Assume you have a patient 68 years old with previous myocardial infarction (Actually patient 201 in MIT-BIT arrhythmia database). Assume that AV node depolarises strongly. However, at the same time, SA node depolarises too but with weaker energy but with its normal frequency. Assume this happens only during extrasystole.
I think the results of this extrasystole are
- SA node stimulus halts AV node stimulus in the middle of depolarisation so it cannot depolarise fully
- the preceding depolarisation of SA node causes a weak ventricular contraction but still sufficient to open the pulmonary valve
- depending on the situation, the blood flow caused SA node depolarisation can pass the pulmonary valve or not (backflow)
- in both cases, there is a little gap between two flows i.e. a little decrement and increament in the flow rate during the whole action potential
- higher right ventricular pressure
- two times opening of aortic valve during long compensatory pause in action potential and long R wave
- inefficient filling and
My draft drawing what is happening in pressures and ECG
where the pressure level is lower than normal (60 < 100 mmHg), and ECG (in Finnish EKG) graph is not in relative scale. R2 is smaller peak than R1.
So results of this thinking
- lower pressure in ventricles
- higher pressure in atrias
- if RA pressure greater than LA, partially patent foramen ovale
- less blood oxygenated
What is this kind of simultaneous depolarisation of two pacemaker cells called during extrasystole? How can you explain it?