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Pharmacology > Congestive Heart Failure > Flashcards

Congestive Heart Failure Flashcards

1
Q

define positive inotropy, positive chronotropy, positive dromotropy, positive lusitropy

A

positive inotropy - increase in cardiac contractility
positive chronotropy - increase in HR
positive dromotropy - increase in conduction velocity
positive lusitropy - increase in rate of relaxation

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2
Q

what type of drugs have been shown to decrease cardiac remodeling hence attenuating disease progression

A

drugs that reduce ventricular wall stress or inhibit the RAAS system (like ACEIs, ARBS, aldosterone antagonist etc)

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3
Q

drugs to treat heart failure: given to reduce blood volume

A

diuretics: thiazide diuretics, loop diuretics, aldosterone antagonists

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4
Q

drugs to treat heart failure: given to reduce peripheral resistance

A

vasodilator: inhibitors of angiotensin (ACEIs, ARBS, renin inhibitors) and direct vasodilators

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5
Q

drugs to treat heart failure: given to reduce heart rate and contractility

A

cardioinhibitory drugs: beta blockers and calcium channel blockers

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6
Q

drugs to treat heart failure: to stimulate contractility (inotropic agent)

A

inotropic agent: digoxin

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7
Q

drugs to treat heart failure: inotropic agents used in acute heart failure

A

dopamine, dobutamine, inamrinone, glucagon, milrinone

DDIG M

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8
Q

when are diuretics recommended for heart failure patients

A

if there is evidence of fluid retention (because they do not alter disease progression or prolong survival)

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9
Q

mechanism of action of diuretics in HF patients

A
  • reduce venous pressure and ventricular preload
  • reduce pulmonary and/or systemic congestion or edema
  • and associated symptoms –> dyspnea
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10
Q

what do ACEIs do in HF patients

A
  • reduce peripheral resistance hence reduce afterload (resistance against which left ventricle must eject its volume of blood during contraction)
  • reduce Na and H2O retention thereby reducing preload (volume of blood in ventricle after diastole)
  • reduce sympathetic activity by reducing NE release
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11
Q

ARBs approved by FDA for the use of HF

A

candesartan and valsartan

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12
Q

concurrent use of these drugs have been shown to produce sustained improvement in left ventricular ejection fraction

A

hydralazine and nitrates (isosorbide dinitrate)

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13
Q

mechanism of action for hydralazine and isosorbide nitrate

A
  • hydralazine is a vasodilator that reduce peripheral resistance in arterial SM and increases stroke volume and cardiac output –> decrease afterload
  • isosorbide nitrate is a venodilator that reduces preload
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14
Q

adverse effect of combination therapy of hydralazine and isosorbide dinitrate

A

hypotension
reflex tachycardia
sodium and water retention
headache, dizziness, and GI disturbances

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15
Q

drugs used to treat systolic HF

A 
diuretics
spironolactone
inhibitors of angiotensin
direct vasodilators
beta blockers
inotropic agents
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16
Q

drugs used to treat diastolic HF

A

diuretics
beta blocker
calcium channel blockers

17
Q

what are the beta blocker used for HF

A

carvedilol

metoprolol

18
Q

mechanism of beta blockers in HF

A

they block excessive sympathetic influence on the heart –> slows/reverses ventricular remodeling, improve LV systolic function, decreasing heart rate and ventricular wall stress thereby reducing myocardial oxygen demand, and inhibiting plasma renin release

19
Q

clinical application of digoxin

A

decrease symptoms of HF, increase exercise intolerance, decrease rate of hospitalization

DOES NOT INCREASE SURVIVAL

20
Q

when should digoxin be used?

A

patients with HF and supraventricular tachyarrhythmias such as atrial fibrillations

21
Q

mechanism of digoxin

A
  • positively inotropic (increases contractility of heart by increasing cytoplasmic calcium)
  • negatively chronotropic (decreases HR)
  • enhanced vagal tone (decreased oxygen demand)
  • decreased conduction through AV node increases the effective refractory period
22
Q

adverse effects of digoxin

A
  • cardiac arrhythmias esp atrial tachycardias and AV block
  • alteration of color perception and other CNS effects
  • hypokalemia (enhance therapeutic and toxic effect of digoxin)
  • hypercalcemia
  • hypomagnesia
23
Q

drug interaction of digoxin

A

Digoxin is QueeN of VA
quinidine, NSAID, verapamil, and amiodarone compete with digoxin for binding sites and depress renal clearance of digoxin

diuretics can indirectly react with digoxin because of ability to cause hypokalemia

24
Q

contraindications of digoxin

A
  • pts with diastolic or right sided HF –> outflow obstruction
  • uncontrolled hypertension
  • bradyarrhythmias
  • non responders or intolerance
  • hypokalemia
25
Q

tx of digoxin toxicity

A
  • withdraw drug or lower dose
  • adjust electrolyte status (increase K and Mg and reduce Ca)
  • lidocaine and/or Mg for ventricular tachyarrhythmias
  • if real severe, give digitalis antibodies
26
Q

what are the phosphodiesterase III inhibitors and how do they work

A

inamrinone
milrinone

inhibit myocardial phosphodiesterase –> increase in cAMP activity –> positive inotropic activity and arterial and venous vasodilating effects

27
Q

clinical use of phosphodiesterase III inhibitors (name them again)

A

iniamrinone and milrinone

short term therapy in people with intractable heart failure

28
Q

adverse effects of PDE III Inhibitors

A

PDE HAT

Hypotension
Arrhythmias
Thrombocytopenia

29
Q

when is dopamine used for HF

A

in treatment of shock

30
Q

mechanism of dopamine in HF

A

activates dopaminergic and beta 1 receptors –> increase force and rate of contraction and renal vasodilation

31
Q

adverse effect of dopamine

A

cardiac arrhythmias

32
Q

use of dobutamine in HF

A

it is a beta 1 agonist so it is used to increase cardiac output in acute management of HF

33
Q

mechanism of dobutamine in HF

A

increase in cAMP via Gs –> phosphorylation of calcium channels with increased calcium entry into myocardium –> increased contraction

positive inotropic effects and vasodilation

34
Q

use of glucagon in HF

A

cardiac stimulant in management of severe cases of beta blocker overdosage

35
Q

mechanism of glucagon in HF

A

increase in cAMP via Gs leads to increased contractility without using beta receptors

positive inotropic and chronotropic effects

Pharmacology (79 decks)

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