ACS drugs Flashcards
(38 cards)
main targets for CAD management (4)
supply - coronary blood flow, arterial oxygen content;
demand - HR, force of contraction
main drug classes in CAD (6)
reduce cardiac workload (decrease myocardial O2 demand) - B-blockers, CCBs, other channel inhibitors, BP lowering (indirectly, effect afterload);
coronary vasodilators - nitrates, K+ channels openers (e.g.nicorandil)
where are L-type Ca2+ Channels present and what is the effect of blocking them (3)
- arterial smooth muscle - vasodilation
- cardiac muscle - reduced force of contraction
- cardiac pacemaker tissue - reduced heart rate/AVN block
how does Ca2+ cause muscle contraction (mech)
what are the 2 types of CCBs and examples
- non-dihydropiridine (negative ionotropic), useful for arrythmias and angina, veramapil/ diltiazem
- dihydropiridine (non-ionotropic), acts on smooth muscle to reduce BP - used for hypertension, little/no cardiac effect, amolodipine, nifedipine
common adverse affects of CCBs (6)
negative ionotropic - slow HR, reduced contraction (may worsen heart failure);
non-ionotropic - headache (due to increased flood flow), flushing, peripheral oedema, reflex tachy (to counteract increased blood flow)
what does ionotropic mean (in terms of the heart)
contractility - positive inotropy is an increase in contractility (contract with more force)
verapamil vs diltiazem
verapamil - mainly cardiac affects; diltiazem - cardiac and vascular effects; choose appropriate drug depending on the action required
high levels of what NTs (2) result in high mortality levels from heart disease
NA; adrenaline
what does increased NA/adrenaline cause (cardiac + resp)
activates beta-receptors which act on cardiac tissue and pacemaker cells to increase force and rate of contractions (B1); acts of bronchial smooth muscle to dilate airways (B2)
what is the effect of BBlockers
block beta-receptors so they cannot be stimulated by NA/adrenaline release -> stops increase in HR/contraction force; new BBs try to focus on just blocking B1 receptors so that lung function is not affected, otherwise it could be danger out to people with asthma
commonly used BBs
non-specific: propanolol (worsens asthma);
cardioselective: atenolol, bisoprolol, metoprolol;
vasodilator activity: carvedilol, labetelol (alpha blocking properties, causes vasodilation)
what conditions have BBs demonstrated a reduction in mortality in
ACS; MI; chronic heart failure; angina; AF; resistant HTN (small roll in HTN alone)
adverse effects of BBs (4)
cardiac: bradycardia, HF initially worsens (start a low dose);
sympathetic blockade: bronchoconstriction, fatigue/feeling cold (due to decreased adrenaline)
MOA of nitrates
nitrates -> increased nitric oxide -> increased cGMP -> increased dephosphorylation of myosin light chain, decreased Ca2+ influx into cell -> relaxation of vascular smooth muscle (vasodilation)
effects of nitrates (3)
arterial dilation: improves coronary supply by vasodilating coronary artery to reduce BP;
venous dilation: decreased preload and stretching of the heart (decreased venous return to heart), Decreased pressure in ventricles (Especially diastolic wall pressure)
adverse effects of nitrates (4)
hypotension, reflex tachy, headaches, flushing
what are nitrates used for
symptom relief in ischaemic chest pain; relief of acute heart failure (high dose IV required)
commonly used nitrates (2)
glyceryl trinitrate (GTN) - sublingual or spray usually (oral is broken down by liver), rapid relief but short acting;
isosorbide mononitrate - oral, OD, prevention of angina pain
specialist drugs for angina treatment (3)
nicorandil (K+ channel opener, nitrate action); ranolazine (late Na+ current inhibitor); ivabradine (sinus node inhibitor, slows HR, blocks conduction)
when to use CCBs
uncontrolled hypertension; vasoplastic/mixed angina, MI without HF
when to use BBs
previous MI or HF
what are the key targets for hypertension
cardiac output (decrease - slow pumping); vascular resistance (vasodilation to reduce resistance, vol of blood is reduced)
main drug targets in hypertension (and drug types)
intravascular volume - diuretics, thiazides;
sympathetic tone - alpha and B-blockers;
peripheral arteries - CCBs (vasodilation);
neuroendocrine mediators of BP (block) - ACEi, ARBs, renin inhibitors