Heart Lecture 3: Cardiac Refractory Periods

Question 1

What creates refractory periods?

Answer 1

voltage and time-dependence of Na+ (fast response) and Ca++ (slow response) channels

Question 2

What is the difference between the effective and relative refractory periods?

Answer 2

ERP: all Na+ channels are completely inactivated (no APs can be elicited)
RRP: some Na+ channels have partially recovered so abnormal APs can be elicited

Question 3

What effect do anti-arrhythmic drugs have on refractory periods?

Answer 3

lengthens them

Question 4

What determines refractoriness in Fast responses?

Answer 4

voltage

Question 5

What determines refractoriness in Slow responses?

Answer 5

time

Question 6

What is the vulnerable period of the heart?

Answer 6

the relative refractory period (when you can get scary, crazy beats)

Question 7

Do premature beats usually conduct quickly or slowly?

Answer 7

SLOWLY since their upstroke is very slow due to limited Na+ channels available

Question 8

What is R on T phenomena?

Answer 8

a premature beat (R wave) that occurs during the relative refractory period (T wave) of the previous beat

Question 9

repolarization of action potential is consistent with which wave on EKG?

Answer 9

T wave

Question 10

What is commotio cordis and why is it often fatal?

Answer 10

an electrical disruption of the heart rhythm that occurs as a result of a blow to the area directly over the heart. Fatal because it hits the heart right at repolarization (critical stage) of action potential throwing the heart into vfib

Question 11

Why is post-repolarization refractoriness a special feature of the AV node?

Answer 11

the refractory period outlasts the action potential duration (preventing rapid ventricular activation)

Question 12

How is post-repolarization refractoriness different from other refractory periods?

Answer 12

The cell is still refractory even AFTER the voltage has fully repolarized to resting potential. This happens because recovery period of Ca++ is dependent on TIME not voltage.

Question 13

What is the medical definition of atrial fibrillation?

Answer 13

Irregularly irregular ventricular rate (greater than 100bpm)

In other words, it is defined with respect to ventricular activity

Question 14

In atrial fibrillation, what is determining the rate and rhythm of ventricular activation?

Answer 14

the AV node refractory period

Question 15

How do you slow ventricular rate in a patient with A-fib?

Answer 15

1) Ca++ channel blockers

2) beta blockers (blocks beta receptors on AV node, lengthening refractory period - blocks sympathetic input basically.)

Question 16

As heart rate increases, what happens to the duration of the action potential (systole)?

Answer 16

decreases

Question 17

What interval on the EKG represents systole (aka action potential duration)?

Answer 17

Q-T

Question 18

As heart rate increases, AP ______, as heart rate decreases, AP ______.

Answer 18

shortens; lengthens

Question 19

What effect does shortening systole have on diastole?

Answer 19

conserves it (restores some of the loss in diastolic filling times at higher heart rates)

Question 20

What are two ways that prolonged Q-T syndrome (aka prolonged action potentials) can occur?

Answer 20

1) acquired (bradycardia, hypokalemia, drugs like quinidine that block Na+ channel)
2) congenital (due to genetic lesions in Na+ and/or K+ channels)

Question 21

What is Torsades de Pointes?

Answer 21

polymorphic ventricular tachycardia; results from abnormally prolonged QT interval

can result from development of early afterdepolarizations

Question 22

What shortens more when heart rate increases, systole or diastole?

Answer 22

diastole