for b.sc students, and MBBS first years

1. Conduction system and ecg

2. Conduction system:
• Inherent and rhythmical electrical activity is the
reason for the heart’s life long beat.
• Source: network of specialized cardiac muscle fibers
called ‘autorhythmic fibers’ because they are self-
excitable.
• Repeatedly generate action potentials that trigger
heart contractions.
• Continue to stimulate a heart to beat even after its
removed form the body.
• Autorhythmic fibers – 2 important functions:
• 1. act as a pacemaker, setting the rhythm of electrical
excitation that causes contraction of the heart.

3. • 2. form the conduction system, a network of
specialized cardiac muscle fibers that provide a
path for each cycle of cardiac excitation to
progress through the heart.
• Conduction system ensures that cardiac
chambers become stimulated to contract in a
coordinated manner, which makes the heart an
effective pump.

5. • Cardiac action potentials propagate through the
conduction system in the following sequence:
• 1. cardiac excitation normally begins in the SA node,
located in the right atrial wall just inferior to the
opening of the SVC.
• SA node cells do not have a stable resting potential.
• Rather, they repeatedly depolarize to threshold
spontaneously.
• Spontaneous depolarization is a ‘pacemaker potential’.
• When the pacemaker potential reaches threshold, it
triggers an action potential.
• Each AP from the SA node propagates throughout
both atria via gap junctions in the intercalated discs of
atrial muscle fibers.

7. • Following the AP, the atria contract.
• 2. by conducting along atrial muscle fibers, the AP
reaches the AV node, located in the septum between
the 2 atria, just anterior to the opening of the coronary
sinus.
• 3. from the AV node, the AP enters the AV bundle (or
bundle of HIS).
• This bundle is the only site where action potentials can
conduct from the atria to the ventricles.
• 4. after propagating along the AV bundle, the AP
enters both the right and left bundle branches.
• The bundle branches extend through the
interventricular septum towards the apex of the heart.

9. • 5. finally, the large-diameter purkinje fibers rapidly
conduct the AP from the apex of the heart upward to
the remainder of the ventricular myocardium.
• Then the ventricular contract, pushing the blood
upward toward the semilunar valves.
• On their own, autorhythmic fibers in the SA node
would initiate an AP about every 0.6 sec, or 100 times
per minute.
• This rate is faster than that of any other autorhythmic
fibers.

11. • Because AP from the SA node spread through the
conduction system and stimulate other areas before
the other areas are able to generate an AP at their own,
slower rate; the SA node acts as a natural pacemaker
of the heart.
• Nerve impulses from the ANS and blood borne
hormones modify the timing and strength of each
heart beat, but they don’t establish the fundamental
rhythm.
• In a person at rest, Ach released by the
parasympathetic division of the ANS slows SA node
pacing to about 75 APs per minute, or one every 0.8
sec.

13. • Artificial pacemakers:
• If the SA node becomes damaged or diseased, the
slower AV node can pick up the pacemaking task.
• Its rate of spontaneous depolarization is 40-60
times/minute.
• If the activity of both nodes is suppressed, the
heartbeat may still be maintained by autorhythmic
fibers in the ventricles – the AV bundle, a bundle
branch or purkinje fibers.
• Pacing rate is so slow (20-35 beats/min) that blood
flow to the brain is inadequate.

14. • When this condition occurs, normal heart rhythm can
be restored and maintained by surgically implanting
an artificial pacemaker, a device that sends out small
electrical currents to stimulate the heart to contract.
• A pacemaker consists of a battery and impulse
generator and is usually implanted beneath the skin
just inferior to the clavicle.
• Connected to 1 or 2 flexible wires that are threaded
through the SVC and then passed into the right atrium
and right ventricle.
• Many of the newer pacemakers, referred to as ‘activity
adjusted pacemakers’, automatically speed up the
heartbeat during exercise.

16. Action potential and contraction of
contractile fibers:
• AP initiated by the SA node travels along the
conduction system and spreads out to excite the
‘working’ atrial and ventricular muscle fibers, called
contractile fibers.
• An AP occurs in a contractile fiber as follows:
• 1. depolarization:
• Unlike autorhythmic fibers, contractile fibers have a
stable resting membrane potential that is close to -
90mv.
• When a contractile fiber is brought to threshold by an
AP from neighbouring fibers, its ‘voltage gated fast
Na+ channels’ open.

17. • These Na+ ion channels are referred to as ‘fast’
because they open very rapidly in response to a
threshold-level depolarization.
• Opening of these channels allows Na+ inflow because
the cytosol of contractile fibers is electrically more
negative than interstitial fluid and Na+ conc. Is higher
in interstitial fluid.
• Inflow of Na+ down the electrochemical gradient
produces a ‘rapid depolarization’.
• Within a few millisecs, the fast Na+ channels
automatically inactivate and Na+ inflow decreases.

19. • 2. plateau:
• Next phase of an AP in a contractile fiber.
• Period of maintained depolarization.
• Due in part to opening of ‘voltage-gated slow Ca2+
channels’ in the sarcolemma.
• When these channels open, calcium move from the
interstitial fluid into the cytosol.
• This inflow of Ca2+ causes even more Ca2+ to pour
out of the SR into the cytosol through additional Ca2+
channels in the SR membrane.
• Increased Ca2+ conc. In the cytosol ultimately triggers
contraction.
• Several different types of voltage gated K+ channels
are also found in the sarcolemma of a contractile fiber.

21. • Just before the plateau phase begins, some of these K+
channels open, allowing potassium ions to leave the
contractile fiber.
• Therefore, depolarization is sustained during the
plateau because Ca2+ inflow just balances K+ outflow.
• The plateau phase lasts for about 0.25sec, and the
membrane potential of the contractile fiber is close to
0 mV.
• By comparision, depolarization in a neuron or skeletal
muscle is much briefer, about 1 msec, because it lacks
a plateau phase.

23. • 3. repolarization:
• Recovery of the RMP.
• Resembles other excitable cells.
• After a delay, voltage gated K+ channels open.
• Outflow of K+ restores the negative RMP.
• At the same time, the Ca2+ channels in the
sarcolemma and the SR are closing, which also
contribute to repolarization.

26. • Mechanism of contraction is similar in cardiac and
skeletal muscle.
• Electrical activity leads to the mechanical response
after a short delay.
• As Ca2+ conc. Rises inside a contractile fiber, Ca2+
binds to the regulatory protein troponin, which allows
the actin and myosin filaments to begin sliding past
one another, and tension starts to develop.
• Subs. That alter the movement of Ca2+ through slow
Ca2+ channels influence the strength of heart
contractions.
• E.g: epinephrine – increases contraction force by
enhancing Ca2+ inflow into the cytosol.

29. • In muscle, the ‘refractory period’ is the time interval
during which a second contraction cannot be
triggered.
• Refractory period of a cardiac muscle fiber lasts longer
than the contraction itself.
• As a result, another contraction cannot begin until
relaxation is well underway.
• For this reason, tetanus cannot occur in cardiac
muscle as it can in skeletal muscle.
• Imp. For pumping action of heart as alternating
contraction and relaxation are needed to pump blood
flow.

31. ATP production in cardiac muscle:
• Cardiac muscle relies almost exclusively on aerobic
cellular respiration.
• O2 needed diffuses from blood in the coronary
circulation and is released from myoglobin inside
cardiac muscle fibers.
• In a person at rest, the heart’s ATP comes mainly from
oxidation of fatty acids (60%) and glucose (35%), with
smaller contributions from lactic acid, aminoacids,
and ketone bodies.
• During exercise, the heart’s use of lactic acid,
produced by actively contracting skeletal muscles,
rises.

32. • Like skeletal muscle, cardiac muscle also produces
some ATP from ‘creatine phosphate’.
• Creatine kinase – enzyme that catalyzes transfer of a
phosphate group from creatine phosphate to ADP to
make ATP.
• Normally, CK and other enzymes are confined within
cells.
• Blood levels of creatine kinase indicates MI.
• Injured or dying cardiac or skeletal muscle fibers
release CK into the blood.

33. ECG:
• As AP propagate through the heart, they generate
electrical currents that can be detected at the surface
of the body.
• An ECG or EKG is a recording of these electrical
signals.
• The ECG is a composite record of AP produced by all
the heart muscle fibers during each heartbeat.
• The instrument used to record the changes is an
electrocardiograph.
• Electrodes are positioned on the arms and legs (limb
leads) and at 6 positions on the chest (chest leads) to
record the ECG.

36. • The ECG amplifies the heart’s signals and produces 12
different tracings from different combinations of limb
and chest leads.
• Each limb and chest electrode records slightly
different electrical activity because of the difference in
its position relative to the heart.
• By comparing these records with one another and with
normal records, following things can be determined:
• 1. conducting pathway is abnormal.
• 2. if the heart is enlarged.
• 3. if certain regions of the heart are damaged.
• 4. cause of chest pain.

37. • In a typical record, 3 clearly recognizable waves
appear with each heart beat.
• P wave: first wave.
• small upward deflection on the ECG.
• Represents atrial depolarization – spreads from the
SA node thorugh contractile fibers in both atria.
• QRS complex: second wave.
• begins as a downward deflection – continues as a
large, upright, triangular wave and ends as a
downward wave.
• Represents ‘rapid ventricular depolarization’ – AP
spreads through ventricular contractile fibers.

38. • T wave:
• Third wave – dome shaped upward deflection.
• Indicates ventricular repolarization – ventricles are
starting to relax.

39. • T wave is smaller and wider than the QRS complex
because repolarization occurs more slowly than
depolarization.
• During the plateau period of steady depolarization, the
ECG tracing is flat.
• Size of the waves can provide clues to abnormalities.
• Larger P waves indicate enlargement of an atrium.
• Enlarged Q wave may indicate a MI.
• Enlarged R wave indicates enlarged ventricles.
• T wave is flatter than normal when the heart muscle is
receiving insufficient oxygen.
• E.g: CAD
• T wave may be elevated in hyperkalemia.

41. • Analysis of an ECG also involves measuring the time
spans between waves – ‘intervals or segments’.
• P-Q interval: is the time from the beginning of the P
wave to the beginning of QRS complex.
• Represents the conduction time from the beginning of
atrial excitation to be beginning of ventricular
excitation.
• another way: time required for the AP to travel
through the atria, AV NODE, and the remaining fibers
of the conduction system.
• In CAD and RF – AP forced to detour around scar
tissue caused by then – PQ interval lengthens.

43. • ST segment – begins at the end of the S wave and ends
at the beginning of the T wave.
• Represents the time when the ventricular contractile
fibers are depolarized during the plateau phase of the
AP.
• Elevated in acute MI.
• Depressed when the heart muscle receives insufficient
oxygen.

45. • QT interval:
• Extends form the start of QRS complex to the end of
the T wave.
• Time from the beginning of ventricular depolarization
to the end of ventricular repolarization.
• Lengthened by myocardial damage, myocardial
ischemia or conduction abnormalities.