The document summarizes the cardiac conduction system and electrocardiogram (ECG). It describes how the conduction system initiates and propagates electrical signals throughout the heart to coordinate contractions. Specialized pacemaker cells in the sinoatrial node initiate signals that spread through atria and ventricles via pathways like the atrioventricular node and bundle of His. This electrical activity generates currents detectable by ECG, which can provide information on conduction abnormalities and heart health.

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.