Anti arr Flashcards
Describe the phases of Action potential in myocardium cells
Phase 0 = Na enters the cell
Phase 1 = Some K leaves the cell
Phase 2 = Ca enters the cell platue
Phase 3 = all k channels open and k leaves
Phase 4 = resting membrane potential is restored cell is ready to get another stimulus
What Absolute Refractory period ? and it extends from? whats its other name?
ARP is the same as the Action potential duration, its a period where the myocardium cannot be stimulated until its over. extends from phase 0 to phase 3
Whats the main point of antiarrh drugs?
either shorting AP duration or increase it to move phase 4 around, make it so that ectopic focus does not send stimulus during it and time it so it they attack during APR and then it will be pointless.
at which phase do ectopic focus send stimulus that causes problems?
Phase 4
Describe the phases of action potential in SA node
Similar to myocardium except that phase 4 is a slop, the slope is due to Na leaking from HCN funny sodium channels in until it reaches a threshold then it will depolarize ———> this why SA can stimulate on its own called automaticity.
No phase 1 and 2 innit too, only 4, 0,3
Whats the relation between the slope in phase 4 and the firing rate of SA node?
If the slope moves up ( More Na leaking in = shorter time to reach threshold ) then it will increase the firing rate.
If it the slopes moves down (less Na leaking in = takes longer to reach threshold) it will decrease firing rate .
Whats the risk factor of elongating AP/AFP
Torsade de pointe
how do you treat torsade de pointe
magnesium sulfate injection
What are the 4 classes of anti arrhythmic drugs?
Von williams classifications :
Class 1
Class 2
Class 3
Class 4
Others
what is class 1 and its subtypes and give example?
Class 1 are Na channel blockers :
Class 1A they block NA channels and elongate AP duration :- Quinidine, procainamide, disopyramide
Class 1B- they block na channels and shortens the AP duration :-
Lidocaine ( lignocaine/xylocaine ), Mixilletine
Class 1C- block na channels but doesnt affect Ap duration work by different mechanism , flaccind , propafeonone
What is class 2? and give examples
Class 2 are beta blockers :-
Propranolol none selective
Metaprolol selective ( lipophilic metabolized in liver in bile along with propranolol )
atelolol selective ( lipophobic secreted in kidneys unchanged along with sotalol)
What is class 3? and give examples
class 3 are k channels blockers , they elongate ap duration:-
Amiodarone , dronedarone, satolol
what is class 4 and give examples
class 4 are calcium channel blockers, elongate the platue ( phase 2 ), elonagtes AP duration,
Verapmil , diltiam , phenlyalkylamines and benzothiazepines respectively.
Class 1 quinidine what its MOA
1- Block Na channels and elongating AP duration ( cuz its class 1A)
2- Blocks Na channels and moves DOWN the slope in phase 4 in SA node leading to decreased firing rate,
Works on both firing rate and conducting ( chromotopic and dromotopic respectively)
What are the other actions of quinidine ?
1- blocks muscarinic receptors producing atropine like effects ( dry mouth, urine retention, mydrasis, bronchodilation)
2- block alpha –> lead to vasodilation and hypotension
3- negative inotropic effect —> decrease contractility
which forms can quinidine be given as?
IV, IM, Orally
whats the relation between digoxin and quinidine
quinidine displaces digoxin increasing its toxicity
Uses of Quinidine?
its broad spectrum treat many arrhthymia :-
Atrial fibrillation
Venticular arrthymia
Adverse effects of quinidine
1- Hypotension and vasodilation due to alpha blockage
2- cincohism تسمم
3- paradoxical tachycardia ( when given at low doses due to the muscarinic blocking effect including tachycardia) we give verapmil or digoxin to counter this
4- Torsade de pointe and syncope due to elongations of AP duration
5- minimum SLE like symptoms. rash, arthritis, increased creatinine
6- heart failure due to negative inotropic effect ( decreased contractility )
What is the mechanism of procainamide
Same as quinidine
Block na channels and elongate ap duration
block na leaking channels and Move DOWN the slope decreasing firing rate
Whats the difference between procainamide and quinidine in mechanism?
procainamide has less muscarinic blockage effect —> no paradoxical tachycardia –> no need for digoxin or verapmil to counter
how is procainamide administered?
js like quinidine iv, im, orally
Side effects of procainamide?
1- SLE like symptoms —> rash, arhtritis, increased creatinine
2- hematotoxicity –> thrombocytopenia, agranuloctye
3- torsado de pointe and syncome due to elongation of AP duration
what are the 3 drugs that cause SLE like symptoms
1- Procainamide
2- hydralazine —> vasodilator that is used in hypertensive emergencies and pregnancy
3- quinidine
Whats Disopyramides MOA?
sicne its CLASS 1A its similar to quinidine
Bloack Na channels and elongates AP duration
block na leaking during phase 4 moving the slope down and decreasing firing rate
Adverse effects of disopyramide?
heart failure due to negative inotropic effect and decreased contractility
paradoxical tachycardia due to atropine like effects and muscarinic block –> need verapimil and digoxin
Torsade de pointe due to elongated AP duration
What is the MOA of Lidocaine?
Its class 1B :-
Blocks Na channels but DECREASE AP duration ( by speeding up the other phases)
Works primary on dead tissue –> number 1 for arrthymia after MI or ischemia
NO EFFECT ON CONDUCTION COMPARED TO CLASS 1A, NO EFFECT ON SLOPE
