But ultimate pace makers an - (I) AVjunctionat pace making cells, (ii) Bundle of his and it is branches or (iii)the barbarization network

se, it receives an wave of excitation (which has been generated by the SAN) and it becomes excited so that. these other areas of functional tissues, normally, have no scope to genrated impulse Thus, in absence of the impulse generation by the SAN.the Av junchonal tissue may generate impulse When AV junctional pace making cells too. are out of order,the common bundle of has will do so. and so on Therefore, normally SAN is The pace maker (= makes or determines The pace at which the heart is beating pace in this instancemeans the speed in walking I. e. , the heart rate). But ultimate pace makers an - (I) AVjunctionat pace making cells, (ii) Bundle of his and it is branches or (iii)the barbarization network. and in this order Mechanism of spontaneous generation of rhythm Thus, normally, the SAN is generating impulse regularly at an interval of about 0.8 seconds Question is how the SAN is getting depolarized spontaneously, i.e. when it is not stimulated by any external agent . The answer is as follows Outing insole. small number or sodium ions enter the in tenor of the cells of the SAN despite The resistance against it Elsewhere in the body, in other cells (say. in nerve cells}, The same phenomenon (That is slow trickling in of Na+ into the cell) occurs, but that leads to exit of some K+ from ICF to ECF Therefore, over all, the membrane potential does not change (because the effect of entry of Na+is cancelled by the exit of K+) However, in the P cells of the SAN.the exit of K+ ions during diastole does not occur so that the effect of Na+ entry remains eclectically unbalanced. This unbalanced entry of Nations therefore, causes a slow use of membrane potential (that is the membrane potential approaches, from a high negative value towards less negative value, for example, from a value of, say. - 90 mV to a value of, say -60 mV) as shown in fig. 5.2.6. The. slow rise of membrane potential is called diastolic dapolanzation (also called 'pace maker potential1) Fig. 5.2.6. The diastolic depolanzationL which is a characteristic feature of those areas of heart which can generate rhythm At 60 mV, the tinng' occurs (see text) When the diastolic depolanzation has attained a value of about -60 mV(from, say. -90 mV), sudden firing' occurs (fig. 5.2.6.) explosive entry of Na+ ions now occurs development of action potential The action potential, (i.e.the wave of depolarization) propagates onwards, without, normal. any loss of strength Cause of the 'explosive entry' of Na+ is is follows recall (chap 1 sec I, fig.1.1.2.). the Nations can cross the call membrane through Na channels These Na channels may be voltage gated. At a voltage of -60 mV, these voltage gated channels suddenly open in large number massive Na+entry occurs- development of AP (see chap2 sec I for details) In short.fall of resting membrane potential (Vm) of myocardial cell leads to massive opening up of Na channels in the myocardial cell membrane Conductivily Thus, normally, the impules is generated at( sinu atrinal node (SAN), it travels to AVN, from AVU to bundle of His (fig. 5.1.1.) Via the two divisions of the bundle of has the impulse continues to travel onwards ultimately the im pulse spreads via the subenducardial Purkinje network to every part of heart (fig.5.1.1.} Now, the details will be discussed Spread of excitation over the atria from the SAN the impulse spreads ill over the atna (both right and left) It is now known that there are three pathwavs called preferential channels which originate in the SAN and end in the AVN (fig. 5.1.1.) These are -(1) anterior. (2) middle (Wenckebach's) and (3) posterior intermodal (Thorel's) tracts A branch of antienor tract (Bachman'a) supplies the left atrium Through these preferantial channels tht impure reaches The AVN Tasl enough At AVN the speed of the movement o' impulse is slowed down This Blowing down, to someextent is teleologically desirable (i) first it allows the atrinal systole to be completed before the onset of ventricular exitation . (ii) Second in conditions, when the atrinal are contracting with a very high frequency [e.g. attrinal flutter). because of conduction delay in the AVN. all the impulses do not reach the ventricles and the ventricles are spared to soma exetent Unfotunaltly however. AVN it also perhaps the common est site of heart block The frequency of impulse generation by SAN can be altered by, (i) vagal and (ii) sympathetic stimulation The former depresses where as the latter increases the heart rate Similarly the velocity of conduction through the AVN can be altered by vegal or sympathetic stimulation, the sympathetic stimulation increasing but the parasympatatic stimulation reducing the speed of conduction through The AVN Conduction through the ventricls from the lower end of the AVN. a tract, called the bundle, of has. (fig.5.1.1.) arises proceeds onwards remaining on the right side of the interventricular septum and subendocardially divides --> into two branches, the right and left blanches The fight branch is rather the direct continuation of the undivided bundle of is it (the right branch) then leaves the saptum and enters right venttricles near the attachment of papillary muscles, remaining subentiocardially. The left branch comes out from the undivided bundle rather perpendicularly — perforates the septum --> comes ont he left side of the septum, remaining sub endocardially ---> divides into two mam branches, an anterior and another posterior division (fig. 5.1.1.) These divisions Then leave the septum and remaining subendocardially enter the left venttrincle In the ventricles both the right and left branches.