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Anesthesia Pharmacology > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

Nitroprusside Class

A

Nitrate

Direct peripheral arterial vasodilator

Non-selective relaxation of arterial & venous smooth muscle

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2
Q

Nitroprusside MOA

A

As NTP is metabolized, it releases nitric oxide and cyanide. NO activates guanylyl cyclase which synthesizes (cGMP), decreases intracellular calcium, which causes smooth muscle dilation

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3
Q

Nitroprusside Use

A

Reliable antihypertensive

Afterload reducing agent

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4
Q

Nitroprusside Dosing

A

Infusion: 0.3–10 mcg/kg/min

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5
Q

Nitroprusside Onset and DOA

A

Onset: 1 minute
DOA: 3 – 5 minutes

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6
Q

Nitroprusside Metabolism

A

Metabolized in RBC’s to cyanide which is released, then metabolized in the liver and kidneys to thiocyanate (inactive)

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7
Q

Nitroprusside Excretion

A

Thiocyanate (inactive) is slowly excreted by the kidneys

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8
Q

Nitroprusside Admin Considerations (8)

A

Caution in patients with aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure

May cause headache, tachycardia and bronchodilation

Patients with renal failure may experience a build-up of thiocyantate, which may lead to thyroid dysfunction, muscle weakness, nausea, hypoxia, and an acute toxic psychosis

Dilation of coronary arterioles may result in an intracoronary steal

Reductions in pulmonary artery pressure and the hypoxic pulmonary vasoconstriction mechanism may decrease lung perfusion

Large doses of NTP may lead to methemoglobinemia and is treated with methylene blue to reduce methemoglobinemia to hemoglobin

NTP must be protected from light because of photodegradation

Patient’s on NTP infusions benefit from arterial line monitoring

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9
Q

Nitroglycerin Class

A

Nitrate

Peripheral vasodilator with venous dilation predominating over arterial dilation

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10
Q

Nitroglycerin MOA

A

As NTG is metabolized, it releases nitric oxide and cyanide. NO activates guanylyl cyclase which synthesizes (cGMP), decreases intracellular calcium, which causes smooth muscle dilation

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11
Q

Nitroglycerin Uses

A

Relieves

  • Myocardial ischemia
  • Coronary vasospasm
  • Hypertension
  • Ventricular failure

Used for controlled hypotension

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12
Q

Nitroglycerin Dosing

A

IV Infusion: 5 – 200 mcg/min

SL: 0.4 mg

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13
Q

Nitroglycerin Onset and DOA

A

Onset: 2 minutes
DOA: 5 minutes

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14
Q

Nitroglycerin Metabolism

A

Nitroglycerin undergoes rapid reductive hydrolysis in the liver and blood by glutathione-organic nitrate reductase. One metabolic product is nitrite, which can convert hemoglobin to methemoglobin

Also have non-hepatic metabolism via RBCs and Vascular endothelial walls

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15
Q

Nitroglycerin Excretion

A

Kidneys

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16
Q

Nitroglycerin Admin Considerations

A

Headache, tachycardia can occur

Tolerance may develop with prolonged use

Caution in patients with aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure

Ideal agent for MIs

  • Decrease preload will reduce myocardial oxygen demand and increases endocardial perfusion
  • Redistributes coronary blood flow to ischemic areas of the subendocardium
  • Relieves coronary vasospasm
17
Q

Hydralazine Class

A

Direct acting arterial vasodilator

18
Q

Hydralazine MOA

A

Activate guanylate cyclase to increase cGMP, decreases intracellular Ca and causes vasodilation

19
Q

Hydralazine Use

A

Antihypertensive

This is the drug of choice with a normal or low HR

20
Q

Hydralazine Dosing

A

Intermittent boluses: 2.5 – 20 mg

21
Q

Hydralazine Onset and DOA

A

Onset: 15 minutes
DOA: 2 – 4 hours

22
Q

Hydralazine Metabolism

A

Liver

23
Q

Hydralazine Excreted

A

Kidneys

24
Q

Hydralazine Considerations

A

Can result in reflexive tachycardia, bad for CAD

Caution in patients with aortic stenosis, hypertrophic cardiomyopathy, increased ICP, hypotension, heart failure

Can have hypersentivity reactions

Can increase Na retention with resulting hypervolemia

25
Q

Nicardipine Class

A

Calcium channel blocker

26
Q

Nicardipine MOA

A

Depress electrical impulses in the sinoatrial (SA) and atrioventricular (AV) nodes by blocking the influx of Ca, resulting in negative chronotropic and inotropic effects and increasing coronary and systemic vasodilation

Decreases HR, contractility, conduction velocity and vascular smooth muscle relaxation

27
Q

Nicardipine Use (7)

A

Treatment

  • Angina
  • Hypertension
  • Arrhythmias
  • Peripheral vascular disease
  • Esophageal spasm
  • Cerebral vasospasm
  • Controlled hypotension
28
Q

Nicardipine Dosing

A

5 mg/hr, increased by 2.5 mg/h every 15 min up to 15 mg/hr

29
Q

Nicardipine Onset and DOA

A

Onset: 1 min
DOA: 3 hr

30
Q

Nicardipine Metabolism

A

Liver

31
Q

Nicardipine Excretion

A

Kidneys

32
Q

Nicardipine Admin Considerations

A

May cause reflexive tachycardia, bad for CAD

Caution in patients with an acute MI, heart failure, bradycardia, hypotension and on dantrolene (can increase K+ and cause myocardial depression)

Anesthesia Pharmacology (23 decks)

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