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abdominal pressure Se/Sp 73/87% for RA >8 and Se/Sp 55/83% for PCWP >15 ( AJC 1990;66:1002)
Abnl Valsalva response: square wave (↑ SBP w/ strain), no overshoot (no ↑ BP after strain)
S 3 (in Pts w/ HF → ~40% ↑ risk of HF hosp. or pump failure death; NEJM 2001;345:574)
rales, dullness at base 2° pleural effus. ( often absent in chronic HF due to lymphatic compensation) ± hepatomegaly, ascites and jaundice, peripheral edema
• Perfusion (“warm” vs . “cold”)
narrow pulse pressure (<25% of SBP) → CI <2.2 (91% Se, 83% Sp; JAMA 1989;261:884)
soft S 1 (↓ dP/dt), pulsus alternans, cool & pale extremities, ↓ UOP, muscle atrophy
• ± Other: Cheyne-Stokes resp., abnl PMI (diffuse, sustained or lifting depending on cause of HF), S 4 (diast. dysfxn), murmur (valvular dis., ↑ MV annulus, displaced papillary muscles) Evaluation for the presence of heart failure
• CXR (see Radiology insert): pulm edema, pleural effusions ± cardiomegaly, cephalization, Kerley B-lines • BNP/NT-proBNP can help exclude HF; levels ↑ w/ age, ↓ w/ obesity, ↓ renal fxn, AF
• Evidence of ↓ organ perfusion: ↑ Cr, ↓ Na, abnl LFTs • Echo (see inserts): ↓ EF & ↑ chamber size → systolic dysfxn; hypertrophy, abnl MV inflow, abnl tissue Doppler → ? diastolic dysfxn; abnl valves or pericardium; estimate RVSP
• PA catheterization: ↑ PCWP, ↓ CO and ↑ SVR (in low-output failure) Evaluation of the causes of heart failure
• ECG: evidence for CAD, LVH, LAE, heart block or low voltage (? infiltrative CMP/DCMP) • Coronary angio (or noninvasive imaging, eg, CT angio); if no CAD, w/u for CMP
    Precipitants of acute heart failure
• Dietary indiscretion or medical nonadherence (~40% of cases) • Myocardial ischemia or infarction (~10–15% of cases); myocarditis • Renal failure (acute, progression of CKD, or insufficient dialysis) → ↑ preload • Hypertensive crisis (incl. from RAS) , worsening AS → ↑ left-sided afterload • Drugs (bB, CCB, NSAIDs, TZDs), chemo (anthracyclines, trastuzumab), or toxins (EtOH) • Arrhythmias; acute valvular dysfxn (eg, endocarditis), esp. mitral or aortic regurgitation • COPD or PE → ↑ right-sided afterload; anemia, systemic infection, thyroid disease Treatment of acute decompensated heart failure
• Assess degree of congestion & adequacy of perfusion • For congestion : “LMNOP”
L asix IV w/ monitoring of UOP; total daily dose 2.5× usual daily PO dose → ↑ UOP, but transient ↑ in renal dysfxn vs. 1× usual dose;  clear diff between cont gtt vs. q12h dosing ( NEJM 2011;364:797)
M orphine (↓ sx, venodilator, ↓ afterload)
N itrates (venodilator)
O xygen ± noninvasive vent (↓ sx, ↑ P a O 2 ; no ∆ mortality; see “Mechanical Ventilation”)
P osition (sitting up & legs dangling over side of bed → ↓ preload)

• For low perfusion , see below • Adjustment of oral meds
ACEI/ARB: hold if HoTN, consider Δ to hydralazine & nitrates if renal decompensation
βB: reduce dose by at least ½ if mod HF, d/c if severe HF and/or need inotropes
    Treatment of advanced heart failure ( Circ 2009;119:e391)
• Consider PAC if not resp to Rx, unsure re: vol status, HoTN, ↑ Cr, need inotropes • Tailored Rx w/ PAC (qv); goals of MAP >60, CI >2.2 (MVO 2 >60%), SVR <800, PCWP <18
• IV vasodilators : NTG, nitroprusside (risk of coronary steal if CAD; prolonged use → cyanide/thiocyanate toxicity); nesiritide (rBNP) not rec for routine use ( NEJM 2011;365:32) • Inotropes (properties in addition to ↑ inotropy listed below)
dobutamine: vasodilation at doses ≤5 µg/kg/min; mild ↓ PVR; desensitization over time
dopamine: splanchnic vasodil. → ↑ GFR & natriuresis; vasoconstrictor at ≥5 µg/kg/min
milrinone: prominent systemic & pulmonary vasodilation; ↓ dose by 50% in renal failure
• Ultrafiltration : similar wt loss to aggressive diuresis, but ↑ renal failure ( NEJM 2012:367:2296) • Mechanical circulatory support ( Circ