Cardiovascular

System
FAKULTAS FARMASI UAD
YOGYAKARTA

CIRCULATORY SYSTEM

BLOOD
HEART
BLOOD VESSELS

CIRCULATORY
SYSTEM
BLOOD VESSELS

The Blood Vessels

The cardiovascular system has
three types of blood vessels:
Arteries (and arterioles) carry
blood away from the heart
Capillaries where nutrient and gas
exchange occur
Veins (and venules) carry blood
toward the heart.

Blood vessels

BLOOD VESSELS

ARTERIES

CAPILLARIES

CARRY BLOOD FROM THE HEART

ARTERY ARTERIOLES CAPILLARIES
SITE OF GAS AND NUTRIENT EXCHANGE

VEINS

RETURN BLOOD TO THE HEART

CAPILLARIES VENULES VEINS

The Arteries
Arteries and arterioles take blood
away from the heart.
The largest artery is the aorta.
The middle layer of an artery wall
consists of smooth muscle that can
constrict to regulate blood flow and
blood pressure.
Arterioles can constrict or dilate,
changing blood pressure.

The Veins
Venules drain blood from capillaries,
then join to form veins that take
blood to the heart.
Veins have much less smooth
muscle and connective tissue than
arteries.
Veins often have valves that prevent
the backward flow of blood when
closed.
Veins carry about 70% of the bodys
blood and act as a reservoir during
hemorrhage.

ARTERY AND VEIN WALLS

THREE LAYERS (TUNICS)

TUNICA EXTERNA (OUTERMOST)

TUNICA MEDIA
TUNICA INTERNA (INNERMOST)

ARTERY AND VEIN WALLS

TUNICA EXTERNA
OUTERMOST LAYER
LOOSE CONNECTIVE TISSUE

MERGES WITH ADJACENT CONNECTIVE

TISSUES

ANCHORS VESSEL
PASSAGE FOR NERVES, BLOOD & LYMPH
VESSELS

ARTERY AND VEIN WALLS

TUNICA EXTERNA
NOURISHMENT

OUTER HALF NOURISHED BY SMALL

BLOOD VESSELS (VASA VASORUM)
INNER HALF NOURISHED BY DIFFUSION
FROM BLOOD IN LUMEN

ARTERY AND VEIN WALLS

TUNICA MEDIA
MIDDLE LAYER
GENERALLY THE THICKEST LAYER
SMOOTH MUSCLE

VASOCONSTRICTION & VASODILATION

COLLAGEN
SOMETIMES ELASTIC TISSUE

ARTERY AND VEIN WALLS

TUNICA INTERNA
SMOOTH INNER LAYER
EXPOSED TO BLOOD
SQUAMOUS ENDOTHELIUM (EPI)
BASEMENT MEMBRANE
FIBROUS TISSUE

ARTERY AND VEIN WALLS

TUNICA INTERNA
REPELS BLOOD CELLS (& PLATELETS)
SELECTIVELY PERMEABLE BARRIER TO
BLOOD SOLUTES
SECRETES VASOCONSTRICTORS &
VASODILATORS

ARTERIES

MUST WITHSTAND PRESSURE

MORE MUSCULAR THAN VEINS
ROUND IN CROSS SECTION
THREE SIZE CATEGORIES

CONDUCTING (ELASTIC) ARTERIES

DISTRIBUTING (MUSCULAR) ARTERIES
RESISTANCE (SMALL) ARTERIES

ARTERIES
CONDUCTING (ELASTIC) ARTERIES
LARGEST ARTERIES
E.G., AORTA, PULMONARY ARTERIES
TUNICA MEDIA

NUMEROUS ALTERNATING THIN LAYERS OF

PERFORATED ELASTIC TISSUE

SMOOTH MUSCLE, COLLAGEN, AND ELASTIC FIBERS

EXPAND DURING SYSTOLE

RECOIL DURING DIASTOLE

MINIMIZES DOWNSTREAM PRESSURE

FLUCTUATIONS

ARTERIES
DISTRIBUTING (ELASTIC)
ARTERIES
SMALLER BRANCHES
E.G., BRACHIAL &
FEMORAL ARTERIES
FURTHER FROM THE
HEART
25 40 SMOOTH MUSCLE
LAYERS

75% OF WALL THICKNESS

ARTERIES
RESISTANCE (SMALL) ARTERIES
MAINLY UNNAMED
UP TO 25 SMOOTH MUSCLE LAYERS
LITTLE ELASTIC TISSUE
SMALLEST ARE ARTERIOLES

1-3 LAYERS OF SMOOTH MUSCLES

40 200 M DIAMETER

ARTERIES
METARTERIOLES
SHORT VESSELS LINKING ARTERIOLES
AND CAPILLARIES
TUNICA MEDIA DISCONTINUOUS

MUSCLE CELLS FORM PRECAPILLARY

SPHINCTER
ENCIRCLES CAPILLARY ENTRANCE
REGULATES MOVEMENT OF BLOOD INTO
CAPILLARIES

The Capillaries

Capillaries have walls only one cell

thick to allow exchange of gases and
nutrients with tissue fluid.
Capillary beds are present in all
regions of the body but not all capillary
beds are open at the same time.
Contraction of a sphincter muscle
closes off a bed and blood can flow
through an arteriovenous shunt that
bypasses the capillary bed.

CAPILLARIES

CENTRAL TO CIRCULATORY SYSTEM

SITE OF EXCHANGE BETWEEN BLOOD
AND TISSUES
SMALLEST BLOOD VESSELS
ENDOTHELIUM ONLY
THIN WALLS (0.2 M 0.4 M)
5 9 mM DIAMETER (AVERAGE)

CAPILLARY STRUCTURE

~ BILLION IN BODY
HUGE COLLECTIVE SURFACE AREA
6,300 SQUARE METERS (M 2)
> SIZE OF FOOTBALL FIELD
< 80 M FROM ALMOST ALL CELLS

SOME EXCEPTIONS
E.G., TENDONS, LIGAMENTS, ETC.

ORGANIZED INTO CAPILLARY BEDS

CAPILLARY BEDS

UNIT OF CAPILLARY ORGANIZATION

10 100 CAPILLARIES SUPPLIED BY
SINGLE METARTERIOLE
THOROUGHFARE CHANNEL

ARTERIOLE VENULE

PRECAPILLARY SPHINCTER AT ENTRANCE

TO EACH CAPILLARY

OPENED OR CLOSED

Anatomy of a capillary
bed

CAPILLARY BEDS

BLOOD VOLUME
THERE IS NOT ENOUGH BLOOD TO FILL
ALL BLOOD VESSELS
SIMULTANEOUSLY
~75% OF THE BODYS CAPILLARIES ARE
CLOSED AT ANY GIVEN TIME

TYPES OF CAPILLARIES
TWO TYPES OF CAPILLARIES
CONTINUOUS CAPILLARIES
FENESTRATED CAPILLARIES

TYPES OF CAPILLARIES
CONTINUOUS CAPILLARIES
OCCUR IN MOST TISSUES
ENDOTHELIAL CELLS HELD TOGETHER BY
TIGHT JUNCTIONS
FORM CONTINUOUS TUBE
INTERCELLULAR CLEFTS 4 nm WIDE

GLUCOSE, ETC. CAN PASS THROUGH

PLASMA PROTEINS, ETC. CANNOT

TYPES OF CAPILLARIES
FENESTRATED CAPILLARIES
ALLOW RAPID ABSORPTION / FILTRATION
KIDNEYS, SMALL INTESTINE, ETC.
RIDDLED WITH HOLES

FENESTRATIONS / FILTRATION PORES

20 100 nm DIAMETER
USUALLY COVERED WITH DIAPHRAGM
RAPID PASSAGE OF SMALL MOLECULES

CIS dan CES

TYPES OF CAPILLARIES
SINUSOIDS
IRREGULAR BLOOD-FILLED SPACES
BONE MARROW, SPLEEN, ETC.
SOME ARE CONTINUOUS CAPILLARIES
SOME ARE FENESTRATED CAPILLARIES

LARGE PORES
PROTEINS AND BLOOD CELLS CAN PASS
THROUGH
ALBUMIN, CLOTTING FACTORS, RBCs, ETC.

CAPILLARY EXCHANGE
CAPILLARIES
SITES OF EXCHANGE BETWEEN BLOOD
AND SURROUNDING TISSUES
ROUTES OF EXCHANGE

PASSAGE THROUGH FENESTRATIONS

PASSAGE THROUGH INTERCELLULAR
CLEFTS
PASAGE THROUGH ENDOTHELIAL CELL
CYTOPLASM

CAPILLARY EXCHANGE

MECHANISMS OF EXCHANGE

DIFFUSION
TRANSCYTOSIS
FILTRATION
REABSORPTION

CAPILLARY EXCHANGE
DIFFUSION
MOST IMPORTANT MECHANISM
MOVEMENT DOWN CONC GRADIENT
IMPORTANT FOR

O2, CO2, STEROID HORMONES

GLUCOSE, ELECTROLYTES, ETC.

THROUGH PLASMA MEMBRANE

THROUGH CHANNELS / CLEFTS / FENESTRATIONS

NOT IMPORTANT FOR

PROTEINS, ETC. (TOO BIG)

CAPILLARY EXCHANGE
TRANSCYTOSIS
MOVEMENT THROUGH EPITHELIAL CELLS
ENDOCYTOSIS, THEN EXOCYTOSIS
IMPORTANT FOR

FATTY ACIDS
ALBUMIN
SOME HORMONES (E.G., INSULIN)

CAPILLARY EXCHANGE
FILTRATION
CAPILLARY PRESSURE

TISSUE PRESSURE

~30 mmHg AT ARTERIAL END

~-3 mmHg

FLUID LEAVES AT ARTERIAL END

REDUCED, BUT NOT PREVENTED BY
ONCOTIC PRESSURE

CAPILLARY EXCHANGE

ONCOTIC PRESSURE

TISSUE FLUID HAS FEWER SOLUTES THAN

BLOOD
OSMOTIC FORCE PUSHING FLUID INTO
CAPILLARIES
CANNOT OVERCOME PRESSURE
DIFFERENCES AT ARTERIAL END OF CAP.
CAN OVERCOME PRESSURE DIFFERENCES AT
VENOUS END OF CAPILLARIES

CAPILLARY EXCHANGE
REABSORPTION
CAPILLARY PRESSURE

TISSUE PRESSURE

~ 10 mmHg AT VENOUS END

~-3 mmHg

ONCOTIC PRESSURE OVERWHELMS

PRESSURE DIFFERENCE
FLUID ENTERS AT VENOUS END

CAPILLARY EXCHANGE
FILTRATION AND REABSORPTION
FLUID LEAVES CAPILLARY AT ARTERIAL
END
~85% OF FLUID REENTERS CAPILLARY AT
VENOUS END

CAPILLARIES ARE LARGER AND MORE

NUMEROUS AT VENOUS END

~15% REENTERS RETURNED VIA

LYMPHATIC SYSTEM

CAPILLARY EXCHANGE
EDEMA
EXCESS FLUID IN A TISSUE
ACCUMULATION CAUSED BY

INCREASED CAPILLARY FILTRATION

REDUCED CAPILLARY REABSORPTION
OBSTRUCTED LYMPHATIC DRAINAGE

CAPILLARY EXCHANGE
CAUSES OF EDEMA
INCREASED CAPILLARY FILTRATION
CAUSES (E.G.)

INCREASED CAPILLARY B.P.

INCREASED CAPILLARY PERMEABILITY
CONGESTIVE HEART FAILURE
POOR VENOUS RETURN
INSUFFICIENT MUSCULAR ACTIVITY
KIDNEY FAILURE HYPERTENSION

CAPILLARY EXCHANGE
CAUSES OF EDEMA
REDUCED CAPILLARY REABSORPTION
CAUSES (E.G.)

BLOOD ALBUMIN DEFICIENCY

REDUCED ONCOTIC PRESSURE

LIVER DISEASES (LESS ALBUMIN)

HYPOPROTEINEMIA (LESS ALBUMIN)

CAPILLARY EXCHANGE
CAUSES OF EDEMA
OBSTRUCTED LYMPHATIC DRAINAGE

~15% OF FLUID LOST IS RETURNED VIA

LYMPHATIC SYSTEM
OBSTRUCTION OR REMOVAL INTERFERES
WITH THIS RETURN

VEINS

CAPILLARIES VENULES VEINS

RETURN BLOOD TO THE HEART
FURTHER FROM THE HEART
LOWER BLOOD PRESSURE THAN
ARTERIES

AVERAGE 10 mmHg VS. 100 mmHg

NEED NOT WITHSTAND HIGH PRESSURES

VEINS

THINNER WALLS

LESS SMOOTH MUSCLE

LESS ELASTIC TISSUE

COLLAPSE WHEN EMPTY

EXPAND MORE EASILY
PRESSURE NOT HIGH ENOUGH TO RETURN
BLOOD TO HEART
VENOUS VALVES AND MASSAGING ASSIST
RETURN

VEINS
VENULES
15 100 M DIAMETER
PROXIMAL END POROUS

FLUID EXCHANGE WITH TISSUES

GAINS TUNICA MEDIA

SMOOTH MUSCLE SPARSE
TRIBUTARIES VEINS

VEINS
VENOUS SINUSES
ESPECIALLY THIN WALLS
LARGE LUMENS
NO SMOOTH MUSCLE
E.G., CORONARY SINUS OF THE HEART

VENOUS RETURN

FLOW OF BLOOD BACK TO THE HEART

MECHANISMS OF VENOUS RETURN

PRESSURE GRADIENT
THORACIC (RESPIRATORY) PUMP
CARDIAC SUCTION
SKELETAL MUSCLE PUMP
GRAVITY

VENOUS RETURN
PRESSURE GRADIENT
MOST IMPORTANT FORCE IN VENOUS
RETURN
VENULE PRESSURE ~15 mmHg
VENA CAVAE PRESSURE ~ 4.6 mmHg
BLOOD FLOW TO THE HEART FAVORED
BY P

VENOUS RETURN
THORACIC (RESPIRATORY) PUMP
INFERIOR VENA CAVA SPANS
ABDOMINAL AND THORACIC CAVITIES
DURING INHALATION

THORACIC PRESSURE DROPS

ABDOMINAL PRESSURE INCREASES
FLOW OF BLOOD FROM ABDOMINAL TO
THORACIC CAVITY PROMOTED

VENOUS RETURN
CARDIAC SUCTION
DURING VENTRICULAR SYSTOLE

CHORDAE TENDINEAE PULL AV VALVE

CUSPS TOWARD VENTRICLES
ATRIAL SPACE SLIGHTLY INCREASED
BLOOD DRAWN INTO ATRIA

VENOUS RETURN
SKELETAL MUSCLE PUMP
VEINS SURROUNDED AND SQUEEZED
BY SKELETAL MUSCLES
BLOOD SQUEEZED OUT
VALVES

SIMILAR TO SEMILUNAR VALVES

INSURE UNIDIRECTIONAL FLOW

VENOUS RETURN
GRAVITY
BLOOD IN HEAD AND NECK SIMPLY
FLOWS DOWNHILL

VENOUS RETURN
EFFECTS OF EXERCISE
INCREASED CARDIAC OUTPUT

BLOOD VESSEL DILATION

INCREASED FLOW RATE

INCREASED RESPIRATORY RATE

INCREASED BLOOD PRESSURE

ENHANCED THORACIC PUMP

MUSCLE CONTRACTIONS

ENHANCED SKELETAL MUSCLE PUMP

CIRCULATORY ROUTES

HEART
ARTERIES
ARTERIOLES
METARTERIOLES
CAPILLARIES
METARTERIOLES
VENULES
VEINS
HEART

CIRCULATORY ROUTES

TYPICAL CIRCULATORY ROUTE

HEART ARTERIES ARTERIOLES CAPILLARIES

CAPILLARIES VENULES VEINS HEART

USUALLY PASSES THROUGH SINGLE

CAPILLARY BED

EXCEPTIONS?

CIRCULATORY ROUTES
PORTAL SYSTEM
BLOOD FLOWS THROUGH TWO
CONSECUTIVE CAPILLARY BEDS
E.G. KIDNEYS

CIRCULATORY ROUTES
ANASTOMOSIS
TWO VESSELS (VEINS OR ARTERIES)
MERGE WITH EACH OTHER

ARTERIOVENOUS ANASTOMOSIS
ARTERIAL ANASTOMOSIS
VENOUS ANASTOMOSIS

CIRCULATORY ROUTES
ARTERIOVENOUS ANASTOMOSIS
SHUNT
ARTERY VEIN
BYPASSES CAPILLARIES
E.G. FINGERS, TOES, EARS, ETC.
REDUCE HEAT LOSS
MORE SUSCEPTIBLE TO FROSTBITE

CIRCULATORY ROUTES
ARTERIAL ANASTOMOSIS
TWO ARTERIES MERGE
PROVIDE ALTERNATIVE ROUTES OF
BLOOD SUPPLY TO A TISSUE
E.G. CORONARY CIRCULATION,
AROUND JOINTS

CIRCULATORY ROUTES
VENOUS ANASTOMOSIS
TWO VEINS MERGE
MORE COMMON
ALTERNATIVE ROUTS OF DRAINAGE
FROM AN ORGAN

Cardiovascular system
diagram

The Pulmonary Circuit

The pulmonary circuit begins with

the pulmonary trunk from the right
ventricle which branches into two
pulmonary arteries that take oxygenpoor blood to the lungs.
In the lungs, oxygen diffuses into the
blood, and carbon dioxide diffuses
out of the blood to be expelled by
the lungs.
Four pulmonary veins return oxygenrich blood to the left atrium.

The Systemic Circuit

The systemic circuit starts with the
aorta carrying O2-rich blood from
the left ventricle.
The aorta branches with an artery
going to each specific organ.
Generally, an artery divides into
arterioles and capillaries which
then lead to venules.

The vein that takes blood to the vena

cava often has the same name as the
artery that delivered blood to the
organ.
In the adult systemic circuit, arteries
carry blood that is relatively high in
oxygen and relatively low in carbon
dioxide, and veins carry blood that is
relatively low in oxygen and relatively
high in carbon dioxide.
This is the reverse of the pulmonary
circuit.

Major arteries and veins

of the systemic circuit

The coronary arteries serve the

heart muscle itself; they are the
first branch off the aorta.
Since the coronary arteries are
so small, they are easily clogged,
leading to heart disease.
The hepatic portal system carries
blood rich in nutrients from
digestion in the small intestine to
the liver, the organ that monitors
the composition of the blood.

The Heart
The heart is a cone-shaped, muscular
organ located between the lungs
behind the sternum.
The heart muscle forms the
myocardium, with tightly interconnect
cells of cardiac muscle tissue.
The pericardium is the outer
membranous sac with lubricating
fluid.

The heart has four chambers: two upper,

thin-walled atria, and two lower, thickwalled ventricles.
The septum is a wall dividing the right
and left sides.
Atrioventricular valves occur between
the atria and ventricles the tricuspid
valve on the right and the bicuspid valve
on the left; both valves are reenforced by
chordae tendinae attached to muscular
projections within the ventricles.

External heart
anatomy

Coronary artery
circulation

Passage of Blood
Through the Heart

Blood follows this sequence through

the heart: superior and inferior vena
cava right atrium tricuspid valve
right ventricle pulmonary
semilunar valve pulmonary trunk
and arteries to the lungs pulmonary
veins leaving the lungs left atrium
bicuspid valve left ventricle aortic
semilunar valve aorta to the
body.

Internal view of the

heart

The pumping of the heart sends out

blood under pressure to the arteries.
Blood pressure is greatest in the
aorta; the wall of the left ventricle is
thicker than that of the right ventricle
and pumps blood to the entire body.
Blood pressure then decreases as the
cross-sectional area of arteries and
then arterioles increases.

Path of blood through the

heart

The Heartbeat

Each heartbeat is called a cardiac cycle.

When the heart beats, the two atria
contract together, then the two
ventricles contract; then the whole
heart relaxes.
Systole is the contraction of heart
chambers; diastole is their relaxation.
The heart sounds, lub-dup, are due to
the closing of the atrioventricular
valves, followed by the closing of the
semilunar valves.

Intrinsic Control of
Heartbeat
The SA (sinoatrial) node, or pacemaker,
initiates the heartbeat and causes the
atria to contract on average every 0.85
seconds.
The AV (atrioventricular) node conveys
the stimulus and initiates contraction of
the ventricles.
The signal for the ventricles to contract
travels from the AV node through the
atrioventricular bundle to the smaller
Purkinje fibers.

Conduction system of
the heart

Extrinsic Control of
Heartbeat

A cardiac control center in the medulla

oblongata speeds up or slows down the
heart rate by way of the autonomic
nervous system branches:
parasympathetic system (slows heart
rate) and the sympathetic system
(increases heart rate).
Hormones epinephrine and
norepinephrine from the adrenal
medulla also stimulate faster heart
rate.

The Heart
The heart is a cone-shaped, muscular
organ located between the lungs
behind the sternum.
The heart muscle forms the
myocardium, with tightly interconnect
cells of cardiac muscle tissue.
The pericardium is the outer
membranous sac with lubricating
fluid.

The heart has four chambers: two upper,

thin-walled atria, and two lower, thickwalled ventricles.
The septum is a wall dividing the right
and left sides.
Atrioventricular valves occur between
the atria and ventricles the tricuspid
valve on the right and the bicuspid valve
on the left; both valves are reenforced by
chordae tendinae attached to muscular
projections within the ventricles.

External heart
anatomy

Coronary artery
circulation

Passage of Blood
Through the Heart

Blood follows this sequence through

the heart: superior and inferior vena
cava right atrium tricuspid valve
right ventricle pulmonary
semilunar valve pulmonary trunk
and arteries to the lungs pulmonary
veins leaving the lungs left atrium
bicuspid valve left ventricle aortic
semilunar valve aorta to the
body.

Internal view of the

heart

The pumping of the heart sends out

blood under pressure to the arteries.
Blood pressure is greatest in the
aorta; the wall of the left ventricle is
thicker than that of the right ventricle
and pumps blood to the entire body.
Blood pressure then decreases as the
cross-sectional area of arteries and
then arterioles increases.

Path of blood through the

heart

The Heartbeat

Each heartbeat is called a cardiac cycle.

When the heart beats, the two atria
contract together, then the two
ventricles contract; then the whole
heart relaxes.
Systole is the contraction of heart
chambers; diastole is their relaxation.
The heart sounds, lub-dup, are due to
the closing of the atrioventricular
valves, followed by the closing of the
semilunar valves.

Intrinsic Control of
Heartbeat
The SA (sinoatrial) node, or pacemaker,
initiates the heartbeat and causes the
atria to contract on average every 0.85
seconds.
The AV (atrioventricular) node conveys
the stimulus and initiates contraction of
the ventricles.
The signal for the ventricles to contract
travels from the AV node through the
atrioventricular bundle to the smaller
Purkinje fibers.

Conduction system of
the heart

Extrinsic Control of
Heartbeat

A cardiac control center in the medulla

oblongata speeds up or slows down the
heart rate by way of the autonomic
nervous system branches:
parasympathetic system (slows heart
rate) and the sympathetic system
(increases heart rate).
Hormones epinephrine and
norepinephrine from the adrenal
medulla also stimulate faster heart
rate.

HEART VALVES
ATRIOVENTRICULAR (AV) VALVES
ATRIUM VENTRICLE
VENTRICLE RELAXED

VALVE OPEN
ATRIUM VENTRICLE BLOOD FLOW

VENTRICLE CONTRACTS

VENTRICLE PRESSURE INCREASES

VALVE CLOSES
PREVENTS BACK FLOW

HEART VALVES
ATRIOVENTRICULAR (AV) VALVES
PAPILLARY MUSCLES

CONTRACT WITH REST OF VENTRICLE

PULL ON CHORDAE TENDINEAE

CHORDAE TENDINEAE

CONNECT AV VALVE CUSPS TO PAPILLARY

MUSCLES OF
REINFORCE AV VALVES
PREVENT PROLAPSE

HEART VALVES
SEMILUNAR VALVES
VENTRICLE ARTERY
VENTRICLE RELAXED

PRESSURE HIGHER IN ARTERIES

VALVE CLOSED

VENTRICLE CONTRACTS

PRESSURE HIGHER IN VENTRICLE

VALVES FORCED OPEN
BLOOD FLOWS FROM HEART

HEART STRUCTURE
PERICARDIUM
DOUBLE-WALLED SAC
ENCLOSES HEART
CONTAINS PERICARDIAL FLUID (5-30 ML)
GREATLY REDUCES FRICTION

HEART STRUCTURE
HEART WALL
EPICARDIUM (OUTER)

MYOCARDIUM

A.K.A. VISCERAL PERICARDIUM

THICKEST LAYER
CARDIAC MUSCLE

ENDOCARDIUM

SMOOTH INNER LINING

CONTINUOUS WITH BLOOD VESSELS

HEART STRUCTURE
MYOCARDIUM
THICKEST; CARDIAC MUSCLE
MUSCLE FIBERS CONNECTED BY
FIBROUS (PROTEIN) SKELETON

STRUCTURAL SUPPORT
SOMETHING TO PULL AGAINST
ELECTRICAL NONCONDUCTOR

ALLOWS ATRIA AND VENTRICLES TO CONTRACT

SEPARATELY

CARDIAC MUSCLE STRUCTURE

CARDIAC MUSCLE CELLS
MYOCYTES / CARDIOCYTES

STRIATED
SHORT, THICK (50 100 M x 10 - 20 M)
BRANCHED
SINGLE NUCLEUS
LESS DEVELOPED SR (SER)
LARGER T-TUBULES (ADMIT Ca++)
JOINED VIA INTERCALATED DISKS

CARDIAC MUSCLE STRUCTURE

INTERCALATED DISK FEATURES
INTERDIGITATING FOLDS

MECHANICAL JUNCTIONS

INCREASED SURFACE AREA CONTACT

FASCIA ADHERENS (ACTIN)
DESMOSOMES

ELECTRICAL JUNCTIONS

GAP JUNCTIONS
ELECTRICALLY STIMULATE NEIGHBORS

CARDIAC METABOLISM

EXCLUSIVELY AEROBIC
MYOGLOBIN-RICH (STORED O2)
GLYCOGEN-RICH (STORED SUGAR)
LARGE MITOCHONDRIA (25% VS 2%)
MULTIPLE FUELS USABLE
VULNERABLE TO O2 DEFICIENCY
NOT PRONE TO FATIGUE

(AEROBIC, NO O2 DEBT, NO FATIGUE)

GBR SISTEM KONDUKSI

Sistem konduksi

MEKANISME POMPA JANTUNG

CARDIAC RHYTHM
HEARTBEAT
INVERTEBRATES

TRIGGERED BY NERVOUS SYTEM

VERTEBRATES

TRIGGERED BY HEART ITSELF

CARDIAC RHYTHM
CARDIAC MYOCYTES
AUTORHYTHMIC

SPONTANEOUS DEPOLARIZATION AT
REGULAR INTERVALS

SOME SPECIALIZED TO GENERATE ACTION

POTENTIALS

CARDIAC CONDUCTION SYSTEM

SINOATRIAL (SA) NODE
ATRIOVENTRICULAR (AV) NODE

CARDIAC RHYTHYM
SINOATRIAL (SA) NODE
MYOCYTES IN RIGHT ATRIUM
PACEMAKER
INITIATES HEARTBEAT
DETERMINES HEART RATE
FIRING RATE REDUCED BY NERVES
70 80 BEATS PER MINUTE (BPM)

CARDIAC RHYTHYM
SINOATRIAL (SA) NODE
CELLS LACK STABLE RESTING MEMBRANE
POTENTIAL
SPONTANEOUSLY DEPOLARIZE AND
REPOLARIZE AT REGULAR INTERVALS (~0.8
SEC)
EACH DEPOLARIZATION INITIATES ONE
HEARTBEAT
GENERATE ACTION POTENTIAL

CARDIAC RHYTHYM
SA ACTION POTENTIAL
SPREADS THROUGHOUT ATRIAL
MYOCARDIUM
ATRIA CONTRACT ~SIMULTANEOUSLY
SIGNAL REACHES AV NODE (50MSEC)
DELAYED AT AV NODE (100 MSEC)
VENTRICLES FILL DURING DELAY

CARDIAC RHYTHYM
ATRIOVENTRICULAR (AV) NODE
NEAR RIGHT AV VALVE
ELECTRICAL GATEWAY TO VENTRICLES
DISTRIBUTES SIGNAL TO
VENTRICULAR MYOCARDIUM

AV BUNDLE
PURKINJE FIBERS

CARDIAC RHYTHYM

SIGNAL TRAVELS FROM AV THROUGH

VENTRICULAR MYOCARDIUM
VENTRICULES CONTRACT
~SIMULTANEOUSLY
(PAPILLARY MUSCLES CONTRACT
FIRST)

CARDIAC RHYTHYM
CARDIAC ACTION POTENTIALS
PROLONGED DEPOLARIZATION

200 - 250 MSEC VS. 2 MSEC

RESULT OF SLOW Ca++ CHANNELS

SUSTAINED CONTRACTION
LONGER REFRACTORY PERIOD

200 MSEC VS. 1 2 MSEC

PREVENTS WAVE SUMMATION, TETANUS

SYSTOLE / DIASTOLE

SYSTOLE

CONTRACTION OF A HEART CHAMBER

REFERS TO VENTRICLE UNLESS
OTHERWISE NOTED

DIASTOLE

PERIOD DURING WHICH A HEART

CHAMBER RELAXES AND FILLS WITH
BLOOD

HUKUM FRANK STARLING

BLOOD FLOW

AMOUNT OF BLOOD FLOWING

THROUGH A TISSUE/ORGAN/VESSEL IN
A GIVEN TIME

E.G., ML/MIN

SUPPLIES NUTRIENTS AND OXYGEN TO

CELLS
REMOVES WASTES FROM CELLS

BLOOD FLOW
PERFUSION
RATE OF BLOOD FLOW PER GIVEN
MASS/VOLUME OF TISSUE

E.G., ML/MIN/G

BLOOD FLOW

MUST KEEP PACE WITH METABOLIC

RATE OF CELLS

TOTAL FLOW CONSTANT IN RESTING

INDIVIDUAL

NECROSIS (TISSUE DEATH)

EQUAL TO CARDIAC OUTPUT

FLOW TO INDIVIDUAL ORGANS VARIES

CONTINUALLY

BLOOD FLOW
HEMODYNAMICS
PHYSICAL PRINCIPLES OF BLOOD FLOW
BASED UPON

PRESSURE DIFFERENCES (P)

INCREASED PRESSURE DIFFERENCE

INCREASED FLOW

RESISTANCE (R)

INCREASED RESISTANCE DECREASED FLOW

BLOOD PRESSURE

EASILY MEASURED
SYSTOLIC PRESSURE

DIASTOLIC PRESSURE

PEAK PRESSURE DURING SYSTOLE

PRESSURE DURING DIASTOLE

PULSE PRESSURE

SYSTOLIC MINUS DIASTOLIC

MEASURE OF STRESS ON ARTERIES

BLOOD PRESSURE
MEAN ARTERIAL PRESSURE (MAP)
AVERAGE OF CONTINUOUS READINGS
ESTIMATE

DIASTOLIC + 1/3 PULSE PRESSURE

AFFECTED BY GRAVITY

~62 mmHg IN HEAD

~180 mmHg IN ANKLES

BLOOD PRESSURE

HYPERTENSION

CHRONIC RESTING BP > 140/90

CHRONIC, NOT TRANSIENT

CAN WEAKEN SMALL ARTERIES

ANEURYSMS

HYPOTENSION

CHRONIC LOW RESTING BP

RESULT OF ANEMIA, BLOOD LOSS,
DEHYDRATION, ETC.

BLOOD PRESSURE
ANEURYSM
WEAK POINT IN BLOOD VESSEL
PULSATES, MAY RUPTURE

PAIN, DEATH

RESULT FROM

CONGENITAL WEAKNESS
TRAUMA
INFECTIONS (E.G., SYPHILIS)
ATHEROSCLEROSIS AND HYPERTENSION

BLOOD PRESSURE

ARTERIES DISTEND AND RECOIL

ABSORB SOME OF THE FORCE OF THE EJECTED

BLOOD
REDUCE PRESSURE FLUCTUATIONS
MAINTAIN STEADY BLOOD FLOW
CONTINUOUS, YET PULSATILE
AORTA 120 CM/SEC SYSTOLE
AORTA 40 CM/SEC DIASTOLE

DOWNSTREAM B.P. & PRESSURE FLUCTUATIONS

REDUCED

BLOOD PRESSURE
EFFECTS OF AGING
INCREASE IN BLOOD PRESSURE
ARTERIES LESS DISTENDIBLE
ATHEROSCLEROSIS STIFFENS ARTERIES

RESISTANCE
PERIPHERAL RESISTANCE
RESISTANCE BLOOD ENCOUNTERS IN THE
VESSELS
RESULTS FROM FRICTION AGAINST VESSEL
WALLS
PROPORTIONAL TO THREE VARIABLES

BLOOD VISCOSITY
VESSEL LENGTH
VESSEL RADIUS

RESISTANCE
VARIABLES AFFECTING RESISTANCE
BLOOD VISCOSITY

MAINLY DUE TO ERYTHROCYTES AND

PLASMA PROTEINS
INCR VISCOSITY INCR RESISTANCE

RESISTANCE
VARIABLES AFFECTING RESISTANCE
VESSEL LENGTH

FRICTION IS CUMULATIVE
INCR LENGTH INCR RESISTANCE

RESISTANCE
VARIABLES AFFECTING RESISTANCE
VESSEL RADIUS

INNATE RADIUS DIFFERENCES

ALTERATIONS POSSIBLE
VASOCONSTRICTION (NARROWING)
VASODILATION (WIDENING)

INCREASED FRICTION NEAR VESSEL WALL

DECR RADIUS INCR RESISTANCE

RESISTANCE
LAMINAR FLOW
BLOOD TRAVELS IN SHEETS
FASTER NEAR CENTER OF VESSEL

SLOWER NEAR VESSEL WALLS

LESS FRICTION
MORE FRICTION

SIMILAR TO WATER FLOW IN RIVERS

RESISTANCE
LAMINAR FLOW
LARGER VESSELS

SMALLER VESSELS

GREATER FRACTION OF BLOOD IN CENTER

GREATER FRACTION OF BLOOD NEAR
VESSEL WALLS

RESISTANCE = CONSTANT / RADIUS4

FLOW RATE = CONSTANT * RADIUS4

REGULATION OF BLOOD
SUPPLY
VASOCONSTRICTION
WIDESPREAD VASOCONSTRICTION

RESULTS IN INCREASE IN BP
RESULTS IN INCREASED PERFUSION

LOCALIZED VASOCONSTRICTION

INCREASES RESISTANCE IN AREA

REDIRECTS BLOOD FROM ONE ORGAN TO
ANOTHER

REGULATION OF BLOOD
SUPPLY
LOCAL CONTROL
AUTOREGULATION
REACTIVE HYPEREMIA
VASOACTIVE CHEMICALS
ANGIOGENESIS

REGULATION OF BLOOD
SUPPLY
LOCAL CONTROL
AUTOREGULATION

INADEQUATE BLOOD FLOW

BUILDUP OF WASTE PRODUCTS
VASODILATION STIMULATED
INCREASED BLOOD FLOW

REGULATION OF BLOOD
SUPPLY
LOCAL CONTROL
REACTIVE HYPEREMIA

BLOOD SUPPLY CUT OFF, THEN RESTORED

INCREASED BEYOND NORMAL LEVEL OF
FLOW
E.G., AFTER COMING IN FROM COLD
POSSIBLY DUE TO BUILDUP OF WASTE
PRODUCTS

REGULATION OF BLOOD
SUPPLY
LOCAL CONTROL
VASOACTIVE CHEMICALS

RELEASED BY PLATELETS, ENDOTHELIAL

CELLS, ETC.
E.G., HISTAMINE

STIMULATES VASODILATION

E.G., PROSTACYCLIN

STIMULATES VASOCONSTRICTION

REGULATION OF BLOOD
SUPPLY
LOCAL CONTROL
ANGIOGENESIS

GROWTH OF NEW BLOOD VESSELS

LONG-TERM CHANGE
E.G. REGROWTH OF UTERINE LINING
FOLLOWING MENSTRUATION
E.G., MUSCLES OF ATHLETES
E.G., ARTERIAL BYPASSES AROUND
CORONARY OBSTRUCTIONS

REGULATION OF BLOOD
SUPPLY
NEURAL CONTROL
VASOMOTOR CENTER OF MEDULLA
OBLONGATA
NERVE FIBERS

CAN STIMULATE VASOCONSTRICTION IN

MOST BLOOD VESSELS
CAN STIMULATE VASODILATION IN
CARDIAC AND SKELETAL MUSCLE

REGULATION OF BLOOD
SUPPLY
NEURAL CONTROL
THREE AUTONOMIC REFLEXES

BAROREFEXES
CHEMOREFLEXES
MEDULLARY ISCHEMIC REFLEXES

Guyenet Nature Reviews Neuroscience 7, 335346 (May 2006) | doi:10.1038/nrn1902

REGULATION OF BLOOD
SUPPLY
NEURAL CONTROL
BAROREFLEXES

RESPONSE TO D IN BLOOD PRESSURE

DETECTED BY BARORECEPTORS
PRESENT IN AORTIC ARCH AND IN OTHER
ARTERIES ABOVE HEART
NEGATIVE FEEDBACK RESPONSE

REGULATION OF BLOOD
SUPPLY
NEURAL CONTROL
CHEMOREFLEXES

RESPONSE TO IN BLOOD CHEMISTRY

ESPECIALLY pH, [O2], [CO2]

D DETECTED BY CHEMORECEPTORS
PRESENT IN AORTIC ARCH AND IN OTHER
ARTERIES ABOVE HEART
ADJUST RESPIRATION
STIMULATE VASOCONSTRICTION

INCREASE BP INCREASE PERFUSION

REGULATION OF BLOOD
SUPPLY
NEURAL CONTROL
MEDULLARY ISCHEMIC REFLEX

RESPONSE TO INADEQUATE PERFUSION IN

BRAINSTEM
INCREASE HEART RATE & CONTRACTION
FORCE
INDUCE WIDESPREAD VASOCONSTRICTION

INCREASE BP INCREASE PERFUSION

REGULATION OF BLOOD
SUPPLY
HORMONAL CONTROL
ANGIOTENSIN II

VASOCONSTRICTIVE HORMONE

ANGIOTENSINOGEN ANGIOTENSIN I

INCREASE BP INCREASE PERFUSION

CONVERSION STIMULATED BY RENIN
KIDNEYS PRODUCE RENIN IN RESPONSE TO LOW BP

ANGIOTENSIN I ANGIOTENSIN II

CONVERSION STIMULATED BY ACE (ENZYME)

ACE PRESENT IN LUNGS
ACE INHIBITORS TREAT HYPERTENSION

MEKANISME ACE inhibitor

ACE dan AT II
Perubahan angiotensinogen ke AT I & AT II

ANGIOTENSIN II

1.
2.
3.
4.

Angiotensonogen dari hati dirubah

oleh renin menjadi angiotensin I (ATI).
AT I oleh chimase dirubah menjadi AT
II
ATII memiliki efek:
Meningkatkan aktivitas jantung
Meningkatkan tahanan perifer
Memacu sekresi ADH dan aldosteron
Merangsang pusat haus

REGULATION OF BLOOD
SUPPLY
HORMONAL CONTROL
EPINEPHRINE / NOREPINEPHRINE

VASOACTIVE HORMONES

BIND TO -ADRENERGIC RECEPTORS ON SMOOTH

MUSCLE OF MOST BLOOD VESSELS

VASOCONSTRICTION
INCREASE BP INCREASE PERFUSION

BIND TO -ADRENERGIC RECEPTORS ON BLOOD VESSELS

OF SKELETAL MUSCLE AND CORONARY BLOOD VESSELS

VASODILATION
INCREASED BLOOD FLOW TO HEART & MUSCLES

The Electrocardiogram
An electrocardiogram (ECG) is a
recording of the electrical changes
that occur in the myocardium during
a cardiac cycle.
Atrial depolarization creates the P
wave, ventricle depolarization
creates the QRS wave, and
repolarization of the ventricles
produces the T wave.

Electrocardiogram

The Vascular Pathways

1)

2)

3)

The cardiovascular system

includes two circuits:
Pulmonary circuit which circulates
blood through the lungs, and
Systemic circuit which circulates
blood to the rest of the body.
Both circuits are vital to
homeostasis.

Blood Flow
The beating of the heart is
necessary to homeostasis
because it creates pressure that
propels blood in arteries and the
arterioles.
Arterioles lead to the capillaries
where nutrient and gas exchange
with tissue fluid takes place.

Blood Flow in Arteries

Blood pressure due to the pumping

of the heart accounts for the flow of
blood in the arteries.
Systolic pressure is high when the
heart expels the blood.
Diastolic pressure occurs when the
heart ventricles are relaxing.
Both pressures decrease with
distance from the left ventricle
because blood enters more and
more arterioles and arteries.

Cross-sectional area as it
relates to blood pressure and
velocity

Blood Flow in
Capillaries
Blood moves slowly in capillaries
because there are more
capillaries than arterioles.
This allows time for substances to
be exchanged between the blood
and tissues.

Blood Flow in Veins

1)
2)
3)

Venous blood flow is dependent upon:

skeletal muscle contraction,
presence of valves in veins, and
respiratory movements.
Compression of veins causes blood to
move forward past a valve that then
prevents it from returning backward.

Changes in thoracic and abdominal

pressure that occur with breathing
also assist in the return of blood.
Varicose veins develop when the
valves of veins become weak.
Hemorrhoids (piles) are due to
varicose veins in the rectum.
Phlebitis is inflammation of a vein
and can lead to a blood clot and
possible death if the clot is dislodged
and is carried to a pulmonary vessel.

Blood

Blood separates into two main parts:

plasma and formed elements.
Plasma accounts for 55% and formed
elements 45% of blood volume.
Plasma contains mostly water (9092%)
and plasma proteins (78%), but it also
contains nutrients and wastes.
Albumin is a large plasma protein that
transports bilirubin; globulins are plasma
proteins that transport lipoproteins.

Composition of blood

The Red Blood Cells

Red blood cells (erythrocytes or RBCs)

are made in the red bone marrow of
the skull, ribs, vertebrae, and the
ends of long bones.
Normally there are 4 to 6 million RBCs
per mm3 of whole blood.
Red blood cells contain the pigment
hemoglobin for oxygen transport;
hemogobin contains heme, a complex
iron-containing group that transports
oxygen in the blood.

Physiology of red blood

cells

The air pollutant carbon

monoxide combines more readily
with hemoglobin than does
oxygen, resulting in oxygen
deprivation and possible death.
Red blood cells lack a nucleus
and have a 120 day life span.
When worn out, the red blood
cells are dismantled in the liver
and spleen.

Iron is reused by the red bone marrow

where stem cells continually produce
more red blood cells; the remainder of
the heme portion undergoes chemical
degradation and is excreted as bile
pigments into the bile.
Lack of enough hemoglobin results in
anemia.
The kidneys produce the hormone
erythropoietin to increase blood cell
production when oxygen levels are low.

The White Blood Cells

White blood cells (leukocytes) have

nuclei, are fewer in number than
RBCs, with 5,000 10,000 cells per
mm3, and defend against disease.
Leukocytes are divided into granular
and agranular based on appearance.
Granular leukocytes (neutrophils,
eosinophils, and basophils) contain
enzymes and proteins that defend
the body against microbes.

The aganular leukocytes (monocytes

and lymphocytes) have a spherical or
kidney-shaped nucleus.
Monocytes can differentiate into
macrophages that phagocytize
microbes and stimulate other cells to
defend the body.
Lymphocytes are involved in immunity.
An excessive number of white blood
cells may indicate an infection or
leukemia; HIV infection drastically
reduces the number of lymphocytes.

Macrophage engulfing
bacteria

The Platelets and Blood

Clotting

Red bone marrow produces large

cells called megakaryocytes that
fragment into platelets at a rate of
200 billion per day; blood contains
150,000300,000 platelets per mm3.
Twelve clotting factors in the blood
help platelets form blood clots.

Blood Clotting

Injured tissues release a clotting factor

called prothrombin activator, which
converts prothrombin into thrombin.
Thrombin, in turn, acts as an enzyme
and converts fibrinogen into insoluble
threads of fibrin.
These conversions require the
presence of calcium ions (Ca2+).
Trapped red blood cells make a clot
appear red.

Blood clotting

Hemophilia

Hemophilia is an inherited clotting

disorder due to a deficiency in a
clotting factor.
Bumps and falls cause bleeding in the
joints; cartilage degeneration and
resorption of bone can follow.
The most frequent cause of death is
bleeding into the brain with
accompanying neurological damage.

Bone Marrow Stem

Cells
A stem cell is capable of dividing
into new cells that differentiate into
particular cell types.
Bone marrow is multipotent, able to
continually give rise to particular
types of blood cells.
The skin and brain also have stem
cells, and mesenchymal stem cells
give rise to connective tissues
including heart muscle.

Blood cell formation in red

bone marrow

Capillary Exchange

At the arteriole end of a capillary,

water moves out of the blood due to
the force of blood pressure.
At the venule end, water moves into
the blood due to osmotic pressure of
the blood.
Substances that leave the blood
contribute to tissue fluid, the fluid
between the bodys cells.

In the midsection of the capillary,

nutrients diffuse out and wastes
diffuse into the blood.
Since plasma proteins are too large
to readily pass out of the capillary,
tissue fluid tends to contain all
components of plasma except it has
lesser amounts of protein.
Excess tissue fluid is returned to the
blood stream as lymph in lymphatic
vessels.

Capillary exchange

Cardiovascular Disorders

Cardiovascular disease (CVD) is the

leading cause of death in Western
countries.
Modern research efforts have improved
diagnosis, treatment, and prevention.
Major cardiovascular disorders include
atherosclerosis, stroke, heart attack,
aneurysm, and hypertension.

Atherosclerosis
Atherosclerosis is due to a build-up of
fatty material (plaque), mainly
cholesterol, under the inner lining of
arteries.
The plaque can cause a thrombus
(blood clot) to form.
The thrombus can dislodge as an
embolus and lead to
thromboembolism.

Stroke, Heart Attack,

and Aneurysm

A cerebrovascular accident, or stroke,

results when an embolus lodges in a
cerebral blood vessel or a cerebral
blood vessel bursts; a portion of the
brain dies due to lack of oxygen.
A myocardial infarction, or heart
attack, occurs when a portion of heart
muscle dies due to lack of oxygen.

Partial blockage of a coronary artery

causes angina pectoris, or chest pain.
An aneurysm is a ballooning of a
blood vessel, usually in the abdominal
aorta or arteries leading to the brain.
Death results if the aneurysm is in a
large vessel and the vessel bursts.
Atherosclerosis and hypertension
weaken blood vessels over time,
increasing the risk of aneurysm.

Coronary Bypass
Operations

A coronary bypass operation

involves removing a segment of
another blood vessel and replacing
a clogged coronary artery.
It may be possible to replace this
surgery with gene therapy that
stimulates new blood vessels to
grow where the heart needs more
blood flow.

Coronary bypass
operation

Clearing Clogged
Arteries

Angioplasty uses a long tube

threaded through an arm or leg
vessel to the point where the
coronary artery is blocked; inflating
the tube forces the vessel open.
Small metal stents are expanded
inside the artery to keep it open.
Stents are coated with heparin to
prevent blood clotting and with
chemicals to prevent arterial closing.

Angioplasty

Dissolving Blood Clots

Medical treatments for dissolving

blood clots include use of t-PA (tissue
plasminogen activator) that converts
plasminogen into plasmin, an
enzyme that dissolves blood clots,
but can cause brain bleeding.
Aspirin reduces the stickiness of
platelets and reduces clot formation
and lowers the risk of heart attack.

Heart Transplants and

Artificial Hearts
Heart transplants are routinely
performed but immunosuppressive
drugs must be taken thereafter.
There is a shortage of human organ
donors.
Work is currently underway to
improve self-contained artificial
hearts, and muscle cell transplants
may someday be useful.

Hypertension

About 20% of Americans suffer from

hypertension (high blood pressure).
Hypertension is present when systolic
pressure is 140 or greater or diastolic
pressure is 100 or greater; diastolic
pressure is emphasized when medical
treatment is considered.
A genetic predisposition for
hypertension occurs in those who have
a gene that codes for angiotensinogen,
a powerful vasoconstrictor.