Cardiac & Bronchodialators Flashcards
Digitalis MOA
-inhibits Na/K ATPase in myocardium = ↑Na = ↑activity of Na/Ca exchanger = ↑Ca
-Leads to: ↑ino, ↑EF, ↓preload, ↓AV node conduction, ↓SA node automaticity
Digitalis therapeutic index
0.8-2 ng/ml
toxic > 2.4
Digitalis SE
-arrhythmias (Vfib, AV block)
-↓QT
-cardiotoxic (↑risk w/ ↓K)
Digitalis drug interactions
-quinidine
-CCB
-NSAIDS
-amiodarone
-BB
-diuretics
Digitalis and electrolytes
-↓K = ↑dig binding to Na/K ATPase = ↑therapeutic & toxic effects
-↑Ca = ↑digitalis-induced ↑Ca = Ca overload & digitalis-induced arrhythmias
-↓Mg = sensitizes heart to digitalis-induced arrhythmias
Digitalis Contraindications
-↓K
-WPW
-AV block
-renal dysfx
-harmful in pt w/HSS
What sympathomimetics are not metabolized by reuptake and MAO & COMT
-isoproterenol & dobutamine (COMT only)
-ephedrine (liver, mostly excreted renal unchanged)
Epinephrine receptor & dosing
B1>B2, a1
0.01-0.2 mcg/kg/min
1-20 mcg/min
NE receptor & dosing
a1, B1 > B2
0.01-0.2 mcg/kg/min
4-16 mcg/min
Dopamine receptor & dosing
B1>B2, a1
2-20 mcg/kg/min
Isoproterenol receptor & dosing
B1 > B2
0.015-0.15 mcg/kg/min
1-5 mcg/min
Dobutamine receptor & dosing
B1>B2>a1
2-20 mcg/kg/min
Ephedrine receptor & dosing
a, B indirect
bolus 5-25 mg IV
up to 50 mg IM
Isoproterenol clinical effect
Pure beta agonist
- ↑ HR, contractility, CO
-↓ PVR, DBP
-↑MVO2 demand while ↓ O2 supply
Dobutamine clinical effect
Selective B1 agonist
-↑ contractility, CO, cAMP, Ca in SR
-↓ PVR (B2)
-↓ LV filling pressure –> ↑coronary BF
-stimulates SA, AV nodal automaticity
PDE inhibitor MOA
↑cAMP & ↑cGMP
Clinical indication for PDE 3 vs 4 vs 5
-PDE3 = ↑ cAMP & ↑ cGMP (milrinone, cilostazol, amrinone) = inodilators
-PDE4 = ↑ cAMP (roflumilast, apremilast, ibudilast) = help w/ inflammatory states
-PDE5 = ↑ cGMP (sildenafil, tadalafil, vardenafil) = pulm vasodilation
PDE inhibitor SE
-block plt aggregation
-ventricular arrhythmias
-HA
-HoTN
-flushing
Inhaled beta-agonist MOA
b2 agonist = ↑cAMP = ↓Ca; stabilizes mast cell
Inhaled beta-agonist SE
-tremor
-↑HR
-hyperglycemia
-↓K
-↓Mg
-dysrhythmias
Inhaled muscarinic antagonist MOA
M3 antagonist = ↓IP3 = ↓Ca
Inhaled muscarinic antagonist short vs long acting
-ipratropium (short)
-tiotropium (long)
Methylxanthines (theophylline, aminophylline) MOA
PDEi = ↑cAMP & ↑cGMP; inhibit leukotriene; adenosine receptor antagonist
Dose based SE for Methylxanthines
> 20 mcg/ml: N/V/D, HA, insomnia
30 mcg/ml: sz, arrhythmias, CHF
Nonselective vs selective alpha antagonist
Non: phenoxybenzamine, phentolamine
a1: -zosin
a2: yohimbine
Phentolamine dose
bolus: 1-5 mg
infusion: 0.1-0.2 mg/min
Beta antagonist SE
-heart block
-HF
-AV block
-sinus arrest
-HoTN
-bronchospasm (asthma)
What beta antagonist are not metabolized by the liver
Esmolol (hydrolysis of RBCe)
Atenolol (renal)
Labetalol
-a1, B1, B2 (1a:7B)
-mixed blockade↓ PVR, ABP w/o reflex tachy
-IV peak 5 min
-Dose: 0.1-0.25 mg/kg q 10 min
Class I antidysrhythmic SE
-cinchonism
-cardiotoxicity
-arterial embolism
-hypersensitivity rxn
Class I antidysrhythmic MOA
-depresses phase 0
-mixed effects on phase 3 repolarization
Class IA antidysrhythmic
-Quinidine
-procainamine
-disopyraminde
-moricizine
Class IB antidysrhythmic
-Lidocaine
-Tocainide
-Mexiletine
Class IC antidysrhythmic
-Flecanide
-Propafenone
Class II antidysrhythmic
Beta blockers
Class II antidysrhythmic MOA
-slows phase 4 depolarization in SA node
Class III antidysrhythmic MOA
-prolongs phase 3 repolarization (↑QT)
-↑effective refractory period
Class III antidysrhythmic SE
-pulmonary/thyroid/CV/dErm toxic
-optic neuropathy
-corneal microdeposits
Class III antidysrhythmic
↓K
-amiodarone
-sotalol
ibutilide
-dofetilide
-bretylium
Class IV antidysrhythmic
CCB:
-Verapamil
-Diltiazem
Class IV antidysrhythmic MOA
↓conduction velocity through AV node
Adenosine MOA
↓AV node conduction d/t K efflux (hyperpolarizes); 6 > 12 mg
Non-dihydropyridines vs Dihydropyridines
Non-dihydropyridines
-verapamil, diltazem
- Target myocardium = ↓coronary vascular resistance, ↓ino, ↓dromo, ↓chrono
Dihydropyridine
- -dipine
-Targets vascular smooth muscle = ↓SVR
CCB SE
-inhibit inflow of Ca into cells of cardiac & vascular smooth muscle
CCB Drug Interactions
-potentiate NMB & LA
-vasoplegic synd
-may ↑dig levels
-BB
-HoTN, CHF, asystole, high-degree AV block w/ BB and dig