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Weintraub et al

Acute Heart Failure Syndromes


Table 3.

Presenting Profiles in Emergency Department Patients With AHFS

Normal or moderately elevated BP


Develop gradually (days or weeks) and are associated with systemic congestion. Radiographic pulmonary congestion may be minimal in patients with advanced HF

Low BP (90 mm Hg)


Mostly related to low cardiac output and often associated with decreased renal function.

Cardiogenic shock


Rapid onset. Primarily complicating acute MI, fulminant myocarditis, acute valvular disease.

Flash pulmonary edema


Abrupt onset. Often precipitated by severe systemic hypertension. Patients respond readily to vasodilators and diuretics.


25% of ACS have HF signs/symptoms

Rapid or gradual onset. Many such patients may have signs and symptoms of HF that resolve after resolution of ischemia.

Isolated right HF from pulmonary HTN or intrinsic RV failure (eg, infarct) or valvular abnormalities (eg, tricuspid valve endocarditis)


Rapid or gradual onset due to primary or secondary PA hypertension or RV pathology (eg, RV infarct). Not well characterized with few epidemiological data.

Postcardiac surgery HF


Occurring in patients with or without previous ventricular dysfunction, often related to worsening diastolic function and volume overload immediately after surgery and the subsequent early postoperative interval. Can also be caused by inadequate intraoperative myocardial protection resulting in cardiac injury.

Clinical Presentation


Elevated BP (160 mm Hg)


Target: volume management, improve cardiac performance (output) Therapy: diuretic or fluid administration (directed by filling pressures and cardiac index), inotropic support, mechanical assistance (IABP, VAD)

Target: cardiac output

Therapy: inotropes with vasodilatory properties (eg, milrinone, dobutamine, levosimendan); consider digoxin (intravenous and/or orally)vasopressor medicationsmechanical assist devices (eg, IABP)

Target: improve cardiac pump function

Therapy: inotropesvasoactive medicationsmechanical assist devices, corrective surgery

Target: BP, volume management

Therapy: vasodilators, diuretics, invasive or NIV, morphine¶

Target: coronary thrombosis, plaque stabilization, correction of ischemia

Therapy: reperfusion (eg, PCI, lytics, nitrates, antiplatelet agents)

Target: PA pressure Therapy: nitrates, epoprostenol, phosphodiesterase inhibitors, endothelin-blocking agents, coronary reperfusion for RV infarcts, valve surgery


Predominantly pulmonary (radiographic/clinical) with or without systemic congestion. Many patients have

preserved EF

Targets† and Therapies‡ Target: BP and volume management

Therapy: vasodilators (eg, nitrates§, nesiritide, nitroprusside) and loop diuretics

Target: volume management Therapy: loop diureticsvasodilators

ACS indicates acute coronary syndromes; AHFS, acute heart failure syndromes; EF, ejection fraction; HTN, hypertension; IABP, intraaortic balloon pump; MI, myocardial infarction; NIV, noninvasive ventilation; PA, pulmonary artery; RV, right ventricle; VAD, ventricular assist device. *Of all AHFS admissions.

  • Treating etiology or precipitant is of equal of greater importance (eg, arrhythmia, ACS, infection).

  • Represents initial therapies for early management and should be tailored to each patient’s unique presentation.

§Probably preferred in patients with ACS or history of CAD.

  • Its incidence may be related to the definition used (clinical vs radiographic).

¶Avoid if retaining CO2. Data from Gheorghiade and Pang4 and Gheorghiade et al.58

ing or decompensated chronic HF, (2) cardiogenic pulmonary edema, (3) hypertensive AHFS, (4) cardiogenic shock, (5) isolated right HF, and (6) AHFS with ACS.66 Although specific goals for each phenotype have not been well-established, in- creasing evidence suggests that hypotension and tachycardia should be avoided, especially in patients with coronary artery disease.209,210 Whether management by profile leads to im- proved short- or long-term outcomes versus current management requires further study before broad implementation.

Importantly, clinical profiles may not take into account the underlying substrate or etiology of the patient’s chronic HF. For

example, a common clinical profile is hypertensive HF, but should the presence or absence of systolic dysfunction or coronary artery disease further refine management? It has recently been suggested that patients be further classified accord- ing to the ACC/AHA stages of HF (Table 4).5,211 These stages account for the underlying substrate and promote certain thera- peutic options and considerations but whether this is important to consider in the early phase of management is not known. Further, detailed echocardiographic data regarding cardiac struc- ture and function may not be available on all patients, limiting the feasibility of directing therapy based on HF stages.

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