Unit 4 - Heart Failure Flashcards
what is the definition of CHF?
inability of heart to pump blood at rate commensurate w/ requirements of metabolizing tissues, or can only do so from elevated filling pressure
what is the definition of heart failure? main clinical manifestations? what is it usually from?
syndrome from any structural or functional disorder that impairs ability of ventricle to fill or eject blood
- dyspnea, fatigue, fluid retention (central or peripheral)
- may result from normal LV size and function to sever dilation and systolic dysfunction
what are the NY heart association functional classifications for HF?
I: cardiac disease w/o limitations on PA (SOB only if extreme)
II: slight limitation of PA (SOB if climb many stairs)
III: marked limitation of PA (SOB if walk to kitchen)
IV: inability to carry any PA (SOB even at rest)
-end-stage, poorest outcome
why are HF patients unable to exercise?
cardiac function:
- alternations in ventricular distensibility
- valvular regurgitation
- pericardial restraint
- cardiac rhythm
- conduction abnormalities
- RV function
non-cardiac:
- peripheral vascular function
- skeletal muscle physiology
- pulmonary dynamics
- neurohormonal and reflex autonomic activity
- renal Na handling
explain the progression of HF?
LV dysfunction begins with injury to myocardium –> change in LV geometry and structure (cardiac remodeling)
-activation of endogenous neurohormonal systems play major role in this remodeling, thus want to interrupt this cycle
what is the neurohormonal impact in HF patients?
elevated levels of NE, AII, aldosterone, endothelin, ADH, and cytokines, that adversely affect structure and function of heart
what are compensatory mech in HF in ANS?
heart: increased HR, myocardial contractile stimulation (inotropy), relaxation (chronotropy)
peripheral circulation: arterial and venous vasoconstriction (increased afterload and preload, respectively)
what are compensatory mech in HF in kidney?
due to RAAS
- arterial and venous vasoconstriction (increased afterload and preload, respectively)
- Na and water retention (increased preload and afterload)
- increased myocardial contractile stimulation
what are compensatory mech in HF in heart?
- endothelin 1 (increased preload and afterload)
- ADH (increased preload and afterload)
- natriuretic peptides (decreased afterload)
- prostaglandins
- Frank-Starling law (increased EDV/preload, EDP)
- hypertrophy
- peripheral O2 delivery
- -redistribution of CO, altered O2-Hb dissociation, increased O2 extraction by tissues
- anaerobic metabolism
ACEi hemodynamic effects?
- arteriovenous vasodilation
- -decrease PCWP and LVEDP
- -decrease SVR and BP
- -increase CO and exercise tolerance
- no change in HR/contractility
- decreased MVO2
- increased renal, coronary, and cerebral flow
- diuresis and natriuresis
what are advantages of ACEi?
- inhibit LV remodeling post-MI
- modify progression of chronic CHF
- -increase survival
- -decrease hospitalizations
- -improve QOL
- no neurohormonal activation or reflex tachycardia
- tolerance doesn’t develop
what are indications for ARBs?
- used in place of ACEi when cough an issue
- -still causes angioedema
- used in tandem with ACEi
ASE of ARBs?
fewer than ACEi
- deccreases GFR
- raises K+
- hypotension
- angioedema
why do we only use diuretics to treat HF symptoms?
- neurohormonal activation (increases levels of NE and AII)
- contraindicated in hypovolemia
- ASE: volume contraction and electrolyte depletion
what do diuretics do to CO? arteries?
no direct effect on CO (unless excessive preload reduction), but improves arterial distensibility
why are aldosterone antagonists good for HF?
the risk of death is reduced in class IV patients
what is eplerenone?
an aldosterone antagonist that doesn’t cause gynocomasetia
side effects of aldosterone
- hyperkalemia
- metabolic acidosis
- gynecomastia
- gastric disturbances (peptic ulcer)
how should you use beta-blockers?
initiate at very low dose, and gradually increased if tolerated
- will initially increase CO, but will peter out
- can be initiated even if hospitalized for HF, as long as IV therapy for HF not required
what is digoxin? how does it work?
cardiac glycoside; potent inhibitor of cellular Na+/K+ ATPase
- increases intracellular Na+ –> Na+/Ca++ exchange system increases –> intracellular Ca++ increases –> increases contractility
- increases vagal efferent activity to heart
- reduces sinoatrial firing rate
- reduces conduction velocity thru AV node
what are hemodynamic effects of digoxin?
- increase CO, LVEF, exercise tolerance, natriuresis
- decrease LVEDP, neurohormonal activation
what are neurohormonal effects of digoxin?
- increased vagal tone
- decreased plasma NE, peripheral NS activity, RAAS activity
- normalizes arterial baroreceptors
why isn’t digoxin used all the time?
management issue: narrow therapeutic/toxic window can cause easy overdose
- toxicity: cardiac arrythmias (commonly atrial tachycardia and AV block)
- not given to end-stage disease
how is digoxin metabolized?
kidneys
how is dobutamine given?
given as continuous infusion
- short onset of action and half-life
- can develop tolerance after 24 to 48 hours of same dose
- acutely improves symptoms, but increases mortality overall
what is milrinone?
phosphodiesterase IIIa inhibitor
-causes less breakdown of cAMP, so increased contractility (inotropy), HR (chronotropy), and relaxation (lusitropy)
how is milrinone given?
continuous infusion, and must be adjusted for renal function
- no demonstrated tolerance development, but for short term (48 to 72 hours)
- no difference in hospital stay, but increased hypotensive events, atrial arrhythmias, and overall mortality
