Cardiac action potential By: Hina Shaikh May 8th 2009

Introduction Action potential Cardiac muscle action potential Clinical correlations

Introduction Action potential can be defined as the rapid changes in the membrane potential. These changes occur due to the change in membrane permeability to ions. There is a reversal of membrane charge that moves down the axon causing an electrical impulse to be transmitted. 1st: Before jumping into cardiac action potential, we have to understand action potential. So I will briefly go over what is action potential. Draw pic on board

Introduction In the extracellular fluid we see a high concentration of sodium ions with a low concentration of potassium ions. Intracellularly there is high concentration of potassium ions and a low concentration of sodium ions. The sodium-potassium pump present on the membrane, regulates the respective concentration of these ions. 2nd :Remember we learned in class the different types of pumps seen in the body and one of the most important pumps mentioned was the sodium-potassium pump.

As we know from before this pump uses ATP to extrude 3 Na+ ions out of the cell and 2 K+ into the cell thus creating an environment in which intracellularly the cell is negatively charged and extracellularly it is positively charged. Draw pic

Phases - If the membrane potential is at its baseline (about -85 mV), all the fast Na+ channels are closed, and excitation causes them to open. This allows a greater influx of Na+ If, however, the membrane potential is less negative, some of the fast Na+ channels will be opened earlier, causing a lesser response to excitation. There are 5 phases, numbered (0-4) Phase 4: Is the resting membrane potential. Phase 0: is immediate/rapid depolarization Results from a Na+ ion influx into the cell by the fast channels opening. The fast Na+ channels opening is depending on the membrane potential at the time of excitation. Action potential generated by the ventricular cardiomyocyte

Phase 2: plateau of action potential Phase 1: slight repolarization, is due to closure of the fast Na+ channels, causing an end to depolarization. Phase 2: plateau of action potential Phase 3: The potassium channels are open which cause potassium ions to go into the extracellular compartment. The is net loss of positive charge causes the cell to repolarize. Phase 4: back to resting membrane potential will remain in this state unitl anoter action potential is generated. Phase 4: fast sodium channels and slow calcium channels are closed.

Differences 1) Longer action potential 2) Plateau

Comparison In cardiac muscle there are fast sodium channels as well as slow calcium channels which open slowly. These channels are open for tenths of a second. In this time period calcium and sodium ions enter into the cell elongating the depolarization period thus causing the appearance of a plateau. In skeletal muscle the opening of “fast sodium channels” causes generation of action potential. These channels are termed “fast” as they open for thousandths of a second and immediately close. After closure, repolarization occurs.

This is not seen in skeletal muscle. In additon, after the action potential is generated, the permeability of potassium ions to the membrane decreases. This is not seen in skeletal muscle. Decreased permeability of potassium ions and the discontinued entering of sodium and calcium ions into the cell restores the resting membrane potential. This decreased potassium permeability may result from the excess calcium influx through the calcium channels just noted. Summary: When g'K+ is high and g'Na+ and g'Ca++ are low (phases 3 and 4), the membrane potential will be more negative. When g'K+ is low and g'Na+ and/or g'Ca++ are high, the membrane potential will be more positive (phases 0, 1 and 2).

Fast and Slow response Fast Response: - Also known as non- pacemaker action potentials Rapid depolarization Found throughout the heart except for the pacemaker cells.  Happens in Phase 0, the fast sodium channels open causing rapid depolarization to occur. Fast sodium currents cause depolarization. In this same instance potassium channels are closed. 2) Slow Response: Are known to be the pacemaker cells of the heart i.e. SA node and AV node Slower depolarization. Slow calcium currents cause depolarization. Initailly open at Phase 4, which initiates depolarization, giving rise to Phase 0 where there is depolarization. The rate of movement of these ions are slow, thus a slower rate of depolarization. 2 types of action potentials

SA node graph- Phase 4 is the spontaneous depolarization (pacemaker potential) (-40 and -30 mV). Phase 0 is the depolarization phase Phase 3 repolarization.

Clinical aspect There are certain cells of the heart that can undergo spontaneous depolarization, in which an action potential is generated without any influence from nearby cells. This is also known as automaticity. Automaticity is due to the spontaneous electrical activity of the SA node. Electrical impulses generated from the SA node spread through the heart via a nodal tissue. The normal activity of the pacemaker cells of the heart is to spontaneously depolarize at a regular rhythm, generating the normal heart rate. Abnormal automaticity involves the abnormal spontaneous depolarization of cells of the heart.

Clinical aspect cont.. Disorder of irregular or abnormal heart rhythms are called Arrhythmia. Normally the SA node sends the electrical signal throughout the heart where it goes to the AV node AV bundle Purkinjie fibres. However, if this pathway is disrupted, it can result in abnormal heart rhythms. It can be in the form of: 1) Tachycardia: more than 100 beats/min 2)Bradycardia: less than 60 beats/min

Symptoms: ii) Tachycardia: i) Bradycardia: Palpitations Fatigue Rapid heart action chest pain dizziness Light headedness fainting or near fainting i) Bradycardia: Fatigue dizziness light headedness fainting or near-fainting spells

Causes and Factors: Factors: Causes: Coronary artery disease High blood pressure Diabetes Smoking Excess alcohol or caffeine drug abuse and stress. Causes: Normal pathway disrupted Another part of the heart acts as the pacemaker Development of abnormal heart rate

Fibrillation Arhythmias can develop into a more severe state, known as fibrillation. There are two types of fibrillation: Atrial Fibrillation Ventricular Fibrillation Slow and fast response

1) Atrial Fibrillation: Atria quiver Fail to push out enough blood into ventricles The remaining blood in the atria forms a clot A fragment of this clot can travel and obstruct an artery causing stroke. Treatment: Anticoagulant Electric shock to revert heart rhythms back to normal Antiarrhythmic agents

2) Ventricular Fibrillation: ventricles quiver unable to pump enough blood to vital organs (i.e. brain) Leaving untreated can lead to death Treatment: Defribillator: applies electric shock that reverts it to the normal heart beat Antiarrhythmic agents: supress fast heart rhythms

References http://outreach.mcb.harvard.edu/animations/actionpotential.swf http://www.chemistrydaily.com/chemistry/Cardiac_action_potential http://www.phschool.com/science/biology_place/biocoach/cardio1/electri cal.html http://www.americanheart.org/presenter.jhtml?identifier=4469 http://www.chemistrydaily.com/chemistry/Cardiac_arrhythmia http://library.thinkquest.org/C003758/Function/The%20Cardiac%20Acti on%20Potential.htm http://www.nlm.nih.gov/MEDLINEPLUS/ency/imagepages/1056.htm http://www.nlm.nih.gov/MEDLINEPLUS/ency/article/001101.htm http://www.medicinenet.com/atrial_fibrillation/page4.htm#tocm http://www.cvphysiology.com/Arrhythmias/A010.htm http://www.doctorslounge.com/cardiology/drugs/antiarrhythmic/ Guyton