Antiarrhythmics Flashcards
What state do VG channels need to be in for phase 0 to occurs
Resting state
What is the “transition of voltage gates channels from inactive back to resting “?
Recovery
Dependent upon the cell membrane reaching a negative membrane voltage
What process depends on depolarization with a Na+ channel?
Recovery
What type if ion blocker can slow down repolarization?
K+ blocker
Disturbances in impulse conduction may occur due to either _______ or _____.
block or reentry
The ______ interval is very indicative of how well your AV node is working.
P-R
What type of AV block is when you are not really blocking the AV node, you are just slowing it down?
First-degree AV block
What does Torsades de Pointes mean?
“twisting of the points”
What is Third-degree AV block also called?
Complete heart block
_________ occurs when one impulse reenters and excites areas of the heart more than once.
Reentry
__________ ________ may be confined to small areas or large portions of the myocardium.
Reentry circuits
Some reentry circuits may be totally random and meander their way through the myocardial tissues causing ____________.
fibrillation
A block may also cause the depression of one of the bundle branches, resulting in an abnormally slow and uncoordinated ventricular depolarization. Right or left bundle branch block would result in a widened ________ on the EKG.
QRS
WHY does reentry occur?
- obstacle to homogenous conduction (the impulses spreading through the myocytes do NOT travel at the same speed)
- Unidirectional block
- Conduction time around the block
What can cause obstacles to homogenous conduction?
a fast accessory tract or an MI (injury/ischemia) that damaged some conduction tissue
What occurs during unidirectional block?
the impulse will “die out” in one direction, but may continue through if it approaches from the other direction
How can we prevent unidirectional block?
- convert the unidirectional block to bidirectional block
* speed up the time around the block
What are the two primary methods to treating reentry circuits?
- Speed the conduction around the depressed tissue
- Increase the effective refractory period of the depressed area
(both cause bidirectional block)
What is the refractory period?
How long it takes to get a critical amount of VG Na+ channels back to the resting period
What are 2 things that drugs can do to treat reentry arrhythmias?
- delay recovery by prolonging the inactivation state of VG Na+ channels
2, prolong repolarization by blocking K+ channels
(drug classes do one of these)
What is erratic atrial muscle depolarizations with multiple foci and is characterized by an IRREGULARLY-IRREGULAR tracing?
Atrial Fibrillation (A fib)
What classes are responsible for RATE control of A fib?
Class II and IV (slow down AV node)
Digoxin can also slow down AV node at specific doses
Most A fib pts are treated with II and IV
What classes are responsible for RHYTHM control of A fib?
Class I and III (fix re-entry circuits)
What are usually characterized by wide, bizarre QRS complexes, followed by a pause (skipped beat)?
Premature Ventricular Contractions
What drug classes can treat Premature Ventricular Contractions?
Class I and III (fix reentry)
What is rapid succession of depolarizations resulting from ventricular foci?
Ventricular Tachycardia (impulses originate at ventricular pacemaker)
What is sinus bradycardia?
Sinus bradycardia is a rhythm in which fewer than the normal number of impulses arise from the sinoatrial (SA) node. < 60 beats/minute, with sinus bradycardia being defined as a sinus rhythm with a rate below 60 beats per minute. (When the SA node is not sending the signal for HR as quickly as “normal”)
What is Tau-recovery time?
how fast the drug will dissociate from the channel once the channel enters the resting state
______ Na+ channels switch from inactive to resting the more negative the membrane becomes.
A. more
B. less
A. more
VG Na+ channel blockers alter the channel’s:
1.
2.
- Conductance properties
2. Recovery time
What factors can cause arrhythmias?
- disturbances in impulse FORMATION
- disturbances in impulse CONDUCTION
- both FORMATION & CONDUCTION
Where do disturbances in impulse formation usually occur?
SA node, AV node,and Purkinje fibers (because they have funny currents and are where the impulses originate from)
What is the primary pacemaker?
SA node
What are the “latent pacemakers”?
Purkinje fibers
Purkinje fibers are particularly sensitive to _____ stimulation
A. SNS
B. PNS
A. SNS
Excessive _______ stimulation may cause purkinje fibers to fire in the absence of the SA node signal, resulting in ventricular depolarization that is not in sync with the rest of the heart.
SNS
Excessive SNS stimulation of purkinje fibers can cause:
- VENTRICULAR TACHYCARDIA
* VENTRICULAR FIBRILLATION
What can cause disturbances in impulse CONDUCTION?
block or reentry
What can cause block?
HIGH PNS activity that significantly depresses the AV node which slows or prevents conduction from atria to ventricles
What drug class can you give to fix heart block?
antimuscarinic agents
What type of AV block results in abnormally long PR intervals?
First-degree AV Block
What type of AV block?
• Only every-other PR interval is able to conduct through the AV node.
Second-degree AV Block
What type of AV block?
No association of QRS complete to P-waves and cardiac function is ONLY persevered through an escaped junctional or ventricular pacemaker
Third-degree AV Block (Complete Heart Block)
When the AV node is firing fast (normal), the PR interval is_______.
A. short
B. long
A. short
Block can cause the depression of one of the bundle branches, resulting in an abnormally _____ and ______ ventricular depolarization.
Slow and uncoordinated
Right or left bundle branch block would result in a widened _____ on the EKG
QRS
impulses that interrupt phase 3 (EAD) or phase 4 (DAD) of the cardiac myocytes action potential
Afterdepolarizations
frequently occur at low heart rates when the action potential duration (QT interval) is long
Early Afterdepolarization (EAD)
Early Afterdepolarization (EAD) commonly occur due to?
Commonly occur with K+ blockers or due to congenital abnormalities of K+ channels (Long QT interval)
Delayed Afterdepolarizations (DAD)?
usually occur at fast heart rates and are associated with calcium overload
What can cause Delayed Afterdepolarizations (DAD)?
digoxin toxicity, excessive SNS activity
What phase do EADs interrupt?
3
what phase do DADs interrupt?
4
What occurs when one impulse reenters and excites areas of the heart more than once?
reentry
T/F? o Reentry circuits may be confined to small areas or large portions of the myocardium
True
What 3 things must happen for reentry to occur?
- Obstacle to homogenous conduction
- Unidirectional block
- Conduction time around the block
What is Unidirectional block?
When the impulse “dies out” in one direction but may continue through if it approaches from the other direction.
What is an obstacle to homogenous conduction?
•When the impulses spreading through the myocytes do NOT travel at the same speeds
(Can occur due to a fast accessory tract or an MI that damaged some conduction tissue)
What does “Conduction time around the block” mean?
The conduction time around the blocked area must be long enough so that when the impulse reaches the other side, the slow area is no longer refractory and can conduct in a retrograde fashion (if the impulse is going too fast, it will fly past the area where it would reenter, but if it is slow enough, it can enter the area that was blocked from the other side and reenter
What are the two ways to treat reentry circuits?
1.Speed the conduction around the depressed tissue (not normally done pharmacologically)
•“the person is going to fast to stop and open the door”
2.Increase the effective refractor period of the depressed area
•“lock the door”
Drugs that treat reentry arrhythmias do one of two things:
- Delay recovery by prolonging the inactivation state of VG Na+ channel
- Prolong repolarization by blocking K+ channels
________ is the erratic atrial muscle depolarization with multiple foci. It is characterized by “irregularly-irregular” tracing.
Atrial Fibrillation
How can we treat A fib?
We can treat A fib by:
• Fixing the reentry circuits (RHYTHM control of A fib)
• Slow down the AV node (RATE control of A fib)
What drugs can fix the reentry circuits?
Na+ channel blockers (Class I)
K+ channel blockers (Class III)
What are Premature ventricular contractions?
characterized by wide, bizarre QRS complexes, followed by a pause (skipped beat)
What are the two types of Premature ventricular contractions?
- unifocal
2. multifocal
Which type of Premature ventricular contractions is more dangerous?
Multifocal
What class of agents • Primarily mess with VOLTAGE GATED Na+ channels • Will affect myocytes and purkinje fibers more than the nodal tissue • Class Ia, Ib, and Ic (based on affinity for channel and how long the drug remains bound)
Class I Agents: Na+ channel blockers
What class of agents blocks SNS in heart so they decrease HR, decrease in FOC, increase in duration of contraction
Class II agents (BB)
What class of agents prolong the action potential duration usually by blocking K+ channels
Class III agents
What do you need to monitor in pts on class III agents?
QT interval
What class of agents blocks L-type Calcium channels?
Class IV agents (CCBs)
What is Sinus bradycardia?
Sinus bradycardia is a rhythm in which fewer than the normal number of impulses arise from the sinoatrial (SA) node. The normal heart rate has been considered historically to range from 60 to 100 beats per minute, with sinus bradycardia being defined as a sinus rhythm with a rate below 60 beats per minute.
When the SA node is not sending the signal for HR as quickly as “normal”
Sinus bradycardia
When the SA node is sending the signal for HR quicker than “normal”
Sinus tachycardia
What is sinus tachycardia?
a heart rhythm originating from the sinoatrial node with an elevated rate of impulses, defined as a rate greater than 100 beats/min (bpm) in an average adult. The normal resting heart rate in the average adult ranges from 60–100 beats/min.
