Cardiac impulses are produced normally at SA node from the beginning. Heartrate should be from 60 beats to 100 beats per minute in a normal

individual. If heart rate is below 60 brady arrythmia .if heart rate is more than 100

tachy arrythmia Normal counduction order of heart is SA node ,atria,Avnode ,bundle of

his ,purkinjee,venticles finally. Automaticity should be from SA node .

Normal velocity or capability of tissue to conduct impulse in atria is 1 meter per second,Avnode 0.05 meter per sec.conduction through purkinje system is fast conduction 4to 5 meter per second

Heart rate increses 100 to 150 that is simple tachy cardia Some times time tachy cardia suddenly appears and disappear those are

called paroximal tachy cardia .those are from 150 to 250 If heartrate is 250 to 350 those are called flutters .if more than 350

those are called fibrillations. Simple tachycardia is called sinus tachy cardia

automaticity is capability to under go spontaneous depolarisation with out any external stimulus

Myocardial cells have two kinds of cells.capable of producing their automaticity.and non –automaticity cells.

Unpleasant awareness of cardiac out put is known as palitations If node is the problem we call it nodal tachy cardia or junctional

tachy cardia.some cells are capable of producing their natural automaticity is called pacemakers .ex:SA NODE av node purkinje system .atial cells and ventrical cells do not produce automaticity.

Action potentials are same in the SA node ,AV node ,purkinje system .

Atria and ventrical have similar action potential process.Sanode AV NODE PURKINJE cells does not rest .they have a

tendancy to climb over to threshold potential

• Resting membrane potential is -60 mv .threshold potential is -40.in SA node resting membrane potential gradually climb over to threshold cuz SA Nodal cells have leay sodium channels.we call it diastolic current.along with it some potassium is leaking out.some calcium is going in.

• Since cell is being loaded with cataions resting membrane potential moves to threshold potential.nw ca++ channels open and it come in threshold potential moves to” 0”.this is called depolarisation.later k+ channels open and k+ leak out negativity develop in side of the cell repolarisation occurs.actually cell has to come to resting membrane potential and then to threshold potential.since it is SA node no RMP cuz sodium influx, calcium influx,and potassium out flux persistantly.

• SA cellls and atiral cells are connected through gap junctions.during Sanode depolarisation little calcium trigger moves to atria and bring the action potential to RMP to TP.

• In atrial node rmp is -90 tm is -70.ca+ came through gap junctions is responsible for the atrial movement of RMP TO TM .atrial cells are not auto excitable cells but they can be excited.after it reached to TM very fast sodium channels open .it brigs to “0” phase that mean depolarisation.after dat na+ channel closes and k+ moves out ca + come in .in this situation both cations move simaltaneously hence plateau phase occurs.after that ca++ channels closed.and time dependant k+ channels open k+ leaks out hence repolarisation occurs

The reason atial cells cant auto conducted is na+moves in along with it ca ++ moves in also k+ coming out hence equal charge .hence no RMP TO TM .during depolarisation some na+ in atia move to another cell brigs out depolarisation.

the auto excited cells have the sequnce of automaticity SA node>av node>purkinjefibers.if Sanode is working it supresses the actions of AV node and purkinje .this is called over drive supression.

If SA node is underworking means less than 60/min due to strong vagal activity .vagal activity releases acetylcholine.ach binds to M2 receptors (serpentine)and G inhibitory in intracellularly inhibits g protien beta and gama parts opens the k+ channels and alpha part inhibits adenylcyclase and decreases cyclic AMP activation of protien kinase A is down hence sodium and ca++ are less phosporelated .no cationic influx .hence rmp to tm is less .decreased depolarisation .is called sinus bradycardia

In some cases opposite action is also possible when norephinephrine is released during excercize during fever,during hyperthyroidism more norephineprine is released.acts on beta2 receptors stimulates G protien activity increses adenalylcyclase,incresed Protien kinase A Activity,produces incresed phosporelation of cations hence more cations come in and hence more early depolarisation occurs .thats why during exercise heart rate increases.

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• Triggered automaticity in some cells occur .if a normal impulse come to a deseased part of the ventricle it produces two types of abnormality .1)early after depolarisation2)delayed after depolarisations.early after depolarisation occur

• Due to prolonged repolarisation(due to defective k+ channels) .there are three types of sodium channels 1)resting –contains m gate which is active h gate which is inactive both are closed in resting.2)acive both are opened 3)m gate opens but h gate closes in inactive state .the order of these channels open is 1-2-3 .and next3-1, 1-2,2-3.natural cell during repolarisation 3-1 phase trapped until it reaches to resting .hence repolarisation continues.but in prolonged repolarisation cell 3-1 phase of the cell flips back to its original state bit early before repolarisation closes.hence early depolarisation occurs,

Obsolete refractory period :sodium channels from 3-1 stage never come even if you create more energy

Relative refractory period:after purticular point if you give some energy they come 3-1 stage some extent called relative refractory period.

Delayed after repolarisations occur after repolarisation completed+ cationic load ca++.during adrenergic stress more stimulation of beta 2 and more Camp and more PKA activation more phosporelation ca++channels .this ca++ trigger delayed after depolarisation.

Digitalis prevents na K+ ATP ASE and activates na+ ca++ exchanger more ca++ comes in DAD occurs