CARDIAC MUSCLE
Maryam Fida (o-1827)
Source: The Guyton and Hall Physiology

Functional Anatomy and
Properties of Myocardium
Action Potential in Cardiac
Muscle

Physiologic Anatomy of Heart

• In the heart there is Atrial muscle and Ventricular muscle which are
separated from each other by the fibrous AV Rings containing Valves.
• ATRIAL MUSCLE: thin walled. There are two sheets, superficial and deep
sheet. Superficial sheet is common over both atria. Deep sheet is separate for
each atrium. Muscle fibers in the deep sheet are at right angle to the muscle
fibers in the superficial sheet.
• FUNCTIONS OF THE ATRIUM:
• 1. Receive venous blood from large veins. So atria act as reservoir.
• 2. Conduct the blood into the ventricles.
• 3. Atrial contraction is responsible for last 25 % of ventricular filling.
• 4. In the right atrium there is SA Node(Pace maker) and AV node.
• 5. In the wall of the atria, there are low pressure stretch receptors and
these are involved in various reflexes like brain bridge reflex and left atrial
reflex.
• 6. Atria also produce a hormone i.e. Atrial Natriuretic Hormone.
Whenever NaCl increases in ECF, it causes release of ANH which causes
natriuresis.
• VENTRICULAR MUSCLE:
• Much thicker than atrial muscle. Thickness of right ventricle wall is 3-4 mm
and thickness of left ventricle is 8 – 12 mm.

FUNCTIONAL ANATOMY OF MYOCARDIUM
1.Involuntary
2.Has cross striations
3.Each cardiac muscle fiber consists of a
number of cardiac cells, united at ends in
series. Where as in skeletal muscle each
muscle fiber is individual cell.
4.Cardiac muscle cells are branching and
interdigitate.
5.Single central nucleus in each cell.
6. Atrial muscle and ventricular muscle act
as separate functional syncytium and
impulses from atria are conducted to
ventricles through the AV Node and AV
Bundle.
7. Sarcoplasmic system is present. In
skeletal muscle triad is at the junction of A
and I bands. In cardiac muscle T Tubules
are much large and thus in cardiac muscle
if we take a section it may form a diad or a
triad. And these diads and triads are
present at the level of Z Disks.
8.Between adjacent cardiac cells there are
side to side and end to end connections
and these are the intercellular junctions.
These junctions are Gap Junctions. Or
intercalated discs
9.When one part of myocardium is excited
the whole muscle is excited.
10.Whole myocardium obeys all or none
law as a whole.
11.No spike potential but action potential
with plateau.
12.Has got long refractory period.
Absolute refractory period in ventricular
muscle is 250 – 300 milli sec.
In atrial muscle Absolute refractory period
is 150 milli sec
Because of long refractory period cardiac
muscle cannot be tetanized.

METABOLIC PROPERTIES OF CARDIAC MUSCLE
1.Highly vascular having abundant blood supply.
2.Numerous mitochondria and mitochondria may form 25 – 30 % of
whole mass.
3.Increased myoglobin content.
4.Slow ATPase activity
5.At basal conditions heart, gets
• 35% of energy from CHO,
• 60% from fats and
• among fats 50% are free fatty acids
• remaining 5 % is obtained from ketone bodies and amino acids.
• 6.During starvation and in uncontrolled diabetes mellitus , the
energy obtained from CHO decreases and from fats increases.
7.Normally less than 1% of total energy is obtained from the
anaerobic metabolism.
8.In hypoxic conditions, cardiac muscle can obtain up to 10% of
energy from the anaerobic metabolism.

Properties of Myocardium
• Conductivity
• Automaticity & Rhythmicity
• Excitability
• Contractility

Properties of Myocardium
Conductivity
 Ability to conduct AP or cardiac
impulses.
 The property of conductivity
varies in different parts of the
heart.
 Velocity of conduction in:
• Atril Muscle: 0.3 m/sec
• Inter nodal pathway: 1 m/sec
• AV Node: 0.1 m/sec (slowest)
• Purkinge System: 1.5 – 4 m/sec
 Conductivity is affected by
autonomic stimulation.
Sympathetic increase the velocity
of conduction. Vagal stimulation
Slows down. Ischemia slows the
velocity of conduction
Automaticity & Rhythmicity
 Spontaneous generation of action
potential in heart without external
stimulation is called Automaticity. Self
Generation.
 It occurs at regular intervals so it is
called Rhythmicity.
 Automaticity in heart is Myogenic and
not neurogenic.
 SA NODE: 70 -80 Impulses/minute
 AV NODE: 40-60 / min
 AV Bundle/Purkinge system/Ventricles
15-40 /min
 SA Node having the highest rate of
impulse formation is called PACE
MAKER.
 ECTOPIC FOCUS: When a focus or site
other than SA node produces impulses
it is called Ectopic focus.

Properties of Myocardium
 Excitability
 Property to respond to stimuli.
 Heart responds to electrical,
mechanical and chemical stimuli.
 Contractility
 Property to undergo shortening.
 The tension developed during cardiac
muscle contraction is less than that
developed in Skeletal muscle
contraction.
 Shortening is slow as compared to
sk. Muscle
 Cardiac muscle obeys Frank’ s starling
law.
Greater the initial or resting length,
greater will be the force of contraction.
In heart the initial or resting length
depends upon end diastolic volume or
pressure. End diastolic volume depends
upon the venous return.
• Force of myocardial contraction is
increased by:
• Sympathetic stimulation
• Catecholamines
• Calcium ions
• Digitalis
• Thyroxine
• Glucagon
• Theophylline and caffeine.
• Force of myocardial contraction is
decreased by:
• Vagal stimulation
• Acidosis
• Barbiturates, quinidine,
procainamide
• Ischemia.
• The strength of contraction of
cardiac muscle depends to a great
extent on the concentration of
calcium ions in the extracellular
fluids

Action Potentials in Cardiac Muscle
(Ventricular Muscle)
• SA Nodal Action Potential – Pace Maker
potential
• Ventricular Muscle Action Potential
• Atrial Muscle Action Potential
• Purkinje System Action Potential

Phases of Ventricular Muscle Action
Potential
• Phase 0 – Up Stroke
• Phase I – Initial Repolarization
• Phase II – Plateau Phase
• Phase III – Repolarization
• Phase IV – Resting Membrane Potential

PHASE 0 - UPSTROKE
• It is the Upstroke of Action Potential
• Opening of Voltage Gated Sodium Channels at
-70 to -80 mV
• There is transient increase in Sodium
Conductance leading to rapid influx of Sodim
Ions causing membrane Depolarization.
• At the peak of Upstroke, the membrane
potential approaches the sodium Equilibrium
Potential.

PHASE I – Initial Repolarization
• It is a brief period of initial repolarization
• This phase results from
– Closure of voltage gated sodium channels leading
to Decreased sodium influx
– Opening of potassium channels leading to
potassium efflux.

PHASE II – Plateau Phase
• It is the plateau phase of the action potential
• There is slow opening of voltage gated calcium
channels at -30 to -40 mV
• There is excessive calcium influx during this phase
because of transient increase in calcium conductance
• This calcium influx is balanced by the Potassium efflux
leading to the production of plateau i.e. delay in the
repolarization
• During the plateau, outward and inward currents are
nearly equal so that the membrane potenital is stable
in this phase.
• Plateau phase is not part of reploarization. It is
sustained depolarization.

PHASE III – Repolarization
• During this phase, the calcium conductance
decreases due to closure of slow calcium
channels
• There is increase in the potassium
conductance leading to excessive efflux of
potassium and this is the only dominant
current during this phase.
• This results in the repolarization till the
potassium equilibrium potential is reached.

PHASE IV – Resting Membrane
Potenital
• During this phase the Membrane is in resting
state.
• RMP is -85 to -90 mv
• Activation of Na K Atpase pump