Clinical Note

Normally, the long refractory period of the atrioventricular node protects the heart from tachyarrhythmias that commonly originate in the atrium. In Wolf-Parkinson-White syndrome, the atrioventricular node is bypassed by a muscle bridge between the atria and ventricles. Although these patients are normally asymptomatic, a bout of atrial fibrillation, normally a relatively benign and not uncommon arrhythmia, can be life threatening because the ventricle will attempt to follow the rapid atrial rate. The resulting tachycardia can depress cardiac output to the point of circulatory collapse. For that reason it is recommended that these patients get the bypass pathway surgically ablated as soon as it is detected.

an accelerated heart rate, venous pressure simply falls and stroke volume is reduced proportionately. If the heart is electrically paced to a very high rate (tachycardia) or decreases to a very low rate (bradycardia), cardiac output is severely impaired. At heart rates below 50 beats/mm, as might occur in a patient with complete heart block, stroke volume is maximal and can no longer compensate for the reduced rate. At heart rates above 150 beats/min, as might occur in a patient in ventricular tachycardia, the filling time is so short that the heart fails to fill adequately between beats. It is interesting to note that when the heart rate is increased by sympathetic stimulation, the duration of the action potential is reduced in the ventricle so that the systolic period is shortened, thus allowing more time for filling between beats. That phenomenon allows the heart to pump efficiently at rates in excess of 200 beats/min during exercise.

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