Decompensated CHF

3 components of pathophysiology:

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(1) Systemic overload = excess TBW
(2) Acute diastolic dysfunction = sudden increase in LV pressure –> pulmonary congestion. Unrelated to LV contractile function. Occurs via wall stiffening (ex: scarring from old MI) or impaired filling (ex: LVH, tachycardia of any cause).
(3) Low output failure = problem in contractility, leading to poor end-organ perfusion (fatigue, confusion, worsened renal function)

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DDX/etiology of decompensation:
-abrupt: ACS, PE, ruptured valve or chordae tendinae or papillary muscle, ruptured ventricular septum (above evaluated via echo), arrhythmia
-gradual onset: tamponade, copd, sepsis, acidosis, hyperthyroidism, med/dietary noncompliance

Key history: Chest pain/anginal equivalent? History of CHF (or similar episodes)? History of MI or CAD?

Treatment goals:
-reduce preload??
-improve LV outflow
-maintain myocardial perfusion

dyspnea: sit pt upright, supplemental O2, BiPAP if significant WOB, intubation if altered
chest pain: give ASA, supplemental O2, nitroglycerin SL if hypertensive, PCI if STEMI
pulmonary congestion/ADHF: nitroglycerin if hypertensive to reduce afterload
systemic overload: iv lasix if normotensive and no renal dysfunction, bumex drip if hypotensive or soft pressures or any renal dysfunction
cardiogenic shock/low output failure:  determine etiology if acute (STEMI, valve rupture), consider inotropes*, consider bumex gtt if chronic with concomitant diastolic failure/pulmonary edema

Treatment pathway:
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*from Circulation:
“Patients with decompensated HF unresponsive to diuresis often have diminished concomitant peripheral perfusion, clinically apparent as cool extremities, narrowed pulse pressure, and worsening renal function. They may have markedly elevated SVR despite hypotension due to the stimulation of the renal-angiotensin-aldosterone system, as well as release of endogenous catecholamines and vasopressin. In this setting, reversal of systemic vasoconstriction is often achieved through the use of vasodilators (such as sodium nitroprusside) and inotropes with peripheral vasodilatory properties to improve hemodynamic parameters and clinical symptoms.
The most commonly recommended initial inotropic therapies for refractory HF (dobutamine, dopamine, and milrinone) are used to improve CO and enhance diuresis by improving renal blood flow and decreasing SVR without exacerbating systemic hypotension. Dobutamine stimulation of β1– and β2-receptors can achieve this goal at low to medium doses by modestly increasing contractility with usually mild systemic vasodilation. Unfortunately, β-adrenergic receptor responses are often blunted in the failing human heart. A chronic increase in activation of the sympathetic nervous system and increased circulating catecholamine levels results in a phosphorylation signal that leads to uncoupling of the surface receptor from its intracellular signal transduction proteins (desensitization), as well as increased receptor targeting for endocytosis (decreased receptor density). PDIs such as milrinone, acting through a non–β-adrenergic mechanism, are not associated with diminished efficacy or tolerance with prolonged use. This drug causes relatively more significant right ventricular afterload reduction through pulmonary vasodilation and less direct cardiac inotropy, which results in less myocardial oxygen consumption. Milrinone can cause severe systemic hypotension, necessitating the coadministration of additional pressor therapies. Direct randomized comparisons of milrinone and dobutamine have been small and have demonstrated similar clinical outcomes.”

SCAPE management: BIPAP + high dose NTG drip

Categories of CHF pts (Stevenson profile for CHF):
-warm & dry = healthy CHF (well perfused, adequately diuresed)
-warm & wet = well perfused, needs diuresis
-cold & wet = poorly perfused, needs pressors + diuresis = cardiogenic shock (CCU)
—- or CHF + other etiology shock (ex septic shock)


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