Download The Cardiovascular System

THE CARDIO – VASCULAR SYSTEM
Cardiac imaging techniques
1. Plain film
- PA
- Lateral view
- Oblique views
2. Cardiac ultrasound
3. Left ventriculography - femoral artery approach
4. Coronary angiography
5. Scintigraphy
6. MRI
Mitral stenosis
Causes – rheumatic fever, bacterial endocarditis
Clinical findings – dyspnea, atrial fibrillation
Plain film:
- pulmonary venous hypertension (PVH),
- LA enlargement
- RVH,
- pulmonary hemosiderosis
Ultrasound
– increased LA dimensions,
- multiple echoes on MV leaflets (calcifications, vegetations);
- RV enlargement
Mitral regurgitation
Causes – rheumatic fever, mitral valve prolapse, rupture of
papillary muscles, Marfan syndrome, bacterial
endocarditis, rupture of chordae.
Clinical findings: acute presentation – MI, endocarditis;
decompensation by sudden onset of hypertension.
Hemodynamics – movement of leaflet of MV into LA
during systole.
Plain film
– “big heart disease”
– enlarged chambers (LA+LV);
- PVH;
- calcification of mitral annulus.
Ultrasound
- enlarged LA,LV.
– MVP;
Aortic stenosis
Types – valvular + subvalvular + supravalvular
Clinical findings – symptoms of LV failure; angina;
syncope
Plain film
– enlargement of ascending aorta (does not occur with
supravalvular AS), aortic arch is not enlarged
- LVH;
- calcification of aortic valve
Ultrasound
– multiple aortic valve echoes;
- postenotic dilatation of aorta;
- LVH;
Aortic regurgitation
Causes – rheumatic fever, systemic hypertension, aortic
dissection, endocarditis.
Plain film
– cardiomegaly,
- dilated LV,
- dilated aorta (ascending aorta + aortic arch)
Ultrasound
– dilatation of LV and aorta,
- atypical valve leaflets
Coarctation of aorta
Types – infantile (preductal) + adult (postductal)
Clinical findings – differential blood pressure between
arms and legs
Hemodynamics
– preductal type has concomitant R-L shunting via PDA
or VSD;
- postductal coarctation
- L-R flow through PDA;
- collaterals to descending aorta : internal
mammary – intercostals; periscapular arteries – intercostals
Coarctation of aorta
• Plain film
– prestenotic dilatation of aorta proximal to coarctation,
– Small aortic arch
– indentation of aorta caused by the coarctation (3 sign)
– inferior rib notching secondary to dilated intercostal
arteries,
– prominent left cardiac border from LVH,
– normal pulmonary vascularity
• MRI
– study of choice
– shows site and length of coarctation,
– allows evaluation of collaterals
Acute miocardial infarction
Clinical history + ECG + serum enzymes
Angiography – evaluate CAD + therapeutic angioplasty
Plain film – monitoring of pulmonary edema
Scintigraphy (with Thallium, In)– evaluation of segmental
ischemia and scar tissue
Ultrasound, MRI – imaging of complications – left
ventricle anewrism
IRM
Pericardial effusion
Causes – tumor, inflammatory, infectious, metabolic,
trauma, vascular.
Plain film
-  250 ml are necessary to be detectable,
- symmetric enlargement of cardiac silhouette.
- normal pulmonary vessels
Ultrasound
– study of choice,
- echo-free space between epicardium and pericardium.
Ventricular septal defect
Types – membranous (80%), muscular (10%), AV
Clinical findings – small to moderate defects :
asymptomatic; large defects lead to CHF; 75% close
spontaneously by age 10.
Hemodynamics – blood flow from LV into RV
Plain film
– small VSD – normal chest x ray;
- significant shunt – enlargement of LV, pulmonary
arteries and LA.
Ultrasound – diagnostic method of choice.
Angiography – commonly performed preoperatively –
pressure measurement, oxygenation.
11 month old
LV
RV
RV
LV
US
MRI
Atrial septal defect
Hemodynamics – blood flows from LA to RA.
Plain film
– RA,RV and PA enlargement;
- the aortic arch appears small (but in reality is normal)
because of the prominent pulmonary trunk and clockwise
rotation of heart (RV enlargement).
Ultrasound – imaging modality of choice for diagnosis
Angiography –
Atrial septal defect
US
VD
AD
VS
AS
MRI
Patent ductus arteriosus
In the fetus a PDA represents a normal pathway of blood
flow.
PDA closes functionally 48 hours after delivery and
anatomically after 4 weeks.
Hemodynamics – there is an L-R shunt the pressure in
aorta is higher than in the PA.
Plain film
- Small PDA – normal Rx
- large PDA - enlargement of the PA, LA, LV
- increased pulmonary vascularity.
US
– demonstrates Ao-PA shunt,
- enlargement of the LA, LV
Aortography – CM injected into the Ao passes into the PA
A
O
AP
A
C
PDA
AP
B
D
AP
ESOPHAGUS
Methods of examination
Plain film
– foreign bodies,
- cervical or mediastinal emphysema,
- hiatal hernia
Barium meal
– single-contrast
- double-contrast
– water-soluble solutions – when perforation of the
esophagus is suspected
CT – tumour staging
Endoscopic ultrasound – evaluates the extent of the
tumours
CT
Diverticula
Pulsion diverticula
- herniation of mucosa and submucosa
- through cricopharyngeal muscle (Zencker
diverticulum)
- through the esophageal muscles, in the lower
esophagus - epiphrenic diverticula
Traction diverticula
- causes: adenopathies, cancer, TB
– middle esophagus.
Barium meal - addition image
Complications – inflammation, perforation
Esophagitis
May present with erosions, ulcers, strictures, perforations
and fistulas.
Types
– infectious (herpes, candidiasis, cytomegalovirus),
- chemical (reflux, corrosives),
- iatrogenic (radiotherapy, nasogastric tubes),
- other ( HIV, scleroderma, Crohn).
Barium meal
– thickening, nodularity of esophageal folds
- irregularity of mucosa (granularity, ulcerations)
- luminal narrowing and stricture.
- Caustic esophagitis
- Esophageal sticture – long, regular margins
Achalasia
Gastroesophageal sphincter fails to relax because of degeneration
of Auerbach’s plexus.The sphincter relaxes only when hydrostatic
pressure of the column of liquid or food exceeds that of the sphincter:
emptying occurs more in upright than in orizontal position.
Diagnosis – manometry is the most sensitive to diagnose elevated
lower esophageal sphincter pressure.
Plain film - air-fluid level in the esophagus
Barium meal
- primary and secondary peristaltis absent throughout esophagus
- lower esophageal sphincter fails to relax in response to swallowing
- dilated esophagus
- Stricture of the abdominal esophagus
Complications
– reccurent aspiration and pneumonias
- increased incidence of esophageal cancer.
Esophageal cancer
Types – squamos cell carcinoma, adenocarcinoma,
lymphoma, leiomyosarcoma.
Barium meal
– stricture - infiltrative
– irregular filling defect - polypoid
– malignat ulcer - ulcerative.
Staging – CT + endoscopic US
STOMACH
Methods of examination
1. Barium meal – single + double contrast
2. Endoscopic ultrasound
3. CT
Anatomy
Fundus + body + antrum + pylorus + curvatures + gastric
folds
Hiatal hernia - two types:
1. Sliding hernia (95%)
– GEJ is above the diaphragm, part of the fundus is
herniated above the diaphragm
- reflux is more likely with larger hernias
- may be reducible
2. Paraesophageal hernia (5%)
– GEJ is in its normal position
- part of the fundus is herniated above the diaphragm
- reflux is not necessarily associated
- usually nonreducible.
Barium meal – gastric folds above the diaphragm.
Gastric volvulus
Abnormal rotation of stomach
Organoaxial volvulus – 180 rotation around long axis of
the stomach  great curvature is cranially located 
 upside-down stomach
Mesenteroaxial volvulus – stomach rotates around its
short axis, fundus is caudal to antrum
Menetrier’s disease (giant hypertrophic gastritis)
Large gastric rugal folds with protein-losing enteropathy.
Clinical triad – achlorhydria, hypoproteinemia, edema.
Barium meal– giant gastric rugal folds,
- hypersecretion (poor coating, dilution of barium),
- gastric wall thickening,
- small intestinal fold thickening
Zollinger – Ellison syndrome
Syndrome caused by excessive gastrin production.
Clinical – diarrhea, pain.
Barium meal
– ulcers (duodenal bulb, stomach, postbulbar),
– thickened gastric and duodenal folds,
– increased gastric secretion, reflux esophagitis.
Peptic ulcer disease
Cause – oversecretion of acid + helicobacter pylori.
Barium meal – direct + indirect signs.
Ulcer crater seen in profile – barium collection projects
outside the margin of the gastric wall.
Indirect signs –thickened gastric folds, increased gastric
secretion.
Ulcer crater seen “en face”
– round barium collection which persists on different
views, with regular borders
– surrounded by a rim of radiolucency (edema),
– mucosal folds extend up to the margin of the ulcer.
Diferential diagnosis
GASTRIC DIVERTICULUM
Gastric carcinoma
Third most common GI malignancy (colon, pancreas,
stomach).
Risk factors:
pernicious anemia,
adenomatous polyps,
chronic atrophic gastritis
Location – lesser curvature (60%),
– greater curvature (10%),
– GEJ (30%)
Gastric carcinoma
Early gastric cancer - adiographic features:
- polypoid lesions (type 1) - 0,5cm (normal peristaltis
does not pass through lesion)
- superficial lesions ( type 2)
- excavated lesion (type 3)
Advanced gastric cancer - radiographic features:
- malignant ulcer
- infiltrative – rigidity, diffuse narrowing
- polipoid – filing defect
Lymphadenopathy
Hepatic metastases.
Benign tumors
types
– leiomyoma, lipoma, fibroma, schwanoma,
carcinoid - are usually submucosal in location.
- polyp
DUODENUM
Methods of examination
1. Barium meal – single + double contrast
2. Endoscopic ultrasound
3. CT
Duodenal ulcer
- 2-3 times more common than gastric ulcers.
- all bulbar duodenal ulcers are considered benign.
- postbulbar or multiple ulcers raise the suspicion for
Zollinger-Ellison syndrome.
edematous – ulcer + edema
edemato-sclerous – ulcer + edema + deformity
sclerous – deformity and shrinking
ULCER DUODENAL POSTBULBAR
STENOZA PILORICA
ULCEROASA,
DECOMPENSATA
DIVERTICULI DUODENALI
SMALL BOWEL
Methods of examination
1. Plain film
2. Dedicated single contrast small bowel examination
2. Enteroclysis
3. CT
Crohn’s disease
Recurrent inflammatory condition of bowel of unknown etiology.
Lesions are common in small bowel (80%), colon (70%)
Pathologic development: hyperplasia of lymphoid tissue in
submucosa – edema – aphtoid ulcerations – deeper ulcers – fistulas –
abscesses – strictures
Radiographic features – types of lesions:
Thickening of folds (edema)
Nodular pattern (submucosal edema and inflammation)
Ulcerations – grow and fuse with each other in linear fashion,
ulceronodular pattern (“cobblestone”)
Fatty thickening and retraction of mesentery;
Mass effect (lymphadenopathy) may separate bowel loops
String sign – tubular narrowing of intestinal lumen (edema, spasm,
scarring depending on chronicity)
Fibrosis/scarring may result in: rigidity, strictures.
MECKEL
DIVERTICULUM
COLON
Methods of examination
1.Plain films – to detect colonic obstruction, colonic ileus
2. Barium enema – single-contrast + double-contrast
contraindications to BE
– suspected colonic perforation,
- patients at risk for intraperitoneal leakage (severe
colitis, toxic megacolon),
- severe recent disease (myocardial infarction,
cerebrovascular accident)
complications of BE – perforation due to overinflation or
traumatic insertion of balloon
3. Ultrasound – to identify abscesses and bowel-wall
thickening
4. CT – abscess, fistula, diverticulitis, cancer
B
A
Polyps
Familial polyposis
- Most common intestinal polyposis syndrome
- Usually more than 100 polyps
- Screening of family members of familial
polyposis should start at puberty:
malignant degeneration by 40 years;
treatment – total colectomy
Gardner syndrome
- Polyposis – colon 100%, duodenum 90%;
- Hamartomas of stomach
- Soft tissue tumors – inclusion cysts, desmoids, fibrosis
- Osteoma in calvarium, mandible
- Malignant transformation in 100% if untreated
Peutz – Jeghers
- Second most common intestinal polyposis
- Mucocutaneous lesions – buccal mucosa, palm
- Polyps have virtually no malignant potential
- Slightly increased risk of stomach, duodenal, ovarian
cancer
Turcot syndrome – polyps + intracerebral gliomas
Juvenile polyposis
- Usually large polyps in rectum
- Present in children with bleeding, prolapse or
obstruction
COLON CARCINOMA
High-risk groups
- Polyps, polyposis syndromes – especially familial polyposis,
- ulcerative colitis,
- positive family history of colon cancer,
-positive family history of endometrial or breast cancer.
Location
Rectum – 35%, sigmoid – 25%, descending colon – 10%,
ascending colon-10%, transverse colon – 10%, cecum – 10%.
Radiographic features
- Polypoid
- Ulcerative
- infiltrating (stenosing)
Complications
Obstruction, intussusception, perforation, peritoneal spread,
local tumor reccurence
Staging
T1 – mucosa or submucosa only
T2 – muscle or serosa
T3 – extension to contigous structures
T4 – extension beyond contigous structures
N1 – regional lymph nodes
N2 – distant lymph nodes
M - metastases
ULCERATIVE COLITIS
Unknown etiology.
Clinical: diarrhea, rectal bleeding. Disease affects
primarily mucosa and typically starts in rectum. Associated
findings:
Joints – arthritis, arthralgia, ankylosing spondylitis
Liver – sclerosing cholangitis, chronic active hepatitis,
cholangiocarcinoma
Skin – pyoderma gangrenosum, erythema nodosum
Radiographic features
- Granular mucosa, shallow confluent ulcerations
- pseudopolyps
- Circumferential bowel involvement, tubular narrowing
- Ahaustral, foreshortened colon
Complications – toxic megacolon ( transverse colon 
6cm), strictures, obstruction, malignancy
DIVERTICULA