Absolute and Relative Refractory Period


syllabus | home page | BME Home Page | search the web | e-mail Doug


The absolute refractory period is the interval from the beginning of the action potential until the fiber is able to conduct another action potential.                The relative refractory period follows and is the time period in which, although the cell has not fully recovered, a small, weak action potential can be generated as the result of a strong input stimulus.

   The absolute refractory period is the time period during which the rapid influx of Na+ rapidly decreases the negativity of the cardiac cell.  As Vm (membrane potential) approaches zero the electrostatic force pulling Na+ into the cell is neutralized.  The concentration gradient of Na+ however continues to push Na+ into the cell and the cell begins to hyperpolarize as Vm begins to become positive.  This closing of the Na+ channels signals the beginning of the absolute refractory period.  Once these channels close, they cannot reopen for a set period of time.  When Vm becomes positive by about 20mV, Na+ continues to to enter the cell because the concentration gradient overpowers the electrostatic forces.  The influx is slow however, and many of the inactivation gates have already closed.  At about 30mV, Na+ influx ceases.  The channels remain closed until the first half of repolarization, and thus the cell is absolutely refractory during this entire period.  No action potential can be generated by the cell during this time, and the cell will not respond to further excitation.  This mechanism prevents sustained, tetanic contraction of cardiac muscle.  Tetanus would preclude the normal intermittent pumping action of the heart and interrupt the pattern of electrical conduction throughout the cardiac muscle.  The result would be fibrulation.
   The relative refractory period immediately follows the absolute refractory period, and is due to the efflux of K+ ions.  During the second half of repolarization, the excitatory Na+ channels are mostly ready to open, and a small weak action potential can be generated.  However, it is better to wait until the channels are fully ready before continuing with the next excitation.  Full excitability is not regained until the cardiac fiber has been fully repolarized.  In order for an action potential to be generated during the relative refractory period the stimulus must be greater than that which would normally elicit a response.  Unlike the absolute refractory period, the duration of the relative refractory period can change.  As heart rate increases, and systole decreases, the action potential becomes narrower due to a decrease in relative refractory period.  At rest, the heart rate slows, and the action potential becomes wider as the relative refractory period increases.  This allows greater oxygen supply to reach needy areas during exercise and other stress conditions.
   These refractory periods are important because during this time the gradient concentrations of important ions (Na+, K+) are restored.  This allows further excitation of the cardiac fiber.  The results of the refractory periods can be seen in the plateau of the cardiac fiber action potential.


Sample Problems:

What causes the absolute refractory period?

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



The absolute refractory period is caused by the closing of the excitatory Na+ channels.

The duration of the absolute refractory period is fixed while that of the relative refractory period is not.


For more information on this topic, please refer to Berne & Levy , 15,25

Also, check out the following links that may be helpful:


syllabus | home | BME | search the web | e-mail Doug

Or, Jump to Lesson Number:

1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 | Exam #1
17 | 18 | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | Exam #2
28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 | 36 | 37 | 38 | 39 | 40 | 41 | 42 | Exam #3

Please don't make me go to any of those pages!
I want to go somewhere completely different!

This page was written by Ammon Fager , a student in this course.

BME 403 Pages maintained by the T.A., Douglas Miles.