The term “tachycardia” means fast heart rate, which usually is defined as faster than 100 beats/min in an adult. An electrocardiogram (ECG) recorded from a patient with tachycardia is shown in Figure 1. This ECG is normal except that the heart rate, as determined from the time intervals between QRS complexes, is about 150 beats per minute instead of the normal 72 beats per minute.
Fig1. Sinus tachycardia (lead I).
Some causes of tachycardia include increased body temperature, stimulation of the heart by the sympathetic nerves, or toxic conditions of the heart.
The heart rate usually increases about 10 beats/min for each degree (Fahrenheit) increase in body temperature (with an increase of 18 beats/min per degree Celsius), up to a body temperature of about 105°F (40.5°C); beyond this, the heart rate may decrease because of progressive debility of the heart muscle as a result of the fever. Fever causes tachycardia because increased temperature increases the rate of metabolism of the sinus node, which in turn directly increases its excitability and rate of rhythm.
Many factors can cause the sympathetic nervous system to excite the heart, as we discuss at multiple points in this text. For instance, when a patient sustains severe blood loss, sympathetic reflex stimulation of the heart may increase the heart rate to 150 to 180 beats/min.
Simple weakening of the myocardium usually increases the heart rate because the weakened heart does not pump blood into the arterial tree to a normal extent, and this phenomenon causes reductions in blood pressure and elicits sympathetic reflexes to increase the heart rate.
BRADYCARDIA
The term “bradycardia” means a slow heart rate, usually defined as fewer than 60 beats/min. Bradycardia is shown by the ECG in Figure 2.
Fig 2. Sinus bradycardia (lead III).
Bradycardia in Athletes. The well-trained athlete’s heart is often larger and considerably stronger than that of a normal person, which allows the athlete’s heart to pump a large stroke volume output per beat even during periods of rest. When the athlete is at rest, excessive quantities of blood pumped into the arterial tree with each beat initiate feedback circulatory reflexes or other effects to cause bradycardia.
Vagal Stimulation Causes Bradycardia. Any circulatory reflex that stimulates the vagus nerves causes release of acetylcholine at the vagal endings in the heart, thus giving a parasympathetic effect. Perhaps the most striking example of this phenomenon occurs in patients with carotid sinus syndrome. In these patients, the pressure receptors (baroreceptors) in the carotid sinus region of the carotid artery walls are excessively sensitive. Therefore, even mild external pressure on the neck elicits a strong baroreceptor reflex, causing intense vagal-acetylcholine effects on the heart, including extreme bradycardia. Indeed, sometimes this reflex is so powerful that it actually stops the heart for 5 to 10 seconds.
SINUS ARRHYTHMIA
Figure 13 shows a cardiotachometer recording of the heart rate, at first during normal respiration and then (in the second half of the record) during deep respiration. A cardiotachometer is an instrument that records by the height of successive spikes the duration of the interval between the successive QRS complexes in the ECG. Note from this record that the heart rate increased and decreased no more than 5 percent during quiet respiration (shown on the left half of the record). Then, during deep respiration, the heart rate increased and decreased with each respiratory cycle by as much as 30 percent.
Fig3. Sinus arrhythmia as recorded by a cardiotachometer. To the left is the record when the subject was breathing normally; to the right, when the subject was breathing deeply.
Sinus arrhythmia can result from any one of many circulatory conditions that alter the strengths of the sympathetic and parasympathetic nerve signals to the heart sinus node. The “respiratory” type of sinus arrhythmia, as shown in Figure 13-3, results mainly from “spillover” of signals from the medullary respiratory center into the adjacent vasomotor center during inspiratory and expiratory cycles of respiration. The spillover signals cause an alternate increase and decrease in the number of impulses transmitted through the sympathetic and vagus nerves to the heart.
