Congestive heart failure Management of Acute heart failure

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nehal Eid, M.D.[2]

Synonyms and keywords: Acute decompensated heart failure; ADHF; flash pulmonary edema

Overview

Acute heart failure can occur in the setting of new-onset heart failure or worsening of existing chronic heart failure, also known as acute decompensated heart failure (ADHF) or flash pulmonary edema. ADHF commonly presents with acute shortness of breath due to pulmonary edema, which is the rapid accumulation of fluid in the lungs. Other signs and symptoms may include hypotension with impaired end-organ perfusion, worsening renal function, altered mentation, and cold clammy extremities. ADHF is associated with a poor prognosis if not treated promptly and appropriately. Like chronic heart failure therapy, the goal is to improve symptoms, but in the acute setting the additional priorities are to improve oxygenation, restore hemodynamic stability, relieve congestion, and identify the precipitating cause. The mainstays of acute medical treatment include oxygen for hypoxia, diuresis to reduce preload and intravascular volume, and selective use of vasodilators to reduce afterload when blood pressure permits. Chronic heart failure therapies should be continued, initiated, or optimized once the patient is hemodynamically stable.

General Recommendations

Hospitalization

Hospitalization is required for the management of the patient with ADHF with the following signs, symptoms, and laboratory abnormalities:

• Hypotension and/or cardiogenic shock
• Evidence of poor end-organ perfusion such as worsening renal function, cold clammy extremities, or altered mental status
• Hypoxemia with oxygen saturation below 90%
• Atrial fibrillation with rapid ventricular response resulting in hypotension
• Possible acute coronary syndrome or ongoing myocardial ischemia

Priorities During Hospitalization

Hospitalized acute heart failure management should prioritize rapid diagnosis and phenotyping, early decongestion, hemodynamic stabilization, initiation or optimization of guideline-directed medical therapy (GDMT) when stable, and early post-discharge follow-up planning.

Hospitalized acute heart failure management should prioritize:

• Rapid diagnosis and clinical phenotyping
• Early IV loop diuretics to achieve decongestion
• Selective IV vasodilators only when hypertensive or severely congested without hypotension or organ hypoperfusion
• Escalation to inotropes/vasopressors and shock pathways when hypoperfusion is present
• In-hospital initiation or optimization of evidence-based oral GDMT, including SGLT2 inhibitors and ARNI where appropriate, before discharge with early follow-up

Heart Failure Hospitalization Goals

1. Complete decongestion
2. Initiation and optimization of GDMT
3. Transitions of care with early follow-up and a titration plan

Telemetry and Monitoring

The patient should be admitted to a level of care that allows continuous electrocardiographic monitoring, given the risk of arrhythmias, and frequent assessment of vital signs.

• Heart rhythm and oxygen saturation should be monitored continuously.
• Intake and output should be monitored carefully. A daily net fluid balance target should be established, and diuretic dosing should be adjusted to achieve this target.
• Daily weights should be obtained using the same scale at the same time of day, usually before the patient has eaten and after the patient has first voided in the morning. Intake and output measurements may underestimate insensible losses.
• BUN, creatinine, serum sodium, chloride, bicarbonate, serum potassium, and magnesium should be monitored during active diuresis. Potassium and magnesium should be repeated as needed after aggressive diuresis.
• If the patient is hyponatremic, this does not suggest inadequate salt intake, but rather excess free water retention. Free water restriction may be required, especially when sodium is markedly reduced. Intravenous drips should not be administered in D5W in patients with clinically significant hyponatremia unless specifically indicated. Patients with congestive heart failure should generally follow a sodium-restricted diet.

Oxygen

Oxygen improves the patient's status if hypoxemia is present, and the goal is to keep the oxygen saturation above 90%. Continuous positive airway pressure may be applied using a face mask; this has been shown to improve symptoms more quickly than oxygen therapy alone, and has been shown to reduce the risk of death. Severe respiratory failure requires treatment with endotracheal intubation and mechanical ventilation.

Management Considerations

The patient's therapy must be tailored to:

• Whether the patient has acute decompensated systolic or diastolic heart failure
• The patient's intravascular volume status
• The patient's hemodynamic status
• The precipitant of the decompensation

Systolic Versus Diastolic Heart Failure

The management of the patient with acute decompensated heart failure depends partly upon whether the patient has acute decompensated systolic heart failure or acute decompensated diastolic heart failure. Both forms may be treated with oxygen, decongestion, and selective vasodilator therapy when blood pressure permits. Inotropic agents are generally reserved for patients with systolic dysfunction and evidence of hypoperfusion or shock. While initiation of ACE inhibitors or other RAAS inhibitors is generally deferred during the earliest unstable phase of acute decompensation, these agents may be continued or initiated before discharge once the patient is hemodynamically stable and renal function and potassium are acceptable. Control of tachycardia may be particularly useful in patients with diastolic dysfunction to improve ventricular filling time.

Intravascular Volume Status

The aggressiveness of diuresis depends upon the patient's volume status and hemodynamic profile. If the patient is total body and intravascular volume overloaded and normotensive, then diuresis alone is usually appropriate. If the patient is volume overloaded but hypotensive or hypoperfused, then vasodilators should generally be avoided, and inotropes or vasopressors may be required in addition to diuretics. A phenotype-based acute HF treatment algorithm includes hypertensive pulmonary edema, normotensive congestion, and hypotensive or hypoperfused cardiogenic shock phenotypes.

• Hypertensive AHF / flash pulmonary edema often reflects high afterload: prioritize oxygen or NIV as needed, IV vasodilator plus IV diuretic if there is no hypotension.
• Normotensive congestive AHF or “warm/wet” profile: prioritize IV loop diuretic-based decongestion and reassess response frequently.
• Hypotensive/hypoperfused AHF or cardiogenic shock or “cold” profile: avoid routine vasodilators; evaluate for shock, start vasopressor or inotrope as appropriate, and activate shock/advanced HF pathways.

Identification of and Treatment of Underlying Cause of Decompensation

Identification and treatment of precipitants of acute decompensation is a mainstay of therapy. Please see the accompanying chapters for detailed management strategies.

• Hypertension: Vasodilators may be administered if there is no hypotension or end-organ hypoperfusion.
• Acute coronary syndrome: Treat according to ACS guidelines with antiplatelet therapy, anticoagulation, anti-ischemic therapy when appropriate, and urgent coronary angiography/revascularization when indicated. Mechanical circulatory support may be considered in selected patients with refractory cardiogenic shock or mechanical complications.
• Valvular heart disease: Acute mitral regurgitation may require vasodilator therapy and urgent valve intervention when severe. Mitral stenosis requires heart rate control to prolong left ventricular filling. Severe aortic stenosis may require balloon valvuloplasty, TAVR, or surgical valve replacement depending on clinical context.
• Atrial fibrillation can cause acute decompensation of heart failure due to increased heart rate and oxygen demand, and conversely acute decompensation of heart failure can precipitate atrial fibrillation due to left atrial dilation and increased wall stress. Thus, atrial fibrillation and acute decompensated heart failure are often closely related, and successful management of atrial fibrillation is often critical to reversing the acute decompensation.

In the patient with acute decompensated heart failure, management of atrial fibrillation depends on hemodynamic stability, left ventricular systolic function, and whether AF is the precipitant of decompensation. In patients with decompensated HFrEF, nondihydropyridine calcium channel blockers such as diltiazem and verapamil should generally be avoided because of negative inotropic effects. Digoxin or amiodarone may be used for rate control when beta-blockers or calcium channel blockers are not tolerated or are contraindicated. Urgent synchronized cardioversion is indicated when AF causes severe hemodynamic instability.

If a patient is in cardiogenic shock, then cardioversion can be considered in the patient with atrial fibrillation. In the absence of severe hemodynamic compromise, atrial fibrillation will often recur in this setting. Cardioversion can also be undertaken if new-onset atrial fibrillation is the clear precipitant of hemodynamic decompensation. If the patient is going to be cardioverted, anticoagulation should be addressed according to guideline-based cardioversion and stroke-prevention recommendations.

• Ventricular Arrhythmias: The development of either ventricular tachycardia or ventricular fibrillation is a life-threatening complication and must be treated promptly with cardioversion or defibrillation when indicated. Many antiarrhythmics can be pro-arrhythmic in the patient with heart failure and are contraindicated. Amiodarone is commonly used for the management of ventricular arrhythmias in the patient with heart failure. Underlying precipitants such as hypokalemia and hypomagnesemia should be corrected. Inotropic agents can also be pro-arrhythmic; therefore, the lowest effective dose should be used and they should be tapered as soon as possible.

Specific Therapies of Acute Heart Failure

Diuretics

• Usually, but not always, patients with decompensated systolic heart failure are total body and intravascular volume overloaded, and intravenous diuretics are often required in the acute setting. IV loop diuretics are first-line therapy for congestion, with a goal of complete decongestion before discharge because persistent congestion predicts poor outcomes and readmission. Even in the absence of overt volume overload, such as decompensation due to hypertension or valvular heart disease, diuresis may improve the symptoms of congestive heart failure because “dry lungs work better than wet lungs.” These drugs also cause venodilation in the lung vasculature, which may relieve shortness of breath. By reducing volume overload, these drugs can optimize cardiac performance and reduce functional mitral regurgitation and tricuspid regurgitation.
• Diuretics reduce preload and reduce intravascular volume.
• Intravenous preparations are preferred because of more predictable absorption. Severe systemic congestion may cause intestinal edema, which can affect enteral absorption of medications.
• For patients already taking outpatient loop diuretics, an initial IV loop diuretic dose of 1 to 2.5 times the total daily oral home dose may be used. For diuretic-naive patients, an initial dose of furosemide 40 to 80 mg IV twice daily is commonly recommended. The DOSE trial used a high-dose strategy equal to 2.5 times the home daily oral loop diuretic dose and found no significant difference in primary endpoints between bolus and continuous infusion strategies.
• Bumetanide and torsemide may have advantages due to more consistent oral bioavailability and potentially reduced ototoxicity risk at higher doses.
• Torsemide dose is 10 to 20 mg intravenously.

Diuretic Response Monitoring and Escalation

• Track urine output, daily weights, congestion signs, electrolytes, and renal function; reassess early and adjust dosing.
• In case of inadequate response or “diuretic resistance,” escalate loop diuretic therapy and consider sequential nephron blockade, such as a thiazide-type diuretic like metolazone, with close electrolyte monitoring.
• If high doses of furosemide are inadequate, boluses or continuous infusions of bumetanide may be preferred. The DOSE trial showed no significant difference in clinical endpoints between continuous infusion and intermittent bolus dosing. Some patients with very high chronic diuretic requirements may respond better to continuous infusion.
• These loop diuretics may be combined with thiazide diuretics such as oral metolazone, hydrochlorothiazide 25 to 50 mg twice daily, or intravenous chlorothiazide 500 to 1000 mg/day for a synergistic effect to address diuretic resistance. To avoid electrolyte abnormalities, addition of a thiazide is generally reserved for patients who do not respond adequately to moderate- or high-dose loop diuretics.
• Hypotension may result from diuresis if mobilization of fluid from the extravascular space does not keep pace with fluid leaving the intravascular space through diuresis. Patients with diastolic dysfunction and restrictive physiology are also prone to hypotension due to reductions in preload.
• Typically, BUN and creatinine may rise during diuresis. If the rise in creatinine is minimal and the patient remains fluid overloaded, then diuresis can continue with careful attention to renal function. Creatinine elevations in the range of 0.3 mg/dL do not necessarily predict worse outcomes except when patients are discharged with persistent congestion. If the creatinine rises significantly before the patient is euvolemic, this may suggest reduced renal perfusion and is associated with a poorer prognosis. If the creatinine rises significantly, other nephrotoxic drugs should be discontinued, and diuretic dosing may need to be adjusted. Despite a rise in creatinine, continued diuresis may still be required if severe pulmonary edema persists, and consideration should be given to the addition of an inotropic agent when hypoperfusion is present.
• If further efforts to induce diuresis fail and the patient remains volume overloaded, then ultrafiltration or dialysis may be considered in selected cases.
• In patients who have sustained a myocardial infarction and have heart failure, an aldosterone antagonist such as spironolactone or eplerenone can be added if indicated. Given the risk of hyperkalemia, these agents should only be added if renal function and serum potassium can be carefully monitored.

Vasodilator Therapy

In the absence of hypotension or organ hypoperfusion, intravenous vasodilators such as nitroglycerin or nitroprusside may be considered to reduce filling pressures and improve symptoms, particularly when acute heart failure is precipitated by severe hypertension. However, IV vasodilators have not shown a proven benefit on mortality or rehospitalization and should not be used routinely. They should be avoided or discontinued if hypotension or worsening organ perfusion develops.

Nitroglycerin

• Nitroglycerin reduces preload and, at higher doses, also reduces afterload. Nitroglycerin may be helpful in improving symptoms of dyspnea, particularly in hypertensive acute heart failure or acute pulmonary edema.
• Tolerance or tachyphylaxis can develop within hours of continuous high-dose nitroglycerin administration.
• The initial dose of intravenous nitroglycerin is commonly 5 to 10 µg/min, titrated every 3 to 5 minutes in 5 to 10 µg/min increments according to blood pressure and clinical response.

Nitroprusside

• Like nitroglycerin, nitroprusside is both a venodilator and arterial vasodilator, but nitroprusside provides a greater degree of afterload reduction compared with nitroglycerin. Clinical scenarios where rapid and potent arterial dilation may be useful include hypertensive emergency, acute mitral regurgitation, ventricular septal rupture, and aortic insufficiency.
• The initial dose of nitroprusside is usually 0.3 µg/kg/min by continuous intravenous infusion, titrated carefully according to blood pressure and clinical response. Doses above 2 µg/kg/min increase the risk of cyanide toxicity, and prolonged or high-dose infusions require close monitoring, especially in renal or hepatic dysfunction.
• Patients administered nitroprusside can develop accumulation of metabolites including cyanide or thiocyanate, which can be toxic and even fatal. Thus, the duration of a nitroprusside infusion is usually limited and requires close monitoring.

Cardiogenic Shock

• Prompt identification of cardiogenic shock and escalation of level of care are required, including ICU management, invasive hemodynamics when needed, and early involvement of an advanced HF or cardiogenic shock team.
• Inotropes and vasopressors may be used for hypoperfusion as a bridge to recovery, definitive intervention such as revascularization or valve intervention when indicated, or advanced therapies such as temporary mechanical circulatory support, LVAD, or transplant evaluation.

Inotropic Therapy

• Inotropes may be administered if the cardiac output and the systolic blood pressure are low, if there is evidence of end-organ hypoperfusion such as rising creatinine, and if there is evidence of elevated filling pressures, such as elevated pulmonary capillary wedge pressure or elevated jugular venous pressure, which limit diuresis and/or vasodilator therapy.
• Milrinone increases contractility and reduces afterload.
• Dobutamine increases contractility and reduces afterload.
• Dopamine increases blood pressure and, at low doses, may increase renal blood flow, though routine renal-dose dopamine is not recommended.
• There is ongoing concern that inotropes, by increasing heart rate and contractility, may damage hibernating but viable myocardium. These agents are also pro-arrhythmic. Consistent with these concerns, the randomized OPTIME-CHF trial demonstrated that randomization to milrinone versus placebo was associated with increased hypotension, atrial arrhythmias, and a non-significant increase in mortality.
• Because milrinone does not exert its effects through beta receptors, it may be more effective in patients receiving a beta blocker.
• The starting dose of dobutamine is 2.5 µg/kg/min, and the dose can be gradually titrated up according to clinical response.
• The loading dose of milrinone is 50 µg/kg over 10 minutes. The initial maintenance dose is 0.375 µg/kg/min, and the maximum dose is 0.750 µg/kg/min. Loading doses are often avoided in unstable or hypotensive patients.

Vasopressor Support

• In the presence of severe hypotension and impaired end-organ perfusion despite optimal left ventricular filling pressures on invasive monitoring, intravenous norepinephrine, vasopressin, or dopamine at a dose >5 µg/kg/min may be administered.
• Vasopressors increase afterload and may decrease cardiac output; they should be used transiently when possible.

Prophylaxis for Venous Thromboembolism

In the absence of contraindications, low-dose unfractionated heparin, fondaparinux, or a low molecular weight heparin is recommended as DVT prophylaxis in the patient with acute decompensated heart failure.

Morphine

• Morphine may reduce anxiety and perceived dyspnea, but routine use in acute decompensated heart failure is not recommended.
• Observational studies and meta-analyses have associated morphine use in acute heart failure with higher risk of invasive ventilation and short-term mortality, although confounding by severity is possible.
• Morphine should generally be avoided except in selected patients with severe pain or refractory distress after careful risk-benefit assessment.

Guideline-Directed Medical Therapy

Hospitalization should be used to initiate and/or optimize disease-modifying therapy once the patient is hemodynamically stable. The STRONG-HF trial demonstrated that high-intensity care with initiation and rapid up-titration of guideline-directed medical therapy after hospitalization for acute heart failure reduced the risk of heart failure readmission or all-cause death at 180 days in the overall trial population. STRONG-HF enrolled patients across the LVEF spectrum, but subgroup conclusions by LVEF should be interpreted cautiously because the trial was not powered primarily for LVEF subgroup analyses.

ACE Inhibition

Continuation of Chronic ACE Inhibition

• ACE inhibition can be continued in the setting of acute decompensated congestive heart failure if the patient is hemodynamically stable without rising creatinine, clinically significant hyperkalemia, or symptomatic hypotension. The half-life of an ACE inhibitor is relatively long, and persistent hypotension may occur in the setting of aggressive diuresis.

Initiation of Acute ACE Inhibition

• ACE inhibitors or other RAAS inhibitors should generally be initiated or resumed once the patient is hemodynamically stable, without symptomatic hypotension, severe worsening renal function, or clinically significant hyperkalemia. Stability criteria commonly include systolic blood pressure ≥100 mm Hg, no recent need for IV inotropes, and no recent escalation of IV diuretics or vasodilators.
• Intravenous enalaprilat is generally avoided in acute decompensated heart failure because it may cause prolonged hypotension and impaired end-organ perfusion, particularly in unstable patients.
• Hyponatremia and low systolic blood pressure are markers of increased activation of the renin angiotensin system and may be associated with hypotension after administration of an ACE inhibitor.

ARNI Initiation in HFrEF

The ACC and AHA recommend in-hospital initiation of sacubitril/valsartan (ARNI) in patients hospitalized with acute decompensated HFrEF before discharge in the absence of contraindications. This represents a shift from the traditional approach of initiating and uptitrating ACE inhibitors first before switching to ARNI, as early initiation may simplify management. The 2024 ACC Expert Consensus Decision Pathway emphasizes that sacubitril/valsartan can be initiated in both new-onset HF and chronic HF on partial GDMT.

Hemodynamic stability criteria for initiation include:

• Systolic blood pressure ≥100 mm Hg for at least 6 hours
• No increase in IV diuretics or vasodilators for at least 6 hours
• No IV inotropic therapy within the previous 24 hours
• Hemodynamic stability

Initial dosing strategy may include:

• SBP 100-120 mm Hg: Start sacubitril/valsartan 24/26 mg twice daily
• SBP ≥120 mm Hg: Start sacubitril/valsartan 49/51 mg twice daily
• Dose adjustment after discharge every 1-2 weeks according to systolic blood pressure
• Transition from other RAAS inhibitors: Patients on an ARB can be transitioned directly to ARNI, whereas ACE inhibitors should be discontinued for at least 36 hours before initiating ARNI. Previous IV inotropic therapy should have been successfully discontinued at least 24 hours before starting sacubitril/valsartan.

Beta Blockers

Discontinuation

While beta blockers play a central role in the management of chronic heart failure, beta blockade should not be newly initiated during the unstable phase of acute decompensated heart failure.

If the patient is chronically administered a beta blocker, the beta blocker can often be continued in the absence of hypotension, shock, severe bradycardia, or need for escalating inotropic support. If the patient becomes hemodynamically unstable, the beta blocker dose can be reduced or temporarily held. If inotropic agents are required, beta blocker continuation should be individualized.

Evidence regarding beta-blocker continuation or withdrawal includes:

• In the OPTIMIZE-HF cohort study, beta-blocker withdrawal among eligible patients was associated with worse outcomes.
• In the ESCAPE cohort study, withdrawal of beta blockers was associated with adjusted higher mortality.
• The B-CONVINCED randomized controlled trial found no difference in short-term outcomes during hospitalization, but patients randomized to continue beta-blockers were more likely to be taking beta-blockers at 3 months.
• In a retrospective observational analysis of the SURVIVE trial, patients remaining on beta-blockers had lower adjusted mortality at 30 and 180 days.
• The Prins systematic review in 2015 included five cohort studies and the B-CONVINCED randomized trial and found benefit associated with beta-blocker continuation.

Additional studies include:

• A non-randomized analysis of the SENIORS trial found non-significantly reduced hospital mortality with nebivolol.
• The GULF-CARE cohort found reduced hospital mortality, but no benefit at 3 and 12 months.
• The KCHF cohort found reduced hospital mortality with beta-blocker use at admission.

Up Titration

Beta-blocker therapy can be up-titrated as part of guideline-directed medical therapy once the patient is clinically stable. NT-proBNP-guided therapy intensification has not consistently improved outcomes compared with usual guideline-directed care.

Aldosterone Antagonism

• If the patient is chronically receiving an aldosterone antagonist before the episode of decompensated congestive heart failure, the agent may be continued in the absence of hypotension, hyperkalemia, and impaired renal function.
• If the patient meets criteria for initiation of an aldosterone antagonist for the management of chronic heart failure, this can be initiated before hospital discharge when renal function and potassium are acceptable.

SGLT2 Inhibitors In-Hospital Initiation

SGLT2 inhibitors are one of the “4 pillars” of HFrEF medical therapy and reduce the risk of heart failure hospitalization and cardiovascular mortality irrespective of diabetes status. Once clinical stabilization is achieved, the ACC recommends in-hospital initiation of SGLT2 inhibitors for patients hospitalized with acute decompensated heart failure. Trials including SOLOIST-WHF, EMPULSE, EMPA-RESPONSE AHF, EMPAG-HF, DICTATE-AHF, and DAPA-Resist have shown that SGLT2 inhibitors can be safely started during hospitalization in selected stable patients. These medications increase urine output, may augment decongestion, and reduce heart failure events. In-hospital initiation is associated with greater long-term adherence and prescription persistence, and clinical benefits may emerge early after initiation.

Initiation criteria include hemodynamic stability, commonly with the following features:

• Systolic blood pressure ≥100 mm Hg
• No inotropic support for at least 24 hours
• No symptoms of hypotension
• No increase in IV diuretic dose in the previous 6 hours
• No IV vasodilators
• Estimated glomerular filtration rate ≥20 mL/min/1.73 m²
• Safety considerations: SGLT2 inhibitors should not be initiated in patients with hypovolemia, and diuretic requirements should be reassessed because they can decrease acutely and chronically. Monitoring for euglycemic diabetic ketoacidosis, hypoglycemia, and urinary/genital mycotic infections is recommended. Following initiation, an eGFR drop is expected, and clinicians should not necessarily adjust or discontinue medications solely based on this expected change.

Sequencing of GDMT: The 2024 ACC notes that for some patients with less robust blood pressure, the first step may be a low dose of an ARB, with a potential switch to sacubitril/valsartan before discharge once a low dose of beta-blocker has been tolerated. The usual strategy aims for addition of all neurohormonal modulator classes before major uptitration. During GDMT initiation and titration, patients should be monitored for changes in heart rate, blood pressure, electrolytes, renal function, and symptoms, with planned uptitration delayed until adverse effects observed with lower doses have resolved. When patients show progressive kidney dysfunction, temporary down-titration of neurohormonal antagonists may be necessary, particularly in the setting of hypotension and progressive kidney dysfunction.

Guideline-Directed Medical Therapy for Hospitalized Patients with HFpEF/HFmrEF

SGLT2 Inhibitors as Core Therapy Across the EF Spectrum

The 2023 European Society of Cardiology focused update upgraded SGLT2 inhibitors to a Class I recommendation for both HFmrEF and HFpEF. The 2022 AHA/ACC/HFSA guideline provides a Class 2a recommendation for SGLT2 inhibitors in patients with HF and LVEF >40%. Benefits are driven primarily by reduced heart failure hospitalizations rather than cardiovascular mortality, with modest improvements in quality of life. SGLT2 inhibitors can be initiated during hospitalization for acute decompensated heart failure once clinically stable, using similar stability criteria as for HFrEF.

Dosing: Both empagliflozin and dapagliflozin are dosed at 10 mg once daily with no titration required.

For patients with HFmrEF (LVEF 41–49%) and selected patients with HFpEF, particularly those with LVEF closer to the lower end of the preserved EF spectrum, additional therapies may be considered:

Mineralocorticoid receptor antagonists (MRAs): Class 2b recommendation for patients with LVEF on the lower end of the spectrum. Spironolactone may be started at 25 mg daily and titrated according to potassium and creatinine.

Angiotensin receptor-neprilysin inhibitors (ARNIs): Class 2b recommendation for selected patients, particularly women and those with LVEF closer to 40%. Sacubitril/valsartan may be started at 24/26 mg twice daily and titrated as tolerated.

Angiotensin receptor blockers (ARBs): Class 2b recommendation when ARNI is not feasible, particularly for patients with LVEF on the lower end of the spectrum.

Monitoring kidney function and serum potassium is useful 1-2 weeks after initiation when using RAAS blockers and/or SGLT2 inhibitors.

Hypertension Control as a Key Treatment Target

Blood pressure management is a critical therapeutic target in HFpEF, as hypertension is one of the most important causes and comorbidities in HFpEF. Adults with HFpEF should have blood pressure controlled according to contemporary hypertension guidelines, commonly targeting systolic blood pressure <130 mm Hg when tolerated.

Antihypertensive choice: Preferred agents for blood pressure control in HFpEF include:

• Diuretics when required for volume control
• SGLT2 inhibitors, which may lower blood pressure and may require adjustment of other antihypertensives
• MRAs, ARNIs, or ARBs based on modest cardiovascular benefits in HFpEF trials
• Avoid beta-blockers solely for blood pressure lowering unless another indication exists
• Beta-blockers may be considered when a specific non-HFpEF indication exists, such as:
  • Atrial fibrillation requiring rate control
  • Angina pectoris
• For patients with HFmrEF (LVEF 41-49%), there is modest evidence suggesting beta-blockers may improve clinical outcomes, particularly for those with LVEF on the lower end of this spectrum. Analysis from the DELIVER trial showed that beta-blocker use was not associated with harm across the LVEF spectrum from 40-80%, though this does not establish benefit in the absence of other indications.

Contraindicated Medications

Congestive heart failure is considered an absolute contraindication to the use of the following medications:

• Mannitol

Transitional Care Plan

The transitional care plan should include two early post-discharge events:

1. Follow-up phone call within 2-3 days of discharge
2. Clinic visit within 7-14 days of hospital discharge

The first post-discharge appointment provides the opportunity to reassess clinical status, provide additional patient education, review medications and adjust doses, and address issues that might lead to readmission or worsening HF.

Transitional Care Plan Components

Transitional care planning should include:

• Addressing any precipitating causes of worsening HF identified in the hospital
• Adjusting diuretics based on volume status, weight, and electrolytes
• Coordination of safety laboratory checks, such as electrolytes after initiation or intensification of GDMT
• Plans for GDMT optimization, including:
  • Plans for resuming medications held in the hospital
  • Plans for initiating new medications
  • Plans for titration of GDMT to goal doses as tolerated
• Reinforcing HF education and assessing adherence with medical therapy and lifestyle modifications
• Addressing high-risk characteristics, including comorbid conditions, limited psychosocial support, and impaired health literacy
• Referral to cardiac rehabilitation where appropriate
• Referral to palliative care specialists in selected patients