Siklus Jantung (sistole

dan distole)
• Peristiwa mekanis siklus jantung (sistole dan diastole)
• Suara jantung
• Curah jantung / cardiac output
• Pengaturan fungsi jantung
• Autoregulasi intrinsik
• Pengaturan saraf

Topik
Structure of the heart, and course of blood flow
through the heart chambers and heart valves.
Structure of the heart, and course of blood flow
through the heart chambers and heart valves.
PERISTIWA MEKANIS SIKLUS
JANTUNG (SISTOLE DAN DIASTOLE)
• The cardiac events that occur from the beginning of one
heartbeat to the beginning of the next are called the
cardiac cycle.

• Each cycle is initiated by spontaneous generation of an

action potential in the sinus node, the action potential
travels from here rapidly through both atria and then
through the A-V bundle into the ventricles.

The Cardiac Cycle

• The atria act as primer pumps for the ventricles,
and the ventricles in turn provide the major
source of power for moving blood through the
body’s vascular system.

The Cardiac Cycle

• The cardiac cycle consists of :
• a period of relaxation called diastole - during
which the heart fills with blood, followed by
• a period of contraction called systole.

Diastole and Systole

Events of the cardiac cycle for left ventricular function, showing changes in
left atrial pressure, left ventricular pressure, aortic pressure, ventricular
volume, the electrocardiogram, and the phonocardiogram
• Atria as primer pumps
• Ventricle as pumps
• Emptying of ventricle during systole -
Isovolumic (Isometric) contraction
• Period of ejections (fast and slow ejections)
• Period of Isovolumic (Isometric) Relaxation
• End-Diastolic Volume, End-Systolic Volume, and
Stroke Volume Output

Heart cylce
Relationship between left ventricular volume and
intraventricular pressure during diastole and
systole.
• Atrioventricular ValvesThe
• the tricuspid and mitral valves - prevent backflow of blood from
the ventricles to the atria during systole, and
• the semilunar valves (the aortic and pulmonary artery valves)
prevent backflow from the aorta and pulmonary arteries into the
ventricles during diastole
• Function of the Papillary Muscles
• Aortic and Pulmonary Artery Valves

Function of the Valves

Mitral and aortic valves (the left ventricular valves).
SUARA JANTUNG
• When listening to the heart with a stethoscope, one does
not hear the opening of the valves because this is a
relatively slow process that normally makes no noise.

• However, when the valves close, the vanes of the valves

and the surrounding fluids vibrate under the influence
of sudden pressure changes, giving off sound that travels
in all directions through the chest.

Relationship of the Heart

Sounds to Heart Pumping
• When the ventricles contract,
• a sound caused by closure of the A-V valves.
• The vibration is low in pitch and relatively long-lasting and
is known as the first heart sound.

• When the aortic and pulmonary valves close at the end of

systole,
• a rapid snap because these valves close rapidly, and the
surroundings vibrate for a short period.
• This sound is called the second heart sound.

Relationship of the Heart

Sounds to Heart Pumping
• Listening with a stethoscope to a normal heart, one hears a
sound usually described as “lub, dub, lub, dub.
• ”The “lub” is associated with closure of the atrioventricular (A-V)
valves at the beginning of systole, and
• the “dub” is associated with closure of the semilunar (aortic and
pulmonary) valves at the end of systole.

• The “lub” sound is called the first heart sound, and the “dub” is
called the second heart sound, because the normal pumping
cycle of the heart is considered to start when the A-V valves
close at the onset of ventricular systole.

Heart Sounds
• The duration of each of the heart sounds is
slightly more than 0.10 second—the first sound
about 0.14 second, and the second about 0.11
second.
• Vibration of the taut valves immediately after closure,
along with vibration of the adjacent walls of the heart and
major vessels around the heart.
• Contraction of the ventricles first causes sudden backflow
of blood against the A-V valves (the tricuspid and mitral
valves), causing them to close and bulge toward the atria
until the chordae tendineae abruptly stop the back bulging.
• The elastic tautness of the chordae tendineae and of the
valves then causes the back surging blood to bounce
forward again into each respective ventricle

Causes of the First and

Second Heart Sounds
• This causes the blood and the ventricular walls, as well as
the taut valves, to vibrate and causes vibrating turbulence
in the blood.
• The vibrations travel through the adjacent tissues to the
chest wall, where they can be heard as sound by using the
stethoscope.

Causes of the First and

Second Heart Sounds
• The second heart sound results from sudden closure of the
semilunar valves at the end of systole.
• When the semilunar valves close, they bulge backward toward the
ventricles, and their elastic stretch recoils the blood back into the
arteries, which causes a short period of reverberation of blood
back and forth between the walls of the arteries and the semilunar
valves, as well as between these valves and the ventricular walls.
• The vibrations occurring in the arterial walls are then
transmitted mainly along the arteries. When the vibrations of
the vessels or ventricles come into contact with a “sounding
board,” such as the chest wall, they create sound that can be
heard.

Causes of the First and

Second Heart Sounds
Amplitude of different-frequency vibrations in the
heart sounds
and heart murmurs in relation to the threshold of
audibility,
showing that the range of sounds that can be heard
is between
40 and 520 cycles/sec.
Chest areas from which sound from each valve is
best heard.
Phonocardiograms from normal and
abnormal hearts.
• many abnormal heart sounds, known as “heart
murmurs,” occur when there are abnormalities of the
valves
• Systolic Murmur of Aortic Stenosis
• Diastolic Murmur of Aortic Regurgitation
• Systolic Murmur of Mitral Regurgitation
• Diastolic Murmur of Mitral Stenosis

Heart Murmurs Caused by

Valvular Lesions
CURAH JANTUNG (CARDIAC
OUTPUT)
• Cardiac output : quantity of blood pumped into the aorta
each minutes by the heart

• Venous return : quantity of blood flowing from the vein

into the right atrium

• VENOUS RETURN = CARDIAC OUTPUT

Concepts
• Varies with the level of activity
• Factors :
• Level of body metabolism
• Activity (exercise)
• Age
• Body size
• Cardiac index : cardiac output /m2 body surface are

Normal values for cardiac output at

rest and during activity
CARDIAC OUTPUT
• Role of the Frank-Starling mechanism of the heart
• Related to venous return
• Heart has a built-in mechanism to pump automatically
• Heart rate increase  increase of heart  stretch SA
node :
• HR increase
• Brainbridge reflex

Control of cardiac output

by venous return
• Person in rest : 4 – 6 liter / minutes
• Exercise : 4 – 7 times of rest

• Regulated by :
• Intrinsic cardiac regulation of pumping in response to
changes in volume of blood flowing into the heart
• Control of heart rate and strength of heart pumping by the
autonomic nervous system

Heart pumping
• Venous return – rate of blood flow into the heart from the
veins
• Consist of peripheral tissues flow
• Affect to Cardiac output
• Heart will pumps into the systemic arteries

• Intrinsic ability of heart to adapt to changing volumes of

inflowing blood – Frank-Starling mechanism of the heart

Intrinsic regulation of heart pumping –

The Frank-Starling Mechanism
 EXTRA
CARDIAC
AMOUNT OF
MUSCLE
BLOOD TO
STRETCH
VENTRICLE

MUSCLE VENTRICLE
CONTRACT PUMPS EXTRA
WITH INCREASE BLOOD TO
FORCE ARTERIES

Frank-starling mechanism
Cardiac index for the human being (cardiac output
per square meter of surface area) at different ages.
Effect of increasing levels of exercise to increase
cardiac output (red solid line) and oxygen
consumption (blue dashed line).
• Sum of blood flow regulation in all local tissue of body
• tissue metabolism  local blood flow
• Cardiac output = arterial pressure / total peripheral
resistance
• Hypereffective heart
• Nervous stimulation
• Hypertrophy of heart muscle
• Hypoeffective heart
• Inhibition of nervous excitation
• Pathological factors, etc

Cardiac output regulation

Chronic effect of different levels of total peripheral
resistance on cardiac output, showing a reciprocal
relationship between total peripheral resistance
and cardiac output.
Cardiac output curves for the normal heart and for
hypoeffective and hypereffective hearts.
Cardiac output in different pathological conditions.
The numbers in parentheses indicate number of
patients studied in each condition.
Cardiac output curves at different levels of
intrapleural pressure and at different degrees of
cardiac tamponade.
Combinations of two major patterns of cardiac output curves
showing the effect of alterations in both extracardiac pressure and
effectiveness of the heart as a pump.
PENGATURAN FUNGSI JANTUNG
(AUTOREGULASI INTRINSIK DAN
PENGATURAN SARAF)
• What are some of the specific needs of the tissues for
blood flow?
• Delivery of oxygen to the tissues.
• Delivery of other nutrients, such as glucose, amino acids,
and fatty acids.
• Removal of carbon dioxide from the tissues.
• Removal of hydrogen ions from the tissues.
• Maintenance of proper concentrations of other ions in the
tissues.
• Transport of various hormones and other substances to the
different tissues.

Local Control of Blood Flow

in Response to Tissue Needs
Blood Flow to Different Organs and Tissues Under
Basal Conditions
• Increased of arterial pressure cause an immediate rise of
blood flow
• Metabolic theory
• Myogenic theory

• Specific tissue
• Juxtaglomerular apparatus in kidney
• Brain : O2, CO2, H

Auto regulation of blood

flow
• Regulation by substances secreted or absorbed into the
body fluids
• Vasoconstrictor agent
• Norepinephrine – epinephrine
• Angiotensin
• Vasopressin (ADH)
• Vasodilator agents
• Bradykinin
• Histamine

Humoral regulation
• Calcium – vasoconstriction
• Potassium – vasodilatation
• Magnesium – vasodilatation
• Acetate and citrate – vasodilatation
• Hydrogen – dilatation of arterioles

Effect of ion and other chemical

factors on vascular control
• The nervous system controls the circulation almost
entirely through the autonomic nervous system.
• By far the most important part of the autonomic nervous
system for regulating the circulation is
• the sympathetic nervous system
• the parasympathetic nervous system

Nervous Regulation of the

Circulation
• Important : when venous return and cardiac output
increase
• In exercise : providing additional signals to raise the
arterial pressure  increase cardiac output

Role nervous system in

controlling cardiac output
Anatomy of sympathetic nervous control of the circulation.
Also shown by the red dashed line is a vagus nerve that
carries parasympathetic signals to the heart.
Anatomy of sympathetic nervous control of the circulation.
Also shown by the red dashed line is a vagus nerve that
carries parasympathetic signals to the heart.
Sympathetic innervation of the systemic circulation.
• Most arterioles of the systemic circulation are
constricted.
• The veins especially (but the other large vessels
of the circulation as well) are strongly
constricted.
• The heart itself is directly stimulated by the
autonomic nervous system, further enhancing
cardiac pumping.

Role of the Nervous System in

Rapid Control of Arterial Pressure
• The nervous mechanisms for arterial pressure control is
the baroreceptor reflex.
• initiated by stretch receptors, called either baroreceptors or
pressoreceptors
• A rise in arterial pressure stretches the baroreceptors and
causes them to transmit signals into the central nervous
system.
• “Feedback” signals are then sent back through the
autonomic nervous system to the circulation to reduce
arterial pressure downward toward the normal level.

The Baroreceptor Arterial Pressure

Control System—Baroreceptor
Reflexes
• After the baroreceptor signals have entered the tractus
solitarius of the medulla
• secondary signals inhibit the vasoconstrictor center of the
medulla and
• excite the vagal parasympathetic center.

• The net effects are

• (1) vasodilation of the veins and arterioles throughout the
peripheral circulatory system and
• (2) decreased heart rate and strength of heart contraction.

Circulatory Reflex Initiated by the

Baroreceptors
• Therefore, excitation of the baroreceptors by high pressure in
the arteries reflexly causes the arterial pressure to decrease
because of both a decrease in peripheral resistance and a
decrease in cardiac output.

• Conversely, low pressure has opposite effects, reflexly causing

the pressure to rise back toward normal.

• Because the baroreceptor system opposes either increases or

decreases in arterial pressure, it is called a pressure buffer
system, and the nerves from the baroreceptors are called buffer
nerves.

Circulatory Reflex Initiated by the

Baroreceptors
• Sympathetic :
• Increase heart rate
• Increase the force of contraction
• Increase cardiac output
• Parasympathetic (vagal)
• Decrease heart rate
• Decrease the force of contraction

Effect of sympathetic and

parasympathetic
• Potassium  Hyperkalemia :
• heart dilated and flaccid
• slow of heart rate
• block impulse from atria
• abnormal rhythm
• Decrease the resting membrane potential
• Calcium  hypercalcemia :
• Spastic contraction
• Temperature :
• Fever : increase heart rate

Heart function and its

function
• During heavy exercise, the muscles require greatly
increased blood flow. Part of this increase results from
local vasodilation of the muscle vasculature caused by
increased metabolism of the muscle cells.
• Additional increase results from simultaneous elevation
of arterial pressure caused by sympathetic stimulation of
the overall circulation during exercise.
• In most heavy exercise, the arterial pressure rises about 30
to 40 per cent, which increases blood flow almost an
additional twofold.

Increase in Arterial Pressure During Muscle

Exercise and Other Types of Stress
• Abdominal Compression Reflex
• Increased Cardiac Output and Arterial Pressure Caused
by Skeletal Muscle Contraction During Exercise

Role of the Skeletal Nerves and Skeletal

Muscles in Increasing Cardiac Output and
Arterial Pressure
• Most nervous control of blood pressure is achieved by :
• the baroreceptors,
• the chemoreceptors, and
• the low-pressure receptors

• When blood flow to the vasomotorcenter in the lower

brain stem becomes decreased severely enough to cause
nutritional deficiency—that is, to cause cerebral
ischemia—the vasoconstrictor and cardioaccelerator
neurons in the vasomotor center respond directly to the
ischemia and become strongly excited
Central Nervous System Ischemic Response—Control of
Arterial Pressure by the Brain’s Vasomotor Center in
Response to Diminished Brain Blood Flow
• The degree of sympathetic vasoconstriction
caused by intense cerebral ischemia is often so
great that some of the peripheral vessels become
totally or almost totally occluded.

Central Nervous System Ischemic Response—Control of

Arterial Pressure by the Brain’s Vasomotor Center in
Response to Diminished Brain Blood Flow
• With each cycle of respiration, the arterial pressure
usually rises and falls 4 to 6 mm Hg in a wavelike
manner, causing respiratory waves in the arterial pressure.

Respiratory Waves in the

Arterial Pressure
• When the body contains too much extracellular fluid, the
blood volume and arterial pressure rise.
• The rising pressure in turn has a direct effect to cause the
kidneys to excrete the excess extracellular fluid, thus
returning the pressure back toward normal.
• The renal–body fluid system for arterial pressure control,
is the fundamental basis for long-term arterial pressure
control.

Renal–Body Fluid System for Arterial

Pressure Control
Experiment in a dog to demonstrate the importance
of nervous maintenance of the arterial pressure as a
prerequisite for cardiac output control.
• Shock usually results from inadequate cardiac output.
Therefore, any condition that reduces the cardiac output
far below normal will likely lead to circulatory shock.
• Cardiac abnormalities that decrease the ability of the heart
to pump blood
• Factors that decrease venous return

Circulatory Shock Caused by

Decreased Cardiac Output
• Occasionally, the cardiac output is normal or even greater
than normal, yet the person is in circulatory shock.
• (1) excessive metabolism of the body, so that even a normal
cardiac output is inadequate, or
• (2) abnormal tissue perfusion patterns, so that most of the
cardiac output is passing through blood vessels besides
those that supply the local tissues with nutrition.

Circulatory Shock That Occurs

Without Diminished Cardiac Output
Effect of hemorrhage on cardiac output and arterial
pressure.
• Hypovolemia means diminished blood volume.
• Hemorrhage is the most common cause of hypovolemic
shock.
• Hemorrhage decreases the filling pressure of the circulation
and, as a consequence, decreases venousreturn.
• As a result, the cardiac output falls below normal, and shock
may ensue

Shock Caused by
Hypovolemia—Hemorrhagic Shock
Time course of arterial pressure in dogs after
different degrees of acute hemorrhage. Each curve
represents average results from six dogs.
• These reflexes stimulate the sympathetic vasoconstrictor
system throughout the body, resulting in three important
effects:
• (1) The arterioles constrict in most parts of the systemic
circulation, thereby increasing the total peripheral resistance.
• (2) The veins and venous reservoirs constrict, thereby helping to
maintain adequate venous return despite diminished blood
volume.
• (3) Heart activity increases markedly, sometimes increasing the
heart rate from the normal value of 72 beats/min to as high as 160
to 180 beats/min.

Sympathetic Reflex Compensations in

Shock—Their Special Value to Maintain
Arterial Pressure.
Different types of “positive feedback” that can lead
to progression of shock.
Cardiac output curves of the heart at different times
after hemorrhagic shock begins.
Necrosis of the central portion of a liver lobule in
severe circulatory shock
• Loss of plasma from the circulatory system, even without
loss of red blood cells, can sometimes be severe enough
to reduce the total blood volume  hypovolemic shock
• 1. Intestinal obstruction is often a cause of severely reduced
plasma volume.
• 2. In almost all patients who have severe burns or other
denuding conditions of the skin

Hypovolemic Shock
Caused by Plasma Loss
 • an increase in vascular capacity or a decrease in blood
volume reduces the mean systemic filling pressure, which
reduces venous return to the heart. Diminished venous
return caused by vascular dilation is called venous
pooling of blood.
• Deep general anesthesia
• Spinal anesthesia
• Brain damage

Neurogenic Shock—Increased
Vascular Capacity
• Anaphylaxis is an allergic condition in which the cardiac
output and arterial pressure often decrease drastically.
• The histamine causes
• (1) an increase in vascular capacity because of venous
dilation,
• (2) dilation of the arterioles, resulting in greatly reduced
arterial pressure; and
• (3) greatly increased capillary permeability, with rapid loss
of fluid and

Anaphylactic Shock and

Histamine Shock
• A condition that was formerly known by the popular
name “blood poisoning” is now called septic shock

Septic Shock
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