Cardiac Currents and ECG

Conduction pathways in the heart

A. SINO-ATRIAL NODE: where the rhythmical impulse that initiates contraction is normally generated. The impulse passes from the SA node to atrial myocyte (where it spreads via gap junctions) as well as to the internodal pathways. The SA node is normally the pacemaker that drives the heart because its rate of spontaneous depolarization is faster than other regions. However, if the firing rate of the SA node is suppressed, another region of the heart will become the pacemaker. B. INTERNODAL PATHWAYS: specialized conduction paths to rapidly conduct the impulse from the SA node to the AV node and the left atrium. The conduction velocity in the internodal pathways is higher than in atrial muscle, which results in the impulse reaching the AV node before the entire atrial wall has depolarized. The internodal pathways are analogous to the rapidly conducting Purkinje fibers of the ventricle. C. ATRIOVENTRICULAR NODE: conducts the impulse from the atria to the ventricles. The AV node is a narrow bunch of fibers through which conduction is much slower than other areas of the heart (except SA node). The impulse is delayed for ~0.1 sec in the AV node before reaching the ventricles, which allows the atria to contract before the ventricles. D. BUNDLE OF HIS AND BUNDLE BRANCHES: The atria are separated from the ventricle by a ring of fibrous tissue that cannot conduct an electrical impulse. The upper portion of the bundle of His passes through this fibrous tissue, and carries the impulse from the AV node to the left and right bundle. E. PURKINJE FIBERS: the left and right bundle branches subdivide into the Purkinje fibers, which branch extensively over the subendocardial surfaces of both ventricles. The Purkinje fibers have the highest conduction velocity within the heart, and this arrangement facilitates rapid depolarization of the ventricles. F. TRANSMISSION OF THE IMPULSE BETWEEN MYOCYTES: The impulse spreads between myocytes via gap junctions, and the depolarization moves from the endocardium to the epicardium.

Action potentials in different areas of the heart

Action potential configurations in different regions of the mammalian heart. The SA node cells have no stable resting potential and are the intrinsic pacemaker responsible for cardiac excitation. The action potential originates in the SA nodes and spreads to atrial myocytes, the AV node, the Bundle of His, Purkinje fibers, and finally ventricular myocytes.

Summary of neural regulation

As illustrated above, the sympathetic and parasympathetic neural influences have opposing effects on the heart. Sympathetic stimulation acts to increase heart rate, increase conduction velocity through the AV-node, and shorten the duration of the ventricular action potential. Parasympathetic influence is via the vagus nerve. Vagal stimulation acts to decrease heart rate, slow conduction through the AV-node but does has not have a significant effect on the atrial or ventricular myocytes. The opposing effects produced by these neural inputs is to a large extent explained by the fact that they have opposing effects on a common g protein that influences the major cardiac ionic currents.

Gap junctions

Basics of the electrical wave propagation in the heart Basics of electrical wave propagation in the heart. Propagation of the action potential (AP) from cell to cell is mediated via intercellular ion channels formed by arrays of proteins known as connexins, concentrated in gap junctions. Six connexin subunits form a hemichannel (connexon) in the membrane of one myocyte and connect to a hemichannel from an adjacent myocyte to form an intercellular channel.

Effects of autonomic nerves on ionic currents in the SA and AV nodes

Parasympathetic nerves release acetylcholine (ACh), which activates muscarinic receptors on SA and AV node cells. High levels of parasympathetic activity can activate a potassium channel sensitive to ACh (the KACh channel), which increases potassium current. Sympathetic nerves release norepinephrine which activates beta-1 receptors on SA and AV node cells.

Effect of sympathetic nerves on ionic currents in atrial and ventricular myocytes

Release of norepinephrine from sympathetic nerves activates beta-1 receptors on atrial and ventricular myocytes, resulting in increased L-type calcium and delayed rectifier potassium current. There is no change in voltage-gated sodium current in response to activation of beta-1 receptors. The duration of the ventricular action potential is mainly determined by the balance between the calcium and potassium current. An increase in calcium current alone would prolong the duration of the ventricular action potential. However, norepinephrine from sympathetic nerves increases both calcium and potassium currents, resulting in a faster rate of phase 3 repolarization and a decrease in duration of the ventricular action potential (decrease in the QT interval, which reflects the duration of the ventricular action potential).

The SA node is a pacemaker

The SA node does not have a stable resting potential so it is the pacemaker responsible for excitation of the heart. The slope of phase 4 and the value for the maximum diastolic potential will depend on the balance between the funny sodium current (depolarizing current) and the potassium current (repolarizing current).

Typical ECG recording

The changes in electrical activity recorded on the ECG during excitation of the heart reflect the amount of current developed (which depends on the mass of tissue) and also the rate in change of potential. The mass of the SA and AV nodes are so small that it's excitation (i.e., action potentials) cannot be detected on the ECG. The isoelectric line on the ECG is the line recorded before cardiac excitation occurs (the line before the P wave). The PR segment is the time between the end of the P wave to the start of the QRS complex. Excitation of the AV node occurs during the PR segment but this cannot be detected on the ECG (the PR segment is along the isoelectric line). The ST segment corresponds to phase 2 of the ventricular action potential. During this plateau phase, there is a small change in membrane potential so the ST segment also will be seen along the normal isoelectric line.

Ionic currents in SA node action potential

This figure illustrates qualitatively the temporal relationship of the major ionic currents responsible for generating phase 4 depolarization (i.e., pacemaker potential) and the action potential in SA-node cells. Inward current through so-called funny Na channels provides the inward current that drives the early portion of phase 4 depolarization. These Na-conducting channels are "funny" because they become activated (open) at membrane potentials negative to about -50 mV and close at potentials positive to about -50 mV. This is in contrast to the more classic voltage-gated sodium channels that are activated by membrane depolarization. Accordingly, the inward funny Na current is on during phase 4 depolarization and then turns off during phase 0 of the action potential. The depolarization during phase 4 first leads to activation of the T-type calcium current which, in combination with the inward funny Na current, depolarizes the membrane potential into the range where L-type channel activation occurs. When this occurs, the number of open L-type channels increases and the inward L-type calcium current drives phase 0 depolarization. The T-type calcium current is called this because it is a "tiny" current, while the L-type calcium current is "large". Membrane depolarization during phase 0 leads to the activation of delayed rectifier K channels which provide the outward current that drives phase 3 repolarization. Outward current through open delayed rectifier K channels also acts to oppose the inward funny Na current during phase 4 (not well illustrated in this figure). The K channels that opened during the action potential close with time as membrane potential remains negative to about -50 mV. The funny Na channels begin to reopen when membrane potential moves negative to about -50 mV during phase 3 and the sequence of events starts over. The membrane potential reaches its most negative value when the inward funny Na current is exactly opposed by the outward delayed rectifier K current. This most negative potential is referred to as the maximum diastolic potential (MDP). The MDP will be influenced by the magnitudes of the two currents and will become more negative by conditions that enhance the K-current. In contrast, conditions that enhance the funny Na current will act to move MDP to a more positive value.