HTN Drugs Flashcards
ACE-I MOA
Block AII production by preventing ACE from catalyzing AI to AII
Leads to vasodilation and decrease in Na reabsorption
ARB MOA
Directly block AII receptor without blocking breakdown of bradykinin
Cause of cough from ACE-I
ACE usually breaks down bradykinin. ACE-I block ACE, preventing the breakdown of bradykinin, causing it’s buildup and leading to coughing
Renal route to increase BP
Catecholamine release—> renin release —> Angiotensinogen to AI —> ACE converts AI to AII —> AII increase BP via vasoconstriction and retention of Na/H2O
Aldosterone also released increasing NA retention
Renin release is a B1 action
Direct renin inhibitor MOA
Prevents renin release from kidneys which prevents angiotensinogen from becoming AI
Fenoldopam
Class: Dopamine-1 receptor antagonist
Dose: 0.1-1.6 mcg/kg/min
Onset: 4-5 min
Duration: <10 min
Labetalol
Alpha and beta adrenergic blocker
Dose: 5-10 mg increments
Onset: 1-3 mins or less
Duration: 3-6 hrs
Nicardipine
Calcium channel blocker
Dose: 5 mg/hr increased in 2.5 increments up to 15
Onset: 1-5 min
Duration 3-6 hrs
Clevidipine
calcium channel blocker
Dose: infusion 1-2 mg/hr
Onset: 2-4 min
Duration: 5-15 min
Nitroglycerin
Venous vasodilator
Dose: infusion 5-100 mcg/min, 5 mcg/kg/min increase q5min
Onset: 2-5 min
Duration: 5-10 min
Tolerance and reflex tachycardia may develop
Sodium nitroprusside
Arterial and venous vasodilator
Dose: pump 0.3-10 mcg/kg/min, Do not increase more than 2 mcg/min
Onset: seconds
Duration 3-5 min
Cyanide toxicity
Sodium Nitroprusside Metabolism
Direct vasodilator/releases NO
NO goes into vessel wall/vasodilates—> 5 cyanide molecules surround NO —> cyanohg—> cyanides go to blood —> thiosulfate combines with cyanide to make thicyanate —> eliminate in the kidneys
Cyanide toxicity
cytochrome oxidase burns O2 via cellular respiration, cyanide can block tissue respiration and cause hypoxia. Oxygen is not getting to tissues so venous blood looks as red as arterial blood
S/S of Cyanide toxicity
CNS dysfunction: mental status change, seizure, coma
CV instability: tachyphylaxis, hypertension
ECG changes
Metabolic acidosis
Treatment of Cyanide toxicity
Stop infusion 100& O2 Mechanical ventilation as needed to prevent acidosis Correct metabolic acidosis with nabicarb 3% Na nitrate Na thiosulfate Consider B12
Esmolol
Beta Blocker
Dose: 0.5-1.0 mg/kg then 50-300 mcg/kg/min infusion
Onset: 1-2 min
Duration: 10-30 min
Broken down by RBC esterases making it shorter acting
Phentolamine
Dose: 1-5 mg
Onset: 1-2 min
Duration: 3-5 min
ACE-I Examples
-pril
ARB examples
-sartan
Direct Renin Inhibitor Example
Aliskiren
CCB
-Dipine + Verapamil and Diltiazem
BB with Alpha Blocking Activity
Carvedilol and Labetolol
Also cause vasodilation along with BB effects
Alpha Adrenergic Blockers
Vasodilate, mainly used on pots with BPH
Minipress, Doxazosin
Central Alpha Agonists
Clonidine
VERY potent, reserved for most brittle HTN—>pt take prior to surgery
Withdrawal and a lot of side effects
