LOADING AWESOME
CARDIAC ACTION POTENTIAL
www.propofology.com
Dr. David Lyness
@Gas_Craic
ELECTROPHYSIOLOGICAL CHANGES IN CARDIAC MYOCYTE CELLS
Different to that seen in standard nerves.
Prolonged plateau phase lasting around 300 ms compared with 1 ms in nerves.
Prolonged plateau phase lasting around 300 ms compared with 1 ms in nerves.
Negative mV = resting to positive mV = contracting
Depends on the in-out movements of ions to produce positive/negative changes
Five phases: 0-4
Different to the phases seen in the SA and AV nodes
Phase 0—depolarization because of the opening of fast sodium channels. Potassium flux also decreases.
Phase 1—partial repolarization because of a rapid decrease in sodium ion passage as fast sodium channels close.
Phase 2—plateau phase in which the movement of calcium ions out of the cell, maintains depolarization.
Phase 3—repolarization, sodium, and calcium channels all close and membrane potential returns to baseline.
Phase 4—resting membrane potential
(-90 mV), resulting from the activity of the Na/K ATPase pump which creates a negative intracellular potential because of the exchange of three sodium ions for only two potassium ions being brought in.
Phase 2 - plateau phase of the cardiac action potential.
Membrane permeability to calcium increases during this phase, maintaining depolarization and prolonging the action potential. Membrane permeability to Ca decreases towards the end of phase 2, and the plateau is partially maintained by an inward sodium current. Sodium flows into the cell through the
sodium – calcium exchanger. Exchanger transfers three sodium ions into the cell in exchange for one calcium ion flowing out = net inward positive current.
Potassium flows OUT of the cell, except for phase 4, where it's actively being brought in as part of the exchanger.
Much of the calcium influx in the plateau phase occurs through L-type (long opening) calcium channels. Increased activation of L-type channels occurs with catecholamine exposure, whilst they are blocked by calcium channel antagonists such as verapamil.
Calcium Channel Blockade:
By acting on cardiac muscles (myocardium), they reduce the force of contraction of the heart.
By slowing down the conduction of electrical activity within the heart, they slow down the heart beat.
By blocking the calcium signal on adrenal cortex cells, they directly reduce aldosterone production = lower blood pressure.
By slowing down the conduction of electrical activity within the heart, they slow down the heart beat.
By blocking the calcium signal on adrenal cortex cells, they directly reduce aldosterone production = lower blood pressure.
MAGNESIUM
Mg acts as a physiologic Calcium Channel inhibitor by slowing slow
L-Type Calcium channel during PHASE 2. This reduces further Ca release by the Sarcoplasmic Reticulum which leads to reduced automaticity, contractility and conductivity through cardiac tissue, including the AVN.
QUICK-LOOK @ PHASES
0 = Na in = rapid surge in positive charge
1 = K & Cl out causes dip in positivity
2 = Ca comes in and K out, causing plateau
3 = Potassium out and Na/Ca channels close = return to -ve
4 = Na/K exchanger = 3Na out for 2K in = negative charge
http://ceaccp.oxfordjournals.org/content/7/3/85.full.pdf
