p.67 抽出テキスト

Circulation. 2022;145:e895–e1032. DOI: 10.1161/CIR.0000000000001063 May 3, 2022 e961 CLINICAL STATEMENTS AND GUIDELINES

cy of perfusion.1–5 The diagnosis of cardiogenic shock warrants consideration of recommendations in Section 9.5, “Evaluation and Management of Cardiogenic Shock,” but any concern for worsening hypoperfusion should also trigger involvement of the multidisciplinary team for hemodynamic assessment and intervention. Initial triage includes recognition of patients with ACS for whom urgent revascularization may be indicated. In the absence of ischemic disease, recent onset with accelerating hemodynamic decompensation may represent inflammatory heart disease, particularly when accompanied by conduction block or ventricular arrhythmias.7,8 However, most HF hospitalizations for decompensation are not truly “acute” but follow a gradual increase of cardiac filling pressures on preexisting structural heart disease, often with precipitating factors that can be identified3,6 (Table 21). Some patients present with pulmonary edema and severe hypertension, which require urgent treatment to reduce blood pressure, more commonly in patients with preserved LVEF. Patients require assessment and management of ischemia, arrhythmia and other precipitating factors and comorbidities. The presenting profile, reversible factors, appropriate workup for the cause of HF including ischemic and nonischemic causes, comorbidities, and potential for GDMT titration inform the plan of care to optimize the disease trajectory.5

Recommendation-Specific Supportive Text

1.   and 2.  Most patients admitted with HF have clinical evidence of congestion without apparent hypoperfusion.1–5,9,10 Although elevations of right- and left-sided cardiac filling pressures are usually proportional in decompensation of chronic HF with low EF, up to 1 in 4 patients have a mismatch between right- and left-sided filling pressures.9–11 Disproportionate elevation of right-sided pressures, particularly with TR, hinders effective decongestion. Disproportionate elevation of left-sided filling pressures may be underrecognized as the cause of dyspnea in the absence of jugular venous distention and edema. Elevated natriuretic peptides can help identify HF in the urgent care setting but with less utility in certain situations, including decreased sensitivity with obesity and HFpEF and decreased specificity in the setting of sepsis. Resting hypoperfusion is often underappreciated in patients with chronic HF but can be suspected from narrow pulse pressure and cool extremities1,9 and by intolerance to neurohormonal antagonists. Elevated serum lactate levels may indicate hypoperfusion and impending cardiogenic shock.12 When initial clinical assessment does not suggest congestion or hypoperfusion, symptoms of HF may be a result of transient ischemia, arrhythmias, or noncardiac disease such as chronic pulmonary disease or pneumonia, and more focused hemodynamic assessment may be warranted. Assessment of arrhythmia, device profiles such as percent LV pacing versus RV pacing in patients with CRT, and device therapy and shocks in patients with ICD can provide important information. 3.	 Hospitalization for HF is a sentinel event that signals worse prognosis and the need to restore hemodynamic compensation but also provides key opportunities to redirect the disease trajectory. 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.1 Patients require assessment and management of ischemia, arrhythmia, and other precipitating factors and comorbidities. The presenting profile, reversible factors, appropriate work-up for cause of HF including ischemic and nonischemic causes, comorbidities, disease trajectory, and goals of care should be addressed. Establishment of optimal volume status is a major goal, and patients with residual congestion merit careful consideration for further intervention before and after discharge, because they face higher risk for rehospitalization and death.2–5 The disease trajectory for patients hospitalized with reduced EF is markedly improved by optimization of recommended medical therapies, which should be initiated or increased toward target doses once the efficacy of diuresis has been shown.13,14

Table 21.  Common Factors Precipitating HF Hospitalization With Acute Decompensated HF ACS Uncontrolled hypertension AF and other arrhythmias Additional cardiac disease (eg, endocarditis) Acute infections (eg, pneumonia, urinary tract) Nonadherence with medication regimen or dietary intake Anemia Hyper- or hypothyroidism Medications that increase sodium retention (eg, NSAID) Medications with negative inotropic effect (eg, verapamil) ACS indicates acute coronary syndrome; AF, atrial fibrillation; HF, heart failure; and NSAID, nonsteroidal anti-inflammatory drug.

Downloaded from http://ahajournals.org by on October 7, 2026