72‑year‑old male with 20‑year history of hypertension (on enalapril) and type‑2 diabetes (on metformin and gliclazide), recent etoricoxib use, presents with sudden severe dyspnea, tachypnea, severe hypertension, elevated jugular venous pressure, bilateral basal crackles, left ventricular heave, S4 gallop, grade III peripheral edema and confusion. What is the most likely diagnosis and how should it be managed acutely?

Acute Decompensated Heart Failure with Hypertensive Emergency

This patient has acute decompensated heart failure (ADHF) with hypertensive emergency, likely precipitated by NSAID use (etoricoxib), and requires immediate IV vasodilator therapy, oxygen support, and cautious diuresis while discontinuing the offending NSAID.

Most Likely Diagnosis

This clinical presentation represents acute decompensated heart failure with preserved ejection fraction (HFpEF) complicated by hypertensive emergency. The constellation of findings definitively establishes this diagnosis 1:

• Elevated jugular venous pressure (6 cm at 30°) is the most reliable sign of hypervolemia and acute HF 1
• Bilateral basal crackles correlate with elevated pulmonary venous pressure in acute HF 1
• S4 gallop indicates left ventricular diastolic dysfunction 1
• Left ventricular heave suggests chronic pressure overload from longstanding hypertension 1, 2
• Grade III peripheral edema with elevated JVP confirms volume overload 1
• Severe hypertension (180/100 mmHg) with acute dyspnea meets criteria for hypertensive emergency with acute organ damage 1

The disorientation represents hypertensive encephalopathy, and the tachypnea (30/min) with respiratory distress indicates pulmonary edema 1.

Critical Precipitating Factor

Etoricoxib (COX-2 inhibitor) is the primary culprit precipitating this acute decompensation 1, 3:

• NSAIDs cause sodium and water retention, directly antagonizing diuretic effects 1
• NSAIDs increase blood pressure by 5-10 mmHg on average, potentially triggering hypertensive crisis 1
• NSAIDs reduce the efficacy of ACE inhibitors like enalapril 3
• The 5-month history of bipedal edema correlates with his "as needed" NSAID use for knee pain 1

Acute Management Algorithm

Immediate Interventions (First 30 Minutes)

1. Discontinue etoricoxib immediately 1

2. Oxygen therapy to maintain SpO2 >90% 1

3. IV vasodilator therapy for hypertensive emergency 1:

• Nitroglycerin IV starting at 5-10 mcg/min, titrate every 5 minutes to reduce BP by 25% in first hour 1
• Target BP reduction: 160/100 mmHg within 1 hour, then 140/90 mmHg over next 2-6 hours 1
• Avoid excessive BP reduction as this may worsen renal perfusion in chronic hypertensives 1

4. IV loop diuretic for decongestion 1:

• Furosemide 40-80 mg IV bolus (double his usual oral dose if on chronic diuretics, otherwise start with 40 mg) 1
• Monitor urine output; target >100-150 mL/hour initially 1
• Assess spot urine sodium after 2 hours: if <50-70 mEq/L, increase diuretic dose 1

Critical Monitoring Parameters

• Continuous cardiac monitoring for arrhythmias 1
• Hourly vital signs until stable 1
• Strict intake/output monitoring 1
• Daily weights 1
• Serial electrolytes (potassium, sodium, creatinine) every 6-12 hours initially 1

Important Caveats Regarding Worsening Renal Function

Do not panic if creatinine rises modestly during decongestion 1:

• Venous congestion is the primary driver of renal dysfunction in this patient, not low cardiac output 1
• The elevated JVP (6 cm) and warm extremities indicate adequate perfusion with high venous pressure 1
• Creatinine increases of 0.3 mg/dL during decongestion are acceptable and often reflect hemoconcentration from effective diuresis 1
• Continue diuretics unless creatinine rises >0.5 mg/dL or oliguria develops 1

Addressing the Pale Conjunctivae and Diminished Pedal Pulse

The pale conjunctivae warrant hemoglobin assessment but should not delay acute HF management 1. Anemia may be contributing to dyspnea but is not the primary problem 1.

The asymmetric pedal pulses (0-1 left vs. +2 right) suggest peripheral arterial disease from his 40 pack-year smoking history 1. This finding:

• Does not change acute HF management 1
• Requires vascular assessment after stabilization 1
• May explain his knee pain (claudication rather than arthritis), making the NSAID use even more inappropriate 1

Medication Adjustments After Stabilization

Continue enalapril unless creatinine rises significantly or hyperkalemia develops 1, 3. ACE inhibitors are beneficial in HFpEF and should not be discontinued reflexively for modest creatinine elevation 1.

Optimize diabetes management: The combination of metformin and enalapril in renal dysfunction requires monitoring for lactic acidosis, though at current doses risk is low 4. Consider holding metformin temporarily if creatinine worsens significantly 4.

Never restart etoricoxib or any NSAID in this patient with HF 1. For knee pain, consider acetaminophen or, if vascular assessment confirms PAD, address the underlying ischemia 1.

Why This Is Not Pulmonary Hypertension

While the physical findings overlap with pulmonary hypertension (RV heave, elevated JVP), several features exclude primary pulmonary arterial hypertension 1, 5, 2:

• Acute presentation (hours to days) rather than chronic progressive dyspnea 1, 6
• Bilateral crackles are absent in isolated PAH 1, 2
• Severe hypertension is not typical of PAH 1
• Clear precipitant (NSAID use) 1
• S4 gallop suggests left-sided disease, not isolated right heart failure 1

The RV heave and elevated JVP reflect acute right ventricular strain from elevated left-sided filling pressures, not primary pulmonary vascular disease 1, 5.