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Oral Boards J > Beta Antagonists and Vasodilators > Flashcards

Beta Antagonists and Vasodilators Flashcards

1
Q

Esmolol Class

A

selective B1 antagonist

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2
Q

Esmolol Use

A

used to prevent or minimize tachycardia and hypertension in response to perioperative stimuli (such as intubation, surgical stimulation, and emergence)
May decrease post op opioid requirements

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3
Q

Esmolol MOA

A

Competitive antagonist of B1 receptors (inhibits B2 receptors at higher doses)

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4
Q

Esmolol Dose

A

0.5mg/kg or 10mg
Infusion = 50 mcg/kg/min
(Uptitrate q5min to max dose 200 mcg/kg/min)

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5
Q

Esmolol Pharmacokinetics

A 
Onset = 1 - 2 min 
DOA = 5 - 10 min 
Metabolism = rapid hydrolysis by plasma esterase metabolism in RBCs 
Elimination = renal
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6
Q

Esmolol Contraindications

A

Bradycardia, 1st degree heart block, cardiac failure

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7
Q

Esmolol Considerations

A

Caution in patients with hypotension and bronchoconstriction

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8
Q

Labetolol Class

A

Non-selective alpha and beta antagonist

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9
Q

Labetolol Use

A

treat tachycardia and hypertension

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10
Q

Labetolol MOA

A

competitive antagonist of B1, B2, and A1 receptors

Beta blockade to alpha blockade is 7:1

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11
Q

Labetolol Dose

A

Intermittent bolus 5 - 20 mg

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12
Q

Labetolol Pharmacokinetics

A 
Onset = 5 min 
DOA = 3 - 6 hours 
Metabolism = hepatic 
Elimination = hepatic and renal
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13
Q

Labetolol Contraindications

A

Caution in patients with asthma, COPD, bradycardia, hypotension, and CHF

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14
Q

Labetolol Considerations

A

May cause left ventricular failure, orthostatic hypotension, and bronchospasm

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15
Q

Nitroglycerin Class

A

Peripheral vasodilator, venous dilation predominating over arterial dilation

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16
Q

Nitroglycerin Use

A

Relieves myocardial ischemia, coronary vasospasm

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17
Q

Nitroglycerin MOA

A

Comes from it’s metabolism
As NTP is metabolized, it released nitric oxide + cyanide
NO activates guanylyl cyclase, which synthesize cGMP, decreases intracellular calcium, causing SM dilation

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18
Q

Nitroglycerin Dose

A

IV Infusion: 5 - 100 mcg/min

SL: 0.4 mg

19
Q

Nitroglycerin Pharmacokinetics

A

Onset: 2 - 5 minutes
DOA: 5 - 10 minutes
Metabolism: rapid reductive hydrolysis in liver + blood by glutathione-organic nitrate reductase
Produces nitrate, which can convert hemoglobin to methemoglobin
Elimination: Kidneys

20
Q

Nitroglycerin Contraindications

A

Caution: AS, hypertrophic cardiomyopathy, increased ICP, hypotension, CHF

21
Q

Nitroglycerin Considerations

A

Risk for methemoglobinemia
Tolerance may develop with prolonged use
Side effects: headache, tachycardia (rebound from dilated veins)
Ideal for MIs: decreasing preload reduces myocardial oxygen demand & increases endocardial perfusion
Redistributes coronary BF to ischemic areas of subendocardium
Relieves coronary vasospasm

22
Q

Nitroprusside Class

A

Direct peripheral arterial vasodilator, non-selective relaxation of arterial & venous SM

23
Q

Nitroprusside Use

A

Reliable & easily-titrated antihypertensive

24
Q

Nitroprusside MOA

A

As NTP is metabolized, it releases nitric acid + cyanide

NO activates guanylyl cyclase which synthesizes cGMP, decreases intracellular calcium, causing SM dilation

25
Q

Nitroprusside Dose

A

Infusion: 0.3 - 10 mcg/kg/min

26
Q

Nitroprusside Pharmacokinetics

A

Onset: 1 minute
DOA: 3 - 5 minutes
Metabolism: into cyanide then to thiocyanate, which then is eliminated by kidneys
Elimination: Thiocyanate cleared by kidneys

27
Q

Nitroprusside Contraindications

A

Caution in patients w/ AS, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure
Renal failure due to buildup of thiocyanate causing thyroid dysfunction, muscle weakness, nausea, hypoxia, acute toxic psychosis

28
Q

Nitroprusside Considerations

A

Side effects: headache, tachycardia, bronchodilation (due to NO)
Dilation of coronary arterioles may result in an intracoronary steal
Reductions in pulmonary artery pressure & the hypoxic pulmonary vasoconstriction mechanism may decrease lung perfusion
Large doses of NTP may lead to methemoglobinemia
Risk of cyanide toxicity

29
Q

Nitroprusside Considerations

A

Side effects: headache, tachycardia, bronchodilation (due to NO)
Dilation of coronary arterioles may result in an intracoronary steal
Reductions in pulmonary artery pressure & the hypoxic pulmonary vasoconstriction mechanism may decrease lung perfusion
Large doses of NTP may lead to methemoglobinemia
Risk of cyanide toxicity

30
Q

Hydralazine Class

A

Direct acting arterial vasodilator

31
Q

Hydralazine Use

A

Hypertension

32
Q

Hydralazine MOA

A

Activate guanylate cyclase to increase cGMP

33
Q

Hydralazine Dose

A

Intermittent boluses: 2.5 - 20 mg

34
Q

Hydralazine Pharmacokinetics

A

Onset: 15 minutes
DOA: 2 - 4 hours
Metabolism: Liver
Elimination: Kidneys

35
Q

Hydralazine Contraindications

A

Caution in patients who cannot tolerate reflex tachycardia or hypotension (CAD, AS, hypertrophic cardiomyopathy, increased ICP, CHF)

36
Q

Hydralazine Considerations

A

Reflex tachycardia, hypotension

37
Q

Nicardipine Class

A

Calcium channel blocker

38
Q

Nicardipine Use

A

Angina, HTN, arrhythmias, peripheral vascular disease, esophageal spasm, cerebral vasospasm, & controlled hypotension

39
Q

Nicardipine MOA

A
  • Depress electrical impulses in the sinoatrial (SA) + atrioventricular (AV) nodes by blocking the influx of Ca, resulting in negative chronotropic + inotropic effects & increasing coronary + systemic vasodilation – specifically L-type Ca channels
  • Blocks calcium influx into vascular smooth muscle and cardiac muscle
40
Q

Nicardipine Dose

A

5 mg/hr, increase by 2.5 mg/hr every 15 minutes, up to 15 mg/hr

41
Q

Nicardipine Pharmacokinetics

A

Onset: 1 - 5 minutes
DOA: 3 - 6 hours
Metabolism: Liver
Elimination: Kidneys

42
Q

Nicardipine Contraindications

A

Caution in acute MI, HF, bradycardia, hypotension, dantrolene (both work on Ca channels)

43
Q

Nicardipine Considerations

A

Reflex tachycardia, headache

Oral Boards J (11 decks)

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