Heart Lecture 2: Cardiac Conduction

Question 1

What determines the internal resistance of the heart?

Answer 1

Gap junctions

Question 2

How does current flow through cardiac myocytes?

Answer 2

Gap junctions

Question 3

3 types of adhering junctions found in intercalated discs of cardiac cells

Answer 3

1) fascia adherens (anchoring sites for actin)
2) macula adherens/desmosomes (holds cells during contraction by binding intermediate filaments)
3) Gap junctions

Question 4

Definition of Healing Over

Answer 4

increase in internal resistance that results from decrease in number of open gap junctions

Question 5

What causes Healing Over?

Answer 5

Increase in intracellular [Ca++] and/or [H+] (happens in ischemia when blood isnt there to wash those waste ions away)

Question 6

What does Healing Over effectively do to conduction?

Answer 6

Walls off area of damaged tissue either entirely (good) or somewhat (creates arrhythmias)

Question 7

Important structural features of SA and AV node

Answer 7

1) small diameter (HIGH internal resistance, small space constant)
2) few gap junctions (SLOW conduction)
3) few myofibrils (WEAK contraction)

Question 8

Important structural features of atrial and ventricular mucsle

Answer 8

1) medium diameter
2) many gap junctions (FAST conduction)
3) many myofibrils (STRONG contraction)

Question 9

Important structural features of His bundle, bundle branches, Purkinje fibers

Answer 9

1) large diameter
2) the most gap junctions (FASTEST conduction)
3) few myofibrils (WEAK contraction)

Question 10

Two factors that determine cardiac conduction

Answer 10

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)

Question 11

3 conditions that alter resting membrane potential

Answer 11

1) hyperkalemia (more positive RMP)
2) premature excitation during relative refractory period
3) ischemia or myocardial injury (more pos RMP)

Question 12

Can effects of hyperkalemia be reversed?

Answer 12

yes, and that reversibility is important for recovering ischemic areas

Question 13

Two phases of conduction on EKG

Answer 13

1) P-R interval (200ms)

2) QRS interval (100ms)

Question 14

Where does impulse travel in PR interval?

Answer 14

atrial muscle –>AV node –> His Purkinje (does not yet get to ventricle muscle)

Question 15

Where does impulse travel in QRS?

Answer 15

ventricular muscle from endocardium to epicardium

Question 16

What is the importance of the delay in conduction caused by the AV node?

Answer 16

1) permits optimal ventricular filling

2) filters impulses so afib and aflutter do not necessarily pass to ventricles

Question 17

What feature of the AV node protects the ventricles from abnormally high atrial rates?

Answer 17

the long refractory period

Question 18

What is the AV nodal conduction time on the EKG?

Answer 18

the PR interval

Question 19

Main feature of 1st degree heart block

Answer 19

PR interval longer than 200ms (or one box on EKG)

Question 20

2nd degree heart block

Answer 20

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)

Question 21

3rd degree heart block

Answer 21

no communication between atria and ventricles. Only source of QRS comes from latent ventricular pacer

Question 22

normal duration of QRS complex (aka the intra-ventricular conduction time)

Answer 22

100ms

Question 23

What does a slurred QRS complex suggest?

Answer 23

slowed intra-ventricular conduction resulting from abnormal wall motion (impulse does NOT go from endo to epi but instead travels longitudinally)

Question 24

What is a notched QRS complex?

Answer 24

evidence of asynchronous electrical activation of left and right ventricles (bundle branch blocks)

Question 25

Is supraventricular tachycardia normal or pathological?

Answer 25

normal because the impulse is still traveling through the canonical conduction pathway (SA-atria-AV-His Purkinje)

stroke volume is not significantly compromised

Question 26

What does SVT look like on an EKG?

Answer 26

narrow, rapid QRS complexes

Question 27

How does SVT differ from ventricular tachycardia?

Answer 27

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

Question 28

What does Vtac look like on an EKG?

Answer 28

slurred, repeated QRS complexes

Question 29

What does atrial fibrillation look like on an EKG?

Answer 29

no discrete P and T waves but an indecipherable squiggle in between QRS complexes

Question 30

What does ventricular fibrillation look like on an EKG?

Answer 30

craziness, no clean QRS complexes because they are all slurred

Question 31

What is the parasympathetic mediator of the heart?

Answer 31

Acetylcholine released from the vagus nerve

Question 32

What is the sympathetic mediator of the heart?

Answer 32

Norepinephrine released from symp nerves

Question 33

Chemical effects of ACh on the heart

Answer 33

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

Question 34

Functional effects of ACh on heart

Answer 34

1) SLOWS the heart rate (via lengthening the PR-interval)

2) no effect on ventricles

Question 35

Chemical effects of norepinephrine on the heart

Answer 35

1) increases cAMP which increases slow inward Ca++ current. This increases SA node rate and AV node conduction

Question 36

Where does norepinephrine act?

Answer 36

On the beta-1 adrenergic receptors in all areas of the heart

Question 37

What receptors does ACh use on the heart?

Answer 37

muscarinic

Question 38

Which neurotransmitter has a negative ionotropic effect?

Answer 38

ACh (inhibits muscle contraction - makes Vm more negative)

Question 39

Which neurotransmitter has a positive ionotropic effect?

Answer 39

NE (increases atrial and ventricular contraction - makes Vm more positive since it increases Ca++ flow into the cell)