Vasodilators Flashcards
alpha 2 receptor subtypes
alpha 2A: sedation, analgesia, sympatholysis
alpha 2B: vasoconstriction, antishivering
alpha 2C: startle response
Most common SE produces by clonodine
sedation and xerostomia
Alpha 2 agonists produce sedation in what area of the brainstem?
the locus ceruleus
Where to alpha 2 agonists produce analgesia? What does neuraxial placement inhibit?
Site of analgesia is the spinal cord. Substance P and nociceptive neuron firing are inhibited.
alpha 2 agonists decrease anesthetic requirements by how much?
50%
- What can occur with abrupt discontinuation of clonidine therapy?
- What will exaggerate this response and why?
- What would be appropriate intraoperative management?
- rebound hypertension (as soon as 8 hours).
- Will be exaggerated in patients also on beta-blocker: beta 2 is blocked causing vasoconstriction and alpha receptors are unopposed.
- labetalol and clonidine patch
What are the three classes of calcium channel blockers (what is each one most selective for)?
phenylalkylamines: verapamil (AV node), benzothiazepines: cardizem (AV node), dihydropyridines: all the -pines (arteriolar beds)
MOA of CCBs
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+.
Phenylalklyamines and benzothiazepines should not be given in what type of patients?
Patients with heart failure, severe bradycardia, sinus node dysfunction, or AV node block.
Good combination for coronary artery vasopasm
nitrates and calcium channel blockers
Which CCB has the greatest vasodilating effect?
Nicardipine
CCB overdose may be partially reversed by what agents?
IV administration of calcium or dopamine
Drug interactions with CCB
May increase digoxin levels and enhance neuromuscular blocking agents and impair reversal of blockade (calcium is required for presynaptic release of Ach).
First line therapy for HTN, CHF, and mitral regurgitation
ACE inhibitor therapy
Refractory hypotension (not responsive to fluids or administration of phenylephrine) secondary to ACE inhibitor therapy prior to surgery may be treated with which agents?
Vasopression (V1 and V2 receptors) and methylene blue (inhibits production of nitric oxide)
SE of ACE inhibitors
Cough d/t bradykinin, angioedema, hyperkalemia r/t decreased aldosterone secretion, increased insulin sensitivity causing hypoglycemia.
What do phosphodiesterase inhibitors do?
Inhibit the breakdown of cAMP and cGMP causing smooth muscle relaxation
Treatment for cyanide toxicity
100% O2. treat acidosis, and administer THIOSULFATE 150 mg/kg IV over 15 minutes (acts as sulfur donor to convert cyanide to thiocyanate)
Sodium nitroprusside metabolism
In liver and kidney to thiocyanate and cyanomethohemoglobin
Contraindications for nitroglycerin
severe aortic stenosis and hypertrophic obstructive cardiomyopathy
What do high doses of nitroglycerin produce? What is the treatment?
methemoglobinemia, especially in patients with hepatic dysfunction. Methylene blue 1% 1-2 mg/kg over 5 minutes.
Hydralazine
Systemic ARTERIAL vasodilator. Used to treat HTN associated with pregnancy and outpatient CHF (in combo with nitrates).
What is responsible for the vasodilating effect of sodium nitroprusside?
Nitric oxide (NO), which activates guanylate cyclase present in vascular smooth muscle resulting in increased intracellular concentrations of cGMP.
How does sodium nitroprusside (SNP) generate NO? What byproduct accumulates with doses > 2 mcg/kg/min?
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.
