This document discusses cardiovascular physiology, specifically the action potential and conductivity of ventricular muscle fibers. It describes the five phases of the ventricular action potential, from rapid depolarization in Phase 0 to return to resting membrane potential in Phase 4. Abnormal action potentials like early and delayed afterdepolarizations are also discussed. The document then covers excitability changes, the heart's conducting system, conduction through the atrioventricular node, and impulse transmission via the Purkinje system.

1. Cardiovascular Physiology
Dr. Hussein Farouk Sakr

2. Excitability
• The ability of the cardiac muscle to respond to a stimulus, this
response is in the form of action potential which is propagated
to the different muscle fibers to produce contraction.
• The RMP of the cardiac muscle is -90 m.v. due to:
• Selective permeability of the membrane.
• Na+ -K+ pump (an electrogenic pump).

5. Action potential of the ventricular muscle
fiber
Phase 0:
- Fast channels open, Na influx 
depolarization.
- The channels open and close
quickly.

6. Action potential of the ventricular muscle
fiber
Phase 1:
• Partial repolarization is due to closure of
Na channels and transient K efflux
through special type of K channel
(transient outward) and the inactivation
of the Na channel.

7. Action potential of the ventricular muscle
fiber
Phase 2:
- Plateau phase, at which the membrane potential
is kept constant by:
a) Ca influx through the L-type Ca channels.
b) K efflux through the ungated K channels

8. Action potential of the ventricular muscle
fiber
Phase 3:
- Repolarization appear due to closure
of the voltage activated Ca channels
and opening of the voltage gated K
channels  rapid K efflux (delayed
rectifier).

9. Action potential of the ventricular muscle
fiber
Phase 4:
- Return of the membrane potential to the resting
state.

10. Electrical, excitability and mechanical changes in the ventricular
muscle fibers

11. Excitability changes
• Absolute refractory period
• During this period the excitability is
completely lost.
• No stimulus whatever its strength can
stimulate the cardiac muscle during this
period.
• Coincides with rapid depolarization,
repolarization and plateau.
• With the mechanical changes coinciding
with systole.
• No cardiac tetanization.
• Relative refractory period
• During this period the excitability
increases gradually from 0-100%.
• It coincides with the rapid
repolarization and first half of diastole.
• The cardiac muscle can be stimulated
by superminimal stimulus.

12. Abnormal Action Potentials
Early afterdepolarizations
occur during phase 3 and are more likely to occur
when action potential durations are prolonged.
Because these afterdepolarizations occur at a
time when fast Na channels are still inactivated,
slow inward Ca carries the depolarizing current.
Another type of afterdepolarization

13. Abnormal Action Potentials
delayed afterdepolarization,
occurs at the end of phase 3 or early in phase 4. It, too,
can lead to self sustaining action potentials and
tachycardia.
This form of triggered activity appears to be
associated with elevations in intracellular calcium,
as occurs during ischemia, digitalis toxicity,
and excessive catecholamine stimulation

14. Conductivity
• The ability of the cardiac muscle to conduct action potential from one fiber to the
other.

15. Conducting system of the heart
Atrial muscle
fiber 0.3 m/sec.
Internodal fibers 1-4 m/sec.
AVN 0.03 -0.05
m/sec.
4-5 m/sec.
Ventricular muscle
fiber 0.3 m/sec.

16. Conduction of impulse from SAN to AVN
• The impulses arising from the SAN
spread in different directions:
• Through the atrial muscle fibers at rate 0.3
m/sec.
• Through the anterior interatrial band at rate
1 m/sec.
• Through the anterior, middle and
posterior internodal fibers at rate 1-4
m/sec.

17. Conduction of the impulse through the AVN
(AVN delay)
• When the impulse reaches the AVN, there is
delay in impulse conduction.
• The duration of delay is 0.16 sec.
• The velocity of conduction though he AVN is
0.03-0.05 m/sec.
Causes of AVN delay:
• 1- Decreased number of gap junction between the
muscle fibers.
• 2-Small size of the cardiac muscle fibers in contrast
with the atrial muscle fibers.
• 3-The less negative resting membrane potential 
slow depolarization.

18. •Significance of the AVN delay:
• 1-Allows sufficient time for atrial contraction
before ventricular contraction  sufficient
ventricular filling.
• 2-It protects the ventricle from high atrial
rhythm by producing partial block as in atrial
flutter and atrial fibrillation.

19. Transmission in the Purkinje system
• The ventricular muscle fibers is depolarized
from the end of Purkinje fibers and the
impulse is conducted from the inner surface
to the outer surface.
• The conduction velocity is 4-5 met/sec.
• The wave of excitation passes spirally along
the direction of the ventricular muscle fibers.