How should a patient with a history of cardiac arrest, currently experiencing episodes of hypotension, be managed while on dronedarone (antiarrhythmic medication) and furosemide (loop diuretic)?

Management of Hypotension in a Patient on Dronedarone and Furosemide

Discontinue dronedarone immediately, as it is contraindicated in patients with decompensated heart failure and can cause hypotensive shock, then carefully adjust furosemide dosing to address volume status while monitoring for worsening renal function. 1, 2

Immediate Actions: Discontinue Dronedarone

• Dronedarone must be stopped immediately in patients with class IV heart failure or those who have had an episode of decompensated heart failure in the past 4 weeks, especially with depressed left ventricular function (LVEF <35%). 1
• Dronedarone should not be used to control ventricular rate in patients with permanent atrial fibrillation as it increases the risk of stroke, MI, systemic embolism, or cardiovascular death. 1
• Dronedarone can directly cause hypotensive shock, with blood pressure typically normalizing within 24 hours of discontinuation (consistent with its half-life), making it the likely culprit in this clinical scenario. 2
• The combination of dronedarone with digoxin and furosemide in the setting of decompensated heart failure has been associated with life-threatening arrhythmias and worsening hemodynamics. 3
• Dronedarone has been specifically linked to worsening heart failure leading to cardiogenic shock requiring inotropic support, with improvement occurring after drug discontinuation. 4

Assess Hemodynamic Status and Volume State

• If systolic blood pressure (SBP) <90 mmHg with signs of hypoperfusion (cool extremities, altered mental status, oliguria, elevated lactate, worsening renal function), hold diuretics completely until adequate perfusion is restored. 5
• Measure actual blood pressure carefully, as the threshold of SBP <90 mmHg is the key decision point for withholding diuretics. 5
• If SBP ≥90 mmHg without signs of hypoperfusion, the patient likely has isolated low blood pressure readings rather than true cardiogenic shock, and diuretics can be continued with careful monitoring. 5
• Rule out hypovolemia from excessive diuresis by assessing jugular venous pressure, orthostatic vital signs, and recent weight loss patterns. 5

Furosemide Adjustment Strategy

For Hypotension WITH Hypoperfusion (SBP <90 mmHg):

• Hold furosemide initially and address hypotension first before resuming diuretics. 5
• Consider short-term IV inotropic support (dobutamine, dopamine, or levosimendan) if hypoperfusion persists despite adequate volume status. 5
• Once perfusion is restored and SBP improves, reinitiate diuretic therapy at a reduced dose with careful monitoring. 5

For Hypotension WITHOUT Hypoperfusion (SBP ≥90 mmHg):

• Slow the rate of diuresis but maintain it until fluid retention is eliminated, as excessive concern about hypotension can lead to underutilization of diuretics and refractory edema. 5
• If azotemia occurs before treatment goals are achieved, slow the rate of diuresis but continue it cautiously. 5
• Reduce furosemide dose by 25-50% and monitor response, adjusting based on urine output, daily weights (target 0.5-1.0 kg daily loss), and renal function. 5

Critical Monitoring Parameters

• Hold or reduce furosemide if creatinine rises >0.3 mg/dL during hospitalization, as this increases in-hospital mortality nearly 3-fold (OR 2.7,95% CI 1.6 to 4.6). 5
• Hold furosemide if eGFR falls below 30 mL/min/1.73 m² or creatinine exceeds 2.5 mg/dL, as worsening renal function is associated with increased mortality. 5
• Hold furosemide if potassium drops below 3.0 mEq/L until corrected, as severe hypokalemia increases arrhythmia risk. 5
• Monitor urine output hourly initially, daily weights at the same time each day, and daily electrolytes (especially potassium), BUN, and creatinine during active diuresis. 5

Maintain Guideline-Directed Medical Therapy

• Continue ACE inhibitors/ARBs and beta-blockers during the acute episode unless the patient is truly hemodynamically unstable (SBP <90 mmHg with end-organ dysfunction), as these medications work synergistically with diuretics. 5
• The American Heart Association recommends continuing ACE inhibitors or ARBs during exacerbation unless hemodynamically unstable. 5
• Beta-blockers should also be continued during exacerbation unless hemodynamically unstable, as they work synergistically with diuretics. 5

Alternative Antiarrhythmic Selection

• Amiodarone is the preferred antiarrhythmic for patients with heart failure, as it has neutral effects on mortality in clinical trials, unlike dronedarone which is contraindicated. 1
• Most antiarrhythmic agents (particularly class I sodium channel antagonists and class III potassium channel blockers like dronedarone and d-sotalol) should be avoided in patients with heart failure due to increased mortality risk. 1
• Dofetilide is another option with neutral mortality effects in heart failure patients, though it requires careful QT monitoring and dose adjustment for renal function. 1

Common Pitfalls to Avoid

• Do not restart dronedarone in this patient, as the history of cardiac arrest likely indicates structural heart disease or reduced ejection fraction, both of which are contraindications. 1
• Avoid completely stopping diuretics due to fear of hypotension when SBP ≥90 mmHg, as this leads to persistent volume overload and worsening heart failure. 5
• Do not discontinue ACE inhibitors/ARBs or beta-blockers reflexively for isolated low blood pressure readings without evidence of true hypoperfusion. 5
• Recognize that dronedarone-induced hypotension can occur even with the first dose and may require intensive care unit admission with vasopressor support. 2