Chapter 23 Antianginal drugs Flashcards
Under ischemic conditions when the myocardium is deprived of oxygen, the heart shifts to anaerobic metabolism to meet its energy needs. One of the by-products of anaerobic metabolism is lactic acid. Accumulation of lactic acid and other metabolic by-products causes?
pain receptors surrounding the heart to be stimulated, which produces the heart pain know as angina.
Angina pectoris (chest pain) occurs because of a?
mismatch between the oxygen supply and oxygen demand, with either too high a demand for oxygen or too little oxygen delivery.
Coronary artery disease is an abnormal condition of the arteries that delivers oxygen to the heart muscle. These arteries may become narrowed, which results in reduced flow of oxygen and nutrients to the myocardium. Poor blood supply to an organ is referred to as ischemia. The condition is called ischemic heart disease. What happens when the coronary arteries that deliver oxygen to the heart muscle become blocked?
a heart attack or myocardial infarction (MI) occurs.
Many substances and situations can increase heart rate and contractility and oxygen demand, including caffeine, exercise, and stress, and result in stimulation of the?
sympathetic nervous system (SNS), leading to increased heart rate and contractility.
Some of the drugs used to treat angina are aimed at?
correcting the imbalance between myocardial oxygen supply and demand by decreasing heart rate and contractility.
There are three classic types of chest pain, or angina pectoris.
Chronic stable angina
Unstable (preinfarction) angina
Vasospastic angina
-Dysrhythmias and electrocardiogram (ECG) changes often accompany these different types of anginal attacks.
Chronic stable angina has?
atherosclerosis as its primary cause. Chronic stable angina can be triggered by exertion or other stress, as well as nicotine in tobacco, alcohol, coffee, and other drugs that stimulate the SNS. The pain of chronic stable angina is commonly intense but subsides within 15 minutes of either rest or appropriate antianginal drug therapy.
Unstable (preinfarction) angina is usually the?
early stage of progressive coronary artery disease, often ending in an MI in subsequent years. Another term for this type of angina is crescendo angina, because the pain increases in severity, as does the frequency of attacks. Later, pain may even occur while the patient is at rest.
Vasospastic angina results from?
spasms in the layer of smooth muscle that surrounds atherosclerotic coronary arteries, often occurring at rest and without any precipitating cause, but following a regular pattern, such as the same time of day. This type of angina is also called Prinzmetal angina or variant angina.
The three main classes of drugs used to treat angina pectoris are:
(1) nitrates and nitrites
(2) beta blockers
(3) calcium channel blockers (CCBs)
There are three main therapeutic objectives of antianginal drug therapy:
(1) minimizing the frequency of attacks and decrease the duration and intensity of the anginal pain
(2) improving the patient’s functional capacity with as few adverse effects as possible
(3) preventing or delaying the worst possible outcome, MI
The overall goal of antianginal drug therapy is?
to increase blood flow to ischemic myocardium, decrease myocardial oxygen demand, or both.
Nitrates have long been the mainstay for both the?
prophylaxis and treatment for angina.
The rapid- and long-acting nitrates available for clinical use include amyl nitrite (rapid acting), nitroglycerin (both
rapid and long-acting), isosorbide dinitrate (both rapid
and long-acting), and isosorbide mononitrate (primarily long-acting).
.
Antianginal Calcium Channel Blockers (CCBs)
Diltiazem (Cardizem):
Verapamil (Calan):
- Diltiazem (Cardizem): It is the only benzothiazepine CCB; effective for tx of angina pectoris. Available in parenteral form used in atrial fibrillation; Cardizem SR taken twice/day; Cardizem CD taken once/day.
- Verapamil (Calan): Has similar indications as Cardizem
Calcium Channel Blockers CCBs Mechanism of Action:
Inhibits transport of Ca+ into myocardial and vascular smooth muscle cells= inhibition of excitation of muscles and promotes muscle relaxation of smooth muscles surrounding the coronary arteries; this dilates and increases blood flow and lowers SVR (systemic vascular resistance; force against the heart).
CCB Indications:
Angina, HTN, Prinzmetal’s angina, arrhythmias, short-term treatment of Reynaud’s disease.
CCB Contraindications:
Acute MI, 2nd or 3rd degree AV block (unless pt. has pacemaker), hypotension
Adverse Effects for CCBs
Hypotension, arrhythmias, palpitations, syncope, peripheral edema, bradycardia, Rash, dyspnea, and Stevens-Johnson syndrome.
CCBs Drug Interactions:
Grapefruit juice= decreased metabolism of CCBs
Beta Blockers= additive effects
Beta blockers are also used to relieve angina and do so by?
decreasing the heart rate, reducing workload on the heart, and decreasing oxygen demands.
Exercise-induced spasms in atherosclerotic coronary arteries can also be reversed or prevented by?
administration of nitrates, encouraging healthy physical activity in patients.
The nitrates are used to treat?
stable, unstable, and vasospastic (Prinzmetal) angina.
If the goal of treatment is to abort or treat a sudden attack of angina, then rapid onset of action is needed, such as with?
IV infusion, sublingual tablet, and/or translingual spray, with pharmacokinetics that allow quick entry of the drug into the bloodstream.