Vasodilators Flashcards

1
Q

alpha 2 receptor subtypes

A

alpha 2A: sedation, analgesia, sympatholysis
alpha 2B: vasoconstriction, antishivering
alpha 2C: startle response

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2
Q

Most common SE produces by clonodine

A

sedation and xerostomia

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3
Q

Alpha 2 agonists produce sedation in what area of the brainstem?

A

the locus ceruleus

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4
Q

Where to alpha 2 agonists produce analgesia? What does neuraxial placement inhibit?

A

Site of analgesia is the spinal cord. Substance P and nociceptive neuron firing are inhibited.

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5
Q

alpha 2 agonists decrease anesthetic requirements by how much?

A

50%

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6
Q
  1. What can occur with abrupt discontinuation of clonidine therapy?
  2. What will exaggerate this response and why?
  3. What would be appropriate intraoperative management?
A
  1. rebound hypertension (as soon as 8 hours).
  2. Will be exaggerated in patients also on beta-blocker: beta 2 is blocked causing vasoconstriction and alpha receptors are unopposed.
  3. labetalol and clonidine patch
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7
Q

What are the three classes of calcium channel blockers (what is each one most selective for)?

A

phenylalkylamines: verapamil (AV node), benzothiazepines: cardizem (AV node), dihydropyridines: all the -pines (arteriolar beds)

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8
Q

MOA of CCBs

A

blockade of Ca2+ influx through L-type (L for long-lasting) voltage-gated Ca2+ channels in myocardial and vascular smooth muscle cells. Dihydropyridines work EXTRACELLULARLY, phenylalkylamines work INTRACELLULARLY, and benzothiazipines has unknown Ca2+ channel mechanism but may also work on Na-K pump, decreasing intracellular Na available to exchange with Ca2+.

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9
Q

Phenylalklyamines and benzothiazepines should not be given in what type of patients?

A

Patients with heart failure, severe bradycardia, sinus node dysfunction, or AV node block.

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10
Q

Good combination for coronary artery vasopasm

A

nitrates and calcium channel blockers

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11
Q

Which CCB has the greatest vasodilating effect?

A

Nicardipine

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12
Q

CCB overdose may be partially reversed by what agents?

A

IV administration of calcium or dopamine

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13
Q

Drug interactions with CCB

A

May increase digoxin levels and enhance neuromuscular blocking agents and impair reversal of blockade (calcium is required for presynaptic release of Ach).

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14
Q

First line therapy for HTN, CHF, and mitral regurgitation

A

ACE inhibitor therapy

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15
Q

Refractory hypotension (not responsive to fluids or administration of phenylephrine) secondary to ACE inhibitor therapy prior to surgery may be treated with which agents?

A

Vasopression (V1 and V2 receptors) and methylene blue (inhibits production of nitric oxide)

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16
Q

SE of ACE inhibitors

A

Cough d/t bradykinin, angioedema, hyperkalemia r/t decreased aldosterone secretion, increased insulin sensitivity causing hypoglycemia.

17
Q

What do phosphodiesterase inhibitors do?

A

Inhibit the breakdown of cAMP and cGMP causing smooth muscle relaxation

18
Q

Treatment for cyanide toxicity

A

100% O2. treat acidosis, and administer THIOSULFATE 150 mg/kg IV over 15 minutes (acts as sulfur donor to convert cyanide to thiocyanate)

19
Q

Sodium nitroprusside metabolism

A

In liver and kidney to thiocyanate and cyanomethohemoglobin

20
Q

Contraindications for nitroglycerin

A

severe aortic stenosis and hypertrophic obstructive cardiomyopathy

21
Q

What do high doses of nitroglycerin produce? What is the treatment?

A

methemoglobinemia, especially in patients with hepatic dysfunction. Methylene blue 1% 1-2 mg/kg over 5 minutes.

22
Q

Hydralazine

A

Systemic ARTERIAL vasodilator. Used to treat HTN associated with pregnancy and outpatient CHF (in combo with nitrates).

23
Q

What is responsible for the vasodilating effect of sodium nitroprusside?

A

Nitric oxide (NO), which activates guanylate cyclase present in vascular smooth muscle resulting in increased intracellular concentrations of cGMP.

24
Q

How does sodium nitroprusside (SNP) generate NO? What byproduct accumulates with doses > 2 mcg/kg/min?

A

SNP interacts with oxyhemoglobin, dissociating immediately and forming methemoglobin while releasing cyanide and NO. The risk of cyanide toxicity increases with doses > 2mcg/kg/min precipitating anaerobic respiration, lactic acidosis, tissue anoxia, and increased mixed venous O2.

25
Q

SNP infusion rates > 3 mcg/kg/min results in

A

heme-platelet aggregation inhibition and increased bleeding time

26
Q

What vasodilator is contraindicated in patients with glaucoma?

A

Fenaldopam

27
Q

Fenaldopam MOA

A

Dopamine type 1 receptor agonist. Increases cAMP causing arterial vasodilation. Increases renal blood flow and urine output.

28
Q

cerebral effects of SNP

A

increased blood flow and cerebral blood volume. May increase ICP in patients with decreased intracranial compliance. Patients with known inadequate cerebral blood flow associated with increased ICP or carotid artery stenosis should not be treated with SNP.

29
Q

Nitric oxide MOA

A

endogenous vasodilator. Produces relaxation of pulmonary arterial system (administered by inhalation) by increasing cGMP concentrations. It dilates vessels at the alveolar levels, improving V/Q matching and oxygenation.

30
Q

Clinical uses for nitric oxide

A

Pediatric lung injury and persistent pulmonary HTN of the newborn. Also used off-label in adults for heart-to-lung transplant candidates for pulmonary HTN.

31
Q

What happens with discontinuation of NO?

A

A drop in SpO2 occurs. Life-threatening rebound arterial hypoxemia and pulmonary HTN may occur. WEAN OFF.

32
Q

Sildenafil, vardenafil, and tadalafil

A

PDE5 inhibitors. Effective pulmonary vasodilators, great for pulmonary HTN. Also used to treat erectile dysfunction.