Clinical Note

Forty years ago, ventricular fibrillation was a major cause of in-hospital mortality in heart attack patients because the infarcted heart is very prone to fibrillation until it heals. That problem has been largely solved now by the creation of the intensive care unit, where the patient's ECG is continuously monitored. Should ventricular fibrillation occur, it is detected by the monitoring equipment which alerts the staff to quickly use a defibrillator to resuscitate the patient.

can stagnate in the nonbeating atria and become a source for blood clots, putting these patients at risk of stroke. Patients with chronic atrial fibrillation are often put on anticoagulation medicines.

The heart continues to pump blood in atrial fibrillation because a coordinated atrial contraction is not vital to pumping by the ventricle. That is not the case if the ventricles fibrillate, however. Ventricular fibrillation causes an immediate cessation of the rhythmic cycle of contraction and relaxation of the ventricles. Rather they simply quiver. Cardiac output falls to zero with rapid loss of consciousness and ensuing death of the victim. Panel B in Figure 11 shows that all coordinated electrical activity is lost in ventricular fibrillation and only an irregular baseline is seen. The most common causes of ventricular fibrillation are occlusion of a coronary artery (myocardial ischemia), advanced heart failure, drug overdose, or electrocution. If detected early enough, ventricular fibrillation can often be stopped by a high-voltage shock to the heart from a device called a defibrillator. That shock puts all of the heart cells into a refractory period simultaneously so that a coordinated beat can resume. Interestingly, although the electrical energy from a defibrillator can shock a fibrillating heart into a normal rhythm, a higher-voltage shock, it can also cause a normally beating heart to fibrillate.

Suggested Reading

Marriot HJL. Practical electrocardiography. Baltimore: Williams and Wilkins, 1988

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