AKTIVITAS MEKANIK

JANTUNG
Rahmatina B. Herman
Bagian Fisiologi
Fakultas Kedokteran - Unand

Position of Heart in Thoracic Cavity

Structure of Heart

Structure of Heart..

Anatomy - Physiology of Heart

Two separate parts: left and right
Respectively:
- left atrium and ventricle
- right atrium and ventricle
Atrial function: primary pumps for ventricular
Ventricular function: pumping blood to all parts of
body and to the lungs
Ventricles pump more powerful than the atria
Atria contract prior to ventricles

Anatomy - Physiology of Heart..

Function of Valves and Papillary Muscles

The valves open and close passively

AV valves (tricuspid and mitral):

- Prevent backflow of blood from the ventricles into
atria during systole

Semilunar valves (aortic and pulmonary):

- Prevent backflow of blood from aorta and pulmonary
arteries into ventricles during diastole

Papillary muscles:
- Papillary muscles contract when the ventricular walls
contract
- They pull the vanes of valves inward toward the
ventricles to prevent their bulging too far backward
toward the atria during ventricular contraction

Anatomy Physiology of Cardiac Muscles

Myocardium:
- Atrial muscles
- Ventricular muscles
- Specialized excitatory and conductive system
of the heart

Involuntary muscles
Similar manner to skeletal muscle contraction
Syncytium

Structure of Cardiac Muscle Fibers

Sarcolemma
Myofibril
Filaments:

- Actin
- Myosin

Sarcoplasma
Sarcoplasmic reticulum

Structure of Cardiac Muscle Fibers..

Structure of Cardiac Muscle Fibers..

Intercalate Disc

Structure of Cardiac Muscle Fibers..

Electrical Activity of Cardiac Muscle Fibers

Polarization
Depolarization:

- Plateau
- Rhythmicity

Repolarization
Conductivity
Refractory period

Electrical Activity of Cardiac Muscle Fibers..

Electrical Activity of Cardiac Muscle Fibers..

Electrical Activity of Cardiac Muscle Fibers..

Electrical Activity of Cardiac Muscle Fibers..

Electrical Activity of Cardiac Muscle Fibers..

Rhythmicity of Cardiac Action Potential

Rhythmicity of Cardiac Action Potential..

Refractory Period

Conductivity of Cardiac Action Potential

Conduction velocity in atrial and ventricular muscle
fibers:
0,3 0,5 m/second
= 1/250 conduction velocity of action
potential in large nerve fibers
= 1/10 conduction velocity of action potential in
skeletal muscle fibers
Conduction velocity in Purkinye system
0,02 4 m/second depend on location

Mechanism of Contraction

Duration of Contraction
Duration of contraction = duration of action potential:
- In atrial: 0,2 second
- In ventricular 0.3 second
Greatly influenced by frequency of heart rate (HR)

- The faster the frequency of HR, the shorter the

duration of contraction, especially diastolic period
- HR 72x/sec syst period : diast period = 40:60

- HR increased 3x syst period : diast period = 65:35

Oxygen Consumption By Heart

Basal O2 consumption is 2 ml/100g/min
Considerably higher than that of resting skeletal
muscle
O2 consumption by beating heart is 9 ml/100g/min
at rest
Increases during exercise and in a number of different
states
Cardiac venous O2 tension is low, and little additional
O2 can be extracted from the blood in the coronaries
blood flow, so increases in O2 consumption require
increases in coronary blood flow

SIKLUS JANTUNG
(CARDIAC CYCLE)

The Cardiac Cycle

Definition:

The cardiac events that occur from the beginning

of one heartbeat to the beginning of the next
The cardiac cycle consists of:

- Diastole : period of relaxation, during which the

heart fills with blood
- Systole

: period of contraction, during which

the heart ejects blood from its
chambers

Conductive System of Heart

SA Node (sinoatrial node)/ sinus node :
- located in the superior lateral wall of right atrium,
immediately below and slightly lateral to the
opening of the superior vena cava
Internodal pathways:
- conductive system from SA node to AV node
AV node (atrioventricular node):
- located in the posterior septal wall of right atrium,
immediately behind tricuspid valve and adjacent to
the opening of coronary sinus
AV bundle/ His bundle

Purkinje System

Conductive System of Heart..

Conductive System of Heart..

Organization of AV node

Transmission of Cardiac Impulse

Events of Cardiac Cycle

Generating and transmission of cardiac impulses:
1. Generating rhythmical impulses in SA node
2. Conducting the impulses rapidly throughout atria
atria contract

3. Conducting impulses to AV node (delay 0,13 sec)

4. Conducting impulses through AV/ His bundle
5. Finally transmission impulses rapidly throughout
ventricles through Purkinye system ventricle
contract

Events of Cardiac Cycle..

Because of impulses generate in SA node and delay in
transmission to ventricles atria contract (atrial
systole) prior to ventricles
Ventricles still in relaxation period (ventricular
diastole), called diastole

AV valves open and allow blood to flow into ventricles

filling of ventricles

Events of Cardiac Cycle..

Filling of the ventricles during diastole
Rapid filling:
- A-V nodes closed large amount of blood accumulate in
atria immediately push AV valves open blood flow
rapidly into ventricles; lasts for the first third of diastole

Diastasis:
- During the middle third of diastole, only a small amount
of blood that continues to empty into atria from veins and
passes directly into ventricles

Atrial systole:
- During the last third of diastole, atria contract and
give additional thrust to inflow of blood into ventricles

Events of Cardiac Cycle..

Emptying of the ventricles during systole
Period of isovolemic (isometric) contraction:
- Ventricular contraction intraventricular pressures
AV valves close
- But not sufficient to push semilunar valves open no
emptying of blood from ventricles

Period of ejection:
- Semilunar valves opened blood pour out of ventricles

Period of isovolemic (isometric) relaxation:

- Ventricular relaxation intraventricular pressures
semilunar valves close
- But not sufficient to cause AV valves open no blood
flow into ventricles

Events of Cardiac Cycle..

During ventricular contraction:
- Period of ejection
- Ventricular pressure blood pour from ventricles
into arterial system (aorta and pulmonary trunks)
> cardiac output (volume / minute)
> stroke volume (volume/ contraction)

During atrial relaxation:

- Atrial pressure blood flow from veins into atria
venous return (volume/ minute)

Events of Cardiac Cycle..

The greater venous return, the greater the
heart muscle is stretched, the greater will be
the force of contraction and the greater stroke
volume
Within physiological limits, the heart pumps all
the blood that comes to it without allowing
excessive damming of blood in the veins
(Frank-Starling Law)

Events of Cardiac Cycle..

Ventricular Volume
End diastolic volume (EDV): 110 120 cc,
- Can be increased to 150 180 cc
Stroke volume (SV): 70 cc
- SV = EDV ESV (110 cc 40 cc)
Ejection fraction: 60 %
- SV/EDV x 100%
End systolic volume (ESV): 40 50 cc,
- Can be decreased to 10 20 cc
- SV can be increased to 140 - 160 cc

Relationship between left ventricular volume and intraventricular pressure during

diastole and systole. The heavy red lines is volume-pressure diagram.
EW, net external work

Concepts of Preload and Afterload

Preload:
In assessing the contractile properties of muscle, it is
important to specify the degree of tension on muscle
when it begins to contract

After load:
To specify the load against which the muscle exerts
its contractile force

Concepts of Preload and Afterload..

The importance of the concepts of preload and
afterload:
Many abnormal function states of the heart or
circulation, the pressure during filling of
ventricle (the preload), the arterial pressure
against which the ventricle must contract (the
afterload), or both are severely altered from
the normal

BUNYI JANTUNG
(HEART SOUNDS)

Normal Heart Sounds

Using a stethoscope, one hears a sound usually
described as lub, dub, lub, dub
- The lub is 1st heart sound, associated with closure
of atrioventricular (A-V) valves at the beginning of
systole
- The dub is 2nd heart sound, associated with closure
of semilunar (aortic and pulmonary) valves at the
end of systole

Normal Heart Sounds..

1st heart sound:
- Duration: 0.14 seconds
- Low pitch

2nd heart sound :

- Duration: 0.11 detik seconds
- High pitch

3rd heart sound :

- heard at the beginning of the middle third of diastole
- blood oscillation in ventricles initiated by inrushing blood from
atria
- weak, rumbling
- can often be recorded in the phonocardiogram

4th heart sound (atrial heart sound):

- blood oscillation in ventricles when atria contract
- sometimes can be recorded in the phonocardiogram

Normal Heart Sounds..

Phonocardiogram from normal heart

Causes of Heart Sounds

Vibration of the taut valves immediately after closure,
along with vibration of adjacent walls of the heart and
major vessels around the heart
Vibrating is caused by turbulences in blood
1st heart sound:
Contraction of ventricles sudden backflow of blood
against A-V valves closing of valves and bulging toward
atria vibrating turbulence in blood vibrations
2nd heart sound:
Semilunar valves close rapidly at the end of systole
bulge backward toward ventricles vibrating turbulence
in blood vibrations

Causes of Heart Sounds..

3rd heart sound:
Oscillation of blood back and forth between the walls of
ventricles initiated by inrushing from the atria
vibrations of the walls
This sound does not occur until the middle third of
diastole because the ventricles are not filled sufficiently
to create elastic tension necessary for reverberation
4th heart sound (atrial heart sound):
Atria contract inrush of blood into ventricles
vibrations

Mitral and aortic valves (left ventricular valves)

Chest areas from which sound from each valve is best heard

CURAH JANTUNG
(CARDIAC OUTPUT)

Definition
Cardiac output (COP):
- is the quantity of blood pumped into the aorta each
minute by heart
- is also the quantity of blood that flows through circulation

The volume of cardiac output is equal with stroke

volume (SV) multiplied by heart rate (HR) per minute
COP = SV x HR

Venous return:
- is the sum of all the local blood flows through all
individual tissue segments of peripheral circulation

Normal Values for Cardiac Output

COP varies widely with the level of activity of body
Factors that directly affect COP:
1. Venous return (Frank-Starling Law)
2. Basic level of body metabolism
3. Body activity
4. Age
5. Body size

Resting COP: the average 5 L/min for resting adult

- 5.6 L/min for young healthy men
- 4.9 L/min for young healthy women (10-20% lower)

With increasing age, body activity and metabolism

diminishes COP

Cardiac Index
Cardiac index is COP per square meter of body
surface area (COP/surface area)
COP increases approximately in proportion to the
body surface area

The normal human being weighing 70 kg has body

surface area of 1,7 m2, COP 5 L/min.
cardiac index : 5 L/min/1,7 m2 = 3 L/min/m2 of
body surface area

Cardiac index for the human being

Cardiac Reserve
Cardiac reserve is:
- Ratio between maximum COP and resting COP
- Average: 4-5 times
- Athlete: may increase 7-8 times
- In severe heart disease: cardiac reserve 0
not be able to perform physical activity

PENGATURAN
POMPA JANTUNG
(REGULATION
OF HEART PUMPING)

I. Intrinsic Regulation
Intrinsic Regulation by Frank-Starling
mechanism
The amount of blood pumped by heart is
determined by the rate of blood flow into
the heart from veins (venous return)
Within physiology limits, heart pumps all
blood that comes to it

II. Control by Autonomic Nervous System

Excitation of heart by sympathetic nerves:
- Increasing heart rate (to 180 200 bpm)
- Increasing the force of myocardial contraction
stroke volume COP

Parasympathetic (vagal) stimulation:

- Decreasing HR and force of contraction
- Vagal fibers are distributed mainly to atria, but not
much to ventricles
- Strong vagal stimulation can stop heart beats, but
then usually escapes and beats at rate 20-40 bpm

Cardiac sympathetic and parasympathetic nerves

The vagus nerves are parasympathetic nerves

Control of Heart Rate

Effects of strain on right atrial wall

Strain on right atrial wall strain on SA

node increasing SA node rhythmicity
increasing heart rate

Strain on right atrial wall Bainbridge

reflect: increasing heart rate