Beta Antagonists and Vasodilators Flashcards
Esmolol Class
selective B1 antagonist
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
Esmolol MOA
Competitive antagonist of B1 receptors (inhibits B2 receptors at higher doses)
Esmolol Dose
0.5mg/kg or 10mg
Infusion = 50 mcg/kg/min
(Uptitrate q5min to max dose 200 mcg/kg/min)
Esmolol Pharmacokinetics
Onset = 1 - 2 min DOA = 5 - 10 min Metabolism = rapid hydrolysis by plasma esterase metabolism in RBCs Elimination = renal
Esmolol Contraindications
Bradycardia, 1st degree heart block, cardiac failure
Esmolol Considerations
Caution in patients with hypotension and bronchoconstriction
Labetolol Class
Non-selective alpha and beta antagonist
Labetolol Use
treat tachycardia and hypertension
Labetolol MOA
competitive antagonist of B1, B2, and A1 receptors
Beta blockade to alpha blockade is 7:1
Labetolol Dose
Intermittent bolus 5 - 20 mg
Labetolol Pharmacokinetics
Onset = 5 min DOA = 3 - 6 hours Metabolism = hepatic Elimination = hepatic and renal
Labetolol Contraindications
Caution in patients with asthma, COPD, bradycardia, hypotension, and CHF
Labetolol Considerations
May cause left ventricular failure, orthostatic hypotension, and bronchospasm
Nitroglycerin Class
Peripheral vasodilator, venous dilation predominating over arterial dilation
Nitroglycerin Use
Relieves myocardial ischemia, coronary vasospasm
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
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
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
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
