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structure of electrical conducting system of heart

function of elements of conducting system
SAN→ generates electrical impulse
AVN→ mode of passage of impulse from atria to ventricles
bundle of his, right bundle branch, left bundle branch→ specialised conducting system to transmit impulse
action potential
transient depolarisation of a cell as a result of activity of ion channels
types of cardiac action potentials
pacemaker action potential
non pacemaker action potential
pacemaker action potentials
autorhythmic
controlled by If (funny) channels

stages in pacemaker action potential generation
funny channels allow Na+ influx into membrane
depolarises membrane
as membrane potential reached until threshold reached→ action potential generated
Ca2+ channel open
at top of depolarisation, K+ channels open and Ca2+channels close
K+ leave→ causes repolarisation
non-pacemaker action potentials
sodium ions influx into cell membranes, rapidly depolarising membrane
sodium channels close, potassium channels open so K+ moves out of cell
calcium channels open, so lots of calcium moves in, little bit of potassium leaving to allow electrochemical balance
calcium channels close and potassium channels open→ lots of potassium exits to repolarise
potassium leaves channel slowly from potassium channel

pacemaker activity
intrinsic, spontaneous time dependant depolarisation of a cell membrane that leads to an action potential
hierarchy of pacemakers
primary pacemaker→ highest firing frequency (fastest pacemaker):
SAN→ 100bpm
secondary pacemaker:
AVN→ 40bpm
tertiary pacemaker:
purkinje fibres→ 20bpm
SAN under constant vagal stimulation which suppresses its intrinsic frequency to approx. 60 bpm
drugs affecting cardiac action potential
Class 1→ Na+ channel blocker
class 2→ Beta blocker
Class 3→ K+ channel blockers
Class 4→ Ca2+ channel blocker
examples of class 1 channel blockers
1a→ moderate:
quinidine
procainamide
1b→ weak:
lidocaine
phenytoin
1c→ strong:
flecainide
propafenone
examples of class 2 heart drugs
propranolol
metoprolol
examples of class 3 heart drugs
amiodarone
sotalol
examples of class 4 heart drugs
verapamil
diltiazem
conduction of action potentials
pass through gap junctions located at intercalated disks
components of ECG
P wave→ atrial depolarisation
PQ interval→ AV nodal delay
QRS→ ventricular depolarisation
ST→ interval between depolarisation and repolarisation
T wave→ repolarisation
normal sinus rhythm

atrial fibrillation
no ordinated atrial contraction
sinus node no longer in charge
ventricular rate is irregular
AVN important in regulation of atrial signals

atrial flutter
abnormal rhythm in atrium
regular but fast→ 300ppm
AV node is vital

ventricular fibrillation
cardiac arrest rhythm
no regularity
shockable

ventricular tachycardia
associated w cardiac arrest
shockable

1st degree heart block
long time between P wave and QRS
aka 1st degree AV block
AVN takes longer to produce ventricular depolarisation
always QRS after p wave

Second degree AV block→ Mobitz I)
progressive lengthening of PR interval, then missed QRS complex

secondary degree AV block→ Mobitz II
PR interval normal, then absent QRS after P wave

second degree AV block→ 2:1 block
absent QRS after alternate P waves

third degree block with junctional escape
no relationship between P waves and QRS complexes
