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Radiology > Cardiac > Flashcards

Cardiac Flashcards

1
Q

Helpful videos

A

VALVULAR DISEASES LEFT HEART
https://www.youtube.com/watch?v=LP_YTrcrsZA

CYANOTIC CONGENITAL HEART DEFECTS
https://www.youtube.com/watch?v=KjvW59vGlY8

VSD
https://www.youtube.com/watch?v=e7ObXrdtXek

AF
https://www.youtube.com/watch?v=6FLE6HWiImM

RESTRICTIVE CARDIOMYOPATHY
https://www.youtube.com/watch?v=Vwxco4YvxoQ

CARDIAC IMAGING MODALITIES
https://www.youtube.com/watch?v=UCLdHKbaYqo

PERICARDITIS
https://www.youtube.com/watch?v=lxE4xgjE31E

ENDOCARDITIS
https://www.youtube.com/watch?v=9JUdjT7idXM

PULMONARY EDEMA
https://www.youtube.com/watch?v=oRDOUv6dEpE

HEART FAILURE
https://www.youtube.com/watch?v=ypYI_lmLD7g&list=RDQMzyHGNiS0aVQ&start_radio=1

AORTIC VALVE DISEASE
https://www.youtube.com/watch?v=ifSJGLC55SU

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2
Q

Right atrium

A

Defined by IVC. Crista Terminalis is normal structure (not clot or tumour), muscular ridge that runs from entrance of SVC to entrance from IVC. IVC valve or Eustachian valve is little flap in IVC that hooks up to atrium. When this valve is more trabeculated its called Chiari network

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3
Q

Coronary sinus

A

Main drianing vein of myocardium. Runs in AV groove on posterior surface heart and enters RA near tricuspid valve.

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4
Q

Right ventricle

A

Defined by moderator band. Trcuspid papillary muscles insert onto septum. No fibrous connection between AV valve and outflow tract. Pulmonary valve has 3 cusps and is separated from tricuspid valve by thick muscle crista supraventricularis.

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5
Q

Left atrium

A

Most posterior chamber. MCQ like signs of enlargement.

DOUBLE DENSITY
Superimposed second contour on right heart from enlargement of right side of LA.

SPLAYING OF CARINA
angle >90 degrees suggests enlargement.

WALKING MAN SIGN
Posterior displacement of left main stem bronchus on lateral. Upside down V shape with intersection of right bronchus.

ORTNERS SYNDROME
Cardiovocal hoarseness from pressing on RLN by enlarged LA

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6
Q

Left ventricle

A

Leaflets of mitral valve connected to papillary muscles by chordae tendinae. Papillary muscles insert into lateral and posterior walls as well as apex of left ventricle.

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7
Q

Echogenic focus in left ventricle

A

Common sonographic observation. Calcified papillary muscle that goes away by 3rd trimester. Associated with Downs 13% (most of time normal)

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8
Q

Lipomatous hypertrophy of interatrial septum

A

Dumbbell appearance of fat in interatrial septum sparing the fossa ovalis. Can cause supraventricular arrhythmia. Can be hot on PET as made of brown fat.

LIPOMA
Rare, encapsulate, does NOT spare the fossa ovalis, If multiple, tuberous sclerosis. Rarely associated with arrhythmia.

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9
Q

Coronary arteries normal

A

3 coronary cusps, right leg and posterior (non-coronary).

RIGHT CORONARY
RIght main
Conus about 1.2 time first branch supplies RVOT
Nodal branch
Acute marginal
PDA in 65-80% people

LEFT CORONARY
Left main gives off LCX and LAD
LCX gives off obtuse marginals
LAD gives off diagonals and septal branches

RCA perfuses SA node 60%
RCA perfuses AV node 90%

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10
Q

2 vs 3 chamber views

A

Cardiac MRI views based off standard echocardiogram views

2 CHAMBER
Displays LV and LA.
Good for wall motion, global LV function and mitral valve issues. Coronary sinus is adjacent to LA in this veiw and viewed in cross section

3 CHAMBER
Apical long axis view.
Can see LA/LV/RV and LVOT
Ideal for looking at aortic regurg and stenosis

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11
Q

Dominance

A

Coronary dominance determined by which vessel gives rise to PDA and posterior LV branches.

Right sided dominance 85%

Can be codominant if PDA arises from RCA and posterior LV branches are from LCX.

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12
Q

Malignant origin

A

Most common and most serious anomaly. LCA from right coronary sinus coursing between aorta and pulmonary artery. Can get compressed and cause sudden cardiac death.

Anomalous right off left cusp - repair if symptomatic
Anomalous left off right cusp - always repair

Malignant conronary artery with origin from opposite coronary sinus and an interatrial course is second most common cause of sudden cardiac death in young patients (most common HOCM)

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13
Q

ALCAPA

A

Anomalous left coronary from pulmonary artery.

INFNATILE
Die early of CHF and dilated cardiomyopathy

ADULT
Still risk of sudden death. Steal syndrome with reversed flow in LCA as pressure decreases in pulmonary circulation

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14
Q

Coronary artery aneurysm

A

DIameter >1.5x normal lumen. Most common cause is atherosclerosis. Kawasaki disease in children, lots of other vasculitidies also. Iatrogenic from cardiac cath.

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15
Q

Myocardial bridging

A

Intramyocardial course of coronary artery (usually LAD). Can cause symptoms as diameter decreases in systole or may be issue for CABG planning. Can be source of ischaemia.

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16
Q

Coronary fistula

A

Connection between coronary artery and cardiac chaber. Usually RCA with drainage into right cardiac chambers. Associated/result in coronary aneurysm

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17
Q

Coronary CT

A

PATIENTS
Low risk or atypical chest pain - normal will stop cath or stress test being done. Patient with suspected aberrant coronary anatomy.

IDEAL HR
To reduce motion artefacts want <60bpm. Beta blockers used

CONTRAINDICATIONS TO BETA BLOCKADE
Severe asthma, heart block (1st degree ok), acute chest pain, recent cocaine

IF NO BETA BLOCKER
Can have scan but cant use prospective gating, have to use retrospective gating

PROSPECTIVE GATING
Step and shoot. Data acquisition triggered by R wave. Reduced radiation. No functional imaging. Always axial.

RETROSPECTIVE GATING
Scans whole time then back calculates. Can do functional imaging. Higher radiation. Helical.

OTHER DRUGS
Nitroglycerine given to dilate coronaries. Contraindications are hypotension, severe aortic stenosis, HOCM, viagra.

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18
Q

Aortic stenosis

A

Congenital (bicuspid) or acquired (degenerative or rheumatic). Increased afterload can lead to concentric LV hypertrophy. Peak velocity through valve grades severity. Velocity encoded CINE imaging (VENC), velocity mapping/phase contrast imaging is MRI technique for quantifying this. Dilatation of ascending aorta is due to jet phenomenon related to stenotic valve

3 types: valvular (most common 90%), subvalvular and supravalvular

Supravalvular aortic stenosis think Williams syndrome
Bicuspid aortic valve and coarctation think Turners syndrome

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19
Q

Bicuspid aortic valve

A

Very common, 2% popn. Most common congenital heart disease probably this although usually asymptomatic so probably VSD.

Aortic stenosis most common complication.
Bicuspid aortic valve independent risk factor for aortic aneurysm.
Association with cystic medial necrosis.
Association with Turners and coarctation.
Association with PCKD

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20
Q

Aortic regurgitation

A

Seen with bicuspid aortic valves, bacterial endocarditis, Marfans, aortic root dilatation from HTN and aortic dissection. How rapid regurg onset is detemrines haemodynamic impact

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21
Q

Mitral stenosis

A

Rheumatic heart disease is most common cause. Left atrial enlargement on CXR

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22
Q

Mitral regurgitation

A

Most common acute causes are endocarditis or papillary muscle/chordal rupture post MI. Chronic causes are primary (myxomatous degeneration) or secondary (dilated cardiomyopathy leading to mitral annular dilation). Isolated right upper lobe pulmonary oedema associated with mitral regurgitation

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23
Q

Pulmonary stenosis

A

Valvular, subvalvular and supravalvular

VALVULAR
Most common and can lead to ventricular hypertrophy. Associated with Noonan syndrome.

SUPRAVALVULAR 
Williams syndrome (pulmonary and aortic stenosis)

SUBVALVULAR
TOF

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24
Q

Pulmonary regurgitation

A

TOF patient who has been repaired. TOF involves patch repair of VSD and relief of RVOT obstruction. To fix RV obstruction, pulmonary valve integrity must be disrupted.. Eventual failure of this valve via regurg is primary complication,

Cardiac MRI used for timing of pulmonary regurg repair. If valve is repaired before RV is severely dilated the outcomes are good. If RV reaches certain degree of dilatation it wont return to normal and patient doesnt do well.

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25
Q

Tricuspid regurg

A

Most common form of tricuspid disease due to relatively weak annulus. May occur in endocarditis (IV drug use) or carcinoid. Most common cause is pulmonary arterial hyertension. TR causes RV dilatation not hypertrophy.

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26
Q

Rheumatic heart disease

A

Most commonly involves mitral and aortic valves. if there is multivalve disease think Rheumatic fever.

Immune modulated response to group A beta haemolytic strep.

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27
Q

Ebstein anomaly

A

Children whose mums used lithium. Tricuspid valve hypoplastic and posterior leaf displaced apically (downward). Result is large RA, decreased RV and tricuspid regurg. Box shaped heart.

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28
Q

Tricuspid atresia

A

Congenital anomaly that occurs with RV hypoplasia. Almost always has ASD or PFO. Associated with asplenia. Can have right arch (but think Truncus or TOF first with right arch).

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29
Q

Carcinoid syndrome

A

Can result in valvular disease but only after mets to liver. Seretonin degrades heart valves, typically tricuspid and pulmonic. Left sided vavular disease rare as lungs degrade vasoactive substances. If left sided disease think primary bronchial carcinoid or right to left shunt.

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30
Q

Great vessels

A

Most common variant branching is bovine with brachiocephalic and left CCA from common origin

Terminology of arch is based on arch relation to trachea (right arch with mirror branching is congenital heart)

5 types of right arch but 2 worth knowing:
Aberrant left - subclavian from back of arch
Mirror branching- subclavian from front of arch

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31
Q

Right arch with mirror branching

A

Usually asymptomatic although strongly associated with congenital heart disease, most commonly TOF. CLosely associated with truncus

If mirror image right arch, 90% will have TOF (6% truncus)
If person has truncus, 33% have mirror image right arch (TOF 25%)

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32
Q

Right arch with aberrant left subclavian

A

Last branch is aberrant left subclavian. Vascular ring as ligamentum arteriosum completes the ring encircling trachea.

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33
Q

Left arch aberrant right subclavian

A

Most common arch anomaly. Usually asymptomatic but can sometimes have dysphagia lusoria and RSCA passes posterior to esophagus. Last branch is aberrant RSCA. Origin of RSCA may be dilated - diverticulum of Kommerell.

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34
Q

Double aortic arch

A

Most common vascular ring. Symptoms may begin at birth and include tracheal compression and or difficulty swallowing. Right arch larger and higher, left arch smaller and lower. Arches are posterior to esophagus and anterior to trachea

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35
Q

Subclavian steal

A

PHENOMENON
Stenosis and/or occlusion at prox subclavian with retrogreade flow in ipsilateral vertebral

SYNDROME
Stenosis and/or occlusion at prox subclavian with retrogreade flow in ipsilateral vertebral AND ssociated cerebral ischaemic symptoms. Blood “stolen” from posterior circulation. WHen upper limb exercised, blood diverted away from brain to arm resulting in dizziness/syncope etc

Almost always atherosclerosis 98% but others are takayasu arteritis, radiation, preductal aortic coarctation. Teenager will be Takayasu

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36
Q

Congenital heart Aunt Minnies CXRs

A 
Egg on String: Transposition
Snow Man: TAPVR (supracardiac)
Boot shaped: TOF
Reverse 3: Coarctation
Box Shaped Heart: Ebstein, Vein of Galn Malformation
Scimitar Sword: PAPVR with hypoplasia

Right arch: Truncus or TOF

37
Q

Cyanotic vs Not Cyanotic

A

CYANOTIC 5 Ts
TOF (right arch)
Truncus (right arch increased pulm vasc)
TAPVR (left arch, normal heart size, increased pulm flow)
Transposition (left arch, normal heart size, increased pulm flow)
Tricuspic atresia (left arch, normal heart size, decreased pulm flow)

NOT CYANOTIC
ASD
VSD
PDA
PAPVR
Aortic coarctation
38
Q

Congenital heart differentials

A 
CHF IN NEWBORN
TAPVR type 3
Congnital aortic or mitral stenosis
Left sided hypoplastic heart
Cor triatriatum
Infantile coarctation
CYANOTICS 5 Ts
TAPVR (has PFO)
Transposition
Tricuspid atresia (has VSD)
TOF (has VSD)
Hypoplastic left

SMALL HEART
Adrenal insufficiency
Cachectic state
Constrictive pericarditis

39
Q

VSD

A

Most common congenital heart disease. Membranous most common 70%. Outlet subtypes (infundibulum) must be repaired. Big heart, increased vasculature, small aortic knob). Playing of carina. 70% close spontaneously.

40
Q

PDA

A

Normally closes 24 hours after birth functionally, 1 month anatomically. Think 3 things: prematurity, maternal rubella, cyanotic heart disease. CXR big heart, increased vasculature, large aortic arch.

41
Q

ASD

A

Several types with secundum most common (50-70%). Larger subtype is primum (endocardial cushion defect) and more likely to be symptomatic. Secundums will close with treatment, others wont. Primums not amenable to device closure due to proximity to AV valve tissue. CXR either normal or big heart, increased vasculature and small aortic knob. More common female.

Hand/thumb defects and ASD = Holt Oram
Ostium primum ASD = Downs
Sinus venosus ASD = PAPVR

SUBTYPES
Sinus venousus = PAPVR
Ostium secundum = most common
Ostium primum = Downs

42
Q

AV canal

A

Endocardial cushion defect. Secondary to deficient development of portion of atrial septum, interventricular septum and AV valves. Strong association with Downs. Cant use closure devices.

43
Q

Unroofed coronary sinus

A

Rare ASD secondary to fenestrated coronary sinus. Paradoxical emboli and chronic right heart volume overload. Strong associated with persistent left SVC

44
Q

PAPVR

A

Partial anomalous pulmonary venous return defined as one or more of pulmonary veins draining into RA. Associated with ASD.

Right sided PAPVR = sinous venousus ASD
Right sided PAPVR nd Pulmonary hypoplasia = Scimitar syndrome

45
Q

TAPVR

A

Cyanotic heart disease with all pulmonary veins goinginto right heart. Large PFO or ASD needed for survival. Increased pulmonary vasculature. 50% asplenia patients have a congenital heart disease, of those nearly 100% are TAPVR.

TYPE 1 SUPRACARDIAC
Most common. Veins drain above heart. Snowman CXR.

TYPE 2 CARDIAC
Second most common.

TYPE 3 INFRACARDIAC
Veins drain below diaphragm (hepatic veins or IVC)
Obstruction n way through diaphragm is common and causes pulmonary oedema look in newborn.

46
Q

Transposition

A

Most common cause of cyanosis in first 24 hours. Most commonly in infants of diabetic mothers. Aorta from RV and pulmonary trunk from LV. Ventriculoarterial discordance. RV is one with moderator band.

Survival depends on ASD, VSD or PDA.

D TRANSPOSITION
Egg on a string CXR.Discordance between ventricles and vessels. Intra-atrial baffle performed to fix. Ductus only connection between 2 systems. Corrected it has very Aunt Minnie appearance. PA draped over aorta after LeCompte Manouvre

L TRANSPOSITION
Congenitally corrected. Double discordance where trium hooks up to wrong ventricle and ventricle to wrong vessel

47
Q

Tetralogy of Fallot TOF

A

Most common cyanotic heart disease. Symptom severity related to how bad RVOT obstruction is. Pentalogy if ASD added. Likely to have right arch. Fixed with primary repair. If unable to repair, get Blalock Taussig shunt. Most common comlication is pulmonary regurgitation

VSD
RVOT obstruction
Overriding aorta
RV hypertrophy

48
Q

Truncus arteriosus

A

Cyanotic anomaly. Single trunk supplying both pulmonary and systemic circulation. Almost always has VSD. Associated with right arch. Associated with CATCH 22 genetics (DiGeorge syndrome).

49
Q

Coarctation

A

Strong association with Turners 15-20%. Bicuspic aortic valve most common associatd defect 80%. More berry aneurysms. Figure 3 on CXR. Rib notching 4-8th ribs.

INFANTILE
Heart failure in 1st week of life. Preductal (before left subclavian). Hypoplastic aortic arch.

ADULT
Leg claudication. BP differences. Post ductal (after left subclavian). Normal aortic arch. Collaterals more likely

50
Q

Hypoplastic left heart

A

LV and aorta hypoplastic. Present with pulmonary oedema. Must have ASD or large PFO. Large PDA to put blood in arch. Associated with aortic coarctation and endocardial fibroellastosis.

51
Q

Cor triatum sinistrum

A

Rare. Abnormal pulmonary vein draining into LA with an unnecessary fibromuscular membrane causing subdivision of LA. Fives appearance of triatrium heart. Cause of unexplained pulmonary HTN in paeds. Acts like mitral stenosis and can cause pulmonary oedema. Fatal within 2 years unless surgical intervention

52
Q

Ischaemic heart

A

Either cardiac MRI or nuclear imaging.

MI is usually initiated by rupture of unstable coronary atherosclerotic plaque leading to abrupt arterial occlusion. Wavefront of necrosis starts subendocardial and progresses to subepicardium. Destruction of small vessels disallows contrast to area of injury. Island of dark signal in ocean of delayed enhancement.

53
Q

Ischaemic heart continued

A

STUNNED MYOCARDIUM
After acute injury, myocardial dysfunction persists even after restoration of blood flow. Wall motion abnormal. Normal perfusion (thallium or sestamibi). Associated with acute MI.

HIBERNATING MYOCARDIUM
Chronic process. Severe CAD causing chronic hypoperfusion. Areas of decreased perfusion and decreased contractility even when resting. Not an infarct. FDG PET this area will take up tracer more then normal myocardium and will redistribute thallium. Reversible with revascularization. Wall motion abnormal, abnormal fixed perfusion. Associated with high grade CAD. Redistribute with delayed thallium and take up FDG

INFARCT/SCAR
Dead myocardium. Abnormal wall motion. Will not come back to life. Abnormal fixed perfusion. Will not redistribute thallium or take up FDG. Associated with chronic prior MI.

54
Q

Ischaemic heart imaging

A

Diastolic dysfunction = echocardiography
Systolic dysfunction = cardiac MRI

Cardiac MRI contraindications:
ICD/Pacemakers. Cochlear implants. Intracranial shrapnel.

55
Q

Delayed imaging

A

Done using inversion recovery technique to null normal myocardium, followed by gradient echo. T1 shortening from Gad looks bright. Bright is dead. Works because:

Increased volume of contrast material in acute MI and inflammatory conditions. Scarred myocardium washes out more slowly

56
Q

Why stress imaging is done

A

Coronary arteries can autoregulate. Stenosis of up to 85% can be asymptomatic at rest. Demand is increased making a 45% stenosis significant. An inotropic stress agent (dobutamine) is used for wall motion and a vasodilator (adenosine) is used for perfusion analysis.

57
Q

MRI in acute MI

A

Cardiac MRI can be done in the first 24 hours post MI if patient is stable. Late gad enhancement will reflect size and distribution of necrosis. Zone of enhancement that extends from subendocardium toward pericardium in vascular distribution. Microvascular obstruction will be islands od dark signal in enhanced tissue and represent acute and subacute finding. Microvascular obstruction not seen in chronic disease as these will turn to scar.

T2 bright and enhanceing is salvageable tissue

58
Q

Acute vs chronic MI

A

Both have delayed enhancement. If infarct was transmural and chronic may have thinned myocardium. Acute will have normal thickness. T2 signal from oedema may be increased in acute setting. Chronic is T2 dark (scar). No microvascular obstruction in chroic.

MI ON CONTRAST ENHANCED MRI
Delayed enhancement follows vascular distribution. Enhancement extends from endocardium to epicardium

59
Q

Microvascular obstruction

A

Islands of dark tissue in an ocean of late Gad enhancement. Poor prognostic finding associated with lack of functional recovery. NOT seen in chronic infarct.

60
Q

Ventricular aneurysm

A

Rare but can occur as result of MI.

TRUE
Mouth wider than body. Myocardium intact. Anterolateral wall.

FALSE
Mouth is narrow compared to body. Myocardium NOT intact (pericardial adhesions contain rupture). Posterolateral wall. High risk of rupture.

61
Q

Viability

A

Graded based on % of transmural thickness involved in infarct. Segmental imaging over multiple heart beats. T1 post con inversion recovery gradient echo.

25% likely to improve with PCI
25-50% may improve
50-100% unlikely to recover function

62
Q

Bad sequale of MI

A 
Dressler syndrome (effusion) 4-6 weeks
Papillary muscle rupture 2-7 days
Ventricular pseudoaneurysm 3-7 days
Ventricular aneurysm months
Myocardial rupture within 3 days 50% of time
63
Q

Dilated cardiomyopathy

A

Dilatation with end diastolic dimeter >55mm, with a decreased EF. Idiopathic, ischemic or others including alcohol, cyclosporine, Chagas etc. Ischaemic may show sunendocardial enhancement. Idiopathic will show either no enhancement or midmyocardial enhancement. Association with mitral regurgitation.

64
Q

Restrictive cardiomyopathy

A

Anything that causes a decrease in diastolic function. Can be myocaridumreplaced by fibrotic tissue, infiltration of myocardium or damage by iron. Most common cause is amyloid

AMYLOIDOSIS
Deposit in myocardium cause abnormal diastolic function with biatrial enlargement, concentric thickening of left ventricle and reduced systolic function of both ventricles. Bad prognosis. Need long T1, difficult to suppress myocardium.

EOSINOPHILIC CARDIOMYOPATHY (LOEFFLER)
Bilateral ventricular thrombus. Need long T1
65
Q

Constrictive pericarditis

A

Used to be TB or viral. No most common cause is iatrogenic secondary to CABG or radiation.. Pericaridum too thick >4mm and calcified. Ventricular septum moves towards LV in wavy pattern in early diastole (diastolic bounce).

66
Q

Myocarditis

A

Inflammation of heart. Often viral, cocksackie. Late Gd enhancement follows non vascular distribution perferring lateral free wall. Pattern is epicardial or mid wall.

67
Q

Sarcoidosis

A

Cardiac involvement in 5% and associated with increased risk of death. Increased T2 and enhancement. Focal wall thickening from oedema can mimic hypertrophic cardiomyopathy. Often involves septum.

68
Q

Takotsubo cardiomyopathy

A

Takotsubo is a Japanese Octopus trap.\ which looks like a pot with a narrow mouth and large round base. Octopus can go in and turn around but cant get out. Condition with chest pain and ECG changes in someone with stressful event. Transient akinesia or dyskinesia of the LV apex without coronary stenosis. Ballooning of LV apex is a buzzword.

69
Q

Cardiac MRI late Gad enhancement

A

Both diseased and normal myocardium will tale up Gad but depends when imaged. Early 1-3 mins see normal tissue enhance then late 5-20 mins see wash out from normal tissue and retained by pathological tissue.

ISCHAEMIC
Enhancement starts subendocardially and spreads transmurraly toward epicardial surface in distribution of known coronary artery territory

NON ISCHAEMIC
Enhancement located mid wall of ventricle in patchy or multifocal distribution.

70
Q

Arrythmogenic right ventricular cardiomyopathy ARVC

A

Fibrofatty degeneration of RV leading to arrythmia and sudden death. Dilated RV with reduced function and fibrofatty replacement of myocardium. Normal LV. Watch for use of fat sat imaging

71
Q

Hypertrophic cardiomyopathy

A

Abnormaly hypertrophy from disarray of myofibrils. of myocardium that compromises diastole. Asymmetric hypertophy of intraventricular septum. Cause of sudden cardiac death. HOCM has this plus LVOT obstruction. Venturi forces can pull anterior leaflet of mitral valve into the LVOT (SAM systolic anterior motion of mitral valve). Patchy mid wall delayed enhancement of hypertrophied muscle may be seen as is an independent risk factor for sudden death.

72
Q

Noncompaction

A

LV noncompaction is uncommon congenital cardiomyopathy that is result of loosely packed myocardium. LV has spongy appearance with increased trabeculations and deep intertrabecular recesses. Heart failure at young age. Diagnosis based on ratio of non compacted end diastolic myocardium to compacted end diastolic myocardium.

73
Q

Muscular dystrophy

A

X linked neuromuscular conditions. Biventricular replacement of myocardium with connective tissue and fat. Delayed Ga enhancement mid wall. Often have dilated cardiomyopathy. Kid with dilated heart and mid wall enhancement.

BECKER
Mild one

DUCHENNE
Severe one.

74
Q

Cardiac mets

A

30x more common than primary. Pericardium most commonly affected site. Most common manifestation pericardial effusion (second most common is LN). melanoma may involve myocardium. Most common met is lung cancer.

75
Q

Angiosarcoma

A

Most common primary MALIGNANT tumour in adults.Likes RA and pericardium. Can cause right heart failure and/or tamponade. Bulky and heterogenous. ‘sun-ray’ appearance grows along perivascular spaces associated with epicardial vessels.

76
Q

Left atrial myxoma

A

Most common primary CARDIAC tumour in adults. Associated with MEN syndromes. Most often attached to interatrial septum. May be calcified. Enhance with Gad. Distal emboli and fainting spells. Younger people Carney complex.

77
Q

Rhabdomyoma

A

Most common fetal cardiac tumour. Hamartoma. Prefer LV myocardium. Associated with Tuberous Sclerosis. Usually regress spontaneously. Tend to be multiple.

78
Q

Fibroma

A

Second most common cardiac tumour in children. Like IV septum. Dark T1 and T2 and enhance.

79
Q

Fibroelastoma

A

Most common neoplasm to involve cardiac valves (80% aortic or mitral). Systemic emboli common. Usually incidental. Usually <1cm.

80
Q

Thrombus

A

Most common intracardiac ‘mass’. Favours left atrial appendage or LV apex. Thrombus wont enhance.

81
Q

Pericardial effusion

A

Visceral and parietal, normally holding 50cc fluid. Effusion if 50cc exceeded. Renal failure most common cause. Think about Lupus and Dressler SYndrome (effusion post MI)

CXR normal heart comparison, now really big. Giant water bottle heart. Lateral CXR with 2 lucent lines and central opaque line (oreo cookie sign).

82
Q

Cardiac tamponade

A

Percardial effusion can cause elevated pressure in pericardium and result in compromised filling of cardiac chambers. Atria then ventricles. Can occur with as little as 100cc. Rate of accumulation key factor.

Short axis imaging during deep inspiration showing flattening or inversion of the IV septum toward LV.

83
Q

Pericardial cysts

A

Benign incidental finding. Usually right cardiophrenic sulcus. Do not communicate with pericardium. Rarely can get infected or haemorrhage. Water density.

84
Q

Congenital/acquired absence of pericardium

A

Most common is partial absence over LA and adjacent pulmonary artery. When left pericardium absent, heart shifts to left. Herniation can only occur if lung has also been removed. LA appendage most at risk of herniation.

Tongue of lung between aorta and PA anteriorly on left side.

85
Q

Palliative surgery for hypoplastic left heart

A

Not curative, extends life. 3 stage process to protect lungs and avoid right heart overload

NORWOOD (WITHIN DAYS OF BIRTH)
Created unobstructed outflow tract from systemic ventricle. Aorta anastomosed to pulm trunk. ASD enlarged. Blalock Taussig shunt between right subclavian and right PA. Ductus removed (can get oveshunting of blood to lungs and pulmonary oedema).
SANO procedure similar but instead of Blalock Taussig shunt you connect RV to pulm artery.

GLENN CLASSIC (3-6 MONTHS)
Shunt between SVC and right pulm artery, sewing off prox right pulm artery. Decrease right heart workload.
GLENN BIDIRECTIONAL has SVC and RPA shunt as above but leaves RPA open. If this is used can then take down Blalock Taussig or Sano shunt.

FONTAN (1.5 - 5 years)
Glenn Classic as above with closure of ASD and placing shunt from RA to LPA. Lets blood return from systemic circulation to lungs by passive flow and turns RV into a functional LV. Numerous complications atriomegaly arrhythmias and plastic bronchitis.

86
Q

Other surgery

A

CLASSIC BLAOCK TAUSSIG SHUNT
Originally developed for use with TOF. Shunt between subclavian artery and pulmonary artery on opposite side to arch. tehcnically difficult and distorts anatomy of pulmonary artery

MODIFIED BLALOCK TAUSSIG SHUNT
Gortex shunt between subclavian artery and pulmonary artery on same side as arch. Easier to do

GLENN = vein to artery (SVC to pulm artery)
B-T = vein artery to artery (subclav to pulm)
87
Q

Other surgery continued

A

PULMONARY ARTERY BANDING
Done to reduce pulm art pressure. Most common indication CHF in infancy with anticipated delayed repair. SIngle ventricle most common lesion requiring banding

ATRIAL SWITCH
Correct transposition of great arteries. Creates baffle to switch flow. RV becomes systemic LV and LV pumps to lungs. Done in first year of life. SENNING baffle made from RA wall and atrial septal tissue without extrinsic material. MUSTARD resect atrial wall and create with pericardium or synthetic material

RASTELLI
Most commonly used operation for transposition, pulm outflow obstruction and VSD. Plce baffle within RV diverting flow from VSD to aorta. Pulm valve oversewn and conduit made between RV and PA. LV becomes systemic ventricle. Wll need multiple other surgeries as conduits wear out and need replacing.

JATENE
Arterial switch method involving transection of aorta and pulm arteries about valve sinuses, includng removal of coronaries. Great arteries switched and coronareis sewn int new aorta (formerly PA). No onduit to go bad and LV is systemic ventricle.

ROSS
DOne for diseased aortic valves in children. Replaces aortic valve with pulmonary valve and pulmonary vlave with cryopreserved pulmonary valve homograft.

BENTALL
Composite graft replacement of aortic valve, aortic root and ascending aorta with reimplantation of coronary arteries into graft. Done to treat combined aortic valve and ascending aorta disease.

88
Q

Surgery SUMMARY

A

GLENN
Vein to artery.
Bypass right heart and take systemic blood to pulmonary circulation.
SVC syndrome and PA aneurysms

BLALOCK TAUSSIG
Artery to artery
Increases pulmonary blood flow.
Stenosis at shunt pulmonary insertion site.

FONTAN
Complicated with multiple versions.
Bypass RV and direct systemic blood into PAs.
Enlarged RA causing arrhythmia. Plastic bronchitis

89
Q

Heart transplant

A

ORTHOTOPIC
All heart is removed except circular part of LA (part with pulm veins). Donor heart trimmed to fit LA.

HETEROTOPIC
Recipient heart remains in place, donor heart added on top. Double heart. Gives native heart a chance to recover and gives you back up if donor rejected.

Radiology (16 decks)

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