A 49-year-old man presents to his physician complaining of weakness and fatigue. On exam, you note significant peripheral edema. Transthoracic echocardiogram is performed and reveals a preserved ejection fraction with impaired diastolic relaxation. A representative still image is shown in Image A. Which of the following is likely the cause of this patient's symptoms?

Heavy, long-term alcohol consumption

History of myocardial infarction

History of a recent viral infection

Previous treatment with doxorubicin

A 64-year-old man presents to his physician for a scheduled follow-up visit. He has chronic left-sided heart failure with systolic dysfunction. His current regular medications include captopril and digoxin, which were started after his last episode of symptomatic heart failure approximately 3 months ago. His last episode of heart failure was accompanied by atrial fibrillation, which followed an alcohol binge over a weekend. Since then he stopped drinking. He reports that he has no current symptoms at rest and is able to perform regular physical exercise without limitation. On physical examination, mild bipedal edema is noted. The physician suggested to him that he should discontinue digoxin and continue captopril and scheduled him for the next follow-up visit. Which of the following statements best justifies the suggestion made by the physician?

Digoxin is useful to treat atrial fibrillation, but does not benefit patients with systolic dysfunction who are in sinus rhythm.

Long-term digoxin therapy produces significant survival benefits in patients with heart failure, but at the cost of increased heart failure-related admissions.

Both captopril and digoxin are likely to improve the long-term survival of the patient with heart failure, but digoxin has more severe side effects.

Captopril is likely to improve the long-term survival of the patient with heart failure, unlike digoxin.

Digoxin does not benefit patients with left-sided heart failure in the absence of atrial fibrillation.

On cardiology service rounds, your team sees a patient admitted with an acute congestive heart failure exacerbation. In congestive heart failure, decreased cardiac function leads to decreased renal perfusion, which eventually leads to excess volume retention. To test your knowledge of physiology, your attending asks you which segment of the nephron is responsible for the majority of water absorption. Which of the following is a correct pairing of the segment of the nephron that reabsorbs the majority of all filtered water with the means by which that segment absorbs water?

Proximal convoluted tubule via passive diffusion following ion reabsorption

Distal convoluted tubule via passive diffusion following ion reabsorption

Distal convoluted tubule via aquaporin channels

Thick ascending loop of Henle via passive diffusion following ion reabsorption

Collecting duct via aquaporin channels

A 64-year-old male with a history of coronary artery disease, hypertension, hyperlipidemia, and type II diabetes presents to his primary care physician with increasing shortness of breath and ankle swelling over the past month. Which of the following findings is more likely to be seen in left-sided heart failure and less likely to be seen in right-sided heart failure?

Basilar crackles on pulmonary auscultation

Increased ejection fraction on echocardiogram

A 71-year-old woman with a past medical history of type 2 diabetes, hypercholesterolemia, and hypertension was admitted to the hospital 8 hours ago with substernal chest pain for management of acute non-ST-elevated myocardial infarction (NSTEMI). The ECG findings noted by ST-depressions and T-wave inversions on anterolateral leads, which is also accompanied by elevated cardiac enzymes. Upon diagnosis, management with inhaled oxygen therapy, beta-blockers and aspirin, and low-molecular-weight heparin therapy were initiated, and she was placed on bed rest with continuous electrocardiographic monitoring. Since admission, she required 2 doses of sublingual nitroglycerin for recurrent angina, and the repeat troponin levels continued to rise. Given her risk factors, plans were made for early coronary angiography. The telemetry nurse calls the on-call physician because of her concern with the patient's mild confusion and increasing need for supplemental oxygen. At bedside evaluation, The vital signs include: heart rate 122/min, blood pressure 89/40 mm Hg, and the pulse oximetry is 91% on 6L of oxygen by nasal cannula. The telemetry and a repeat ECG show sinus tachycardia. She is breathing rapidly, appears confused, and complains of shortness of breath. On physical exam, the skin is cool and clammy and appears pale and dull. She has diffuse bilateral pulmonary crackles, and an S3 gallop is noted on chest auscultation with no new murmurs. She has jugular venous distention to the jaw-line, rapid and faint radial pulses, and 1+ dependent edema. She is immediately transferred to the intensive care unit for respiratory support and precautions for airway security. The bedside sonography shows abnormal hypodynamic anterior wall movement and an ejection fraction of 20%, but no evidence of mitral regurgitation or ventricular shunt. The chest X-ray demonstrates cephalization of pulmonary veins and pulmonary edema. What is the most appropriate next step in the stabilization of this patient?

Initiate dopamine therapy and diuresis

Obtain blood cultures and start preliminary broad-spectrum antibiotics

Start intravenous fluids and epinephrine therapy

Intubate the patient and perform an emergency cardiocentesis

Insert two large-bore intravenous catheters and start rapid fluid resuscitation

A 72-year-old woman comes to the emergency department because of a 2-week history of worsening shortness of breath, lower extremity swelling, and a 3-kg (6.6-lb) weight gain. Crackles are heard on auscultation of the chest. Cardiac examination shows a dull, low-pitched early diastolic sound at the 5th left intercostal space that becomes louder in the left lateral decubitus position at end-expiration. Which of the following is the most likely cause of these auscultation findings?

Decreased left myocardial compliance

Increased ventricular contractility

Increased capacity of the pulmonary circulation

Decreased left-ventricular filling pressure

Increased left ventricular end-systolic volume

Background: Beta-blockers reduce mortality in patients who have chronic heart failure, systolic dysfunction, and are on background treatment with diuretics and angiotensin-converting enzyme inhibitors. We aimed to compare the effects of carvedilol and metoprolol on clinical outcome. Methods: In a multicenter, double-blind, randomized parallel group trial, we assigned 1511 patients with chronic heart failure to treatment with carvedilol (target dose, 25 mg twice daily) and 1518 to metoprolol (target dose, 50 mg twice daily). The patients were required to have chronic heart failure (NYHA II-IV), the previous admission for a cardiovascular indication, an ejection fraction of < 0.35, and to have been treated optimally with diuretics and angiotensin-converting enzyme inhibitors unless not tolerated. The primary endpoints were all-cause mortality and the composite endpoint of all-cause mortality or all-cause admission. The analysis was done by intention-to-treat. Findings: The mean study duration was 58 months (SD, 6). The mean ejection fraction was 0.26 (SD, 0.07) and the mean age was 62 years (SD, 11). The all-cause mortality was 34% (512 of 1511) for carvedilol and 40% (600 of 1518) for metoprolol (hazard ratio, 0.83 [95% CI 0.74-0.93], p = 0.0017). The reduction in all-cause mortality was consistent across pre-defined subgroups. The incidence of side effects and drug withdrawals did not differ significantly between the 2 study groups. Based on the best interpretation of the results of this clinical trial, which of the following statements is most accurate?

Carvedilol demonstrated a significant improvement in all-cause mortality in patients with heart failure as compared to metoprolol.

The study was underpowered and unable to arrive at a statistically significant conclusion.

Metoprolol demonstrated a significant improvement in all-cause mortality in patients with heart failure compared to carvedilol.

The results are likely biased due to trial design, and therefore non-generalizable.

There is no appreciable, statistically significant difference in overall mortality between the 2 treatment arms.

Classification of heart failure (HFrEF vs HFpEF) for USMLE Step 1: High-Yield Internal Medicine Lessons

Heart Failure Classification - The Pump Problem

Heart Failure (HF) is a clinical syndrome of dyspnea, fatigue, and fluid retention. Left Ventricular Ejection Fraction (LVEF) is the primary metric for classification, dividing HF into distinct categories based on the heart's pumping ability.

Heart Failure Classification (HFrEF, HFmrEF, HFpEF) and LVEF

HFrEF (Reduced EF): Systolic dysfunction (a "pumping" problem).
- LVEF ≤ 40%.
HFpEF (Preserved EF): Diastolic dysfunction (a "filling" problem).
- LVEF ≥ 50%.
HFmrEF (Mildly Reduced EF):
- LVEF 41-49%.

⭐ HFpEF is increasingly common and is often associated with older age, female sex, hypertension, and obesity.

HFrEF - The Weak Pump

Systolic Dysfunction: Characterized by Left Ventricular Ejection Fraction (LVEF) ≤ 40%.
Pathophysiology: Impaired contractility → ↓ Stroke Volume → ↓ Cardiac Output.
Ventricular Remodeling: Eccentric hypertrophy (dilated chamber, thin walls).
Auscultation Hallmark: S3 gallop (early diastole) from rapid ventricular filling into a dilated, compliant ventricle.
Primary Causes:
- Ischemic Heart Disease (post-MI)
- Dilated Cardiomyopathy
- Chronic Volume Overload

⭐ Guideline-directed medical therapy (GDMT) with ACEi/ARB/ARNI, β-blockers, MRAs, and SGLT2 inhibitors is proven to reduce mortality in HFrEF.

HFpEF - The Stiff Pump

Pathophysiology (Diastolic Dysfunction): Impaired ventricular relaxation and filling leads to ↑ left ventricular end-diastolic pressure (LVEDP). The ventricle can't relax, so it can't properly fill.
Ventricular Remodeling: Characterized by concentric hypertrophy-thickened ventricular walls with a smaller chamber size.
Primary Causes:
- Chronic Hypertension (most common)
- Aortic Stenosis
- Hypertrophic & Restrictive Cardiomyopathy
Auscultation Hallmark: An S4 gallop is often heard, representing atrial contraction into a stiff, noncompliant ventricle.

Cardiac Hypertrophy and Heart Failure Classification

⭐ Despite significant heart failure symptoms, the ejection fraction remains normal or near-normal (EF ≥ 50%), as the systolic 'squeeze' function is preserved.

Head-to-Head - Tale of Two Failures

Feature	HFrEF (Systolic Failure)	HFpEF (Diastolic Failure)
Ejection Fraction	≤ 40%	≥ 50%
Primary Problem	↓ Contractility	↓ Compliance / Impaired Relaxation
Ventricular Geometry	Eccentric Hypertrophy (Dilated)	Concentric Hypertrophy (Thickened)
Classic Auscultation	S3 Gallop (Volume Overload)	S4 Gallop (Stiff Ventricle)
Common Etiologies	Ischemia, MI, Dilated Cardiomyopathy	Hypertension, Aortic Stenosis, HOCM

High‑Yield Points - ⚡ Biggest Takeaways

HFrEF (systolic HF) is defined by an ejection fraction (EF) < 40% due to impaired contractility, commonly post-MI.

HFpEF (diastolic HF) has an EF ≥ 50% from impaired ventricular relaxation and stiffness, often due to chronic hypertension.

An S3 gallop is a classic sign of HFrEF (volume overload), while an S4 gallop suggests HFpEF (atrial kick against a stiff ventricle).

Guideline-directed therapies (e.g., beta-blockers, SGLT2i) show significant mortality benefit in HFrEF.

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