Anatomy

Systema Cardiovascular

dr. Dodik Nursanto, M.Biomed

The cardiovascular system is mesodermally
derived

Specifically, lateral
splanchnic mesoderm…
The cardiogenic field is established in the mesoderm just after gastrulation (~18-19
days) and develops into a fully functional, multi-chambered heart by the 8th week

angiogenic cell clusters

(angioblasts/hemangioblasts)

(right endocardial tube)

(right dorsal aorta)

blood islands
(developing blood vessels)
pericardial cavity

cardiogenic field
Carlson fig 6-14

Establishment of
the heart fields
BMP2 & 4 in mesoderm

WNT inhibition (from

“Anterior” Visceral
Endoderm) in anterior
mesoderm

BMP2,4+/Wnt- expression
pattern specifies cardiac
tissue (evidenced by
expression of NKX-2.5,
aka tinman)
Langman’s fig 12-9
Repositioning the cardiogenic field
(mammals)

Larsen’s fig 12-6

Langman’s fig 12-6

 Cranial folding

Cranial folding rotates

cardiogenic area,

moves it ventrally and caudally,

and orients heart tube
and pericardial cavity

Moore & Persaud fig 13-9

 Lateral
folding

Moore & Persaud fig 13-8

Lateral folding apposes paired heart tube primordia

and brings dorsal aortae to midline
Heart primordia fuse to form tubular heart
 Ductus
Arterial end Arterial end Aorta arteriosus
4a Superior
4 Tubular vena Pulmonary
heart Ventricle cava trunk
Foramen
3 Atrium ovale
2
Ventricle
1 Inferior Ventricle
Venous end Venous end vena cava
(a) Day 20: (b) Day 22: (c) Day 24: Heart (d) Day 28: Bending (e) Day 35: Bending
Endothelial Heart continues to continues as ventricle is complete.
tubes begin starts elongate and moves caudally and
to fuse. pumping. starts to bend. atrium moves cranially.

Figure 18.23
 Fusing cardiac primordia

“conotruncus”
(outflow tract)

future
ventricles

future
atria

21 days 22 days
Langman’s fig 12-7

septum transversum
(liver & diaphragm primordium)
 Retinoic acid (RA) and other
factors determine the cranio-
caudal axis of heart primordia

• Primary heart field: left ventricle

• Posterior segment of primary heart
field: atria
• Secondary heart field: right ventricle
& outflow tract
• EXOGENOUS RETINOIDS CAN
INTERFERE WITH THIS PROCESS!

Carlson fig 17-17

Heart tube and dorsal aortae in place

Transverse pericardial sinus

Langman’s fig 12-5

 Heart folding
How do you get from this…

22 days Langman’s fig 12-7 30 days Carlson fig 17-19

…to this?
 Folding and rotation of heart tube
aortic roots

truncus arteriosus

bulbus cordis

ventricle

atrium

sinus venosus

22 days 23 days 24 days Langman’s fig 12-6

• Ventricle moves ventrally

and to right

• Atrium moves dorsally

and to left
Looped heart anatomy

Carlson fig 17-18

 At 30 days…
• Atrial partitioning just
beginning to happen
• Primary interventricular
foramen undivided
• Outflow tract (bulbus
cordis/truncus arteriosus)
undivided
• Proximal portion of bulbus
cordis becomes
trabeculated and forms
the right ventricle
• Atrioventricular canal
undivided
Langman’s fig 12-8
 Partitioning the AV canal

Moore & Persaud fig 13-11

Atrioventricular Endocardial Cushions
• Retinoic acid (and many other factors) dependent* conversion of
endocardial endothelium in the AV canal into mesenchyme that proliferates
to form “cushions” of tissue
• Dorsal and ventral cushions fuse in the middle to form a block of tissue that
divides right and left AV canals

*can be disrupted by exogenous retinoids and/or in many genetic disturbances (e.g. trisomy 21 –aka Down Syndrome)
 Partitioning the AV canal

based on Larsen’s fig 12-27

QuickTime version

Atrioventricular Endocardial Cushions

• Expansion of tissue around periphery of AV canal
• Dorsal and ventral cushions fuse to form right and left AV canals divided by
septum intermedium (failure of cushions to fuse causes “persistent AV canal”)
• Remodeling brings right and left AV canals into alignment with future right and
left ventricles –movement driven by differential growth (failure of this process
leads to “double inlet” defects)
 Persistent A-V canal
• Failure of A-V endocardial cushions to fuse
• Common in Down syndrome

View of A-V canal looking down into

ventricles with atria removed
(e.g. at dotted line on left)

Carlson fig 17-32

Fig 174, Nishimura & Okamoto (1976)
 • septum primum
– ostium primum
– ostium secundum
• septum secundum
– foramen ovale

33

40

Atrial septum formation

Larsen’s figs 12-24, 12-25, 12-26 43
 • septum primum
– ostium primum
– ostium secundum
• septum secundum
– foramen ovale

QuickTime version
from Larsen’s figs 12-24, 12-25, 12-26

Atrial septum formation

 Why is a right-left
shunt necessary?

In the fetus, blood is oxygenated in

the placenta and delivered to the
heart via the inferior vena cava:
• Shunted to left atrium via
foramen ovale
• Also shunted from pulmonary
outflow via ductus arteriorsus

Carlson fig 17-19

 Atrial Septal Defects (ASDs)
Multi-factoral, so many etiologies, but one well-known example is mutation
in NKX2-5 characterized by:
– Incomplete septum secundum
– AV “bundle block” (disruption of conducting fibers, evidenced by prolonged P-R
interval on ECG) –typically worsens with age

Schott et al. (1998).

Science. 281:108-111
Doppler flow echo-CG ECG showing progressive AV block
showing RA to LA shunt (normal P-R int. 0.13-0.2s)
 Late
5th week

Moore & Persaud fig 13-17

• Atrium in process of septal formation

• Interventricular septum still incomplete
– muscular septum present
– membranous septum ABSENT
• Outflow tract still undivided
membranous septum will form here
muscular septum Langman’s fig 12-17
 Outflow Tract Partitioning
Truncoconal ridges
• Neural crest-derived endocardial cushions
R
L form in truncus arteriosis and conus
(bulbus) cordis region
• Fuse at truncoconal transition and “zip”
proximally and distally to form
aorticopulmonary septum.
Membranous septum formed by contributions
from AV cushions and truncoconal cushions.

5th wk 7th wk

8th wk 9th wk QuickTime version Larsen’s fig 12-33

 Outflow Tract Defects
• Typically due to failure of neural crest-derived
conotruncal cushions
• Associated with other disorders affecting neural crest:
DiGeorge syndrome, fetal alcohol syndrome,
chromosome 22 mutations (e.g. Tbx-1)
• Can also arise due to defects in secondary heart field
(e.g. Hand-2, retinoids)
• Examples include: persistent truncus arteriosus,
transposition of the great vessels, aortic and/or
pulmonary stenosis (tetrology of Fallot)
Persistent Truncus Arteriosus (left)
Great Vessel Transposition (right)

Carlson fig 17-31

Pulmonary Stenosis: Tetrology of Fallot
• Pulmonary stenosis
• Overriding aorta
• Intraventricular septal defect
• Hypertrophy of right ventricle
• (Patent ductus arteriosus)… so really a “pentology”

Carlson fig 17-40

 Other signs of Tetrology of Fallot

• Respiratory distress (dyspnea),

with rapid breathing
• Characteristic squatting posture,
at rest, to relieve dyspnea
• Coeur en sabot
(boot-shaped heart) in Xray
• Cyanosis develops gradually,
with intermittent severe “spells”
• Clubbed fingers and toes with cyanosis
 Formation of semilunar valves
also outflow cushion dependent… P

L
Pulmonary R

Aorta
valve
A
tubercles

Pulmonary
artery
Truncoconal Larsen’s fig 12-34
septum

Tricuspid
valve

Langman’s fig 12-27

Mitral valve
Langman’s fig 12-23
 Formation of AV valves
dependent on AV cushions and ventricular myocardium…

Moore & Persaud fig 13-19

 Mitral stenosis/hypoplastic left ventricle

• Failure of left A-V valve (tricuspid

valve) to form: LV and aorta becomes
hypoplastic because of reduced load.
• OK in embryo since oxygenated blood
is coming from IVC and can be
distributed systemically via ductus
arteriosus.
• But, this arrangement doesn’t work so
well in a breathing infant since
oxygenation occurs in the lungs.
 Fontan Repair of Single Ventricle

• Reroute systemic venous

blood to lungs for oxygenation
• Reroute right ventricle outflow
to aorta
• Oxygenated blood from lungs
flows from LA in RA via patent
foramen ovale and RV pumps
oxygenated blood out to body.
Blood Vessel Development

Langman’s fig 16-04

 Aortic arches at pharyngeal arches and pouches
7 weeks Each pharyngeal arch has aortic arch,
cranial nerve, and cartilage components…

4th arch

6th arch

1st arch 2
2nd arch 3
• Five aortic arches are forming 4
3rd arch
during the 4 and 5 weeks.
th th

• 5th arch fails to form;

arches are numbered: 6
1, 2, 3, 4, and 6 “branchial” = pharyngeal
Langman’s fig 16-04
 Changes in the aortic arch pattern
Animation: http://www.indiana.edu/~anat550/cvanim/aarch/aarch.html

6 months postnatal

6 weeks

From this… …to this

Moore & Persaud fig 13-39
 Changes in the aortic arch pattern (AS,1,2,3,5)
Animation: http://www.indiana.edu/~anat550/cvanim/aarch/aarch.html

Aortic Sac (AS):

• proximal part of aortic arch
• brachiocephalic a.

1st arch mostly disappears

• maxillary a.
• (part of external carotid a.?)
Aortic sac
2nd arch mostly disappears
• stapedial a.
• (hyoid a.?)

3rd arch:
• common carotid a.
• part of internal carotid a.
• internal and external
carotid aa. sprout from 3rd arch
Moore & Persaud fig 13-39

5th arch fails to form

 Changes in the aortic arch pattern (4)
Animation: http://www.indiana.edu/~anat550/cvanim/aarch/aarch.html

4th arch on right: 4th arch on left:

– proximal segment of right
subclavian a. (rest of subclavian
a. from 7th intersegmental a. and
R dorsal aorta)
Moore & Persaud fig 13-39
– arch of aorta
(from left common carotid a.
to left subclavian a. only)
 Changes in the aortic arch pattern (6)
Animation: http://www.indiana.edu/~anat550/cvanim/aarch/aarch.html

(6th arch = pulmonary arch)

6th arch on right: 6th arch on left: Moore & Persaud fig 13-39

– right pulmonary artery – left pulmonary artery

– distal segment regresses – distal segment persists as ductus arteriosus
 Aortic Arch
Anomalies
(A) Double aortic arch
abnormal persistence of right normally
distal segment regresses
~1:1000 incidence –often assoc.
with dysphagia and/or dyspnea
(B) Right aortic arch
abnormal persistence of right
distal segment & regression of left normally
distal segment persists
~1:1000 incidence –usually
asymptomatic
(C) Aberrant right subclavian normally
persists
(from aortic arch)
(abnormal regression of right
proximal segment & persistence of
right distal segment)
~1:100 incidence –often assoc.
with dysphagia and/or dyspnea;
also, R radial pulse may be weak
Carlson fig 17-42
 Interrupted aortic arch (IAA)
• Abnormal regression of proximal left 4th arch
• Output to left upper limb, trunk, and both lower limbs is via pulmonary trunk (connected to
descending aorta via ductus arteriosus)
• Rather asymptomatic at first, but ductus starts to close during first 2 weeks of life, so needs to
be caught and fixed (via surgical reconstruction) by then
• Neural crest etiology: Rare (1:50,000) in general population, but rather common (~10%) in
patients with DiGeorge syndrome (22q deletion)

R and L common
carotid arteries
and right limb*

R subclavian a.

*The R subclavian is shown here

L subclavian a.
as a separate branch from the
arch of the aorta; the middle
vessel is the R common
cartotid; the remaining vessel
coming from the arch of the
aorta is the L common carotid.

Carlson fig 17-44

 Coarctation of aorta

• Collateral circulations
can compensate for
postductal coarctation
– But, not perfect, so blood
pressure in upper limbs is
higher compared to lower
limbs
• Preductal coarctation is
MUCH less common (5% of
coarctations)

~1:3000 incidence overall, but

commonly coincident w/
Turner’s syndrome (~20%) and
neural crest disorders

Moore & Persaud, Fig 15-29;

ref to Sadler, Fig 11-37
 Venous system development
sinus venosus cardinal veins

vitelline veins umbilical veins

Langman’s fig 12-41
 Vitelline and umbilical veins change
sinus
venosus
cardinal V during liver development
L hepatocardiac
channel

hepatic
L vitelline V sinusoids

duodenum

umbilical V
hepatic portion of
inferior vena cava

hepatic V
4 weeks duodenum 5 weeks (R vitelline V) hepatic V
yolk sac
Langman’s fig 12-42 R hepatocardiac
channel
ductus
venosus
• R hepatocardiac channel
 hepatic portion of IVC
portal V
• R umbilical V regresses
• proximal L umbilical V regresses superior
mesenteric V
6 weeks
• distal L umbilical V persists 8 weeks
and then  round ligament of the liver (ligamentum teres hepatis) splenic V
• ductus venosus  ligamentum venosum Langman’s fig 12-43
 Systemic venous development
anterior cardinal veins posterior cardinal veins

Langman’s fig 12-41

Systemic venous development: shift to the right

5.5 weeks
5 weeks 6 weeks Moore & Persaud
Systemic venous development: shift to the right
L. brachiocephalic anastomosis

7 weeks Adult
Moore & Persaud

What if the brachiocephalic anastomosis fails?

 Left superior Double superior
vena cava vena cava

Langman’s fig 12-46

viewed from behind

 Double inferior Absent inferior
vena cava vena cava

Langman’s fig 12-45

 Heart Anatomy

Figure 19.1
49
50
51
52
53
54
 Heart Covering

• Pericardial physiology
– Protects and anchors heart
– Prevents overfilling

55 Figure 19.2
 External Heart: Anterior View

Figure 19.4b
56
57
58
 External Heart: Posterior View

Figure 19.4d
59
 Gross Anatomy of Heart: Frontal Section

60
 Gross Anatomy of Heart: Frontal Section

Figure 19.4e
61
62
 Coronary Circulation

Figure 19.7a
63
 Coronary Circulation

Figure 19.7b
64
 Heart Valves

Figure 19.9
65
66
67
68
 Heart Valves

Figure 19.10
69
Thank You
Slide Title
 Superior vena cava
Right atrium
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.

Internodal pathway
2 The impulses Left atrium
pause (0.1 s) at the
atrioventricular
(AV) node.
3 The atrioventricular Purkinje
(AV) bundle
fibers
connects the atria
to the ventricles.
4 The bundle branches
conduct the impulses Inter-
through the
interventricular septum.
ventricular
5 The Purkinje fibers
septum
depolarize the contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
Figure 18.14a
Heart Excitation Related to ECG

Chapter 18, Cardiovascular System

Figure 72
18.17
The vagus nerve Dorsal motor nucleus of vagus
(parasympathetic) Cardioinhibitory center
decreases heart rate.

Medulla oblongata
Cardio-
acceleratory Sympathetic trunk ganglion
center
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.

AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
Figure 18.15
 CopyrightThe McGraw-Hill Companies, Inc. Permission required for reproduction or display.

G. Regulation of the Cardiac Cycle

1. The amount of blood pumped at any
one time must adjust to the current
needs of the body (more is needed
during strenuous exercise).
2. The S-A node is innervated by
branches of the sympathetic and
parasympathetic divisions, so the
CNS controls heart rate.

74
 CopyrightThe McGraw-Hill Companies, Inc. Permission required for reproduction or display.

a. Sympathetic impulses increase the

speed of heart rate.
b. Heart rate is decreased by
parasympathetic impulses.

75
 CopyrightThe McGraw-Hill Companies, Inc. Permission required for reproduction or display.

3. The cardiac control center of the

medulla oblongata maintains a
balance between the sympathetic
and parasympathetic divisions of
the nervous system in response to
messages from baroreceptors which
detect changes in blood pressure.

76
 CopyrightThe McGraw-Hill Companies, Inc. Permission required for reproduction or display.

4. Impulses from the cerebrum or

hypothalamus may also influence
heart rate, as do body temperature
and the concentrations of certain
ions.

77
78
 Heart Sounds

• Heart sounds (lub-

dup) are associated
with closing of
heart valves

Figure 19.20
79
80
 Factors Involved in Regulation of Cardiac Output

81
82
83
By-pass Graft

Chapter 18, Cardiovascular System 84

Walls of the
Heart
 Chambers & Valves

Trace the blood flow through the heart

 Blood Supply to the Heart
• After traveling through the capillaries of the
heart, blood empties into the Right atrium via
the vena cavas
Types of Blood Vessels
Types of Blood Vessels
Aorta
 Pericardium Disorders
• Pericarditis – inflammation of the heart
– Causes: trauma, viral or bacteria infection, tumor
– Edema causes visceral and parietal layers to rub
together = chest pain
– Pus or blood build up in pericardial space
– S/S
• Pain with respirations or coughing, dyspnea, restlessness
– Complications: Pericardial Effusion, Cardiac
Tamponade
– Treatment:
• Antibiotics, pain meds, antiinflammatory meds,
pericardiocentesis (Cardiac Tamponade)
 Heart Valve Disorders

• General Principles:
– Congenital defect: decreased pumping
efficiency
– Incompetent valve leak: allows backflow
into previous chamber
– Stenosed valves: narrowed valve; slowing
blood from out of chamber
 Heart Valve Disorders

• Mitral Valve Prolapse (MVP)

– Flaps of mitral valve extend back into L
atrium causes leaking
– Mostly genetic basis
– 1 in 20 people
– S/S: most asymptomatic; chest pain,
fatigue
– Treatment: valvuloplasty
Mitral Valve Prolapse
 Heart Valve Disorders

• Aortic Regurgitation
– Blood leaks back into L ventricle during
ejection into the aorta
– Volume overload in L ventricle,
hypertrophy, dilation of L ventricle
– Complications: myocaridal ischemia
– Treatment: valvuloplasty
 Myocardium Disorders

• Atherosclerosis
– Type of arteriosclerosis
– Lipids build up on the inside of vessel walls
 calcify  vessels hard & brittle
– Risk factors: cigarette smoking, high
fat/cholesterol diet, hypertension
Atherosclerosis
 Myocardium Disorders
• Congestive Heart Failure (CHF)
– “Left-sided Heart Failure”
– Inability of the L ventricle to pump blood
efficiently
– Causes: myocardial infarction
– S/S: decreased pumping pressure in
systemic circulation; retained fluids
• Can lead to congestion in pulmonary circulation 
pulmonary edema  right-sided heart failure
– Treatment: heart transplant
Congestive Heart Failure
Angioplasty
 Disorders of Veins

• Varicose Veins
– Enlarged veins caused by pooling
– Results in varicosities or varices (“spider
veins”)
– Risk factors: standing for long periods
• Semilunar valves widen  more pooling
– Treatment: compression stockings, surgical
removal
Varicose Veins
 Disorders of Veins
• Phlebitis – vein inflammation
– Causes: irritation by IV catheter
• Thrombophlebitis
– Deep vein thrombosis (DVT)
– Phlebitis caused by a clot
– S/S
• Pain, redness, swelling
– Complications
• Pulmonary embolism
DVT
Pulmonary Embolism
 Venous Stasis Ulcers
• Result of chronic
vein insufficiency
• Lack of oxygen to
peripheral tissues
• Elevate leg & apply
pressure
• Irregular edges
• “Aching” pain

Occurs in
about 1 in
every
500 births
(a) Ventricular septal defect.
The superior part of the inter-
ventricular septum fails to
form; thus, blood mixes
between the two ventricles.
More blood is shunted from
left to right because the left
ventricle is stronger.
Narrowed
aorta
Occurs in Occurs in
about 1 in about 1 in
every 1500 every 2000
births births
(b) Coarctation of the (c) Tetralogy of Fallot.
aorta. A part of the Multiple defects (tetra =
aorta is narrowed, four): (1) Pulmonary trunk
increasing the workload too narrow and pulmonary
of the left ventricle. valve stenosed, resulting
in (2) hypertrophied right
ventricle; (3) ventricular
septal defect; (4) aorta
opens from both ventricles.
Figure 18.24
111
112
113
 Cardiopathologies

114
115
 Arteries

• Arteries are thick-

walled, and lined
with smooth
muscle.
• Arteries expand
with each heart
beat, and contract
afterwards,
helping to move
blood.
117
 Arterioles

• Arterioles branch off of arteries.

• Arterioles can constrict to direct and control blood
flow. They may, for example, increase blood supply to
the skin to allow more heat to dissipate, or constrict
during stress to redirect blood to the heart and
muscles.
 Capillaries

• Body tissues contain a

vast network of thin
capillaries.
• Capillary walls are only
one cell thick, allowing
exchange of gases,
nutrients, and wastes.
• Capillaries are so fine
that RBCs must line up
single-file to go through
them.
120
 Venules

• Venules are thin-walled collectors of blood.

• Low pressure in the venules allows the capillary
beds to drain into them.
 Veins

• Veins have thinner

walls than arteries.
• Contraction of
skeletal muscles helps
move blood up the
limbs and back to the
heart.
• Valves in the veins
prevents backflow of
blood.
 Electrical System of Heart

1. Bundle of His
2. Sinoatrial Node
3. Intraatrial Pathway
4. Inernodal Pathway
5. Atrialventricular Node
6. Right Bundle Branch
7. Purkinje Fibers
8. Left Bundle Branch
The Vascular System

Figure 11.8b
 Movement of Blood Through Vessels

• Most arterial blood is

pumped by the heart
• Veins use the milking action
of muscles to help move
blood

Figure 11.9
Diffusion at Capillary Beds

Figure 11.20
Circulation to the Fetus

Figure 11.15
Pulse

• Pulse – pressure
wave of blood
• Monitored at
“pressure points”
where pulse is easily
palpated

Figure 11.16
Measuring Arterial Blood Pressure

Figure 11.18
 Cardiac Output Regulation

Figure 11.7

Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide