Cardiovascular Physiology and Pathophysiology
PhysiologyStructure and Function4 Topics
Lymphatics and Edema Formation
Vascular Control3 Topics
The Cardiac Cycle
Compensation for Circulatory Failure
Determinants of Myocardial Performance7 Topics
Neuro-Control of Heart and Vasculature4 Topics
Electro-Mechanical Association4 Topics
Electrical Side of the Heart4 Topics
Causes of Heart Failure
PathophysiologyDefining Heart Failure
MVO2 and Heart Failure
Cardiac Output and Heart Failure7 Topics
Vascular Tone in Heart Failure
The Action Potential
The action potential describes the changes in cellular membrane potential that occur as a result of specific ion movements as a muscle cell depolarizes and repolarizes as a wave of excitation passes over it.
Components of the myocardial action potential
- Phase 0: phase of rapid depolarization; due mainly to the influx of Na+ into the cell. The slope of Phase 0 determines the speed of conduction of the wave of excitation. The greater the slope, the greater the speed of conduction.
- Phase 1: short phase of repolarization; due mainly to the loss of K+ from the cell (Ito).
- Phase 2: the plateau phase; due mainly to the influx of Ca2+ into the cell (L-type Ca2+ channel).
- Phase 3: the repolarization phase; due mainly to the outward movement of K+ from the cell (Ik).
- Phase 4: the resting membrane phase for working myocardial cells: no net gain or loss of ions. In pacemaker cells phase 4 involves a process of gradual depolarization due to the influx of mainly Na+ and K+ ions (If).
The refractory period
The refractory period (RP) represents a time period after the onset of phase 0 of the action potential during which another stimulus, no matter how strong, cannot induce another depolarization within that cell.
The RP prevents a cell from being depolarized at an extremely high rate. For myocardial muscle cells it prevents the heart muscle from experiencing tetany.
For all cardiac cells except the SA and AV nodal cells, the RP ends during Phase 3 of the action potential. For cells of the SA and AV node, the RP ends after the end of Phase 3 (during phase 4) of the action potential.
Relative to the surface ECG, the RP ends during the first half of the T wave. It should be finished by the middle of the T wave.
Automatic and non-automatic myocardial cells
Automatic cells include those of the SA node, some cells in the leaflets of the AV valves, some cells around the coronary sinus, cells of the distal AV node, and cells of the His bundle, bundle branches and Purkinje system.
Automaticity is determined by the ability of cells to spontaneously depolarize during Phase 4 of the action potential.
Cells that are not normally automatic may gain automaticity a result of disease or electrolyte disturbance. Thus these cells with a normally flat Phase 4 develop a Phase 4 that gradually depolarizes.
The autonomic nervous system can alter automaticity:
- The sympathetic nervous system increases automaticity
- The parasympathetic nervous system reduces automaticity
Myocardial action potentials differ from skeletal muscle action potentials
The duration of the action potential:
- In skeletal muscle: very short; order of milliseconds
- In myocardial muscle: very long; order of 100’s of milliseconds
Length of the refractory period:
- In skeletal muscle: shorter than the length of the action potential
- In myocardial muscle: lasts almost the length of the action potential
- In skeletal muscle: repetitive stimulation can induce tetany
- In myocardial muscle: repetitive stimulation cannot induce tetany. Tetany for the heart would cause death. The heart needs a pause between each contraction to allow for filling. The long duration of the action potential and refractory period allows the contraction of the heart to end before the next excitation can induce a second contraction. Hence between two repetitive beats, filling of the heart can occur.