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Acute Dyspnea in a Patient with Preserved Ejection Fraction

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Acute Dyspnea in a Patient with Preserved Ejection Fraction

A 69-year-old woman with a history of hypertension and obesity (BMI 34) presents with 3 days of progressive dyspnea, orthopnea, and bilateral ankle swelling. She has no chest pain. Vitals: BP 156/92 mmHg, HR 96/min, respiratory rate 26/min, SpO2 91% on room air, temperature 37.1 °C. Exam: bibasilar crackles to mid-lung fields, JVP elevated at 12 cm, 2+ pitting edema to mid-shin, and an S3. Chest radiograph shows pulmonary vascular congestion and small bilateral effusions. ECG shows sinus rhythm with left ventricular hypertrophy and no ST elevation. BNP is 980 pg/mL. Troponin is mildly elevated at 32 ng/L (URL 14). Creatinine is 1.3 mg/dL (baseline 1.0).

1. What is the likely diagnosis and how would you distinguish among the main possibilities using bedside and laboratory data?

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The picture is acute decompensated heart failure, likely with preserved ejection fraction given hypertension, obesity, and LVH. Key discriminators:

  • HFpEF vs HFrEF: echocardiography is required; the exam alone cannot determine ejection fraction. The S3 and elevated JVP support elevated filling pressures.
  • Acute coronary syndrome: mild troponin elevation can occur in HF from demand ischemia; without chest pain or dynamic ECG changes, serial troponins and clinical correlation are needed before labeling it ACS.
  • Pulmonary embolism: possible with dyspnea and hypoxemia, but bilateral crackles, orthopnea, elevated JVP, and congestion on imaging favor HF; D-dimer/CTPA if clinical suspicion persists.
  • Pneumonia: afebrile, no focal consolidation, so less likely but not excluded.
  • Renal worsening: creatinine rise may reflect cardiorenal congestion or diuretic effect; track urine output and electrolytes.

The combination of orthopnea, JVD, bibasilar crackles, S3, congestion on radiograph, and BNP >900 strongly supports HF.

2. Outline your initial treatment and monitoring plan, including what you would avoid and what would prompt escalation.

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Initial management:

  • Oxygen to keep SpO2 ≥90–94%, upright positioning, continuous pulse oximetry and telemetry.
  • IV loop diuretic (e.g., furosemide) guided by congestion and renal function; monitor urine output, daily weights, electrolytes, and creatinine.
  • Blood pressure control with nitrates if hypertensive and not hypotensive; avoid aggressive fluid boluses.
  • Treat precipitating factors: uncontrolled hypertension, medication nonadherence, arrhythmia, infection, ischemia.
  • Echocardiography to define ejection fraction and valve disease; serial troponins if ACS suspected.

Avoid: routine inotropes (not indicated without low output), NSAIDs, and rapid large-volume fluids. Caution with nephrotoxins.

Escalate to ICU/telemetry if: worsening hypoxemia requiring high-flow oxygen or noninvasive ventilation, hypotension, oliguria, rising creatinine, or arrhythmia. Reassess diuretic response within 6–12 hours; if inadequate, consider escalating diuresis or nephrology/cardiology involvement.