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NUNA 681(pharm) > CV Drugs- Dig and Inotropic Drugs > Flashcards

CV Drugs- Dig and Inotropic Drugs Flashcards

1
Q

digitalis- plant family from which many

A

cardiac glycosides are derived

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2
Q

digitalis- is an inotrope used for

A

patients with CHF and to slow ventricular response of patients with SVT (PAT, afib, aflutter)

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3
Q

digitalis- decreases the risk of

A

death due to heart failure, but increases the incidence of sudden death (arrhythmias)

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4
Q

in the treatment of SVT, dig can be given in combo with

A

a beta-antagonist at smaller doses of each and yet obtain more rapid control

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5
Q

contraindications for digitalis

A
  1. Wolff-Parkinson-White (30% develop vfib from increased conduction down the alternate path)
  2. hypertrophic cardiomyopathy (sub aortic stenosis) (increased obstruction with increased contractility)
  3. acute myocardial infarction (increase oxygen demand with increased contractility)
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6
Q

digitalis- has been shown to improve

A

morbidity without any benefit on mortality

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7
Q

digitalis- may act by

A

decreasing sympathetic activity

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8
Q

digitalis- may not be effective in patients who have

A

normal left ventricular systolic function

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9
Q

digitalis- the benefits of dig therapy are greatest in patients with

A

severe heart failure, an enlarged heart and a third heart sound gallop

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10
Q

digitalis- may be used in patients with

A

mild to moderate heart failure if they do not respond to an angiotensin converting enzyme inhibitor or a beta blocker

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11
Q

__ of dig can be effective

A

low dosage

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12
Q

__ and __ must be considered in deciding on an approatire dosage of dig

A

renal function and possible drug interaction

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13
Q

in general, dig therapy should be avoided in

A

the acute phase after myocardial infarction

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14
Q

digitalis- directs effects, inhibition of

A

Na/K ATPase ion transport system- causing increased Na inside the cell

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15
Q

digitalis- direct effects, increased intracellular Na then effects

A

the Na/Ca exchanger and less Ca is taken out of the cardiac cell; more Ca inside the cell accounts for increased contraction force

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16
Q

digitalis- decrease (less negative) __

A

resting membrane potential (automaticity)

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17
Q

digitalis- increase in the slopes of

A

phase 4 (automaticity)

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18
Q

digitalis- decrease in duration of

A

action potential due to shortening of phase 2 (corresponds to vent contraction)

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19
Q

digitalis- MOA on ANS activity

A

enhanced parasympathetic nervous activity; SA node activity decreased, slowed conduction through the AV node

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20
Q

digitalis CV effects-

A
  1. increased myocardial contractility
  2. increased CO
  3. improve tissue perfusion
  4. increased parasympathetic activity
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21
Q

digitalis CV effects- increased myocardial contractility from

A

increase SV, decreased heart size(preload), decreased LVEDP

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22
Q

digitalis CV effects- increased CO from

A

increased renal perfusion, diuresis of newly mobilized edema

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23
Q

digitalis CV effects- improved tissue perfusion

A

decreased sympathetic outflow, decreased SVR (afterload) leading to even better stroke volume

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24
Q

digitalis CV effects- increased parasympathetic activity

A

slowed HR- negative chronotropic and negative dromotropic (better coronary artery perfusion)

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25
Q

digitalis CV effects- in the normal heart, increased contractility is offset by decreases in __. __ may remain unchanged or even decrease

A

heart rate and direct vasoconstriction

CO

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26
Q

digitalis changes in EKG- ___ causes changes shown on EKG

A

cardiac glycosides

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27
Q

digitalis changes in EKG- prolonged PR

A

delay through the AV node

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28
Q

digitalis changes in EKG- shortened QT

A

more rapid ventricular repolarization

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29
Q

digitalis changes in EKG- ST segment depression

A

decreased slopes of phase 3

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30
Q

digitalis changes in EKG- smaller or inverted T wave

A

decrease slope and duration of phase 2 and 3

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31
Q

digoxin- onset

A

5-30 minutes

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32
Q

digoxin- admin route

A

IV

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33
Q

digoxin- clearance

A

35% excreted daily via kidneys

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34
Q

digoxin- elimination 1/2 life

A

31-33 hours

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35
Q

digoxin- prolonged with renal failure to up to

A

4.4 days

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36
Q

digoxin- __ to protein (skeletal muscle) decreased muscle mass in elderly

A

25% bound

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37
Q

digitalis toxicity- narrow therapeutic range

A

0.5-2.5 ng/ml

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38
Q

digitalis toxicity- incidence

A

20% of patients on digoxin will have some form of toxicity

39
Q

digitalis toxicity- MOA

A

inhibition of Na/K ATPase ion transport system; Ca accumulates in the cell causing dysrhythmias

40
Q

digitalis toxicity- causes

A
  1. most commonly renal dysfunction
  2. hypokalemia (due to diuretic) increase myocardial binding of drug (may also be due to hyperventilation)
  3. increased sympathetic activity related to hypoxemia
  4. hypercalcemia, hypomagnesia, decreased muscle mass (elderly)
41
Q

symptoms of digitalis toxicity

A
  1. arrhythmias
  2. increased automaticity
  3. delayed AV conduction
42
Q

first symptoms of arrhythmias from digitalis toxicity is

A

worsening of pre-existing CHF

43
Q

arrhythmias associated with digitalis toxicity

A
  1. PVCs
  2. junctional tachycardia
  3. Wenckebach’s AV block
  4. sinus bradycardia or arrest
  5. atrial tachycardia
  6. bidirectional vtach- most common with dig toxicity
  7. atrial flutter
  8. vfib
44
Q

most common arrhythmias with digitalis toxicity

A

atrial tachycardia

45
Q

most frequent cause of death with digitalis toxicity

A

vfib

46
Q

digitalis toxicity GI symptoms

A

N/V, diarrhea, increased salivation

47
Q

digitalis toxicity CNS symptoms

A

fatigue, confusion, blurred vision, green halos (CNS symptoms seen in elderly)

48
Q

digitalis toxicity- life threatening ___

A

hyperkalemia; with severe toxicity, related to paralysis of Na/K pump and leakage of K out of cell

49
Q

digitalis toxicity treatment

A
  1. postpone case unless most urgent toxicity is corrected
  2. stop digoxin
  3. check electrolytes
  4. correction of cause (hypokalemia, hypomagnesemia, arterial hypoxemia); supplemental K only after checking level
  5. anti-arrhythmic administration (lidocaine, atropine, digibind)
  6. temporary pacemaker (complete AV block)
50
Q

prophylactic digitalis for surgical procedures- __ hearts, without signs of __

A

healthy

failure, the diagnosis of cause of arrhythmias might be muddy

51
Q

prophylactic digitalis for surgical procedures- events common under anesthesia that increase risks of toxicity

A
  1. altered renal function
  2. hyperventilation causing hypokalemia
  3. increased sympathetic activity during anesthetic
52
Q

prophylactic digitalis for surgical procedures- thoracic surgery

A

in elderly patients, 1 mg over four doses the day before and am of surgery decreased SVT incidence

53
Q

prophylactic digitalis for surgical procedures- cardiac disease

A

decreased incidence of impaired cardiac function in patients with CAD during recovery

54
Q

prophylactic digitalis for surgical procedures- __ continue digitalis therapy especially if for __

A

DO

HR control

55
Q

drug interaction with digitalis- succ

A

additive parasympathetic effect of cause dysrhythmias due to catecholamine release (theoretical)

56
Q

drug interaction with digitalis- beta-adrenergic agonists (pavulon)

A

increased cardiac dysrhythmias

57
Q

drug interaction with digitalis- calcium IV

A

dysrhythmias

58
Q

drug interaction with digitalis- diuretics causing loss of K

A

digitalis toxicity due to hypokalemia

59
Q

drug interaction with digitalis- halothane

A

dysrhythmias

60
Q

drug interaction with digitalis- fentanyl, enflurane, isoflurane

A

decrease automaticity

61
Q

selective phosphodiesterase inhibitors (PDE III) are

A

noncatecholamine, nonglycoside

62
Q

selective phosphodiesterase inhibitors (PDE III) MOA

A

decreased hydrolysis of cAMP and cGMP, increasing the cAMP and cGMP in the myocardium and vascular smooth muscle

63
Q

selective phosphodiesterase inhibitors (PDE III) effect

A

positive inotropic effect with diastolic relaxation and vascular smooth muscle relaxation

64
Q

selective phosphodiesterase inhibitors (PDE III) clinical use

A

acte cardiac failure

65
Q

selective phosphodiesterase inhibitors (PDE III)- amrinone: effect

A

inotropic effects and vasodilation

66
Q

selective phosphodiesterase inhibitors (PDE III)- amrinone: increases CO within

A

5 minutes

67
Q

selective phosphodiesterase inhibitors (PDE III)- amrinone: side effects

A

hypotension due to vasodilation, thrombocytopenia, dysrhythmogenic

68
Q

selective phosphodiesterase inhibitors (PDE III)- amrinone: advantage

A

safety with therapeutic index is 100:1 compared to 1.2:1 for cardiac glycosides

69
Q

selective phosphodiesterase inhibitors (PDE III)- milrinone (Primacor): effect

A

inotropic and vasodilation; little effect on HR and myocardial oxygen consumption

70
Q

selective phosphodiesterase inhibitors (PDE III)- milrinone (Primacor): use

A

acute LV dysfunction after cardiac surgery; used in weaning from CBP

71
Q

selective phosphodiesterase inhibitors (PDE III)- milrinone (Primacor): dose

A

bolus 50mcg/kg, infusion of 0.5 mcg/kg/min

72
Q

nonselective phosphodiesterase inhibitors inhibit

A

all fraction of PDE isoenzymes I-V

73
Q

nonselective phosphodiesterase inhibitors- theophylline: uses

A

treatment of bronchospasm (recommended to reserve the use of theophylline after beta 2 agonists and corticosteroids have been tried)

74
Q

nonselective phosphodiesterase inhibitors- theophylline: side effects

A
  1. can cross placenta
  2. may relax GE sphincter
  3. narrow therapeutic range of 10-20 mcg/ml
75
Q

nonselective phosphodiesterase inhibitors- theophylline: toxic effects

A

dysrhythmias

76
Q

nonselective phosphodiesterase inhibitors- theophylline: metabolism

A

liver metabolism negatively affected by alcoholism, cimetidine or extremes of age; smoking (speeds metabolism)

77
Q

calcium effect

A

inotropic effect of increased SV, decreased LVEDP (especially in hypocalcemic)

78
Q

calcium effects

A

HR and SVR decrease

79
Q

calcium- be careful when patient receiving __ and also __; can cause __

A

digitalis

hypokalemic

arrhythmias

80
Q

calcium uses

A

coming off CBP (cardioplegia with K, citrate in blood, sodium bicarb)

81
Q

__ contains more calcium than __

A

CaCl

CaGluconate

82
Q

glucagon is a

A

polypeptide hormone produced in the pancreas

83
Q

glucagon stimulates

A

the formation of cAMP

84
Q

glucagon causes the release of

A

catecholamines- secondary

85
Q

glucagon increases

A

the contractility and HR in the presence of beta blockers

86
Q

glucagon can cause

A

tachycardia- significantly high enough to interfere with filling an offsetting ability to increase CO (tachycardia especially if atrial fib)

87
Q

glucagon adult dose

A

1-5 mg rapid bolus

88
Q

glucagon elimination 1/2 time

A

3-6 min

89
Q

glucagon may cause

A

N/V, hyperglycemia, paradoxical hypoglycemia, hypokalemia

90
Q

glucagon in smooth muscle,

A

increased cAMP decreased intracellular Ca by facilitating the uptake of Ca into the sarcoplasmic reticulum, leading to smooth muscle relaxation

91
Q

methylene blue is a

A

potent inhibitor of NO synthase in vascular endothelial cells; resulting decreased NO release and increased systemic vascular resistance

92
Q

methylene blue binds to

A

guanylate cyclase (GC) in the vascular smooth muscle- blocking cGMP action in the vascular smooth muscle

93
Q

methylene blue is useful in

A

septic shock, endocarditis, transplant, protamine reaction, post CPB to counteract excessive vasodilation of vasoplegic syndrome

94
Q

methylene blue bolus

A

2mg/lg over 30 mins, followed by 0.5-1 mg/kg/hr if needed

NUNA 681(pharm) (12 decks)

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