Management of HFrEF Patients Presenting with Sepsis
In patients with HFrEF who develop sepsis, continue guideline-directed medical therapy (GDMT) in the absence of hemodynamic instability or contraindications, while simultaneously implementing aggressive fluid resuscitation targeting adequate tissue perfusion. 1
Acute Sepsis Management in HFrEF
Fluid Resuscitation Strategy
Aggressive fluid resuscitation remains the cornerstone of sepsis management even in HFrEF patients, with evidence suggesting traditional fluid resuscitation targets do not increase adverse events and likely improve outcomes. 2
Target adequate tissue perfusion as the principal endpoint rather than arbitrary blood pressure goals, using clinical variables including mental status, capillary refill, urine output, and lactate clearance. 1
Infuse fluids aggressively with more than 4 liters potentially required during the first 24-48 hours in adult septic patients, continuing liberal infusions as needed. 1
The concern about fluid overload in HFrEF should not prevent appropriate sepsis resuscitation, as patients with sepsis and preexisting HF who receive adequate fluid resuscitation have better outcomes despite theoretical concerns. 2
Vasopressor and Inotrope Selection
Norepinephrine remains the most well-supported vasopressor for patients with sepsis and preexisting HFrEF, while dopamine may induce more cardiac adverse events and should be avoided. 2
Dobutamine should be used cautiously given its generally detrimental effects but may have application when combined with norepinephrine in patients with low cardiac output states. 2
In patients with clinical evidence of hypotension associated with hypoperfusion and elevated cardiac filling pressures, intravenous inotropic or vasopressor drugs should be administered to maintain systemic perfusion while more definitive therapy is considered. 1
GDMT Management During Sepsis
Continuation of Chronic HF Medications
Continue GDMT including ACE inhibitors/ARBs and beta-blockers during septic episodes in most patients, unless hemodynamic instability or specific contraindications exist. 1
Beta-blockers may be appropriate to continue in the absence of acute hemodynamic decompensation and may provide independent benefits in sepsis, particularly for atrial fibrillation management after acute hemodynamic stabilization. 2
SGLT2 inhibitors and mineralocorticoid receptor antagonists should generally be continued as they have minimal blood pressure effects and provide ongoing benefit. 1
Medication Adjustments
Temporarily discontinue or reduce diuretics during the acute septic phase when aggressive fluid resuscitation is required, then resume once hemodynamic stability is achieved and volume status is optimized. 3
Reconcile all medications on admission and adjust as appropriate, stopping non-HF antihypertensive medications that may contribute to hypotension. 1
Consider decreasing or stopping antiarrhythmic therapy and other non-class I HFrEF medications that may exacerbate hypotension. 1
Hemodynamic Monitoring
Invasive hemodynamic monitoring should be performed in patients with respiratory distress or impaired perfusion when adequacy of intracardiac filling pressures cannot be determined from clinical assessment. 1
Monitor for signs of fluid overload including pulmonary edema using bedside thoracic ultrasound for interstitial edema when available. 1
Assess volume status continuously through clinical examination, recognizing that clinical signs of dehydration are rare in acute sepsis and should prompt consideration of subacute or chronic disease processes. 1
Common Pitfalls and Caveats
The most critical error is withholding adequate fluid resuscitation due to fear of worsening HF, as sepsis-induced tissue hypoperfusion carries higher immediate mortality risk than volume overload. 2, 4
Avoid using blood pressure alone as the resuscitation endpoint, as normal blood pressure does not guarantee adequate tissue perfusion in HFrEF patients. 1
Do not automatically discontinue all GDMT during sepsis—this represents clinical inertia that worsens long-term outcomes without improving acute management. 1, 2
Recognize that infection increases metabolic demands and sepsis syndrome causes reversible myocardial depression mediated by cytokine release, requiring aggressive supportive care. 1
Post-Acute Management
Transition from intravenous to oral diuretic therapy with careful attention to dosing and monitoring of electrolytes once hemodynamic stability is achieved. 1
Resume or initiate beta-blocker therapy after optimization of volume status and successful discontinuation of intravenous diuretics, vasodilators, and inotropic agents, starting at low doses only in stable patients. 1
For patients not previously on GDMT, initiation of all four core medication classes should occur prior to hospital discharge in stable patients, beginning with SGLT2 inhibitors and MRAs due to minimal blood pressure effects. 5
Monitor supine and upright blood pressure, renal function, electrolytes, and HF signs/symptoms closely with all medication changes during the recovery phase. 1