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

CV Drugs- Dig and Inotropic Drugs Flashcards

(94 cards)

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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
digitalis CV effects- in the normal heart, increased contractility is offset by decreases in __. __ may remain unchanged or even decrease
heart rate and direct vasoconstriction CO
26
digitalis changes in EKG- ___ causes changes shown on EKG
cardiac glycosides
27
digitalis changes in EKG- prolonged PR
delay through the AV node
28
digitalis changes in EKG- shortened QT
more rapid ventricular repolarization
29
digitalis changes in EKG- ST segment depression
decreased slopes of phase 3
30
digitalis changes in EKG- smaller or inverted T wave
decrease slope and duration of phase 2 and 3
31
digoxin- onset
5-30 minutes
32
digoxin- admin route
IV
33
digoxin- clearance
35% excreted daily via kidneys
34
digoxin- elimination 1/2 life
31-33 hours
35
digoxin- prolonged with renal failure to up to
4.4 days
36
digoxin- __ to protein (skeletal muscle) decreased muscle mass in elderly
25% bound
37
digitalis toxicity- narrow therapeutic range
0.5-2.5 ng/ml
38
digitalis toxicity- incidence
20% of patients on digoxin will have some form of toxicity
39
digitalis toxicity- MOA
inhibition of Na/K ATPase ion transport system; Ca accumulates in the cell causing dysrhythmias
40
digitalis toxicity- causes
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
symptoms of digitalis toxicity
1. arrhythmias 2. increased automaticity 3. delayed AV conduction
42
first symptoms of arrhythmias from digitalis toxicity is
worsening of pre-existing CHF
43
arrhythmias associated with digitalis toxicity
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
most common arrhythmias with digitalis toxicity
atrial tachycardia
45
most frequent cause of death with digitalis toxicity
vfib
46
digitalis toxicity GI symptoms
N/V, diarrhea, increased salivation
47
digitalis toxicity CNS symptoms
fatigue, confusion, blurred vision, green halos (CNS symptoms seen in elderly)
48
digitalis toxicity- life threatening ___
hyperkalemia; with severe toxicity, related to paralysis of Na/K pump and leakage of K out of cell
49
digitalis toxicity treatment
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
prophylactic digitalis for surgical procedures- __ hearts, without signs of __
healthy failure, the diagnosis of cause of arrhythmias might be muddy
51
prophylactic digitalis for surgical procedures- events common under anesthesia that increase risks of toxicity
1. altered renal function 2. hyperventilation causing hypokalemia 3. increased sympathetic activity during anesthetic
52
prophylactic digitalis for surgical procedures- thoracic surgery
in elderly patients, 1 mg over four doses the day before and am of surgery decreased SVT incidence
53
prophylactic digitalis for surgical procedures- cardiac disease
decreased incidence of impaired cardiac function in patients with CAD during recovery
54
prophylactic digitalis for surgical procedures- __ continue digitalis therapy especially if for __
DO HR control
55
drug interaction with digitalis- succ
additive parasympathetic effect of cause dysrhythmias due to catecholamine release (theoretical)
56
drug interaction with digitalis- beta-adrenergic agonists (pavulon)
increased cardiac dysrhythmias
57
drug interaction with digitalis- calcium IV
dysrhythmias
58
drug interaction with digitalis- diuretics causing loss of K
digitalis toxicity due to hypokalemia
59
drug interaction with digitalis- halothane
dysrhythmias
60
drug interaction with digitalis- fentanyl, enflurane, isoflurane
decrease automaticity
61
selective phosphodiesterase inhibitors (PDE III) are
noncatecholamine, nonglycoside
62
selective phosphodiesterase inhibitors (PDE III) MOA
decreased hydrolysis of cAMP and cGMP, increasing the cAMP and cGMP in the myocardium and vascular smooth muscle
63
selective phosphodiesterase inhibitors (PDE III) effect
positive inotropic effect with diastolic relaxation and vascular smooth muscle relaxation
64
selective phosphodiesterase inhibitors (PDE III) clinical use
acte cardiac failure
65
selective phosphodiesterase inhibitors (PDE III)- amrinone: effect
inotropic effects and vasodilation
66
selective phosphodiesterase inhibitors (PDE III)- amrinone: increases CO within
5 minutes
67
selective phosphodiesterase inhibitors (PDE III)- amrinone: side effects
hypotension due to vasodilation, thrombocytopenia, dysrhythmogenic
68
selective phosphodiesterase inhibitors (PDE III)- amrinone: advantage
safety with therapeutic index is 100:1 compared to 1.2:1 for cardiac glycosides
69
selective phosphodiesterase inhibitors (PDE III)- milrinone (Primacor): effect
inotropic and vasodilation; little effect on HR and myocardial oxygen consumption
70
selective phosphodiesterase inhibitors (PDE III)- milrinone (Primacor): use
acute LV dysfunction after cardiac surgery; used in weaning from CBP
71
selective phosphodiesterase inhibitors (PDE III)- milrinone (Primacor): dose
bolus 50mcg/kg, infusion of 0.5 mcg/kg/min
72
nonselective phosphodiesterase inhibitors inhibit
all fraction of PDE isoenzymes I-V
73
nonselective phosphodiesterase inhibitors- theophylline: uses
treatment of bronchospasm (recommended to reserve the use of theophylline after beta 2 agonists and corticosteroids have been tried)
74
nonselective phosphodiesterase inhibitors- theophylline: side effects
1. can cross placenta 2. may relax GE sphincter 3. narrow therapeutic range of 10-20 mcg/ml
75
nonselective phosphodiesterase inhibitors- theophylline: toxic effects
dysrhythmias
76
nonselective phosphodiesterase inhibitors- theophylline: metabolism
liver metabolism negatively affected by alcoholism, cimetidine or extremes of age; smoking (speeds metabolism)
77
calcium effect
inotropic effect of increased SV, decreased LVEDP (especially in hypocalcemic)
78
calcium effects
HR and SVR decrease
79
calcium- be careful when patient receiving __ and also __; can cause __
digitalis hypokalemic arrhythmias
80
calcium uses
coming off CBP (cardioplegia with K, citrate in blood, sodium bicarb)
81
__ contains more calcium than __
CaCl CaGluconate
82
glucagon is a
polypeptide hormone produced in the pancreas
83
glucagon stimulates
the formation of cAMP
84
glucagon causes the release of
catecholamines- secondary
85
glucagon increases
the contractility and HR in the presence of beta blockers
86
glucagon can cause
tachycardia- significantly high enough to interfere with filling an offsetting ability to increase CO (tachycardia especially if atrial fib)
87
glucagon adult dose
1-5 mg rapid bolus
88
glucagon elimination 1/2 time
3-6 min
89
glucagon may cause
N/V, hyperglycemia, paradoxical hypoglycemia, hypokalemia
90
glucagon in smooth muscle,
increased cAMP decreased intracellular Ca by facilitating the uptake of Ca into the sarcoplasmic reticulum, leading to smooth muscle relaxation
91
methylene blue is a
potent inhibitor of NO synthase in vascular endothelial cells; resulting decreased NO release and increased systemic vascular resistance
92
methylene blue binds to
guanylate cyclase (GC) in the vascular smooth muscle- blocking cGMP action in the vascular smooth muscle
93
methylene blue is useful in
septic shock, endocarditis, transplant, protamine reaction, post CPB to counteract excessive vasodilation of vasoplegic syndrome
94
methylene blue bolus
2mg/lg over 30 mins, followed by 0.5-1 mg/kg/hr if needed

NUNA 681(pharm) (12 decks)

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