CARDIOVASCULAR
SYSTEM
Group 4
Terms
 Ischemia-refers to an interference with blood supply to an
organ or part of an organ, depriving the organ’s cells and
tissues of oxygen and nutrients.
 Causes:
 Narrowing of arterial structures
 Thrombotic or embolic occlusions
 Infarction- is tissue death (necrosis) due to inadequate
blood supply to the affected area. It may be caused by
artery blockages, rupture, mechanical compression, or
vasoconstriction. The resulting lesion is referred to as an
infarct
 Haemorrhage- ilocalized area of ischemic necrosis within a
tissue or organ produced by occlusion and rupture of a
blood vessel
Causes
 Injury such as trauma
 Atherosclerosis
 Inflammatory or neoplastic erosions of the vessel wall.
CONGENITAL HEART DISEASES
 DEF: Abnormalities of the heart or great vessels that are
present at birth and result in either shunting of blood
between the Rt and Lt circulation and/or cause outflow
obstruction.
 They originate from faulty embryogenesis during week 3-8
when major CVS structures develop.
 Cause unknown in 90%,
 Environmental factors e.g congenital rubella, maternal
DM, alcohol, drugs e.g thalidomide.
 Genetic factors e.g trisomies 13,15,18,21, Turners
syndrome
CLASSIFICATION
1.An abnormal communication: ASD, VSD, PDA. atreal septal defect,
ventricular septal defect, patent ductus arteriousus
2. An obstruction eg. tricuspid atresia, pulmonary, mitral, aortic valve
stenosis, coarctation of aorta.
3. Common chambers- common atrium, common ventricle
4. Abnormal connections (discordance)- Transposition of great
arteries.
5. Abnormal situs (position) of heart chambers.
LEFT-TO-RIGHT SHUNTS
Atrial septal defect(ASD)
 The most common congenital cardiac lesions are left-to-right shunts
which permit mixing of blood in the systemic and pulmonary
circulations.
 Is the most common congenital cardiac lesion which permits free
communication btw the two atria as a result of either lack of closure
of the foramen ovale after birth or its improper
closure during gestation
 Because the left atrium pressure is usually higher than the pressure in
the right atrium, the resulting shunt is from left to right and causes
increased pulmonary blood flow and overloading of the right
ventricle.
 This produces the radiographic appearance of enlargement of the
rt ventricle, rt atrium and pulmonary outflow tract
Apical 4 chamber view echo.
Note the enlarged right chambers.
Ventricular septal defect(VSD)
 In pts with vsd, the resulting shunt is also from left to
right because the left ventricular pressure is usually
higher than the pressure in the right ventricle
 The shunt causes increased pulmonary blood flow and
consequently increased pulmonary venous return.
 This leads to diastolic overloading and enlargement of
the lt atrium and lt ventricle
 Because shunting occurs primarily in systole and any
blood directed to the rt ventricle immediately goes
into the pulmonary artery, there is no overloading of
the rt ventricle and radiographically no right
ventricular enlargement is seen.
Patent ductus arteriosus(PDA)
 Is the third major type of lt-to-rt shunts
 The ductus arteriosus is a vessel that extends from the
bifurcation of the pulmonary artery to joint the aorta
just distal to the left subclavian artery.
 It serves to shunt blood from the pulmonary artery into
the systemic circulation during intrauterine life.
 Persistence of the d.a, which normally closes soon
after birth results in a lt-to-rt shunt.
 The flow of blood from the higher-pressure aorta to the
lower-pressure pulmonary artery causes increased
pulmonary blood flow, and an excess volume of
blood is returning to the lt atrium and ventricle.
 Radiographically, there is enlargement of the lt atrium,
lt ventricle and the central pulmonary
arteries, along with diffuse increase in pulmonary
vascularity
 The increased blood flow through the aorta proximal
to the shunt produces a prominent aortic knob in
contrast to a small- or normal size aorta seen in atrial
and ventricular SD
 All lt-to-rt shunts can be complicated by development
of pulmonary hypertension(Eisenmenger’s syndrome)
 R/A
 PA chest
 ASD-enlarged rt ventricle, rt atrium and pulmonary
outflow tract
 VSD-pulmonary trunk enlargement, no rt ventricular
enlargement
 PDA- enlargement of lt atrium, lt ventricle with an
increase in pulmonary vascularities
 US- atrial defect has common atria; ventricular defect
demonstrate lack of closure
 MRI- spin echo MRA breath-hold and cine to
investigate morphological and functional anomalies
when US is not visible or not diagnostic
Tetralogy of Fallot
 Is the most common cause of cynotic congenital
heart disease.
 It consists of four( thus “tetra”) abnormalities:
 i) high ventricular septal defect
 ii) pulmonary stenosis
 iii) overriding of the aortic orifice above the ventricular
defect and
 iv) right ventricular hypertrophy
 Pulmonary stenosis cause an elevation of pressure in
the rt ventricle and hypertrophy of that chamber
 Because of the narrow opening of the pulmonary
valve, an inadequate amount of blood reaches the
lungs to be oxygenated.
 The VSD and the overriding of the aorta produce rt-to-
lt shunting of unoxygenated
 blood into the lt ventricle and the into the systemic
circulation, thus increasing degree of cyanosis
 R/A
 PA chest- enlarged right ventricle causes upward and
lateral displacement of the heart apex
 Echocardiography- demonstrates the four
abnormalities of the disease.
 MRI- demonstrates the morphological conditions; spin-
echo scans to identify abnormalities, and cine to
demonstrate flow void in pulmonary stenosis
TETRALOGY OF FALLOT(TOF)
Boot shaped heart -.
Due to uplifting of the cardiac apex
due to right ventricular hypertrophy and
concavity of the main pulmonary artery.
Coarctation of the aorta
 Refers to narrowing or constriction of the aorta that
most commonly occurs just beyond the branching of
the blood vessels to the head and arms ( just beyond
the origin of LSA)
 The blood supply and the pressure to the upper
extremities are higher than normal
 As a result, there is decreased blood flow through the
constricted area to the abdomen
 and legs.
 Classically the pt has normal blood pressure in the
arms, but very low blood pressure in the legs.
 It is the most common frequent cause of hypertension
in children.
 The relative obstruction of aortic blood flow leads to
progressive development of
 Collateral circulation- the enlargement of normally
tiny vessels in an attempt to compensate for the
inadequate blood supply to the lower portion of the
body
 R/A
 PA chest- rib notching
 Ba. Swallow- opposite of above
 Echo – demonstrate the severity of the stricture
 Doppler echo-determines flow gradient and possible
collateral vessels
 Aortography( angiography)- localizes obstruction,
determines length of coarctation and identifies an
associated malformation
 MRI-demonstrate narrowing, used for follow-up of
corrective surgery
Oblique-sagittal ‘black
blood’
Turbo-spin echo showing
severe discrete coarctation
Transposition of the great arteries
 The common form is the D-loop transposition in which
the ventricular anatomy is normal.
 There is simple reversal of connection of the great
arteries, with the aorta arising from the
morphologically right ventricle and the pulmonary
artery arising from the morphologically left ventricle.
 The exact orientation is variable, but the most
common arrangement is with aortic valve arising from
a high anterior position from the rt ventricle, and the
pulmonary valve arising from the lower position behind
the rt ventricular outflow tract.
 The normal arrangement where the rt ventricular
outflow tract and main pulmonary artery twists around
the lt ventricular outflow tract and the
 aorta, is lost and the two great arteries run upwards parallel
to their respective chambers
 R/A
 PA chest- heart is slightly enlarged and rounded
 Echo- clearly show the two great vessels but care must be
taken to correctly identify the great arteries, which usually
lie in parallel
 Angiography- will clearly show the abnormal connections
and clarify other associated anomalies
TGA( TRANSPOSITION OF GREAT ARTERIES)EGG ON STRING, EGG ON SIDE SIGN
TRANSPOSITION OF THE GREAT
ARTERIES(TGA)
MR sagittal:
Aorta arises
anteriorly from
hypertrophied
right ventricle.
Posterior PA arises
from left
ventricle.
 Read other congenital anomalies
 Double inlet left ventricle
 Double outlet left ventricle
 Dextrocardia
 Tricuspid atresia
 Pulmonary stenosis
 Aortic stenosis
 Congenital cardiomyopathies
 Truncus arteriosus etc
Coronary Artery Disease(CAD)
 Narrowing of coronary arteries causes oxygen
deprivation of the myocardium and ischemic heart
diseases.
 In most patients, narrowing of the lumen of one or
more of the coronary arteries is attributable to the
deposition of fatty material on the inner arterial wall
(atherosclerosis)
 Predisposing factors to development of CAD;
 HTN
 Obesity
 Smoking
 A high-cholesterol diet
 Lack of exercise.

 The speed and degree of luminal narrowing
determine whether an atherosclerotic lesion causes
significant and clinically evident ischemia.
 Temporary oxygen insufficiency causes angina
pectoris, a feeling of severe chest pain that may
radiate to the neck, jaw and left arm( sometimes both
arms), and that is often associated with the sensation
of chest tightness or suffocation
 Occlusion of coronary arteries deprives an area of
myocardium of its blood supply and leads to the
death of muscle cells (myocardial infarction) in the
area of vascular distribution.
 The size of the coronary artery that is occluded and
the myocardium that it supplies determine the extent
of heart muscle damage.
 The greater the area affected, the poorer the
prognosis because of the increase loss of pumping
function that may result in CHF
.
 A favourable prognosis is the development of
collateral circulation, through which blood from
surrounding vessels is channeled into the damaged
tissue.
 if pt survives, the infarcted region heals with fibrosis.
 Long term complication include the development of
thrombi on the surface of the damage area
 and the production of a local bulge ( ventricular
aneurysm)at the site of weakness of the myocardial
wall
 R/A
 PA chest- vessel calcifications
 SPECT- classifies myocardial necrosis
 CT-decreased attenuation in the affected myocardial
tissue
 Calcium scoring to visualized hard plaque , CTA to
visualize soft plague
 MRI- increased T2W signal intensity in affected
myocardial tissue
 NM- focal defects(cold spots) after exercise with filling
at rest indicate stenosis
 IVUS( intravascular ultrasound)- vessel size and length
of lesion
 Angiogram- strictures or narrowing are filling defects
CT
With MDCTA
imaging of the
more proximal
coronary
arteries allows
reliable
exclusion or
detection CAD.
Oblique coronal MIP reconstruction
shows Ca++ of LAD
 Congestive Cardiac Failure(CCF)
 Refers to the inability of the heart to propel blood at a
volume sufficient to the tissues.
 Causes
 Intrinsic cardiac abnormality( include insufficient or
defective cardiac filling and impaired contractions for
emptying)
 HTN hypertension
 Any obstructive process that abnormally increases the
peripheral resistance to bood flow
 PA chest-
 CTR > 50%
 Left sided cardiac enlargement, pulmonary oedema,
pulmonary effusion
 Right sided widened mediastenum and elevated right
hemidiaphragm
 Echo – measuring left ventricular performance,
ejection fraction and filling pressures of the pulmonary
artery and ventricles
 Hypertension
 Blood pressure is the function of cardiac output ( the
amount of blood pumped per unit time by the heart)
and the total peripheral resistance, which reflects the
condition of the walls of the blood vessels throughout
the body
 Although the peripheral resistance and the cardiac
output may fluctuate rapidly
 Depending on such factors as whether a person sits or
stands and is quiet or excited, the systemic bp remains
remarkably constant in a healthy person.
 Bp reading consists of systolic(highest pressure in the
peripheral arteries that occurs when the lt ventricle
contracts), and diastolic ( pressure in the peripheral
arteries when the lt ventricle is relaxing and filling with
the blood form the lt atrium
 HTN is defined as elevation of systolic pressure above
140mmHg and of diastolic pressure above 90mmHg
 Forms
 Most pts with elevated bp has essential or idiopathic
htn – characterized by gradual onset and a
prolonged course, often of many years
 A much less common malignant form characterised
by abrupt onset, runs a rapid cause
and often leads to renal failure or cerebral
haemorrhage
 About 6% of pts have secondary htn resulting from
another disease.
 Underlying causes:
 renal parenchyma disease
 Vascular disease
 Adrenal abnormalities
 Abnormality involving the secretion of a substance the
increases vascular tone and and peripheral arterial
substance
 R/A
 P/A chest- aortic knuckle prominence
 Arteriography detects renovascular lesions
 RN renogram-demonstrate lesions
 Hypertensive heart disease
 Long standing HTN causes narrowing of systemic
blood vessels and an increase resistance in blood
flow.
 The left ventricle is forced to assume a larger
workload, which initially causes hypertrophy and little
if any change in radiographic appearance of cardiac
silhoutte.
 R/A
 PA chest- enlarged lt ventricle, inferior displacement
of cardiac apex, aortic tortuosity
 Aneurysm
 Is a localized dilatation of an artery that most
commonly involves the aorta, especially its abdominal
portion
 It represents a weakness in the wall (decrease elastin
and increased collagen production)

Types
 Saccular aneurysm- involves only one side of the
arterial wall
 Fusiform aneurysm
 Is bulging of the entire circumference of the vessel
wall
 Of a blood vessel caused by atherosclerosis , syphilis or
other infection, trauma, or a congenital defect such
as Marfan’s syndrome
 Presence of multiple small anerysms is suggestive of a
generalized arterial inflammation (arteritis)
 R/A
 Radiograph- calcification outlining vessel
Extensive calcification of the Aorta
53
54
 Atherosclerosis
 Arteriosclerosis occurs when arteries become marked
by thickening, hardening and lack of elasticity in the
arterial wall. Atherosclerosis is one form of
arteriosclerosis
 The major cause of vascular disease of the extremities
is atherosclerosis, in which fatty deposits called
plaques develop in the intima and produce
progressive narrowing and often
 And often complete occlusion of large and medium
size arteries.
 R/A
 Plain- calcification demonstrating hardening of the
artery
 Colour Doppler- demonstrates plaque and degree of
luminal stenosis
 MRA- two-dimensional time-of-flight view
 Demonstrates narrowing and flow changes in
infrapopliteal vessels
 3-D images demonstrate narrow occlusions as signal
absence
 Traumatic rupture of the aorta
 Is potentially a fatal complication of closed-chest
trauma.
 In almost all cases(90-95%), the aortic tear occurs just
distal to the left subclavian artery at the site of the
ductus venosus
 R/A
 PA chest – widened mediastinum, deviation of the NG
tube to right, apical pleural cap
 C TA/Aortography- demonstrates tear and
heamorrhage
A traumatic pseudoaneurysm at
the isthmus on arch aortography.
A. Aortogram – shows
aortic laceration at the
isthmus
59
 Dissection of the aorta
 Is a potentially life threatening condition in which
disruption of the intima( inner layer) permits the blood
to enter the wall of the aorta and separate its layers.
 As a result of the disruption, the aorta is divided into
true and false lumens
 Most occur in pts with arterial HTN, some are a result of
trauma or congenital defect
 Radiographic appearance
 Plain.- widening of aortic shadow which may be
irregular
 CT- double-barrel channel with linear filling defect
within the lumen(intimal flap)
 MRI- intimal flap causes medium intensity signal
separating true and false lumina; blood flow causes
signal void
 TEE(transesophageal echocardiography)-
demonstrates intimal tear, extension of dissection and
pleural effusion
 Aortography-extend of true and false lumina
VALVULAR DISEASES
 Review anatomy of major valves
 Rheumatic Heart Disease(RHD)
 Rheumatic fever is an autoimmune disease that results
from reactions of a pts antibodies against antigens
from a previous streptococci infection(of throat and
ear).
 The symptoms( fever, rash, inflamed and painful joints)
typically develop several weeks after the
streptococcal infection
 The major damage of RF is to the valves of the heart,
most frequently the mitral and aortic valves.
 It is the major cause of acquired valvular disease.
 The allergic response causes inflammation of the
valves
 Deposits of blood platelets and fibrin from blood
flowing over the valve produce small nodules
(vegetations) along the margins of the valve cusps.
 The thickened valves may stick together, so that the
valvular opening remains permanently
narrowed(stenosis) rather than opening properly when
blood flows through.
 Fibrous scarring may cause retraction of the valves
cusps so that the cusps are unable to meet when the
valves tries to close; this is insufficiency, and blood
leaks through the valve when it should be closed.
 Imaging
 Doppler echocardiography- quantify valvular
insufficiencies
 Mitral stenosis
 Almost always a complication of rheumatic disease,
results from diffuse thickening of the valve by fibrous
tissue, calcific deposits, or both.
 R/A
 PA chest- left atrium enlargement
 Lateral,RAO- posterior displacement of oesophagus,
left main bronchus and calcification of valves
 Echocardiography-chamber enlargement, wall
thickness and size of valvular orifices
 Sine MRI- demonstrates and quantitates abnormal
flow patterns
 Read mitral insufficiency
 Aortic stenosis
 May be caused by:
 RHD
 Congenital valvular deformity(esp of bicuspid origin)
 Degenerative process of aging( idiopathic calcific
stenosis
 The obstruction to lt ventricular outflow in aortic
stenosis increases the workload of the lt ventricle
 R/A
 PA chest- enlargement of lt ventricle, rounding of the
cardiac apex
 Posterior displacement of the cardiac apex in the
lateral projection
 Lateral- posterior displacement of cardiac apex ,
bulging of ascending aorta
 Aortic valve calcification
 Read aortic insufficiency
 Infective endocarditis
 Refers to the formation of nodules or vegetations on
heart valves by deposits of bacteria or fungi.
 Unlike the small nodules in rheumatic fever, the
vegetations in I.E are filled with bacteria and tend to
break easily to enter the bloodstream and form septic
emboli that
 Travel to the brain, kidney, lung or other vital organs.
 R/A
 Echocardiography- shaggy echoes produce by
irregular thickening of affected valves
 Electron-beam CT- vegetations in valve,valvular
calcifications, distirted orifices
 Pericardial effusion
 Refers to accumulation of fluid within the pericardial
space surrounding the heart.
 Causes include:
 Bacteria
 Viruses
 Neoplastic involvement
 idiopathic
 Imaging
 PA chest- enlargement of cardiac silhouette
 Echocardiography- posterior sonolucent fluid
collection
 CT- loculated fluid accumulation around the heart
 MRI- differentiate serous from hemorrhagic fluid as
decreased signal intensity
2.PERICARDIAL EFFUSSION
Pericardial
effusion in a 40year-old
woman with
shortness of
breath. Axial
contrastenhanced CT
scan shows an
effusion (∗) with
the same
attenuation as
water (0 HU).
 Deep venous thrombosis
 DVT which is primarily the major source of potentially
fatal pulmonary embolism.
 Risk factors are related to Virchow's triad:
stasis,
hypercoagulability,
and venous injury.
VENOUS DISEASES
 At times, DVT may be the earliest symptom of an
unsuspecting malignancy of the pancreas, lung or
G.I.T
 R/A
 Venography- constant filling defects or an abrupt
ending of the opaque column in a vein, nonfilling of
one or more veins, extensive
SONOGRAPHIC FEATURES
1.
Noncompressibility of vein (loss of “wink”
sign)
2.
Echogenic lumen
3.
Enlarged vein
4.
Color Doppler allows differentiation of
occlusive and nonocclusive thrombi.
5.
Indirect iliac evaluation is possible by
evaluating the pulse wave Doppler form.
The waveform changes with respiration,
augmentation, and Valsalva.
80
 Varicose veins
 Are dilated, elongated and tortuous vessels that most
commonly involve the superficial veins of the leg just
under the skin.
 If the venous dilatation becomes extreme, the valves
that normally prevent backflow of blood due to
gravity become incompetent and cease to function,
thus increasing the volume of blood in these slowflowing vessels
 R/A
 Venography- demonstrates patency of the deep
venous system and degree of collateral circulation
from the superficial to deep veins.
THANK YOU
END