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Cardiovascular Unit > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

cardiac output equation?

A

CO = HR x SV

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2
Q

3 major determinants of stroke volume?

A

contractility, preload, afterload

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3
Q

how is preload measured?

A

LV end diastolic volume (or pressure)

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4
Q

what is afterload?

A

resistance ventricle must overcome to empty its contents (largely consequence of aortic pressure)

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5
Q

causes of afterload increase?

A

higher pressure load (HTN) or increased chamber size (dilated LV)

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6
Q

contractility influenced by?

A

intracellular Ca

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7
Q

on PV loop: what is a?

A

mitral valve opening, beginning of diastole

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8
Q

on PV loop: what is a-b?

A

diastolic filling, blood into L ventricle. also, compliance.

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9
Q

on PV loop: what is b?

A

mitral valve closure (end diastolic volume)

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10
Q

on PV loop: what is b-c?

A

isovolumic contraction (increase in P with no change in vol)

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11
Q

on PV loop: what is c?

A

aortic valve opening

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12
Q

on PV loop: what is c-d?

A

ejection (afterload)

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13
Q

on PV loop: what is d?

A

aortic valve closure (end systolic volume)

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14
Q

on PV loop: what is d-a?

A

isovolumic relaxation

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15
Q

what happens to curve if compliance is reduced?

A

gets steeper (decreased SV)

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16
Q

effect of afterload on pressure? ESV?

A

greater afterload results in greater ESV.

pressure generated during ejection increases, more work expended to overcome resistance to eject, less fiber shortening.

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17
Q

effect of contractility on ESPVR line? stroke volume?

A

increasing contractility = steeper line. ventricle empties more completely so get smaller end systolic volume and increased stroke volume

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18
Q

things that increase SV?

A

increase preload, decreased afterload, increased contractility

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19
Q

EDV influenced by?

A

chamber compliance. more stiff means less dilation.

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20
Q

what factors does ESV depend on?

A

afterload and contractility. not preload.

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21
Q

general causes of HF w reduced ejection fraction?

A

systolic dysfunction: impaired contractility or increased afterload

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22
Q

general causes of HF w preserved ejection fraction?

A

diastolic dysfunction: impaired diastolic filling

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23
Q

specific causes of HF w reduced ejection fraction?

A

destruction of myocytes, abnormal myocyte function, fibrosis. increased resistance to flow d/t pressure overload.

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24
Q

specific causes of HF w preserved ejection fraction?

A

acute ischemia, hypertrophy, fibrosis, pericardial dz, etc

25
Q

precipitating factors for HF?

A

increased cardiac workload. increased metabolic demands, increased circulating vol (preload), conditions that increase afterload (like HTN), conditions that impair contractility, very slow HR

26
Q

goals of treatment of HF with reduced EF? aka systolic HF

A

correct underlying condition, eliminate acute precipitating cause of stx, manage HF stx, modulate neurohormonal response, prolong survival

27
Q

drugs used for treatment of HF with reduced EF?

A

diuretics, RAA inhibitors (ACE-I, ARBs, aldo antagonists), B-blockers, vasodilators, positive inotropic agents (digoxin)

28
Q

direct effects of digoxin?

A

positive inotropic: increases contractile state of myocardium, increases SV
increases vagal tone: slows HR

29
Q

digoxin secondary effects?

A

decreased HR, arterial and venous dilation, decreased venous P, normalizes arterial baroreceptors.

30
Q

digoxin molecular site of action?

A

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

31
Q

digoxin electrophysiological actions?

A

increased vagal nerve activity: reduced firing rate of SA node, decreased conduction velocity in AV node, heart block possible.
ECG shows: increased PR interval

32
Q

digoxin pharmacokinetics?

A

daily dose. oral. renal elimination (excreted unchanged). higher dose (1.4) gives max increase in contractility. lower (.5-.8 gives neurohormonal benefits)

33
Q

digoxin toxicity? CI with which drugs?

A

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

34
Q

digoxin overall? mortality effect?

A

no real benefit. maybe stx relief. not first line.

35
Q

when is digoxin useful?

A

HF patients w/ LV systolic dysfunction in atrial fibrillation. only oral positive inotrope.

36
Q

other inotropic drugs?

A

dobutamine, dopamine, milrinone

37
Q

how are B agonists used for HF? which?

A

dobutamine, dopamine. IV for acute decompensated HF (stabilize)

38
Q

how are phosphodiesterase inhibitors used? which?

A

milrinone. IV for acutely ill. + inotrope and vasodilation.

39
Q

effect of diuretics?

A

reduce fluid volume and preload. reduction in heart size improves efficiency and reduces wall stress. reduce edema.

40
Q

loop diuretics use?

A

furosemide. widely used. maintain euvolemia. promote K loss (hypokalemia)

41
Q

thiazide diuretics used?

A

chlorothiazide. rarely alone. combination w loop for resistance. also promote hypokalemia.

42
Q

K sparing diuretics used?

A

amiloride, triamterene. weak diuretic but limited K and Mg wasting.

43
Q

vasodilator actions?

A

venodilators. arterial vasodilator. balanced or mixed.

44
Q

venodilators used? effect on LV EDV?

A

nitroglycerin, isosorbide dinitrate. decrease LV EDV.

45
Q

arterial vasodilators used? effects?

A

hydralazine. reduce systemic vasc resistance. increased SV. no change in LV EDV

46
Q

mixed/balanced vasodilators used? effects?

A

ACE-I, ARBs, isosorbide dinitrate/hydralazine combo. decreased LV EDV.

47
Q

what does angiotensin do?

A

potent arterial constrictor. increases afterload. Na/H2O retention. aldosterone secretion. promotes sympathetic activation. arrhythmogenic. promotes fibrosis.

48
Q

what does aldosterone do?

A

promotes Na and water retention, K secretion. stimulates fibrosis in heart and vasculature. cardiac hypertrophy

49
Q

ACE inhibitors’ actions in heart failure?

A

decrease systemic vascular resistance (afterload). reduce left ventricular filling pressure (preload). reduce fluid vol, cardiac fibrosis, hypertrophy. increase survival.

50
Q

ACE-I side effects?

A

ACE cough (d/t bradykinin), angioedema, hypotension. hyperkalemia esp if used w aldo agonist.

51
Q

angiotensin receptor blockers? actions?

A

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.

52
Q

what does isosorbide dinitrate/hydralazine combo do?

A

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.

53
Q

aldo antagonist therapy?

A

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.

54
Q

B-antagonists?

A

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).

55
Q

are all B blockers useful?

A

no. metoprolol (extended release form), carvedilol. some genetic variability.

56
Q

which drugs used in chronic HF improve stx?

A

furosemide, digoxin, inotropes, B-blockers, ACE-I/ARBs, spironolactone.

57
Q

which drugs used in chronic HF decrease mortality?

A

B-blockers, ACE-I/ARBs, spironolactone. not sure about furosemide. digoxin does not. inotropes increase mortality.

58
Q

what are some non-drug therapies?

A

diet (salt restriction). bi-ventricular pacing. ICD. LVAD. heart transplant. cell therapy?

59
Q

goals of treatment of HF with preserved EF? (aka diastolic HF)

A

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.

Cardiovascular Unit (16 decks)

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