Jack, an apartment superintendent, grabbed a quick cup of coffee and then put on his coat to shovel snow off the front sidewalk

Question

He is 56 years old and has experienced two episodes of angina over the past 3 years. This time when he was shoveling the snow, he felt palpitations in his chest. It was as though his heart had stopped and then began to beat rapidly as if to catch up. Afraid of what he was feeling, he went inside and called for an ambulance. When the paramedics arrived, they took an ECG and told Jack he was going to be fine. He was taken to hospital to be seen by an emergency physician and was released later that afternoon.

The ECG taken by the paramedics showed Jack was experiencing premature ventricular contractions. In general terms, how do PVCs appear on an ECG? What factors contributed to the onset of PVCs in Jack's situation?

Describe the physiologic events in PVC. How is cardiac output disrupted with the presence of PVCs?

Because of Jack's history, his PVCs leave him at risk for events such as ventricular tachycardia or ventricular fibrillation. Compare and contrast these two arrhythmias. Why are they particularly dangerous?

Answer 1

Premature ventricular contractions present with normal beats interspersed by distorted QRS complexes. The PVCs in Jack's situation may have been triggered by the increased physical activity that generated an increased sympathetic response and heart rate. The coffee might have acted as an additional sympathetic stimulant. Finally, his history of previous cardiac events can be a predisposing factor to arrhythmia.

A premature ventricular contraction begins with an electrical event by a ventricular ectopic pacemaker. Because of the ectopic beat, the ventricles are unable to complete repolarization before the next SA impulse. The result is a delay, or compensatory pause, in ventricular systole. PVCs cause a decrease in diastolic filling and therefore a reduction in cardiac output.

Ventricular tachycardia originates within the conduction system and/or the muscles of the ventricular wall. It involves abnormal QRS complexes on the electrocardiograph and a heart rate falling within 70 to 250 beats/minute. It may be sustained or may spontaneously rectify itself. Ventricular fibrillation creates a series of sine-wave patterns on the electrocardiograph and involves a "quivering" of the ventricular walls instead of contraction.
Ventricular tachycardia is clinically significant because it inhibits the proper function of the atrial pacemaker and decreases the diastolic filling time. With ventricular fibrillation, cardiac output and pulses are nonexistent.