anti-arrythmics + anti-angina + cardiac glycosides Flashcards
what is a non-pacemaker blockade
suppress abnormal atrial or ventricular cells to restore normal sinus rhythm (RHYTHM control)
- Na channel blocker and potassium channel blocker
what is an AVN blockade
suppress AV node to prevent high atrial rate from causing high ventricular rate (RATE control)
- beta blocker and calcium channel blocker
types of sodium channel blocker
increasing degree of blockade of Na channel: B,A,C
MOA of Class 1C Na channel blocker
eg flerainide
MOA: slows phase 0 depolarisation
use: refractory ventricular tachycardia
1C=no change
MOA of Class 1A Na channel blocker
eg procainamide
MOA: slow phase 0 depolarisation
prolonged effective refractory period (moment cell starts repolarising) and action potential duration becase drug has K channel blockade
1A = after = prolong AP
MOA of CLass 1B Na channel blocker
eg lidocaine
MOA : slow phase 0 depolarisation and shorten phase 3 repolarisation
decrease action potential duration but ERP unchanged
1B=before=shorten AP
MOA of K channel blocker
eg SAD
Sotalol
Amiodarone
Dofelitide
MOA: slow down phase 3 repolarisation -> increase ERP and APD
use of K channel blocker
- atrial fibrillation
- prevent reentrant ventricular tachycardia => instead of completing normal circuit, electrical signal has alt loop back upon itself (self perpetuating rapid and abnormal activation)
special quality about K channel blocker
Amiodarone is metabolised by liver into active metabolites
this means that effect persist even after discontinuation of the drug (long half life: effect maintained 1-3mths after discontinuation)
MOA of beta blockers
block binding of NE to beta receptor so voltage gated Ca channels cannot open and calcium cannot enter
reduced slope of 4 (depolarisation to threshold potential and slope of 0 (when calcium channels supposed to open)
takes longer time before can depoalrise so reduced frequency of action potential moving through AV node -> decrease HR and contractility
uses of beta blockers
tachycardia
atrial fibrillation
protective effect after MI
AE of beta blockers
bradycardia
hypotension -> decrease contractility if beta blockers block contractile portion of myocardium
MOA of calcium channel blocker
non dihydropridine calcium channel blockers: (primarily affect myocardium)(IV)
diltiazem
verapamil
block calcium entry into cell -> decrease slope of 4 and 0 in AV node
block atrial signals from processing through AV node and into ventricles
- prolonged ERP and APD (prolong both depol and repol)
use of calcium channel blockers
supraventricular tachycardia
hypertension
angina
AE of calcium channel blockers
hypotention
contraindicated: pre-existing depressed cardiac output -> further inhibit AV nodal conduction
types of anti angina drugs
- vasodilators: nitrates, calcium channel blockers
- cardiac depressants: calcium channel blockers, beta blockers
- ivabradine
MOA of nitrates
form NO which activates guanylyl cyclase which phosphorylates GTP to cGMP
inactivates myosin-LC so relaxation, causing vasodilation
effect of vasodilation on
- veins: decrease venous return, hence preload (at low conc)
- arteries: reduce peripheral resistance, decrease afterload (at high conc)
- coronary arteries: lower pressure in arteries because heart does not stretch as much so improvement in subendocardial blood flow
decreased workload on heart so increase supply of blood and oxygen to coronary arteries
types of nitrates
glycerol nitrate
PK: injecton-> slow onset but long DOA
sublingual (under tongue) -> quick onset but slow DOA
isosorbide dinitrate
isosorbide mononitrate
PK: oral -> slow onset but long DOA
how are nitrates angina pectoris prophylaxis
if end diastolic pressure and volume is high, heart would enlarge and press on coronary arteries. This would affect subendocardial blood flow.
nitrates would dilate coronary arteries so it is able to receive greater blood flow
AE of nitrates
reflex tachycardia (baroreflex)
hypotension
headache -> meningeal artery vasodilation
MOA of calcium channel blockers in anti-angina
decrease contractility -> decrease O2 requirement -> decrease workload on heart
ranking of calcium channel blockers as cardiac depressants
verapamil> diltiazem > nifedipine
MOA of ivabradine
inhibit cardiac pacemaker current that controls spontaneous diastolic depolarization in SA node -> lower HR
results in decreased cardiac workload -> decreased myocardial o2 consumption
Uses: stable angina, chronic HF
AE of ivabradine
visual problems
bradycardia associated symptoms: hypotension, dizziness, fatigue, malaise
what are cardiac glycosides (digitalis)
late stage HF drug
- goal: increase HR
PK:
oral
digitoxin
- extensive metabolism in liver and excreted through faeces
- slow onset, long DOA
digoxin
- not metabolised in liver and excreted through urine
- quick onset, short DOA
MOA of digitalis
inhibit Na/K ATPase. Efflux of Na from cell through the pump maintains the sodium gradient across the cell membrane and Na-Ca exchanger ruses energy from sodium gradient to pump calcium out of cell.
by inhibiting Na/K ATPase, cannot maintain sodium gradient so calcium cannot be pumped out and accumulates in cell. More calcium available for contraction, resulting in stronger contractions
effects of digitalis
mechanical effect: increase contractility -> increase CO -> decrease sympathetic activity and increase renal blood flow which would release more renin -> decrease preload and afterload
electrical effect: increase contractility -> more parasympathetic activity ->decrease AV conduction -> decrease ventricular rate
AE of digitalis
dysrhythmia (AV block, A F, VF)
GI effects
CNS effects
digitalis toxicity
increased intracellular Ca can lead to
- tachycardia, atrial fibrillation, automaticity, extra systole
what to do
- discontinue
- anti-arrthymic drugs (eg lidocaine, propanaol)
- digoxin antibody
for angina, which drug is the most appropriate for long term therapy aimed at reducing the incidence and severity of vasospasm
Diltiazem
anti-arrthymatics drug classes
some block potassium channels
class 1- sodium blocker
class 2- beta blockers
class 3- potassium
class 4- Ca2+ channel
