nifedipine/dopamine/dobutamine/verp Flashcards

1
Q
nifedipine effects
systemic BP
Heart rate
myocardial depression
sinoatrial node
av node conduction
coronary artery dilation
peripheral artery dilation
A
decrease BP
increase to no change HR
moderate myocardial depression
no sa
no av
marked coronary artery dilation
marked peripheral artery dilation
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2
Q

nifedipine oral dose

iv odse

A

10-30mg oral every 8 hrs

5-15mcg/kg-iv

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3
Q

nifedipine side effects

A

flushing, vertigo, and headache are most common

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4
Q

dopamine clinical uses

A

increase cardiac output in patients with decreased contractility, low systemic blood pressure and low urine output as may be present after cardiopulmonary bypass or chronic heart failure.

increases myocardial contractility
renal blood flow
GFR
excretion of sodium and urine output

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5
Q

when is dopamine not preferred

A

pulmonary HTN

right ventricular function

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6
Q

dopamine d1 receptors

A

postsynaptically -vasodilation in renal, mesenteric, coronary and cerebral vascular beds and inhibition of sodium potassium pump.

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7
Q

dopamine

receptors stimulated

A

d1=d2>b>a

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8
Q

dopamine d2 receptors

A

presynaptically- inhibit adenylate cyclase. inhibit release of NE. nausea and vomiting and reward.

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9
Q

dopamine at infusion of 0.5-3mcg/kg/min

A

d1 and d2 receptors. vasodilation diuresis and natriuresis.

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10
Q

dopamine at 3-10mcg/kg/min

A

beta receptors and some alpha induces NE release - increases co by increasing chronotropy and contractility.

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11
Q

dopamine at greater than 10mcg/kg/min

A

predominantly stimulates alpha 1 receptors. leading to arterial nd venous vasoconstriction. increases SVR BP CO and reflex bradycardia may occur

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12
Q

what is the variability of dopamine

A

10-75 fold variability in dopamine plasma concentrations.

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13
Q

dopamines increase coronary perfusion and cardiac output while decreasing after load is similar to what device

A

intraaortic balloon pump

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14
Q

elimination of atracurium

A

hoffman elimination

nonspecific esterase

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15
Q

elimination of cisatracurium

A

hoffman elimination

nonspecific esterase

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16
Q

elimination of rocuronium

A

hepatic renal

liver- excreted in the bile-per hammon

17
Q

elimination of vecuronium

A

renal 30%

hepatic 40-80%

18
Q

elimination of pancuronium

A

renal primarily some hepatic

19
Q

elimination of succs

A

plasma cholinesterase

20
Q

elimination of mivacurium

A

plasma cholinesterase

21
Q

ketamine receptors

A
NMDA
Opioid receptors
monoaminergic receptors 
muscarinic receptors
voltage sensitive sodium
L type Calcium channels
neuronal nicotinic acetylcholine receptors.
22
Q

what is ketamine actions on gaba a receptors

A

weak actions

23
Q

what does ketamine suppress

A

neutrophil production of inflammatory mediators and improves blood flow.

24
Q

direct inhibition of cytokines in blood by ketamine contributes to what

A

contributes to the analgesic effects of ketamine

25
Q

ketamine inhibits action of NMDA receptors by using what neurotransmitter

A

glutamate- and decreases presynaptic release of glutamate

26
Q

what antagonizes ketamine

A

anti cholinesterase drugs

27
Q

what does ketamine do with sodium channels

A

mild local anesthetic like properties sharing binding site with local anesthetics.

28
Q

what does ketamine have to do with the nicotinic acetylcholine receptors

A

may play a role in its analgesic effects

29
Q

why is ketamine a good choice IM (what type of patients)

A

induction drug in children and difficult to manage mentally challenged patients regardless of age

30
Q

why is ketamine a good choice for rapid induction for asthma patients

A

it has drug induced bronchodilation

31
Q

patients with increased ICP and ketamine why dont we want to use it

A

nystagmus

32
Q

the side effect of ketamine is increase cerebral blood flow by how much

A

60%

33
Q

administration of what medication can blunt ketamine induced increases in cerebral blood flow

A

thiopental, diazepam, midazolam,