Depolarisation diastolic

SA node Digitalis sensitizes the SA node to normal vagal impulse resulting in bradycardia. In a patient suffering from paroxysmal supraventricular tachycardia, it decreases the heart rate due to vagal action on SA node which is associated with decrease in the slope of slow diastolic depolarisation and increase in the transmembrane negativity and, also lower the SA rate by antiadrenergic action. 

The electrocardiographic pattern of injury is recorded from the myocardial area in which, as a consequence of diminished blood supply (more important than the one that generates the ECG pattern of ischaemia) or other non-ischaemic causes, an evident diastolic cellular depolarisation exists (Figure 2.1(3)). This leads to the formation of a low-quality TAP in the injury area which is expressed in the ECG as ST-segment depression or elevation (see Experimental point of view - below - and Figure 4.5). This ECG pattern usually represents especially in the setting of ACS and especially, when the changes are dynamic, the existence of active ischaemia. 

In human beings, the electrocardiographic injury pattern is seen in the presence of evident and persistent clinical ischaemia. When we extrapolate the findings in the experimental field to clinical practice, it could be considered that when the ischaemia is important, persistent and predominant in a certain area (subendocardium or subepi-cardium), an evident diastolic depolarisation in that area generates a low-quality TAP (slower... 

Calcium channels are responsible for the genesis of APs in cardiac pacemaker cells (diastolic depolarisation) and the propagation of slow APs in sino-atrial and atrioventricular node cells and are equally important in the control of depolarisatiOTi-induced Ca entry responsible for the plateau (phase 2) of the AP (see Fig. 1). 

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