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M2 Pharmacology Jen > Cardiotonic > Flashcards

Cardiotonic Flashcards

1
Q

Atropine: class

A

Muscurinic blocker

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2
Q

Atropine: indication

A

Cholinergic syndrome, Bradycardial, organophosphate poisoning, cardiac rescessatation & more…to dilate pupils, bradycardia (raises HR), to decrease secretions, organophosphate poisoning (insecticide, etc – blocks action of ACh; given with Pralidoxime)

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3
Q

Atropine: PD

A

lowers the parasympathetic activity of all muscles and glands regulated by the parasympathetic nervous system (dilates eye, increases HR, reduces airway secretions, etc)

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4
Q

Atropine: PK

A

effect lasts 4-8 hours (except in eye, where they can last up to 72 hrs

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5
Q

Atropine: Tox

A

Atropine poisoning (intensification of sympathetic effects in same end organs):
Mad as a hatter: delirium, hallucinations
Blind as a bat: mydriasis, photophobia, blurred vision (cycloplegia)
Dry as a bone: block of secretions (salivary, sweat)
Red as a beet: prostaglandins?, fever, anhidrosis (inability to sweat), dilation of vessels
Hot as a hare: hyperthermia resulting from anhidrosis; can be lethal in infants
Other side effects of atropine include:
urinary retention (block of detrusor muscle)
bronchodilation
constipation
tachycardia

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6
Q

Atropine: excr

A

both liver and kidney

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7
Q

Atropine: special

A

lipid soluble (can cross BBB); use with caution in infants because of risk of hyperthermia; don’t use in men with prostatic hyperplasia

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8
Q

Epinephrine: class

A

direct-acting adrenergic agonist

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9
Q

Epinephrine: indication

A

vasopressor, cardiac stimulant, bronchodilator, adjunct to local anesthetics, treatment for anaphylaxis

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10
Q

Epinephrine: PD

A

major action is to stimulate peripheral alpha-1 adrenoceptors, thereby leading to vasoconstriction (resistance arterioles, increase SVR) and venoconstriction (in capacitance vessels, increase preload); beta-1 receptors leading to tachycardia and increased contractility; and beta-2 receptors leading to bronchodilation; these actions are also helpful in severe allergic reactions (e.g. anaphylaxis) by stabilizing mast cells

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11
Q

Epinephrine: PK

A

can be given iv (immediate), IM (variable), SC 5-15 min), and via inhalation (1-5 min onset), ophthalmic topical; metabolized by COMT and then renally excreted

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12
Q

Epinephrine: tox

A

excessive vasoconstriction, HTN, hemorrhagic stroke, angina, arrhythmias

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13
Q

Epinephrine: interactions

A

risk of excessive hypertension in patients taking propranolol

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14
Q

Epinephrine: special

A

utility with local anesthetics; drug of choice in severe anaphylactic reactions (along with others)

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15
Q

Epinephrine: monitor

A

BP, HR, rhythm, infusion site, evidence of extravasation

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16
Q

Dopamine: class

A

Adrenergic & dopaminergic agonist

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17
Q

Dopamine: indication

A

inotropic agent; vasopressor –> shock, CHF.

Note: not useful in treatment of Parkinson’s Disease, why not???

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18
Q

Dopamine: PD

A

stimulates DA (renal blood flow), beta-1, and alpha-1 receptors at different concentrations (low, med, high infusion rates)

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19
Q

Dopamine: PK

A

can only be infused IV; acts quickly within minutes; half-life brief (minutes), hence continuous infusion

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20
Q

Dopamine: tox

A

ectopy, tachycardia, angina, nausea

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21
Q

Dopamine: special

A

correct hypovolemia first; administer through large vein; prevent extravasation; monitor patient closely

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22
Q

Lisinopril: class

A

Angiotensin converting enzyme inhibitor

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23
Q

Lisinopril: indication

A

Antihypertensive, CHF

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24
Q

Lisinopril: PD

A

inhibits conversion of AT I to AT II by ACE; diminishes both vasocontriction and stimulation of aldosterone secretion by AT II

25
Q

Lisinopril: PK

A

well absorbed; onset 1 h, peak 6 h, duration 24 h; once a day is fine; excreted primarily in urine as unchanged drug

26
Q

Lisinopril: tox

A

orthostatic hypotension; use with caution in patients with impaired renal function, or renal artery stenosis; be careful in patients on diuretics, or those with aortic stenosis; angioedema, cough; acute renal failure

27
Q

Lisinopril: interactions

A

additive effects with most other antihypertensives; NSAIDs may reduce ability to lower BP; hyperkalemia with KCL, others

28
Q

Lisinopril: special

A

often discontinue diuretics prior to beginning use to reduce hypotension; Category C/D in pregnancy, abnormal cartilage development

29
Q

Lisinopril: monitor

A

BP, weight, edema, K, BUN, creatinine!!!!!

30
Q

Hydralazine: class

A

Arterial vasodilator

31
Q

Hydralazine: indication

A

Antihypertensive, CHF

32
Q

Hydralazine: PD

A

“direct” acting vasodilator; seems to act by inducing endothelium to produce NO, which then passes to SM cells and induces production of cGMP, minimal venodilating effect

33
Q

Hydralazine: PK

A

given po, im, iv; metabolized extensively in GI mucosa and in liver, eventually excreted as metabolites in urine; F ~40%; onset 30 after po dose, 10 min after iv dose; persist for 2-6 hours

34
Q

Hydralazine: tox

A

more dangerous in patients with renal disease, prior stroke, angina; watch for hypotension, edema, occasionally drug-induced lupus

35
Q

Hydralazine: interactions

A

additive effects with most other antihypertensives

36
Q

Hydralazine: special

A

never use as chronic oral monotherapy for treatment of hypertension, since edema and reflex tachycardia will result; concern giving to patients with CAD

37
Q

Hydralazine: monitor

A

BP, weight, edema, BUN, creatinine, symptoms of lupus or angina

38
Q

Hydralazine: pregnancy

A

Lowers BP in 3rd tri. Used only for that amt of time won’t cause lupus.

39
Q

Prazosin: class

A

a1 blocker

40
Q

Prazosin: indication

A

Antihypertensive, Rx for BHP, tx for kidney stones, raynaud’s sx.

41
Q

Prazosin: PD

A

blocks alpha-1 receptors on arterioles and veins, thereby inhibiting NE-mediated vasoconstriction and venoconstriction

42
Q

Prazosin: PK

A

available po or transdermal; variable oral bioavailability (~60%), onset 2 h, duration 12-24 h; extensively metabolized in liver

43
Q

Prazosin: tox

A

excessive hypotension with passing out, especially orthostatic, especially in patients on diuretics

44
Q

Prazosin: interactions

A

additive effects with most other antihypertensives, especially diuretics

45
Q

Prazosin: special

A

start gradually, and at bedtime, to avoid first-time passing out ; male patients with BPH?

46
Q

Prazosin: monitor

A

BP, weight, edema,

47
Q

Nitroprusside: class

A

Venous and arterial vasodilator

48
Q

Nitroprusside: indication

A

Antihypertensive, CHF

49
Q

Nitroprusside: PD

A

acts “directly” on vascular smooth muscle to cause dilatation of both veins and arterioles; metabolized to release CN- and NO, which activates guanylate cyclase, leads to production of cGMP from GTP, which then leads to vasodilation; cGMP then hydrolyzed to GMP by PDE

50
Q

Nitroprusside: PK

A

only route is iv; rapid onset (minutes) and cessation (minutes), thereby allowing minute-by-minute titration; CN- metabolite is converted to SCN in liver, then excreted in urine; must be given by continuous infusion

51
Q

Nitroprusside: tox

A

excessive hypotension; accumulation of CN- and thiocyanate; headache; decreased blood flow to brain

52
Q

Nitroprusside: interactions

A

additive effects with most other antihypertensives

53
Q

Nitroprusside: special

A

monitor patient VERYclosely—must be in ICU with arterial line; avoid high infusion rates or prolonged infusions, to prevent accumulation of CN-; use with caution in patients with increased intracranial pressure

54
Q

Nitroprusside: monitor

A

BP, HR, metabolic acidosis; most often requires arterial line

55
Q

Carvedilol: class

A

a1 and b blocker, antioxidant

56
Q

Carvedilol: indication

A

CHF

57
Q

Carvedilol: PD

A

order of affinity for binding is β1 & β2 > α1 > α2 (highest affinity for beta receptors)

58
Q

Carvedilol: special

A

has antioxidant effects; improves survival in patients with heart failure

M2 Pharmacology Jen (11 decks)

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