Looking at the case in a 6-second strip is soooo scary.
Strip # 1 - before the non-conducted beat is the gradual slowing of the rate (longer RR interval) and there is prolongation of the PRI before the non-conducted beats.
Strip # 2 - there is a conducted beat followed by non-conducted P waves. This is called ventricular standstill or paroxysmal AV block.
Strip # 3 is the continuation of the ventricular standstill/paroxysmal AV block.
Strip # 4 - if seen in isolation can be mistaken at Mobitz II. It should be properly labeled as 2:1 AV block.
Strips # 5 and 6 also showed 2:1 AV conduction but here it is clear that this a type 1 mechanism due to the PRI prolongation before the dropped beat.
This case has a brain mass. It impaired the swallowing function, so the nurse is regularly suctioning the patient. The RR prolongation (slowing of the heart rate and PRI prolongation are characteristics of vagally-induced event.
So this is vagal-induced.
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Paroxysmal AV block can be initiated by a conducted on non-conducted PAC, PVC, acceleration or deceleration of sinus beats. According to Fisch, the electrophysiology of paroxysmal AV block is unclear. One proposed mechanism is repetitive concealed conduction. Concealed conduction is the failure of a cardiac impulse to traverse the entire AV conducting system. Another mechanism is the prolonged PP interval after the PAC associated with deceleration-dependent (Phase 4) depolarization of the lower part of the junction and resultant AV block.
Again according to Dr. Fisch, "resumption of normal AV conduction has been ascribed to conduction during the supernormal period of recovery following idioventricular impulse, summation of anterograde or retrograde impulses, and Wedensky facilitation. In which a properly timed retrograde impulse makes it possible for an otherwise non-threshold anterograde impulse to conduct and "peel" back the refractory period".
Reference:
Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical Arrhythmia. New York. Futura Publishing Co.
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