Flashcards in Antiarrhythmic Basics Deck (32)
What is cardiac arrhythmia?
Loss of cardiac rhythm
What is cardiac excitability?
Ease with which cardiac cells undergo a series of events characterized by:
--sequential depolarization and repolarization
--communication with adjacent cells
-propagation of the electrical activity with a normal or abnormal manner
What are the fast response and slow response action potentials?
Fast Response (initiate depolarization):
ventricular and atrial muscle as well as purkinje fibers
Sinoatrial (SA) node and atrioventricular (AV) node
The resting potential (80-95) of the cell is set by what?
1. Balance of inward (sodium and calcium) and
2. Outward (potassium) currents and
3. The corresponding equilibrium potentials of these currents
--altering the balance of these ions (Via antiarrhythmics) will affect the excitability of the cardiac myocytes
There are 5 phases of the fast response action potential. In general what are these phases?
Phase 0: initial rapid depolarization of the cell membrane
Phase 1: Subsequent partial repolarization of the membrane
Phase 2: unique to cardiac muscle is called the plateau
Phase 3: rapid repolarization phase of the action potential
Phase 4: Resting membrane potential
Now each card will go through the phases of the fast response action potential. Phase 0, what are the features?
Action potential begins: myocyte is depolarized to a potential of about -50mV
--at this threshold potential voltage gated Na channel open and an influx of Na comes into the cell --- resulting in a self reinforcing depolarization of the cell
Now, the same depolarization that cases the channels to open also inactivates the channels several milliseconds later.
Calcium channels also open during depolarization but the inward calcium flux is much slower
Phase 1, what are some features?
K+ conductance is responsible for the resting membrane potential and is suppressed during depolarization, therefore impairing repolarization of the tissue.
--some enhanced K conductance during depolarization which causes opening and then closing of potassium channels that only allow K to exit the cell
-this coupled with inactivation of the Na channels in the membrane causes a temp repolarization of the cell
Phase 2, what are some features?
L-type Ca2+ channels open once the membrane is depolarized to about -50mV (positive charge rushes into cell)
--during this phase of the action potential, the hyperpolarizing effects of K efflux are diminished because of inactivation of K channels by membrane depolarization.
The influx of positive current from Ca2+ matches the remaining positive efflux carried by K exiting through a few open K channels. --- this causes the membrane potential to remain constant at a positive value and present as plateu.
Phase 3, what are some features?
Outward K channels open during phase 3
--Na and Ca channels because inactivated
---outward movement bring about rapid repolarization of the cell
Phase 4, what are some features?
Inward K channels which permit outflux of K at highly negative membrane potentials keeps the resting membrane potential maintained.
--Na channels become activated
While depolarized the cell is resistant to a subsequent depolarizing event called absolute refractory period. What is relative refractory period?
After partial but incomplete repolarization a subsequent depolarization is possible but occurs slowly
Moving on to the slow response cardiac action potentials. What are the phases?
Phase 4: spontaneous depolarization which triggers the action potential
Phase 0: depolarization
Phase 3: repolarization
Nodal tissues does not contain fast voltage gated Na channels. The action potential is therefore dependent on what?
L-type Ca channels
--the slow opening and closing of these channels upon depolarization creates a phase 0 that is slower than that seen in ventricular cells
Once an action potential in the SA node is triggered, the electrical impulse spreads rapidly through the atria and enters the AV node. Conduction through the AV node is slow (allowing time for atrial contraction to propel blood into the ventricles). What happens next?
The impulse then propagates through the His-Purkinge system to all parts of the ventricles
Moving on to the basics of Arrhythmias, Arrhythmias can be classified as either supraventricular (Atrial or AV junctional) or Ventricular. What are factors for an arrhythmia?
2. Electrolyte imbalances
3. Changes in your heart muscle
4. Injury following a heart attack
5. Irregular heart rhythms
All arrhythmias result from disturbances in impulse formation, disturbances in impulse conduction or both. First what does disturbances in impulse formation mean?
SA role: normal impulse formation
--AV node will take over if SA node is not producing impulses.
two MOA associated with impulse formation: altered automaticity and afterdepolarizations
What are factors for why altered automaticity can occur?
Occurs at the SA node and AV node
--due to many factors: beta adrenergic stimulation, hypokalemia, and hypoxia
Sympathetic and Parasympathetic affect the discharge of the pacemaker cells
Automatic behavior at other cardiac sites that ordinarily lack spontaneous pacemaker activity can show enhanced automaticity.
--both enhanced normal (autonomics) or abnormal automaticity lead to arrhythmias
Some individuals posses accessory electrical pathways that bypass the AV node. Thus what happens?
The ventricular tissue receives impulses from both the normal and the accessory pathways
The second mechanism associated with disturbances in impulse formation is afterdepolarizations, when does this occur?
Normal action potential triggers abnormal depolarizations
--if this reaches threshold, it may give rise to secondary upstrokes that can propagate and create abnormal rhythms.
There are two types of afterdepolarizations, early and delayed. What are early depolarizations?
Depolarizations that interrupt phase 2 or phase 3.
--phase 2: inward Ca2+ current
--phase 3: inward Na channels
Can lead to arrhythmias --- aka torsade de points
Marked prolongation of the cardiac action potential
What are delayed afterdepolarizations?
Interrupt phase 4
--shortly after repolarization is complete
Finally the last thing at all arrhythmias result from is disturbances of impulse conduction. Re-entry tachyarrhythmias, what does this mean?
Myocardial ischemia and injury can induce severe ventricular arrhythmias
There are various types of Arrhythmias. Each card will go through the types. First are premature atrial contractions, what is this?
Early beats that originate in the atria
--harmless and do not require treatment
Premature Ventricular Contractions (PVCs) are the next type of arrhythmias. What are some features?
Most common arrhythmias
--skipped beats caused by stress, nicotine, exercise, heart disease or electrolyte imbalance.
Next arrhythmia is atrial fibrillation, what are some features?
Irregular heart rhythm results in the atria contracting abnormally
Next arrhythmia is atrial flutter, what are some features?
Caused by one or more rapid circuits in the atrium
--often converts to a-fib
next arrhythmia is paroxysmal supraventricular tachycardia, PSVT. What are some features?
Rapid heart rate
--from above the ventricles
--begins and ends suddenly
two main types: accessory path tachycardias and AV nodal reentrant tachycardias
Next arrhythmia is ventricular tachycardia (V-tach), what are some features?
Rapid heart rhythm originating from the ventricles
Next arrhythmia is ventricular fibrillation, what are some features?
Erratic, disorganized firing of impulses from the ventricles
--emergency because the ventricles quiver and are unable to contract or pump blood to the body.
The last arrhythmia is sinus node dysfunction, what are some features?
Slow heart rhythm due to abnormal SA node
--results in pacemaker
A quick review on EKG. what do the various waves represent?
P wave: atrial depolarization
QRS: ventricular depolarization
T wave: ventricular repolarization
PR: beginning of atrial depolarization to beginning of ventricular depolarization
QT: duration of ventricular depolarization