Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

S5 - Anesthesia Pharm II - Test 2 > Digoxin & Inotropes > Flashcards

Digoxin & Inotropes Flashcards

1
Q

use of digoxin

A
  • CHF
  • slow ventricular response of pts with supraventricular tachydysrhytmias (PAT, afib, aflutter)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

digoxin decreases the risk of death due to heart failure but still might make the patient die because of what adverse effect?

A

increased incidence of sudden death d/t arrhytmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

digoxin can be combined with what other drug class in the treatment of SVT

what is the benefit of this?

A

beta antagonist

can give smaller doses of each and yet obtain more rapid control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

contraindications for digoxin

A
  • Wolff-Parkinson White (WPW)
  • Hypertrophic cardiomyopathy
  • Acute MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

why is digoxin contraindicated in pts with WPW?

A

30% develop Vfib from increased conduction down alternate path

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why is digoxin contraindicated in pts with hypertrophic cardiomyopathy?

A

increased contractility = increased obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why is digoxin contraindicated in acute MI?

A

increases O2 demand and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T/F - Digoxin is effective for patients with normal LV systolic function

A

false - may not be effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when might digoxin be used in a patient with mild to moderate heart failure?

A

pt doesn’t respond to ACE inhibitor or beta blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

patient comorbidities that must be considered when dosing digoxin

A

renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

patients who benefit the most from digoxin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

MOA of digoxin

A
  • Inhibits Na+/K+-ATPase ion transport system (more Na+ inside cell)
  • Increased intracellular Na+ then affects the Na+/Ca2+ exchanger (more Ca2+ inside the cell for increased force of contraction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does digoxin affect resting membrane potential

why?

A

decreases

(less negative, increased automaticity)

d/t changes in K+ gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does digoxin affect phase 4 of cardiac action potential?

A

increases slope

(increased automaticity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does digoxin affect the duration of action potential?

A

decreased duration d/t shortening of phase 2

(corresponds to ventricular contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

effect of digoxin on cardiac output

what effects does this have?

A

increases

  • increased renal perfusion
  • diuresis of newly mobilized edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how does digoxin affect ANS activity?

A
  • enhanced PNS activity
  • SA node activity decreased
  • slowed conduction through AV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effect of digoxin on contractility

how does this affect SV, preload, and LVEPD?

A

increased contractility

  • increased SV
  • decreased heart size (decreased preload)
  • decreased LVEDP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

effect of digoxin on tissue perfusion

A

improved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how does digoxin affect SVR

A

decreases (leading to even better stroke volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how does digoxin affect HR?

why?

A

slowed HR d/t negative chronotropic and dromotropic effects

(increased PNS activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how is increased contractility offset in a normal heart?

how does digoxin affect CO in a normal heart?

A

decreases in HR and direct vasoconstriction in arterial smooth muscle

CO may be unchanged or even decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

effects of positive inotropic effects with no change in HR on a failing heart

A
  • decreased preload
  • decreased afterload
  • decreased wall tension
  • decreased O2 consumption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

EKG changes assoc. with cardiac glycosides

A
  • prolonged PR
  • shortened QT
  • ST segment depression
  • smaller or inverted T wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

dose of digoxin

A

up to 10 mcg/kg over 30 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

onset and elimination ½ life of digoxin

A

onset 5-30 minutes

elim. ½ life: 31-33 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does renal failure affect elimination time of digoxin?

A

can be prolonged up to 4.4 days in renal failure pts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how is digoxin excreted

A

daily via kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

protein binding of digoxin

A

25% bound to protein (skeletal muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

therapeutic range of digoxin

A

0.5 - 2.5 ng/mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how common is digoxin toxicity?

A

20% of pts taking it will have some form of toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

causes of digoxin toxicity

A
  • renal dysfunction (most common)
  • hypokalemia
  • increasing myocardial binding of drug
  • hypoxemia (increased SNS activity)
  • hypercalcemia, hypomagnesemia
  • decreased muscle mass (elderly)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

for every 10 mmHg increase in PaCO2, serum K decreases an average of:

A

0.5 mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

most frequent cause of death with digoxin toxicity

A

Vfib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what EKG change confirms digoxin toxicity?

A

no 1 specific change confirms toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

patient population most likely to have CNS symptoms with digoxin toxicity

A

elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

GI symptoms of digoxin toxicity

A
  • N/V
  • Diarrhea
  • increased salivation
38
Q

CNS symptoms of digoxin toxicity

A
  • fatigue
  • confusion
  • delirium
  • blurred vision
  • green halos
39
Q

electrolyte imbalance seen with digoxin toxicity

A

life-threatening hyperkalemia

40
Q

correctable causes of digoxin toxicity

A
  • hypokalemia
  • hypomagnesemia
  • arterial hypoxemia
41
Q

treatment of complete AV block associated with digoxin toxicity

A

temporary pacemaker

42
Q

antiarrhythmics used to treat digoxin toxicity

A
  • lidocaine
  • atropine
43
Q

common events under anesthesia that increase risks of digoxin toxicity

A
  • altered renal function
  • hyperventilation causing hypokalemia
  • increased sympathetic activity
44
Q

use of prophylactic digoxin in thoracic/abd surgeries

A

in elderly patients, 1mg over 4 doses the day before and morning of surgery decreased SVT incidence

45
Q

use of prophylactic digoxin for surgical procedures in pts with cardiac disease

A

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

46
Q

how does digoxin interact with succinylcholine?

A

additive PNS effects or cause dsrhythmias d/t catecholamine release (theoretical)

47
Q

how does digoxin interact with beta agonists?

A

increased dysrhythmias

48
Q

how does digoxin interact with IV calcium

A

causes dysrhythmias

49
Q

how is digoxin affected by diuretics

A

diuretics causing loss of K+ can lead to digoxin toxicity

50
Q

which volatile is associated wtih dysrhythmias when used with digoxin?

A

halothane

due to sensitization of myocardium to catecholamines

51
Q

2 meds we’ll use a lot that decrease automaticity of digoxin

A
  • fentanyl
  • isoflurane
52
Q

MOA of PDE-3 Inhibitors

A

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

53
Q

effect of PDE-3 inhibitors

A

positive inotropic effect with diastolic relaxation and vascular smooth muscle relaxation

54
Q

clinical use of PDE-3 inhibitors

A

acute cardiac failure

55
Q

how does increased cAMP affect the myocardium vs. vascular smooth muscle?

A
  • myocardium: increases intracellular Ca2+
  • vascular smooth muscle: decreases intracellular Ca2+ by facilitating uptake into sarcoplasmic reticulum (smooth muscle relaxation and dilation)
56
Q

PDE-3 inhibitors

A
  • Amrinone
  • milrinone (Primacor)
57
Q

nonselective PDE3 inhibitor

A

theophylline

58
Q

effects of amrinone?

A
  • inotropic effect, vasodilation
  • increases CO within 5 minutes
59
Q

side effects of amrinone

A
  • hypotension d/t vasodilation
  • thrombocytopenia
  • dysrhytmogenic
60
Q

advantage of amrinone over cardiac glycosides

A

therapeutic index is 100:1 vs. 1.2:1

61
Q

effects of milrinone

A
  • inotropic effect, vasodilation
  • little effect on HR and myocardial O2 consumption
62
Q

uses of milrinone

A
  • acute LV dysfunction after cardiac surgery
  • weaning from CBP
63
Q

PDE-3 inhibitor that has 30x the inotropic potency of amrinone with less side effects

A

milrinone

64
Q

dosing of milrinone for bolus vs. infusion

A

bolus 50 mcg/kg

infusion 0.5 mcg/kg/min

65
Q

uses of theophylline

A

treatment of bronchospasm

(recommended to reserve use after beta 2 agonists and steroids have been tried)

66
Q

side effects of theophylline

A
  • may relax GE sphincter
  • can cross placenta
  • toxic effects: dysrhytmias
67
Q

metabolism of theophylline

what things can negatively or positively affect its metabolism?

A
  • liver metabolism
  • negatively affected by alcoholism, cimetidine, or age extremes
  • smoking speeds metabolism
68
Q

CV effects of IV calcium admin

A
  • inotropic effect of increased SV, decreased LVEDP (especially in patients with hypocalcemic)
  • HR and SVR decrease
69
Q

which contains more calcium - CaCl or CaGluconate?

A

CaCl

70
Q

AE of giving IV calcium to pts receiving digoxin and also hypokalemic

A

arrhytmias

71
Q

what is inotropy?

A

the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload

72
Q

contractility is related to the rate of myocardial muscle shortening, which is dependent on:

A

intracellular Ca2+ concentration during systole

73
Q

MOA of glucagon

A
  • stimulates cAMP production
  • causes catecholamine release
74
Q

positive chronotropic effects of glucagon are useful for what treatment?

A

symptomatic bradycardia, especially in cases of calcium blocker or beta blocker overdose

increases HR and contractility

75
Q

AE of glucagon

A

tachycardia - can be significant enough to interfere with filling and offset ability to increase CO (causing heart failure)

76
Q

dose and elimination ½ time of glucagon

A
  • 1-5 mg rapid bolus
  • elim ½ time 3-6 min
77
Q

adverse effects of glucagon

A
  • N/V
  • hyperglycemia
  • paradoxical hypoglycemia
  • hypokalemia
78
Q

how does glucagon cause smooth muscle relaxation

A

increased cAMP in smooth muscle decreases intracellular Ca2+

decreased intracellular Ca2+ by facilitating uptake into SR, leading to smooth muscle relaxation

79
Q

MOA of methylene blue

A

potent NO synthase inhibitor in vascular endothelial cells

binds to guanylate cyclase in vascular smooth muscle, blocking cGMP action

80
Q

how does methylene blue increase SVR

A

by inhibiting NO synthase release in vascular endothelial cells

decreased NO release = increased SVR

81
Q

uses of methylene blue

A
  • septic shock
  • endocarditis
  • transplant
  • protamine reaction
  • post CPB to counteract excessive vasodilation of vasoplegic syndrome
82
Q

methylene blue dose

A

2 mg/kg over 30 min followed by 0.5-1 mg/kg/hr if needed

83
Q

why does digoxin cause a prolonged PR interval

A

delay through AV node

84
Q

why does digoxin shorten the QTc

A

soo the book says more rapid repolarization and her notes say depolarization..at this moment I do not have the brain cells to know which is correct

85
Q

why does digoxin cause ST segment depression

A

decreased slope of phase 3 depolarization of cardiac action potential

~of note phase 3 is repolarization so i think she had a typo?~

86
Q

why does digoxin cause a smaller or inverted T wave

A

decreased slope and duration of phases 2 & 3

87
Q

T/F - if your pt who takes digoxin has ST segment or T wave changes, no need to be alarmed because that’s a normal change with digoxin

(info from book)

A

false - changes in ST and T don’t correlate with therapeutic plasma concentrations of cardiac glycosides

may indicate myocardial ischemia

88
Q

what is the most frequent cause of digoxin toxicity in the absence of renal dysfunction?

(book)

A

concurrent admin. of diuretics that cause K+ depletion

89
Q

how can supplemental potassium help in digoxin toxicity?

(book)

A

decreases binding of digoxin to cardiac muscle - directly antagonizes cardiotoxic effects

(still check a K+ before you give!)

90
Q

what is digibind?

(book/google)

A

digoxin antibodies that decrease plasma concentration of digoxin

used to treat life-threatening digoxin toxicity

S5 - Anesthesia Pharm II - Test 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions