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Inpatient management of acute decompensated heart failure
  1. Leah Raj1,
  2. Samuel David Maidman2,
  3. Bhavin B. Adhyaru3
  1. 1 Medicine – Cardiovascular Medicine, University of Southern California, Los Angeles, California, USA
  2. 2 Emory University School of Medicine, Atlanta, Georgia, USA
  3. 3 Medicine, Emory University, Atlanta, Georgia, USA
  1. Correspondence to Samuel David Maidman, Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA; samuel.maidman{at}


Acute decompensated heart failure (ADHF) is the leading cause of hospital admissions in patients older than 65 years. These hospitalisations are highly risky and are associated with poor outcomes, including rehospitalisation and death. The management of ADHF is drastically different from that of chronic heart failure as inpatient treatment consists primarily of haemodynamic stabilisation, symptom relief and prevention of short-term morbidity and mortality. In this review, we will discuss the strategies put forth in the most recent American College of Cardiology/American Heart Association and Heart Failure Society of America guidelines for ADHF as well as the evidence behind these recommendations.

  • Heart failure
  • acute decompensated heart failure
  • heart failure exacerbation
  • Inpatient heart failure

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Heart failure is the leading cause of hospitalisation in patients older than 65 years and hospitalisations for acute decompensated heart failure (ADHF) are associated with high risk for poor outcomes.1 In fact, more than one-third of patients die or require rehospitalisation within 90 days of discharge after treatment for ADHF.2

The Heart Failure Society of America (HFSA) enumerates therapy goals for patients admitted with ADHF, which include improving symptoms, restoring oxygenation, optimising volume status, identifying aetiology, addressing precipitating factors, optimising chronic oral therapy, minimising side effects, identifying people who would benefit from revascularisation or device therapy, identifying risk of thromboembolism and need for anticoagulation therapy and finally, effectively educating patients.1 Management of

ADHF is drastically different from the management of chronic heart failure. The latter is centred on therapies that have shown to reduce long-term mortality. For this reason, many recent heart failure-related reviews focus on evidence surrounding pharmacotherapy.3–7 In contrast, management of ADHF is based on haemodynamic stabilisation, support of oxygenation and ventilation, and symptom relief.8 Furthermore, to our knowledge, there are limited recent reviews that specifically address in-hospital management of ADHF. In this review, we present current guidelines and results of recent studies in an effort to provide a comprehensive, evidence-based approach to managing ADHF.

Indications for hospitalisation

Per HFSA guidelines (table 1), patients with heart failure and the following constellation of signs and symptoms should be admitted: hypotension, worsening renal function, altered mentation, dyspnoea at rest, haemodynamically significant arrhythmia and acute coronary syndrome (ACS).1 Admission should be considered in patients with worsening congestion, major electrolyte disturbance or associated comorbidities such as pneumonia, pulmonary embolism, diabetic ketoacidosis, symptoms suggestive of transient ischaemic accident or cerebral vascular accident, repeated implantable cardioverter-defibrillator (ICD) firings and previously undiagnosed heart failure.1 Many of these variables correlate with impending poor outcomes and, as such, are included in the Get with the Guidelines-Heart Failure (GWTG-HF) Risk Score used to predict in-hospital all-cause heart failure mortality.9

Table 1

Admission criteria based on HFSA guidelines


The most common presentation of ADHF is congestion. Often, these patients present with new or worsening dyspnoea associated with rapid accumulation of fluid in the lung. Of note, although this may be a chief complaint of the patient and relief remains a primary goal of therapy for this group of patients, it has not been found to be a reliable marker for long-term patient-centred clinical outcomes.10 Other symptoms include a swollen abdomen or extremities and the inability to lay flat. A history of orthopnoea and/or paroxysmal nocturnal dyspnoea is both sensitive and specific in ADHF. Anorexia or early satiety can be a complication of abdominal swelling and should always be inquired about, along with any change in exercise tolerance.

In regard to the physical examination, changes in vital signs can be telling of ADHF, such as tachycardia or blood pressure different from baseline. Importantly, hypotension can be a sign of severe ventricular dysfunction and cardiogenic shock (this will be discussed in the 'Low output' section). When examining the patient, signs of dyspnoea, tachypnoea and accessory muscle use should be evaluated for. Extra heart sounds, specifically S3 and S4, or changes in murmurs can be present.11 Crackles audible on lung examination would be indicative of interstitial pulmonary oedema. However, the absence of crackles does not exclude decompensated heart failure as many patients develop lymphatic drainage avoiding audible crackles on auscultation. An examination significant for wheezing can be indicative of cardiac asthma, which is associated with worse hypercapnia, but studies have shown it does not change in hospital and 1-year mortality in the elderly.12 Signs of volume overload also include elevated jugular venous pressure, which is a marker of elevated right-sided filling pressures. This is the most sensitive and specific sign of elevated left-sided filling pressures. However, this can also be found in both right or left heart dysfunction and can be absent in one-third of patients with elevated left-sided filling pressures. Unfortunately, lower extremity oedema is not as reliable and can be either present or absent in ADHF.

Imaging, such as chest radiographs, should be performed on all patients and can be used to aid in the diagnosis of congestion and as well as demonstrate the stages of heart failure in terms of lung findings. Briefly, in the acute phase, there is congestion of the vascular bed from increased capillary hydrostatic pressure.13 As this progress, fluid begins to accumulate in the interstitium around vessels and airway—protecting the alveolar spaces from alveolar oedema.13 As severity worsens, there is redistribution of fluid to upper lobes and distention of pulmonary veins, enlargement of hilar structures, Kerley lines (septal lines in the lower lung), blurring of peribronchial and perivascular margins.14 15 Cephalisation, known as redistribution, occurs with chronic pulmonary venous hypertension. Of note, cardiomegaly and pleural effusions can also be visualised.

In recent years, point-of-care ultrasound (US) has also gained popularity as an imaging modality to determine volume status for heart failure patients.16 A chest US finding of ‘lung comets’, hyperechoic reverberation artefacts, is equivalent to the standard chest X-ray finding of Kerley B lines.17 Additionally, US measurements of inferior vena cava diameter and collapsibility have been shown to provide a more accurate estimate of central venous pressures as well as possibly be a better predictor of rehospitalisation than brain natriuretic peptide (BNP) levels at presentation.18 19

Low output

ADHF can manifest as a low cardiac output state. Here, the patient complains of fatigue, decreased exercise tolerance, anorexia. The pertinent examination findings include hypotension, cognitive changes, narrow pulse pressure, pulsus alternans and cool extremities. Abnormal laboratory values include declining serum sodium and worsening renal function.


Cardiac enzymes, specifically troponins, can be measured if a myocardial infarction is suspected; however, these can also be elevated in ADHF from subendocardial ischaemia, inflammatory marker activation and increased myocardial demand from fixed coronary disease. BNP and N-terminal pro-BNP can be incredibly helpful in aiding clinical judgement when cause of symptoms is uncertain, particularly when heart failure is unlikely.20 When the ventricular myocytes are under stress, they secrete pro-hormone pre-proBNP, which is cleaved into BNP and NT-proBNP.21 Secretion of these peptides induces vasodilation, diuresis and inhibits renin and aldosterone production.21 Elevated BNP has been associated with increased mortality and cardiovascular events in all heart failure patients and can be used as a prognostic tool.22–24 In-hospital mortality is higher in patients admitted for decompensated heart failure with a BNP >1730 pg/mL compared with those with BNP <430 pg/mL.25 Additionally, a low BNP level has been demonstrated to be an effective metric in ruling out heart failure and may serve to guide against further cardiac imaging.26

Echocardiography allows visual information about left ventricle (LV) size, global and regional systolic dysfunction, diastolic dysfunction, valvular disease and pericardial disease. Some echocardiograms allow physicians to estimate right-sided heart pressures, providing more data about haemodynamics of the patient. The imaging modality also provides measurements of cardiac anatomy and function, especially left ventricular ejection fraction (LVEF). While the finding of an LVEF less than or equal to 40% is important in the classification of systolic (HFrEF) versus diastolic (HFpEF) dysfunction, in-hospital management of ADHF is symptom-driven. Nevertheless, the classification of dysfunction based on LVEF should be noted and shared with outpatient providers as no medical therapies have been definitively proven to have a mortality benefit in HFpEF.27–30


EKG findings such as negative T waves, global T wave inversions and marked QT interval prolongation are common. They are found in patients with subendocardial ischaemia from increased wall stress, high end-diastolic pressure or dressed coronary artery flow. Other aetiologies include increased sympathetic tone or electrical heterogenicity exacerbated by ischaemia, metabolic changes or catecholamines. Evidence of left ventricular hypertrophy, left atrial abnormalities or presence of atrial fibrillation can also be found on EKG.

Laboratory abnormalities

Routine laboratory tests include complete blood count to evaluate for infection or anaemia and chemistry to identify renal dysfunction from low output state or elevated pressures. Electrolyte abnormalities can be indicative of outcomes as low serum chloride at admission has been associated with impaired decongestion.31 Hypochloraemia noted 2 weeks after admission was also associated with reduced survival.31 Although not routinely used, spot urine sample has been shown to predict natriuretic response after diuretics was given.32

Aetiology of exacerbation


Dietary indiscretion and non-adherence to guideline-directed medical therapy (GDMT), especially diuretics, should always be inquired about. Non-compliance increases mortality, morbidity and the need for hospitalisation. Reviews have shown that compliance ranges from 10% to 90% in patients diagnosed with heart failure.33 Issues with compliance are incredibly multidimensional and include financial cost, access to care, access to transportation, social support and health literacy.

Cardiac deterioration

Potential life-threatening conditions, such as myocardial infarction, can also cause ADHF. Other cardiac-related aetiologies include valvular disease, either new or progressive or arrhythmias and commonly atrial fibrillation. Specifically, this arrhythmia will lead to loss of coordinated atrial contraction, compromising ventricular filling, affecting myocardial oxygenation and contractility. There could also be progression of the underlying cardiac dysfunction or transient stress-induced heart failure, known as takotsubo cardiomyopathy. Dyssynchrony caused by right ventricular pacing can also lead to ADHF. Using data from the ADHERE (Acute Decompensated Heart Failure National Registry) registry, uncontrolled hypertension was shown to be present in approximately 50% of patients admitted with ADHF.1 34 Of note, recent changes or additions of medications such as negative inotropic drugs (verapamil, nifedipine, diltiazem, certain beta-blockers) and use of non-steroidal anti-inflammatory drugs or steroids should also be investigated as they can lead to ADHF.


Cardiotoxic agents such as alcohol, cocaine and chemotherapy drugs can be found to be the culprits of ADHF, and a thorough history should be done to elicit this information.


In the hospital setting, iatrogenic causes such as intravenous fluid administration should be on the differential. The following conditions should also be considered: renal failure, anaemia, thyroid disorders, infections, uncontrolled diabetes mellitus and pulmonary emboli. Small amounts of congestion may cause significant dyspnoea in patients with pulmonary disease, such as chronic obstructive pulmonary disease (COPD). Obstructive sleep apnoea can also exacerbate heart failure (HF) by haemodynamic changes, hypoxia and fluid retention so should be screened for and treated while inpatient.1 24

In-hospital modifications to standard therapy

Salt and fluid restriction

Similar to the home setting, a low sodium diet (2 g daily) is recommended for hospitalised patients.35 36 A fluid restriction of <2 L per day should also be implemented. Evidence for salt and fluid restriction, in addition to other non-pharmacological interventions for ADHF, is presented in table 2.

Table 2

Evidence-based non-pharmacological interventions


Supplemental oxygen therapy via a nasal cannula, facemask or assisted ventilation should be given to patients to treat hypoxaemia with SpO2 <90%. If there is concern for respiratory distress or evidence of respiratory acidosis or persistent hypoxia on a nasal cannula or facemask, then non-invasive ventilation (NIV) should be attempted (if there are no contraindications such as altered mental status, facial or neurological surgery/trauma, upper airway obstruction, inability to protect airway or clear secretions or risk for aspiration).37 It has been shown that in patients with cardiogenic pulmonary oedema, NIV improves dyspnoea, hypercapnia and acidosis, decreases incidence of intubation and decreases mortality. Multiple meta-analysis have examined the outcomes of utilising NIV in patients suffering from cardiogenic pulmonary oedema and have shown that compared with standard therapy, NIV reduces the need for intubation and decreases mortality.38–40 If patients with respiratory failure have contraindications to NIV or do not improve, they should be intubated for mechanical ventilation in attempts to keep arterial oxygen saturation >90%.41

Oxygen supplementation is not recommended in patients without hypoxaemia as it has been shown to cause vasoconstriction and decreased cardiac output. In a small trial of 13 patients diagnosed with left ventricular systolic dysfunction, supplemental oxygen was studied compared with mechanical air. These patients were randomised into a double-blinded study either receiving supplements oxygen 40% FiO2 with non-rebreather mask or mechanical air. First, it was found that cardiac output fell by 0.5 L on high flow oxygen compared with 0.02 L on mechanical air. Second, supplemental oxygen also increased systemic vascular resistance.42


During hospital stay for ADHF, home oral diuretics are held as most patients receive intravenous diuretics. This will be discussed below.

Intravenous iron supplementation

The most recent American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend intravenous iron supplementation in all heart failure patients with iron deficiency.24 Patients do not necessarily need to be anaemic to have improvement in heart failure symptoms.43 While cheaper and more accessible, oral iron supplementation has unfortunately not been demonstrated to provide similar benefits.44

Guideline-directed medical therapy

In patients with HFrEF experiencing a symptomatic exacerbation of heart failure requiring hospitalisation, it is recommended that GDMT be continued in the absence of haemodynamic instability or contraindication.24 ACE inhibitors, angiotensin receptor blockers (ARB), angiotensin receptor-neprilysin inhibitors (ARNI), aldosterone antagonists and beta-blockers have been shown to be well tolerated and result in better outcomes.45–48 ARNI is a new drug class that prevents the breakdown of vasoactive proteins, including natriuretic peptide and bradykinin levels, thereby preventing maladaptive remodelling, vasoconstriction and sodium retention. Compared with ACE inhibitors, ARNIs are superior in decreasing symptoms and physical limitations of heart failure as well as HF-related rehospitalisation and death.48 Initiation of beta-blocker therapy is recommended after optimisation of volume status and successful discontinuation of intravenous diuretics, vasodilators and inotropic agents. When initiated, it should be at low dose and only in stable patients. The most recent ACC/AHA guidelines also recommend starting the ‘funny current’ inhibitor, Ivabradine, in cases where heart rate remains >70 beats per minute on the maximally tolerated dose of beta-blockers or if this drug class is contraindicated.24 This new addition comes after the SHIFT Trial (Systolic Heart failure treatment with the I f inhibitor ivabradine Trial) found Ivabradine use to have lower rates of cardiovascular death and HF-related hospital admission compared with placebo.49

ACE inhibitors, ARBs, ARNIs or aldosterone antagonists can be temporarily held if patients suffer from renal dysfunction and should be restarted when kidney function has improved. Withholding beta-blocker therapy should be considered only in those patients that have been hospitalised after initiation of a beta-blocker, recent up titration of dose, significant volume overload or low cardiac output. The 2009 B-CONVINCED Trial (Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode) demonstrated that continuing beta-blockers in patients who had been on a stable dose for more than 1 month was not associated with delayed or lesser improvement.50

Management of heart failure

The haemodynamic profile of patients with heart failure can help guide management. All patients can be classified into one of four groups (figure 1).51

Figure 1

Patients with acute decompensated heart failure can be classified by congestion and perfusion status based on information collected through history and physical examination. Proper identification of haemodynamic status is crucial in guiding clinical decision-making and selection of medical therapies.

As described above, patients who present with congestion will have evidence of orthopnoea, high jugular venous pressure, increasing S3, loud P2, oedema, ascites or rales.51 Patients with low perfusion will have signs of narrow pulse pressure, pulsus alternans, cool extremities, poor mentation, symptomatic hypotension, declining serum sodium level or worsening renal function.51 Each patient should be evaluated for congestion and perfusion, and based on these findings, appropriate therapies can be initiated. For example, those without signs of congestion and adequate perfusion (‘warm and dry’) can be treated with GDMT outpatient. Those with congestion and appropriate perfusion (‘warm and wet’) are treated with diuretics and vasodilators in the inpatient setting. Inotropes should be started in those patients presenting without congestion, but with poor perfusion (‘cold and dry’). Diuretics should be added to inotropic therapy when patients have signs of poor perfusion in addition to congestion (‘cold and wet’). Evidence-based pharmacological therapies are presented in table 3.

Table 3

Evidence-based pharmacological treatment strategies

Inpatient monitoring

HFSA guidelines recommend daily monitoring of vital signs (including orthostatic blood pressure) and at least daily monitoring of weight, fluid intake and output, symptoms and signs of congestion, serum electrolytes, blood urea nitrogen (BUN), serum creatinine, signs of metabolic alkalosis and oxygen saturation until values are stable. Telemetry is continued for at least 24–48 hours and discontinued once the patient’s haemodynamics, medication regimen and electrolytes are stable.1


Patients with ADHF and evidence of volume overload should be treated with intravenous diuretics.24 36 It has been shown that with each 4-hour delay in initiation of intravenous diuretics, the risk of in-hospital death increases for patients with BNP >865.52 First-line diuretic therapy for patients with ADHF is intravenous loop diuretics compared with oral diuretics since the bioavailability of oral furosemide (loop diuretic) is variable depending on situation and patient. In the ADHERE database, 88% of patients received intravenous loop diuretics during their hospitalisation.53 Loop diuretics increase natriuresis and diuresis by acting at the thick ascending limb of the loop of Henle. By inhibiting reabsorption of sodium and chloride via the sodium, potassium and chloride pump, they shift the balance of osmotic forces towards fluid secretion in the collecting system.54 Intravenous furosemide has a short duration of action—peak effect in 1–2 hours and lasts for ~6 hours. Often, dosing the intravenous diuretic at least two times per day is the best approach. Typically, patients treated with loop diuretics chronically will need a higher dose in the acute setting, roughly 2.5 times their oral dose at home. However, careful use of loop diuretics is important. In the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE), there was an increase in mortality with escalating loop diuretic doses, especially above 300 mg/day of furosemide.55 There are other loop diuretics including torsemide and bumetanide. Furosemide is the least expensive; however, bumetanide produces more natriuresis than either furosemide or torsemide. Unfortunately, there are no significant clinical trials to guide practice.56

Some patients will present with renal dysfunction causing the effects of diuretics to be diminished. In these cases, higher diuretic doses can be used or even adding a second diuretic, typically a thiazide can also be considered. Thiazides act on the distal convoluted tube to block Na, K, ATPase and NaCl transport.57 They are less potent than loop diuretics, but have a synergistic effect with them where sodium reabsorption is blocked in two sections of the nephron leading to more diuresis.58 Chlorothiazide is the only thiazide that can be dispensed intravenously. Hydrochlorothiazide and metolazone are oral thiazides. Unfortunately, there are limited data studying the use of thiazide diuretics and loop diuretics as combination therapy and these studies are limited by power, design, population and primary endpoints.59

Instead of bolus dosing as described above, a continuous infusion of the loop diuretic can be an option in patients. This method provides a steady drug level in the renal tubules. The Diuretic Optimisation Strategies Evaluation (DOSE) Trial examined the effect of various doses of furosemide as well as bolus versus continuous infusion on patients’ symptoms, changes in body weight, net fluid loss, renal function, biomarkers, rehospitalisation and death. The study found no difference in patient’s symptoms or renal function in those who received bolus versus continuous infusions of diuretics. Second, there was no trend towards greater improvement in symptoms in the high-dose group than in the low-dose group. However, high-dose furosemide resulted in greater net fluid loss, weight loss and relief from dyspnoea.60 Overall, diuretics need to be carefully monitored as they can cause excessive urine output, hypotension, rise in BUN and creatinine concomitantly with reduced potassium and magnesium levels.

Vasopressin antagonists, most commonly tolvaptan, were developed to block arginine vasopressin receptors at the renal tubules to enhance aquaresis.61 In addition to promote diuresis, vasopressin antagonists improve serum sodium in hypervolaemic, hyponatremic states. The Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Congestive Heart Failure (ACTIVCHF) trial evaluated the effect of tolvaptan in ADHF as adjunct therapy. It showed that tolvaptan resulted in greater weight reduction at 24 hours without adverse renal effects compared with placebo.62 The EVEREST trial (Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study With Tolvaptan) examined adding tolvaptan to conventional diuretics.63 Here, Tolvaptan improved some heart failure symptoms such as weight, peripheral oedema and dyspnoea. However, on day 7, ‘global clinic status’ had not improved. Compared with placebo, serious adverse events, including renal dysfunction, hypotension and electrolyte abnormalities were similar in both groups.63 One of the most recent trials examining the effects of vasopressin antagonists as adjunct therapy in patients with ADHF, the Targeting Acute Congestion with Tolvaptan in Congestive Heart Failure trial (TACTICS), showed no improvement in dyspnoea in those patients treated with tolvaptan. This therapy remains controversial given that the long-term safety and benefits are unknown. According to the ACC/AHA guidelines, short-term use of vasopressin antagonist in patients with volume overload and severe hyponatremia with cognitive symptoms is reasonable.24 36

Relaxin is a natural human peptide vasodilator. It acts in multiple ways, but it has been studied in heart failure given its ability to activate nitric oxide and cause vasodilation leading to increased cardiac output and renal perfusion. The Efficacy and Safety of Relaxin for the Treatment of Acute Heart Failure trial (RELAX-HF) looked at serelaxin (recombinant human relaxin-2) in patients diagnosed with ADHF, with variable left ventricular function, and systolic blood pressure >125 mm Hg. Patients received serelaxin compared with placebo in addition to standard care. It showed that in patients treated with serelaxin, the length of hospital stay was reduced and cardiovascular death and all-cause mortality were decreased, but improvements in dyspnoea were variable.64 65 However, this pharmacological therapy is not yet approved by the ACC/AHA or HFSA for treatment of ADHF.

The synthetic renal natriuretic peptide analogue, ularitide, has been the subject of more recent studies. Like others of the same class, the agent results in vasodilation, inhibition of the renin–angiotensin–aldosterone system and inhibition of renal sodium reabsorption.66 The Trial of Ularitide Efficacy and Safety in Acute Heart Failure (TRUE-AHF) sought to determine whether early administration of the drug would sufficiently reduce myocardial-wall stress to provide a mortality benefit. Compared with placebo, ularitide showed significant decreases in systolic blood pressure as well as NT-proBNP levels. Increases in serum creatinine and hematocrit at the time of infusion also suggest a hemoconcentration effect. However, the drug did not demonstrate a benefit in cardiac troponin T levels nor mortality.67 Accordingly, ularitide use has not yet been adopted in any society guidelines.


Based on current guidelines, ultrafiltration is reserved for patients with fluid overload who do not achieve an adequate response to an aggressive diuretics regimen.24 36 68 It works via moving water and solutes across a semipermeable membrane. The efficacy of this therapy has been evaluated in several trials. In the Ultrafiltration vs Intravenous Diuretics for Patients Hospitalised for Acute Decompensated Heart Failure trial (UNLOAD), 200 patients hospitalised for ADHF were randomly assigned to ultrafiltration or intravenous diuretics. At 48 hours, patients assigned to ultrafiltration had greater fluid loss, 4.6 L compared with 3.3 L. At 90 days, patients assigned to ultrafiltration had fewer rehospitalisations and fewer unscheduled clinic visits.69 However, in the Ultrafiltration in Decompensated Heart Failure with Cardiorenal Syndrome trial (CARRESS-HF), ultrafiltration was inferior to pharmacological therapy due to increase in serum creatinine in the ultrafiltration group in contrast to a fall in mean serum creatinine in the pharmacological therapy group.70 Based on these inconsistent findings, use of ultrafiltration has diminished.

Indications for haemodynamic monitoring

There are several methods of monitoring haemodynamics—non-invasive arterial blood pressure, central venous pressure and use of a pulmonary artery catheter are among a few. The pulmonary artery catheter is able to measure central venous pressure, pulmonary artery pressure, cardiac index and mixed venous oxygen saturation. As a class I recommendation, invasive haemodynamic monitoring with a pulmonary artery catheter should be performed to guide therapy in patients who have respiratory distress or clinical evidence of impaired perfusion where the adequacy or excess of intracardiac filling pressures cannot be determined from examination. The routine use of invasive haemodynamic monitoring in patients with ADHF is not recommended by the HFSA or recent ACC/AHA guidelines.


In patients with elevated filling pressures or increased LV afterload, vasodilators can be used. Nitrates, which are known to dilate the venous more than arterial circulation, are the most commonly used vasodilators in this population. At higher doses, nitrates lower systemic vascular resistance and LV afterload. This benefits the patient by increasing stroke volume and cardiac output. Per ACC/AHA guidelines, if symptomatic hypotension is absent, intravenous nitroglycerin nitroprusside or nesiritide may be considered an adjuvant to diuretic therapy for relief of dyspnoea in patients admitted with ADHF.24 36 Furthermore, a combination of isosorbide dinitrate and hydralazine is recommended for African–Americans due to a shown reduction in morbidity and mortality.71

Nitroglycerin is a typical intravenous nitrate that can be used for this by venodilating, lowering preload and reducing pulmonary congestion. Tachyphylaxis can occur within hours of high-dose nitroglycerin, which can lead to significant haemodynamic changes and it is sometimes avoided in patients with right ventricle infarctions or aortic stenosis, when side effects of hypotension can also lead to serious decompensation.

Another nitrate, nitroprusside, affects both arterial and venous vessels similarly. Its effects lead to decreased pulmonary capillary wedge pressure (PCWP) almost instantly leading to decrease LV filling pressure and decreased systemic vascular resistance (SVR). In patients, where SVR is elevated, the decrease in afterload will cause increased stroke volume while maintaining blood pressure. In contrast to patients with normal SVR, it can cause hypotension. In patients with depressed stroke volume from elevated LV afterload, such as acute aortic and mitral regurgitation, ventricular septal rupture or hypertensive emergency, nitroprusside’s ability to arterial dilatation and afterload reduction can be crucial. Side effects include the metabolism of nitroprusside to cyanide, reflex tachycardia and rebound vasoconstriction after discontinuing the therapy.72 Therefore, it is only used for 24–48 hours before discontinuing.

Similarly, nesiritide dilates both arterial and venous systems. It is less potent than nitroprusside, but has a longer half-life. It is a peptide similar to human BNP, which leads to dose-dependent reductions in filling pressures, systemic and pulmonary vascular resistance, and increased cardiac output.73–76 The largest randomised trial of the routine use of nesiritide in patients with ADHF is ASCEND-HF (Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure). It found that nesiritide helped reduce dyspnoea, but had increased rates of hypotension, and did not alter rates of death, rehospitalisation at 30 days or renal function.77 The Vasodilator in the Management of Acute Heart Failure (VMAC) study was a multicentre, randomised, double-blinded controlled trial of nesiritide, nitroglycerin and standard therapy in patients hospitalised for worsening HF. The primary endpoints of the VMAC trial were a change in PCWP and dyspnoea score. Trial results showed that the combination of nesiritide plus standard therapy significantly decreased PCWP and dyspnoea score at 3 hours compared with standard therapy alone. It also lowered the PCWP more than nitroglycerin.78 Side effects of nesiritide to monitor for include hypotension, headache and worsening renal function.

Thus far, there are no data to suggest that intravenous vasodilators improve outcomes in patients with ADHF; therefore, its use is limited to improving dyspnoea in patients with normal blood pressure.


Intravenous inotropes can be considered in patients with advanced heart failure and poor peripheral perfusion to relieve symptoms and improve end-organ function. In this low output state, patients with ADHF usually have systolic blood pressure <90 mm Hg or are unresponsive/intolerant of intravenous vasodilators. Based on the ACC/AHA guidelines, temporary intravenous inotropic support is recommended in patients with cardiogenic shock to maintain systemic perfusion and preserve end-organ performance until definitive therapy or resolution of the acute precipitating problem.24 36 Short-term inotropic support may be reasonable as bridge therapy while awaiting mechanical circulatory support or cardiac transplantation in patients with stage D heart failure refractory to GDMT and device therapy.24 36 Finally, long-term continuous inotropes may be considered as palliative therapy for symptom control in those who are not eligible for either mechanical circulatory support or cardiac transplantation who suffer from stage D HF despite optimal GDMT and device therapy.24 36

Use of this therapy requires continuous or frequent blood pressure monitoring and continuous monitoring of cardiac rhythm. If symptomatic hypotension or worsening tachyarrhythmias develop, dose reduction or discontinuation is suggested. Inotropes are not indicated for patients with ADHF with preserved systolic function. Side effects of inotropes include ischaemia from an increased heart rate and myocardial oxygen consumption. It can also lead to atrial and ventricular arrhythmias.79 80

Dopamine dilates renal and mesenteric artery beds by acting on dopamine-1 receptors. It also stimulates β1 adrenergic receptors to increase stroke volume and therefore cardiac output. However, at higher doses it can stimulate α-adrenergic receptors leading to increased heart rate and peripheral vasoconstriction. In the Dopamine in Acute Decompensated Heart Failure (DAD-HF) trial, it was shown that low-dose furosemide and low-dose dopamine may be as effective as high-dose furosemide for diuresis and dyspnoea reduction and can also reduce worsening renal function in patients with ADHF.81 Most recently, the Low-Dose Dopamine or Nesiritide in Acute Heart Failure (ROSE-HF) trial showed that neither inotrope in addition to diuretics improves markers of decongestion or renal function in patients with ADHF.82

Dobutamine acts mainly on β1 adrenergic receptors and minimally on β2 and α1 receptors. These effects lead to increases in stroke volume and cardiac output with decreases in systemic vascular resistance and PCWP. There are limited data studying dobutamine’s effect on patients with ADHF. However, a non-randomised retrospective study from ADHERE registry showed that milrinone and dobutamine were associated with increased mortality compared with vasodilators in patients being treated for ADHF.83

Milrinone is a phosphodiesterase inhibitor that increases myocardial inotropy by inhibiting degradation of cyclic AMP. It can also reduce systemic and pulmonary vascular resistance and improve LV diastolic compliance. These effects lead to increases in cardiac index and decreases in LV afterload and filling pressures. Of note, beta-blocker therapy can be continued since milrinone does not act on β-receptors such as dobutamine and dopamine. Side effects of this drug include tachyarrhythmias, hypotension and thrombocytopenia. Like all inotropes, the role of milrinone is limited and is used for temporary symptomatic improvement or as bridge to cardiac transplantation. The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) study showed that milrinone has no apparent clinical benefit in patients with decompensated systolic heart failure.84


Norepinephrine, high-dose dopamine or vasopressin can be used in patients with ADHF and hypotension in attempts to preserve systemic blood pressure and end-organ perfusion. It should be noted that this would increase afterload and then consequently decrease cardiac output.85

Discharge planning

Deliberate discharge planning will reduce the risk of postdischarge mortality and readmission. Reducing potential exacerbation factors, achieving a euvolemic state and optimising GDMT should be prioritised on discharge.68 Often an outpatient diuretic regimen must be improved and some suggest transitioning from intravenous to oral diuretics 1 to 2 days before discharge. A study examining 30 000 patients hospitalised for decompensated heart failure showed that the rate of 30-day hospital readmission was higher in hospitals with the lowest rates of early follow-up.86 In 2016, another study was published showing that outpatient follow-up within 14 days after emergency department visit or hospitalisation is associated with better outcomes.87 Finally, all medications, dietary fluid and salt restriction, appropriate follow-up, adherence, daily weight measurements should be discussed with the patient as well as provided as written instructions.


Even with it being an exceptionally frequent reason for admission and a core condition taught during internal medicine training, ADHF remains one of the most difficult inpatient conditions to appropriately manage. Following a detailed work-up consisting of a history, physical, laboratory studies and imagining studies, all patients should be evaluated for congestion and perfusion status. Evidence-based pharmacological therapy should then be selected accordingly, with inotropes used in cases of decreased perfusion and preload reducing agents directed towards congestion. Once haemodynamically stabilised, GDMT and reoccurrence prevention should be prioritised during discharge planning.

Self-assessment questions

  • Which of the following is not an indication for admission based on HFSA guidelines?

    1. Hypotension

    2. Worsening renal function

    3. Altered mental status

    4. Dyspnoea on exertion

  • All of the following can be an aetiology of decompensated heart failure except for

    1. Arrhythmia

    2. Cocaine

    3. Obesity

    4. Infection

  • What type of diuretic is first-line therapy for a patient admitted for ADHF?

    1. Furosemide

    2. Hydrochlorothiazide

    3. Lisinopril

    4. Zaroxolyn

  • In regard to discharge planning, evidence has shown that 30-day readmission rates are lower with which of the following intervention?

    1. Outpatient follow-up within 14 days

    2. Weight loss

    3. Fluid and salt restriction

    4. Exercise

  • Name one indication for invasive haemodynamic monitoring:

    1. Clinical evidence of impaired perfusion where the adequacy or excess of intracardiac filling pressures cannot be determined from physical examination

    2. All patients with ADHF

    3. New onset heart failure

    4. Cardiogenic shock

Main messages

  • Therapy for patients with heart failure should be based on the status of their perfusion and congestion. Patients with low perfusion will have signs of narrow pulse pressure, pulsus alternans, cool extremities, poor mentation, symptomatic hypotension, declining serum sodium level or worsening renal function. Patients who present with congestion will have evidence of orthopnoea, high jugular venous pressure, increasing S3, loud P2, oedema, ascites or rales.

  • Based on recent data, there is no difference in patient’s symptoms or renal function when given bolus versus continuous infusions of diuretics.

  • There are no data to suggest that intravenous vasodilators improve outcomes in patients with acute decompensated heart failure; therefore, its use is limited to improving dyspnoea in patients with normal blood pressure.

  • Several studies have shown that close follow-up in clinic helps to reduce readmission rates and is associated with better outcomes.

Current research questions

  • Acute decompensated heart failure (ADHF) encompasses several forms of heart failure including new-onset heart failure, worsening chronic heart failure, decompensated heart failure caused by comorbidities, non-adherence or toxins. To make this diagnosis even more complicated, patients that present with symptoms of ADHF can also be linked to other conditions such as acute coronary syndrome and chronic obstructive pulmonary disease. Unfortunately, this can cause delays in diagnosing and initiating therapies. Early identification is a vital area for future research. Which research approach should this be targeting, whether it be laboratory tests or imaging modality?

  • Prognostic models have been developed from trials and registries to aid with the management of heart failure. Wouldn’t further development and utilisation of these tools aid in identifying patients at high risk for short-term or long-term mortality? These patients can benefit from more aggressive therapies that are available.

  • Almost $40 billion was spent in the USA for management of heart failure. A significant majority of this expense comes from hospitalisations. As the number of patients diagnosed with heart failure increases every year, leading to more admissions. What areas of research can we turn attention towards to limit costs of this life-threatening condition?

Key references

  • Heart Failure Society of A, Lindenfeld J, Albert NM, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail 2010;16:e1-194.

  • Writing Committee M, Yancy CW, Jessup M, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation 2013;128:e240-327.

  • Felker GM, Lee KL, Bull DA, et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med 2011;364:797–805.

  • McAlister FA, Youngson E, Kaul P, et al. Early Follow-Up After a Heart Failure Exacerbation: The Importance of Continuity. Circ Heart Fail 2016;9.

  • Yancy CW, Jessup M, Bozkurt B, et al. 2017ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. J Card Fail 2017;23:628–51 doi: 10.1016/j.cardfail.2017.04.014.


  • (A) True (B) True (C) True (D) False

  • (A) False (B) False (C) True (D) False

  • (A) True (B) False (C) False (D) False

  • (A) True (B) False (C) True (D) False

  • (A) True (B) False (C) False (D) False



  • Contributors LR wrote the review article. SDM wrote, edited and submitted the review article. BBA conceived of, supervised and edited the review article.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.