CONDUCTION SYSTEM

The heart regul ates the rate and strength of contracti on through an intrinsic conduction system, modi fi ed by
external sympathetic and parasympathetic pathways.
A maj or porti on of the heart i s made up of 'worki ng' cardi omyocytes, al so known as contracti l e fi bers. Action
potentials, i ni ti ated by autorhythmic cells i n the sinoatrial node, spread throughout the i ntri nsi c conducti on
system and exci te the contractile fibers, causi ng atri al and ventri cul ar contracti on.
AUTORYTHMIC CELLS
Duri ng embryoni c devel opment, about 1% of the cardi omyoctes (cardi ac muscl e fi bers) that make up the
muscul ar wal l s of the heart become hi ghl y speci al i zed autorhythmi c muscl e cel l s (sinoatrial node,
atrioventricular node, atrioventricular bundle, and Purkinji fibers), capabl e of spontaneous depol ari zati on.

These groups of cel l s act to i ni ti ate acti on potenti al s that propagate (spread) through the i ntri nsi c conducti on
system of the heart, causi ng al l four chambers to contract i n a co-ordi nated sequence of events.
Sinoatrial (SA) node
A group of speci al i zed autorhythmi c cel l s l ocated under the epi cardi um, i n the ri ght atri um, j ust
superol ateral to where the superi or vena cava opens i nto the heart.
Function: The SA node acts as the natural pacemaker of the heart, i ni ti ati ng acti on potenti al s that then
propagate through the atri a, vi a gap j uncti ons i n the i ntercal ated di scs of atri al muscl e fi bers.
The speci al i st cel l s of the SA node do not have a stabl e resti ng potenti al . Instead, they
spontaneousl y depol ari ze creati ng a pacemaker potential, whi ch i ni ti ates an acti on potenti al
around 100 ti mes per mi nute.
Atrial conduction pathways
A group of speci al i sed conducti ng cel l s arranged i n bands that are l ocated i n the wal l of the ri ght
atri um. They ori gi nate from the SA node, and consi st of internodal tracts, Bachmann's bundle
and a number of other pathways, whi ch propagate acti on potenti al s from the SA node to the rest
of the heart.
Function: The i nternodal tracts faci l i tate the transmi ssi on of el ectri cal si gnal s from the SA node to the AV
node and ri ght atri um, At the same ti me, the Bachmann's bundl e transmi ts pacemaki ng i mpul ses
from the SA node to the l eft atri um. The transmi ssi on of el ectri cal si gnal s al ong both of these
pathways sti mul ate the ri ght and l eft atri a to contract i n uni son.
Atrioventricular (AV) node
A group of speci al i zed autorhythmi c cel l s l ocated next to the right atrioventricular valve, at the
i nferi or aspect of the i nteratri al septum, anteri or to the openi ng of the coronary si nus. The
conducti on speed of the node i s i mportant i n sl owi ng the acti on potenti al , whi ch i s why there i s a
del ay between atri al contracti on, and ventri cul ar contracti on.
Primal Pictures Ltd. 2010
Function: The AV node sl ows the acti on potenti al to approxi amtel y 40-60 ti mes per mi nute, so that atri al
systol e can compl ete pri or to ventri cul ar systol e. Atri al contracti on i s then tri ggered by
depol ari zai on of the atri um through Bachmann's fi bers, and contracti on fi bers i n the atri um.
Atrioventricular (AV) bundle
Al so known as the 'Bundle of His', the AV bundl e i s a group of speci al i zed autorhythmi c cel l s
l ocated i n the i nterventri cul ar septum. They pass from the the AV node and branch i nto l eft and
ri ght fasci cl es before passi ng to the apex of the heart.
Function: It recei ves acti on potenti al s from the AV node, and propagates them to both ri ght and l eft bundl e
branches, extendi ng through the i ntraventri cul ar septum towards the apex of the heart.
Purkinj e fibers
Purki nj e fi bers, run from the apex of the heart upwards through the ventricular myocardium.
Function: They rapi dl y conduct acti on potenti al s upwards, tri ggeri ng ventricular contraction, whi ch pushes
bl ood through the semi -l unar val ves.
The autorhythmi c cardi omyocytes i n the SA node act as the heart's pacemaker. They are self-excitable and
repeatedl y generate acti on potenti al s, whi ch i ni ti ate rhythmi c cardi ac contracti ons. They provi de a path for
exci tati on to spread throughout the wal l s of the heart, ensuri ng co-ordi nated contracti on of al l four chambers.
MEMBRANE POTENTIALS
Membrane potential i s the vol tage across a pl asma membrane, measured i n mi l l i vol ts (mV), resul ti ng from the
rel ati ve concentrati ons of posi ti ve and negati ve i ons, such as sodi um (Na
+
), cal ci um (Ca
2+
), and potassi um
(K
+
) on the i nsi de and outsi de of the pl asma membrane.
Resting potential
Al l cel l s wi th an uneven charge di stri buti on across thei r pl asma membrane have a resti ng membrane
potenti al . A resti ng membrane potenti al occurs when there i s a bui l d up of negati vel y charged i ons (ani ons)
i n the cytosol i mmedi atel y i nsi de the pl asma membrane, and an equal bui l d up of posi ti vel y charged i ons
(cati ons) i n the extracel l ul ar fl ui d i mmedi atel y outsi de the membrane. The separati on of these opposi te
charges causes potential energy (voltage) to be produced and hence a resti ng membrane potenti al i s
establ i shed.
A greater di fference i n charge across the membrane wi l l produce a l arger membrane potenti al , wi th the
di fference i n charge across the pl asma membrane dependent upon the selective permeability of the cel l
membrane to vari ous i ons.
There are a number of factors that contri bute to the resti ng membrane potenti al .
There i s a l arger number of K
+
i ons l eavi ng the cel l than Na
+
i ons enteri ng i t due to there bei ng more K
+
leakage channels on the pl asma membrane than Na
+
leakage channels. As a resul t, the i nsi de of the
membrane becomes more negati ve, whi ch contri butes to the negati vi ty of the resti ng membrane potenti al .
Na
+
/K
+
/ ATPase pumps present on the pl asma membrane al so contri bute to the resti ng membrane
potenti al , si nce these acti ve transport pumps remove more posi ti ve charges from the cel l , than those
brought i nto the cel l .
Threshold potential
The threshol d potenti al i s the membrane potenti al requi red to i ni ti ate depolarization to form an action
potential.
An acti on potenti al i s when the resti ng membrane potenti al of the cel l undergoes depolarizaton and then
repolarization returns i t to i ts ori gi nal resti ng membrane potenti al .
Action potential: depolarization
Depol ari zati on i s a change i n a cel l 's membrane potenti al , where the cytopl asmi c si de of the pl asma
membrane becomes l ess negati vel y charged than at resti ng membrane potenti al . Thi s i s usual l y due to an
influx (i nfl ow) of posi ti vel y charged i ons maki ng the i nsi de of a cel l more posi ti ve/l ess negati ve compared to
the outsi de of the cel l (e.g. a change from -60 mV to -40 mV or from -90 mV to +20 mV). The pl asma
membrane i s sai d to become l ess pol ari zed or depolarized.
Action potential: repolarization
Repol ari zati on i s a change i n membrane potenti al , where the membrane potenti al i s returned to a negati ve
resti ng val ue after depol ari zati on. The pol ari ty of the pl asma membrane i s restored: i t i s repolarized.
MEMBRANE POTENTIALS OF AUTORHYTHMIC CELLS
Cardi omyocytes contai n sodi um, cal ci um, and potassi um i on channel s, thus al l owi ng sodi um (Na
+
), cal ci um
(Ca
2+
) and potassi um (K
+
) i ons to enter and l eave the cel l . Movement of these i ons across the cel l pl asma
membrane affects the cel l 's membrane potential.
Gap junctions connect adj acent cardi omyocytes, al l owi ng i ons to pass between cel l s, thus i ni ti ati ng the
spread of depol ari zati on from one cel l to the next. Many transport channel s are voltage-gated, meani ng they
open and cl ose i n response to a speci fi c vol tage l evel across the pl asma membrane.
Resting potential of autorhythmic cells
Resti ng membrane potenti al of autorhythmi c cardi omyocytes i s about -60 mV, whereas i t ranges from -85
mV to -95 mV i n contracti l e cardi omyocytes; the negati ve val ue denoti ng a more negati vel y charged
cytopl asmi c si de compared to outsi de the pl asma membrane.
Pacemaker potential of autorhythmic cells
The autorhythmi c cel l s of the si noatri al (SA) node undergo a spontaneous, gradual depol ari zati on due to a
smal l i nward current of posi ti ve sodi um i ons (Na
+
), al ong wi th a progressi ve decl i ne i n potassi um i on (K
+
)
efflux and a sl ow but gradual l y i ncreasi ng cal ci um i on (Ca
2+
) influx.
Thi s resul ts i n the i nsi de of each cel l gradual l y becomi ng l ess negati ve compared to the outsi de,
generati ng a vol tage known as the pacemaker potential, whi ch dri ves the rhythmi c fi ri ng of the heart.
Threshold potential of autorhythmic cells
A cel l membrane depol ari zes towards i ts threshol d potenti al of about -40 mV, whi ch i ni ti ates an acti on
potenti al .
Depolarization of autorhythmic cells
When a threshol d potenti al i s reached i t tri ggers the openi ng of fast calcium channels, causi ng an i nfl ux of
posi ti ve cal ci um i ons i nto the autorhythmi c cel l . Thi s i n turn causes rapi d depol ari zati on of the cel l
membrane, l eadi ng to the reversal of membrane potenti al . Depol ari zati on peaks at about +10 mV.
Repolarization of autorhythmic cells
Reversal of membrane potenti al tri ggers potassium channels to open, generati ng a rapi d i ncrease i n the
effl ux of posi ti ve potassi um i ons. Thi s causes repol ari zati on of the cel l membrane, bri ngi ng i t back down
from +10 mV to a resti ng membrane potenti al of about -60 mV.
MEMBRANE POTENTIALS OF CONTRACTILE CELLS
The maj ori ty of cardi omyocytes that make up the muscul ar wal l s of the heart are contractile cells. They are
the so-cal l ed 'worki ng' cardi ac muscl e fi bers. Contracti l e cel l s rel y on autorhythmi c cel l s to generate and
propagate an action potential before they can contract. The two cel l types are l i nked and communi cate vi a
gap junctions.
Resting potential of contractile cells
Contracti l e cardi omyocytes have a stabl e resti ng potenti al of -90 mV; the negati ve val ue denoti ng a more
negati vel y charged cytopl asmi c si de compared to outsi de the pl asma membrane.
Threshold potential of contractile cells
The cel l membrane depol ari zes towards i ts threshol d potenti al of about -40 mV, whi ch i ni ti ates an acti on
potenti al .
Depolarization of contractile cells
Depol ari zati on of an adj acent cel l (autorhythmi c or contracti l e) causes connecti ng gap j uncti ons to open,
al l owi ng posi ti ve i ons (Ca
2+
and Na
+
) to move i nto the contracti l e cel l .
A smal l vol tage change resul ts, bri ngi ng the cel l membrane up to threshol d potenti al and sti mul ati ng the
openi ng of fast voltage-gated Na
+
channels. Rapi d i nfl ux of posi ti ve Na
+
i ons down an el ectrochemi cal
gradi ent causes fast depol ari zati on of the cel l membrane, reversi ng the membrane potenti al from -90 mV to
about +25 mV.
Thi s i s known as the 'depolarization phase' or 'phase 1' of an acti on potenti al i n contracti l e cel l s.
Plateau of contractile cells
The 'plateau phase' or 'phase 2' of an acti on potenti al i n contracti l e cel l s i s a peri od of mai ntai ned
depol ari zati on l asti ng approxi matel y 0.25 seconds.
Depol ari zati on causes the openi ng of slow voltage-gated Ca
2+
channels i n the sarcol emma, generati ng
the movement of posi ti ve Ca
2+
i ons down a concentrati on gradi ent from extracel l ul ar fl ui d, i nto the cel l .
Thi s Ca
2+
i nfl ux tri ggers a further Ca
2+
i nfl ux from an i nternal store of Ca
2+
i n the sarcopl asmi c reti cul um.
An i ncrease i n i ntracel l ul ar Ca
2+
ul ti matel y tri ggers contracti on of the cel l .
Synchroni zed openi ng of K
+
channel s at the peak of depol ari zati on, i ni ti ates K
+
effl ux. The pl ateau phase
i s therefore mai ntai ned by Ca
2+
i nfl ux bal anci ng K
+
effl ux.
Repolarization of contractile cells
As cal ci um channel s cl ose, addi ti onal voltage gated K
+
channels open, causi ng K
+
efflux to i ncrease. Thi s
resul ts i n repol ari zati on restori ng a resti ng membrane potenti al of about -90 mV, where the i nsi de of the cel l
i s more negati ve than the outsi de.
Thi s phase i s known as the 'repolarization phase' or 'phase 3' of an acti on potenti al i n contracti l e cel l s.
ELECTROCARDIOGRAM (ECG)
An el ectrocardi ogram (ECG, or EKG) i s a composi te recordi ng of the el ectri cal acti vi ty of the heart duri ng the
cardi ac cycl e.
A typi cal ECG traci ng of a heartbeat i s made up of the fol l owi ng features, whi ch al l rel ate to a speci fi c peri od
of conducti on wi thi n the cardi ac cycl e: P wave, PR segment, QRS complex, ST segment, T wave, PR
interval, ST interval, QT interval, U wave.
ECG paper i s di vi ded i nto 1 mm squares, each square representi ng 0.04 seconds (sec) al ong the hori zontal
axi s and 0.1 mV al ong the verti cal axi s. The ECG traci ng di spl ays the heart's el ectri cal acti vi ty i n mi l l i Vol ts per
second.
P wave
The P wave represents depol ari zati on of the atri al contracti l e fi bers; a wave of depol ari zati on
spreads from the SA node to the AV node, and from the ri ght to the l eft atri um i n about 0.03
sec. After the P wave begi ns, there i s a del ay of about 0.1 sec as the acti on potenti al reaches
the AV node. Duri ng thi s ti me the atri a contract (atri al systol e).
PR segment
The PR segment, al so commonl y referred to as the 'PQ segment', represents conducti on of
the el ectri cal si gnal from the AV node to the AV bundl e, through the ri ght and l eft bundl e
branches and then to the Purki nj e fi bers, towards the ventri cl es. Thi s does not di rectl y cause
contracti on and i s therefore seen as a fl at regi on on the ECG.
QRS complex
The QRS compl ex represents rapi d depol ari zati on of the ventri cul ar contracti l e fi bers,
fol l owed shortl y by ventri cul ar contracti on (ventri cul ar systol e). Contracti on advances from the
apex of the heart upwards, pushi ng the bl ood to fi rst cl ose the AV val ves, then towards the
semi l unar val ves to open them.
Atri al repol ari zati on i s smal l i n ampl i tude and occurs duri ng ventri cul ar depol ari zati on; there
i s no di scerni bl e wave i n an ECG as i t i s masked by the more domi nant QRS compl ex.
ST segment
The ST segment, al so referred to as the isoelectric period, represents the peri od i n whi ch the
enti rety of both ventri cl es i s depol ari zed. Thi s roughl y corresponds to the pl ateau phase of a
ventri cul ar acti on potenti al .
T wave
The T wave represents the repol ari zati on of the ventri cl es whi ch i s l onger i n durati on than
depol ari zati on, due to the sl ower conducti on of
the repol ari zati on wave compared to the depol ari zati on wave.
Repol ari zati on begi ns at the apex of the heart, proceedi ng upwards, spreadi ng throughout the
ventri cl es. Ventri cul ar rel axati on (ventri cul ar di astol e) occurs shortl y after the T wave begi ns.
Ventri cl es are repol ari zed, reachi ng thei r resti ng potenti al and compl ete rel axati on by 0.6 sec.
U wave
Someti mes a smal l posi ti ve U wave may be seen after the T wave due to repol ari zati on of papi l l ary muscl e
or Purki nj e fi bers. Thi s represents the remnants of ventri cul ar repol ari zati on.
PR interval
The PR i nterval , al so commonl y referred to as the 'PQ interval', represents the peri od of ti me
between the onset of atri al depol ari zati on (P wave) and the onset of ventri cul ar depol ari zati on
(QRS compl ex); thi s i s usual l y about 0.12 to 0.20 sec i n durati on.
QT interval
The QT i nterval represents the ti me that i t takes for both ventri cul ar depol ari zati on and
repol ari zati on to occur; roughl y equal to the durati on of an average ventri cul ar acti on
potenti al .
Hi gher heart rates si gni fy shorter ventri cul ar acti on potenti al s and therefore a decreased QT
i nterval wi l l show on an ECG trace.