Organ dysfunction, injury and failure in acute heart failure: from pathophysiology to diagnosis and management. A review on behalf of the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC)

Abstract

Organ injury and impairment are commonly observed in patients with acute heart failure (AHF), and congestion is an essential pathophysiological mechanism of impaired organ function. Congestion is the predominant clinical profile in most patients with AHF; a smaller proportion presents with peripheral hypoperfusion or cardiogenic shock. Hypoperfusion further deteriorates organ function. The injury and dysfunction of target organs (i.e. heart, lungs, kidneys, liver, intestine, brain) in the setting of AHF are associated with increased risk for mortality. Improvement in organ function after decongestive therapies has been associated with a lower risk for post-discharge mortality. Thus, the prevention and correction of organ dysfunction represent a therapeutic target of interest in AHF and should be evaluated in clinical trials. Treatment strategies that specifically prevent, reduce or reverse organ dysfunction remain to be identified and evaluated to determine if such interventions impact mortality, morbidity and patient-centred outcomes. This paper reflects current understanding among experts of the presentation and management of organ impairment in AHF and suggests priorities for future research to advance the field.

Keywords: Heart failure; Multiple organ failure; Venous congestion.

Figure 1

Relationships between congestion and end-organs. LV, left ventricle.

Figure 2

The pharmacological management of congestion in heart failure. Patients without congestion (i.e. normal filling pressures and no volume overload) should be managed with neurohumoral blockers, the lowest possible dose of loop diuretics, and selected therapies in cases of persistent symptoms. In congestion, it is pivotal to distinguish between the phenotype of volume overload: cardiac-type fluid accumulation (i.e. oedema, ascites, pleural effusion) or vascular-type fluid redistribution. In volume overload, the goal is to remove extracellular fluid through the use of loop diuretic therapy, which should be adequately dosed and administered i.v. Loop diuretics should often be used in combination with diuretic agents acting in other segments of the nephron. Vasodilators may be added cautiously in low cardiac output and systolic blood pressure of >90 mmHg, while avoiding a decrease in mean arterial blood pressure to <65 mmHg. Inotropes are to be used only in severe hypoperfusion. The use of ultrafiltration is limited to selected cases of refractory volume overload. In contrast, vasodilating agents (with a considerably lower dose of diuretics) are the preferred pharmacological option in vascular fluid redistribution. ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; ARNI, angiotensin receptor neprilysin inhibitor; CKD, chronic kidney disease; CRT, cardiac resynchronization therapy; GFR, glomerular filtration rate; HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction; HR, heart rate; MRA, mineralocorticoid receptor antagonist; NT-proBNP, N-terminal pro-B-type natriuretic peptide; SBP, systolic blood pressure.