Properties of heart muscles, valves & Blood

Vessels (I)

Dr Gauhar Hussain
Assistant Professor of Physiology

College of Medicine, Dawadimi

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 Objectives
1. Define the four specific characteristics of cardiac muscle and explain their
importance.
3. State the origin of the electrical activity of the heart and describe the
myogenic nature of the cardiac action potential, and the mechanism and
route of spread of electrical activity through myocardium.
4. Describe the ionic basis of each phase of the action potential, and the
characteristics of the action potential in different regions of the heart.
5. State the temporal relationship between mechanical and electrical events.

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 Cardiac Muscle
• Involuntary, Striated

• Individual cell= 100 micro-meter long, 15 micro-meter

broad

• Exhibit branching

The heart is composed of 3 types of muscles:

1. Atrial muscle,

2. Ventricular muscle, and

3. Specialized excitatory and conductive fibers.

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 Cardiac Muscle
• Intercalated discs: Gap junctions (nexus) allow ions to
move easily – provide low resistance bridges.

• Heart function as syncytium: cardiac cells are so

interconnected that when one of these cells becomes excited,
the action potential spreads to all of them.

Two separate syncytium:

1. Atrial syncytium and

2. Ventricular syncytium

Connected with each other by A-V bundle.

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 Properties of cardiac muscle
Electrical properties

1. Excitability:

2. Rhythmicity

3. Conductivity:

Mechanical properties:

4. related to Contractility:

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 Action potential in
different regions of the heart
• Variability in the shape of the action potential at each location.

• There are two types of action potentials in the heart.

• Fast/long action potentials are produced in working cells (atria & ventricles)

and Purkinje fibers.

Working cells do not exhibit automaticity.

• Slow/brief action potentials are produced

in the SA & AV nodes. These are the cells

that exhibit automaticity.

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 1. Excitability
Working Cardiac muscle is excitable.
Definition : It is the ability of the cardiac muscle to respond to an
adequate stimulus by generation of action potential i.e. excitation
impulse.

Transmembrane resting potential (RMP)

- At rest myocardial fibers (atrial and

ventricular) show RMP -80 to - 95 mV

RMP of Ventricular fiber = -90mV

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 Action potential (Fast)-working cells
Phase 0: Depolarization

Phase 1: Initial repolarization (brief)

Phase 2: Plateau (slow repolarization)

Phase 3: Rapid repolarization

(later & long)

Phase 4: Resting membrane potential

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 Ionic basis for excitability (Fast AP)
Depolarization: Phase 0: stimulation by an adequate stimulus causes
overshoot (1-2 ms) due to increased permeability to Na+ ions.

• Voltage-gated sodium channels (fast sodium channels) open and permit

sodium to rapidly flow into the cell .

• The membrane potential reaches

about +20 millivolts before the

sodium channels close.

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 Ionic basis for excitability (Fast AP)
Repolarization: {b} Plateau: Phase 2 (100-150 ms)

{a} Initial repolarization. Phase 1 (10 ms) • Ca2+ channels open and fast K +channels close.

i. Small slow inflow of Ca++ and Na+

• The potential changes from + 20 to + 5 mv.
ii. Small outflow of K+
• fast sodium channels close and
(maintains membrane potential at about 0 mV)
• potassium ions leave the cell through open
potassium channels (K+ efflux).

{c} Rapid repolarization Phase 3-(100-150 ms)

• Ca2+ channels close and slow K + channels

open: rapid K+ efflux (out flow).
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 Ionic basis for excitability (Fast AP)
Phase 4: Resting membrane potential

• The permeabilities for sodium, potassium and calcium return to their

resting levels. Because PK is the highest. The membrane potential is
about -90 mV.

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 2. Rhythmicity (Automaticity)
Definition: It is the ability of the heart to initiate its own impulses (beat)
continuously and regularly independent of nervous connection.
It describes the origin of the electrical activity of the heart.

Myogenic nature of the cardiac action potential

• The contraction of the heart is myogenic – meaning that the signal for
cardiac compression arises within the heart tissue itself.

• In other words, the signal for a heart beat is initiated by the heart muscle
cells (cardiomyocytes) rather than from brain signals.
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 2. Rhythmicity (Automaticity)
Origin of the cardiac impulses:
initiated in the automatic cells/ Autorhythmic cells or nodal tissues :
 SA node = (sinus rhythm) = 90-110/min., (highest rhythm = pacemaker)
 AV node = (nodal rhythm)= 45- 60 / min.
 Purkinje fiber = 30/min.
 Ventricular muscle = 20 – 40/ min.
Idioventricular rhythm if SA node & AV node are damaged or inhibited by vagal stimulation.

Abnormal Pacemakers—“Ectopic” Pacemaker : Occasionally some other part of the heart

develops a rhythmical discharge rate that is more rapid than that of the sinus node.
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 Mechanism of Autorythmicity
Ionic basis for slow cardiac AP
Shows spontaneous pacemaker potential or
prepotential followed by spontaneous AP.
Stages of slow AP in automatic cells
Rapid depolarization:
0
When the potential reaches a threshold voltage of
3
about –40 millivolts, the L-type calcium channels 4

become activated, causing the action potential.

(mainly)
Increase in Na influx (little)
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 Mechanism of Autorythmicity
Ionic basis for slow cardiac AP
Plateau absent
Repolarization upto -40 mV.

• within about 100 to 150 milliseconds after opening

L-type calcium channels closes and second, at
about the same time greatly increased numbers of
potassium channels open & large quantities of
potassium ions diffuse out of the fiber. Both these
effects reduce the intracellular potential back
to its negative resting level (-40 mV).
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 Mechanism of Autorythmicity
Ionic basis for slow cardiac AP
Then continuous hyperpolarization:
-40 to – 60 mV

• potassium channels remain open for another

few tenths of a second, temporarily continuing
movement of positive charges out of the cell,

• with resultant excess negativity inside the

fiber; this process is called hyperpolarization
at the termination of the action potential.
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 Mechanism of Autorythmicity
Ionic basis for slow cardiac AP-: Pacemaker potential
Why is this new state of hyperpolarization not
maintained forever? = unstable RMP. (-55 to - 60 mV)

• The reason is that during the next few tenths of a second

after the action potential is over, progressively more and
more potassium channels close.

• The inward-leaking sodium (“funny” current) and

calcium ions once again overbalance the outward flux of
potassium ions, which causes the resting potential to drift
upward once more, finally reaching the threshold level for
discharge at a potential of about –40 millivolts.
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 Mechanism of Autorythmicity
Ionic basis for slow cardiac AP-: Pacemaker potential
• This unstable RMP is called prepotential or
"pacemaker potential”.

Definition : It is slow diastolic depolarization

between the action potential, when reaches the firing
level spontaneous regular action potentials are
generated= triggers the next impulse.

Cause : It is due to continuous Na+ & Ca++ +influx

(LEAKY /FUNNY Channels=Natural leakiness to Na+ &
Ca++) and decreased K+ efflux
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• Because this channel is activated following
hyperpolarization, it is referred to as an “h”
channel;

• however, because of its unusual (funny)

activation it is called as “f” channel and the
current produced as “funny current.”

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 Importance of Pacemaker potential or
Prepotential
1. It is the cause of rhythmicity (automaticity).

2. The rate of slope of prepotential determines the heart rate. The more is the slope, the more
will be the heart rate).

(i.e. the speed with which it is reached to the firing level determine the rate of the tissue
discharge.)

• Note-: Although SA nodal rhythm is more than 90 beat/min. yet the heart rate (as measured by
counting the radial pulsations) is only 70 beat/min.

• This is due to the effect of vagus nerve on rhythmicity of SA node decreasing it to about 70
beat/min (vagal tone).

• Factors affecting Heart rate and rhythmicity = chronotropic effect

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 3. Conductivity
• Definition : It is the ability of the cardiac muscle to conduct (transmit) the excitation
waves (action potential) initiated in the SA node to all parts of the heart in (the form
of depolarization).

• This is mediated through the conductive system of the heart

• Rapid Transmission in the Ventricular Purkinje System

• Caused by a very high level of permeability of the gap junctions at the intercalated discs
between the successive cells that make up the Purkinje fibers

• One-Way Conduction Through the A-V Bundle

• In only 0.03 second: cardiac impulse passes from the bundle branches in the ventricular
septum to the terminations of the Purkinje fibers
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Route of spread of electrical activity
through myocardium.
SA node

AV node

Bundle of His

Bundle Branches

Conducting System of Heart

Purkinje fibers
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Rate of propagation of cardiac impulses
Delay of Impulse Conduction from
Tissue Conduction rate the Atria to the Ventricles
(m/s)
Atrial muscle 0.4

Atrial pathways 1

AV node 0.05

Bundle of His 1

Purkinje system 4-5

Ventricular muscle 0.5-1

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 Temporal relationship between mechanical
and electrical events.
Excitation-Contraction Coupling in Cardiac muscle
• Cardiac mechanical
contraction is triggered by
electrical activation via an
intracellular calcium-
dependent process known as
excitation–contraction
coupling

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 Mechanical properties
(1) Contractility : It is the ability of the heart to pump blood against the peripheral
resistance.

(2) All or none law: “Stimuli causes the cardiac muscle to contracts maximally or not
at all, provided that all factors affecting contraction are kept constant”.

• This is because the cardiac muscle acts as a functional syncytium (as one unit).

(3) The cardiac muscle cannot be tetanized:

• This is due to long absolute refractory period in the cardiac muscle during which its
excitability is completely lost.

• ARP ends by the end of systole, and first part of diastole.

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 Mechanical properties
(4) Length - tension relationship (Starling law) :

• “The force of contraction of the cardiac muscle is directly proportional to the

initial length of the cardiac muscle fiber within limit”

• i.e. the greater the initial length of the cardiac muscle fiber, the stronger will be
the force of its contraction.

• Initial length of cardiac muscle fibers is determined by the degree of

diastolic filling.

Note: Factors affecting myocardial contractility (Force)= Ionotropic factors.

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 Mechanical properties
(5) Force - velocity relationship : The velocity of contraction is inversely proportional to
afterload and directly proportional with preload.

• Pre-load: The load on muscle before it begins to contract. It means the force which stretch the
muscle fibers and increase its length before contraction.

• In the heart the preload is the amount of blood returns to the heart and fill the ventricle at
end of diastole (EDV=end diastolic volume ).

• After-load: the force which act on the muscle after its beginning of contraction and resist the
contraction and decreases its velocity.

• In the heart the increase in the mean aortic pressure opposes the contraction power of the
ventricle.
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 Mechanical properties
(6) Force-frequency relationship
(i) Staircase (or treppe ) phenomenon :

• When the isolated heart is stimulated by successive maximal stimuli (constant), the force of

contraction increases gradually for the first few contractions and then it remains
the same.
• Explanation:

• The increase in contractility is due to: (Beneficial effect)

• 1. Increase the availability of Ca++ inside muscle cytoplasm.

• 2. Increase in the warmth --> increases the rate of metabolic processes and chemical reactions.
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 Mechanical properties
(6) Force-frequency relationship

(ii)-Extrasystole: Following an interval of constant frequency, if an impulse comes

early (in diastole), it causes a weak contraction called extrasystole then followed
by compensatory pause

(iii)-Beat loss:

• Following an interval of constant frequency of beats if an impulse is absent, the

following contraction after this period of rest becomes more powerful.
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 Reference:

• Guyton and Hall Textbook of Medical Physiology: 13th edition

Thank You

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