Many cardiac excitation problems can be diagnosed from the information in a single lead of an electrocardiogram. The lead II electrocardiogram traces at the top of Figures 5–1
are identified as normal sinus rhythms based on the following characteristics: (1) the frequency of QRS complexes is approximately 1/s, indicating a normal beating rate; (2) the shape of the QRS complex is normal for lead II and its duration is less than 120 ms, indicating rapid depolarization of the ventricles via normal conduction pathways; (3) each QRS complex is preceded by a P wave of proper configuration, indicating sinoatrial (SA) nodal origin of the excitation; (4) the PR interval is less than 200 ms, indicating proper conduction delay of the impulse propagation through the atrioventricular (AV) node; (5) the QT interval is less than half of the R-to-R interval, indicating normal ventricular repolarization; and (6) there are no extra P waves, indicating that no AV nodal conduction block is present. The subsequent electrocardiographic tracings in Figures 5–1
represent irregularities commonly found in clinical practice. Examination of each of these traces with the above characteristics in mind will aid in the differential diagnosis.
The physiological consequences of abnormal excitation and conduction in the heart depend on whether the electrical abnormality evokes a tachycardia
, which will limit the time for cardiac filling between beats; evokes a bradycardia
, which is inadequate to support sufficient cardiac output; or decreases the coordination of myocyte contraction, which will reduce stroke volume.
Traces 2 through 6 below the normal trace in Figure 5–1
represent typical supraventricular arrhythmias (ie, originating in the atria or AV node). Supraventricular tachycardia
(shown in trace 2 in Figure 5–1
and sometimes called paroxysmal atrial tachycardia
) occurs when the atria are abnormally excited and drive the ventricles at a very rapid rate. These paroxysms often begin abruptly, last for a few minutes to a few hours, and then, just as abruptly, disappear and the heart rate reverts to normal. QRS complexes appear normal (albeit frequent) with simple paroxysmal atrial tachycardia because the ventricular conduction pathways operate normally. The P and T waves may be superimposed because of the high heart rate. Low blood pressure and dizziness may accompany bouts of this arrhythmia because the extremely high heart rate does not allow sufficient diastolic time for ventricular filling.
There are two mechanisms that may account for supraventricular tachycardia. First, an atrial region, often outside the SA node, may become irritable (perhaps because of local interruption in blood flow) and begin to fire rapidly to take over the pacemaker function. Such an abnormal pacemaker region is called an ectopic focus.
Alternatively, atrial conduction may become altered so that a single wave of excitation does not die out but continually travels around some abnormal atrial conduction loop. In this case, the continual activity in the conduction loop may drive the atria and AV node at a very high frequency. This self-sustaining process is called a reentry phenomenon
and is illustrated in Figure 5–3
. This situation may develop as a result of abnormal repolarization and altered refractory periods in local areas of the myocardium. Atrial flutter
is a special form of tachycardia of atrial origin in which a large reentrant pathway drives the atria at very fast rates (250-300 beats/min) and normal refractory periods of AV nodal tissue are overwhelmed. Thus, ventricular rate is often some fixed ratio of the atrial rate (2:1, 4:1) with frequencies often 150 to 220 beats/min. The electrocardiogram often shows a saw-tooth pattern of merged P waves with intermittent normal QRS complexes.
Normal and reentrant (circus) cardiac excitation pathways.
occur at the AV node and generally represent impaired conduction through this tissue. In a first-degree heart block
(trace 3 in Figure 5–1
), the only electrical abnormality is unusually slow conduction through the AV node. This condition is detected by an abnormally long PR interval (>0.2 s). Otherwise, the electrocardiogram may be completely normal. At normal heart rates, the physiological effects of the first-degree block are inconsequential. The danger, however, is that the slow conduction may deteriorate to an actual interruption of conduction.
A second-degree heart block (trace 4 in Figure 5–1) is said to exist when some, but not all, atrial impulses are transmitted through the AV node to the ventricle. Impulses are blocked in the AV node if the cells of the region are still in a refractory period from a previous excitation. In this situation, the primary problem is a slower-than-normal conduction through the AV nodal region and thus the second-degree block is aggravated by high atrial rates. In the second-degree block, some, but not all, P waves are accompanied by corresponding QRS complexes and T waves. Atrial rate is often faster than ventricular rate by a certain ratio (eg, 2:1, 3:1, and 4:1). This condition may not represent a serious clinical problem as long as the ventricular rate is adequate to meet the pumping needs.
In a third-degree heart block (trace 5 in Figure 5–1), no impulses are transmitted through the AV node. In this event, some area in the ventricles—often in the common bundle or bundle branches near the exit of the AV node—assumes the pacemaker role for the ventricular tissue. Atrial rate and ventricular rate are completely independent, and P waves and QRS complexes are totally dissociated in the electrocardiogram. Ventricular rate is very likely to be slower than normal (bradycardia) and is often slow enough to impair cardiac output.
Atrial fibrillation (trace 6 in Figure 5–1) is characterized by a complete loss of the normally close synchrony of the excitation and resting phases between individual atrial cells. Cells in different areas of the atria depolarize, repolarize, and are excited again randomly. Consequently, no P waves appear in the electrocardiogram, although there may be rapid, irregular, small waves apparent throughout diastole. The ventricular rate is often very irregular in atrial fibrillation because impulses enter the AV node from the atria at unpredictable times. Fibrillation is a self-sustaining process. The mechanisms behind it are not well understood, but impulses are thought to progress repeatedly around irregular conduction pathways (sometimes called circus pathways, which imply a reentry phenomenon as described earlier and in Figure 5–3). However, because atrial contraction usually plays a negligible role in ventricular filling, atrial fibrillation may be well tolerated by most patients as long as ventricular rate is sufficient to maintain the cardiac output.1
Traces 2 through 6 below the normal trace in Figure 5–2
show typical ventricular electrical abnormalities. Conduction blocks called bundle branch blocks
(trace 2 in Figure 5–2
) can occur in either of the branches of the Purkinje system of the intraventricular septum, often as a result of a myocardial infarction. Ventricular depolarization is less synchronous than normal in the half of the heart with the nonfunctional Purkinje system. This results in a widening of the QRS complex (>0.12 s) because a longer time is required for ventricular depolarization to be completed. The direct physiological effects of bundle branch blocks are usually inconsequential.
Premature ventricular contractions (PVCs) (trace 3 in Figure 5–2) are caused by action potentials initiated by and propagated away from an ectopic focus in the ventricle. As a result, the ventricle depolarizes and contracts before it normally would. A PVC is often followed by a missed beat (called a compensatory pause) because the ventricular cells are still refractory when the next normal impulse emerges from the SA node. The highly abnormal ventricular depolarization pattern of a PVC produces the large-amplitude, long-duration deflections on the electrocardiogram. The shapes of the electrocardiographic records of these extra beats are highly variable and depend on the ectopic site of their origin and the depolarization pathways involved. The volume of blood ejected by the premature beat itself is smaller than normal, whereas the stroke volume of the beat following the compensatory pause is larger than normal. This is partly due to the differences in filling times and partly to an inherent phenomenon of the cardiac muscle called postextrasystolic potentiation. Single PVCs occur occasionally in most individuals and, although sometimes alarming to the individual experiencing them, are not dangerous. Frequent occurrence of PVCs, however, may be a signal of possible myocardial damage or perfusion problems.
(trace 4 in Figure 5–2
) occurs when the ventricles are driven at high rates, usually by impulses originating from a ventricular ectopic focus. Ventricular tachycardia is a very serious condition. Not only is diastolic filling time limited by the rapid rate, but also the abnormal excitation pathways make ventricular contraction less synchronous and therefore less effective than normal. In addition, ventricular tachycardia often precedes ventricular fibrillation.
Prolonged QT intervals (the left side of trace 5 in Figure 5–2) are a result of delayed ventricular myocyte repolarization, which may be due to inappropriate opening of sodium channels or prolonged closure of potassium channels during the action potential plateau phase. Although the normal QT interval varies with heart rate, it is normally less than 40% of the cardiac cycle length (except at very high heart rates). Long QT syndrome is identified when the QT interval is greater than 50% of the cycle duration. It may be genetic in origin (mutations influencing various ion channels involved with cardiac excitability), may be acquired from several electrolyte disturbances (low blood levels of Ca2+, Mg2+, or K+), or may be induced by several pharmacological agents (including some antiarrhythmic drugs). The prolongation of the myocyte refractory period, which accompanies the long QT syndrome, extends the vulnerable period during which extra stimuli can evoke tachycardia or fibrillation. Patients with long QT syndrome are predisposed to a particularly dangerous type of ventricular tachycardia called torsades de pointes (“twisting of points,” as shown on the right side of trace 5 in Figure 5–2). This differs from the ordinary ventricular tachycardia in that the ventricular electrical complexes cyclically vary in amplitude around the baseline and can deteriorate rapidly into ventricular fibrillation.
In ventricular fibrillation (trace 6 in Figure 5–2), various areas of the ventricle are excited and contract asynchronously. The mechanisms are similar to those in atrial fibrillation. The ventricle is especially susceptible to fibrillation whenever a premature excitation occurs at the end of the T wave of the previous excitation, that is, when most ventricular cells are in the “hyperexcitable” or “vulnerable” period of their electrical cycle. In addition, because some cells are repolarized and some are still refractory, circus pathways can be triggered easily at this time. Because no pumping action occurs with ventricular fibrillation, the situation is fatal unless quickly corrected by cardiac conversion. During conversion, the artificial application of large currents to the entire heart (via paddle electrodes applied across the chest) may be effective in depolarizing all heart cells simultaneously, thus allowing a normal excitation pathway to be reestablished.
1 The real danger with atrial fibrillation lies in the tendency for blood to form clots in the atria in the absence of the normal vigorous coordinated atrial contraction. These clots can fragment and move out of the heart to lodge in small arteries throughout the systemic circulation. These emboli can have devastating effects on critical organ function. Consequently, anticoagulant therapy is usually prescribed for patients in atrial fibrillation.