Perioperative Management of Heart Failure Patients: A Contemporary Review

Dr Neeraj Manikath , claude.ai

Abstract

Heart failure (HF) remains a significant predictor of perioperative morbidity and mortality, with an estimated 3-5% of surgical patients having established HF. The perioperative period presents unique challenges due to hemodynamic stress, fluid shifts, and inflammatory responses that can precipitate acute decompensation. This review synthesizes current evidence on optimizing perioperative care for HF patients, with emphasis on phenotype-specific management strategies for heart failure with reduced ejection fraction (HFrEF) versus heart failure with preserved ejection fraction (HFpEF), diuretic timing, and surveillance protocols for early detection of postoperative decompensation.

Introduction

The surgical patient with heart failure represents a complex clinical scenario requiring meticulous perioperative planning. With approximately 6.2 million adults in the United States living with HF, anesthesiologists and intensivists increasingly encounter these patients in surgical settings. Perioperative mortality in HF patients undergoing non-cardiac surgery ranges from 4-15%, compared to <1% in patients without cardiac disease.

The physiological stress of surgery—characterized by sympathetic activation, inflammatory cytokine release, fluid shifts, and altered ventricular loading conditions—can unmask compensated HF or precipitate acute-on-chronic decompensation. Understanding the distinct pathophysiology of HFrEF and HFpEF is crucial for tailoring perioperative strategies that minimize cardiac complications while ensuring adequate tissue perfusion.

Optimizing Volume Status in Patients with Reduced vs Preserved Ejection Fraction

Pathophysiologic Considerations

HFrEF (LVEF <40%) is characterized by impaired systolic contractility, reduced cardiac output, and compensatory neurohormonal activation. These patients operate on the steep portion of the Frank-Starling curve, where small increases in preload may significantly augment stroke volume, but excessive volume loading risks pulmonary congestion without commensurate cardiac output improvement.

HFpEF (LVEF ≥50%) involves diastolic dysfunction with impaired ventricular relaxation and increased chamber stiffness. These patients are exquisitely sensitive to both hypovolemia and volume overload. Their non-compliant ventricles require higher filling pressures to maintain stroke volume, yet tolerate volume excess poorly, rapidly developing pulmonary edema with modest fluid accumulation.

Preoperative Volume Optimization

For HFrEF patients, preoperative assessment should focus on clinical euvolemia. Physical examination findings—jugular venous pressure, hepatojugular reflux, peripheral edema, pulmonary rales—remain valuable despite limitations. Natriuretic peptides (BNP >100 pg/mL or NT-proBNP >300 pg/mL) indicate volume overload and predict perioperative complications, with elevated levels associated with 3-fold increased risk of postoperative cardiac events.

Pearl: Target "dry weight" preoperatively using home diuretic regimens, but avoid aggressive diuresis within 24 hours of surgery that might compromise renal perfusion and increase renin-angiotensin-aldosterone system (RAAS) activation.

Point-of-care ultrasound (POCUS) provides objective assessment: inferior vena cava (IVC) diameter >2.1 cm with <50% inspiratory collapse suggests elevated right atrial pressure, while B-lines on lung ultrasound indicate extravascular lung water. For HFrEF patients, 2-3 B-lines per intercostal space across multiple lung zones suggests significant pulmonary congestion requiring optimization.

For HFpEF patients, volume assessment is more nuanced. These patients often have preserved forward flow despite elevated filling pressures. Clinical examination may underestimate congestion, as pulmonary edema can develop rapidly with surgical stress. Elevated filling pressures are sometimes necessary to maintain adequate stroke volume from their stiff ventricles.

Hack: Use tissue Doppler echocardiography (E/e' ratio) if available. E/e' >15 indicates elevated left ventricular end-diastolic pressure and identifies HFpEF patients at highest risk for perioperative pulmonary edema. These patients benefit from more conservative intraoperative fluid strategies.

Intraoperative Fluid Management

HFrEF Strategy: Goal-directed fluid therapy (GDFT) using dynamic parameters proves superior to liberal or restrictive fixed-volume approaches. Stroke volume variation (SVV) and pulse pressure variation (PPV) guide fluid responsiveness in mechanically ventilated patients (tidal volumes ≥8 mL/kg). Maintain SVV <13% and PPV <12% to avoid fluid overload while ensuring adequate preload.

Oyster: Static parameters like central venous pressure (CVP) correlate poorly with fluid responsiveness in HF patients. A CVP <8 mmHg doesn't predict fluid responsiveness, while CVP >12 mmHg doesn't reliably indicate volume overload. Trending CVP changes may be more useful than absolute values.

For HFrEF patients requiring vasopressor support, norepinephrine is preferred over phenylephrine due to its inotropic properties. Consider low-dose dobutamine (2-5 mcg/kg/min) or milrinone (0.25-0.5 mcg/kg/min) if signs of low cardiac output persist despite adequate preload.

HFpEF Strategy: Restrictive fluid management prevents rapid elevation of left ventricular filling pressures. Target mean arterial pressure >65-70 mmHg to maintain coronary perfusion pressure, crucial for their hypertrophied, non-compliant myocardium. Maintain diastolic pressure >60 mmHg, as HFpEF patients rely heavily on diastolic coronary perfusion.

Avoid tachycardia aggressively (maintain HR 60-70 bpm if possible), as reduced diastolic filling time precipitously reduces stroke volume in non-compliant ventricles. Beta-blockers, if not contraindicated, help control heart rate while reducing myocardial oxygen consumption.

Pearl: For HFpEF patients developing intraoperative hypotension, vasopressors (phenylephrine, norepinephrine) are preferred over aggressive fluid boluses. Small volume challenges (200-250 mL crystalloid over 10 minutes) with hemodynamic assessment prevent fluid overload.

Perioperative Transfusion Considerations

Both HF phenotypes tolerate anemia poorly, but transfusion thresholds require careful consideration. While restrictive strategies (hemoglobin <7-8 g/dL) are standard for most surgical patients, HF patients may benefit from higher thresholds (8-9 g/dL), particularly those with ongoing ischemia or hemodynamic instability. However, each unit transfused carries volume load; administer slowly (over 2-4 hours if not actively bleeding) with concurrent diuresis if necessary.

Timing of Diuretic Management Before and After Surgery

Preoperative Diuretic Management

The decision to continue or hold diuretics perioperatively lacks robust evidence and requires individualized assessment balancing decompensation risk against hypotension and acute kidney injury (AKI).

General Principles:

• Continue loop diuretics in patients with NYHA Class III-IV symptoms or recent decompensation (<3 months)
• Consider holding loop diuretics on the morning of surgery for NYHA Class I-II patients in stable outpatient regimens, particularly for procedures with significant fluid shifts
• Continue aldosterone antagonists (spironolactone, eplerenone) given their modest diuretic effect and favorable neurohormonal modulation
• Continue thiazides unless significant volume depletion expected

Pearl: For patients on high-dose loop diuretics (furosemide ≥80 mg daily), continue at 50% of home dose on the morning of surgery to prevent rebound sodium retention while minimizing hypotension risk. Resume full dose within 24 hours postoperatively.

Hack: Convert oral to IV diuretics perioperatively using 1:2 ratio (e.g., furosemide 40 mg PO = 20 mg IV), accounting for increased bioavailability. Enterally absorbed diuretics have 50% bioavailability; parenteral administration ensures consistent effect when gut perfusion may be compromised.

Intraoperative Considerations

Loop diuretics are rarely necessary intraoperatively unless overt pulmonary edema develops. Prophylactic intraoperative diuresis is NOT recommended, as it complicates fluid management and may precipitate hypotension requiring vasopressors and additional fluids—a dangerous cycle in HF patients.

Exception: Patients receiving massive transfusion protocols or those undergoing procedures with obligatory large-volume resuscitation (major vascular, hepatobiliary surgery) may benefit from concurrent loop diuretic administration to prevent volume overload. Administer furosemide 20-40 mg IV after each 4-6 units of blood products if urine output inadequate.

Postoperative Diuretic Management

Timing of Resumption: Resume maintenance diuretics within 12-24 hours postoperatively once hemodynamically stable, oral intake tolerated, and no ongoing bleeding. Delayed resumption (>48 hours) increases risk of fluid accumulation and pulmonary congestion.

Early Postoperative Period (0-48 hours): Use IV loop diuretics for reliable absorption and titratable effect. Continuous infusion (furosemide 5-20 mg/hour) provides more predictable diuresis than intermittent boluses and reduces risk of ototoxicity from peak concentrations. For bolus dosing, administer every 6-12 hours based on response.

Pearl: Patients receiving chronic loop diuretics develop tolerance. If inadequate response to usual dose, double the dose before adding second agent. Furosemide doses up to 160-200 mg IV may be necessary in diuretic-resistant patients.

Combination Diuretic Therapy: For inadequate response to loop diuretics alone, add thiazide-type diuretic (metolazone 2.5-10 mg daily, chlorothiazide 500-1000 mg IV) to achieve sequential nephron blockade. This synergistic approach is particularly effective but requires close monitoring for hypokalemia, hyponatremia, and renal dysfunction.

Hack: Administer metolazone 30-60 minutes before loop diuretic to maximize synergistic effect. Monitor electrolytes every 12-24 hours with combination therapy.

Transition to Oral Therapy (48-72 hours): Once stable, transition to oral formulations. Use home medication doses initially, adjusting based on clinical assessment and daily weights. Target neutral to negative 0.5-1 kg daily fluid balance until euvolemic.

Diuretic Resistance Management: If diuresis inadequate despite high-dose loop diuretics plus thiazide:

1. Increase loop diuretic dose further or convert to continuous infusion
2. Add acetazolamide 250-500 mg IV/PO to enhance bicarbonate excretion and overcome metabolic alkalosis
3. Consider ultrafiltration if medical management fails and patient remains overloaded

Special Considerations: Surgery-Specific Protocols

Major Abdominal Surgery: Expect third-spacing and inflammatory-mediated capillary leak. Liberal intraoperative fluids may be necessary; aggressive diuresis typically deferred until postoperative day 2-3 when third-spaced fluid mobilizes.

Cardiac Surgery: Resume diuretics early (within 6-12 hours) given significant bypass-related fluid accumulation. Target negative fluid balance by postoperative day 1-2.

Thoracic Surgery: Balance adequate fluid restriction (prevent pulmonary edema in remaining lung tissue) with diuretic therapy. Often require diuretics despite restrictive fluid strategy due to inflammatory lung injury.

Monitoring for Postoperative Decompensation and Acute Pulmonary Edema

Risk Stratification

Identify high-risk patients preoperatively using validated risk scores. The Revised Cardiac Risk Index (RCRI) includes HF as major predictor (adjusted OR 2.4 for major cardiac complications). Additional risk factors include:

• Recent HF hospitalization (<6 months)
• NYHA Class III-IV symptoms
• BNP >200 pg/mL or NT-proBNP >600 pg/mL
• Severe valvular disease
• Atrial fibrillation
• Chronic kidney disease (eGFR <30 mL/min/1.73m²)
• High-risk surgery (intraperitoneal, intrathoracic, vascular)

Patients with ≥2 risk factors warrant intensive monitoring protocols.

Clinical Surveillance

Physical Examination (Every 4-6 hours):

• Respiratory rate and oxygen saturation trending
• Jugular venous distension assessment
• Cardiac auscultation (new S3 gallop indicates volume overload; S4 common in HFpEF at baseline)
• Lung auscultation (bibasilar crackles extending above bases suggests pulmonary edema)
• Peripheral perfusion (cool extremities, delayed capillary refill, altered mentation indicate low cardiac output)
• Daily weights (>1-2 kg increase concerning for fluid retention)
• Strict intake-output monitoring

Pearl: Orthopnea and paroxysmal nocturnal dyspnea are highly specific for HF decompensation but may be obscured by postoperative analgesia and supine positioning. Serial questioning about dyspnea on minimal exertion (standing, walking to bathroom) provides better sensitivity.

Laboratory Monitoring

Serial Natriuretic Peptides: BNP or NT-proBNP measured preoperatively and on postoperative days 1-3 detect subclinical decompensation before overt pulmonary edema. Rising levels (>30% increase from baseline) predict clinical deterioration and warrant preemptive intervention.

Hack: NT-proBNP levels >1000 pg/mL on postoperative day 1 in previously compensated HF patient indicate significant risk (75% probability of clinical decompensation within 72 hours). Intensify monitoring and consider preemptive diuresis.

Electrolytes and Renal Function: Monitor daily initially, then every 2-3 days. Watch for:

• Hypokalemia (<3.5 mEq/L) and hypomagnesemia (<1.8 mg/dL) from diuretic therapy—increase arrhythmia risk
• Rising creatinine (>0.3 mg/dL increase) suggesting cardiorenal syndrome or prerenal azotemia
• Hyponatremia (<135 mEq/L), particularly with thiazide diuretics

Troponin Monitoring: Perioperative myocardial injury (PMI) occurs in 8-18% of HF patients undergoing non-cardiac surgery. Check troponin on postoperative days 1-2 in high-risk patients; elevations warrant cardiology consultation and optimization of anti-ischemic therapy.

Point-of-Care Ultrasound (POCUS) Protocol

POCUS provides rapid, objective assessment of hemodynamic status and should be incorporated into routine HF monitoring where available.

Lung Ultrasound (Every 12-24 hours or when clinical change):

• Scan 8 zones (bilateral anterior, lateral, posterior, superior, and inferior)
• B-line quantification: 0-5 per zone = mild, 6-15 = moderate, >15 = severe pulmonary edema
• Increasing B-line count indicates extravascular lung water accumulation before clinical symptoms
• Sensitivity 93%, specificity 93% for pulmonary edema detection

Inferior Vena Cava Assessment:

• IVC diameter >2.1 cm with <50% respiratory variation suggests elevated right atrial pressure (>15 mmHg)
• Serially increased IVC diameter with reduced collapsibility indicates progressive volume overload

Cardiac Function Assessment:

• Left ventricular systolic function (eyeball ejection fraction)
• Right ventricular size and function (RV dilation suggests pulmonary hypertension or RV failure)
• Pericardial effusion (can complicate perioperative HF)
• IVC/RV ratio >1 suggests severe pulmonary hypertension

Pearl: "Dry" lung ultrasound (0-2 B-lines per zone) doesn't exclude HFpEF decompensation in early stages. Combined assessment with IVC, natriuretic peptides, and clinical findings provides optimal sensitivity.

Advanced Hemodynamic Monitoring

Indications for Pulmonary Artery Catheterization:

• Cardiogenic shock or severe low-output state
• Uncertainty about volume status despite less invasive monitoring
• Mixed shock states (cardiogenic plus septic/hypovolemic)
• Refractory pulmonary edema requiring tailored therapy
• High-risk procedures in NYHA Class IV patients

PAC-guided therapy targets:

• Pulmonary capillary wedge pressure (PCWP) 12-18 mmHg
• Cardiac index ≥2.2 L/min/m²
• Mixed venous oxygen saturation >60%

Minimally Invasive Cardiac Output Monitoring: Pulse contour analysis, esophageal Doppler, or bioreactance provide continuous cardiac output trending without PAC risks. Useful for goal-directed therapy in intermediate-risk patients.

Chest Radiography

Daily portable chest X-rays in ICU setting, or obtained based on clinical suspicion in floor patients. Radiographic findings lag clinical presentation by 6-12 hours.

Typical progression:

1. Vascular redistribution (cephalization)
2. Interstitial edema (Kerley B lines, peribronchial cuffing)
3. Alveolar edema (bilateral perihilar infiltrates, "bat wing" pattern)
4. Pleural effusions (bilateral more common; unilateral suggests alternative diagnosis)

Oyster: Supine portable films underestimate pulmonary edema severity. If clinical suspicion high despite "normal" film, obtain upright PA and lateral views or rely more heavily on POCUS findings.

Protocols for Early Intervention

Mild Decompensation (Increased B-lines, minimal symptoms):

• Increase loop diuretic dose by 50-100%
• Restrict sodium (<2 g daily) and fluids (<1.5 L daily)
• Optimize medical therapy (restart ACE inhibitors/ARBs/ARNI if held)
• Increase monitoring frequency

Moderate Decompensation (Clinical dyspnea, moderate B-lines, hypoxemia):

• IV loop diuretics (continuous infusion preferred)
• Supplemental oxygen to maintain SpO₂ >92%
• Consider non-invasive positive pressure ventilation (CPAP/BiPAP) early—reduces preload, afterload, and work of breathing
• Cardiology consultation
• Consider ICU transfer

Severe Decompensation (Acute pulmonary edema, respiratory failure):

• Immediate ICU transfer
• High-dose IV loop diuretics
• Non-invasive or invasive mechanical ventilation
• Consider IV vasodilators (nitroglycerin 10-200 mcg/min) if adequate blood pressure
• Rule out acute coronary syndrome (troponin, ECG)
• Echocardiography to assess precipitating factors

Hack: The "Rule of 2s" for acute pulmonary edema: Furosemide 2× home dose IV, nitroglycerin 200 mcg sublingual (can repeat every 2 minutes ×3), high-flow O₂, sitting position at 45°, BiPAP if available—initiate simultaneously for rapid symptom relief while awaiting ICU transfer.

Prevention Strategies

Multidisciplinary Approach: Preoperative optimization by cardiology, anesthesiology, and surgical teams reduces complications. Preoperative clinics identifying high-risk HF patients enable:

• Medication optimization (initiate GDMT if not already on)
• Coordination of perioperative medication management
• Appropriate monitoring level planning
• Patient education regarding symptoms warranting immediate reporting

Enhanced Recovery Pathways: ERAS protocols adapted for HF patients balance early mobilization and oral intake (reduce complications) with careful volume management:

• Goal-directed fluid therapy intraoperatively
• Multimodal analgesia (minimize opioids, reduce ileus and sedation)
• Early mobilization (improves venous return, prevents deconditioning)
• Structured diuretic protocols

Perioperative Medical Optimization:

• Beta-blockers: Continue throughout perioperative period; withdrawal precipitates rebound tachycardia and ischemia
• ACE inhibitors/ARBs: Hold morning of surgery (prevent refractory hypotension), resume within 24-48 hours postoperatively when stable
• Aldosterone antagonists: Continue perioperatively
• SGLT2 inhibitors: Emerging data suggests continuing through surgery may reduce HF events, though some centers hold 24 hours prior due to ketoacidosis concerns (data evolving)
• Sacubitril-valsartan (ARNI): Hold 24 hours preoperatively, resume when stable postoperatively

Conclusion

Perioperative management of heart failure patients demands phenotype-specific strategies, meticulous volume optimization, and vigilant postoperative surveillance. Understanding the distinct pathophysiology of HFrEF versus HFpEF guides tailored fluid management—goal-directed therapy with dynamic parameters for HFrEF, restrictive approaches for HFpEF. Strategic diuretic management, balancing decompensation prevention against hypotension and renal injury risk, requires individualized timing decisions. Incorporating objective monitoring tools—natriuretic peptides, POCUS, and validated clinical assessments—enables early detection and intervention before overt decompensation. As surgical populations age and HF prevalence increases, evidence-based perioperative protocols integrating these principles will prove essential for optimizing outcomes in this high-risk population.

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