THE CARDIO – VASCULAR SYSTEM

Cardiac imaging techniques

1. Plain film
- PA
- Lateral view
  - Oblique views
2. Cardiac angiography – technique for left
ventriculography:
-  Femoral approach
-  Pigtail for ventricular injections
-  Straight cathether for pressure measurements
3. Coronary angiography
4. Cardiac ultrasound
5. Scintigraphy
6. MRI
 Mitral stenosis

Causes – rheumatic fever, bacterial endocarditis

Clinical findings – dyspnea, atrial fibrillation
Plain film: pulmonary venous hypertension, RVH, LAH,
pulmonary hemosiderosis
Ultrasound – increased LA dimensions, RV enlargement,
multiple echoes on MV leaflets (calcifications,
vegetations); Doppler: velocity measurements
 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”(volume overload,
cardiomegaly), enlarged chambers (LA+LV); PVH;
calcification of mitral annulus.
Ultrasound – MVP; enlarged LA,LV.
 
 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), 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 structures – LV, aorta
Ultrasound – dilatation of LV and aorta, atypical valve
leaflets, high-frequency vibrations of the anterior mitral
leaflet.
 Ventricular septal defect

Types – membranous (80%), muscular (10%), AV (5%)

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 RX; significant shunt –
enlargement of heart, pulmonary arteries and LA.
Ultrasound – diagnostic method of choice.
Angiography – commonly performed preoperatively –
pressure measurement, oxygenation.
 
Atrial septal defect

Hemodynamics – blood flows from LA to RA.

Plain film – RA,RV and PA enlargement; no LA
enlargement; the AA 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 – useful for identifying anomalous
pulmonary veins.
 Patent ductus arteriosus

In the fetus a PDA represents a normal pathway of blood

flow.
Fetal circulation – flow from PA to aorta as intrauterine
bypass of nonaerated lungs.
PDA closes functionally 48 hours after delivery and
anatomically after 4 weeks.
Hemodynamics – there is an L-R shunt because the
pressure in aorta is higher than in the pulmonary circulation.
Small PDA – normal Rx
Enlargement of the aorta and AA, enlargement of LA, LV,
increased pulmonary vascularity.
 Coarctation of aorta
Types – infantile (preductal) + adult (periductal)
Clinical findings – differential blood pressure between
arms and legs
Hemodynamics – preductal type has concomitant R-L
shunting via PDA or VSD; postductal coarctation has L-R
flow through PDA; collaterals to descending aorta : internal
mammary – intercostals; periscapular arteries – intercostals
Plain film – prestenotic dilatation of aorta proximal to
coarctation, indentation of aorta caused by the coarctation,
posstenotic dilatation, inferior rib notching secondary to
dilated intercostal arteries, reverse 3 sign of barium-filled
esophagus, 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
Thallium – evaluate for segmental ischemia and scar tissue
Ultrasound, MRI – imaging of complications
 Pericardial effusion

Causes – tumor, inflammatory, infectious, metabolic,

trauma, vascular.
Plain film -  250 ml are necessary to be detectable,
symmetric enlargement of cardiac silhouette.
Ultrasound – study of choice, echo-free space between
epicardium and pericardium.
 ESOPHAGUS
Methods of examination

Plain film – foreign body, cervical or mediastinal

emphysema, hiatal hernia
Barium meal – single-contrast ( medium-density barium:
50-60%weight/volume) or double-contrast ( heavy or
dense barium: 200%)
Alternative to barium – water-soluble solutions – when
perforation of the esophagus is suspected
CT – staging
Endoscopic ultrasound – evaluate the depth and extent of
submucosal and mural lesions.
 Diverticula

Zencker diverticulum – pulsion diverticulum with

herniation of mucosa and submucosa through
cricopharyngeal muscle. Location: posterior to esophagus
at pharyngeo-esophageal junction.

Kilian –Jamieson diverticulum – lateral to esophagus

below the cricopharyngeus.

Traction diverticula (adenopathies, cancer, TB) –

middle esophagus.
 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).

Radiographic features – thickening, nodularity of

esophageal folds + irregularity of mucosa ( granularity,
ulcerations) + luminal narrowing and stricture.
 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.
Types – primary (idiopathic), secondary (destruction of myenteric
plexus by tumor cells), infectious.
Diagnosis – manometry is the most sensitive to diagnose elevated
lower esophageal sphincter pressure.
Radiographic features: primary and secondary peristaltis absent
throughout esophagus + lower esophageal sphincter fails to relax in
response to swallowing + dilated esophagus typically curves to right and
then back to midline before passing through diaphragm + air-fluid level
in esophagus on plain film.
Complications – reccurent aspiration and pneumonias + increased
incidence of esophageal cancer.
 
 Esophageal cancer

Types – squamos cell carcinoma, adenocarcinoma,

lymphoma, leiomyosarcoma.

Spectrum of appearance – infiltrative, polypoid,

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,

reflux is more likely with larger hernias, may be reducible in
erect position.
2.Paraesophageal hernia (5%) – GEJ is in its normal
position, part of the fundus is herniated above the diaphragm
through esophageal hiatus and lies to the side of the
esophagus, reflux is not necessarily associated, usually
nonreducible.
Radiographic features – gastric folds above the
diaphragm.
 Gastric volvulus

Abnormal rotation of stomach

Organoaxial volvulus – rotation around long axis of
stomach: 180 so 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.
Radiographic features – giant gastric rugal folds,
hypersecretion ( poor coating, dilution of barium), gastric wall
thickening, small intestinal fold thickening due to
hypoproteinemia.

Zollinger – Ellison syndrome

Syndrome caused by excessive gastrin production.
Clinical – diarrhea, recurrent PUD, pain.
Radiographic features – ulcers (duodenal bulb, stomach,
postbulbar), thickened gastric and duodenal folds, increased
gastric secretions, reflux esophagitis.
 Peptic ulcer disease

Cause – oversecretion of acid + helicobacter pylori.

Rx – direct + indirect signs.
Ulcer crater seen en face – distinct collection of barium
which persists on different views: opacity, regular borders,
surrounded by a rim of radiolucency (edema), mucosal folds
extend up to the margin of ulcer crater.
Ulcer crater seen in profile – barium collection projects
outside the projected margin of the gastric wall.
Indirect signs – gastritis, Barclay triad, rigidity of the
lesser curvature.
 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%)
Radiographic features: early gastric cancer
- polypoid lesions (type 1) - 0,5cm (normal peristaltis
does not pass through lesion)
- superficial lesions ( type 2)
- excavated lesion (type 3) – malignant ulcer
Radiographic features: advanced gastric cancer
- malignant ulcer
- infiltrative – rigidity, diffuse narrowing
- polipoid – filing defect

Lymphadenopathy – gastrohepatic ligament, gastrocolic

ligament, perigastric.
Hepatic metastases.
 Benign tumors

- are usually submucosal in location.

- types – leiomyoma, lipoma, fibroma, schwanoma,
carcinoid.
 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
 SMALL BOWEL
Methods of examination

1. Conventional small bowel follow-through (SBFT)

2. Enteroclysis
3. CT
 Crohn’s disease
Recurrent inflammatory condition of bowel of unknown etiology.
Lesions are most common in small bowel (80%), colon (70%)
Pathologic development: hyperplasia of lymphoid tissue in
submucosa – lymphedema – aphtoid ulcerations – deeper ulcers –
fistulas – abscesses – strictures
Radiographic features – types of lesions:
Thickening of folds (edema)
Nodular pattern (submucosal edema and inflammation)
String sign – tubular narrowing of intestinal lumen (edema, spasm,
scarring depending on chronicity)
Ulcerations – grow and fuse with each other in linear fashion
ulceronodular pattern (“cobblestone”)
Fatty thickening and retraction of mesentery; mass
(lymphadenopathy) effect may separate bowel loops or make loops
display a concentric shape (omega sign).
Fibrosis/scarring may result in: pseudodiverticula, rigidity,
strictures.
 COLON
Methods of examination
1. Barium enema – single-contrast + double-contrast
contraindications to BE – suspected colonic perforation,
patients at risk for intraperitoneal leakage (severe colitis, toxic
megacolon), colonoscopy needs to follow enema, severe
recent disease (myocardial infarction, cerebrovascular
accident)
complications of BE – perforation due to overinflation or
traumatic insertion of balloon, appearance of gas in portal
venous system
2. Plain films – to detect colonic obstruction, colonic ileus
3. Ultrasound – to identify abscesses and bowel-wall
thickening
4. CT – abscess, fistula, diverticulitis, cancer
 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
Polyp – polyposis syndromes – especially familial
polyposis,ulcerative colitis, positive family history of colon
cancer, positive family history of endometrial or breast cancer,
rectosigmoidoscopy.
Location
Rectum – 35%, sigmoid – 25%, descending colon – 10%,
ascending colon-10%, transverse colon – 10%, cecum – 10%.
Radiographic features
- Polypoid
- Ulcerative
- Annular constricting – apple core
- Plaquelike
- Scirrhous carcinoma – long circumferential spred
Complications
Obstruction, intussusception,local 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
Uveitis, episcleritis
Radiographic features
- Ahaustral, foreshortened colon
- Granular mucosa, shallow confluent ulcerations
- Polyps
- Circumferential bowel involvement
Complications – toxic megacolon ( transverse colon 
6cm), strictures, obstruction, malignancy