Physiology of the

heart

Department of Human Physiology

Medical University of Lublin
Physiology of the heart

The heart
Heart muscle
Rhythmical excitation of the heart
The heart as a pump
The function of the heart valves
Heart sounds
 Physiology of the heart
Functions of the heart are:
– beating (due to
automaticity)
– pumping blood (due to
muscle contraction)

- weight of the heart – 450 g

- it pumps 80 milion gallons in
lifetime
 Normal anatomy of the myocardium

Left lateral view

Left anterior oblique view

Anterior view
 Functionaly heart is divided into:

a right heart that pumps blood through the

lungs,
a left heart that pumps blood through the
peripheral organs
Right and left heart is a pulsatile two-chamber
pump composed of an atrium and a ventricle
Anatomy of the heart

Anterior view
Anatomy of the heart

Left lateral view

Anatomy of the heart

Left anterior oblique view

Anatomy of the heart

Cardiac anatomy - Short axis view

 Gross anatomy of the heart, oblique view

The ventricles supply the main pumping force that propels the
blood either
(1) through the pulmonary circulation by the right ventricle
(2) through the peripheral circulation by the left ventricle.
Anatomy of the heart

Gross anatomy of the heart, exterior and venticles

 Anatomy of the heart

• Gross
anatomy of
the heart,
valves and
coronary
arteries
Anatomy of the heart
Anatomy of the heart
Normal cardiothoracic imaging landmarks,
AP view
Normal cardiothoracic imaging landmarks,
lateral view
X-RAY EXAMINATION
Gross structure of the myocardium
 Physiology of Cardiac Muscle

types of cardiac
muscle:
- atrial
- ventricular

cross-section

longitudinal section
 Physiologic Anatomy of
Cardiac Muscle

cardiac muscle fibers arranged in a

latticework, with the fibers dividing,
recombining, and then spreading again
cardiac muscle is striated in the same
manner as in typical skeletal muscle.

cardiac muscle has typical myofibrils that contain

actin and myosin filaments
almost identical to those found in skeletal muscle
 Physiologic Anatomy of Cardiac Muscle

Cardiac Muscle is a Syncytium

It has the intercalated discs: they are actually cell

membranes that separate individual cardiac muscle cells
from one another.

At each intercalated disc the cell membranes fuse with one

another in such a way that they form permeable
"communicating" junctions (gap junctions)
that allow almost totally free diffusion of ions.

The action potentials travel easily from one cardiac

muscle cell to the next, through the intercalated discs
 Cardiac muscle
longitudinal section

cross-section

intercalated discs
"gap junctions"
nucleus
 Conductive muscle fibres
specialised excitatory
and conductive muscle
longitudinal section fibres
(96x)

Purkinje
fibre cross-section
(96x)
 Physiology of Cardiac Muscle
The atrial and ventricular types of muscle contract in
much the same way as skeletal muscle,
except that the duration of contraction is much longer.

The specialized excitatory and conductive fibers contract

only feebly because they contain few contractile fibrils

they exhibit either automatic rhythmical electrical

discharge in the form of action potentials or
conduction of the action potentials through the
heart, providing an excitatory system that controls the
rhythmical beating of the heart.
 Anatomy of the heart

The heart actually is composed of two syncytiums:

the atrial syncytium that constitutes the walls of the two
atria,
the ventricular syncytium that constitutes the walls of the
two ventricles
Normally, potentials are not conducted from the atrial
syncytium into the ventricular syncytium directly through
this fibrous tissue.
they are conducted only by way of a specialized
conductive system called the A-V bundle.
 Action Potentials in Cardiac Muscle
the intracellular potential rises
from
a very negative value, about
-85 millivolts,
to a slightly positive value,
about +20 millivolts
After the initial spike, the
membrane remains
depolarized for about 0.2
second, exhibiting a plateau, The presence of this plateau
causes ventricular contraction to
followed at the end of the last much longer (15 times)
plateau by abrupt than contraction of the skeletal
repolarization muscle.
 Action Potentials in Cardiac Muscle
In cardiac muscle, the action potential is caused by
opening of two types of channels:
(1) fast sodium channels - the same as those in skeletal
muscle
(2) slow calcium channels, which are also called calcium-
sodium channels
remain open for several tenths of a second.
During this time, a large quantity of calcium and sodium ions
flows to the interior of the cardiac muscle fiber,
this maintains a prolonged period of depolarization, causing the
plateau in the action potential.
Further, these calcium ions activate the muscle contractile process
 Action Potentials in Cardiac Muscle

Immediately after the onset of the action

potential, the permeability of the cardiac muscle
membrane for potassium ions decreases about
fivefold, an effect that does not occur in
skeletal muscle.

the decreased potassium permeability during

the action potential plateau prevents early
return of the action potential voltage to its
resting level
 Velocity of Signal Conduction
in Cardiac Muscle

The velocity of conduction of the excitatory action potential

signal along both atrial and ventricular muscle fibers
is about 0.3 to 0.5 m/sec,

The velocity of conduction in the specialized heart conductive

system-in the Purkinje fibers - is as great as 4 m/sec in most
parts of the system,
which allows reasonably rapid conduction of the excitatory
signal to the different parts of the heart.
 Refractory Period of Cardiac Muscle
The refractory period of the heart is the interval of time,
during which a normal cardiac impulse cannot re-excite an
already excited area of cardiac muscle.
The normal refractory period of the ventricle is 0.25 to 0.30
second, which is about the duration of the prolonged plateau
action potential.
There is an additional relative refractory period of about
0.05 second during which the muscle is more difficult than
normal to excite but nevertheless can be excited by a very
strong excitatory signal (the early "premature" contraction).
The refractory period of atrial muscle is much shorter (about
0.15 second for the atria compared with 0.25 to 0.30 second
for the ventricles).
Refractory Period of Cardiac Muscle
 Duration of Contraction

Cardiac muscle begins to contract a few milliseconds

after the action potential begins and continues to
contract until a few milliseconds after the action
potential ends.

Therefore, the duration of contraction of

cardiac muscle is mainly a function of the
duration of the action potential, including the
plateau - about 0.2 second in atrial muscle
and 0.3 second in ventricular muscle.
 Excitatory and conductive system of the heart
(1) generating rhythmical electrical impulses to cause
rhythmical contraction of the heart muscle and
(2) conducting these impulses rapidly through the
heart.
When this system functions normally,
the atria contract about one sixth of a second ahead of
ventricular contraction,
which allows filling of the ventricles before they pump
the blood through the lungs and peripheral circulation.
it allows all portions of the ventricles to contract almost
simultaneously which is essential for most effective
pressure generation in the ventricular chambers.
 Rhythmical Excitation of the Heart

This rhythmical and conductive system of the heart is

susceptible to damage by heart disease,

especially by ischemia of the heart tissues resulting

from poor coronary blood flow.
The result is often:
-a bizarre heart rhythm or
- abnormal sequence of contraction of the
heart chambers,
-the pumping effectiveness of the heart often
is affected severely
-even to the extent of causing death.
 Excitatory and conductive system
This system contains:
The sinus node (sinoatrial node)
in which the normal rhythmic impulse is generated.

Internodal pathways
that conduct the impulse from sinus node to the A - V node.

The A - V node (atrioventricular node)

in which the impulse from the atria is delayed before passing into
the ventricles

The A - V bundle
which conducts the impulse from the atria into ventricles

The left and right branches of A - V bundle

which conduct the cardiac impulse to all parts of the ventricles
Excitatory and conductive system
 Sinus (Sinoatrial) Node

A small, flattened, ellipsoid

strip of specialized cardiac
muscle about 3 millimeters
wide, 15 millimeters long, and
1 millimeter thick.

It is located in the superior posterolateral wall of the

right atrium immediately below and slightly lateral to
the opening of the superior vena cava.

the sinus nodal fibers connect directly with the atrial

muscle fibers, so that any action potential that begins
in the sinus node spreads immediately into the atrial
muscle wall.
Automatic Electrical Rhythmicity of the Sinus
Fibers

Some cardiac fibers have the capability of self-excitation,

a process that can cause automatic rhythmical discharge and
contraction.

This is especially true of the fibers of the heart's specialized

conducting system, including the fibers of the sinus node.

For this reason, the sinus node ordinarily controls the rate of
beat of the entire heart,
 Mechanism of Sinus Nodal
Rhythmicity

the "resting membrane potential" of the sinus nodal fiber between

discharges has a negativity of about -55 to -60 millivolts, in
comparison with -85 to -90 millivolts for the ventricular muscle fiber.

At this level of -55 millivolts, the fast sodium channels mainly

have already become "inactivated,"
which means that they have become blocked.

Therefore, only the slow sodium-calcium channels

can open (i.e., can become "activated") and thereby
cause the action potential.
the atrial nodal action potential is slower to develop than the
action potential of the ventricular muscle.
after the action potential does occur, return of the potential to
its negative state occurs slowly as well, rather than the abrupt
return that occurs for the ventricular fiber.
 Self-Excitation of
Sinus Nodal Fibers

Because of the high sodium ion concentration in the

extracellular fluid outside the nodal fiber,
as well as a moderate number of already open sodium channels,
positive sodium ions from outside the fibers normally tend to
leak to the inside.

Therefore, between heartbeats, influx of positively charged

sodium ions causes a slow rise in the resting membrane
potential in the positive direction.

the "resting" potential gradually rises between each two heartbeats

When the potential reaches a threshold voltage of about -40 millivolts,

the sodium-calcium channels become "activated,"

thus causing the action potential

Therefore,
the inherent leakiness of the
sinus nodal fibers to sodium
and calcium ions causes their
self-excitation.
 Why does this leakiness to sodium and calcium ions not cause the

sinus nodal fibers to remain depolarized all the time?

First, the sodium-calcium channels become inactivated (i.e., they close)

within about 100 to 150 milliseconds after opening,
Second, at about the same time, greatly increased numbers of potassium
channels open.

Therefore, influx of positive calcium and sodium ions through the sodium-
calcium channels ceases, while at the same time large quantities of positive
potassium ions diffuse out of the fiber.
Both of these effects reduce the intracellular potential back to its negative
resting level and therefore terminate the action potential.

Furthermore, the 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 is called
hyperpolarization. The hyperpolarization state initially carries the "resting"
membrane potential down to about -55 to -60 millivolts at the termination
of the action potential.
 Internodal Pathways and Transmission of the Cardiac
the anterior
Impulse Through the Atria middle
The ends of the sinus nodal fibers posterior internodal
pathways.
connect directly with surrounding
atrial muscle fibers.

Action potentials originating in the

sinus node travel outward into
these atrial muscle fibers.

The velocity of conduction in most

atrial muscle is about 0.3 m/sec

but conduction is more rapid, about

1 m/sec, in several small bands of
atrial fibers

The cause of more rapid velocity of conduction in these bands is the

presence of specialized conduction fibers.
 Atrioventricular Node, and Delay of Impulse
Conduction from the Atria to the Ventricles
The atrial conductive system is organized so that the cardiac impulse does not travel
from the atria into the ventricles too rapidly;
this delay allows time for the atria to empty their blood into the ventricles before
ventricular contraction begins.
It is primarily the A-V node and its adjacent conductive fibers that delay
this transmission into the ventricles.
The A-V node is located in the posterior wall of the right atrium
immediately behind the tricuspid valve
the impulse, after traveling through the internodal pathways, reaches the A-V
node about 0.03 second after its origin in the sinus node.
Then there is a delay of another 0.09 second in the A-V node itself before the
impulse enters the penetrating portion of the A-V bundle, where it passes into the
ventricles.
A final delay of another 0.04 second occurs mainly in this penetrating A-V
bundle, which is composed of multiple small fascicles passing through the fibrous
tissue separating the atria from the ventricles.
 Atrioventricular Node, and Delay of Impulse
Conduction from the Atria to the Ventricles

Thus, the total delay in the A-V nodal and A-V bundle system
is about 0.13 second.

The slow conduction in the transitional, nodal, and penetrating A-V

bundle fibers is caused mainly by diminished numbers of gap
junctions between successive cells in the conducting pathways,
 Rapid Transmission in
the Ventricular Purkinje System
They are very large fibers, even larger than the normal ventricular muscle
fibers, and they transmit action potentials at a velocity of 1.5 to 4.0
m/sec,
a velocity about 6 times that in the usual ventricular muscle,
and 150 times that in some of the A-V nodal fibers.
This allows almost instantaneous transmission of the cardiac impulse
throughout the entire remainder of the ventricular muscle.

The rapid transmission of action potentials by Purkinje fibers is

believed to be 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.
Therefore, ions are transmitted easily from one cell to the next,
thus enhancing the velocity of transmission.
 One-Way Conduction
Through the A-V Bundle

A special characteristic of the A-V bundle is

the inability, except in abnormal states,

of action potentials to travel backward from the
ventricles to the atria.

This prevents re-entry of cardiac impulses by this route from

the ventricles to the atria, allowing only forward conduction
from the atria to the ventricles.
that everywhere, except
at the A-V bundle, the
atrial muscle is
separated from the
ventricular muscle by a
continuous fibrous
barrier

This barrier normally acts as an insulator to prevent

passage of the cardiac impulse between atrial and
ventricular muscle through any other route besides
forward conduction through the A-V bundle itself.
Distribution of the Purkinje Fibers in the Ventricles:
The Left and Right Bundle Branches

Then the A-V bundle divides into left and right bundle branches that
lie beneath the endocardium on the two respective sides of the
ventricular septum.
Each branch spreads downward toward the apex of the ventricle,
progressively dividing into smaller branches.
These branches in turn course sidewise around each ventricular
chamber and back toward the base of the heart.
The ends of the Purkinje fibers penetrate about one third the way
into the muscle mass and finally become continuous with the cardiac
muscle fibers.

From the time the cardiac impulse enters the bundle branches in the
ventricular septum until it reaches the terminations of the Purkinje
fibers, the total elapsed time averages only 0.03 second
Transmission of the Cardiac Impulse in the Ventricular
Muscle
Once the impulse reaches the ends of the Purkinje fibers, it is
transmitted through the ventricular muscle mass by the
ventricular muscle fibers themselves.
The velocity of transmission is now only 0.3 to 0.5 m/sec,
one sixth that in the Purkinje fibers.
The cardiac muscle wraps around the heart in a double spiral, with fibrous
septa between the spiraling layers;
therefore, the cardiac impulse does not necessarily travel directly outward
toward the surface of the heart but instead angulates toward the surface
along the directions of the spirals.

the total time for transmission of the cardiac impulse from

the initial bundle branches to the last of the ventricular
muscle fibers in the normal heart is about 0.06 second.
the impulse spreads at
moderate velocity
through the atria but is
delayed more than 0.1
second in the A-V nodal
region before appearing
in the ventricular septal
A-V bundle.

Once it has entered this bundle, it spreads very rapidly

through the Purkinje fibers to the entire endocardial
surfaces of the ventricles.
Excitatory and conductive system

Isochronic surfaces of the ventricular activation.gif

Normal conduction pathway
Normal conduction pathway
 The Sinus Node
as the Pacemaker of the Heart

the A-V nodal fibers, when not stimulated from some outside source,
discharge at an intrinsic rhythmical rate of 40 to 60 times per
minute,
the Purkinje fibers discharge at a rate somewhere between 15 and
40 times per minute.
These rates are in contrast to the normal rate of the sinus
node of 70 to 80 times per minute.

the sinus node controls the beat of the heart because its rate of
rhythmical discharge is faster than that of any other part of the
heart.
Therefore, the sinus node is virtually always
the pacemaker of the normal heart.
 A pacemaker elsewhere than the sinus node is
called an "ectopic" pacemaker

An ectopic pacemaker causes an abnormal

sequence of contraction of the different parts of
the heart and can cause significant debility of
heart pumping.
Role of the Purkinje System in Causing Synchronous
Contraction of the Ventricular Muscle
normally the cardiac impulse arrives at almost all portions of the
ventricles within a narrow span of time, exciting the first
ventricular muscle fiber only 0.03 to 0.06 second ahead of
excitation of the last ventricular muscle fiber.

This causes all portions of the ventricular muscle in both

ventricles to begin contracting at almost the same time and then
to continue contracting for about another 0.3 second.

Effective pumping by the two ventricular chambers

requires this synchronous type of contraction.
Control of Heart Rhythmicity and Impulse Conduction
by the Cardiac Nerves:
The heart is supplied with both sympathetic and
parasympathetic nerves,
 Nervous regulation of
action of heart
The heart is supplied with both
sympathetic and parasympathetic nerves

The parasympathetic nerves (the

vagi)
are distributed mainly to
the sinus
the A - V nodes The sympathetic nerves,
the atrial muscle are distributed to
but very less to the ventricular all parts of the heart
muscle. with strong representation to
the ventricular muscle
as well as to the other parts.
 Myocardial action potential
Phase 0 – rapid upstroke
(voltage – gated Na+ channels open)

Phase 1 – initial repolarisation

(inactivation of voltage – gated Na+ channels;
voltage gated K+ channels begin to open)

Phase 2 – plateau
(Ca2+ influx through voltage – gated Ca2+ channels
balances K+ –efflux;
Ca 2+ influx triggers myocyte contraction)

Phase 3 – rapid repolarisation

massive K+ efflux
due to opening of voltage – gated slow K+ channels
closure of voltage – gated Ca 2+ channels

Phase 4 – resting potential

(high K+ permeability through K+ channels)
Premature contraction and compensatory pause
 Nervous regulation of
action of heart
Parasympathetic Sympathetic
Effect stimulation stimulation
Inotropic effect negative positive
(strength of contraction)

Chronotropic effect negative positive

(frequency of contractions)

Tonotropic effect negative positive

(tonus of heart wall)
Bathmotropic effect negative positive
(excitability)

Dromotropic effect
(velocity of conduction negative positive
through the conductive system)
 Cardiac cycle
The cardiac cycle includes
all events realted to the flow of blood through the
heart during one complete heart beat.

The cardiac events that occur from the

beginning of one heartbeat
to the beginning of the next.
 The cardiac cycle

Each cycle is initiated by

spontaneous generation of an action potential
in the sinus node
The cardiac cycle consists of

a period of relaxation called diastole

during which the heart fills with blood

a period of contraction called systole

 Function of the Atria
as Primer Pumps

Blood normally flows continually

from the great veins into the atria

about 80 per cent of the blood

flows directly through the atria into the ventricles

atrial contraction usually causes

an additional 20 per cent filling of the ventricles

the atria simply function as primer pumps that increase

the ventricular pumping effectiveness as much as 20 per cent
 Pressure Changes
in the Atria
The a wave is caused by atrial
contraction
the right atrial pressure increases 4 to 6 mm Hg during atrial contraction
the left atrial pressure increases about 7 to 8 mm Hg

The c wave occurs when the ventricles begin to contract

it is caused:
by slight backflow of blood into the atria at the onset of ventricular
contraction
by bulging of the A-V valves backward toward the atria
because of increasing pressure in the ventricles
The v wave occurs toward the end of ventricular contraction
it results from slow flow of blood into the atria from the veins
while the A-V valves are closed during ventricular contraction
 Function of
the Ventricles as Pumps
Filling of the Ventricles
during ventricular systole,
large amounts of blood accumulate
in the right and left atria because of the closed A-V valves

as soon as systole is over

the ventricular pressures fall again to their low diastolic values

the moderately increased pressures that have developed in

the atria during ventricular systole immediately push the A-V
valves open and

allow blood to flow rapidly into the ventricles

This is called the period of rapid filling of the ventricles

 Diastole

1/3 The period of rapid filling lasts for about the first third of diastole.

During the middle third of diastole

1/3 only a small amount of blood normally flows into the ventricles

(blood that continues to empty into the atria

from the veins and passes through the atria
directly into the ventricles)

1/3 During the last third of diastole

the atria contract and give an additional thrust to the inflow
of blood into the ventricles;
about 20 per cent of the filling of the ventricles during each heart cycle
Emptying of the Ventricles During Systole

1. Period of Isovolumic (Isometric) Contraction

2. Period of Ejection
3. Period of Isovolumic (Isometric) Relaxation
 Period of Isovolumic Contraction
Immediately after ventricular contraction
begins the ventricular pressure rises
abruptly causing the A-V valves to close.

Then an additional 0.02 to 0.03

second is required for the ventricle to
build up sufficient pressure to push
the semilunar (aortic and pulmonary)
valves open against the pressures in
the aorta and pulmonary artery.
during this period,
contraction is occurring in the ventricles,
but there is no emptying
The tension is increasing in the muscle
but little or no shortening of the muscle fibers is occurring.
 Period of Ejection
the right ventricular pressure the left ventricular pressure rises
slightly above 8 mm Hg slightly above 80 mm Hg

the ventricular pressures push the semilunar valves open

 Period of Ejection
the left ventricular pressure
above 80 mm Hg
 Period of Ejection
the right ventricular pressure
above 8 mm Hg
 Period of Ejection

about 70 per cent of the blood emptying

1/3
occurring during the first third of the period of ejection

the period of rapid ejection

2/3 the remaining 30 per cent emptying during the next two thirds

the period of slow ejection

 Period of Isovolumic Relaxation

At the end of systole

ventricular relaxation begins suddenly

the right and left intraventricular pressures

decrease rapidly
 Period of Isovolumic Relaxation
The elevated pressures in the distended large arteries
immediately push blood back toward the ventricles

which snaps the aortic and

pulmonary valves closed

For another 0.03 to 0.06 second,

the ventricular muscle continues to relax

even though the ventricular

volume does not change
 Period of Isovolumic Relaxation
During this period:

the intraventricular pressures

decrease
rapidly back
to their low diastolic levels

Then the A-V valves open

to begin a new cycle of ventricular pumping
 Volumes …
During diastole, normal filling of the ventricles increases the
volume of each ventricle to about 110 to 120 milliliters.

This volume is called the end-diastolic volume

As the ventricles empty during systole,

the volume decreases about 70 milliliters

It is called the stroke volume output

The remaining volume in each ventricle, about 40 to 50 milliliters,

is called the end-systolic volume.
The fraction of the end-diastolic volume that is ejected
is called the ejection fraction equal to about 60 per cent
 Volumes …

when the heart contracts strongly

the end-systolic volume
can be decreased to as little as 10 to 20 milliliters

when large amounts of blood flow into the

ventricles during diastole
the ventricular end-diastolic volumes can become
as great as 150 to 180 milliliters in the healthy heart

the stroke volume output

can be increased to more than double normal
 Function of the Valves

The A-V valves (the tricuspid and mitral valves)

prevent backflow of blood
from the ventricles to the atria during systole

The semilunar valves (the aortic and pulmonary artery valves)

prevent backflow
from the aorta and pulmonary arteries
into the ventricles during diastole

Valves close and open passively

 Function of the Valves

Pulmonic
valve
 Function of the Papillary Muscles
The papillary muscles attach
to the vanes of the A-V valves
by the chordae tendinae

The papillary muscles contract

when the ventricular walls
contract,
they do not help the valves to
close!
they pull the vanes of the valves inward toward the
ventricles to prevent their bulging toward the atria during
ventricular contraction
 Aortic and Pulmonary Artery Valves

the high pressures in the arteries at the end of systole

cause the semilunar valves to snap to the closed position
because of smaller
openings,
the velocity of blood ejection
through the aortic and
pulmonary valves is far
greater than that through the
much larger A-V valves
because of the rapid closure and rapid
ejection
the edges of the aortic and pulmonary valves are
subjected to much greater mechanical abrasion
than are the A-V valves
 The heart sounds
The first heart sound is caused by
- vibration of atrio – ventricular valves immediately after
closure,
- vibration of walls of the heart and
- vibration of major vessel walls
The second heart sound is caused by
- vibration of semilunar valves when they closure
The third heart sound is caused by
rumbling motion of blood flowing into the ventricles

The fourth heart sound occurs when the atria contract

and is caused by inrush of blood into the ventricles
Areas of auscultation of Listening to the sounds of
the body
normal heart sounds with the aid of stethoscope
is called auscultation.
aortic area
pulmonic area

mitral area

tricuspid area
(Erb point)
The heart sounds
Heart murmurs
Mitral
stenosis
Mitral
regurgitation
Aortic
stenosis
Aortic regurgitation
Thank you !