Heart Failure Flashcards
cardiac output equation?
CO = HR x SV
3 major determinants of stroke volume?
contractility, preload, afterload
how is preload measured?
LV end diastolic volume (or pressure)
what is afterload?
resistance ventricle must overcome to empty its contents (largely consequence of aortic pressure)
causes of afterload increase?
higher pressure load (HTN) or increased chamber size (dilated LV)
contractility influenced by?
intracellular Ca
on PV loop: what is a?
mitral valve opening, beginning of diastole
on PV loop: what is a-b?
diastolic filling, blood into L ventricle. also, compliance.
on PV loop: what is b?
mitral valve closure (end diastolic volume)
on PV loop: what is b-c?
isovolumic contraction (increase in P with no change in vol)
on PV loop: what is c?
aortic valve opening
on PV loop: what is c-d?
ejection (afterload)
on PV loop: what is d?
aortic valve closure (end systolic volume)
on PV loop: what is d-a?
isovolumic relaxation
what happens to curve if compliance is reduced?
gets steeper (decreased SV)
effect of afterload on pressure? ESV?
greater afterload results in greater ESV.
pressure generated during ejection increases, more work expended to overcome resistance to eject, less fiber shortening.
effect of contractility on ESPVR line? stroke volume?
increasing contractility = steeper line. ventricle empties more completely so get smaller end systolic volume and increased stroke volume
things that increase SV?
increase preload, decreased afterload, increased contractility
EDV influenced by?
chamber compliance. more stiff means less dilation.
what factors does ESV depend on?
afterload and contractility. not preload.
general causes of HF w reduced ejection fraction?
systolic dysfunction: impaired contractility or increased afterload
general causes of HF w preserved ejection fraction?
diastolic dysfunction: impaired diastolic filling
specific causes of HF w reduced ejection fraction?
destruction of myocytes, abnormal myocyte function, fibrosis. increased resistance to flow d/t pressure overload.
specific causes of HF w preserved ejection fraction?
acute ischemia, hypertrophy, fibrosis, pericardial dz, etc
precipitating factors for HF?
increased cardiac workload. increased metabolic demands, increased circulating vol (preload), conditions that increase afterload (like HTN), conditions that impair contractility, very slow HR
goals of treatment of HF with reduced EF? aka systolic HF
correct underlying condition, eliminate acute precipitating cause of stx, manage HF stx, modulate neurohormonal response, prolong survival
drugs used for treatment of HF with reduced EF?
diuretics, RAA inhibitors (ACE-I, ARBs, aldo antagonists), B-blockers, vasodilators, positive inotropic agents (digoxin)
direct effects of digoxin?
positive inotropic: increases contractile state of myocardium, increases SV
increases vagal tone: slows HR
digoxin secondary effects?
decreased HR, arterial and venous dilation, decreased venous P, normalizes arterial baroreceptors.
digoxin molecular site of action?
positive inotropic effect due to inhibition of Na/K ATPase: increased intracellular Na decreases Ca extrusion by Na/Ca exchanger. increased intracellular conc of Ca.
K also competes w digoxin for binding of Na/K ATPase
digoxin electrophysiological actions?
increased vagal nerve activity: reduced firing rate of SA node, decreased conduction velocity in AV node, heart block possible.
ECG shows: increased PR interval
digoxin pharmacokinetics?
daily dose. oral. renal elimination (excreted unchanged). higher dose (1.4) gives max increase in contractility. lower (.5-.8 gives neurohormonal benefits)
digoxin toxicity? CI with which drugs?
low TI (2). affects all excitable tissues (GI, visual disturbances, neurologic, muscular, cardiac arrhythmias). enhanced toxicity w hypokalemia (re: diuretics). CI w quinidine, verapamil, amiodarone
digoxin overall? mortality effect?
no real benefit. maybe stx relief. not first line.
when is digoxin useful?
HF patients w/ LV systolic dysfunction in atrial fibrillation. only oral positive inotrope.
other inotropic drugs?
dobutamine, dopamine, milrinone
how are B agonists used for HF? which?
dobutamine, dopamine. IV for acute decompensated HF (stabilize)
how are phosphodiesterase inhibitors used? which?
milrinone. IV for acutely ill. + inotrope and vasodilation.
effect of diuretics?
reduce fluid volume and preload. reduction in heart size improves efficiency and reduces wall stress. reduce edema.
loop diuretics use?
furosemide. widely used. maintain euvolemia. promote K loss (hypokalemia)
thiazide diuretics used?
chlorothiazide. rarely alone. combination w loop for resistance. also promote hypokalemia.
K sparing diuretics used?
amiloride, triamterene. weak diuretic but limited K and Mg wasting.
vasodilator actions?
venodilators. arterial vasodilator. balanced or mixed.
venodilators used? effect on LV EDV?
nitroglycerin, isosorbide dinitrate. decrease LV EDV.
arterial vasodilators used? effects?
hydralazine. reduce systemic vasc resistance. increased SV. no change in LV EDV
mixed/balanced vasodilators used? effects?
ACE-I, ARBs, isosorbide dinitrate/hydralazine combo. decreased LV EDV.
what does angiotensin do?
potent arterial constrictor. increases afterload. Na/H2O retention. aldosterone secretion. promotes sympathetic activation. arrhythmogenic. promotes fibrosis.
what does aldosterone do?
promotes Na and water retention, K secretion. stimulates fibrosis in heart and vasculature. cardiac hypertrophy
ACE inhibitors’ actions in heart failure?
decrease systemic vascular resistance (afterload). reduce left ventricular filling pressure (preload). reduce fluid vol, cardiac fibrosis, hypertrophy. increase survival.
ACE-I side effects?
ACE cough (d/t bradykinin), angioedema, hypotension. hyperkalemia esp if used w aldo agonist.
angiotensin receptor blockers? actions?
losartan. similar to ACE inhibitors. alternative for ppl who can’t tolerate ACE-I therapy.
decrease systemic vascular resistance (afterload). reduce left ventricular filling pressure (preload). reduce fluid vol, cardiac fibrosis, hypertrophy. increase survival.
what does isosorbide dinitrate/hydralazine combo do?
mixed arterial and venous dilation: decreases preload and afterload, increases SV. improve survival (esp african americans). used when ACE-I or ARBs not tolerated. less tolerance in combo.
aldo antagonist therapy?
spironolactone, eplerenone. reduce edema, decrease fibrosis in myocardium/vessels (counteract adverse remodeling). improves mortality rate and stx (even w ACE-I). can cause hyperkalemia. added later on.
B-antagonists?
improves stx, ventricular fxn, mortality rate. decrease arrhythmias, O2 demand, BP. prevent remodeling. can initially worsen cardiac fxn (start at low dose and gradually increase).
are all B blockers useful?
no. metoprolol (extended release form), carvedilol. some genetic variability.
which drugs used in chronic HF improve stx?
furosemide, digoxin, inotropes, B-blockers, ACE-I/ARBs, spironolactone.
which drugs used in chronic HF decrease mortality?
B-blockers, ACE-I/ARBs, spironolactone. not sure about furosemide. digoxin does not. inotropes increase mortality.
what are some non-drug therapies?
diet (salt restriction). bi-ventricular pacing. ICD. LVAD. heart transplant. cell therapy?
goals of treatment of HF with preserved EF? (aka diastolic HF)
relief of pulmonary and systemic congestion. address correctable causes of impaired diastolic function. diuretics (reduce pulm congestion/peripheral edema). no mortality benefit of ACE-I, B-blockers or ARBs. no role for inotropic drugs.
