Heart Lecture 2: Cardiac Conduction Flashcards
What determines the internal resistance of the heart?
Gap junctions
How does current flow through cardiac myocytes?
Gap junctions
3 types of adhering junctions found in intercalated discs of cardiac cells
1) fascia adherens (anchoring sites for actin)
2) macula adherens/desmosomes (holds cells during contraction by binding intermediate filaments)
3) Gap junctions
Definition of Healing Over
increase in internal resistance that results from decrease in number of open gap junctions
What causes Healing Over?
Increase in intracellular [Ca++] and/or [H+] (happens in ischemia when blood isnt there to wash those waste ions away)
What does Healing Over effectively do to conduction?
Walls off area of damaged tissue either entirely (good) or somewhat (creates arrhythmias)
Important structural features of SA and AV node
1) small diameter (HIGH internal resistance, small space constant)
2) few gap junctions (SLOW conduction)
3) few myofibrils (WEAK contraction)
Important structural features of atrial and ventricular mucsle
1) medium diameter
2) many gap junctions (FAST conduction)
3) many myofibrils (STRONG contraction)
Important structural features of His bundle, bundle branches, Purkinje fibers
1) large diameter
2) the most gap junctions (FASTEST conduction)
3) few myofibrils (WEAK contraction)
Two factors that determine cardiac conduction
1) space constant (membrane resistance inversely based on K+ permeability; internal resistance inversely based on # gap junctions and cell diameter)
2) rate of rise and amplitude of AP (depends on # of Na+ channels available which depends on the resting membrane potential)
3 conditions that alter resting membrane potential
1) hyperkalemia (more positive RMP)
2) premature excitation during relative refractory period
3) ischemia or myocardial injury (more pos RMP)
Can effects of hyperkalemia be reversed?
yes, and that reversibility is important for recovering ischemic areas
Two phases of conduction on EKG
1) P-R interval (200ms)
2) QRS interval (100ms)
Where does impulse travel in PR interval?
atrial muscle –>AV node –> His Purkinje (does not yet get to ventricle muscle)
Where does impulse travel in QRS?
ventricular muscle from endocardium to epicardium
What is the importance of the delay in conduction caused by the AV node?
1) permits optimal ventricular filling
2) filters impulses so afib and aflutter do not necessarily pass to ventricles
What feature of the AV node protects the ventricles from abnormally high atrial rates?
the long refractory period
What is the AV nodal conduction time on the EKG?
the PR interval
Main feature of 1st degree heart block
PR interval longer than 200ms (or one box on EKG)
2nd degree heart block
All QRS complexes are preceded by P wave but not all P waves are followed by a QRS complex (atrial impulses fail to generate ventricular impulses)
3rd degree heart block
no communication between atria and ventricles. Only source of QRS comes from latent ventricular pacer
normal duration of QRS complex (aka the intra-ventricular conduction time)
100ms
What does a slurred QRS complex suggest?
slowed intra-ventricular conduction resulting from abnormal wall motion (impulse does NOT go from endo to epi but instead travels longitudinally)
What is a notched QRS complex?
evidence of asynchronous electrical activation of left and right ventricles (bundle branch blocks)
Is supraventricular tachycardia normal or pathological?
normal because the impulse is still traveling through the canonical conduction pathway (SA-atria-AV-His Purkinje)
stroke volume is not significantly compromised
What does SVT look like on an EKG?
narrow, rapid QRS complexes
How does SVT differ from ventricular tachycardia?
Vtac conduction through the ventricles is NOT normal. Impulse originates within the ventricle and therefore does not travel through the His-Purkinje system (does not go endo-epi but longitudinally)
stroke volume IS compromised
What does Vtac look like on an EKG?
slurred, repeated QRS complexes
What does atrial fibrillation look like on an EKG?
no discrete P and T waves but an indecipherable squiggle in between QRS complexes
What does ventricular fibrillation look like on an EKG?
craziness, no clean QRS complexes because they are all slurred
What is the parasympathetic mediator of the heart?
Acetylcholine released from the vagus nerve
What is the sympathetic mediator of the heart?
Norepinephrine released from symp nerves
Chemical effects of ACh on the heart
1) rapidly increases K+ permeability allowing K+ to flee the cell, making the resting membrane potential more NEGATIVE, away from threshold. Therefore, hyperpolarizes it making it harder to contract
2) inhibits adenylyl cyclase and cAMP synthesis effectively decreasing slow inward Ca++ current and slowing the conduction of the SA and AV nodes
Functional effects of ACh on heart
1) SLOWS the heart rate (via lengthening the PR-interval)
2) no effect on ventricles
Chemical effects of norepinephrine on the heart
1) increases cAMP which increases slow inward Ca++ current. This increases SA node rate and AV node conduction
Where does norepinephrine act?
On the beta-1 adrenergic receptors in all areas of the heart
What receptors does ACh use on the heart?
muscarinic
Which neurotransmitter has a negative ionotropic effect?
ACh (inhibits muscle contraction - makes Vm more negative)
Which neurotransmitter has a positive ionotropic effect?
NE (increases atrial and ventricular contraction - makes Vm more positive since it increases Ca++ flow into the cell)
