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"Medical Journeys" is a set of clinical resources reviewed by physicians, meant for the medical team as well as the patients they serve. Each episode of this 12-part journey through a disease state contains both a physician guide and a downloadable/printable patient resource. "Medical Journeys" chart a path each step of the way for physicians and patients and provide continual resources and support, as the caregiver team navigates the course of a disease.

While patients may present to the hospital with acute heart failure for a variety of reasons, including acute coronary syndrome requiring urgent revascularization or inflammatory heart disease, most cases of decompensation are due to the toll of gradually rising cardiac filling pressures with preexisting structural heart disease.

Identification of common precipitating factors and the overall patient trajectory should guide therapy. These factors may include uncontrolled hypertension, atrial fibrillation, pneumonia or other acute infection, nonadherence to medications or diet, anemia, thyroid dysfunction, use of nonsteroidal anti-inflammatory drugs or other medications that increase sodium retention, and use of medications like verapamil that have a negative inotropic effect.

The primary goals of inpatient care are hemodynamic stabilization, symptom relief, and preventing short-term morbidity and mortality. The first step in triage centers on hemodynamic assessment to determine the severity of congestion and the adequacy of perfusion.

Cardiogenic Shock

Acute decompensation of chronic heart failure has overtaken acute myocardial infarction as the predominant etiology of cardiogenic shock, defined as a systolic blood pressure under 90 mm Hg along with end-organ injury.

Early recognition of cardiogenic shock is key, with initial measures including vasopressors for pharmacologic support in hypotension, followed by pulmonary artery catheterization to define hemodynamic subsets and guide management. Addition of mechanical circulatory support (MCS) is also reasonable if drugs alone aren't enough to maintain end-organ function, taking into calculation the vascular, bleeding, and neurologic complication risks along with the patient's wishes, overall prognosis, and trajectory. One recent noted MCS use in 45% of cases.

Randomized trials comparing temporary MCS devices have been hampered by small sample sizes, open-label designs, short follow-up, and use of surrogate endpoints. While randomized clinical trials have yet to show a mortality benefit from MCS in cardiogenic shock, trials are comparing intra-aortic balloon pump use, extracorporeal membrane oxygenation, the Impella device, or combinations thereof against optimal medical therapy alone.

Intravenous inotropes to increase cardiac output and improve hemodynamics are typically used, with a class 1 recommendation in the 2022 American Heart Association for treatment of heart failure. Despite limited prospective data and a "paucity" of randomized trials to guide use of IV inotropic agents, as the guidelines note, "broad availability, ease of administration, and clinician familiarity favor such agents as the first therapeutic consideration when signs of organ hypoperfusion persist despite empiric volume replacement and vasopressors."

Even without "robust evidence" of clear benefit of one inotropic agent over another in this setting, choice of agent can be guided by blood pressure, concurrent arrhythmias, and availability.

Guidelines also recommend use of multidisciplinary shock teams and early transfer to an MCS-capable center in cases of worsening end-organ perfusion.

Tackling Volume

Some research has supported the potential for of acute decompensated heart failure with ambulatory or clinic-based diuretic use, and the FDA recently approved an IV-equivalent formulation of furosemide (Furoscix) for treatment of heart failure congestion at home using a pre-filled cartridge for 5-hour subcutaneous self-administration.

However, IV diuretics are the predominant reason for admission.

In that regard, loop diuretics are the fastest and most effective to cut congestion. Optimizing decongestion often requires doubling of patients' prior oral doses, adding a thiazide diuretic, or adding a mineralocorticoid receptor antagonist with diuretic effects.

In the , bolus dosing of furosemide was similar to continuous infusion for symptoms and serum creatinine levels. A high dose 2.5 times what the patient usually took outside of the hospital was not significantly better than leaving patients on the equivalent of their prior oral dose for either symptoms or creatinine levels, but there were trends for greater improvement in symptoms and greater diuresis, albeit with transient renal function worsening.

The TRANSFORM-HF trial showed no difference in outcomes between furosemide and torsemide for hospitalized heart failure patients. However, the ADVOR trial showed that adding IV acetazolamide to loop diuretics boosted early decongestion in patients with acute decompensated heart failure.

Guidelines suggest use of IV nitroglycerin or nitroprusside as reasonable to consider for patients without systemic hypotension as an add-on to diuretic therapy for relief of dyspnea.

As these medications are adjusted with daily laboratory testing for serum electrolytes, urea nitrogen, and creatinine concentrations, treatment is also guided by careful monitoring of fluid intake and output, vital signs, standing body weight at the same time each day, along with clinical signs and symptoms of congestion and hypoperfusion.

Successful decongestion has been defined as the absence of signs of volume overload; in the trial, for example, that meant no more than trace edema, no residual pleural effusion, and no residual ascites. However, in the DOSE trial, only 15% of the patients were free from clinical congestion after 72 hours of treatment.

Even after the signs and symptoms of congestion resolve sufficiently for discharge, patients typically need to be discharged on loop diuretics, and some 25-50% need to be considered for further intervention to address residual congestion, which is linked to elevated risk for rehospitalization and death.

Chronic HF Treatment

Beyond just stabilizing patients, hospitalization is an opportunity to redirect the disease trajectory. Patients often come in on lower-than-recommended doses of guideline-directed medication for heart failure and the doses patients leave the hospital with are not often titrated after discharge.

"During the HF hospitalization, the approach to management should include and address precipitating factors, comorbidities, and previous limitations to ongoing disease management related to social determinants of health," the guidelines note.

In heart failure with reduced ejection fraction (HFrEF), the guidelines note better outcomes with optimization of recommended medical therapies, "which should be initiated or increased toward target doses once the efficacy of diuresis has been shown."

For example, the EMPULSE trial showed more than a 15 percentage point reduction in composite all-cause mortality, HF events, and HF symptoms with the SGLT2 inhibitor empagliflozin (Jardiance) started in the hospital. And starting sacubitril/valsartan (Entresto) during hospitalization for acute HFrEF improved key prognostic biomarker N-terminal pro–B-type natriuretic peptide (NT-proBNP) with a possible halving of rehospitalizations too in the PIONEER-HF trial.

While registry data have suggested slow uptake, a viewpoint article in JAMA Cardiology noting the "strong culture of clinical inertia" around HFrEF medical therapy made the case for of all of the pillars of medication, as this "may improve tolerance, adherence, and persistence."

And recent data show that's not true just for HFrEF. Starting heart failure medications before sending patients home from an acute heart failure hospitalization and rapid uptitration afterward safely improved outcomes across heart failure categories in the STRONG-HF trial, cutting 180-day heart failure readmission or death from any cause by a relative 34% compared with usual care.

A clinical decision-support intervention in the electronic medical record didn't improve prescription of heart failure medications at discharge, the placement of an implantable cardioverter-defibrillator, or referral to palliative care in the randomized trial.

Read previous installments in this series:

Part 1: Cardiomyopathy: What are the Signs, What are the Symptoms?

Part 2: Diagnosing Cardiomyopathy: History, Examination, and Testing

Part 3: Cardiomyopathy: Epidemiology, Etiology, and Pathophysiology

Part 4: Case Study: Cardiomyopathy From Epinephrine in Anesthesia

Part 5: Cardiomyopathy: Cascade Screening for Families

Part 6: Cardiomyopathy: Outside the Office

Part 7: Deciding on Implantable Cardiac Devices for Cardiomyopathy

Part 8: Case Study: The Dangerous Habit That Led to Non-Ischemic Cardiomyopathy in a Healthy Man

Part 9: What to Know About Medical Therapy for Cardiomyopathy

Up next: Common Comorbidities