Pocket Medicine

CARDIOLOGY

HEART FAILURE

Definitions (Braunwald’s Heart Disease, 9th ed., 2012)

•  Failure of heart to pump blood forward at sufficient rate to meet metabolic demands of peripheral tissues, or ability to do so only at abnormally high cardiac filling pressures

•  Low output (↓ cardiac output) vs. high output (↑ stroke volume ± ↑ cardiac output)

•  Left-sided (pulmonary edema) vs. right-sided (↑ JVP, hepatomegaly, peripheral edema)

•  Backward (↑ filling pressures, congestion) vs. forward (impaired systemic perfusion)

•  Systolic (inability to expel sufficient blood) vs. diastolic (failure to relax and fill normally)

•  Reduced (HFrEF) vs. preserved (HFpEF) left ventricular ejection fraction

•  Some degree of systolic and diastolic dysfxn, may occur regardless of ejection fraction

Figure 1-3Approach to left-sided heart failure

History

•  Low output: fatigue, weakness, exercise intolerance, Δ MS, anorexia

•  Congestive:  left-sided → dyspnea, orthopnea, paroxysmal nocturnal dyspnea right-sided → peripheral edema, RUQ discomfort, bloating, satiety

Functional classification (New York Heart Association class)

•  Class I: no sx w/ ordinary activity; class II: sx w/ ordinary activity; class III: sx w/ minimal activity; class IV: sx at rest

Physical exam (“2-minute” hemodynamic profile; JAMA 1996;275:630 & 2002;287:628)

•  Congestion (“dry” vs. “wet”)

↑ JVP (~80% of the time JVP >10 → PCWP >22;  J Heart Lung Trans 1999;18:1126)

 hepatojugular reflux: >4 cm ↑ in JVP for ≥15 sec w/ 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)

S3 (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 S1 (↓ 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), S4 (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”

Lasix 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 (NEJM2011;364:797)

Morphine (↓ sx, venodilator, ↓ afterload)

Nitrates (venodilator)

Oxygen ± noninvasive vent (↓ sx, ↑ PaO2; no ∆ mortality; see “Mechanical Ventilation”)

Position (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 (MVO2 >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 2011;123:533)

Intra-aortic balloon pump (IABP): inflates in diastole & deflates in systole to ↓ impedance to LV ejection of blood, ↓ myocardial O2 demand & ↑ coronary perfusion

ventricular assist device (LVAD ± RVAD): as bridge to recovery (NEJM 2006;355:1873) or transplant (some temporary types can be placed percutaneously = PVAD), or as destination therapy (45–50% ↓ mort. vs. med Rx; NEJM 2009;361:2241)

•  Cardiac transplantation: 15–20% mort. in 1st y, median survival 10 y

•  Utility of BNP-guided Rx remains debated (Circ 2013;301:500 & 509)

•  Implantable PA pressure sensor in NYHA III → ~30% ↓ risk of hosp (Lancet 2011;377:658)

Heart failure with preserved EF (HFpEF; “Diastolic HF”) (Circ 2011;124:e540)

•  Epidemiology: ~½ of Pts w/ HF have normal or only min. impaired systolic fxn (EF ≥40%); risk factors for HFpEF incl ↑ age, , DM, AF. Mortality  to those w/ systolic dysfxn.

•  Etiologies (impaired relaxation and/or ↑ passive stiffness): ischemia, prior MI, LVH, HCMP, infiltrative CMP, RCMP, aging, hypothyroidism

•  Precipitants of pulmonary edema: volume overload (poor compliance of LV → sensitive to even modest ↑ in volume); ischemia (↓ relaxation); tachycardia (↓ filling time in diastole), AF (loss of atrial boost to LV filling); HTN (↓ afterload → ↓ stroke volume)

•  Dx w/ clinical s/s of HF w/ preserved systolic fxn. Dx supported by evidence of diast dysfxn:

(1) echo: abnl MV inflow (E/A reversal and Δs in E wave deceleration time) & ↓ myocardial relax. (↑ isovol relax. time & ↓ early diastole tissue Doppler vel)

(2) exercise-induced ↑ PCWP (± ↓ response chronotropic & vasodilator reserve)

•  Treatment: diuresis for vol overload, BP control, prevention of tachycardia and ischemia;

no benefit to: ACEI/ARB (NEJM 2008;359:2456), PDE5 inhib ( JAMA 2013;309:1268)

spironolactone improves LV fxn, but not sx ( JAMA 2013;309:781)

combined ARB/neprilysin (neutral endopeptidase) inhib under study (Lancet 2012;380:1387)