arrhythmias Flashcards
how many phases are in the action potential of a purkinje cell
5
What happens during phase 0 in the action potential of a purkinje cell
- opening of the sodium channels, rapid depolarization, inactivation of the sodium channels
what happens during phase 1 of action potential of purkinje fibers
– rapid partial repolarization due to the inactivation of fast sodium channels and increased K+ channel permeability.
what happens during phase 2 of action potential of purkinje fibers
plateau phase, Ca2+ (main effector, L-type) and some Na+ (aka: “window” or late current) channels are open
what happens during phase 3 of action potential of purkinje fibers
repolarization, Ca2+ channels inactivated, K+ channels open, Na+ channels turning to rested state
what happens during phase 4 of action potential of purkinje fibers
– resting membrane potential
Effective Refractory Period (ERP)
- ERP is the shortest interval at which a premature stimulus results in a propagated response. The ERP usually includes phase 0, 1, 2 and most of 3.
- it is due to the availability of resting Na+ channels
What phases are present in action potential of SA node cell
- 0, 3, 4
What is happening during phase 0 in SA node cell action potential
- opening of the Ca2+ channels (T-type depolarize early, but are not responsible for action potential, but L-type channels are) causing a slow depolarization.
What is happening during phase 3 in SA node cell action potential
repolarization, Ca2+ channels inactivated, K+ channels open
what is happening during phase 4 in SA node action potential
- resting membrane potential never static like in the Purkinje cell, rather a spontaneous depolarization occurs because of a slow Na+ current (If, or “funny” current), at a more depolarized potential, T- and L-type Ca 2+ channels also open and cause phase 0
is there ever a static resting potential in the SA node
resting membrane potential never static like in the Purkinje cell, rather a spontaneous depolarization occurs because of a slow Na+ current (If, or “funny” current),
The fraction of Na+ channels available for opening in a purkinje fiber in response to a stimulus is determined by
the membrane potential immediately preceding the stimulus.
Action Potential Duration (APD)
Action potential duration is the time interval between the point of depolarization and repolarization. Normally, the ERP and APD are closely linked with the ERP being roughly 85% of APD.
what are the basic causes of cardiac arrhythmias
- disturbances in impulse formation
- disturbances in impulse conduction
- both
SA node reaches threshold at what potential
-40 mV
SA node is at resting membrane potential at what value
-65 mV
List the 4 factors that determine rate of pacemaker cells
- maximum diastolic potential
- slope of phase 4 depolarization
- threshold potential
- duration of action potential
list the two causes of simple block disturbance of impulse conduction
- AV nodal block
- bundle branch block
list the two causes of reentry mechanism disturbance of impulse conduction
*major mechanism
- obstacle to homogenous condution
- unidirectional block at some point
- condution time along the circuit is long enough to find excitable tissues
Explain what happens in normal electircal impulse condution
- two impulses meet and extinguish eachother due to trying to activate cells in the effective refractory period
- all electrical activity stops and allows for resetting of the channels
explain what occurs during unidirectional block and reentry
- the impulse traveling through the unidirectional block is extinguished in the anterograde direction
- the conduction pathway can now re-enter in the retrograde direction and will cause a reentry arrhythmia circuit
Remember the Gaussian distribution of patient responses! Antiarrhythmic agents can precipitate what
lethal arrhythmias
- at higher doses, antiarrhythmic agents can depress conduction in normal tissues and produce drug induced arrhthymias
list the drugs in class 1A of sodium channel blockers
- Quinidine (Quinora)
- Procainamide (Pronestyl)
list the drugs in class 1B of sodium channel blockers
Lidocaine
MOA of drugs in class 1A of sodium channel blockers
- preferentially block open or activated Na+ channels
- slows rate of rise of action potential
-
Blocks K+ channels
- lengthen the duration of action potential and ERP
- **will completely block damaged cells
MOA of drugs in class 1B of sodium channel blockers
- Block inactivated sodium channels
- preferentially affects damaged tissue; blocks “window” current
- shorten the duration of action potential and ERP
MOA of drugs in class 1C of sodium channel blockers
- Binds to ALL sodium channels; no effect on the duration of action potential (ERP stays the same)
List the drugs in class 1C of sodium channel blockers
Flecainide
what are the class II antiarrhythmic drugs
- beta blockers
- reduce adrenergic activity on the heart
MOA of drugs in class III antiarrhythmic agents
- inhibit K+ channels and Prolong repolarization (ERP increases)
list drugs in class III antiarrhythmic agents
- Amiodarone
- Sotalol
list drugs in class IV antiarrhythmic agents
- verapamil
- diltiazem
MOA of drugs in class IV antiarrhythmic agents
- calcium channel blockers
- block slow L-type cardiac Ca2+ channels
- decrease HR and contractility
When is Quinidine used
- broad spectrum
- acute or chronic tx of atrial and ventricular arrhythmias
adverse effects of Quinidine
- low theraputic index
- cardiac toxicity
- blocks alpha receptors -> severe hypotension and reflex tachycardia
- paradoxical tachycardia
- increase QT interval -> Torsade de pointes -> Quinidine syncope
- Diarrhea (top 5 drug to cause this)
- Cinchonism: loss of hearing, angioedema, tinnitus, visual disturbances
What is different about Procainamide from Quinidine even though they are both in Class 1A drugs
procainamide can cause lupus erythematosus in slow acetylators
DOC for acute ventricular arrhythmias
Lidocaine
route of administration of Lidocaine
IV
adverse effects of Lidocaine
- least negative inotropic
- convulsions
when is Flecainide used
- last ditch effort drug
- atrial arrhythmias
- life threatening ventricular arrhythmias
adverse effects of Flecainide
strong pro-arrhythmic effect
which beta blocker is B1 specific, given IV, and has a short half life
Esmolol
use of Esmolol
acute treatment of PSVTs-2nd line
- Paroxysmal supraventricular tachycardia (PSVT)
DOC for ventricular arrhythmias -> ACLS
Amiodarone
when is Amiodarone used
- effective against both atrial and ventricular arrhythmias
even though Amiodarone prolongs QT, what stands out about it
Does not cause Torsade de pointes
adverse effects of Amiodarone
- pulmonary fibrosis
- deposited in tissues, cornea (yellow-brown), skin (grayish blue)
- thyroid disfunction
MOA of Sotalol
- class III
- K+ blocker -> prolongs APD
- also non-selective beta blocker
when is Sotalol used
- in tx of ventricular and atrial arrhythmias
adverse effects of Sotalol
Torsade de pointes
When is Verapamil and Diltiazem used
- Reentrant supraventricular tachycardia
- PSVT
-
Atrial fibrillation and flutter
- marked effects on SA and AV nodes
which drug class is only effective in the atria
CCB
MOA of adenosine
- enhance K+ conductance and inhibition of cAMP-induced Ca2+ influx
- hyperpolarizes everything and resets the heart
when is adenosine used
- reentry arrhytmias
- acute PSVT
- WPW syndrome
DOC for acute PSVT and WPW syndrome
adenosine
acute PSVT treatment order
- adenosine
- Esmolol
- CCB
chronic PSVT treatment order
- B-blocker
- CCBs
DOC for torsade de pointes
Magnesium
MOA of potassium in treatment of arrhythmias
- increased serum K has membrane potential stabilizing action by increasing K+ permeability (hyperpolarizes)
- decreases ADP
- decreases conduction
- decreases pacemaker rate
which drug class only works for ventricular arrhythmias
class 1B: lidocaine
- because that’s the only place where there is a plateau phase where the “window” current is functioning.
Lidocaine, adenosine and magnesium are administered
IV only
- are useful only in acute therapy.
