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NUNA 681 Pharm II > Exam II: CV Drugs Inotropes > Flashcards

Exam II: CV Drugs Inotropes Flashcards

1
Q

Plant family from which many ___ ___are derived.

[Digitalis]

A

cardiac glycosides

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2
Q

Inotrope used for patients with ___ and to slow ventricular response of patients with ___(PAT, afib, aflutter).

[Digitalis]

A

congestive heart failure, supraventricular tachydysrhythmias

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3
Q

Digoxin decreases the risk of ___ due to heart failure, but increases the incidence of ___ ___(arrhythmias).
[Digitalis]

A

death, sudden death

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4
Q

Digoxin probably still plays a role in patients with ____ with evidence of congestion who are unable to tolerate ___ ___ of disease-modifying agents due to borderline blood pressure/renal function.

[Digitalis]

A

severe HF, high doses

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5
Q

Digoxin should be used with the aim of ___ ___ ___, while SDC and ___ and ___levels should be closely monitored to minimize the risk of toxicity.

[Digitalis]

A

reducing hospital readmissions, creatinine and potassium

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6
Q

In the treatment of SVT, ___ can be given in combination with a ___-___ at smaller doses of each and yet obtain more rapid control.

[Combination therapy]

A

digoxin, beta-antagonist

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7
Q

Contraindications:
Wolff-Parkinson-White – ___% develop ___ from increased ___ down the alternate path

[Combination therapy]

A

30, Vfib, conduction

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8
Q

Contraindications:
Hypertrophic cardiomyopathy (subaortic stenosis) –___

[Combination therapy]

A

increased obstruction with increased contractility

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9
Q

Contraindications:
Acute myocardial infarction – increase ___ ___ with increased ____
[Combination therapy]

A

oxygen demand, contractility

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10
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin has been shown to improve ____ without any benefit on _____.

A

morbidity
mortality

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11
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin may act by ____ sympathetic activity.

A

decreasing

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12
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin may not be effective in patients who have normal ___ ___ ____ function.

A

left ventricular systolic

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13
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

The benefits of digoxin therapy are greatest in patients with ___ ___ ____, an enlarged heart and a ___ ___ ____ ____.

A

severe heart failure
3rd heart sound gallop

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14
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

Digoxin may be used in patients with mild to moderate heart failure if they do not respond to an ___-___ ___ ___ or a ___ ____.

A

angiotensin-converting enzyme inhibitor
beta blocker

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15
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

___ dosages of digoxin can be effective.

A

Low

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16
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

___ function and possible ___ ____ must be considered in deciding on an appropriate dosage of digoxin.

A

Renal
drug interactions

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17
Q

[Digoxin (Lanoxin) Therapy in Congestive Heart Failure]

In general, digoxin therapy should be _____ in the acute phase after myocardial infarction.

A

avoided

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18
Q

Digoxin MOA:
___ Effects
Inhibition of ______ ion transport system – causing increased Na inside the cell
Increased intracellular Na then affects the Na/Ca exchanger and ___ ____ is taken out of the cardiac cell.
More ___ inside the cell accounts for increased contraction force.

A

Direct
Na/K ATPase
less Ca++
Ca++

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19
Q

Decrease (less negative) resting membrane potential (automaticity)
Increases in the slope of phase 4 (automaticity)
Decrease in duration of action potential due to shortening of phase 2 (corresponds to vent contraction)

A

Decreased resting membrane potential (less negative) and increased automaticity are due to changes in the potassium gradient.

Phase 2 reflects closure of sodium ion channels and inward flux of calcium ions through specific slow calcium ion channels. Phase 2 corresponds to ventricular contraction.

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20
Q

Digoxin ANS activity -
Enhanced _____ activity
___ node activity decreased
Slowed conduction through the ___ node

A

PNS
SA
AV

(Enhanced PNS - activation of vagal nuclei and the nodose ganglion in the CNS. Results in slowed HR – especially with a fib)

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21
Q

Digoxin CV effects: Increased ____ ____, ____, decreased heart ____, ____, ______

A

myocardial contractility, SV
size, preload, LVED pressure

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22
Q

Digoxin CV: increased CO, ____ perfusion, and diuresis of newly ___ ____

A

renal
metabolized edema

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23
Q

Digoxin CV effects: Improved ____ perfusion, decreased _____ outflow, decreased ____ (____) leading to even better SV

A

tissue
sympathetic
SVR (afterload)

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24
Q

Digoxin CV: increased PNS activity, slowed HR - negative ____ and negative ____

A

chronotropic
dromotropic

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25
Q

Digoxin CV: In the normal heart, increased contractility is offset by decreases in ___ and direct _____ in the arterial smooth muscle. Cardiac output may remain unchanged or even ____.

A

HR
vasoconstriction
decrease

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26
Q

Digoxin CV: In the failing heart, no change in HR with positive inotropic effects - decreased p____, a____, wall tension, and oxygen c_____.

A

preload, afterload
consumption

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27
Q

Cardiac glycosides cause changes shown on the EKG:
Prolonged ___ – delay through the AV node

A

PR

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28
Q

Cardiac glycosides cause changes shown on the EKG:
Shortened QT – more rapid ____ ____

A

ventricular repolarization

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29
Q

Cardiac glycosides cause changes shown on the EKG:
___ segment depression – decreased slope of ___ ___

A

ST
phase 3

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30
Q

Cardiac glycosides cause changes shown on the EKG:
Smaller or inverted __ wave – decreased slope and duration of phases __ and __

A

T
2 and 3

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31
Q

Digoxin -
Dose:
Onset:
Route:
Clearance:
Elimination 1/2 life:

A

Dose: up to 10 mcg/kg over 30 minutes
Onset: 5 to 30 minutes
Route: IV
Clearance: 35% excreted daily via kidneys
Elimination ½ life: 31-33 hours

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32
Q

Dig - Prolonged with ___ failure to up to ___ days

A

renal
4.4 days

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33
Q

Dig - ___% bound to protein (skeletal muscle) – decreased muscle mass in ___

A

25%
elderly

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34
Q

Digitalis Toxicity: ____ therapeutic range 0.5 – 2.5 ng/ml

A

narrow

TC says we dont need to know this range

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35
Q

Digitalis Toxicity: Incidence: __% of patients on digoxin will have some form of toxicity

A

20%

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36
Q

Digitalis Toxicity: MOA - inhibition of ____ ion transport system; Ca accumulates in the cell causing ____.

A

Na/K ATPase
dysrhythmias

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37
Q

Digitalis Toxicity: Causes: most commonly ____ dysfunction; hypo____ (due to diuretic) increases myocardial ____ of drug (may also be due to hyperventilation); increased sympathetic activity related to hypo___; hyper____, hypo____, decreased muscle mass (elderly).

A

renal
hypokalemia
binding
hypoxemia; hypercalcemia, hypomagnesia

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38
Q

Digitalis Toxicity: Hyperventilation related to hypokalemia – for every __ mm Hg decrease in PaCO2, serum potassium decreases an average of __ mEq/L

On the other hand, increased serum potassium ___ ___ of cardiac glycosides to the ____ enzyme complex

A

10
0.5
inhibits binding
Na-K ATPase

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39
Q

Digitalis Toxicity: Symptoms
Arrhythmias – first symptom of arrhythmia is worsening of pre-existing CHF (8)

A

PVCs
junctional tachycardia
Wenckebach’s AV block
sinus bradycardia or arrest
atrial tachycardia – most common w dig toxicity
bidirectional Vtach – two different foci
Atrial flutter
Vfib – most frequent cause of death with dig toxicity

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40
Q

Digitalis Toxicity: what one specific EKG change confirms toxicity?

A

No one specific EKG change confirms toxicity
Increased automaticity, delayed AV conduction

41
Q

Digitalis Toxicity: ____ symptoms seen most commonly in the elderly.

A

CNS

42
Q

Digitalis Toxicity: GI symptoms -

A

Nausea and vomiting, diarrhea, increased salivation

43
Q

Digitalis Toxicity: CNS symptoms. -

A

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

44
Q

Digitalis Toxicity: Life-threatening ____ – with severe toxicity, related to paralysis of Na/K pump and leakage of ___ out of cell.

A

hyperkalemia
K

45
Q

Digitalis Toxicity: Treatment -
___ ____ unless most urgent until toxicity is corrected.

A

postpone case

46
Q

Digitalis Toxicity: treatment -
___ digoxin

A

stop

47
Q

Digitalis Toxicity: treatment -
check _____

A

electrolytes

48
Q

Digitalis Toxicity: Treatment -
Correction of cause (hypo____, hypo____, arterial hypo____)

A

(hypokalemia, hypomagnesemia, arterial hypoxemia)

*supplement K only after checking level

49
Q

Digitalis Toxicity: Treatment -
Anti-arrhythmic administration (3)

A

lidocaine, atropine, digibind

Per Dr. Cahoon’s notes:
Lidocaine 1-2 mg/kg IV
Phenytoin 0.5-1.5 mg/kg IV over 5 mins
Atropine 35-70 mcg/kg IV
Propranolol – suppress increased automaticity – but may increase AV node refractoriness

50
Q

Digitalis Toxicity: Treatment -
temporary ____ (complete ___ ___)

A

pacemaker
AV block

51
Q

Prophylactic Digitalis for Surgical Procedures:
___ ____, ____ signs of failure, the diagnosis of cause of arrhythmias might be muddy.

A

Healthy hearts, without

(Events common under anesthesia that increase risks of toxicity – altered renal function, hyperventilation causing hypokalemia, increased sympathetic activity during anesthetic)

52
Q

Prophylactic Digitalis for Surgical Procedures:
Thoracic/abd surgery – in elderly patients, __ mg over ___ doses the day before and am of surgery decreased ___ incidence.

A

1 mg
four doses
SVT

53
Q

Prophylactic Digitalis for Surgical Procedures:
Cardiac disease – decreased incidence of ___ ____ ____ in patients with ___ during recovery

A

impaired cardiac function
CAD

54
Q

Prophylactic Digitalis for Surgical Procedures:
___ continue digitalis therapy esp. if for HR control

A

DO

55
Q

Drug interactions with Digitalis:
______ – additive parasympathetic effect or cause dysrhythmias due to catecholamine release (theoretical)

A

Succinylcholine

56
Q

Drug interactions with Digitalis:
Beta-adrenergic ____ – (pavulon) – increased cardiac dysrhythmias.

A

agonists

57
Q

Drug interactions with Digitalis:
C____ ____ – dysrhythmias

A

Calcium IV

58
Q

Drug interactions with Digitalis:
Diuretics causing loss of K + lead to digitalis toxicity due to _____

A

hypokalemia

59
Q

Drug interactions with Digitalis:
Halothane – ______

A

Halothane – dysrhythmias

60
Q

Drug interactions with Digitalis:
F____, e____, i____ – decrease automaticity

A

Fentanyl, enflurane, isoflurane – decrease automaticity

61
Q

Selective phosphodiesterase inhibitors (PDE III):
non_____, non_____

A

Noncatecholamine, nonglycoside

62
Q

Selective phosphodiesterase inhibitors (PDE III):
MOA: decreased hydrolysis of ___ & ____, increasing the ___ & _____ in the myocardium and vascular smooth muscle

A

cAMP and cGMP
cAMP and cGMP

63
Q

Selective phosphodiesterase inhibitors (PDE III):
Effect: ___ ____ effect with diastolic _____ and vascular smooth muscle _____

A

positive inotropic
relaxation
relaxation

64
Q

Selective phosphodiesterase inhibitors (PDE III):
clinical use: ___ ____ ____

A

Clinical use: acute cardiac failure

65
Q

Selective phosphodiesterase inhibitors (PDE III):

Increases cAMP, increases intracellular Ca and contractility in the myocardium

In vascular smooth muscle, increased cAMP decreases intracellular Ca by facilitating the uptake of Ca into the ___ ____, leading to smooth muscle ____ & _____.

A

sarcoplasmic reticulum
relaxation and vasodilation

66
Q

Selective phosphodiesterase inhibitors - Amrinone:
____ effect and vaso____

A

Inotropic effect and vasodilation

67
Q

Selective phosphodiesterase inhibitors - Amrinone:
increases CO within __ ____

A

5 mins

68
Q

Selective phosphodiesterase inhibitors - Amrinone:
Initial dose ___-___ mg/kg IV, then infusion of __-__ mcg/kg/min

A

0.5-1.5 mg/kg IV
2-10 mcg/kg/min

69
Q

Selective phosphodiesterase inhibitors - Amrinone:
Side effect: ____ due to vasodilation, t______, dysrhythmogenic

A

hypotension
thrombocytopenia

70
Q

Selective phosphodiesterase inhibitors - Amrinone:
Advantage: Safety with therapeutic index is 100:1 compared to 1.2:1 for ____ ____.

A

cardiac glycosides

71
Q

Selective phosphodiesterase inhibitors - Milrinone (Primacor):
____ effect and vasodilation
____ effect on HR and myocardial oxygen consumption

A

inotropic
little

72
Q

Selective phosphodiesterase inhibitors - Milrinone (Primacor):
Use: acute ___ ____ ____ after cardiac surgery; used in weaning from CBP

A

left ventricular dysfunction

73
Q

Selective phosphodiesterase inhibitors - Milrinone (Primacor):
Bolus ___ mcg/kg, infusion of ___ mcg/kg/min

A

50
0.5

74
Q

Selective phosphodiesterase inhibitors - Milrinone (Primacor):
__X the inotropic potency of amrinone w less side effects

A

30

75
Q

Nonselective phosphodiesterase inhibitors -
Inhibits all fractions of PDE isoenzymes __-__

A

I-V

76
Q

Nonselective phosphodiesterase inhibitors - Theophylline:
Uses: treatment of ____ (recommended to reserve the use of theophylline after beta2 agonists and corticosteroids have been tried)

A

bronchospasm

77
Q

Nonselective phosphodiesterase inhibitors - Theophylline:
Side effects: can cross ____, may relax ____ sphincter, narrow therapeutic range of __-__ mcg/ml; toxic effects: dysrhythmias

A

placenta
GE
10-20

78
Q

Nonselective phosphodiesterase inhibitors - Theophylline:
Metabolism: liver metabolism negatively affected by ____, _____ or extremes of age; smoking (____ metabolism)

A

alcoholism, cimetidine
smoking

79
Q

Calcium: Inotropic effect of increased ___, decreased ____ pressure (especially in hypocalcemic)

A

SV
LVED

80
Q

Calcium: ___ and ___ decrease

A

HR and SVR

81
Q

Calcium: Be careful when patient receiving digitalis and also _____; can cause arrhythmias

A

hypokalemic

82
Q

Calcium:
Uses: coming off ____ (cardioplegia with K, citrate in blood, sodium bicarbonate)

A

CPB

83
Q

Calcium: CaCl contains more calcium than _____

A

CaGluconate

84
Q

Calcium:
____ – effect

A

NMB

increased contractility causes reflex decrease svr. “a number of signals (acetylcholine, bradykinin, calcium)” stimulate constitutive nitric oxide synthase in the endothelial cells of the vascular wall (which converts arginine to NO–>–>smooth muscle relaxation.)

85
Q

Cardiac contractility (_____) is the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload. Contractility is related to the rate of myocardial muscle ____, which is, in turn, dependent on the ____ ____ _____ during systole. Increases in heart rate can also enhance contractility under some conditions, perhaps because of the increased availability of intracellular Ca2+.

A

inotropy
shortening
intracellular Ca++ concentration

86
Q

Glucagon: ___ ___ produced in the pancreas

A

Polypeptide hormone

87
Q

Glucagon: Stimulates the formation of ____

A

cAMP

88
Q

Glucagon: Causes the release of ______ – secondary

A

catecholamines

89
Q

Glucagon: Increases the contractility* and HR in the presence of ___ ____

A

beta blockers

90
Q

Glucagon: Can cause tachycardia – significantly high enough to interfere with ___ and offsetting ability to increase ___

A

filling
CO

tachycardia esp if atrial fib

91
Q

Glucagon: “In summary, the available evidence is against a positive inotropic effect of glucagon in the human heart. Thus, it should not be given as an inotropic agent for treating ___ ____ ___ ___ such as acute heart failure or cardiogenic shock. However, experimental and clinical evidence supports its positive _____ effect, which could prove useful for treating symptomatic bradycardia, particularly in cases of calcium or β-receptor antagonist overdose.”

A

low cardiac output states
chronotropic

92
Q

Glucagon: adult dose

A

1 – 5 mg rapid bolus

93
Q

Glucagon: Elimination ½ time is ___-____

A

Elimination ½ time is 3-6 mins

94
Q

Glucagon: side effects

A

May cause n & v, hyperglycemia, paradoxical hypoglycemia, hypokalemia

95
Q

Glucagon: In smooth muscle, increased cAMP decreases intracellular Ca by facilitating the uptake of Ca into the ___ ____, leading to smooth muscle _____

A

sarcoplasmic reticulum
relaxation

96
Q

Methylene Blue:
Potent inhibitor of ___ ___ (__) synthase in vascular endothelial cells; resulting in decreased ___ ____ and increased ____

A

nitric oxide (NO)
NO release
SVR

97
Q

Methylene Blue:
Binds to guanylate cyclase (GC) in the vascular smooth muscle – blocking ___ action in the ____ ___ ____

A

cGMP
vascular smooth muscle

98
Q

Methylene Blue:
Useful in septic shock, endocarditis, transplant, protamine reaction, post ____ to counteract excessive ____ of vasoplegic syndrome

A

CPB
vasodilation

99
Q

Methylene Blue: dosing
Bolus __ mg/kg over __ mins, followed by ____ mg/kg/hr if needed

A

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

NUNA 681 Pharm II (12 decks)

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