Nejm 2003;348:20; Circ 2001;104:2996

Cause: Acute MI; mitral stenosis; rupture of chordae, papillary muscle, or intraventricular septum; myocarditis; LV diastolic dysfunction; hypoalbuminemia; infectious or aspiration pneumonia; radiation pneumonitis; ARDS; phosgene, chlorine or smoke inhalation; septic shock; massive pulmonary embolus; hemorrhagic pancreatitis; DIC; snake venom

Pathophys: Imbalance of Starling forces (pulmonary edema develops when mean PCWP exceeds 20-25 mm Hg), increased negative interstitial pressure (edema post-rx of pneumothorax) or primary alveolar-capillary membrane damage. Noncardiogenic causes of pulmonary edema of uncertain mechanism include high-altitude pulmonary edema, neurogenic pulmonary edema, heroin overdose, eclampsia, and pulmonary edema post-cardioversion.

Sx: Acute severe dyspnea, air hunger, anxiety, terror

Si: Cough, pink sputum, diaphoresis, pallor, cyanosis, tachycardia, HT, rales, rhonchi, wheezing

Crs: Course may vary depending on etiology. Potentially reversible conditions include HT, ischemia, valvular disease, pulmonary embolus, alcohol use, and noncompliance with a diet or drug regimen.

Lab: CBC, electrolytes, BUN, creatinine and cardiac enzymes, B-type naturetic peptide (Arch IM 2004;164:1978; Nejm 2002;347;161; Jama 2002;287:1531), oximetry or ABG, echocardiogram, cardiac catheterization if ASHD is clinically likely and if an acute intervention is planned

Right heart catheterization is indicated for cardiogenic shock not improved by the administration of iv fluid, for CHF that is complicated by hypotension/shock, and for pulmonary edema suspected to be of noncardiogenic origin; see also the section in Chapter 4.

X-ray: For frank pulmonary edema. Cardiomegaly may not be present in acute cardiac disease (eg, acute MI or acute mitral regurgitation).

Rx: Acute pulmonary edema: O2 to maintain saturation > 90%; MS 2-6 mg iv q 5-10 min initially; iv loop diuretics (initial dose: furosemide 40-160 mg; bumetanide 1-2 mg; torsemide 10-20 mg iv); TNG (0.4 mg sl, 1-2 in 2% paste topically, 10-500 μgm/min iv) for angina or pre- and afterload reduction, but recall that nitrate tolerance develops rapidly with continuous administration; iv dobutamine (0.5-20 μgm/kg/min) if CO is low; dopamine (1-3 μgm/kg/min) to improve/maintain renal perfusion; iv nitroprusside (0.5-8 μgm/kg/min) for severe HT and refractory CHF (titrate dose to maintain systolic BP > 100 mm Hg); digoxin (0.25-1 mg iv loading dose) requires > 3 hr to take effect; for enalaprilat 1.25 mg iv, data on use in acute CHF are limited; thrombolytic rx or primary PTCA for acute MI; neseritide forpts unresponsive to diuretics (Lancet 2003;362:316)

Intubation/mechanical ventilation for severe hypoxia and/or respiratory acidosis; intra-aortic balloon counterpulsation for CHF and cardiogenic shock not responding to above rx, forpts with severe MR or ruptured ventricular septum, for support before/during catheterization/PTCA/CABG, or forpts with CHF awaiting heart transplantation

Circ 2000;101:558; Nejm 2000;342:1120; 1999;341:1276

Cause: See preceding section. In addition, high output failure can be seen with anemia, systemic AV fistula, hyperthyroidism, beriberi heart disease (severe thiamine deficiency), Paget’s disease, and multiple myeloma.

Afib can cause severe but reversible LV dysfunction (Circ 2004;109:2839).

Inpts with severe lung disease, RV dysfunction is present in 66%, most of whom had pulmonary vascular disease. LV dysfunction (EF < 45%) is present in only 6% (Chest 1998;113:576).

LV diastolic dysfunction is seen in hypertrophic/constrictive cardiomyopathy, constrictive pericarditis, and HT. As many as 40% ofpts with diastolic dysfunction also have systolic EF > 35% (Circ 2002;105:1387; 2002;105:1505).

Epidem: Over the past 50 yr, the incidence of CHF has declined among women but not among men (Nejm 2002;347:1397). Approximately 50% ofpts with chronic CHF are older than 70 yr. More than 50% of cases are due to ASHD. Diastolic dysfunction is also more common in elderlypts. An elevated homocysteine level is an independent predictor of development of CHF in adults without h/o prior MI (Jama 2003;289:1251).

Pathophys: Salt/water retention; constriction of peripheral resistance vessels; increased sympathetic activity and circulating catecholamines; reduction in cardiac norepinephrine stores and reduced myocardial β-adrenergic receptors; activation of renin-angiotensin-aldosterone system; redistribution of cardiac output; in diastolic dysfunction, abnormal ventricular relaxation and altered ventricular pressure/volume relationships and ventricular filling (Circ 2003;107:659; Nejm 2003;348:2007)

Sx: Fatigue, orthopnea, PND, nocturnal cough, dyspnea on exertion New York Heart functional classification:

Note that these are different stages from those in the AHA/ACC Practice Guidelines, in which Stage A representpts at risk for development of CHF, Stage Bpts have structural heart disease without CHF, Stage Cpts have heart disease with current/prior sx of CHF, and Stage Dpts have severe rest sx (Circ 2001; 104:2996).