Timecourses and amplitudes of events

When voltage is recorded between two points in an excitable tissue, the electrode towards which a wave of membrane depolarization is moving becomes positive relative to the other electrode, while a wave of repolarization causes the reverse voltage difference. During excitation of the heart, the sequence of electrical events is highly predictable. Continual measurement of voltage difference across the heart can, therefore, be used to identify the timing of depolarization of atria and ventricles, while the magnitude of voltage changes indicates the volume of muscle that is involved. The characteristic voltage record obtained is termed the electrocardiogram, or ECG, and the sequence of electrical events that occurs during cardiac excitation can be tracked by identifying each of the phases of the ECG waveform with a specific letter (Fig. 2.2).

Figure 2.2 Timing of sinoatrial and ventricular endocardial and epicardial action potentials, relative to the ECG.

With normal excitation originating from the sinoatrial node, measurement of the time between the beginning of atrial depolarization (beginning of P wave) and the entry of action potentials into the muscle of the ventricular apices (beginning of R wave) is always between 120 and 200 ms. Most of this delay is due to action potential travel through the slowly conducting A/V pathway, producing the so-called P–R interval which provides an index of the efficiency of this path. Ventricular excitation occurs by simultaneous entry of action potentials into both apices and coordinated spread of depolarization over both ventricles. This process takes only 60–80 ms and is indicated by the duration of the QRS complex. Once ventricular depolarization is complete the muscle cells all remain depolarized for the duration of the action potential plateau and then progressively repolarize, producing the T wave. This sequence produces an initial isoelectric period typically around 150 ms in duration while all cells are depolarized, and then a T wave whose timecourse of around 200 ms represents the range of action potential durations in different regions of the ventricular wall.

Since the endocardial cells have longer plateau durations than the epicardial cells, the sequence of repolarization between the different muscle layers is in the reverse order to the sequence of depolarization. For this reason, the voltage polarity of the T wave is usually the same as that of the R wave. In hearts with hypertrophied ventricles, however, greater epicardial intramural pressure is produced during contraction and the differences in plateau duration between epicardial and endocardial regions are reduced. As a result the ventricular cells tend to repolarize in the same sequence as they depolarized, producing an inverted T wave.

Orientations of ECG recording

The voltage changes occurring across the heart spread without diminution throughout the highly conductive medium of the body interior and can be detected from the body surface, so long as electrolyte-rich liquid is rubbed into the skin under the recording electrodes in order to overcome the high electrical resistance of the epidermis. Recording can be made most simply between right and left arms (Lead II) or between one arm and the left leg (Leads I and III). This so-called frontal lead system allows detection of impulse movement across the heart either horizontally or in a semi-vertical direction. Usually, the primary concerns for human physiologists are simply to have a signal large enough for you to be certain whether or not the sequence of excitation is normal, and to be able to reliably trigger a ratemeter from the R wave. Lead II usually provides the best record for these purposes but, because different people’s hearts have different vertical-horizontal orientations, larger signals are seen with one of the other lead orientations in some individuals.

Electrical activity moving at right angles to the orientation of the ECG electrodes produces no voltage signal, so frontal leads provide only limited information on the three-dimensional spread of activity through the heart. For this purpose, it is necessary to also record voltage differences between the heart and different points along the ventrodorsal diameter of the chest. The standard points used are six locations ranging from the right side of the sternum overlying the right ventricle (Lead V₁), to the left axilla overlying the left ventricle (Lead V₆). With these leads, one would expect to see a positive R wave in V₆, but a reversed R wave in V₁ reflecting the relative muscle masses in the two ventricles. So it is not surprising that at one or two of the intermediate locations, where the recording electrodes overlie the interventricular septum, the R wave appears bipolar. The chest leads are particularly useful for recognizing changes in absolute muscle volume in one or other ventricle, which alters the pattern of R wave polarity between the six locations. In addition, the R wave in V₆ is the largest in amplitude of any lead but never normally exceeds 2.5 mV. An R wave from this lead that is 3 mV or more in height can, therefore, be used as a reliable index of left ventricular hypertrophy, and constitutes one of the indices for assessing training-induced cardiovascular adaptation in athletes (see Chapter 11, p. 131).

Effects of local temperature

The membrane events that determine the slope of the pacemaker potential in sinoatrial cells depend on metabolic pumps and all metabolic processes are temperature-dependent. Therefore, changes in deep body temperature will affect heart rate by a direct effect on sinoatrial discharge frequency, with a rise in blood temperature of 0.5° C increasing heart rate by about 8 beats/min. It is not possible to know how much this process affects the efficiency of cardiac output changes in response to exercise or to hot environments, but it has to be considered when evaluating the absolute magnitude of tachycardia that occurs under these conditions.

Exercise tachycardia

The descending pathways that travel from motor cortex to spinal motor neurons and produce muscle movement also provide inputs to the cardiovascular control centre in the hindbrain, inhibiting vagal and increasing sympathetic drive to the sinoatrial node. Thus, heart rate increases proportionately to exercise intensity, with even very low workloads producing heart rates of above 100 beats/min.

At heart rates of 150 beats/min or higher, successive T and P waves follow each other without time for any isoelectric period. The absence of an isoelectric period makes the record look as if there is some irregularity of excitation (Fig. 2.3A). However, inspection will confirm that there is a regular sequence of P, QRS and T waves.

Figure 2.3 Typical ECG records from normal subjects near the extremes of the heart rate range. As in all ECG recordings, each large grid square represents 200 ms and 0.5 mV. In (A) the subject is exercising and heart rate is once every 400 ms or 150 beats/min. Note the loss of an isoelectric interval between T and P waves, but the maintenance of a stable P–R interval of just under 200 ms and a regular sequence of P, QRS and T waves. (B) This shows a heart rate of 35 beats/min in a highly trained athlete at rest. Note that the P–R interval is still less than 200 ms. These two records also show the considerable shortening of the ventricular action potential with increased heart rate, as measured by the time between the R and T waves.

Training bradycardia

Chronic aerobic activity results in a progressive fall in resting heart rate. With moderate activity the reduction is typically only 5–10 beats/min and occurs over several weeks’ activity. With the more intense levels of training associated with competitive aerobic exercise, resting rate continues to fall to values that may be as low as 30–35 beats/min in elite athletes. The mechanisms that underlie this progressive training bradycardia will be examined in Chapter 11 (p. 133). As with exercise tachycardia, extreme bradycardia makes the ECG record look strange (Fig. 2.3B). However, its normality can be confirmed easily by checking that the PR interval is normal and that there is a consistent sequence of P, R and T waves. Note that, without an ECG, it would be impossible to know whether somebody with a very slow heart rate is a normal, athletically fit person or has some cardiac abnormality that slows down the heart beat.

Respiratory sinus arrhythmia

Heart rate shows a sinusoidal oscillation during the respiratory cycle, with a relative tachycardia developing during inspiration and waning during expiration. This oscillation is due to the fact that vagal drive to the sinoatrial node falls progressively as inspiration progresses. Two inhibitory inputs to the vagal centre in the hindbrain are involved, one from stretch receptors in the lung and one from inspiratory neurons in the hindbrain respiratory centre. As the discharges of both these inhibitory pathways are proportional to the amount of inspiratory effort, the magnitude of sinus arrhythmia is much greater during deep than shallow breathing. Even at rest, however, there is typically a variation of at least 5–10 beats/min in individuals below the age of 30. A representative example of sinus arrhythmia can be seen in Figure 4.3 (p. 37).

By middle age, little or no heart rate variability is seen except during deep breathing and with further ageing the variability disappears altogether. This decline is not due to alteration in resting vagal tone (since resting heart rate does not change substantially with age), but probably involves changes in gain of the central input pathways to the vagal centre. Damage to the vagus is a common early component of peripheral nerve degeneration in patients with type I diabetes and, therefore, the magnitude of sinus arrhythmia in younger diabetics is a useful index in assessing their clinical status.

The bradycardia that results from chronic physical training is accompanied by increased magnitude of sinus arrhythmia, probably reflecting the increased range over which altered vagal tone can alter heart rate. In fact, the absolute magnitude of the arrhythmia has been suggested to provide a quantitative index of fitness, similar to that derived from measurement of (Lopes & White 2006).

Absence of P waves

Normal atrial muscle can only be activated once by a single sinoatrial impulse, because the prolonged plateau phase of the atrial action potential maintains it in a refractory state. If, however, the conduction velocity of the action potential is slowed by local hypoxia, or the distance needed for the action potential to travel around the atrial wall is increased because the atria have been stretched, or the action potential plateau phase duration is reduced by altered channel cycling, then a single action potential may circulate through the tissue over and over again and cause repetitive but uncoordinated contractions. This phenomenon is termed atrial fibrillation.

Atrial fibrillation has relatively little effect on the efficiency of cardiac pumping because most ventricular filling has occurred before atrial systole (Fig. 2.1). But it does create a potential problem. Instead of the atrial contents being regularly ejected, some blood tends to lie stationary in the extremities of the atrial chambers. When blood is stagnant, it tends to form clots and cell aggregates (thrombi) (see also Chapter 5, p. 48). If these thrombi are mobilized into the cardiac output, for instance during the vigorous respiratory effort of exercise, then they may occlude vessels in the coronary or cerebral circulation, causing a heart attack or stroke. Individuals with evidence of atrial fibrillation should, therefore, not be recruited into exercise programmes without careful clinical assessment.

Atrial fibrillation can be identified by two characteristics. First, no P wave exists because the action potentials that spread through the atria do not all travel in the same direction and so do not produce a reproducible voltage deflection on the ECG trace. Second, heart rate varies widely from beat to beat, in an unpredictable pattern (Fig. 2.4). This is because the disorganized direction of action potential travel means that they arrive at the A/V node at irregular intervals, with some arriving while the node cells are still in their refractory period from the previous action potential. In all other arrhythmias that involve varying heart rate there is either a progressive rise and fall in frequency (see Sinus arrhythmia, above) or intermittent insertion of extra R waves into an otherwise regular sequence (see Ventricular extrasystole, below).

Figure 2.4 ECG recording from a patient with atrial fibrillation. As in all ECG recordings, each large grid square represents 200 ms and 0.5 mV. The relationship between R and T waves is normal, but no P waves exist and heart rate varies dramatically from beat to beat, between about 100 beats/min (1) and 190 beats/min (2). Note that when heart rate is high, it is essential to identify the matching of R to T waves in order to avoid misinterpreting T waves as P waves.

Abnormal relationship between P and R waves

Damage to the cells of the A/V node may occur due to local ischaemia, inflammation, physical pressure by scar tissue or local calcification. This can have either of two separate effects on impulse conduction. In some cases there is slowing of action potential propagation with prolongation of the P–R interval beyond the normal upper limit of 200 ms, typically to 300–400 ms (Fig. 2.5A). In other cases, the effect of the damage is not to slow conduction velocity, but instead to slow calcium channel cycle time, so that following passage of one action potential the node is still refractory when the next impulse arrives. As a result, only every second or third action potential enters the ventricle and the ECG shows QRS complexes and T waves associated only with every second or third P wave (Fig. 2.5B).

Figure 2.5 ECG records demonstrating different degrees of atrioventricular block. As in all ECG recordings, each large grid square represents 200 ms and 0.5 mV. (A) First degree block. Every P wave (arrowed) is associated with ventricular excitation but the P–R interval is prolonged – here to around 360 ms. (B) Second degree block. Only every second P wave (arrowed) causes ventricular excitation. Note the consistent duration of the P–R interval in these cycles. (C) Third degree (complete) block. In contrast with (B), there is no consistent time linkage of P and R waves. The identifiable P waves are arrowed, but the irregular rhythm indicates that there are additional events masked by the T waves, giving a true atrial excitation rate of around once every 500 ms (120/min).

If the nodal cells are damaged severely enough then they are unable to propagate impulses at all, and ventricles and atria become electrically insulated from each other. Although the sinoatrial node continues to discharge and, therefore, P waves occur at their normal frequency, ventricular activation can originate only from within the ventricular system. The intraventricular Purkinje system contains a number of cells that have similar membrane properties to those of the sinoatrial cells but depolarize much more slowly. These cells normally never reach action potential threshold before they are activated by an impulse arriving from the A/V node. When this is prevented, however, these slower pacemakers can take over control of ventricular rhythm with frequencies in the range of 30–45 beats/min. The result is QRS complexes and T waves at a much lower frequency than that of the P waves and with no consistent association between P and R waves (Fig. 2.5C).

Clearly, lack of synchrony between atrial and ventricular pumping frequency denotes a heart that is not likely to be able to accommodate efficiently to demands for increased output. Individuals in whom you suspect A/V block should, therefore, not be recruited into exercise programmes without referral to a cardiologist.

Abnormal QRS complexes

Normally, action potentials travel from the A/V node down the Purkinje fibres on left and right sides of the interventricular septum. This produces simultaneous depolarization of both ventricles, with a QRS complex that is never more than 80 ms in duration. The synchronization of ventricular depolarization can be disrupted by damage to one of the branches of the Purkinje system, so that one ventricle is activated before the other. Alternatively, arrival of impulses through the conducting system may be normal, but an area of ventricular muscle may be damaged (usually by ischaemia) so that the sequence of spread of action potentials through the ventricular syncytium is disrupted. Any of these changes will result in a longer period being taken for ventricular depolarization, with concomitant widening of the QRS complex and usually some loss of the sharp ‘spikiness’ of the R wave.

Sometimes in a normal heart, the membrane of a cell within the ventricular Purkinje system or the ventricular muscle becomes hyperexcitable and generates an action potential. This causes an additional QRS complex and an extra ventricular contraction. Such a so-called extrasystole can be distinguished by two characteristics. First, the fact that it originates from a site distal to the Purkinje system means that activation of the myocardium follows a different route to normal, producing a QRS complex that has a different shape and is longer in duration. Second, the action potential plateau produces a refractory state in the myocardial cells that prevents activation by the next normal action potential, so an extrasystole is followed by a longer than normal pause before the next contraction. This is termed a compensatory pause.