Initial plan

• Vitals + trajectory: oxygen need, telemetry when appropriate, standing weight, strict I/Os, JVP, edema, perfusion exam, and recent dry weight.
• Core testing: EKG, chest X-ray, BMP, Mg, CBC, LFTs, BNP or NT-proBNP. Add troponin when ischemia or myocardial injury matters clinically.
• New or unexplained HF: review TSH and iron studies, medications/toxins, family history, ischemic risk, valve disease, and possible inflammatory/infiltrative cardiomyopathy when the phenotype suggests it.
• TTE: obtain for new HF, unknown EF, meaningful clinical change, new murmur/valve concern, new wall-motion concern, RV failure, or a course that does not fit the known cardiac history.
• Do not repeat a good recent TTE automatically when the admission is straightforward and nothing clinically important has changed.

Decongestion

• Diuretic-naive: furosemide about 40 to 80 mg IV daily is a usual starting range, adjusted for congestion, kidney function, age, and prior response.
• Already on a loop: convert the total daily outpatient dose to oral furosemide equivalent and give about 1 to 2.5 times that total daily dose IV.
• Bolus vs infusion: either is reasonable. Bolus every 8 to 12 hours is common. Continuous infusion is not automatically superior.
• Do not repeat a clearly ineffective dose. Escalate the dose and reassess.

Diuretics

When loop is not enough

The creatinine bump

• Still wet + still warm: keep decongesting while following the full trajectory.
• Creatinine rising + cold/hypotensive/oliguric: reassess perfusion and hemodynamics immediately.
• Creatinine rising unexpectedly: check nephrotoxins, obstruction, sepsis, contrast, medication changes, and whether the patient is actually intravascularly depleted.

Hypertensive pulmonary edema and vasodilators

• IV nitroglycerin can be useful as an adjunct to diuresis when there is no systemic hypotension, particularly with marked hypertension, ischemia, or acute pulmonary edema.
• Nitroprusside is a selected afterload-reduction strategy for severe afterload excess or regurgitant valve physiology when BP and monitoring permit.
• These are primarily symptom/hemodynamic tools. They have not shown a durable mortality benefit in routine ADHF.
• If the patient is cold or hypotensive, vasodilators are usually the wrong direction.

When RHC actually helps

Routine invasive hemodynamics do not improve outcomes in every HF admission. Use RHC when the answer will actually change management.

• Shock or low-output physiology with unclear filling pressures or cardiac output
• Persistent symptoms despite escalating diuresis when congestion vs underfilling is unclear
• Worsening renal function when the hemodynamic cause is unclear
• Suspected severe pulmonary HTN, RV failure, or mixed pre/postcapillary physiology
• Need for inotropes/vasopressors or planning advanced HF therapy, transplant, LVAD, or mechanical support

GDMT during the admission

• HFrEF: Once the patient is hemodynamically stable, aim to leave with low tolerated doses of the major disease-modifying classes rather than maximizing one drug while the others remain absent.
• HFpEF: decongest first, then use disease-modifying therapy and comorbidity treatment deliberately
  • The July 2026 ACC HFpEF pathway includes SGLT2 inhibitors, MRAs, selected ARNI/ARB use, and phenotype-directed cardiometabolic therapy, including GLP-1's
  • Control HTN, AF, CAD, CKD, obesity, diabetes, and OSA

Discharge