FCPS Part 1 AnatomyRadiology Paper 2

Heart and great vessels

Heart, valves, great vessels and coronary arteries on imaging

The heart is judged by its borders and size on the chest film, and by chambers, valves and coronary arteries on echo, CT and MRI. CPSP asks which chamber forms each border, how chambers enlarge, coronary anatomy and variants, and arch anomalies.

One of the most tested topics in past papers

Surfaces, borders and size

ViewBorderChamber
PA filmRight borderRight atrium (SVC above)
PA filmLeft borderAortic knuckle, pulmonary trunk, left atrial appendage (normally flat), left ventricle
Lateral filmAnteriorRight ventricle (also the main sternocostal surface)
Lateral filmPosteriorLeft atrium above (the base, in front of the oesophagus), left ventricle below
  • Cardiothoracic ratio is reliable only on a PA film: an AP film magnifies the heart, which is further from the detector. In late pregnancy the heart is pushed up and left.
  • On a lateral film, a line from the carina to the anterior costophrenic angle has the aortic valve above it and the mitral valve below. The pulmonary valve lies highest.
  • Because the left atrium lies directly in front of the oesophagus, transoesophageal echo shows its appendage best, and a giant left atrium causes dysphagia and hoarseness.
Enlarged chamberSigns
Left atrium (mitral stenosis)Double density behind the right heart border, splayed carina, elevated left main bronchus, bulging appendage on the left border, posterior oesophageal indentation
Right ventricleUpturned apex, retrosternal space filled on lateral film
Left ventricleApex displaced down and out
Pulmonary trunkBulge below the knuckle: post-stenotic dilatation in valve stenosis; trunk wider than the aorta in pulmonary hypertension
  • An ASD gives plethoric lungs and a large right heart but a normal left atrium, because the left atrium decompresses through the defect.
  • LV aneurysm after anterior infarction: apical bulge of thin scar, sometimes with mural thrombus.

Valves, sounds and valve disease

AreaSite
AorticRight 2nd intercostal space at the sternal edge
PulmonaryLeft 2nd intercostal space
TricuspidLeft lower sternal edge, 4th–5th space; right-sided murmurs louder on inspiration
MitralApex, left 5th space in the midclavicular line
  • S1 is mitral and tricuspid closure; S2 is aortic and pulmonary closure at the start of isovolumetric relaxation, higher pitched than S1 and splitting more on inspiration. S3 comes from ventricular wall vibration during rapid passive filling (when about two-thirds of filling occurs).
Valve lesionPathology and imaging
Rheumatic mitral stenosisThickened leaflets that dome in diastole, fish-mouth orifice from fusion of the commissures, short fused chordae; balloon valvotomy splits the commissures
Calcific aortic stenosis (elderly)Heavy nodular calcium on the aortic side of three cusps, no commissural fusion (age-related degeneration); bicuspid valves calcify a decade or two earlier
Ebstein anomaly (maternal lithium)Septal tricuspid leaflet displaced towards the apex, atrialised right ventricle, huge box-shaped heart, oligaemic lungs; WPW often coexists
Marfan aortic rootPear-shaped root dilatation with loss of the sinotubular waist; cystic medial degeneration (fragmented elastic fibres, mucoid matrix); lens dislocates upwards (downwards in homocystinuria)

Chamber identity

  • Morphological right ventricle: moderator band (carries the right bundle branch), coarse trabeculation, tricuspid valve inserted more apically on the septum, muscular infundibulum (from the conus cordis). Morphological left atrium: narrow finger-like appendage; the right appendage is broad and triangular.
  • Venae cordis minimae (Thebesian veins) drain myocardium straight into the chambers, including the left heart, adding a little desaturated blood to arterial blood (part of the normal anatomical shunt).
  • Right atrium: crista terminalis with the SA node near the SVC; coronary sinus opening between the IVC and tricuspid orifice, with the AV node close by (at risk in tricuspid repair).

Pericardium

  • Fibrous and serous layers; the parietal layer is supplied by the phrenic nerve (shoulder-tip pain); the visceral layer is insensitive.
  • Transverse sinus: behind the aorta and pulmonary trunk, in front of the atria (clamp passed here). Oblique sinus: behind the left atrium, bounded by pulmonary veins and IVC. The superior pericardial recess is a fluid crescent behind the ascending aorta, not a node or dissection.
  • The pericardial stripe between the fat lines on a lateral film is up to 2 mm. About 200–250 mL of fluid is needed before the heart shadow enlarges. On echo pericardial fluid lies in front of the descending aorta.

Coronary arteries and veins

ArteryCourse and supply
Right coronaryFrom the right aortic sinus, in the right AV groove; conus artery, SA nodal (about 60%), AV nodal, posterior descending in about 70% (right dominance)
Left anterior descendingAnterior interventricular groove; anterior two-thirds of the septum (septal branches, the first used for alcohol septal ablation), anterior wall and apex; V1–V4 changes
CircumflexLeft AV groove; lateral and posterior left ventricle
Ramus intermediusThird branch when the left main trifurcates
  • Dominance depends on which artery gives the posterior descending artery. The RCA usually supplies the AV node, so inferior infarction causes heart block.
  • Veins: great cardiac with the LAD, middle cardiac with the posterior descending artery, both into the coronary sinus; anterior cardiac veins enter the right atrium directly.
  • Dangerous variants: an anomalous coronary running between the aorta and pulmonary trunk (exercise syncope or death); left coronary from the pulmonary trunk, which becomes symptomatic as pulmonary resistance falls and flow reverses. A myocardial bridge covers a short tunnelled segment.
  • Coronary CT: nitrate dilates the arteries; calcium is counted above 130 HU. The left internal thoracic artery to the LAD is the best graft; vein grafts are reversed because of their valves.
  • Perfusion and MRI: a defect at stress but not rest is ischaemic viable muscle. Late gadolinium in a coronary territory is infarct; patchy mid-wall suggests sarcoidosis. Diffuse global subendocardial enhancement with a dark blood pool means amyloid (for example in myeloma): thick walls on echo but low QRS voltages, because the walls are infiltrated, not muscular.
  • Adenosine stress: adenosine dilates normal coronary arterioles and steals flow from stenosed beds. Bronchospasm is reversed by aminophylline, a methylxanthine adenosine-receptor blocker; caffeine is avoided before the test for the same reason. Inferior wall defects may be diaphragm attenuation artefact.

Great vessels and their anomalies

FindingExplanation
Bovine archCommon origin of brachiocephalic and left common carotid; commonest variant
Aberrant right subclavianLast arch branch, passes behind the oesophagus (oblique posterior indentation); right laryngeal nerve non-recurrent
Double aortic archPersistent right dorsal aorta; ring round trachea and oesophagus
Right arch with mirror-image branchingTetralogy of Fallot (upturned apex, oligaemic lungs) or truncus
Pulmonary slingLeft pulmonary artery from the right, passing between trachea and oesophagus
Persistent left SVCVein lateral to the arch draining into a dilated coronary sinus
Egg on its side, narrow pedicleTransposition: aorta from the right ventricle in front of the pulmonary trunk, because the aorticopulmonary septum failed to spiral; severe cyanosis from birth
Figure-of-eight heartSupracardiac total anomalous pulmonary venous drainage
Small right lung, heart shifted right, curved tubular shadow widening down beside the right heart borderScimitar syndrome: anomalous right pulmonary vein draining into the IVC
  • Fetal three-vessel view, left to right: pulmonary trunk, aorta, SVC.
  • Aortic dissection: Stanford A involves the ascending aorta wherever the tear begins (rupture into the pericardium causes tamponade); type B spares it. Intramural haematoma: hyperdense wall crescent on plain CT, no flap. A smooth ductus diverticulum at the isthmus is not a tear.

Masses and pulmonary vascular disease

FindingDiagnosis
Several echogenic masses in fetal ventricular walls; later infantile spasms and ash-leaf patchesRhabdomyomas of tuberous sclerosis; most regress, so no early surgery
Atrial septum thickened by fat (about −95 HU), dumbbell shape sparing the fossa ovalis, obese elderly patientLipomatous hypertrophy of the interatrial septum; benign, may cause arrhythmia
Left atrial mass on a stalk from the fossa ovalisMyxoma
Eccentric wall-adherent clot, webs, enlarged bronchial arteries, mosaic lungs after a past embolusChronic thromboembolic pulmonary hypertension; potentially curable by endarterectomy
Saddle embolus with right ventricle wider than left, septum bowed left, contrast reflux into hepatic veins, hypotensionAcute right ventricular pressure overload: the dilated RV pushes the septum into the LV and cuts LV filling, so output falls; large fluid boluses can worsen it

Remember On the PA film the right border is right atrium and the left border is mostly left ventricle; the right ventricle is the front and the left atrium the back.

Exam trap Cardiothoracic ratio from an AP film overestimates heart size.

Exam trap Dominance is decided by the origin of the posterior descending artery, not by which artery is larger.

How FCPS asks about this

  • Right heart border on a PA film: right atrium; left border mostly left ventricle.
  • Where the tricuspid valve is heard: left lower sternal edge.
  • Fish-mouth mitral valve: rheumatic commissural fusion.
  • Marfan aortic root: cystic medial degeneration.
  • Thick walls with low ECG voltage and diffuse subendocardial enhancement: cardiac amyloidosis.
  • Transposition of the great arteries: failed spiralling of the aorticopulmonary septum.
  • Scimitar vein drains into: inferior vena cava.

Test yourself on this topic

5 of the 101 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.

Question 1Medium

A 78-year-old man has exertional syncope and an ejection systolic murmur. At valve replacement, the excised aortic valve has three cusps with heavy nodular calcification on their aortic surfaces and no fusion of the commissures. What is the pathology?

Question 2Medium

Three months after a large anterior myocardial infarction, a 60-year-old man has persistent ST elevation in V1–V4 and a localised, thin-walled, dyskinetic bulge at the left ventricular apex. What forms the wall of this bulge?

Question 3Hard

A 28-year-old woman with a fixed split second sound has a large ostium secundum atrial septal defect. Her right atrium, right ventricle and pulmonary trunk are enlarged and her lungs plethoric, but her left atrium is normal in size. Why is the left atrium not enlarged?

Question 4Hard

In a child with heterotaxy, where venous connections may be abnormal, which feature of an atrium most reliably identifies it as the morphological left atrium?

Question 5Hard

A 60-year-old man has had one heart valve replaced. On his lateral chest film, a line drawn from the carina to the anterior costophrenic angle passes below the prosthetic ring, which lies above and in front of it. Which valve has been replaced?

Practise all 101 questions on this topic

Where this sits in the CPSP syllabus

  • Diagnostic Radiology, Paper 2: Thorax, Heart, great vessels and coronary arteries

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