitation can occur secondary to right heart failure, the most immediate and common auscultatory finding for overall heart failure with volume overload is an S3.
Question 15: A 67-year-old woman presents with progressive shortness of breath, lower extremity swelling, and early satiety. These symptoms started 4 months ago and have been progressively worsening. She has had type 2 diabetes mellitus for 25 years and hypertension for 15 years; for these, she takes metformin and captopril. She had an anterolateral ST-segment elevation myocardial infarction 6 years ago. Her blood pressure is 110/60 mm Hg, the temperature is 36.3°C (97.3°F), and the pulse is 95/min and regular. On examination, she has a laterally displaced apical impulse with a loud 4/6 holosystolic murmur at the apex, which increases in intensity with breath-holding for 3–5 seconds. Jugular veins are distended to the angle of the jaw. Some basilar crackles are present on both sides. There is a history of increased abdominal girth, and the patient presents with shifting dullness on percussion. There is 2–3+ pitting edema in both lower extremities. Echocardiography shows a left ventricular ejection fraction of 40% and moderate mitral and tricuspid regurgitation. Which of the following is the mechanism that applies to this patient’s illness?
A. Progressive myxomatous degeneration of the mitral valve leaflets
B. Streptococcal infection followed by mitral valve dysfunction
C. Left ventricular dysfunction with functional mitral regurgitation following myocardial infarction (Correct Answer)
D. Right-ventricular dilatation with subsequent functional tricuspid valve dysfunction
E. Thickening of the parietal pericardium with impaired filling of the heart
Explanation: ***Left ventricular dysfunction with functional mitral regurgitation following myocardial infarction***
- This is the **primary mechanism** underlying this patient's illness. The patient had an **anterolateral STEMI 6 years ago**, which caused **left ventricular dysfunction (LVEF 40%)**.
- The **laterally displaced apical impulse** indicates **LV dilatation**, and the **4/6 holosystolic murmur at the apex that increases with breath-holding** (increased afterload) is characteristic of **functional mitral regurgitation** due to LV dilatation and papillary muscle displacement.
- **Chronic LV failure** leads to **pulmonary hypertension**, which subsequently causes **RV dilatation and functional tricuspid regurgitation** (explaining the right-sided heart failure symptoms: JVD, ascites, peripheral edema).
- The question asks for the mechanism that applies to the patient's illness—the **root cause** is **ischemic cardiomyopathy with functional MR**, with right heart failure being a **secondary consequence**.
*Right-ventricular dilatation with subsequent functional tricuspid valve dysfunction*
- While the patient does have **RV dilatation and functional TR** (as evidenced by JVD, ascites, and peripheral edema), this represents a **downstream consequence** of chronic left heart failure, not the primary mechanism.
- This option does not explain the **laterally displaced apex**, **reduced LVEF (40%)**, or the **holosystolic apical murmur** (which is MR, not TR; TR murmur is heard at the left lower sternal border).
- The **primary pathology** is on the left side of the heart from the previous MI.
*Thickening of the parietal pericardium with impaired filling of the heart*
- This describes **constrictive pericarditis**, which presents with **equalization of diastolic pressures**, **Kussmaul's sign**, **pericardial knock**, and often a **normal ejection fraction**.
- The patient has **reduced LVEF (40%)** and **valvular regurgitation**, indicating **myocardial dysfunction** rather than a restrictive filling pattern from pericardial disease.
*Progressive myxomatous degeneration of the mitral valve leaflets*
- This describes **mitral valve prolapse (MVP)** or **degenerative MR**, a primary valvular disorder typically seen in younger patients or those with connective tissue disorders.
- The patient's **history of MI** and **LV dysfunction** make **functional (secondary) MR** much more likely than primary valvular degeneration.
- Primary valvular disease would not explain the **reduced LVEF** or the **biventricular failure**.
*Streptococcal infection followed by mitral valve dysfunction*
- This describes **rheumatic heart disease**, which typically causes **mitral stenosis** (more common than pure MR) and occurs after childhood **group A streptococcal pharyngitis**.
- The patient's age (67), absence of rheumatic fever history, **history of ischemic heart disease**, and **LV systolic dysfunction** make this diagnosis highly unlikely.
- Rheumatic MR is usually chronic and stable, not progressively worsening over 4 months in the setting of recent cardiac history.
Question 16: A 53-year-old woman visits her physician with complaints of shortness of breath and fatigue over the last few weeks. Her past medical history includes hypertension diagnosed 20 years ago. She takes hydrochlorothiazide and losartan daily. Her mother died at the age of 54 from a stroke, and both of her grandparents suffered from cardiovascular disease. She has a 13 pack-year history of smoking and drinks alcohol occasionally. Her blood pressure is 150/120 mm Hg, pulse is 95/min, respiratory rate is 22/min, and temperature is 36.7°C (98.1°F). On physical examination, she has bibasilar rales, distended jugular veins, and pitting edema in both lower extremities. Her pulse is irregularly irregular and her apical pulse is displaced laterally. Fundoscopy reveals ‘copper wiring’ and ‘cotton wool spots’. Which of the following echocardiographic findings will most likely be found in this patient?
A. Ejection fraction: 55% with dilated chambers and thin walls
B. Ejection fraction: 60% with normal left ventricular wall thickness
C. Ejection fraction: 65% with rapid early diastolic filling and slow late diastolic filling
D. Ejection fraction: 40% with increased left ventricular wall thickness (Correct Answer)
E. Ejection fraction: 80% with regurgitant aortic valve
Explanation: ***Ejection fraction: 40% with increased left ventricular wall thickness***
- This patient presents with **chronic, poorly controlled hypertension** (20-year history, BP 150/120, hypertensive retinopathy with copper wiring and cotton wool spots) leading to **decompensated heart failure**.
- Clinical signs of heart failure include **shortness of breath, fatigue, bibasilar rales, jugular venous distension, and bilateral pitting edema**.
- The **irregularly irregular pulse suggests atrial fibrillation**, a common complication of hypertensive heart disease and left atrial enlargement.
- The **laterally displaced apical pulse** indicates left ventricular enlargement, and combined with **reduced ejection fraction (40%)** confirms **heart failure with reduced ejection fraction (HFrEF)**.
- In **advanced hypertensive heart disease**, the ventricle may show **mixed/eccentric hypertrophy** with both **increased wall thickness** (from chronic pressure overload) and **chamber dilatation** (from decompensation), resulting in reduced systolic function.
- This represents **stage D hypertensive heart disease** with progression from concentric LVH to eccentric remodeling with systolic dysfunction.
*Ejection fraction: 55% with dilated chambers and thin walls*
- An EF of 55% is **borderline normal/preserved** and would be inconsistent with the **severely reduced systolic function** suggested by the clinical presentation of decompensated heart failure.
- **Dilated chambers with thin walls** is the classic pattern of **non-ischemic dilated cardiomyopathy**, which typically presents with **EF <40%**, not 55%.
- While this patient may have some chamber dilatation, the combination of long-standing hypertension with preserved/increased wall thickness makes this less likely than hypertensive heart disease.
*Ejection fraction: 60% with normal left ventricular wall thickness*
- An EF of 60% is **normal** and **normal LV wall thickness** would not explain the clinical picture.
- This finding would be incompatible with the **severe decompensated heart failure** evident from bibasilar rales, JVD, and pitting edema.
- The **laterally displaced apical pulse and irregularly irregular rhythm** indicate significant cardiac remodeling, not a structurally normal heart.
*Ejection fraction: 65% with rapid early diastolic filling and slow late diastolic filling*
- An EF of 65% indicates **preserved systolic function**, which contradicts the clinical evidence of **systolic heart failure** (laterally displaced apex, severe volume overload).
- While **diastolic dysfunction** can occur in hypertensive heart disease, the described filling pattern doesn't clearly indicate the **impaired relaxation** pattern (reduced E/A ratio) typically seen in hypertensive heart disease.
- The severity of this patient's presentation (bibasilar rales, JVD, peripheral edema) suggests **systolic dysfunction**, not isolated diastolic dysfunction.
*Ejection fraction: 80% with regurgitant aortic valve*
- An EF of 80% is **supranormal/hyperdynamic** and inconsistent with the clinical presentation of **decompensated heart failure**.
- While **chronic aortic regurgitation** can cause LV dilatation and eventual heart failure, it typically presents with a **wide pulse pressure** and **bounding pulses**, and the history strongly points to **hypertensive etiology** rather than primary valvular disease.
- Aortic regurgitation would not explain the **hypertensive retinopathy** or the **20-year history of hypertension** as the primary pathology.
Question 17: A 63-year-old man presents to the emergency room because of worsening breathlessness that began overnight. He was diagnosed with asthma 3 years ago and has been using albuterol and steroid inhalers. He does not have a prior history of cardiac disease or other respiratory diseases. The man is a retired insurance agent and has lived his entire life in the United States. His vital signs include: respiratory rate 40/min, blood pressure 130/90 mm Hg, pulse rate 110/min, and temperature 37.0°C (98.6°F). Physical examination shows severe respiratory distress, with the patient unable to lie down on the examination table. Auscultation of the chest reveals widespread wheezes in the lungs and the presence of S3 gallop rhythm. The man is admitted to hospital and laboratory investigations and imaging studies are ordered. Test results include the following:
WBC count 18.6 × 109/L
Eosinophil cell count 7.6 × 109/L (40% eosinophils)
Troponin T 0.5 ng/mL
Anti-MPO (P-ANCA) antibodies positive
Anti-PR3-C-ANCA negative
Immunoglobulin E 1,000 IU/mL
Serological tests for HIV, echovirus, adenovirus, Epstein-Barr virus, and parvovirus B19 are negative. ECG shows regular sinus tachycardia with an absence of strain pattern or any evidence of ischemia. Transthoracic echocardiography reveals a dilated left ventricle with an ejection fraction of 30% (normal is 55% or greater). Which of the following diagnoses best explains the clinical presentation and laboratory findings in this patient?
A. Extrinsic asthma
B. Chagas disease
C. Primary dilated cardiomyopathy
D. Loeffler's endocarditis
E. Eosinophilic granulomatosis with polyangiitis (EGPA) (Correct Answer)
Explanation: ***Eosinophilic granulomatosis with polyangiitis (EGPA)***
- This patient's presentation with late-onset **asthma**, prominent **eosinophilia**, evidence of **cardiac involvement** (dilated cardiomyopathy, elevated troponin, S3 gallop), and positive **anti-MPO (P-ANCA) antibodies** are all highly characteristic of EGPA (Churg-Strauss syndrome).
- EGPA is a systemic vasculitis that typically affects individuals with a history of asthma and allergic rhinitis, leading to inflammation and damage in various organ systems, including the lungs, heart, and skin.
*Extrinsic asthma*
- While the patient has asthma and high IgE, **extrinsic asthma** alone does not explain the profound **eosinophilia (40%)**, **cardiac dysfunction (dilated cardiomyopathy, S3 gallop, elevated troponin)**, and positive **anti-MPO antibodies**.
- Worsening asthma symptoms in this context suggest a systemic underlying condition rather than just a typical asthma exacerbation.
*Chagas disease*
- **Chagas disease** is caused by *Trypanosoma cruzi* and can lead to **dilated cardiomyopathy**, but it is primarily endemic to Central and South America, which is inconsistent with the patient's lifelong residence in the United States.
- It would not explain the prominent **eosinophilia**, **asthma**, or **positive anti-MPO antibodies**.
*Primary dilated cardiomyopathy*
- **Primary dilated cardiomyopathy** can explain the cardiac findings (dilated left ventricle, reduced ejection fraction, S3 gallop), but it does not account for the patient's severe **eosinophilia**, **asthma**, and positive **anti-MPO antibodies**.
- This diagnosis would be considered if other systemic causes were ruled out.
*Loeffler's endocarditis*
- **Loeffler's endocarditis** (also called eosinophilic endomyocardial disease) presents with marked **eosinophilia** and eosinophilic infiltration of the endocardium leading to restrictive cardiomyopathy.
- However, this patient has **dilated** (not restrictive) cardiomyopathy, and Loeffler's does not explain the **positive anti-MPO antibodies** or the systemic vasculitis. In fact, Loeffler's endocarditis can occur as a **cardiac manifestation of EGPA**, making EGPA the more comprehensive and accurate diagnosis in this case.
Question 18: A 60-year-old man presents to the emergency department with progressive dyspnea for the last 3 weeks. He complains of shortness of breath while lying flat and reports nighttime awakenings due to shortness of breath for the same duration. The patient has been a smoker for the last 30 years. Past medical history is significant for myocardial infarction 7 months ago. Current medications include metoprolol, aspirin, and rosuvastatin, but the patient is noncompliant with his medications. His temperature is 37.2°C (98.9°F), the blood pressure is 150/115 mm Hg, the pulse is 110/min, and the respiratory rate is 24/min. Oxygen saturation on room air is 88%. Chest auscultation reveals bilateral crackles and an S3 gallop. On physical examination, the cardiac apex is palpated in left 6th intercostal space. Bilateral pitting edema is present, and the patient is in moderate distress. Which of the following is the best next step in the management of the patient?
A. Intravenous beta blockers
B. Intravenous diuretics (Correct Answer)
C. Echocardiography
D. Cardiac stress testing
E. Intravenous inotropes
Explanation: ***Intravenous diuretics***
- The patient presents with classic signs and symptoms of **acute decompensated heart failure**, such as progressive dyspnea, orthopnea, paroxysmal nocturnal dyspnea, bilateral crackles, S3 gallop, pitting edema, and elevated blood pressure with elevated heart rate due to fluid overload.
- **Intravenous loop diuretics** (e.g., furosemide) are the most appropriate initial therapy to reduce preload, alleviate pulmonary and systemic congestion, and improve oxygenation.
*Intravenous beta blockers*
- While beta-blockers are a cornerstone of chronic heart failure management, **starting or acutely increasing beta-blocker dosage in acute decompensated heart failure** can worsen cardiac output and lead to symptomatic hypotension or cardiogenic shock.
- Beta-blockers should generally be withheld or reduced during acute exacerbations and reinstituted once the patient is stable.
*Echocardiography*
- While an **echocardiogram** is essential for diagnosing the underlying cause and assessing cardiac function in heart failure, it is not the *best next step* in a patient presenting with acute, severe symptoms requiring immediate stabilization.
- The patient's acute respiratory distress and hypoxemia necessitate immediate medical intervention to reduce fluid overload before detailed diagnostic imaging.
*Cardiac stress testing*
- **Cardiac stress testing** is used to evaluate for inducible ischemia in stable patients and is not appropriate in the setting of acute decompensated heart failure.
- Performing a stress test on a patient with signs of fluid overload and respiratory distress would be dangerous and could exacerbate their condition.
*Intravenous inotropes*
- **Intravenous inotropes** (e.g., dobutamine, milrinone) are typically reserved for patients with evidence of **cardiogenic shock** or severe heart failure with persistent hypoperfusion despite optimal fluid management and diuretic therapy.
- This patient, while acutely ill, primarily exhibits signs of fluid overload without clear evidence of severe hypoperfusion compromising end-organ function.
Question 19: A 59-year-old African-American man presents with dyspnea on exertion and bilateral lower leg edema. The patient had a myocardial infarction 2 years ago, in which he developed chronic heart failure. Also, he has type 2 diabetes mellitus. His medications include bisoprolol 20 mg, lisinopril 40 mg, and metformin 2000 mg daily. The vital signs at presentation include: blood pressure is 135/70 mm Hg, heart rate is 81/min, respiratory rate is 13/min, and temperature is 36.6℃ (97.9℉). The physical examination is significant for bilateral lower leg pitting edema. The cardiac auscultation demonstrated an S3 and a systolic murmur best heard at the apex. Which of the following adjustments should be made to the patient’s treatment plan?
A. Increase the dose of lisinopril
B. Add hydralazine/isosorbide dinitrate (Correct Answer)
C. Add amlodipine
D. Add valsartan
E. Increase the dose of bisoprolol
Explanation: ***Add hydralazine/isosorbide dinitrate***
- This patient is an **African-American** with **chronic HFrEF** who remains symptomatic despite ACE inhibitor and beta-blocker therapy.
- The **A-HeFT trial** demonstrated that **hydralazine/isosorbide dinitrate** reduces mortality and hospitalization in **African-American patients** with **NYHA class III-IV heart failure**.
- This combination is a **Class I recommendation** specifically for **self-identified African-American patients** with HFrEF who remain symptomatic on standard therapy (ACC/AHA guidelines).
- Among the options provided, this is the most appropriate addition, though in current practice, consideration would also be given to adding an **aldosterone antagonist** (spironolactone/eplerenone) or **SGLT2 inhibitor** if not yet prescribed.
*Increase the dose of lisinopril*
- The patient is already on **lisinopril 40 mg daily**, which is the **maximal recommended dose** for heart failure.
- Increasing the dose further would not provide additional benefit and could increase the risk of **hypotension**, **hyperkalemia**, or **renal dysfunction**.
*Add amlodipine*
- Amlodipine is a **dihydropyridine calcium channel blocker** that is generally **not recommended** for routine use in **HFrEF**.
- While it is **safe** in HFrEF (unlike non-dihydropyridines), it does **not improve mortality or morbidity** and does not address the underlying heart failure pathophysiology.
- It may be considered for refractory hypertension or angina in HFrEF patients, but this patient's BP is adequately controlled.
*Add valsartan*
- Valsartan is an **ARB** that would serve as an **alternative** to lisinopril (ACE inhibitor), not as an additional agent.
- **Combining ACE inhibitor + ARB** is generally **avoided** due to increased risk of **hyperkalemia**, **hypotension**, and **renal impairment** without significant mortality benefit.
- If an ARB were to be added, it would be in the form of **sacubitril/valsartan (ARNI)**, which would **replace** the ACE inhibitor, not supplement it.
*Increase the dose of bisoprolol*
- The patient is on **bisoprolol 20 mg**, but the typical **target dose for HFrEF is 10 mg daily**.
- The patient is already at or above the recommended target dose, and further increases would risk **bradycardia**, **hypotension**, and **fatigue** without clear additional benefit.
- Heart rate is already 81/min, suggesting adequate beta-blockade.
Question 20: A 76-year-old woman seeks evaluation at a medical office for chest pain and shortness of breath on exertion of 3 months' duration. Physical examination shows bilateral pitting edema on the legs. On auscultation, diffuse crackles are heard over the lower lung fields. Cardiac examination shows jugular venous distention and an S3 gallop. Troponin is undetectable. A chest film shows cardiomegaly and pulmonary edema. Which of the following medications would be effective in lowering her risk of mortality?
A. Propranolol
B. Digoxin
C. Lisinopril (Correct Answer)
D. Furosemide
E. Verapamil
Explanation: ***Lisinopril***
- The patient presents with classic signs and symptoms of **heart failure**, including dyspnea on exertion, bilateral pitting edema, jugular venous distention, S3 gallop, cardiomegaly, and pulmonary edema. **ACE inhibitors** like lisinopril are cornerstone therapy for **heart failure with reduced ejection fraction (HFrEF)** and significantly reduce mortality.
- They work by blocking the **renin-angiotensin-aldosterone system (RAAS)**, leading to **vasodilation**, reduced preload and afterload, and prevention of cardiac remodeling.
*Propranolol*
- While beta-blockers are used in heart failure, **non-selective beta-blockers** like propranolol are generally not preferred due to potential for exacerbating symptoms in acutely decompensated heart failure and lack of evidence for mortality benefit in this context.
- **Cardioselective beta-blockers** (e.g., carvedilol, metoprolol succinate) are used in stable heart failure, but propranolol's broad effects make it less suitable for this specific indication, especially when there are signs of decompensation.
*Digoxin*
- Digoxin can improve symptoms and reduce hospitalizations in heart failure, but it **does not demonstrate a mortality benefit** in patients with heart failure.
- It is primarily used for **symptom control** in patients with HFrEF, especially those with coexisting **atrial fibrillation**.
*Furosemide*
- Furosemide is a **loop diuretic** that is highly effective at reducing fluid overload and improving symptoms like pulmonary edema and peripheral edema in heart failure.
- However, while it improves symptoms and quality of life, furosemide **does not independently reduce mortality** in heart failure.
*Verapamil*
- Verapamil, a **non-dihydropyridine calcium channel blocker**, is generally **contraindicated** in heart failure with reduced ejection fraction (HFrEF) because it can worsen cardiac function and increase mortality.
- It has **negative inotropic effects**, which can further impair the already weakened pumping ability of the heart.
