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Pharmacology Test 3 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is heart failure?

A

chronic, progressive condition; enlarged heart & inability to pump normally; impaired contraction of LV, organs not adequately perfused; can occur w/ low or high CO

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2
Q

What are the manifestations of heart failure?

A

dyspnea
fatigue/exercise intolerance
fluid retention/pulmonary congestion/peripheral edema

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3
Q

New York Heart Association quantification of HF

A

I: symptoms at levels of exertion that would limit normal individuals
II: symptoms on ordinary exertion
III: symptoms on less than ordinary exertion
VI: symptoms at rest

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4
Q

relate the Starling relationship to myocardial contractility

A

Increased sarcomere length during diastole increased the force of contraction. Muscle length is determined by end diastolic volume which is related to end diastolic filling pressure (preload). Preload recruitment augments CO.
*ppl w/ HF operate on a plateau phase of the Starling curve

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5
Q

factors affecting stroke volume

A

preload: increases stretch & engages Starling mechanism
afterload: ABP, increased resistance in small vessels
inotropic state: contractile state based on autonomic nerves & circulating catecholamines

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6
Q

How does calcium affect heart function?

A

promotes interaction of actin and myosin

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7
Q

steps of myocyte depolarization

A

Na enters via Na channel and changes membrane potential; Ca enters cell through VGCaC; Ca entry signals RyR to release more Ca from SR; Na/Ca exchanger reverses briefly to bring more Ca into cell; contraction happens; Ca pumped back into SR by SERCA for repolarization, also Ca ATPase & Na/Ca exchanger remove more Ca

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8
Q

systolic dysfunction

A

impairment in Ca-mediated contraction

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9
Q

diastolic dysfunction

A

problem with Ca re-sequestration needed for normal relaxation

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10
Q

What do myofibroblasts do?

A

maintain heart’s structural integrity; promote matrix formation by producing molecules promoting fibrosis (fibrotic remodeling)

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11
Q

compensatory responses for a decreased CO

A

*neurohumoral systems

baroreceptors activate SNS; SNS increases renin production; macula densa triggered by afferent arteriole

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12
Q

How does the SNS, AII, and aldosterone directly affect the myocardium?

A

promotes unfavorable remodeling via myocyte apoptosis and changes in gene expression

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13
Q

adaptation mechanisms in HF

A

abnormal baroreflex control: receptors interpret high pressure as normal so fail to inhibit SNS
cardiac hypertrophy
altered renal function: SNS vasoconstriction shunts blood from glomeruli, stimulates renin release
vasoconstriction: by SNS, RAS, vasopressin
edema

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14
Q

American College of Cardiology/AHA classification for HF

A

Stage A: at risk
Stage B: at risk
Stage C: existing HF
Stage D: existing HF

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15
Q

Stage A

A

risk of HF; no structural heart disease or symptoms; pts w/ HTN, atherosclerosis, DM, obesity, chemo, fam hx

therapy: treat HTN, dyslipidemia, smoking cessation
drugs: ACEIs or ARBs

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16
Q

Stage B

A

risk for HF; structural heart disease w/ no S/S; pts w/ prior MI, LV remodeling, asymptomatic vascular disease

therapy: everything under Stage A
drugs: ACEIs or ARBs, beta blockers

17
Q

Stage C

A

HF; structural heart disease w/ prior or current symptoms; pts w/ known heart disease, dyspnea, fatigue, low exerc. tolerance
therapy: add a salt restriction
drugs: diuretic, ACEIs, beta blockers
addtl drugs: aldosterone antagonists, digitalis, hydralazine/nitrates

18
Q

Stage D

A

refractory HF; requires specialized interventions; pts have symptoms at rest, may be hospitalized
therapy: same as others, add palliative care or transplant/mechanical support

19
Q

drugs that reduced mortality of HF when used alone

A

*ACEIs, ARBs, beta blockers

20
Q

other drugs for HF treatment

A

nitrates/hydralazine
loop diuretics/thiazides/spironolactone
adrenergic agonists, cAMP phosphodiesterase inhibitors, Dig

21
Q

How do ACEIs treat HTN?

A
  • -suppress AII, AII, aldosterone
  • -increase Ang1-7
  • -prevent degradation of bradykinin, a vasodilator
  • -reduce afterload and increase SV & CO b/c they are potent arterial dilators
22
Q

What is the first line of therapy for HF?

A

ACEIs

  • for all HF and reduced LVHF
  • often used in combo w/ beta blockers in stage A & B
23
Q

mechanism of action of ARBs

A

competitive antagonism of AT1R suppressing effects of AII and AIII; allow residual AT2R stimulation by AII and AIII to promote vasodilation & natriuresis; increase Ang1-7 activity

24
Q

Which diuretics are best for HF?

A

loops are preferred

thiazides preferred in HTN pts

25
Q

How do beta blockers help in HF?

A

although they impair inotropic performance, they improve exercise tolerance & increase LVEF over a period of several mths; impair hypokalemia; prevent remodeling of heart; prevent hyperphosphorylation of RyR that causes Ca leak from SR

26
Q

mechanism of action of digoxin

A

increases force of contraction by increasing intracellular Ca; increased CO decreases reflex SNS and increases renal perfusion; *inhibits Na/K ATPase

27
Q

non-cardiac mechanism of action of digoxin

A

sensitizes cardiac baroreceptors (they sense pressure as higher); increases vagal tone and increases SA nodal cell sensitivity to ACh (decrease SNS activity on heart); inhibit Na/K ATPase in kidney which reducing renin release

28
Q

mechanism of action of venodilators

A

decrease filling pressure & intracardiac volume

29
Q

mechanism of action of arteriodilators

A

decrease SVR to increase CO; increase renal perfusion to promote diuresis (decreases filling pressure)

30
Q

mechanism of action of isosorbide dinitrate

A

venodilation; increases venous capacitance to reduce preload; increases coronary artery flow

31
Q

mechanism of action of hydralazine

A

reduces renal vascular resistance & increases renal blood flow
*added to ACEIs, dig, diuretics for HF

32
Q

mechanism of action of sodium nitroprusside

A

reduces ventricular filling pressure & SVR; used in ICU setting

33
Q

mechanism of action of nitroglycerin

A

selective for venous capacitance vessels

34
Q

mechanism of action of positive inotropic agents

A

improve cardiac performance, facilitate diuresis, promote stability in the short term

35
Q

mechanism of action of dopamine

A
  • -stimulates beta receptors on heart to stimulate contractility
  • -stimulates alpha receptors at high infusion rates to stimulate peripheral arterial/venous constriction (helps critical circulatory failure by increasing afterload)
36
Q

mechanism of action of dobutamine

A

stimulates beta 1 (inotropic) & beta 2 (vasodilation) receptors; increase renal bloodflow to increase CO

37
Q

mechanism of action of milrinone

A

stimulate myocardial contraction & accelerate myocardial relaxation by increasing cAMP (preventing degradation); cAMP activates protein kinase A (PKA) to increase Ca in the cell

Pharmacology Test 3 (10 decks)

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