Pharmacology of stable coronary artery Flashcards
(35 cards)
drugs can help by
reducing heart rate, reducing myocardial contractility, afterload
purpose of drug treatment
relieve symptoms, halt the disease process, regression of disease process, prevent myocardial infarction, prevent death
vasodilators
calcium channel blockers, nitrates- oral and sublingual
rate limiting drugs
beta adrenoceptor antagonists, calcium channel blockers, ivabradine
common beta blockers used
bisoprolol, atenolol
beta blockers
reversible antagonists of the B1 and B2 receptors, newer drugs are cardioselective acting primarily on the B1 receptors, block the sympathetic system
beta blockers decrease what three determinants of myocardial oxygen demand
heart rate, contractility, systolic wall tension and also allow improved perfusion of the subendocardium by increasing diastolic perfusion time. this increases the exercise threshold at which angina occurs
contraindications of beta blockers
asthma, peripheral vascular disease (relative contraindication), raynauds syndrome, heart failure (those patients who are dependent on sympathetic drive), existing bradycardia/ heart block
adverse drug reactions of beta blockers
tiredness/ fatigue, lethargy, impotence, bradychardia, bronchospasm, rebound- sudden cessation of beta blocker therapy may precipitate myocardial infarction
drug- drug interactions
primarily pharmacodynamic
what happens when beta blockers with verapamil or diltiazem
bradycardia or cardiac failure
what happens when beta blockers with insulin or oral hypoglycaemics
exaggerate and mask hypoglycaemic actions
what happens when beta blockers with other hypotensive drugs
hypotension
examples of calcium channel blockers
diltiazem, verapamil, amlodipine
calcium channel blockers
prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L type calcium channel
rate limiting calcium channel blockers
CCBs like diltiazem and verapamil reduce heart rate and force of contraction
vasodilators calcium channel blockers
CCBs like amlodipine reduce BP and after load
why never use nifedipine immediate release
may precipitate acute MI or stroke
post MI CCB use
may increase morbidity and mortality in patients with impaired LV function
unstable angina CCB use
evidence that dihydropyridines may increase infarction rate and death in the unstable patient
adverse drug reactions CCBs
ankle oedema, headache, flushing, palpitation
nitrovasodilators examples
glyceryl trinitrate GTN, isosorbide mononitrate, isosorbide dinitrate
how do nitrovasodilators work
relax almost all smooth muscle by releasing NO which then stimulates the production of cGMP which produces smooth muscle relaxation. reduce preload and after load so reduce myocardial oxygen consumption
how do nitrovasodilators relieve angina
arteriolar dilatation and so reducing cardiac after load and thus myocardial work and oxygen demand. peripheral venodilatation and so reducing venous return, cardiac preload and thus myocardial workload