Cardiac Muscle Tissue And The Cardiac Conduction System

Course Objectives

➤ Based on the lecture and text material, you should be able to

do the following:
➤ understand and describe the electrical basis for cardiac
muscle contraction
➤ understand and describe the electrical connections between
cardiac myocytes
➤ describe the pathway that conducts pacemaker signals
throughout the heart
➤ outline the basic points of an ECG trace
Cardiac Cells

➤ There are five functionally and anatomically separate types:

➤ Sino-atrial node
➤ Atrio-ventricular node
➤ His-Purkinje system
➤ Atrial muscle
➤ Ventricular muscle
Properties Of Cardiac Muscle
➤ These are
➤ Automaticity (chronotropy): the ability to initiate an
electrical impulse.
➤ Conductivity (dromotropy): the ability to conduct an
electrical impulse.
➤ Contractility (inotropy): the ability to contract.
➤ Lusitropy: the ability to relax and to fill.
Properties Of Cardiac Muscle
➤ Like skeletal muscle, cardiac muscle is striated and
contraction occurs using the same sliding filament
mechanism.

➤ In contrast to skeletal muscle, cardiac muscle fibers are short,

fat, branched and interconnected.

➤ Cardiac muscle fibers also have only one or two nuclei,

contain more mitochondria, have fewer T-tubules, and much
less sarcoplasmic reticulum.
Properties Of Cardiac Muscle
➤ Cardiac muscle cells form a structural and functional syncytium (a complex
three-dimensional network), being linked by low-resistance intercalated
discs.
➤ The intercalated discs serve the following functions:
➤ The connection of adjacent cells via desmosomes.
➤ The connection of actin filaments of adjacent cells.
➤ Tight intercellular coupling through low-resistance gap junctions.
➤ Each gap junction consists of a cluster of several ion channels.
➤ Each channel comprises two hemi-channels or connexons.
➤ Each connexon is made up of six connexin molecules that traverse the
lipid bilayer and form a central pore which allow the ions of the action
potential to pass freely from cell to cell so that the whole heart
contracts instead of just a few cells.
CARDIAC ELECTROPHYSIOLOGY
➤ In cardiac muscle, there are two types of cells:
➤ contractile cells & autorhythmic (or automatic or pacemaker)
cells.
➤ Contractile cells contract when stimulated and autorhythmic cells, on
the other hand, are self-stimulating & contract without any external
stimulation.

➤ Thus, the autorhythmic cells are self excitable and can start their own
depolarization which leads to depolarization of the rest of the heart in
a spontaneous and rhythmic way.

➤ This is called auto-rhythmicity and these cells pace the heart.

1. Pacemaker Potentials
➤ The heart does not depend on the nervous system to depolarize
and contract, it has an inbuilt mechanism called the intrinsic
cardiac conduction system, which consist of specialized non-
contractile cells called pacemaker (autorhythmic) cells.

➤ Pacemaker cells are self-excitatory and they initiate and

distribute impulses throughout the heart in a consistent,
orderly fashion.

➤ They have gap junctions that pass APs from one cell to the
next, but only along a specific conduction pathway.
 Autorhythmic cells do not have a stable resting membrane potential.

➤ They are constantly

depolarizing and drift toward
action potential.

➤ These are called pacemaker

potentials ( s l o w,
spontaneous depolarization).

➤ The pacemaker potential is

characterised by a less
HCN= Hyperpolarization- activated
Cyclic Nucleotide gated Channel negative threshold potential
and a less steep slope.
 Pacemaker potential involves the gradual reduction of membrane
permeability to K+.

➤ Since Na+ permeability

remains unchanged, it
continues to diffuse slowly
into the cell.
➤ The inner membrane becomes
less negative (more positive)
and eventually threshold is
reached.
➤ The fast voltage - gated Ca2+
channels open at -40mV and it
HCN= Hyperpolarization- activated is the explosive influx of Ca2+
Cyclic Nucleotide gated Channel that causes a complete reversal
of membrane potential.
Pacemaker cells depolarize spontaneously, but the rate at
which they do so can be modulated by:

➤ Epinephrine and norepinephrine increase the production of

cAMP, which keeps Na+ channels open.
➤ Speeds heart rate.
➤ Parasympathetic neurons secrete acetylcholine, which opens
K+ channels.
➤ Slows heart rate.
2. Cardiac Action Potential
➤ The cardiac action potential is generated independently of
extrinsic innervation. Five phases are recognised:
1.Phase 0: Initial rapid membrane
depolarisation
2.Phase 1: Initial Repolarisation; rapid
but limited depolarisation (spike)
3.P h a s e 2 : P l a t e a u o r p r o l o n g e d
depolarisation
4.Phase 3: Final rapid repolarisation
5.Phase 4: Electrical diastole

TP = threshold potential
Phase 0–Initial rapid membrane depolarisation
➤ This is represented by the upstroke of action potential.

➤ It is triggered by a decrease in the potential gradient across the

membrane to the threshold potential of –70 to –60 mV.

➤ This leads to voltage-dependent opening of the fast Na+ channels,

resulting in the rapid influx of positively charged ions (the inward
+
Na current) and rapid reversal of membrane polarity.

➤ The transmembrane potential above 0mV is referred to as the

overshoot.
Phase I–Initial Repolarisation; rapid but limited depolarisation (spike)
➤ Activation of a transient outward K+ current and rapid closure
of fast inward Na+ current.

➤ The transient outward K+ current has two components: one

component is voltage-gated and the other is activated by a
local rise in Ca2+.
Phase 2–Plateau or prolonged depolarisation
➤ This is characteristic of the cardiac action potential and is the main
determinant of the duration of the action potential.

➤ The net current is apparently small, as the flow of outward current and
the inward flow of current are almost equal.

➤ The inward currents include: the slowly activating Na+ current, a slow
2+ +
inward Ca current through voltage sensitive channels and an Na /
Ca2+-exchange current.

➤ Outward currents include a slowly activating K+ current, a more

+ + +
rapidly activating K current and the Na /K -electrogenic pump.
Phase 2–Plateau or prolonged depolarisation
➤ During this time, repolarization is already occurring, but the
Ca2+ surge across the membrane prolongs the depolarization,
which is called a plateau.

➤ This plateau leads to the muscle contraction (action potential)

lasting 200 - 300 ms (as compared to the skeletal muscle
contraction lasting 15 to 100 ms).
➤ This provides the heart with the capability needed to eject
blood from the heart.
➤ As long as Ca2+ is entering cardiac cells, they will continue to
contract
Phase 3 – Final rapid repolarisation
2+ +
➤ After the 200 ms, the action potential falls rapidly, Ca channels close; K
channels open and the cells are repolarized.
+ 2+ +
➤ Deactivation of inward Na and Ca currents occurs earlier than the K
currents.

+
➤ When the membrane is sufficiently repolarised, an inward K rectifier current
is progressively activated, resulting in a regenerative increase in outward
currents and an increasing rate of repolarisation.

+ +
➤ Repolarisation is also achieved by the function of the Na /K -ATPase pump.

2+
➤ During this time, the Ca ions are pumped back into the sarcoplasmic
reticulum and extracellular space.
Phase 4 – Electrical diastole
➤ This is represented by a stable resting membrane potential in
atrial and ventricular muscle cells.
➤ The ionic events which occur in contractile cardiac cells are
significantly different from the ionic events which happen in the
pacemaker cells.
➤ The primary difference is a lack of a fast inward Na+ current in the
Pacemaker potential.
Refractory Period
➡ Because the atria and ventricles
contract as single units, they
cannot sustain a contraction.

➡ Because the action potential of

cardiac cells is long, they also
have long refractory periods
before they can contract again.

➡ This is to prevent tetanic

contractions, which would stop
the heart from pumping.
3. Conduction System Of The Heart

➤ Most of the muscle cells in

the heart are contractile cells.
The autorhythmic cells are
located in the following
areas::
➤ Sinoatrial (SA) Node - a
group of specialized cells
located in the right atrium
where the superior vena
cava enters the atrium
➤ Internodal Tracts or Pathways specialized cells that act as a direct
pathway from the SA Node to the AV Node. These pathways do not use gap
junctions to send impulses.
 ➤ Atrioventricular (AV) Node a
group of specialized cells located at
the fibrous septum between the
right atrium and the right ventricle.

➤ Atrioventricular Bundle- this group of cells runs from the AV Node

through the atrioventricular septum and then splits into two major
branches that run down the septum between the two ventricles.
 ➤ Purkinje Fibres these
specialized cells branch off of the
AV bundle at the apex of the
heart and run up the walls of the
heart.

➤ The cells of the conduction pathways are autorhythmic

➤ The vagus nerve provides beat-to-beat control of the SANode.
 Conduction Of Cardiac Impulses
➤ The order of action potential of a heartbeat starts at
SANode

Inter-nodal pathways

AVNode

Bundle of His

Left & Right bundle branches

Purkinje fibers

Ventricles
Conduction Of Cardiac Impulses
➤ The SA Node generates the action potential as it has the fastest rate of
depolarization.

➤ It is the heart’s pacemaker and its rhythm is called sinus rhythm.

Average sinus rhythm is about 75 beats per minute, but of course this
is variable.

➤ The action potential generated will the spread to two places; the gap
junctions to the neighboring cells of atria (which in turn send to their
neighbors in the atria), and to the internodal pathways.

➤ The internodal pathways quickly conduct APs to the AV node.

Conduction Of Cardiac Impulses
➤ The impulse is delayed momentarily which allows the atria
complete their contraction before the ventricle contracts.
➤ The AV node has small diameter fibers and fewer gap
junctions to allow this delay.

➤ The impulse then goes to the AV Bundle (Bundle of His).

➤ There are no gap junctions between cardiomyocytes of the

atria and the ventricles.
Conduction Of Impulses
➤ The AV Bundle is the only electrical connection between the atria and
the ventricles.

➤ The AV bundle branches out into two paths that connect to the
Purkinje Fibers.

➤ Conduction along here is very rapid due to large fibers and a large
number of gap junctions, and allows the ventricles to contract as a
unit.

➤ Defects in the conduction system that cause irregular heart rhythms

are called arrhythmias.
Conduction Velocities

➤ Sino-atrial node: 0.05 m/s

➤ Atrial muscle: 0.8–1.0 m/s
➤ Atrio-ventricular node: 0.03–0.05 m/s
➤ Bundle of His: 0.8–1.0 m/s
➤ Ventricular muscle: 0.8–1.0 m/s
Cardiac Muscle Contraction
➤ 90% of cardiac cells are contractile muscle fibers, which are
responsible for pumping the heart.

2+
➤ 10-20% of Ca need for contraction enters from extracellular space.
Once inside, this calcium stimulates the release of much larger
2+
amounts (80%) of Ca from the sarcoplasmic reticulum.

➤ Cardiac muscle contraction is very similar to that of skeletal muscle

with the difference arising from the presence of slow voltage-gated
2+
Ca channel in the plasma membrane.

➤ In a resting state, ionic calcium cannot enter the cardiac fibers.

➤ Cardiac muscles have much more mitochondria than other
cells, which is why it is absolutely dependent on oxygen for
its metabolism. It relies exclusively on aerobic aspiration.

➤ When a region of the heart is deprived of oxygen, the oxygen-

starved cells begin to metabolize anaerobically.

➤ This produces lactic acid, which causes pH to fall (H+ rises)

and impairs the cardiac cells ability to produce ATP that is
needed to pump Ca2+ out of the cell.
Cardiac Muscle Contraction
➤ The rising levels of intracellular Ca2+ and H+ cause the gap
junctions to close and isolate the damaged cells.

➤ The action potentials look for other paths to reach the cardiac
cells beyond them, and the damaged cells become ischaemic.

➤ If the ischaemia persists, then the cells die, resulting in a

myocardial infarction (a common type of heart attack).
THE ELECTROCARDIOGRAM
➤ An electrocardiogram, or ECG, is a diagnostic test that records
electrical activity in the heart by picking up the movement of ions in
body tissues in response to this activity.
➤ Placing electrodes on the surface of the body does this.

➤ Standard, 12 Chest Leads is the most common ECG, three bipolar leads
(electrodes) on two arms and one leg, and nine chest leads are used.
➤ The electrocardiograph is essentially a record of impulse formation in
the primary pacemaker (sino-atrial node), transmission through
specialised conduction tissues, depolarisation and repolarisation of the
myocardium.
➤ The electrocardiograph has three distinctive peaks or waves:
➤ The first is a small peak called
the P wave that is the result of
the depolarization of the atria.

➤ This is followed by the QRS

complex.
➤ This is associated with the
depolarization of the
ventricle and the
repolarization of the atria
which are occurring at the
same time.
➤ The third wave is the T
wave.
➤ It is a small deflection
associated with
repolarization of the
ventricle.

➤ The interval between the P

wave and the QRS
complex is called the P-R
interval.
➤ P-R interval represents the time is takes for the impulse to
travel from the SA Node to the AV node, through the
penetrating fibers and down the AV Bundle and Purkinje
Fibers.

➤ The interval between the QRS complex and the T wave is

called the Q-T or S-T interval. It represents the time it takes
for the ventricle to contract and relax again.
 The following types of information
can be obtained by interpreting the
different segments of the ECG :

a. Heart rate and rhythm

i. Atrial rate and rhythm
ii. Ve n t r i c u l a r ra te a n d
rhythm
b. Evidence of Axis Deviation
c. Evidence of abnormal Q
wave and S – T segment
changes.
This information, taken with the clinical picture will help to conGirm common
cardiac conditions like: Cardiac irregularities and blocks and Position or
Hypertrophy of the Heart
 Bipolar limb leads record voltage between
electrodes placed on wrists and legs.

Lead I: between right arm and right leg

Lead II: between right arm and left leg

Lead III: between left arm and left leg

Unipolar leads record voltage between a single electrode on the body and
one built into the machine (ground).

Limb leads go on the right arm (AVR), left arm (AVL), and left leg (AVF).

There are six chest leads.

THE ELECTROCARDIOGRAM

•V1 at the fourth intercostal space, at the right

margin of the sternum
•V2 at the fourth intercostal space, at the left
margin of the sternum
•V3 midway between the position of leads V2
and V4 (in a straight line)
•V4 at the Gifth intercostal space at the junction
of the left mid-clavicular line
•V5 midway between the position of leads V4
and V6 (straight down from the axillary line
on the same horizontal position as V4 and V6
• V6 at the horizontal position of V4, at the left
of the mid-axillary line.
ECG And Heart Sounds

➤ Lub occurs after the QRS

wave.
➤ Dub occurs at the beginning
of the T wave.
Case Problems
➤ Charles Doucette, who is 68 years old, retired from a middle
management position in the automotive industry following an
acute myocardial infarction. He was recovering in a local
hospital, where the physicians closely monitored his ECG.
➤ Mr. Doucette’s PR intervals were normal and his QRS
complexes had a normal configuration.
➤ However, occasional P-waves occurred that were not followed
by QRS complexes (non-conducted P-waves). He fainted twice
in the hospital.
Case Problems
➤ The physicians believed that the myocardial infarction caused
a block in his AV conduction system called a Mobitz type II
AV block.
➤ Since Mr. Doucette’s conduction block could become more
severe, his physicians planned to treat him by implanting a
pacemaker.
Case Problems
1. Describe and explain the physiology of the waves and
intervals of the normal ECG.
2. What does the PR interval on the ECG represent? What units
are used to express the PR interval?
3. What is the normal value?
4. What does the term “conduction velocity” mean, as applied
to myocardial tissue? What is the normal conduction velocity
through the AV node? How does conduction velocity in the
AV node compare with conduction velocity in other portions
of the heart?
 Case Problems

How does AV nodal conduction velocity correlate with PR

interval? Since Mr. Doucette’s physicians believe he has a
block in his AV conduction system, why are his PR intervals
normal (rather than increased)?
What does the QRS complex on the ECG represent? What is
implied in the information that the QRS complexes on Mr.
Doucette’s ECG had a normal configuration?
How is it possible to have a P-wave that is not followed by a
QRS complex, as seen on Mr. Doucette’s ECG? Propose a
mechanism to explain the P-wave that is not followed by a
QRS complex.
Why did Mr. Doucette faint?
“
End.