Cardiac Conduction and the EKG (L6)

Question 1

What are intercalcated discs?

Answer 1

Specialized regions of intercellular connections between cardiac cells

Question 2

What are the three types of adhering junctions within an intercalcated disc?

Answer 2

Fasica adherens, macula adherens, and gap junction

Question 3

Define fascia adherens

Answer 3

Anchoring sites for actin that connect to the closest sarcomere

Question 4

What is the function of Macula adherens

Answer 4

Holds cells together during contraction by binding intermediate filaments, joining the cells together
Also called desmosomes

Question 5

What are gap junctions?

Answer 5

Low resistance connections that allow current (action potentials) to conduct between cardiac cells

Question 6

What are gap junctions sensitive to?

Answer 6

Intracellular Ca2+ concentration and the concentration of H+ ions (pH)

Question 7

What is “healing over”?

Answer 7

When there is an increase in internal resistance that results from a decrease in the number of open gap junctions. This is caused by an increase in intracellular (cytosolic) Ca2+ and/or H+ ions (decreased pH).

Question 8

What is the structure and function of the SA node and AV node?

Answer 8

They have a small diameter (5-10 um), tapered ends, with few gap junction connections and few myofibrils. They are the pacemakers, with slow conduction and weak contraction

Question 9

What is the structure and function of the atrial and ventricular muscle?

Answer 9

Medium in diameter (10-20 um), rectangular abundant gap junction connections, with abundant myofibrils. Their function is conduction and contraction, so they have rapid conduction and strong contraction

Question 10

What is the structure and function of the His bundle, bundle branches, and Purkinje fibers?

Answer 10

Large in diameter (50 um), cylindrical, abundant gap junction connections and few myofibrils. They have very rapid conduction but weak contraction

Question 11

Where does the SA node fire in relation to the EKG?

Answer 11

Right before the P wave

Question 12

What is happening (in the heart) during the p-wave of the EKG?

Answer 12

Atrial depolarization is the p-wave on the EKG

Question 13

When does the AV node fire, during the EKG?

Answer 13

You can’t measure it on the EKG but it fires right after atrial depolarization, so sometime between the P-wave and before the QRS complex, but it wouldn’t be shown on the actual EKG

Question 14

What does the QRS complex indicate is happening in the heart?

Answer 14

Ventricular depolarization

Question 15

What two factors impact the conduction of the cardiac action potential?

Answer 15

The length (space) constant and the rate of rise and amplitude of the action potential

Question 16

What is the formula for the space (length) constant for cardiac conduction?

Answer 16

(Rm/Ri)^1/2

Question 17

In the space constant, define Rm and how it affects the conduction of the signal

Answer 17

Rm is the membrane resistance, and its inversely related to K+ permeability. So you want high membrane resistance to keep the signal from leaking out

Question 18

In the space constant, define Ri and how it affects the conduction of the signal

Answer 18

Ri is internal resistance, and its inversely related to the number of nexal connections, as well as cell diameter. You want low internal resistance for high conduction of the signal

Question 19

Explain the H infinity curve and how it affects conduction

Answer 19

The H infinity curve is showing the number of available fast Na+ channels and the membrane potential BEFORE stimulation of an action potential. At very negative mV, the number of Na+ channels available is maximal, and is about ZERO at -50 mV. Small increases in RMP leads to inactivation of VG Na+ channels, thus making the cell LESS excitable

Question 20

What conditions would influence the action potential upstroke as a result of changes in the RMP?

Answer 20

Hyperkalemia (Kelly’s favorite)
Premature excitation during relative refractory period
Ischemia or myocardial injury

Question 21

What is hyperkalemia and how does it effect the conduction of an action potential?

Answer 21

Hyperkalemia is when there is increased extracellular K+ concentration, so this leads to the activation of the inward rectifying K channels (since they are activated by K+). This allows K+ to leak out of the cell, bringing the RMP more positive. This increase in RMP then reduces the number of VG Na+ channels available, so the threshold increases. So there is a slower rate of rise and smaller amplitude of the action potential, meaning there is slow conduction of the action potential

Question 22

Where is the P-R interval on the EKG and what does it show?

Answer 22

The P-R interval is from where the P-wave starts to the start of the QRS complex. This shows conduction time from atria to the ventricular muscles

Question 23

Where is the QRS interval on an EKG and what does it show?

Answer 23

That is the big spikey boi and it shows intra-ventricular conduction time, so conduction through the ventricles.

Question 24

What segment of an EKG is a good diagnostic region and can get a “tombstone”?

Answer 24

ST segment, its where the whole heart should be depolarized. If its altered, then good luck buddy

Question 25

Specifics of AV node conduction

Answer 25

There is a delay in conduction to permit optimal ventricular filling. The action potential is a slow response due to slow inward Ca2+ current. There is a long refractory period, which protects the ventricles from abnormally high atrial rates. The AV nodal conduction time is clinically determined by P-R interval

Question 26

Define 1st degree heart block and what does it look like on an EKG

Answer 26

Abnormal prolongation in P-R interval greater than 0.20 sec, so the signal is getting through the AV node, its just taking longer

Question 27

Define 2nd degree heart block

Answer 27

Some atrial impulses fail to activate ventricles, so not all P waves are followed by QRS complexes. Wenckebach is progressive P-R intervals until a beat is dropped, Mobitz type II does not progress, it just drops a beat

Question 28

Define 3rd degree heart block

Answer 28

AV node is non-functional, can occur when a heart attack kills the AV node. This means the ventricles are no longer being paced by the AV node, so they could be paced by some other ectopic pacemaker, if you’re lucky

Question 29

Specifics of Ventricular Conduction

Answer 29

Rapid conduction through the His-Purkinje system, brings the electrical impulse to the endocardial surface, resulting in endocardial to epicardial activation of the ventricles. Results in a normally narrow QRS complex (less than 100 ms in duration). Synchronizes ventricular activation (contraction), and intra-ventricular conduction time is clinically determined by the duration of QRS complex

Question 30

What does a slurred QRS complex show?

Answer 30

Slowed intra-ventricular conduction, associated with abnormal wall motion. Possible causes are hyperkalemia, ischemia, ventricular tachycardia

Question 31

What does a notched QRS complex indicate?

Answer 31

Asynchronous electrical activation of left and right ventricles. Possible causes are left and/or right bundle branch blocks

Question 32

What happens during supraventricular tachycardia?

Answer 32

Conduction through the ventricles is normal because the impulse comes from the atria and travels through the AV node into the His-Purkinje system. So QRS duration is normal, ventricular wall motion is normal and stroke volume is not significantly compromised

Question 33

What happens during ventricular tachycardia?

Answer 33

Conduction through the ventricles is NOT normal because the impulse originates within the ventricular muscle and does not travel through the His-Purkinje system. So the QRS duration is slurred, ventricular wall motion is abnormal and stroke volume is compromised

Question 34

What happens during atrial fibrillation?

Answer 34

Conduction is abnormal due to re-entry of excitation. Contractile activity of the atria becomes asynchronous and pumping action stops

Question 35

Why is atrial fibrillation not life-threatening?

Answer 35

The SA node is not coordinating with all the cells, but the AV node is still functioning so it will “filter” out the noise and stop it from reaching the ventricles, so the ventricles are still contracting at their normal rate

Question 36

Why is ventricular fibrillation rapidly fatal?

Answer 36

In this case, the cardiac output is 0 because the contractile activity of the ventricles is asynchronous. So you will die very quickly, no coordinated contraction of the heart

Question 37

Effects of Acetylcholine (ACh)

Answer 37

Released from the parasympathetic nerves (vagus nerve), and acts on the muscarinic receptors. Will increase K+ permeability directly via G-proteins, so ACh will hyperpolarize the membrane potential away from threshold. Will also inhibit adenylate cyclase activity and cAMP synthesis, so it will decrease slow inward Ca2+ current indirectly through inhibition of cAMP synthesis. It will also directly inhibit atrial muscle, SA node, and AV node. For atrial muscle contraction, will inhibit it, so negative inotropic effect. For SA node, inhibits the pacemaker activity, slows the heart rate and lengthens the R-R interval. It will also inhibit AV node conduction, lengthening the P-R interval. There is no direct effect on basal ventricular muscle function

Question 38

Effect of Norepinephrine (NE)

Answer 38

Released from sympathetic nerves, affects all areas of the heart. Acts primarily through beta 1 adrenergic receptors to increase cAMP, and increases slow inward Ca2+ current. Will increase atrial and ventricular muscular contraction, so positive inotropic effect. Will also increase SA node rate, so increase heart rate and decrease R-R interval. Will increase AV node conduction, so decreases the P-R interval