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Lecture 3

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University of Toronto Scarborough
Biological Sciences
Stephen Reid

1    Lecture 3: The Electrocardiogram, (pt. II), the Electrical Axis of the Heart, and the Cardiac Cycle See lecture 2 notes for pre-mature beats 1. Heart Block and Branch Bundle Block The previous lecture concluded with examples of three different types of heart block (types I, II and II). There are other possible blockages of electrical activity in the heart. For example, branch bundles too can be blocked. The two branch bundles (left and right), if you remember, take the waves of depolarization down from the AV node, though the bundle of His, and then down to either side of the heart until it reaches the Purkinje fibers. So, it is possible for conduction to be slowed in either one of the branches, creating either a right or left branch bundle block. The ECG traces created by this condition are very strange - the lines are saw-tooth, or 'm' shaped. One of the consequences of a branch bundle block is that the ventricles will no longer contract simultaneously; instead, the ventricle that has the block on its side will contract slightly after the ventricle that does not. 2    2. Flutter and Fibrillation A relatively common form of arrhythmia is heart flutter; fibrillation is less common but more serious. Flutter and fibrillation can occur in the atria, ventricles or both. Very rapid rates of electrical excitation and contraction in either the atria or the ventricles can produce these conditions. Flutter is more benign, whilst fibrillation is much more dangerous, particularly in the ventricles. In atrial flutter, the rapid rate of electrical excitation leads to an enhanced number of P-waves. If each of these P-waves were to triggera QRS complex, then heart rate would be highly elevated (between 200 and 300 beats per minute). The appearance of P-waves can become so fast that the isoelectric interval between the end of the T-wave and the beginning of the P-wave disappears. However, in reality the AV node, and thereafter the ventricles, are generally only activated by every second or third atrial impulse (P-wave); thus actual heart (ventricular) function is not affected to a huge extent by atrial flutter. Whilst atrial flutter produces many P-waves, overall the effect is quite measured. During atrial fibrillation the electrical activity in the atria becomesextremely chaotic and rapid. This can result in different parts of the atria depolarising and contracting at different times. However, the function of the heart is not particularly dependent upon the contraction of the atria (see the cardiac cycle below), and as long as the QRS complex remains intact, then the ventricles will continue to contract properly, at least for the most part. Heart rate will, however, likely be irregular. Ventricular fibrillation can become dangerous as it can lead to uncoordinated and inefficient 3    pumping. During ventricular fibrillation, the electrical activity in the ventricles becomes chaotic and extremely rapid. It is generally caused by the recycling of electrical activity in the ventricular myocardium (muscle). This recycling of electrical activity produces what are calledcircus waves. Normally, waves of depolarisation travel in one direction along a relatively defined path. Once an area of the heart depolarises, it goes into a refractory period. This refractory period of the myocardial muscle prevents recycling of electrical activity (under normal conditions). However, if some cardiac cells emerge from their refractoryperiod before others (in an abnormal manner), the waves of depolarization can be continuously regenerated and conducted though the heart. This causes the contraction of different areas of muscle at different times making coordinated pumping action impossible. It is in a situation of ventricular fibrillation that the padded electrical defibrillators are brought into play in order to reset the heart's natural rhythm. The recycling of electrical activityin the ventricle, which leads toventricular fibrillation, takes the form of what we call are-entry circuit. Under normal conditions, electrical activity moves up the Purkinje fibers into the myocardial muscle causing it to contract. Let us imagine an upwards, equilateral triangle made of three branches, with each intersection of branches leading off into another pathway (see the re-entry circuit slide). Inthe normal pathway, a single wave of electrical activity moving downward splits and moves down both of the two downward branches (labeled 1 and 2 in the slide). When these two waves of depolarisation reach the bottom two corners of the triangle, they can either move offto the right (on the right-hand sideaway from the triangle) or left (on the left-hand side away fromthe triangle), or they can travelthrough the bottombranch toward the middle. If the activity moves through the bottom branch, (i.e., it goes right out of the left-hand downward branch, and left out of the right-hand downward branch), the two currents will collide in the middle of the bottom branch, essentially canceling each other out, and the tissue will go into a refractory period. Thus, the wave of depolarisation can never (normally) travel around the triangle, only through it; from the top pathway, it can only go into either the left-hand pathway through the left hand branch, or the right-hand pathway through the right-hand branch, but it cannot cycle around and around through the triangle. 4    In a heart with ventricular fibrillation, this is not the case. There tends to be a unidirectional block somewhere along the conduction pathway, meaning that electrical activity can only travel in one direction through this block. In the slide there is a unidirectional block in branch 2. Electrical activity can move up this branch but it cannot movedown it. Branch 1 is nor mal. When the original downward moving wave of depolarisation reaches branches 1 and 2, it splits into two waves. A wave of conduction is transmitted down branch 1 in the normal manner. The unidirectional block in branch 2 prevents the downward movement of electrical activityin this branch. When the wave of depolarisation reaches the bottom of branch 1, itsplits into two and can travel either away from the triangle or toward the middle of the triangle along the bottom branch. Normally, the wave of depolarisation traveling from branch 1, into the middle of the triangle via the bottom branch, would encounter muscle cells that are in a refractory period due to waves of depolarisation coming down branch 2. However, no waves of depolarisation have come down branch 2 due to the unidirectional block. In this case, the wave of depolarisation that hadcome from branch 1 is free to move along the bottom branch and up branch 2. It moves through the unidirectional block (at a slow speed) up toward the top of th e triangle. Once at the top, thiswave of depolarisation can move down branch 1 (i.e., it is being recycled). There are no “opposing waves of electricity” to cause cells to become refractory and electricity begins to cycle around and around - this happens throughout the ventricle, and causes the fibrillation. Numerous waves of depolarisation (circus waves) “move in circles” through various parts ofthe ventricle causing theseregions of ventricular muscle to contract independently of other regions of the ventricle. Ventricular fibrillation can lead to death within minutes - however, fibrillation can be stopped, or reset, with a defibrillator. An electrical discharge is placed across the chest, and the electrical activity generated by the defibrillator essentially resets the heart. The overwhelming burst of electricity wipes out all of the re-entry circuits, and puts the heart back onto a normal cycle in which a normal rhythm is established by an endogenous pacemaker (the SA node or an ectopic pacemaker; depending upon the situation). 5    3. The Electrical Axis of the Heart 3a. What is the Electrical Axis of the Heart? The electrical axis of the heart is, essentially, a vectoral analysis of the direction and magnitude of current flow at various instances during the heart's cycle. It is defined as the average of all the instantaneous mean electrical vectors occurring sequentially during depolarisation of the ventricles. Note that atrial depolarisation and repolarisation does not contribute a lot to the mean electrical axis as they are much less muscular than the ventricles. At any one instant as waves of depolarisation are flowing through the conduction system in the ventricles and the ventricular myocardium itself, there is a general direction (vector) in which electrical activity is flowing. If we take all of the directional vectors that electrical activity is flowing in, during the time that the ventricle is depolarising (i.e., during the QRS complex), we can get the mean axis (or direction) of electrical flow during the ventricular contraction phase. During the first phase of the contraction of the ventricles, in which the wave of depolarization is travelling downward through the branch bundles, the general movement of electrical activity is left-to-right - this is becauseas the waves go down the branch bundles, the left bundle depolarizes slightly faster than the right. This is shown on an ECG as a slight dip - the Q-wave. As the ventricle continues to depolarize, the primary movement of electrical activity is downward toward the apex of the heart. It is, in fact, almost the identical direction as the positive electrode on a standard limb lead II ECG. This accounts forthe large upswing of the R-wave on the ECG trace. The large downswing of the R-wave is caused by the third phase of the contraction of the ventricles, when the primary movement of electricity shifts from flowing downwards to flowing right-to-left across the frontal plane of the body. This is due to the full depolarization of the ventricles. Finally, the electrical activity flows backward (“into the body) toward the left, causing the negative S-wave. So if we look at all of these instantaneous vectors and sum them in a vectoral analysis over the entire QRS complex, we find that theaverage direction of electrical flow in the heart is oriented at about 60 degrees - almost exactly the same as the orientation of lead II. 6    3b. Diagnostic Uses of the Electrical Axis Although the electrical axis of the heart is normally oriented around 60 degrees, it can shift depending upon physiological conditions or disease states. It can shift tothe left or the right - there is some normal variation (indeed the axis shifts with inspiration and expiration), but generally a serious shift is considered to be about 60 degrees in either direction (so the axis is at either 0 degrees or 120 degrees). Deviations to the left orthe right are usually the result of increased tissue mass in the ventricles. So if something increases the mass of the right ventricle, it means there is more muscle in the right ventricle to depolarize, and the mean electrical axis shifts to the right. If we look at the circulatory system and the relationship of the heart to the pulmonary an
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