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THE ELECTRIC ACTIVITY OF THE HEART

CONTRACTION OF CARDIAC MUSCLE INITIATION & SEQUENCE OF CARDIAC ACTION CONDUCTION SYSTEM OF THE HEART
POTENTIALS
1. Structure of Cardiac Muscle Fibres: 1. Myocardial Contractile Cells:  Conduction system consists of 4 components:
 Characteristics of Cardiac Muscle Fibres:  AP’s  similar to those in neurons & skeletal muscle cells 1. Sino-atrial (SA) Node:
 Striated; uni- or binucleate, branched with  Main difference between cardiac & skeletal muscle cell /  Sited in wall of RA near superior vena cava
intercalated discs neuron AP’s  lengthening of AP due to Ca2+ entry i.e.  Function  primary pacemaker of heart 
 Intercalated discs  desmosomes & gap plateau phase average impulse frequency at rest = 70/min
junctions  Myocardial cells  resting potential of about –90mV  Innervation:
 Desmosomes  allow forces created in one  Wave of depolarisation moves into contractile cell  potential  Parasympathetic  ACh  decreases HR
cell to be transferred to adjacent cell becomes more positive  voltage gated Na+ channels open 
 Sympathetic  adrenaline & NA  increases
 Gap junctions  electrically couple rapid depolarisation
HR & contraction force
myocardium  rapid spread of wave of  Channels close when potential reaches +20mV  cell begins  Sensitive for temperature, stretching,
depolarisation throughout myocardium to repolarise due to K+ leaving through open K+ channels
touch & chemical stimulation
 Two types of cardiocytes:  AP flattens into plateau due to  decrease in K+
1. Contractile myocardiocytes: permeability & increase in Ca permeability (Ca2+
2+
2. Atrio-ventricular (AV) Node:
 Make up bulk of heart channels open slowly during phase 0 & 1)
 Sited in floor of RA adjacent to interatrial
 Responsible for cardiac contraction   Combination of Ca2+ influx & decreased K+ efflux  plateau septum
phase
mechanical action  Impulse frequency = 40 – 60/min
 Striated & contain contractile proteins  Plateau ends when Ca2+ channels close & K+ permeability  Functions:
2. Autorhythmic cardiocytes: increases again  cell returns to resting potential
1. Slows heart impulse  allows for optimal
 Make up about 1% of myocardial cells  Longer AP  helps prevent sustained contraction ventricular filling
 Specialised cardiocytes  “pacemaker tetanus  important muscles must relax between 2. Controls frequency of impulse discharge
contractions to allow ventricular filling
cells” 3. Reserve pacemaker  in event of SA node
 Able to generate action potentials  Tetanus  cannot occur in cardiac muscle  refractory period failure
spontaneously & contraction end almost simultaneously due to longer
AP 3. AV Bundle (Bundle of His):
 Three cell types form electrical conduction
system: 2. Myocardial Autorhythmic Cells:
 Runs from AV node to interventricular
septum
1. P-cells  sited in SA & AV nodes  set  Property of spontaneous AP generation  results from unstable
pace of cardiac contraction  Right bundle branch  runs from septum up
membrane potentials of pacemaker cells  “pacemaker to apex of heart
2. Moderator cells  “switch” between P- potential”
cells & contractile cells  Left bundle branch  posterior / inferior
 Potential starts at about –60mV  slowly drifts toward threshold branch & anterior / superior branch
3. Purkinje cells  electrophysiological of about –40mV  whenever potential reaches threshold  AP
connection between atria & ventricles firing  Function  functional “switch” between
atria & ventricles
 Unstable potential  arises from “funny channels”  If
2. The Force of Cardiac Muscle Contraction: channels 4. Purkinje Fibre System:
 Rhythmic & co-ordinated contraction of cardiac  If channels  permable to both K+ & Na+; also allow
muscle  dependent on rhythmic discharge of  Branches of left & right bundles branches
current (I) to flow
pacemaker cells in SA node & conduction &  Function  impulse conduction to
distribution of impulse to contractile cells  When channels open at negative membrane potentials  Na+ contractile cells in ventricles
influx exceeds K+ efflux  net positive influx slowly depolarises
 Amount of tension generated by cardiac cell
muscle  proportional to number of  Conduction pathway:SA node  AV node 
crossbridges formed  As potential becomes more positive  If channels gradually bundle of His  Purkinje system  ventricular
close & set of Ca channels opens  slow Ca influx 
2+ 2+
contractile cells
 If cytosolic [Ca2+] too low  some crossbridges continuation of depolarisation until threshold is reached
are not activated  lower tension generated
by heart  Threshold  many Ca2+ channels open  calcium rushes  Ectopic Pacemakers:
into cell  rapid depolarisation
 If additional [Ca2+] enters cell from ECF  more  Impulse  can be initiated by other cardiac cells,
Ca2+ from SR released (calcium-induced calcium  Ca2+ channels close at peak of AP  K+ has already started occurs when:
release)  greater tension generated by slowly leaving cell  repolarisation 1. Rhythmicity of SA node decreases
heart  Modulation of Heart Rate by NS: 2. Conduction pathways between SA node &
 Catecholamines: adrenaline & NA  regulated  Timing of pacemaker cells  can be altered by altering other heart areas are blocked
amount of Ca2+ available for cardiac contraction  permeability of cells to various ions 3. Impulse discharge frequency of
greater tension  NA from sympathetic neurons & adrenaline from myocardium increases  e.g. with intake of caffeine &
 Force of cardiac contraction  also adrenal medulla  increase flow of ions through If during increased sympathetic activities such as exercise
dependent on sarcomere length prior to channels & Ca2+ channels  speeds up rate of pacemaker
contraction  i.e. stretch of myocardial cells depolarisation  heart rate increases
 Stretch on individual fibres 
depends on  ACh from parasympathetic neurons  increases K+
volume of blood in heart chambers permeability  hyperpolarizes cell  pacemaker potential
begins at more negative value; Ca2+ permeability also
reduced  slow depolarisation rate of pacemaker potential
 decreases heart rate