CIRCULATORY SYSTEM Physiology-8

LEARNING OBJECTIVES
Completing this course, students should be able to
Describe the structure and function of the conduction system
of the heart and compare the action potentials in each
part.
 Describe the way the electrocardiogram (ECG) is recorded,
the waves of the ECG, and the relationship of the ECG to
the electrical axis of the heart.
Name the common cardiac arrhythmias and describe the
processes that produce them.
 List the principal early and late ECG manifestations of
myocardial infarction and explain the early changes in
terms of the underlying ionic events that produce them.
 Describe the ECG changes and the changes in cardiac
function produced by alterations in the ionic composition of
the body fluids
REQUIRED KNOWLEDGE FROM PREVIOUS TOPICS
Structure of the heart
Membrane potentials
Action potentials
https://1da29564ffc94212c5733ac3ef259e6b1ca3e3c0.vetisonline.com/#!/browse/book/3-s2.0-C20170004883

Muscle contraction
https://1da29564ffc94212c5733ac3ef259e6b1ca3e3c0.vetisonline.com/#!/browse/book/3-s2.0-C20170004883
ITS RELEVANCE WITH CLINICAL TOPICS
In particular;
Cardiac failure
Dysrhythmias
CONTENTS
Physiology of Cardiac Muscle
Cardiac Cycle
Diastole and Systole
Relationship of the Electrocardiogram to the Cardiac Cycle
The Atria Function as Primer Pumps for the Ventricles
Pressure Changes in the Atria—a, c, and v Waves.
The Heart Valves Prevent Backflow of Blood During Systole
Aortic Pressure Curve
Graphic Analysis of Ventricular Pumping
Regulation of Heart Pumping
PHYSIOLOGY OF CARDIAC MUSCLE
PHYSIOLOGY OF CARDIAC MUSCLE
The heart, is actually two separate pumps
 a right heart that pumps blood through the lungs
 a left heart that pumps blood through the systemic circulation
 that provides blood flow to the other organs and tissues of the body.

Each of these is two-chamber

 Atrium/atria - a weak primer pump for the ventricle
 Ventricles- The main pump.
 per!kard !le çevr!l! kalb!
etrafı
>
- -
Koruya ve
yer!nde
tuten !k! katmanlı
PHYSIOLOGY OF CARDIAC MUSCLE Kese

The heart is surrounded by pericardium

 a two-layer sac
 which protects the heart and holds it in place.
>
-
e

e
PHYSIOLOGY OF CARDIAC MUSCLE
Cardiac rhythmicity >
-
kard!yak r!tm!kl!k
 a continuing succession of contractions *surekl! devam eden kasılmalar
 Regulated by special mechanisms,
 transmitting action potentials throughout the cardiac muscle to
cause the heart’s rhythmical beat.
PHYSIOLOGY OF CARDIAC MUSCLE
The heart has 3 types of muscle fibers:
 atrial muscle>
-
atr!yum kası
 ventricular muscle -
> ventr!küler
kas

 Specialized excitatory and conductive muscle fibers. >

- özelleşm"ş uyarıcı
ve !let!c! kas
↓
!letken
uyarıcı ve
PHYSIOLOGY OF CARDIAC MUSCLE
 Atrial muscle
 Ventricular muscle
 The first two contract in much the same way as skeletal muscle
 except that the duration of contraction is much longer.
 The plato phase
PHYSIOLOGY OF CARDIAC MUSCLE
 Specialized excitatory and conductive muscle fibers.
 They are excitatory and conductive fibers of the heart
 Their contraction is feeble.
 they discharge automatical rhythmical electrical activity as action potentials
 Or conduct the action potentials through the heart,
 providing an excitatory system that controls the rhythmical
beating of the heart.
CARDIAC MUSCLE ANATOMY
Cardiac muscle fibers looks like a lattice-work
 the fibers divide and recombine and then spread again.
They are striated like skeletal muscle.
 *A reflection of centromere organization.
Cardiac muscle has intercalated discs that connect
cytoplasms of muscle fibers
 Which give the muscle properties of syncytium
CARDIAC MUSCLE
ANATOMY
Ara d!sk
sol ventr!kuler kas kasılması
THE LEFT VENTRICULAR
MUSCLE CONTRACTION
The left ventricle’s muscle fiber layers have complex
organization
• The subepicardial layer spirals leftward and the
subendocardial layer spirals in the opposite
direction
• causing counterclockwise rotation of the apex of
the heart and clockwise rotation of the base of
the left ventricle during systol
• pulling the base downward toward the apex
during systole
• At the end of systole, the left ventricle recoils or
untwists during diastole to allow blood to enter
the pumping chambers rapidly.
 -

CARDIAC MUSCLE IS A SYNCYTIUM

The Intercalated discs enable the muscle fibers like one.
But atrial and ventricular fiber are seperated.
So A heart has 4 seperated syncytium
Although electricial discharges from excitatory fiber travel
free in each syncytium, they need special conductive fibers
to be conveyed to the others
 A-V bundle , a bundle of conductive fibers several millimeters in
diameter
ACTION POTENTIALS IN
CARDIAC MUSCLE
The action potential recorded in a
ventricular muscle fiber
≈105 millivolts (from −85 to +20
millivolts)
the membrane remains depolarized for
about 0.2 sec.
exhibiting a plateau , followed by abrupt
repolarization.
So the action potential lasts 15x of
skeletal muscle.
THE CAUSES THE LONG ACTION POTENTIAL AND
PLATEAU IN CARDIAC MUSCLE
1. the action potential of SM is caused by the sudden
opening of fast sodium channels
 that allow tremendous numbers of sodium ions to enter the skeletal muscle fiber from the
extracellular fluid.
 they remain open for only a few msec. and then abruptly close,
 After that repolarization occurs, and the action potential ends in a few msec.
THE CAUSES THE LONG ACTION POTENTIAL AND
PLATEAU IN CARDIAC MUSCLE
The action potential is caused by opening of two types of
channels:
a) voltage-activated fast sodium channels
 as those in skeletal muscle
b) L-type calcium channels
 They also called: slow calcium channels/calcium-sodium channels.
THE CAUSES THE LONG ACTION POTENTIAL AND
PLATEAU IN CARDIAC MUSCLE
This second type of channels differs from the first:
 slower to open
 remain open for several tenths of a second,
 allowing a large quantity of both calcium and sodium ions to flow
in the cardiac muscle fiber
 maintaining a prolonged depolarization
 causing the plateau in the action potential.
THE CAUSES THE LONG ACTION POTENTIAL AND
PLATEAU IN CARDIAC MUSCLE
2. After the onset of the action potential, the permeability
of the cardiac muscle membrane for potassium ions
decreases X5
 The origin of this effect is the excess calcium influx through the
calcium channels
 they close at the end of 0.2 to 0.3 second.
 The membrane permeability for potassium ions increases rapidly.
 This immediately returns the membrane potential to its resting
level
 Başlangıç repolar!zasyonu
PHASES OF CARDIAC
1
O -Kals!yum !yon geç!rgen
Osplato l!ğ! orlar
.

MUSCLE ACTION ↳
potasyum !yon gen!r-
senl!ğ! azal!t

POTENTIAL
·
hızlı repolar!zasyo
T
O

Faz
Phase 0 (Depolarization): Fast Sodium
Channels Open -
> hızlı
sodyum kanalları açılır O
d!nlev!m
Phase 1 (Initial Repolarization): Fast 20

hızlı sodyum kanalları kapaır

Sodium Channels Close hüre repolar!ze olmaya başlar
-
potans!yel!
K+ !yonları hurey! ferk eder
kallrıyla
>
-
12 +
Phase 2 (Plateau): Calcium Channels >
-
hall
Kals!yum kanalları açılır ve

Open and Fast Potassium Channels Close Potasyum knalları kapaır

E
Phase 3 (Rapid Repolarization): Calcium >
- kals!yum kanalları
kapaır ve
yavas potasyum
Channels Close and Slow Potassium kanalları açılı

Channels Open
Phase 4 (Resting Membrane Potential):
-go
↳ my
VELOCITY OF SIGNAL CONDUCTION IN CARDIAC
MUSCLE
Excitatory action potential signal contruction velocities
atrial and ventricular muscle fibers: ≈ 0.3 to 0.5 m/sec
≈ 1/250 of the velocity in very large nerve fibers
≈ 1/10 the velocity in skeletal muscle fibers.
≈ 4 m/sec in Purkinje fibers

>
REFRACTORY PERIOD OF CARDIAC MUSCLE
Cardiac muscle, is refractory to restimulation during the
action potential.
 The impulse cannot re-excite an already excited area of cardiac
muscle.
 The absolut refractory period of the ventricles: 0.25 to 0.30 sec,
 The relative refractory period: ≈0.05 second
 The refractory period of the atria: ≈0.15 sec
EXCITATION-CONTRACTION COUPLING
As it is skeletal muscle,
 action potatial cardiac myofibrils to contract
 This is Excitation-Contraction Coupling
But there are similarities and differences between two
types of muscle
EXCITATION-CONTRACTION COUPLING
Similar part
 The action potential spreads to the interior of the cardiac muscle
fiber along the membranes of the transverse (T) tubules.
 The membranes of the longitudinal sarcoplasmic tubules to cause
release of calcium ions into the muscle sarcoplasm.
 These calcium ions diffuse into the myofibrils and catalyze the
chemical reactions that promote sliding of the actin and myosin
filaments along one another.
EXCITATION-CONTRACTION COUPLING
The Differences
 The action potential opens voltage-dependent calcium channels in
the membrane of the T tubule
 Calcium ions also diffuse into the sarcoplasm from the T-tubule.
 The calcium activates calcium release channels, also called
ryanodine receptor channels, in the SR membrane
 triggering the release of calcium into the sarcoplasm.
E-C COUPLING

Mechanisms of excitation-
contraction coupling and
relaxation.
• ATP, Adenosine
triphosphate
• RyR, ryanodine receptor
Ca2+ release channel
• SERCA, sarcoplasmic
reticulum Ca2+-ATPase
EXCITATION-CONTRACTION COUPLING
In cardiac muscle
 the sarcoplasmic reticulum is less well developed.
 The T tubule volume is 25x greater.
 Quantity of mucopolysaccharides that store Ca+2 is larger.
⭣
The strength of muscle contraction largely depends on extracellular
fluid Ca+2 concentration
EXCITATION-CONTRACTION COUPLING
At the end of the plateau of the cardiac action potential
 the calcium influx to the of the muscle fiber stops.
 Calcium ions in the sarcoplasm are pumped into the SR and T tubule
by a calcium–ATPase pump
 Calcium ions are also removed from the cell by a sodium-calcium
exchanger.
 The resulting excess sodium is then transported out by the sodium-potassium ATPase pump.

The contraction ceases until a new action potential comes

along.
DURATION OF CONTRACTION
Cardiac muscle contraction follows the start of action
potential with a few msec.
 It continues to contract until a few msec. after it ends.
Therefore, the duration of the contraction is
 a function of the duration of the action potential, including the
plateau
 ≈ 0.2 sec. in the atria
 ≈ 0.3 sec. in ventricules.
CARDIAC CYCLE
CARDIAC CYCLE
A single loop of heart’s continuous constriction (sistole) and
relaxation (diastole).
Each cycle is initiated by the sinus node
 That creates the spontaneous an action potential
 It is located in the superior lateral wall of the right atrium
 near the opening of the superior vena cava.
 The action potential travels from here
 rapidly through both atria and
 then through the A-V bundle into the ventricles
CARDIAC CYCLE
 SA node is located in the superior lateral wall of the right atrium
 near the opening of the superior vena cava.
 The action potential travels from here
 rapidly through both atria and
 then through the A-V bundle into the ventricles
CARDIAC CYCLE
The atria act as primer pumps for the ventricles
 there is a delay of more than 0.1 second during passage of the
cardiac impulse from the atria into the ventricles.
 During that period,
 Atrial contraction is completed.
 Ventricules are filled rapidly.
DIASTOLE AND SYSTOLE
The total duration of the cardiac cycle is the reciprocal of
the heart rate.
 For example, if the heart rate is 72 beats/min
 the duration of the cardiac cycle is 1/72 min/beat
 about 0.0139 min/beat, or 0.833 sec/beat.
DIASTOLE AND SYSTOLE

1. The pressure of aorta

2. Left ventricular pressure
3. Left atrial pressure
4. Left ventricular volume
5. The electrocardiogram
6. The phonocardiogram
• a recording of the sounds
produced by the heart valves
DIASTOLE AND SYSTOLE
Cardiac cycle shortens as cardiac rhythm increases and
vice versa. But diastole is effected more deeply.
 For 72 beats/min, systole is ≈ 0.4 of the cardiac cycle.
 If the rhythym is 3x of the normal heart rate, systole is ≈ 0.65.
⭣
 When rhythym is high, the diastole is too short to allow complete
filling of the cardiac chambers before the next contraction.
 Also, cardiac muscle fibers are fed by blood in systole.
RELATIONSHIP OF THE ECG TO THE
CARDIAC CYCLE
RELATIONSHIP OF THE ECG
TO THE CARDIAC CYCLE
P-Atrial depolarization
QRS-Ventricular depolarization
 ≈ 0.16 sec. after the onset of the P
wave
T-Ventricular repolarization
 when the ventricular muscle fibers
begin to relax.
 slightly before the end of
ventricular contraction.
THE ATRIA FUNCTION
AS PRIMER PUMPS
THE ATRIA FUNCTION AS PRIMER PUMPS FOR THE
VENTRICLES
≈ 80% of the blood flows directly into the ventricles before
the atria contract.
≈an additional 20% fills the ventricles by atrial contraction.
 Primer pump effect of The atria
The heart can function without the aid of atria to ventricules
 Since Ventricules are capable of pumping 3-4X of blood the body
needs when it is resting.
PRESSURE CHANGES IN THE ATRIA:
A, C, AND V WAVES.
PRESSURE CHANGES
IN THE ATRIA
«a»-waves
 atrial contraction.
 the right atrial pressure: 4-6
mm Hg
 the left atrial pressure: 7-8
mm Hg
att!yumdak! bas!ng
değ"ş"kl"kler"
PRESSURE CHANGESa -
C
-
Y

dalgaları
IN THE ATRIA
«c» -waves
 At the start of ventricle
contraction
 Due to bulging of the A-V
valves
 + slight backflow of blood
into the atria
PRESSURE CHANGES
IN THE ATRIA
«v»-waves
 At the end of ventricular
contraction
 Due to slow flow of blood
into the atria from the veins
while the A-V valves are
closed
FUNCTION OF THE VENTRICLES
AS PUMPS
FUNCTION OF THE VENTRICLES AS PUMPS
The stages of ventricular contraction according changes of ventricular volume:

During diastole During systole

1. Isovolumic (Isometric) 4. Isovolumic (Isometric)
Relaxation Contraction
2. Rapid filling of the 5. Ejection
ventricles
3. Diastasis
4. Atrial systole
FUNCTION OF THE VENTRICLES AS PUMPS
Rapid filling of the ventricles
 First 1/3 of diastole.
 The moderately increased atrial pressures during ventricular
systole
 immediately push the A-V valves open and
 allow blood to flow rapidly into the ventricles
FUNCTION OF THE VENTRICLES AS PUMPS
Diastasis
 Second 1/3 of diastole.
 only a small amount of blood normally flows into the ventricles

Atrial systole
 Last 1/3 of diastole.
PERIOD OF ISOVOLUMIC (ISOMETRIC)
CONTRACTION
Immediately after the beginning of ventricular contraction
 A-V valves are closed yet, semilunar valves are not open.
 Pressure rises rapidly but the volume stays same
 It takes 0.02 to 0.03 sec
PERIOD OF EJECTION
The ventricular pressures push the semilunar valves open.
Blood is ejected out of the ventricles into the aorta and
pulmonary artery
≈60% of the ventricular blood volume end of diastole is
ejected.
 70% is ejected in first 1/3 -rapid ejection period
 30% is ejected in remaining 2/3 -slow ejection period
PERIOD OF ISOVOLUMIC (ISOMETRIC)
RELAXATION
At the end of systole,
ventricular relaxation begins suddenly
While both type of valves closed
It takes 0.03-0.06 sec
CARDIAC VOLUMES
CARDIAC VOLUMES
End-Diastolic Volume
 The ventricular volume at end of diastole, before the start of
systole
 ≈110 to 120 ml
End-Systolic Volume
 The remaining volume at the of systole
 ≈ 40 to 50 ml
CARDIAC VOLUMES
Stroke Volume Output
 The volume that is ejected from the ventricule during systole
 ≈ 70 ml
The ejection fraction
 The fraction of the end-diastolic volume that is ejected
 ≈ 60%.
 Often used clinically to assess cardiac systolic (pumping)
capability
CARDIAC VOLUMES
In strong cardiac contraction
 the end-systolic volume may decrease
 to as little as 10 to 20 ml.

Conversely, when venous return increases too much

 the ventricular end-diastolic volumes can increse also
 150 to 180 ml in the healthy heart.

The stroke volume output can be increased > 2x

 Increasing the end-diastolic volume
 Decreasing the end-systolic volume
THE HEART VALVES PREVENT BACKFLOW OF
BLOOD DURING SYSTOLE
THE HEART VALVES

Atrioventricular Valves
• prevent backflow of blood from the
ventricles to the atria during systole
• close and open passively
• The papillary muscles
• contract when the ventricular walls
contract but,
• But they do not help the valves to
close
• they prevent bulging of valves too
far backward
THE HEART VALVES

In the cases of a chorda tendina

rupture, or papillary muscle
paralysis.
• the valve bulges far backward
during ventricular contraction,
• Resulting in severe or even
lethal cardiac incapacity.
THE HEART VALVES
 The semilunar valves
 They are forced to close under higher pressures
 Their openings are smaller.
 The velocity of ejected blood is much greater
 Their edges are subjected to much greater mechanical abrasion
 They are not supported by the structures like chordae tendineae.
 But they are constructed of an strong, pliable, fibrous tissue
THE HEART VALVES
Right ventricular external work output is
 1/6 of left ventricle
 because of the 6x difference in systolic pressures
The additional work output to create kinetic energy of
blood flow is proportional
 to the mass of blood ejected times
 the square of velocity of ejection.
HEART SOUNDS
HEART SOUNDS
First heart sound (S1) Second heart sound (S2)
 Closure of the A-V valves.  Closure of semilunar valves
 At the begining of systol.  At the end of systole.
 The vibration pitch is relatively  A rapid snap because these
low valves close rapidly
WORK OUTPUT OF THE HEART
WORK OUTPUT OF THE HEART
The stroke work output of 1. Volume-pressure work /
the heart External work.
 The major proportion.
 The amount of energy that the
 Used to move the blood from the low-
heart converts to work during pressure veins to the high-pressure
each heartbeat while pumping arteries.
blood into the arteries. 2. Kinetic energy of blood
 It has two forms> flow
 A minor proportion of the energy
 Used to accelerate the blood to its
velocity of ejection
WORK OUTPUT OF THE HEART
The work output of the left ventricle required to create
kinetic energy of blood flow is
 only ≈ 1% of the total work output of the ventricle
 generally ignored in the calculation
In certain abnormal conditions
 like aortic stenosis-in which blood flows with great velocity
 This percentage can rise to 50% of the total work output.
GRAPHIC ANALYSIS OF VENTRICULAR
PUMPING
GRAPHIC ANALYSIS OF
VENTRICULAR PUMPING
End-diastolic pressure
 the diastolic pressure just
before ventricular contraction
occurs
The systolic pressure curve
 the systolic pressure achieved
during ventricular contraction
at each volume of filling
GRAPHIC ANALYSIS OF
VENTRICULAR PUMPING
≤ ≈150 ml
 the diastolic pressure does not
increase much
 blood can flow easily from the
atrium into the ventricle.
GRAPHIC ANALYSIS OF
VENTRICULAR PUMPING
> ≈150 ml
 the ventricular diastolic
pressure increases rapidly,
due to 2 reasons:
 fibrous tissue in the heart that will stretch
no more
 the pericardium that surrounds the heart
becomes filled nearly to its limit
GRAPHIC ANALYSIS OF
VENTRICULAR PUMPING
> ≈150-170 ml
 Systolic Pressure begins to fall.
 Actine-myosine interaction
reaches its limit
 no additional contractil force
can be gained
GRAPHIC ANALYSIS OF
VENTRICULAR PUMPING
For the normal left ventricle
 The maximum systolic pressure
is between 250-300 mm Hg,
 but this varies:
 Each person’s heart strength
 Degree of heart stimulation by cardiac
nerves

For the right ventricle, it is

between 60-80 mm Hg.
The volume-pressure
diagram of the cardiac
cycle for normal function of
the left ventricle
1. Period of filling
2. Isovolumetric contraction
3. Period of ejection
4. Isovolumetric relaxation
↓ doluş
.
dönem!

1. Period of filling

The ventricular volume

>

increases:
 50 ->120 ml
 End-systolic volume ->
End-diastolic volume
# = =>

>
=>
Diastolic pressure increases
briefly:
 2-3 mm Hg > 5-7 mm Hg.
2. Isovolumetric filling

 Volume remains same.

 The pressure rises to the levels
of the pressure at the aorta
 5-7 mm Hg > 80 mm Hg &
 3. Period of ejection

 The left ventricular volume

decreases
 120 ml > 50 ml
 But during this period left nac
!mde s!stol!k basınçta meydana gelen değ"
ve
ventricular
!ş!kl!kler! göster!r .
pressure reaches to
the max
 80 mm Hg > 120 mm Hg
 Then false again
 Aortic pressure is higher when the valve
closes the elastic fibers’ capacity
4. Isovolumetric relaxation

 The left ventricular volume remains

same since the both valves are
closed.

 The left ventricular pressure

decreases fast with relaxing
ventricular wall.
 100 mm Hg > 2-3 mm Hg
 The shaded area, labeled “EW”)
represents
 the net external work output of the ventricle
during its contraction cycle

 When the heart pumps large

quantities of blood, the area of
the work diagram becomes much
larger.
1. The extension far to the right > the
ventricle fills with more blood during
diastole
2. Higher pressure increase > the ventricle
contracts with greater pressure
3. The extension to the farther left > smaller
end-systolic volume > The increased
symphatetic activity
PRELOAD AND AFTERLOAD
Preload Afterload
 The degree of tension on the  The load against which the
muscle when it begins to muscle exerts its contractile
contract force
 usually considered to be the  The pressure in the aorta.
end-diastolic pressure  Sometimes it is loosely
considered to be the resistance
in the circulation.
CHEMICAL ENERGY
REQUIRED FOR CARDIAC
CONTRACTION
The energy comes from
• 70-90% - oxidative metabolism of
fatty acids
• 10-30% - other nutrients
• especially glucose and lactate.
CHEMICAL ENERGY
REQUIRED FOR CARDIAC
CONTRACTION
The shaded portion consists of
• the external work (EW)
• the potential energy (PE)
• The aadditional work that could
be accomplished by contraction
of the ventricle
• If the ventricle could completely
empty all the blood in its
chamber with each contraction.
CHEMICAL ENERGY REQUIRED FOR CARDIAC
CONTRACTION
Oxygen consumption is nearly proportional to
 the tension that occurs in the heart muscle during contraction
 multiplied by the duration of contraction time
 this is called the tension-time index.
The law of Laplace
 ventricular wall tension (T) is related to the left ventricular
pressure (P) and the radius (r):
T = P × r
>
CHEMICAL ENERGY REQUIRED FOR CARDIAC
CONTRACTION
T=P×r
 Systolic pressure ↑ > Ventricular pressure ↑ > wall stress and
cardiac workload ↑
 >>> thickening of the ventricular walls > the ventricular chamber radius ↓ (concentric
hypertrophy) >>> partially relieve the increased wall tension
 Dilated ventricules (eccentric hypertrophy) > the ventricular
chamber Radius ↑ > work output ↑
CARDIAC EFFICIENCY
Cardiac efficiency
 The ratio of work output to total chemical energy used to perform
the work
the chemical energy
 The most converted into heat,
 20-25% converted into work output- at max
 ≈5%, in heart failure
REGULATION OF HEART PUMPING
REGULATION OF HEART PUMPING
The pumping of the heart
 At rest- 4-6 litre
 In effort- 3-7x

Basic mechanisms for regulating heart pumping

 Intrinsic: By the blood volume returning to heart
 Extrinsic: By autonomic nervous system
INTRINSIC REGULATION
-THE FRANK-STARLING MECHANISM
Venous return
 Blood flow into the heart from the veins
THE Frank-STARLING Mechanism:
 Venous return increases cardiac contructility
 Because of the interaction between actine-miyosin flaments
Bainbridge Reflex
 Stretch of the right atrial wall directly increases the heart rate by
10% to 20%
-THE FRANK-STARLING
MECHANISM
The ventricular volume output
curve.
• The right and left atrial
pressures ↑
• ventricular volume output/min
↑
• Up-to a certain level
EXTRINSIC REGULATION

The pumping
effectiveness of the heart
also is controlled by
 the sympathetic nerves
 can rise cardiac output 2x
 parasympathetic (vagus)
nerves
 can decrease cardiac output to
almost zero
EXCITATION OF THE HEART BY THE SYMPATHETIC
NERVES
The Sympathetic innervation
 can increase heart rythym
70 beats/min > 200-250 beats min
 also can increase contraction force
2x
 Has a tonic/continious effect on heart. When it’s supressed
 Cardiac output can decrese 30%
EXCITATION OF THE HEART BY THE SYMPATHETIC
NERVES
Parasympathetic (Vagal) Stimulation
 can stop the heartbeat for a few seconds
 but then the heart usually “escapes”
 beats at a rate of 20 to 40 beats/min
 can decrease the strength of heart muscle contraction by 20% to
30%
 With a total decrease in cardiac output of 50%
Vagal innervation of ventricules is weak.
 That is why effect on cardiac contractility is weak
EFFECTS OF IONS, TEMPERATURE &
ARTERIAL PRESSURE
EFFECTS OF IONS- POTASSIUM
Excess potassium in the extracellular fluids
 the heart dilation & bradykardia.
 Also, block conduction of the cardiac impulse from the atria to the
ventricles through the A-V bundle.
EFFECTS OF IONS- POTASSIUM
↑ Potassium concentration (8-12 mEq/L, 2x-3x the normal
value) can cause
 severe weakness of the heart, abnormal rhythm, and death.
↑ Potassium concentration in the EC fluids,
 the membrane potential ↓
 the intensity of the action potential ↓
 the strenght of contraction ↓
EFFECTS OF IONS- CALCIUM
Excess calcium ions cause effects almost exactly opposite
to those of potassium ions
 causing the heart to move toward spastic contraction.
This effect is caused by a direct effect of calcium ions to
initiate the cardiac contractile process
EFFECTS OF IONS
Deficiency of calcium ions causes cardiac weakness
 similar to the effect of high potassium.
Calcium ion levels in the blood normally are regulated
within a very narrow range.
 Cardiac effects of abnormal calcium concentrations are seldom of
clinical concern.
EFFECT OF TEMPERATURE ON HEART FUNCTION
↑ Body temperature, ↑ the heart rate (up-to 2x)

↓ Body temperature, ↓ the heart rate

 Up-to a few beats/min in hypothermia (15.5°–21°C). T

The heat increases the permeability of the cardiac muscle

membrane to ions that control heart rate,
 resulting in acceleration of the self-excitation process.
vucut egzers!z! sırasında meydana gelen sıcaklık artısı

↳EFFECT OF
Kalb!n
TEMPERATURE ON
kasılma
HEART FUNCTION
gücünü attırır
.

A moderate increase in temperature

 such as that which occurs during body exercise
 enhances contractile strength of the heart
sürel! sıcaklık otsı
-uzun
The prolonged temperature elevation
 exhausts the metabolic systems of the heart
 eventually causes weakness
> kalb!n
- metabol!k s!stem!n! yora
-sonunda zayızlığa
.
neden olur
THE ARTERIAL PRESSURE LOAD ↑
DOES NOT DECREASE CARDIAC OUTPUT
The increasing the arterial pressure in the aorta
 does not decrease cardiac output
 until the mean arterial pressure rises > ≈160 mm Hg.
During normal heart function at normal systolic arterial
pressures (80–140 mm Hg)
 cardiac output is determined almost entirely by the ease of blood
flow through the body’s tissues
 which in turn controls venous return of blood to the heart
REFERENCES
Ed., Hall, JE., Hall, ME, Guyton and Hall textbook of
medical physiology, English, 2021, Edition:14th internatial
edition, Publisher: Elsevier, Philadelphia, PA, 2021
VIDEOS
Berne & Levy Physiology, Eighth Edition
The cardiac cycle
The cross-bridge cycle
https://www.clinicalkey.com/#!/browse/book/3-s2.0-C20
200000472
RECOMMENDED READING

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