What is the best management approach for a 57-year-old male with HFrEF (Heart Failure with Reduced Ejection Fraction) and hyperlipidemia, presenting with acute decompensated heart failure, volume overload, and AKI (Acute Kidney Injury)?

Management of Acute Decompensated HFrEF with Volume Overload and AKI

Continue aggressive intravenous loop diuretics at doses equal to or exceeding the patient's chronic oral daily dose (at least 80 mg IV furosemide given his home dose of 40 mg PO BID), maintain guideline-directed medical therapy including bisoprolol and spironolactone, and temporarily reduce or hold ACE inhibitor/ARB initiation until renal function stabilizes, while closely monitoring daily weights, fluid balance, electrolytes, and renal function. 1

Immediate Diuretic Management

Initial IV Diuretic Dosing

• Start with IV furosemide at a dose equal to or exceeding the total chronic oral daily dose (this patient was on 80 mg/day oral, so start with at least 80-100 mg IV) 1
• The 2013 ACC/AHA guidelines specifically state the initial IV dose should equal or exceed chronic oral daily dose, given as either intermittent boluses or continuous infusion 1
• Recent evidence from the DOSE trial supports using 2.5× the home oral dose (which would be 200 mg IV in this case) for more effective decongestion, showing improved net fluid loss and weight change despite only a trend toward symptom improvement 1
• Either continuous infusion or intermittent boluses are acceptable, as the DOSE trial showed no significant difference in efficacy between these approaches 1, 2

Escalation Strategy for Inadequate Response

• If diuresis remains inadequate after initial dosing, intensify the regimen by either increasing loop diuretic doses or adding a second diuretic (thiazide) 1
• Sequential nephron blockade with addition of a thiazide diuretic (metolazone or IV chlorothiazide) is reasonable when loop diuretics alone are insufficient 2, 3
• Low-dose dopamine infusion may be considered in addition to loop diuretics to improve diuresis and preserve renal function, though this is a Class IIb recommendation 1

Continuation of Guideline-Directed Medical Therapy

Beta-Blocker Management

• Continue bisoprolol 5 mg daily unless the patient has marked volume overload, marginal/low cardiac output, or hemodynamic instability 1
• The ACC/AHA guidelines explicitly state that in the majority of HFrEF patients admitted to hospital, oral HF therapy should be continued or even uptitrated during hospitalization 1
• Withholding or reducing beta-blocker therapy should only be considered in patients hospitalized after recent initiation/increase in beta-blocker therapy or with marked volume overload or marginal/low cardiac output 1
• This patient has been on bisoprolol chronically and has adequate blood pressure (BP 91/61 initially, improved to 106/75), so continuation is appropriate 1

Mineralocorticoid Receptor Antagonist

• Continue spironolactone 25 mg daily but monitor potassium and renal function closely 1
• Patients admitted with significant worsening of renal function should be considered for reduction in or temporary discontinuation of aldosterone antagonists until renal function improves 1
• Given this patient's creatinine of 1.6 mg/dL (elevated from baseline) and normal potassium (within normal limits per labs), temporary dose reduction or holding may be prudent until creatinine stabilizes 1

ACE Inhibitor/ARB/ARNI Considerations

• Defer initiation of ACE inhibitor/ARB/ARNI until renal function stabilizes and volume status is optimized 1
• The patient is not currently on an ACE inhibitor or ARB, and with creatinine at 1.6 mg/dL and evidence of cardiorenal syndrome, initiation should wait 1
• Once renal function improves and the patient is euvolemic, initiate an ACE inhibitor at low doses with close monitoring of renal function and potassium within 1-2 weeks 1
• Consider sacubitril/valsartan (ARNI) as preferred over ACE inhibitor/ARB once stable, as PARADIGM-HF demonstrated reduced cardiovascular and all-cause mortality in HFrEF 1

SGLT2 Inhibitor Resumption

• Resume dapagliflozin 10 mg daily once the patient is hemodynamically stable and euvolemic 1
• The patient was reportedly non-adherent to dapagliflozin prior to admission, but this medication has demonstrated mortality and morbidity benefits in HFrEF regardless of diabetes status 1, 4
• SGLT2 inhibitors reduce all-cause mortality, cardiovascular mortality, and HF hospitalization in patients with HF regardless of ejection fraction 4

Management of Acute Kidney Injury

Approach to Cardiorenal Syndrome

• Continue diuresis despite rising creatinine if congestion persists, as venous congestion is the primary driver of renal dysfunction in this setting 1, 5
• The elevated hematocrit (55.9%) and hemoglobin (18.4 g/dL) suggest hemoconcentration from aggressive diuresis, which is expected and acceptable during decongestion 5
• European Society of Cardiology guidelines recommend continuing aggressive diuretic therapy if congestion persists, regardless of rising hematocrit 5

Monitoring Parameters

• Monitor daily weights, strict intake/output, serum electrolytes, creatinine, and BUN daily during IV diuretic therapy 1, 2, 3
• Assess urine output serially to guide dose titration, with goal of negative fluid balance of 500-1000 mL daily 1, 2
• This patient achieved appropriate negative balance of -700 mL in the monitoring period, which should continue 2
• Monitor for electrolyte depletion (potassium, magnesium) which can predispose to arrhythmias, especially when using combination diuretic therapy 1

Temporary Medication Adjustments

• Consider temporary dose reduction or holding of spironolactone if creatinine continues to rise or potassium becomes elevated 1
• The current potassium is normal, but close monitoring is essential given the AKI 1

Management of Congestive Hepatopathy

Addressing Elevated Liver Enzymes

• The elevated ALP (268 U/L) and ALT (62.7 U/L) likely represent congestive hepatopathy from elevated right-sided pressures and hepatic congestion 1
• Aggressive decongestion with diuretics is the primary treatment for congestive hepatopathy, as it addresses the underlying venous congestion 1
• Liver enzymes should improve as volume status normalizes and venous pressures decrease 1

Blood Pressure Management

Addressing Hypotension

• Initial BP of 91/61 mmHg is relatively low but improved to 106/75 mmHg with diuresis, suggesting the hypotension was related to volume overload and reduced cardiac output 1
• Continue current management as BP has improved with decongestion 1
• The transient hypertensive episode (147/86 mmHg) with tachycardia and mild hypoxia suggests inadequate decongestion at that time point 1
• Avoid aggressive vasodilator therapy given baseline low-normal blood pressures 1

Addressing Precipitating Factors

Medication Non-Adherence

• The patient's non-adherence to dapagliflozin is a major precipitating factor for this decompensation 1
• Medication non-adherence for financial or other reasons is a major cause of hospital admission in HF 1
• Address barriers to medication adherence before discharge, including financial concerns, understanding of medication importance, and simplification of regimen 2, 3

Possible Infection

• The productive cough with whitish sputum and chest X-ray showing right lower lung zone reticular opacity concerning for interstitial pneumonia suggests concurrent infection 1
• Pulmonary infections are common in HF patients and add hypoxia to increased metabolic demands, associated with worse outcomes 1
• Treat any identified infection appropriately, as infection is a common precipitant of acute decompensation 1, 3

Transition Planning and Discharge Criteria

Achieving Euvolemia

• Do not discharge until clinical euvolemia is achieved: resolution of peripheral edema (currently grade I pitting edema), clear lung fields (currently decreased air entry right lower third), normal jugular venous pressure, and stable weight 2, 3
• Continue IV diuretics until these clinical endpoints are met 2, 3

Oral Diuretic Transition

• Transition to oral loop diuretics only after achieving euvolemia and demonstrating stable oral diuretic response 2, 3
• The oral dose should be approximately 2-2.5 times the total IV dose that achieved euvolemia, accounting for ~50% oral bioavailability of furosemide 1
• Consider switching to torsemide or bumetanide if absorption concerns exist, as these have better oral bioavailability than furosemide 1

GDMT Optimization Before Discharge

• Ensure all four pillars of GDMT are initiated or optimized before discharge: beta-blocker (already on bisoprolol), ACE inhibitor/ARB/ARNI (needs initiation once stable), MRA (on spironolactone), and SGLT2 inhibitor (resume dapagliflozin) 1, 2, 3
• Initiate ACE inhibitor at low doses once creatinine stabilizes, with plan to uptitrate as outpatient 1

Patient Education

• Provide comprehensive discharge instructions covering: daily weight monitoring (call if weight increases >2-3 lbs in 1 day or 5 lbs in 1 week), sodium restriction (2 grams daily), fluid restriction (approximately 2 liters daily or 30 mL/kg body weight), signs of worsening HF (increased dyspnea, orthopnea, edema), and when to seek immediate medical attention 1, 2, 3
• Emphasize medication adherence, particularly for dapagliflozin which the patient was not taking 2, 3

Common Pitfalls to Avoid

• Do not discontinue beta-blockers abruptly, as this can lead to clinical deterioration and rebound tachycardia 1
• Do not withhold diuretics due to rising creatinine if congestion persists, as venous congestion is the primary driver of renal dysfunction in cardiorenal syndrome 1, 5
• Do not initiate ACE inhibitors/ARBs during active AKI with significantly elevated creatinine, wait until renal function stabilizes 1
• Do not use fixed fluid restrictions without considering body weight, as weight-based restrictions (30 mL/kg) are more reasonable 5
• Do not discharge before achieving clinical euvolemia, as persistent congestion is associated with early readmission 2, 3
• Do not use calcium channel blockers (verapamil, diltiazem, nifedipine) or NSAIDs, as these can precipitate acute HF decompensation 1