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frcr 2a (crack the frcr 2a) > 1. Cardiac (Ischaemic, Non-ischaemic, Genetic conditions, Tumours, Pericardial, Cardiac surgeries) > Flashcards

1. Cardiac (Ischaemic, Non-ischaemic, Genetic conditions, Tumours, Pericardial, Cardiac surgeries) Flashcards

1
Q

Progression of ischaemic necrosis in MI

A

Starts subendocardial, progresses to subepicardium

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2
Q

Microvascular obstruction - definition/imaging

A

Dark islands where destroyed capillaries don’t let contrast through

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3
Q

Significance of microvascular obstruction

A

Independent predictor of death and adverse LV remodelling

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4
Q

Stunned Myocardium - definition (2)

A

Days to weeks after acute injury (ischaemia or reperfusion injury)
Dysfunction of myocardium persists

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5
Q

Stunned Myocardium - Imaging (2)

A

Abnormal wall motion (reduced contractibility)
Normal perfusion (Sestamibi or Thallium)

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6
Q

Hibernating myocardium - Definition (2)

A

Due to chronic hypoperfusion from chronic artery disease.
Areas of decreased perfusion and contractility.

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7
Q

Hibernating myocardium - Imaging (4)

A

Wall motion abnormality
Abnormal fixed perfusion
Will take up FDG more intensely than normal myocardium.
Will demonstrate redistribution of thallium.

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8
Q

Scar - Definition (2)

A

Dead myocardium
Associated with prior, chronic MI

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9
Q

Scar - Imaging (4)

A

Abnormal wall motion.
Abnormal fixed perfusion.
No FDG uptake.
No redistribution of thallium.

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10
Q

Delayed imaging - uses (2)

A

Increased contrast in acute MI and inflammation.
Scarred myocardium washes out more slowly.

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11
Q

Delayed imaging - technique

A

Inversion recovery to dull normal myocardium, followed by gradient echo

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12
Q

Delayed imaging - findings

A

T1 shortening from gadolinium looks bright (bright = dead)

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13
Q

Why stress imaging? (2)

A

Cornaries can autoregulate. 85% stenosis at rest can be asymptomatic. Under stress, 45% stenosis is significant.

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14
Q

Stress imaging - how (2)

A

Inotropic agent (dobutamine) for wall motion.
Vasodilator (adenosine) used for perfusion analysis.

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15
Q

MRI in acute MI - when

A

Can be done in first 24hrs

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16
Q

MRI in acute MI (findings) (2)

A

Late gadolinium enhancement will reflect size and distribution of necrosis (vascular distribution).
Characteristically - zone of enhancement extending from subendocardium towards epicardium in vascular distribution.

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17
Q

Microvascular obstruction - findings (2)

A

Islands of dark signal in delayed gadolinium enhancement
Best seen in first pass imaging (25 seconds)

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18
Q

Microvascular obstruction - cause (2)

A

Acute and subacute finding
NOT seen in chronic infarct, this turns to scar

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19
Q

Microvascular obstruction - clinical

A

Poor prognostic finding, associated with lack of functional recovery.

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20
Q

Acutely injured myocardium (1 week) findings

A

T2 bright - bright = salvagable tissue

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21
Q

Acute vs chronic MI (4)

A

Both delayed enhancement
Acute will always have normal thickness, chronic can be thinned (if infarct was transmural)
Acute may have microvascular obstruction
Acute is T2 bright (oedema), Chronic is T2 dark (scar)

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22
Q

Ventricular aneurysm - association

A

Can occur as result of MI (5%)

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23
Q

True ventricular aneurysm - anatomy (3)

A

Mouth is wider than body.
Myocardium is intact.
Usually antero-lateral wall.

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24
Q

False ventricular aneurysm - anatomy (4)

A

Mouth is narrower than body.
Myocardium is NOT intact (pericardial adhesions contain the rupture).
Higher risk of rupture.
Usually postero-lateral wall.

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25
Q

Viability predictor post MI (3)

A

Depends on thickness involved:
<25%: likely to improve with PCI
25-50%: may improve
>50%: unlikely to improve function

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26
Q

Complications of MI (timing) (5)

A

Papillary muscle rupture - 2-7 days
Ventricular pseudoaneurysm - 3-7 days
Myocardial rupture - within 3 days (50% of time)
Dressler syndrome - 4-6 weeks
Ventricular aneurysm - months (requires remodelling and thinning)

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27
Q

Dilated cardiomyopathy - definition

A

Dilatation with end diastolic diameter of >55mm and reduced EF

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28
Q

Dilated cardiomyopathy - imaging (2)

A

Idiopathic: No enhancement OR linear mid-myocardial enhancement
Ischaemic: May show subendocardial enhancement.

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29
Q

Dilated cardiomyopathy associated with

A

Mitral regurg due to mitral ring dilatation

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30
Q

Restrictive cardiomyopathy - definition

A

Anything that causes a decrease in diastolic function.

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31
Q

Restrictive cardiomyopathy - cause (3)

A

Commonest: Infiltration of myocardium (amyoid)
Myocardium replaced with fibrous tissue (fibroelastosis)
Damage by iron (haemochromatosis)

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32
Q

Amyloidosis (cardiac) - definition & trivia (2)

A

Abnormal deposits in the myocardium causing abnormal diastolic function.
Seen in 50% of cases of systemic amyloid

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33
Q

Amyloidosis (cardiac) (anatomy) (3)

A

Biatrial enlargement,
Concentric thickening of left ventricle,
Reduced systolic function of both ventricles

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34
Q

Amyloidosis (cardiac) (imaging) (3)

A

Sometimes circumferential subendocardial enhancement.
Long T1 needed (350ms vs 200), so long the blood pool is darker than myocardium.
“Difficult to suppress myocardium”

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35
Q

Eosinophillic cardiomyopathy (Loeffler) - buzzword

A

Bilateral ventricular thrombi (long T1 to show)

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36
Q

Constrictive pericarditis - cause (2)

A

Commonly iatrogenic due to CABG or radiation.
Used to be TB or viral

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37
Q

Constrictive pericarditis - imaging (3)

A

CT: Thick pericardium >4mm.
If calcified, this is diagnostic. Calcification usually runs in AV groove.
“Sigmoidisation” seen on SSFP imaging: Ventricular septum moves left in a wave during early diastole “diastolic bounce” - suggests interventricular dependence

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38
Q

Constrictive vs Restrictive pericarditis (2)

A

Constrictive has thicker pericardium.
Constrictive features diastolic septal bounce

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39
Q

Myocarditis - cause

A

Usually viral (e.g. Coxsackie)

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40
Q

Myocarditis - imaging (2)

A

Late enhancement over non-vascular distribution.
Either midwall or epicardial distribution (not subendocardial)

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41
Q

Sarcoidosis - trivia (2)

A

Cardiac involvement in 5% of systemic cases
carries increased risk of death.

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42
Q

Sarcoid - Imaging & distribution (5)

A

High T2, early and late Gd enhancement.
Late Gd enhancement is middle or epicardial, non-coronary distribution.
Focal wall thickening from oedema can mimic hypertrophic cardiomyopathy.
Often affects septum.
RV and papillaries are rarely affected

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43
Q

Takotsubo cardiomyopathy - clinical (2)

A

Post-menopausal women post stressful event.
Chest pain and ECG changes

44
Q

Takotsubo cardiomyopathy - imaging (3)

A

Balooning of left ventricle is buzzword.
Transient akinesia or dyskinesia of left ventricle apex WITHOUT coronary stenosis.
No delayed enhancement.

45
Q

Subendocardial enhancement on MRI

A

Infarct

46
Q

Transmural enhancement on MRI

A

Infarct

47
Q

Subendocardial circumferencial enhancement on MRI

A

Amyloid

48
Q

Midwall, non linear enhancement on MRI

A

HOCM

49
Q

Midwall, linear enhancement on MRI (septal) (2)

A

Myocarditis,
Idiopathic DCM

50
Q

Midwall, linear enhancement on MRI (lateral) (2)

A

Myocarditis,
Sarcoid

51
Q

Epicardial enhancement on MRI (2)

A

Myocarditis,
Sarcoid

52
Q

Arrhythmogenic Right Ventricular Cardiomyopathy - definition

A

Fibrofatty degeneration of RV leading to arrhythmias and sudden death

53
Q

ARVC - anatomy (3)

A

Dilated RV with reduced function
Fibrofatty replacement of myocardium
Normal LV

54
Q

ARVC - imaging

A

Fat-sat MRI to demonstrate far in RV wall

55
Q

Hypertrophic cardiomyopathy - definition/trivia (2)

A

Abnormal hypertrophy of myocardium that compromises diastole.
Cause of sudden death.

56
Q

Hypertrophic cardiomyopathy - types (2)

A

Multiple types, asymmetric hypertrophy of myocardial septum is commonest in exam.
Subset associated with LVOT (hypertrophic Obstructive cardiomyopathy).

57
Q

Hypertrophic cardiomyopathy - imaging (2)

A

HOCM: Anterior leaflet of mitral valve pulled into LVOT (Systolic Anterior Motion (SAM) of mitral valve)
Patchy, midwall delayed enhancement of hypertrophic muscle.

58
Q

Noncompaction - definition/trivia (3)

A

Rare, genetic cardiomyopathy.
Loosely packed myocardial fibres.
Heart failure at young age

59
Q

Noncompaction - imaging (2)

A

LV spongey appearance, increased trabeculations and deep intertrabecular recesses.
Defined as ratio of noncompacted to compacted myocardium of >2.3:1 at end diastole.

60
Q

Muscular dystrophy - definition/trivia (2)

A

X-linked.
Biventricular replacement of myocardium with connective tissue and fat

61
Q

Muscular dystrophy - types (2)

A

Becker (mild), Duchenne (severe)

62
Q

Muscular dystrophy - imaging (2)

A

Delayed enhancement of midwall.
Often also dilated cardiomyopathy.

63
Q

Cardiac mets - trivia (4)

A

30x more common than primary cardiac malignancy.
Pericardium is commonest site affected.
Commonest primary is lung
Melanoma may involve myocardium.

64
Q

Cardiac mets - association (2)

A

Commonest manifestation is pericardial effusion.
Second commonest - pericardial lymph node

65
Q

Angiosarcoma - trivia

A

Commonest cardiac primary in adults

66
Q

Angiosarcoma - anatomy (3)

A

Commonly RA and tend to involve pericardium
Right sided heart failure and/or tamponade.
Bulky and heterogenous.

67
Q

Angiosarcoma - imaging (2)

A

Sun-ray appearance
enhancement of diffuse subtype as it grows along perivascular spaces associated with epicardial vessels.

68
Q

Left atrial myxoma - trivia

A

Commonest malignant primary cardiac tumour in adults (rare in kids)

69
Q

Left atrial myxoma - association (2)

A

MEN syndromes,
Blue nevi (carney complex).

70
Q

Left atrial myxoma - imaging (4)

A

Attached to interatrial septum.
May be calcified.
May prolapse through mitral valve.
Will enhance with Gd

71
Q

Rhabdomyoma - trivia

A

Commonest fetal cardiac tumour.

72
Q

Rhabdomyoma - anatomy (2)

A

They are hamartomas.
Prefer left ventricle

73
Q

Rhabdomyoma - association

A

Tuberous sclerosis.

74
Q

Rhabdomyoma - prognosis (2)

A

Most regress spontaneously.
more likely to regress if associated with tuberous sclerosis.

75
Q

Fibroma - trivia

A

Second commonest cardiac tumour in children

76
Q

Fibroma - imaging (3)

A

Prefer IV septum.
Dark on T1 and T2.
Enhance brightly on perfusion and late Gd.

77
Q

Fibroelastoma - trivia (2)

A

Commonest neoplasm to involve cardiac valves.
Systemic emboli common, esp if left side.

78
Q

Fibroelastoma - imaging (2)

A

80% on left valves.
Highly mobile on SSFP cine.

79
Q

Pericardial anatomy (2)

A

2 layers (visceral and parietal).
Usually about 50ml fluid between.

80
Q

Pericardial effusion - definition

A

More than the normal 50ml fluid between pericardial layers.

81
Q

Pericardial effusion - causes (3)

A

Renal failure (uraemia),
Lupus,
Dressler syndrome

82
Q

Pericardial effusion - imaging (3)

A

CXR:
Increased cardiac size,
Giant water bottle heart,
Lateral CXR with 2 lucent lines (epicardial and pericardial fat) either side of the effusion (Oreo cookie sign)

83
Q

Cardiac tamponade - definition

A

Compromised filling of the chambers (atria first) due to increased pressure in the pericardium, due to effusion.

84
Q

Cardiac tamponade - cause (2)

A

Can occur with >100ml of fluid.
Rate of filling is key, slower filling gives myocardium time to stretch.

85
Q

Cardiac tamponade - imaging (2)

A

Flattening or inversion of IV septum due to augmented RV filling in inspiration.
Reflux of contrast into IVC and azygous system on CT

86
Q

Pericardial cyst - anatomy (3)

A

Benign.
Usually right pericardial sulcus.
Don’t communicate with pericardium.

87
Q

Pericardial cyst - imaging

A

Water density along with right cardiophrenic sulcus

88
Q

Congenital absence of pericardium - anatomy (3)

A

Can be total
More commonly partial, over the left atrium and adjacemtn pulmonary artery.
Heart shifts towards missing side.

89
Q

Congenital absence of pericardium - imaging

A

CT or MRI showing heart contacting left chest wall.

90
Q

Congenital absence of pericardium - trivia (2)

A

Cardiac herniation and volvulus can occur in pts who undergo partial pneumonectomy.
Left atrial appendage is most at risk of strangulation.

91
Q

Palliative surgery for hypoplastic left heart - trivia (4)

A

Not curative.
Done in 3 stages to protect lungs and avoid right heart overload.
Norwood or Sano - within days of birth
Glenn - 3-6 months
Fontan - 1.5-5 years

92
Q

Norwood procedure - anatomy (5)

A

Aims to create unobstructed outflow tract from the systemic ventricle.
Tiny native aorta is anastamosed to pulmonary trunk, and arch augmented by graft.
ASD enlarged to create non-restriced atrial flow.
Blalock-taussig shunt between right subclavian and right PA.
Ductus removed to prevent overshunting to the lungs.

93
Q

Sano procedure - anatomy (2)

A

Same as norwood, but Blalock-taussig shunt replaced with conduit connected right ventricle to pulmonary artery.

94
Q

Classic Glenn procedure - anatomy (2)

A

End-end shunt between SVC and right PA.
Proximal end of right PA closed to reduce right ventricular work, so all venous return is directed straight to lung.

95
Q

Bi-directional Glenn - anatomy (3)

A

end-to-side shunt between SVC and RPA.
RPA left open, allowing blood flow to both lungs.
If done as part of left hyperplasia treatment, blalock-Taussig shunt will be removed.

96
Q

Fontan operation - anatomy (5)

A

Used for hypoplastic heart
Closure of ASD,
Glenn shunt,
Shunt between right atrium and left PA.
Aim to let blood flow passively, no pump, from systemic veins to lungs.
Then turn the right ventricle into a functional left ventricle.

97
Q

Blalock-Taussig shunt (3)

A

Originally for use with TOF.
Subclavian artery to pulmonary artery.
On opposite side to arch.

98
Q

Modified Blalock Taussig shunt

A

Performed on the SAME side as the arch. technically easier to do.

99
Q

Pulmonary artery banding (3)

A

Done to reduce pulmonary artery pressure (aim 1/3 of systemic).
Common indication is CHF in infancy with expected delayed repair
Single ventricle is commonest lesion requiring banding

100
Q

Atrial switch - purpose (3)

A

Used to correct transposition, by creating a baffle within the atria to switch back blood flow at the level of in-flow.
Right ventricle becomes systemic, left pumps to lungs.
Usually done in first year of life.

101
Q

Atrial switch - types (2)

A

Mustard and Senning procedures:
Senning: Baffle created from right atrial wall and septum WITHOUT extrinsic material
Mustard: Involves resection of atrial septum and creation of baffle using pericardium or extrinsic material

102
Q

Rastelli operation - purpose (3)

A

Most commonly used operation for
- transposition
- pulmonary outflow obstruction
- VSD

103
Q

Rastelli operation - anatomy (4)

A

Placement of baffle within the RV, diverting flow from the VSD to the aorta (using the VSD as part of the LVOT).
Pulmonary valve is oversewn, conduit inserted between RV and PA.
Left ventricle becomes the systemic ventricle.
Conduit wears out, committing the child to multiple future surgeries.

104
Q

Jatene procedure - anatomy (2)

A

Arterial switch, transection of the aorta and pulmonary arteries about the valve sinuses, including removal of coronaries.
Great arteries switched, coronaries sewn onto new aorta (formerly PA).

105
Q

Ross procedure - anatomy (3)

A

Done to repair diseased aortic valves in children.
Replaces aortic valve with patient’s pulmonary valve.
Replaces pulmonary valve with cryopreserved pulmonary valve homograft.

106
Q

Bentall procedure (2)

A

Used to treat combined aortic valve and ascending aorta disease. Including marfans lesions.
Composite graft replacement of aortic valve, aortic root and ascending aorta, with reimplantation of coronary arteries onto the graft.

107
Q

Heart transplant types (2)

A

Orthotopic heart transplant:
All of the heart is removed, except circular part of left atrium (where pulmonary veins attach). New heart is trimmed to fit into left atrium.
Heterotopic heart transplant:
Recipient heart remains in place, donor heart placed on top.
Gives back-up if donor is rejected and gives recipient heart chance to recover.

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