Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine (10 page)

BOOK: Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine
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• 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 1-3 
Approach 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)
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
2011;123:533)
Intra-aortic balloon pump (IABP): inflates in diastole & deflates in systole to ↓ impedance to LV ejection of blood, ↓ myocardial O
2
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.
BOOK: Pocket Medicine: The Massachusetts General Hospital Handbook of Internal Medicine
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