Univ. of Maryland School of Medicine Emergency Medicine Interest Group

This brief introduction to cardiac electrophysiology will help you understand how an electrocardiogram works. The heart beats at a relatively constant rate and rhythm due to special properties of cardiac pacemaker cells. These pacemakers depolarize at regular intervals without any external stimuli from neighboring cells. Pacemaker cells are said to display automaticity. Only certain cells in the heart normally possess these properties. These include: Sinoatrial Node (SA), the Atrio-Ventricular Node (AV), the His Bundle, and Purkinje System. Pacemaker cells depolarize in rhythmic fashion. After a depolarization, the cells repolarize. Then inward sodium currents slowely begin flowing and the cells begin to depolarize again. Eventually the cells reach threshold, and an action potential fires. Because of the regular inward currents, pacemaker cells maintain a resting potential of -50 to -60mV. This is higher than regular myocytes which have a resting potential of approximately -90mV. This increased membrane potential deactivates fast Sodium channels. Pacemakers therefore rely on Calcium as the primary cation which triggers action potentials.

Although there are several different types of pacemaker cells, the SA node is the primary pacemaker. This is because the SA node depolarizes at the fastest rate of all the pacemaker sites. As long as the SA node continues to depolarize at a rate faster than the inherent rate of secondary pacemakers, the secondary cells will remain dormant. Other factors decrease the automaticity of secondary pacemaker cells. When they are depolarized by an action potential from the SA node, they experience an upregulation in Na/K+ ATPase activity which hyperpolarizes the cell. The lowered resting potential decreases automaticity. Another factor which diminishes spontaneous depolarization is coupling of secondary pacemakers with dormant myocytes. The gap junction coupling provides tonic inhibition of pacemaker cells in the AV node and His-Purkinje system.

		When the SA node depolarizes, the action potential spreads thoroughout the atria, rapidly causing atrial depolarization and contraction. The action potential rapidly enters the AV node where it is delayed for 120 to 200 msec. The AV node conducts slowly because it depends on slow inward calcium currents to depolarize cells. The AV node also must conduct the action potential through thin fibers which slow conduction. This delay is deliberate and allows the ventricles time to fill following atrial contraction. The action potential spreads to the Bundle of His and then rapidly down the three bundle branches. There is one RIGHT BUNDLE BRANCH and both ANTERIOR and POSTERIOR LEFT BUNDLE BRANCHS. These rapidly depolarize both ventricles. The left ventricle depolarizes slighly before the right. The cells repolarize following depolarization. Atrial depolarization is not seen in an ECG because the higher magnitude ventricular depolarization occurs simultaneously. Ventricular repolarization is seen as the T wave. (Discussed later).
		This diagram correlates with the above heart drawing. The initial inflection (purple) corresponds to atrial depolarization. The large blue inflection corresponds to ventricular depolarization. The atrial repolarization is buried in this complex. The green inflection corresponds to ventricular repolarization. This is a positive inflection because the repolarization begins at the epicardial surface and progresses through the ventricular walls to the endocardium. Depolarization progresses from endocardium to epicardium. This combination of change in direction and change in polarity results in a double negative and a positive inflection for repolarization.
		Each inflection has a name and signifies a stage in the cardiac contraction cycle. P wave SA (atrial contraction) QRS complex Ventricular depolarization and contraction T wave Ventricular repolarization U wave Represents final stage of ventricular repolarization
		This drawing shows the correlation of muscle depolarization and ECG tracings at corresponding times. Phase 0 denotes ventricular depolarization. This is seen on the ECG as the beginning of the QRS complex. Phase 1 denotes the initial rapid repolarization due to closing of fast sodium channels. This is seen as the large drop in mV on the ECG. Phase 2 represents the plateau stage during which inflow and outflow currents are balanced. The ECG returns to baseline. Phase 3 is repolarization. Potassium channels open and calcium closes. The ECG shows the repolarizing T wave. Phase 4 is the recover phase. Both the muscle tracing and ECG return to baseline levels.
		Once the myocardial cells have depolarized, there is a period in which they are refractory to further depolarizations. During phase 1 and most of phase 2, the depolarized cells can not invoke another action potential. This is due to continued inactivation of sodium channels. In phase 3, the sodium channels are reactivated and limited numbers of cells may be depolarized. An effective refractory period exists. In this phase, individual cells may be depolarized, but they are unable to propagate an action potential.
		Normally an action potential will propagates in an antergrade or orthodromic fashion. It will pass through parallel conducting pathways leading from the atria to the ventricles by way of the AV node. If these pathways do not pass the action potential at the same rate, the slower pathway is functionally blocked. This is because the faster pathway would have already excited cells distal to the slow fibers. This drawing shows two parallel pathways functioning normally with anterograde conduction. Re-entrant excitation is inhibited because the entire population of cardiac muscle fibers have been excited and are refractory.
		Reentry is a condition which occurs when a impulse propagates in a retrograde fashion and completes a circular path. Delayed conduction noted by the squiggly line allows time for the proximal (closer to SA node) tissue to repolarize. Once repolarized, the tissue will support a circus rhythm created by the looping action potential. Circus rhythms can occur in the AV node, ischemic tissue, or between an accessory pathway and the AV node. Circus rhythms require: 1. two parallel pathways. 2. unidirectional block. 3. slowed of delayed conduction.
		Uni-directional blocks occur in regions of increased resting membrane potential such as ischemia or infarct. The increased membrane potential is associated with inactive sodium and T-calcium channels. This slow depolarization leads to a block. Tissue distal to the block may generate larger currents. This leads to a circus rhythm. The conduction is blocked in the anterograde direction, but can conduct via retrograde conduction.
		The retrograde conduction is slow, allowing time for the proximal healthy tissue to repolarize. If it depolarizes the healthy tissue after the effective refractory period, an action potential will be conducted. These action potentials are self-sustaining. They can produce increased rate of ventricular firing leading to conditions such as Supraventricular Tachycardias.