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BIO120H1 Lecture Notes - Aortic Stenosis, Diastole, Aortic Valve

Course Code
Stephen Reid

of 8
Lecture 3: The Electrocardiogram, (pt. II), the Electrical Axis of the Heart, and the
Cardiac Cycle
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. 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 trigger a 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 becomes extremely 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
Ventricular fibrillation can become dangerous as it can lead to uncoordinated and inefficient
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 called circus
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 refractory period 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 activity in the ventricle, which leads to ventricular fibrillation, takes
the form of what we call a re-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). In the 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 off to the right (on the right-hand side away from
the triangle) or left (on the left-hand side away from the triangle), or they can travel through the
bottom branch 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.
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 move down it. Branch 1 is normal.
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 activity in this
branch. When the wave of depolarisation reaches the bottom of branch 1, it splits 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
had come 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 the triangle. Once at the
top, this wave 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 of the ventricle
causing these regions of ventricular muscle to contract independently of other regions of the
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).
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 because as 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 for the 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
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 the average direction of electrical flow in the heart is oriented
at about 60 degrees - almost exactly the same as the orientation of lead II.