1.

Ghina Muthmainnah
2. Ufaira Nabila Luthfiani Adriswan
3. Melvinia Savitri
4. Ufaira Nabila
5. Wahyu Fadilla Perkasa
6. Rifty zhafira Maharani
7. Yenny Handayani Sihite
8. Zakiya Zulviyanda
9. Elsa Yosephin Siahaan
10. Nur Fadhliatun ‘Adlin Bt. H. Adnan
 Infarkmiokardium
(ghina): adalah kondisi terhentinya aliran darah yang menyebabkan
kekurangan oksigen, lalu sel – sel jantung mati. Atau lebih dikenal dengan
serangan jantung
 EKG
(ufaira) : adalah grafik yang dibuat oleh sebuah elektro kardiograf yang
merekam aktivitas kelistrikan jantung dalam waktu tertentu. Merupakan tes
medis untuk menilai kelainan jantung.
 Electrode
(yenny): adalah konduktor yang digunakan untuk bersentuhan dengan bagian
atau media non logam dari sebuah sirkuit
 Gelombang p
(nur): merupakan gambaran proses depolarisasi.
(yeyen):merupakan defleksi positif/penyimpangan arah pertama pada suatu
gelombang, makna depolarisasi atrium
 Disosiasi
(chacha):pemecahan molekul dalam proses ilmiah yang menghasilkan satu
atau lebih molekul lain.
 Kompleks QRS
(wahyu): merupakan gelombang defleksi yang terjadi setelah gelombang p,
gelombang ini mempresentasikan aktivtas listrik dari ventrikal
•Atrial septal defect
(ufaira nabilla):lubang abnormal yang terdapat pada sekat yang
memisahkan atrium kanan dan kiri.
•Rongga mediastinum
(vini): adalah rongga diantara paru – paru kanan dan kiri yang berisi
jantung, aorta, ateribesar, pembuluh darah vena besar, kelenjar timus,
trakea, saraf, jaringan ikat, kelenjar getah bening dan salurannya.
•Elephantiasis
(elsa): penyakit kaki gajah. Penyakit menular yang disebabkan oleh
cacing filarial, yang ditularkan oleh nyamuk.
•Inguinalis
(rifty):daerah pangkal paha.
•Pembuluhlimfe
(ghina):adalah pembuluh yang mengangkut cairan dari jaringan menuju
darah untuk dirombak ke noduslimfe.
Interstitium
(rifty): cairan yang mengisi sel didalam tubuh makhluk multiseluler
seperti manusia atau hewan yang memiliki fungsi fisiologi tertentu.
1. Embriogenesis jantung dan pembuluh darah
2. Anatomi jantung dan rongga thorax
3. Histologi pembuluh darah dan jantung
4. Aktivitas listrik jantung
5. Kelainan jantung
6. Embriogenesis sistem limfatik
7. Anatomi sistem lmfatik
8. Histologi pembuluh limfe
9. Kelainan sistem limfatik
 Occurs towards the end of the 3rd week
 Day I8 - cardiac precursor cells seen in the form
of blood islands
 Day 20 - first intraembryonic blood vessels
seen
 Day 21- Folding, heart tube formation,looping
 Day 22 – heart starts to beat, ebb and flow
initially
 Day 28 – embryonic circulation established
 Early development
Formation of trilaminar embryo
Origin of cardiogenic cells
Formation of bilateral heart fields
Formation of the heart tube
Folding of the heart tube
Looping of the heart tube
Cardiac developmental abnormalities
 The developing blood vessels and heart tube
can be seen in an embryo at approximately 18
days .

 When looking down at this early embryo you

can see multiple blood islands dispersed
throughout the embryo.
 The heart primordium arises predominantly
from the mesoderm in the cardiogenic
region of the trilaminar embryo.
 First heart field (FHF)

 Second heart field (SHF)

 Proepicardium

 Cardiac neural crest cells

 FHF

 SHF

 CNC

 Proepicardium
 Early development
Origin of cardiogenic cells
Formation of bilateral heart fields
Formation of the heart tubes
Folding of the heart tube
Looping of the heart tube
Cardiac development abnormalities
 Two distinct mesodermal heart fields that
share a common origin appear to contribute
cells to the developing heart in a temporally
and spatially specific manner.
 Using special technologies to mark
progenitor cells two heart fields (the primary
and secondary) have been characterised.
 The heart tube derived from the primary
heart field may predominantly provide a
scaffold that enables a second population of
cells to migrate and expand into cardiac
chambers .
 These additional cells arise from an area
often referred to as the secondary heart field
(SHF), or anterior heart field, based on its
location anterior and medial to the crescent-
shaped primary heart field
 SHF cells cross the pharyngeal mesoderm
into the anterior and posterior portions,
contributing to the formation of the outflow
tract, future right ventricle, and atria
 Early development
Origin of cardiogenic cells
Formation of bilateral heart fields
Formation of the heart tube
Folding of the heart tube
Looping of the heart tube
Cardiac developmental abnormalities
 The flat germ disk transforms into a tubular
structure during the fourth week of
development
 This is achieved through a process of
differential growth causing the embryo to
fold in two different dimensions
 The heart initially forms
from two tubes located
bilaterally (on either side)
of the trilaminar embryo
in the cranial (head)
 This primitive, bilateral heart tubes each
contains an inner layer of endocardium, a
middle layer of cardiac jelly, and an outer
layer of myocardium region
 1. Craniocaudal axis due to the more rapid
growth of the neural tube forming the brain
at its cephalic end. Growth in this direction
will cause the embryo to become convex
shaped.

 2.Lateral folding, causing the two lateral

edges of the germ disk to fold forming a
tube-like structure
Heart Tube
 The primitive heart tubes
then fuse in the ventral
midline to form the linear
or straight heart tube in a
cranial to caudal direction
 Simultaneously the heart
tube shows a series of
dilatations.
From cranial to caudal
these are:
Bulbous cordis
Ventricle
Atrium
Sinus venosus
 The arterial trunk will divide to separate the pulmonary and systemic
supply.
 The bulbus and the ventricle will later differentiate into the right and left
ventricle
 Bulbus cordis represents
the arterial end of heart. It
consists of

 proximal part called the conus

 a distal part called truncus
arteriosus.
 The truncus continues distally
with the aortic sac.
 The sinus venosus
represents the venous end
of the heart. One vitelline
vein from the yolksac; one
umbilical vein from the
placenta and one common
cardinal vein from the
bodywall ,joins each horn
of the sinus venosus.
 After the formation of the head fold, this
tube lies dorsal to the pericardial cavity and
ventral to the foregut.

 Splanchnopleuric mesoderm lining the dorsal

side of the pericardial cavity proliferates to
forma thick layer called the myoepicardial
mantle.
 When the invagination is complete, the
myoepicardial mantle completely surrounds
the heart tube

 It gives rise to the cardiac muscle

(MYOCARDIUM) and also to the visceral layer
of the pericardium (EPICARDIUM)
 Heart tube is
suspended from the
dorsal wall of the
pericardial cavity by 2
layers of pericardium
that constitutes dorsal
mesocardium
 A hole forms in the dorsal
mesocardium which
increases in size.
 Gradually Mesocardium
disappears and the heart
tube lies free within the
pericardial cavity
 Mesocardium disappears to
form the transverse sinus
of the pericardium
 Early development
Origin of cardiogenic cells
Formation of bilateral heart fields
Formation of the heart tube
Folding of the heart tube
Looping of the heart tube
Cardiac developmental abnormalities
 Looping of the heart tube allows the straight
heart tube to form a more complex structure
reminiscent of the adult heart. Most cardiac
looping occurs during the fourth week and
completes during the fifth week of
development
 The linear heart tube develops differential
growth of the heart tube in comparison with
the foregut
 The direction of cardiac looping is
determined by an asymmetric signalling
system which affects the position of both
thoracic and abdominal contents
 In all vertebrates, there is differential growth
within the heart tube itself resulting in
posterior, leftward, slower growth and
anterior, rightward, faster growth resulting
in rightward looping. This positioning results
in the future right ventricle taking an anterior
and rightward location with reference to the
future left ventricle
 Further disproportionate growth of the heart
tube in comparison to the foregut results in
bending of the heart tube at the inflow as
well as within the ventricular segment
eventually positioning the inflow and future
left ventricular segments posteriorly and to
the left, with the future right ventricle and
outflow segments anteriorly and to the right
 The straight heart tube begins to
elongate with simultaneous growth
in the bulbus cordis and primitive
ventricle

 This forces the heart to bend

ventrally and rotate to the right,
forming a C-shaped loop with
convex side situated on the right.

 The ventricular bend moves

caudally and the distance between
the outflow and inflow tracts
diminishes.

 The atrial and outflow poles

converge and myocardial cells are
added, forming the truncus
arteriosus
 Hence an S-shape is formed with the first
bend of the 'S' being the large ventricular
bend while the bend at the junction of the
atrium and sinus venosus forms the second
'S' bend
The cardiac tube grows at a greater
longitudinal rate then the rest of the
embryo, causing it to fold. As it does
this
it falls to the right. This is known as
d-looping. It may fall to the left in an
l-loop: this will lead to a malformed
heart.
Below are chick embryo dissections
showing
the two types of loop.

normal d-loop l-loop

•The fold of the loop is principally at the junction of bulbus cordis and
ventricle. Note in panel C that the two end up side by side.
•The left ventricle will develop from the ventricle, and the right ventricle
will develop from the bulbus cordis. (And an l-loop will
result in ventricular inversion with the left ventricle on the right.
•Note also that the arterial trunk is above the developing right ventricle.
 Transcriptional regulators

 Epigenetic regulation by microRNAs (miRNA)

 HENSON’S NODE which contains retinoic
acid, serves as an embryonic organizer that
confers information required to direct the
ultimate fate of mesodermal cells during
early embryogenesis.
 Exogenous retinoic acid is extremely
teratogenic at that stage
 Greatest effect is on the arterial pole.
 Early development
Origin of cardiogenic cells
Formation of bilateral heart fields
Formation of the heart tubes
Folding of the heart tube
Looping of the heart tube
Cardiac development abnormalities
 Abnormal left-right signalling

 Looping defects

 Defects due to abnormal migration of cells of

primary and secondary heart fields and of
cardiac neural crest
 From Fertilization to Primitive Heart Tube
Abnormal development at this stage of
embryogenesis almost always results in
embryonic death because of the critical
nature of the early circulation to the further
growth and development of the embryo and
fetus.
 Absence of Hand2 (dHAND) – results in
RV HYPOPLASIA or ABSENT RV
 HETEROTAXY SYNDROMES

 DORV

 DILV
 In humans, mirror-image reversal of left-right
asymmetry is often associated with normal
organ development ( simple dextrocardia or
situs inversus totalis) but discordance of
thoracic and visceral asymmetry universally
results in defective organogenesis, the most
common being heterotaxy syndrome.
 Ventricular Inversion with Transposition of
the Great Arteries
 There is currently considerable research in
animate models on the genes known to
control left-right development. Similarly,
congenitally corrected transposition of the
great arteries is thought to result from both
an abnormality of looping and of outflow
tract development.
 Many other complex abnormalities
involving both ventricles and outflow tract
are thought to have at least some
abnormality in the looping process.
 HYPOPLASIA OF RVOT/MPA - TOF
 ABSENCE OF RVOT/MPA- TA
 ABSENCE OF AORTO-PULMONARY
SEPTUM – TA
 MALALINGMENT OF AORTA AND LV –
ABNORMAL WEDGING -TOF
 ABNORMAL MYOCARDIAL
TRABECULATION- LV/RV NON
COMPACTION
 Cardiovascular = Heart, Arteries, Veins, Blood

 Function:
 Transportation
 Blood = transport vehicle
 Carries oxygen, nutrients, wastes, and hormones
 Movement provided by pumping of heart
 Outermost = Pericardium & Epicardium
 Pericardium is a membrane anchoring heart to
diaphragm and sternum
 Pericardium secretes lubricant (serous fluid)
 Epicardium is outermost muscle tissue

 Middle = Myocardium
 Contains contractile muscle fibers

 Innermost = Endocardium
 Lines Cardiac Chambers
 Human heart has 4 chambers
 2 Atria
▪ Superior = primary receiving chambers, do not actually pump
▪ Blood flows into atria
 2 Ventricles
▪ Pump blood
▪ Contraction = blood sent out of heart + circulated

 Chambers are separated by septum…

 Due to separate chambers, heart functions as double
pump
 …To the rest
of the body
Deoxygenated …To the
Blood lungs

Oxygenated
Blood
 Pulmonary = Deoxygenated Blood
 Involves Right Side of Heart

 Pathway:
1. Superior / Inferior Vena Cava
2. Right Atrium  Tricuspid Valve
3. Right Ventricle  Pulmonary Semilunar Valve
4. Left Pulmonary Artery
5. Lungs
 Systemic = Oxygenated Blood
 Involves Left Side of Heart

 Pathway:
1. Left Pulmonary Vein
2. Left Atrium  Bicuspid Valve
3. Left Ventricle  Aortic Semilunar Valve
4. Aorta
5. All Other Tissues
 [4 main valves]

 When the heart is relaxed…

 Blood passively fills atrium
 Flows right past tricuspid / bicuspid valves
 Semilunar Valves remain shut

 When the heart contracts (pumps)…

 Tricuspid / Bicuspid valves swing up and shut
 Blood ejected out of ventricle
 Semilunar Valves open up
1. Artery  big artery
 medium artery
 small artery (arteriol)
2. Capillary
3. Vein  Big Vein
 medium vein
 small vein (venulla)
  Tunnica Intima : Endotel and Subendotel layer
 Interna Ellastic Membran :
{Big} 40-70 layers, distances ; 5-
15 µm
{medium} waves
{small} very thin; nope
 Tunnica Media :
{big} muscle plain cell (>>),
fibroblas, colagen fiber
{medium} mix with ellastin fibers
and reticular
{small} 5-8 layers, arteriol ≤2
layers
 Externa Ellastic Membran : thin
 Tunnica Adventisia :
{big} bundle tissue, colagen fiber,
vasa vasorum
{medium} + Fibroblast
{small} thin bundle loose tissues
  Tunnica Intima :
{big} endotels, thin spundle
tissues
{medium} + a little ellastic fibers
{venulla} + several spain muscle
cells
 Tunnica Media :
{big} thin/never exist
{medium} more thin than medium
artery, especially
circular spain muscle
{venulla} one or several layers of
spain muscle cells
 Tunnica Adventisia :
{big} thick, spundle tissue,
elongated spain muscle
cells
{medium} more thick than T.
Media, thick spundle
loose tissue
{venulla} thin spundle loose tissue
 Variation structure
 Endotel with basalis membran layer
 In several place, exist pericit outer of endotel
 Type : continue capillary (somatic)
: fenestra capillary with diaphragma
(viseral)
: fenestra capillary without
diaphragma
: sinusoid capillary
 Ductus thoracicus et ductus lymphaticus
dexter (bigger)
 Three layers :
 Tunnica Intima : Endotel, collagen fibers and
ellastic
 Tunnica media : spain muscle cells
 Tunnica adventisia : elongated spain muscle cells
 Ateroschlerosis : accumulation of fat in the
duct wall
 Varises : enlargement of vein duct
 Arterioschlerosis : accumulation of lime i the
duct
 Coroner embolism : the duct filled by blood
clot suddenly
 Elephantiasis : from larva filaria, distributed
by mosquito, culex sp. Hamper the blood way
and make an enlargement of leg like elephant
 Lymphedema : cronic swelling on leg ,
accumulation of liquid caused limfe system
broke and unfunction
 Limfoma Hodgkin : cancer when leukosit
broken
 Castleman : benign that influenced glandula
 Lymphangiomatosis : cista or lesi formed by
limfatik duct
 Lymphangiosarcoma : soft tissue cronic
cancer
 The Sinoatrial node (SA node), is a group of autorhythmic cells
(main pacemaker of the heart) in the right atrium near the entry of
the superior vena cava.
 An internodal pathway connects the SA node to the
atrioventricular node (AV node), a group of autorhythmic cells
found near the floor of the right atrium.
 From the AV node action potentials move into fiber known as the
bundles of his or atrioventricular bundle. The bundle passes
from the AV node into the wall of the septum between the
ventricles.
 A short way down the septum the bundle divides into left and
right bundle branches.
 These fibers continue downward to the apex where they divide
into many small purkinje fibers that spread outward among the
contractile cells.
 If the electrical signals from the atria were conducted
directly into the ventricles, the ventricles would start to
contraction at the top. Then the blood would be squeezed
downward and trapped at the bottom of the ventricle.
 The apex to base contraction squeezes blood toward the
arterial opening at the base of the heart.
 The AV node also delays the transmission of action
potentials slightly, allowing the atria to complete their
contraction before the ventricles begin their contraction.
This AV node delay is accomplished by slowing
conduction through the AV node cells.
 Composite of all action potentials of nodal
and myocardial cells detected, amplified
and recorded by electrodes on arms, legs
and chest
 P wave
 SA node fires, atrial depolarization
 atrial systole
 QRS complex
 atrial repolarization and diastole (signal
obscured)
 AV node fires, ventricular depolarization
 ventricular systole
 T wave
 ventricular repolarization
1)atria begin to
depolarize
2) atria depolarize
3)ventricles begin to
depolarize at apex;
atria repolarize
4)ventricles depolarize
5) ventricles begin to
repolarize at apex
6) ventricles repolarize
 Invaluable for diagnosing abnormalities in
conduction pathways, MI, heart enlargement
and electrolyte and hormone imbalances
No P waves
Arrhythmia: conduction failure at AV node

No pumping action occurs

 One complete contraction and relaxation of
heart
 Atrial systole
 Atrial diastole
 Ventricle systole
 Ventricle diastole
 Quiescent period
 Measurement: compared to force generated by
column of mercury (mmHg) - sphygmomanometer
• Change in volume creates a
pressure gradient

• Opposing pressures
– always positive blood
pressure in aorta, holds
aortic valve closed
– ventricular pressure must
rise above aortic pressure
forcing open the valve
 Auscultation - listening to sounds made by
body
 First heart sound (S1), louder and longer
“lubb”, occurs with closure of AV valves
 Second heart sound (S2), softer and sharper
“dupp” occurs with closure of semilunar
valves
 S3 - rarely heard in people > 30
 Quiescent period
 all chambers relaxed
 AV valves open
 blood flowing into ventricles
 Atrial systole
 SA node fires, atria depolarize
 P wave appears on ECG
 atria contract, force additional blood into
ventricles
 ventricles now contain end-diastolic volume
(EDV) of about 130 ml of blood
 Atria repolarize and relax
 Ventricles depolarize
 QRS complex appears in ECG
 Ventricles contract
 Rising pressure closes AV valves
 Heart sound S1 occurs
 No ejection of blood yet (no change in
volume)
 Rising pressure opens semilunar valves
 Rapid ejection of blood
 Reduced ejection of blood (less pressure)
 Stroke volume: amount ejected, about 70
ml
 SV/EDV= ejection fraction, at rest ~ 54%,
during vigorous exercise as high as 90%,
diseased heart < 50%
 End-systolic volume: amount left in heart
 T wave appears in ECG
 Ventricles repolarize and relax (begin to
expand)
 Semilunar valves close (dicrotic notch of aortic
press. curve)
 AV valves remain closed
 Ventricles expand but do not fill
 Heart sound S2 occurs
 AV valves open
 Ventricles fill with blood - 3 phases
 rapid ventricular filling - high pressure
 diastasis - sustained lower pressure
 filling completed by atrial systole
 Heart sound S3 may occur
 Quiescent period
 Atrial systole
 Isovolumetric
contraction
 Ventricular
ejection
 Isovolumetric
relaxation
 Ventricular filling
 Atrial systole, 0.1 sec
 Ventricular systole, 0.3 sec
 Quiescent period, 0.4 sec
 Total 0.8 sec, heart rate 75 bpm
End-systolic volume (ESV) 60 ml
Passively added to ventricle
during atrial diastole 30 ml
Added by atrial systole 40 ml
Total: end-diastolic volume (EDV) 130 ml
Stoke volume (SV) ejected
by ventricular systole -70 ml
End-systolic volume (ESV) 60 ml
Both ventricles must eject same amount of blood
 Amount ejected by each ventricle in 1 minute
 CO = HR x SV
 Resting values, CO = 75 beats/min x70 ml/beat
= 5,250 ml/min, usually about 4 to 6L/min
 Vigorous exercise  CO to 21 L/min for fit
person and up to 35 L/min for world class
athlete
 Cardiac reserve: difference between
maximum and resting CO
 Diastole - the time during which cardiac muscle relaxes.
 Systole - the time in which cardiac muscle is contracting.

I - The Heart at Rest : Atrial and Ventricular Diastole

 While both atria and ventricles are relaxing, the atria begin filing with blood
from the veins while the ventricles have just completed a contraction
 As the ventricles relax the AV valves between the atria and ventricles open,
and blood flows from the atria to the ventricles.
II - Completion of Ventricular Filling : Atrial Systole
 The last 20% of the filling of the ventricles is accomplished when the atria
contract. Atrial systole begins following depolarization of the SA node.
 Atrial contraction can aid filling of the ventricles in stenosis of the AV valves.
 The force of atrial contraction can also push blood back into the vein. This
can be observed by the pulse in jugular vein of a normal person lying w/ the
head and chest elevated about 30 degrees. If there is an observable jugular
pulse higher on the neck of a person sitting upright, it is indication that the
pressure in the atria is higher than normal.

III- Early Ventricular Contraction and the 1st Heart Sound

 Ventricular Systole begins at the apex of the heart as spiral bands of muscle
squeeze the blood upward toward the base. Blood pushing upward on the
underside of the AV valve forces them closed so that blood cannot flow back
into the atria.
 Vibrations following closure of the AV valves creates the 1st heart sound, the
“lub” of “lub-dup”.
IV - The heart pumps: Ventricular Ejection
 As the ventricles contract, they generate enough pressure to open the
semilunar valves and the blood is pushed into the arteries.
 The pressure created by ventricular contraction becomes the driving force
for blood flow.

V - Ventricular Relaxation and the 2nd Heart Sound

 As the ventricles begin to relax, ventricular pressure decreases.
 Once ventricular pressure falls below the pressure in the arteries blood
starts to flow backward into the heart. This backflow fills the cusps of the
semilunar valves, forcing them together into the closed position.
 The vibrations of the semilunar valve closure is the 2nd heart sound, the
“dup” of “lub-dup”.
 The AV valves open once the pressure in the ventricles falls below the
pressure in the atria and the cycle starts again.
 Coronary artery disease, famous as “the silent killer” This
serious condition is a result of plaque buildup in your arteries.
 Myocardial infarction, or well known as heart attack is the
irreversible death (necrosis) of heart muscle secondary to
prolonged lack of oxygen supply (ischemia).
 Heart failure, is a condition in which the heart can't pump
enough blood to meet the body's needs.
 Cardiomyopathy, refers to diseases of the heart muscle, in
cardiomyopathy the heart muscle becomes enlarged, thick, or
rigid. In rare cases, the muscle tissue in the heart is replaced
with scar tissue.
 Atrial fibrillation (also called AFib or AF), is a quivering or
irregular heartbeat (arrhythmia) that can lead to blood
clots, stroke, heart failure and other heart-related
complications.
 Heart valve disease, occurs if one or more of your heart
valves don't work well.
 Congenital heart defect, is a problem with the structure of
the heart. It is present at birth. It may have had a small
hole in it or something more severe. Although these can
be very serious conditions, many can be treated with
surgery.
 Cerebrovascular disease, refers to a group of conditions
that affect the supply of blood to the brain, causing
limited or no blood flow to the affected areas.
 Rheumatic heart disease (RHD), is a chronic heart
condition caused by rheumatic fever that can be
prevented and controlled. Rheumatic fever is caused by a
preceding group A streptococcal (strep) infection.