Anti-anginal Drugs

For treatment of angina pectoris (chest pain)
What causes angina? inadequate blood flow to the myocardium due to either plaque occlusions w/in or spasms of the coronary arteries. Decreased blood flow = decreased O2 to myocardium results in pain.
Anti-anginal drugs increase blood flow either by increasing oxygen supply or decreasing demand by the myocardium.
3 Types: Nitrates, Beta blockers, and Calcium Channel Blockers
Nitrates— major systemic effect is a reduction of venous tone, which decreases the workload of the heart and promotes vasodilation. Cause generalized vascular and coronary vasodilation, w/c increases blood flow through the coronary arteries to the myocardial cells. Reduces myocardial ischemia but can cause hypotension.
  • Prototype drug: Nitroglcerin (Nitrostat, Nitrobid) - vasodilator; sublingual, the effects of SL last for 10minutes; client can use a maximum of 3 tablets, if pain is not relieve call 911.
  • client may experience dizziness, faintness or headache as a result of peripheral vasodilation.
  • causes relaxation and dilation, reduces cardiac preload and afterload and reduces myocardial 02 demand.
  • ONSET: SL and IV, rapid 1-3mins; Trandermal 30-60minutes, patch should be removed nightly to avoid tolerance, 8-12 hour nitrate free interval. TD should be tapered.
  • HA, hypotension, dizziness, weakness, faintness
Beta blockers—Why are they effective for angina? because by decreasing the heart rate and myocardial contractility, they reduced the need for oxygen consumption and consequently reduce anginal pain.
  • decrease the workload of the heart and decrease oxygen demand.
  • blocks beta-1 and beta-2
  • decrease the effects of SNS by blocking the action of cathecolamines (epinephrine, norepinephrine), thereby reducing heart rate and BP
  • used as antianginal, antidysrhythmic, and antihypertensive drugs
  • should be tapered of to avoid reflex tachycardia and recurrence of anginal pain
Review side effects, contraindications:
  • Contraindicated: pts who have low HR and BP; clients who have 2nd or 3rd degree AV block  
Calcium channel blockers—Why are they effective for angina?
  • decrease workload of the heart, which decreases oxygen demand.
  • Blocks influx of calcium into cardiac cells
  • relax coronary artery spasm
  • relax peripheral arterioles
  • decrease cardiac contractility
  • decrease afterload
  • decrease peripheral resistance
Common side effects: Headache, peripheral edema, bradycardia, flushing, constipation, dizziness, hypotension
Nitrates and calcium channel blocker - effective in treating variant angina pectoris.
Beta blockers- for stable angina
Unstable angina, immediate medical care. Nitrates are usually given SQ and IV as needed. If cardiac pain continues, a beta blocker is given intravenously, if bblocker is not tolerated, calcium channel blocker can be used as substitute.

Cardiac Glycosides: Digoxin

Use: Increases contractility of cardiac muscle fibers
Indications: heart failure; heart rate control in atrial fibrillation
Desired results: Slows heart rate; decreases rate of cardiac electrical conduction; increases strength of cardiac muscle contraction. Improves heart failure symptoms by improving peripheral circulation, which increases fluid excretion.

Prototype drug: Digoxin (Lanoxin)—long half-life
  • Narrow Therapeutic Window: therapeutic range = 0.5 (to treat HF) - 2.0 (best for atrial flutter or fibrillation) ng/ml
  • Low serum potassium level (<3.5) can result in drug toxicity
    • Bradycardia, N/V, visual “halos”, confusion
  • Antidote: Digoxin immune Fab (Digibind)
Maintenance dose: 0.125 - 0.5 mg/dl. For older adults, dose is usually 0.125 mg/dl
Pulse rate should be above 60 beats/min.
Does not convert atrial fibrillation to normal heart rhythm. For mngmt. of atrial fibrillation, a calcium channel blocker, such as Calan may be prescribed. To prevent thromboemboli resulting from atrial fibrillation, Warfarin is prescribed concurrently w/ other drugs.
In clients w/ failing heart, cardiac glycosides increases myocardial contraction, w/c increases cardiac output and improves circulation and tissue perfusion. Because it decrease conduction through the AV node, the heart rate decreases.
Phenytoin and lidocaine are effective in treating digoxin induced ventricular dyshrythmias.
Lasix, HCTZ and systemic cortisone can cause hypokalemia. Patient should consume potassium rich foods or take potassium supplements.
Antacid can reduce Digoxin absorption so avoid taking it on the same time.
PHOSPHODIESTERASE INHIBITORS - Positive inotropic drug used for acute heart failure treatment
Promotes increase in cardiac muscle contraction, vasodilation
  • IV drugs: inamrinone (Inocor), milrinone (Primacor) - increase stroke volume and cardiac output and promote vasodilation. Administered for no longer than 48-72 hours.
Used for short-term acute management of heart failure, requires cardiac monitoring during therapy for severe dysrhythmias can occur.

ATRIAL NATIURETIC PEPTIDE HORMONE
Nesiritide (Natrecor)— diuresis for heart failure treatment
Inhibits  ADH by increasing urine sodium loss. Promote vasodilation, diuresis and natriuresis. Useful for treating clients who have acute decompensated HF w/ dyspnea at rest or who have dyspnea w/ little exertion.