Beta Antagonists and Vasodilators Flashcards by Jackie Agranat

Esmolol Class

selective B1 antagonist

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Esmolol Use

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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Esmolol MOA

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

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Esmolol Dose

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

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Esmolol Pharmacokinetics

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

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Esmolol Contraindications

Bradycardia, 1st degree heart block, cardiac failure

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Esmolol Considerations

Caution in patients with hypotension and bronchoconstriction

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Labetolol Class

Non-selective alpha and beta antagonist

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Labetolol Use

treat tachycardia and hypertension

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Labetolol MOA

competitive antagonist of B1, B2, and A1 receptors

Beta blockade to alpha blockade is 7:1

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Labetolol Dose

Intermittent bolus 5 - 20 mg

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Labetolol Pharmacokinetics

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

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Labetolol Contraindications

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

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Labetolol Considerations

May cause left ventricular failure, orthostatic hypotension, and bronchospasm

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Nitroglycerin Class

Peripheral vasodilator, venous dilation predominating over arterial dilation

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Nitroglycerin Use

Relieves myocardial ischemia, coronary vasospasm

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Nitroglycerin MOA

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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Nitroglycerin Dose

IV Infusion: 5 - 100 mcg/min

SL: 0.4 mg

Nitroglycerin Pharmacokinetics

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

Nitroglycerin Contraindications

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

Nitroglycerin Considerations

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

Nitroprusside Class

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

Nitroprusside Use

Reliable & easily-titrated antihypertensive

Nitroprusside MOA

As NTP is metabolized, it releases nitric acid + cyanide

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

Nitroprusside Dose

Infusion: 0.3 - 10 mcg/kg/min

Nitroprusside Pharmacokinetics

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

Nitroprusside Contraindications

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

Nitroprusside Considerations

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

Nitroprusside Considerations

Hydralazine Class

Direct acting arterial vasodilator

Hydralazine Use

Hypertension

Hydralazine MOA

Activate guanylate cyclase to increase cGMP

Hydralazine Dose

Intermittent boluses: 2.5 - 20 mg

Hydralazine Pharmacokinetics

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

Hydralazine Contraindications

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

Hydralazine Considerations

Reflex tachycardia, hypotension

Nicardipine Class

Calcium channel blocker

Nicardipine Use

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

Nicardipine MOA

- 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

Nicardipine Dose

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

Nicardipine Pharmacokinetics

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

Nicardipine Contraindications

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

Nicardipine Considerations

Reflex tachycardia, headache