 Metoprolol

o Selective B1 blocker (but B2 effects at higher doses), no intrinsic sympathomimetic activity, has
membrane stabilising effects (but not at clinical doses)
o B adrenoreceptors are Gs, thus B blockers decrease AC, cAMP, decreases protein kinase activity,
decreases IC [Ca], causing decreased inotropy/chronotropy/dromotropy
o Used in MI because it
 reduces myocardial oxygen demand by decreasing HR, inotropy, dromotropy
 increases oxygen supply by increasing diastolic time
 prevents LV remodelling a/w MI
o adverse side effects
 CVS – hypotension (blunts BRR, decreases CO, decreases renin release), bradycardia, heart
block, asystole, blunts sympathetic response to hypoglycaemia
 Resp – can cause bronchoconstriction at high doses
 CNS – has high lipid solubility, thus can cause depression, fatigue, confusion
 Other – can get rebound tachycardia and HTN if suddenly ceased, decreases effectiveness of
inotropes/vassopressors, additive –ve inotropy with ketamine/volatiles/IV anaesthetic
agents
 GTN
o Organic nitrate, relies on nitrate reductase in liver and vascular smooth muscle to release NO. NO
acts on VSM to increase GC, increase cGMP, increase activity of protein kinases, decrease IC [Ca]
causing venodilation > vasodilation
o Used in MI because it venodilates, decreases VR, decreases CO and LV wall tension, thus
decreasing myocardial oxygen demand. Also vasodilates large coronary arteries to increase supply,
without coronary steal
 In high doses will also vasodilate, decrease SVR/MAP, trigger BRR with increased HR and
inotropy, thus can decrease CBF (due to decreased diastolic time and decreased diastolic
pressure), and increase myocardial O2 demand
o Adverse effects
 CVS – hypotension, at high doses can decrease coronary BF
 Resp – impairs HPV, worsens VQ mismatch, hypoxia
 CNS – headache, NV, flushing, increased ICP/CBF
 Haem – decreased platelet aggregation
 Other – rarely MetHb, tolerance after 24 hours, contraindicated in HOCM/AS/hypovolaemia
 Diltiazem
o L type calcium channel blocker, with equal effects on heart and periphery
o Binds to cytoplasmic site of Ca channel when it is open, keeps it in inactive/closed state, decreases
Ca influx, decreases IC [Ca], thus decreases inotropy, SAN automaticity, and AVN conduction/HR
(decreases myocardial oxygen demand), and causes vasodilation (decreases afterload). Note: less
venodilation
o Adverse effects
 CVS – hypotension, bradycardia, heart block, asystole, LVF failure
 Resp – impairs HPV, worsens VQ mismatch
 CNS – increased CBF/ICP, NV, headache, prolongs NDNMBs
 Other – decreases inotropy with other anaesthetic agents