Arrhythmia Recognition: The Art of Interpretation

In one pound of fat tissue in the human body there is one-quarter mile of tubing (Figure 1-8). We can assume that this is true for other types of tissue as well.

How many miles of tubing are in your entire vascular system? A lot! The pump needed to push blood through such a tubing system, if it were rigid, would need to be very strong indeed. What do you suppose such strong forces would do to your red cells, white cells, and platelets? They would destroy them. Therefore, this type of system would not work in our bodies.

Instead of rigid tubing, the human body is composed of elastic tubing. Elastic tubing can bend and allow us to move without any difficulty. It is compressible, allowing external muscle movement to help pump the blood by compressing or milking the tube, causing the fluid to be pushed along. The main advantage to this type of tubing, however, is its elastic properties. Its elasticity allows the blood vessel to simply distend in order to accommodate for the extra fluid whenever the heart pumps (Figure 1-9).

What would happen to the pressure inside the tube now? It would build up inside the tube, but the distention would distribute the pressure a bit more smoothly. What happens to an elastic band when you stretch it? It wants to go back to its original shape. This built-up energy places constant, smooth pressure on the blood, causing it to flow forward in a smooth fashion, avoiding high shearing pressures and turbulence (Figure 1-9). The distended arterial walls are, in essence, acting like an additional pump helping to push the blood forward through the circulatory system.

The slow, constant pressure of a distended elastic arterial system wanting to return to normal is the passive way in which the circulatory system functions. Now let’s go over the active system that causes the arterial distention in the first place.

After the rapid ventricular filling phase of diastole, the ventricles are full with blood. If the ventricles were to contract at this point, the stroke volume of the heart would be at the lower end of normal for most people. Why? Because the ventricles are filled, but not overfilled. It is a well-known fact in muscle physiology that a muscle contracts much more efficiently if it is stretched just a bit (see the Additional Information box). So, how can we overfill the ventricles to allow a bit of muscle stretching? Passive inflow of blood just wouldn’t do it. The answer is made clear when we think about atrial contraction.

If you look at Figure 1-12, you will notice that the atria are completely full of blood during the middle of diastole. They have been filled by the venous blood that is constantly flowing back to the heart. At the end of diastole, when the ventricles are almost full, the atria contract and push the extra blood into the ventricles in order to overfill them (Figure 1-13). The overfilling provided by the atrial contraction stretches the ventricular muscle, allowing for maximal contractility and maximal stroke volume. Better stroke volume means better control over the cardiac output.

You may be asking why we are spending so much time on basic physiology when this is a book on arrhythmias. The reason is that the heart rate is one of the most important variables in the maintenance of cardiac output. As we saw earlier, the other main variable is the stroke volume. In many cases, arrhythmias will affect either one or both of these variables profoundly. In order to understand the clinical implications of arrhythmias, you need to understand the concept of cardiac filling and cardiac output very clearly. We will constantly refer back to this section throughout the book.

Additional Information

Muscle Tension

When a muscle is at its normal length (Figure 1-14), the amount of tension that it can produce is a set amount. In other words, a muscle can only produce just so much tension. On the other hand, if the muscle were stretched, the amount of tension that it could produce would be increased (Figure 1-15).

An illustration shows low tension in an unstretched muscle. — Figure 1-14 Unstretched muscle has less tension than stretched muscle.

© Jones & Bartlett Learning.

An illustration shows high tension in a stretched muscle. — Figure 1-15 Stretched muscle has better functionality.

© Jones & Bartlett Learning.

The heart muscle is no exception to this rule. If the heart were allowed to fill only by passive means such as the inflow of blood, the heart muscle would not be stretched. The amount of force that the heart could use to contract would be less than if the muscle were stretched somewhat. (Textbooks on physiology refer to this finding as the Frank-Starling mechanism or law.) The atrial kick allows the heart to “overfill” a bit and stretch the muscle, maximizing myocardial contraction.

Now let’s take a closer look at how heart rate affects stroke volume. What do you think happens to the stroke volume of the heart at very fast heart rates? Remember from our previous discussion on the rapid filling phase that most of the blood volume entering the ventricle occurs during very early diastole right after the AV valves open up (Figure 1-16). At very fast ventricular rates, the ventricles do not have time to fill adequately because the rapid filling phase is shortened (Figure 1-17). The net result is that the ventricles are not filled to capacity or overfilled at the end of diastole. Now when they contract, the amount of blood that is expelled is less than optimal. Less than optimal ejection means a decrease in cardiac output. In other words, the cardiac output will diminish because the stroke volume will be greatly decreased. Decreased cardiac output could very easily cause or lead to hemodynamic instability. That is how and why a tachycardia or rapid heart rate can kill.