Cardiac Exam Lecture 2 Flashcards
Explain the Effective Refractory Period and the Relative Refractory Periods of the Heart
Effective Refractory Period (ERP): channels responsible for the action potential upstroke are completely inactivated and therefore no APs can be fired during this time
Relative Refractory Period: channels responsible for the action potential upstroke are partially recovered and therefore abnormal APs can be ellicited at this time
Refractory Periods are due to voltage- and time dependence of Na+ (fast response) and Ca++ (slow response)
Explain the difference in refractory periods between slow and fast response (aka are they voltage or time dependent)
Fast Response: primarily voltage dependent
Slow Response: primarily time dependent
Explain premature beats for fast response
Premature Beats Ellicited at Different TImes during the relative refractory period:
Premature beats are usually benign, but if it’s really early, some of the Na channels haven’t recovered yet, leads to a slow upstroke and abnormal conduction. This can lead to reentry of excitation.
Explain what an “R on T” is
R on T- premature beat (R wave) that occurs during the relative refractory period (T wave) of previous beat
Explain what commotio cordis is
Commotio cordis: often lethal disruption of heart rhythm caused by blow to area directly above heart aka the precordial region (driveline baseball for example) at a critical time during the cycle of a heart beat causing cardiac arrest. It is a form of VFib. Can sometimes be reveresed by Defib.
Mostly happens in boys and teenagers during sports.
Explain post repolarization refractoriness (slow response)
Post Repolarization Refractoriness - The refractory period of a slow response is significantly longer than the AV node AP duration. Even though the voltage fully repolarizes, cell is still refractory BECAUSE refractory period of slow calcium channels is more dependent on time than on voltage. This mechanism is reponsible for the fact that conduction through the AV node slows when stimulated at higher rates (short cycle lengths). This mechanism also prevents rapid ventricular activation during atrial tachy-dysrhythmias such as AFib or flutter
What happens when you try to excite the AV node at various times after a slow response AP
AV nodal APs… early impulses are abnormally small because there aren’t enough Ca channels available to support a normal AP
Explain Atrial Fibrillation.
In AFib, what is determining the rate and the rhythm of ventricular activation?
How do you slow ventricular rate in a patient with AFib?
In AFib, the ventricular rate is too rapid (> 100 beats per minute) and the ventricular rate is irregularly irregular
In AFib, the AV node refractory period is what determines the rate and rhythm of ventricular activation
In Afib, you can slow the ventricular rate with a calcium channel blocker… lengthen the refractory period, slow AV node conduction. Can also give a beta blocker
AFib is the number one most common arrhythmia, the major risk factor is age. What is the major risk of AFib?
AFib leads to clotting because the blood is stagnant in certain appendages of the atira. If you cardiovert the pt, you can send the clot into the coronary arteries (heart attack) or up to the brain (stroke) or into the lungs (pulmonary embolism).
Treat with anticoagulants, agents that lengthen the refractory period, and also you can ablate the site of arrhythmogenesis
As the heart rate increases, what happens to the AP duration?
What phase of the cardiac cycle shortens more with increased HR, systole or diastole?
As the HR increases, the AP duration gets SHORTER/DECREASES
Diastole shortens (resting period shortens)
Systole has to shorten too but not as much
Explain the hierarchy of pacemaker activity
The SA node is the primary pacemaker and has the fastest inherent beating rate.
Atrial and ventricular subsidary pacemakers
Hierarchy of pacemaker activity means that pacemakers in the heart are anatomically arranged based on their inherent beating rate
SA node > latent atrial pacemakers > AV Node/His bundle > Bundle Brances > Purkinje Fibers
What are the four things that cause diastolic depolarization/ (phase 4) depolarization of the SA node
(Explain the four mechanisms that underlie the SA node)
SA node - multiple mechanisms underlie the SA node pacemaker activity/ These are the four mechanusms that cause diasolic depolarization
- T type Ca++ current
- hyperpolarization-activated inward current/ “funny current” (letting in Na)
- Deactivation of K+ current
- Inward Na/Ca exchange current activated by intracellular SR calcium release
The funny current is the one channel that is activated by hyperpolarization.
Draw the AP of the SA node. Explain the ionic current mechanisms of the SA node. Draw a dot where the maximum diastolic potential is on the graph. Which of the four ionic mechanisms do purkinje fibers have?
Black dot on the graph shows where the maximum diastolic potential is
What are the mechanisms for changes in heart rate?
Mechanisms for changes in heart rate:
a) slope of diastolic depolarization
b) level of maximum diastolic potential
c) threshold potential
d) pacemaker shifts - changes in pacemaker site can cause aburpt changes in heart rate because of the hierarchy of pacemaker activities
What does ACh do to the slope and the maximum diastolic potential (of the SA node AP)?
ACh changes the slope and increases the maximum negative potential… slower to threshold and farther to go.
