1. Inotropes
A. Digitalis
1) Inhibit Na-K-ATPase - positive inotropic effect
2) Parasympathomimetic and anti-adrenergic mechanisms
3) Drug interaction - Quinidine, Verapamil, Amiodarone
4) Conditions that increase sensitivity
2. Inotropes, Vasoconstricting
A. Dopamine
1) Low doses - D1 receptors in renal vasculature
2) Increasing doses - b-1 receptors activated
3) High doses - a-adrenergic receptor activation
B. Epinephrine
1) Potent b and a effects
C. Norepinephrine
1) Potent alpha effects
3. Inotropes, Vasodilating
A. Dobutamine
1) Beta > alpha effect
2) Reduces LV filling pressures
3) Decreases afterload
B. Milrinone, Amrinone
1) Phosphodiesterase inhibitors
C. Isoproterenol
1) Inotropic (beta), chronotropic effects
4. Vasodilators & Vasoconstrictors
A. Vasodilators
B. Nitroprusside
1) Generalized vasodilatation
2) "Steal phenomena"
3) Indications - hypertension, acute heart failure
4) (thiocyanate toxicity - rare; with renal failure)
C. Nitroglycerine
1) General vasodilatation
2) Low doses - venous; high doses - arterial
3) Preload reduction and coronary vasodilation
4) Useful in management of ischemia
5) Decrease LVEDP and pulmonary vascular congestion
D. NO and Isoproterenol - pulmonary effects
E. Vasoconstrictors
F. Neosynephrine (pure alpha)
5. Calcium Antagonists
A. Mechanisms
B. Interference of Ca2+ - mediated smooth muscle contraction - coronary and peripheral smooth muscle relaxation
C. Selective Ca2+ channel inhibition
1) Treatment of angina pectoris / supraventricular tachycardia / hypertension
D. Agents
1) Verapamil
2) Nifedipine
3) Diltiazem
6. ACE Inhibitors
A. Mechanisms
1) Prevent conversion of Angiotensin I to Angiotensin II - vasodilation
2) Decreased Aldosterone secretion
3) Indication - hypertension, heart failure, prophylactically after MI
B. Agents
1) Captopril
2) Low cardiac output states - improvement in renal blood flow
3) Angioedema/cough/neutropenia/nephrotic syndrome
4) Increase in creatinine - RAS
C. Enalapril
1) Enalaprilat (liver) - delay - long duration
2) Less side-effects
7. Beta Blockers
A. Mechanisms
1) b-1 and b-2; cardioselectivity
B. Indications
1) Hypertension, angina pectoris, arrhythmias, prophylactically after MI
C. Adverse effects
1) Bronchospasm, Inhibition of myocardial contractility
D. Drug interactions
1) Lidocaine/Verapamil/Cimetidine/Diltiazem
E. Agents
1) Propanolol, metropolol, atenolol
2) Esmolol - very short half-life
8. Anti-arrhythmic Drugs and Their Actions Class Action Agents
Class Action Agents
IA---------------Inhibit Na+ transport----------------------Quinidine
IA---------------Reduced dV/dT of action potential--------Procainamide
IB---------------Slow dV/dT of phase 0-------------------Disoprymadine
IB---------------Moderate prolongation of repolarization---Lidocaine
IB---------------Prolongs PR, QRS, and QT intervals------Phenytoin
IB---------------Limited effect on dV/dT of phase O-------Mexiletine
IB---------------Shortens repolarization--------------------Tocainide
IB---------------Shortens QT in clinical dose
IB---------------Elevates fibrillation threshold
9. Anti-arrhythmic Drugs and Their Actions
Class Action Agents
IC--------------Markedly slows dV/dT--------------------Flecainide
IC--------------Little effect on repolarization---------------Ecainide
IC--------------Markedly prolongs PR and QRS
II---------------Beta-adrenergic blockers------------------Metoprolol
II---------------Decrease nodal conduction----------------Atenolol
Propanolol
III--------------Prolongs repolarization--------------------Amiodarone
III--------------Alters membrane response----------------Bretylium
IV-------------Calcium channel blockers------------------Verapamil
IV-------------Decrease nodal conduction----------------Nifedipine
Diltiazem
10. Thrombolytic Agents
A. Streptokinase - Indirectly activate plasminogen to plasmin => fibrin into FDP's (non-specific)
B. Urokinase - Indirectly - thrombolysis (non-specific)
C. tPA (Alteplase) - Clot specific thrombolytic - binds directly to clot via fibrin
D. APSAC - Like Streptokinase
