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AA ST2 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

prev of angina

A

2% population

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2
Q

Information is obtained about: - CT cardiac

A

Cardiac morphology and chamber size
Coronary anatomy and disease

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3
Q

when in cardiac cycle to do the scan

A

late diastole

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4
Q

optimal heart rate

A

<60s - ideal 55 - 60

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5
Q

Benefit of retrospective imaging

A

evaluate myocardial wall motion and EF

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6
Q

CT cardiac - contrast delivery parameters

A

During a single breath-hold, 25 ml of IV contrast is injected at a rate of between 4-6 ml/s.

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7
Q

dosing of metroprolol

A

5- 75mg but really up to 40mg

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8
Q

which is worse calcified or non calcified

A

Non-calcified plaque may be more unstable and prone to acute rupture leading

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9
Q

what kind of HU are plaques going to be

A

Soft 14
intermediate 91
Calcified 419

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10
Q

when is CT CA used?

A

if cant do the procedure due to anatomy - large aortic root
or pathology such as dissection

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11
Q

why is calcium scoring dubious

A

may have limited impact due to effects of remodelling

if no calcium then unlikely to have any plaque
if calcium - likely underestimates amount of plaque

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12
Q

Coronary calcium load has been found to progress over time, increasing by

A

15-25% per year

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13
Q

Agatston scoring system for calcium

A

3 mm slice thickness is a product of the area of calcification per coronary segment and a factor rated 1 through 4 dictated by the maximum calcium CT density within that segment

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14
Q

minimum density to be considered a plaque on the scoring system

A

130HU

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15
Q

What is a step artefact

A

Step artefact are forms of reconstruction artefact which may occur particularly as a consequence of cardiac arrhythmia. This results in visible ‘step’ increments on a single image which is reconstructed from several data sets.

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16
Q

CT CA artefacts

A

motion artefact
step artefact
partial voluming next to calcium
IV contrast timing or poor output in cardiomyopathy

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17
Q

what is ectopic origin of the artery - why is it important

A

exclude it in the young
second commonest cause of sudden death in young

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18
Q

.

A

.

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19
Q

Ao

A

Aorta

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20
Q

LA

A

left atrium

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21
Q

LCA

A

left coronary artery

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22
Q

Max intensity projection

A

MIP

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23
Q

PA

A

pulmonary artery

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24
Q

RVOT

A

right ventricle ouflow track

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25
Q

what is the difference between normal variant and anomaly?

A

Normal variant - seen in more than 1% of the population

Anomaly - seen in less than 1% of population

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26
Q

An anomalous coronary artery origin is considered when the ostium is located

A

not within the sinus

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27
Q

patients with clinically significant anomalies will usually present when

A

before midlife

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28
Q

the most common major congenital malformation of the coronary circulation

A

Anomalous origin of the left coronary artery from the pulmonary trunk is the most common major congenital malformation of the coronary circulation (~1:300 000 live births), but this manifests itself in infancy.

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29
Q

anomalies of intrinsic coronary arterial anatomy

A

number of anomalies of intrinsic coronary arterial anatomy such as
ostial stenosis,
atresia,
single, absent or hypoplastic coronary arteries,

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30
Q

What is myocardial bridging?

most common place

A

epicardial segment of a coronary artery that courses through the myocardium.

mid LAD

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31
Q

aetiology of spontaneous dissection is unknown; however, SCAD has been reported, especially in

A

young women during the peripartum period or in association with oral contraceptive use

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32
Q

Features of Kawasaki

A

Conjunctivitis
Erythematous
Lips
Oral cavity
Palms and soles
Polymorphous exanthema of the body trunk
Swelling of the cervical lymph nodes

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33
Q

Kawasaki - Acute/early phase complications

A

Include: pericarditis, myocarditis, endocarditis, inflammation of the conduction system and coronary artery involvement with 1-2% of patients presenting with sudden death due to cardiac failure.

Myocardial infarction is also a potential complication that usually occurs in the first year. At post-mortem, these infants are found to have coronary arteritis with associated thrombosis and aneurysm formation. In a large Japanese study 25% of patients with acute Kawasaki disease were shown by coronary angiography to have coronary aneurysms.

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34
Q

Kawasaki - chronic complications

A

Chronic/long-term phase
In the chronic phase, the long-term complications relate to the persistence of these aneurysms, the development of thrombotic occlusion, the risk of ischaemic heart disease and premature atherosclerosis. Aneurysms detected after the acute stage regress in about 50% of cases with small (<5 mm) to moderate (5-8 mm) sized aneurysms more likely to regress with approximately 1% of patients who recover from acute Kawasaki disease developing giant coronary artery aneurysms (>8 mm in diameter) or coronary artery obstruction due to thrombosis or stenosis. Giant coronary aneurysms have the lowest regression rate, the highest risk of stenosis and strongest association with myocardial infarction.

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35
Q

Should CTCA be done on low to intermediate trop rises

A

debated

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36
Q

How to prepare patients for CT CA

A

Heart rate control
- aim less than 60
- B block
- GTN

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37
Q

how does GTN work?

A

smooth muscle relaxant

severe aortic stenosis contraindicated
contraindicated in phosphodiasterase inhibitors

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38
Q

How long do patients need to breath hold for?

A

10 - 15 seconds

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39
Q

how to get the contrast into the coronary at the right time?

A

ROI to define a peak enhancement of the arteries

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40
Q

left atrial appendage should be looked for what>

A

clots

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41
Q

LV thickness can only be reviewed in relation to what?

A

Diastole or systole.

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42
Q

how to tell systole or diastole

A

based on whether the mitral valve is open or closed

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43
Q

third branch of the left stem

A

ramus or intermeidate branch

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44
Q

obtuse marginal come from

A

circumflex

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45
Q

diagnosal branches come from

A

LAD

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46
Q

dose of CTCA

A

often as low as 1mSv

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47
Q

what views do you need to show?

A

2 3 4 chamber views

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48
Q

plaques are classififed as

A

calcified
non clafieid
mixed morphology

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49
Q

CAD RADS uses what to measure the plaques?

A

3 - 50% stenosis
4 - 70 - 99%

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50
Q

presence of contrast distally implies what

A

doesn’t necessarily mwan there is NOT complete occlusion.

Can still have complete occlusion

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51
Q

What are the distincive features of the right ventricle?

A

APICAL MODERATOR BAND
papillaries attached to interventricular septum and free wall
course trabeculae

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52
Q

What are the distinctive features of the left ventricle?

A

Papillary muscles attached ONLY to ventriclar free wall
thin and delicate trabeculae

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53
Q

Hypoplastic left heart? what is it?

A

born with a crap left heart

small ascending aorta, retrograde flow to the great vessels

Flow from pulmonary trunk into aorta

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54
Q

Hypoplastic left heart surgery outcomes?

A

Palliative option. 3 stage process to protect the lungs and avoid right heart overload

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55
Q

Hypoplastic surgeries - what are they?

A

Norwoord - days
Glenn - 6 months
Fontain - 5 years

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56
Q

NOrwood surgery

A

Creat less restriction the systemic blood flow

Anastomose the aorta to the right ventricle.
Increase the size of the arch
increase the size of the VSD

shunt between the right subcalvian ARTERY and right PA to get blood into the lungs

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57
Q

Glenn procedure

A

Goal: blood return to be passive rather than arterial

Vein to artery. SVC to right PA. Passive blood return.

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58
Q

Fontan procedure

A

GOAL: passive return of blood

Close ASD.
Shunt between RA and left PA

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59
Q

Transposition of arteries - what is it?

A

Different types.
Double issue swap is fine.
If loops are interconenct between each side of th ehart then needs surgery.

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60
Q

L type vs d type for transposition?

A

L type is on the left
D is on the right

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61
Q

Wayts to correct transposition of the arteries.

A

Senning and Mustard - RV is the systemic pump

Rastelli - LV is systemic pump. Uses a baffle.
Jatene - LV systemic pump. Direct switch

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62
Q

LeCompte manuever

A

switching of the aorta and pulmonary artery in transposition of the great arteries

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63
Q

Ross procedure

A

Performed in diseased aortic valve
Pulmonary is placed into the aortic valve

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64
Q

Aortic dilatation from marfans - what procedure is done?

A

Bentell procedure
replaces the valve and ascending aorta

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65
Q

Caridac MR - white is

A

dead

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66
Q

Cardiac MR sweet spot

A

scar enhances late - 10 minuetes to 30 minutes after contrast

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67
Q

how to seperate types of heart disease on MR

A

ischaemic (vascular distribution - sub endocaridal) vs non ischaemic

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68
Q

Cx is supply to which bit of the wall?

A

Lateral

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69
Q

subendocardial is the first to be seen in ischaemic injury - why?

A

wave of ischaemia goes from inside out base on hopw bad the ischaemia is

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70
Q

Viability - 50%

A

less than 50% myocardiam involved thickness then good result ith PCI

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71
Q

Normal vs akinesia vs dyskinesia

A

Normal - myocardium should thicken.
Akinesia - part doesnt contract at all
dyskinesia - bulges in the wrong direction

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72
Q

types of cardiac ventricular aneurysm?

A

True ventricular

False ventricular aneurysm

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73
Q

False ventricular aneurysm - what happens

A

doesn’t go through all layers
body wider than the mouth
posterolateral position

takes 3- 7 days after MI

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74
Q

myocarditis will affect which part of the wall

A

mid wall or epicardial
favours lateral free wall

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75
Q

myocarditis caused by what virus

A

coxsackie virus

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76
Q

what will MR amyloid look like

A

circumferential
sub endocardial distribution
myocardium hard to null (long inversion time)

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77
Q

eosinophilic cardiomyopathy causes what?

A

bilateral ventricular thrombus

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78
Q

MR dose some bouncing of the septum. Sigmoidization

A

Constrictive pericarditis.
calcified pericardium

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79
Q

Causes of constrictive pericarditis

A

CABG or radiation

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80
Q

Causes of contsrictive vs restrictive pericarditis

A

Restrictive is amyloid or esoinophils IN THE MUSCLE

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81
Q

What causes HCM?

A

cardiac sarcomere is retarded

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82
Q

What does HCM look like?

A

thickened myocardium

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83
Q

What is SAM stand for in HCM

A

Systolic anteriror movement of mitral valve

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84
Q

MR distribution of pathology is subendocardial and circumferential

A

Amyloidosis

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85
Q

MID wall MR cardiac spots of apthology

A

HOCM

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86
Q

Midwall, epicardialCardiac MR pathology

A

myocarditis, sarcoidosis

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87
Q

thrombus vs tumour? Which imaging to tell the difference

A

Cardiac MR with contrast. Tumour will enhance

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88
Q

most common caridac tumour?

What about kids?

A

Primary is a myxoma

Mets is pericardial

kids - tubosclerosis. Rhabdomyeloma

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89
Q

ischaemic or scarred cardiac tissue will behave how with Nuclear studies?

A

They wont take up the tracer.

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90
Q

How do you work out the difference between ischaemic or scar?

A

cold on only stress - ischaemia

cold on stress and normal - scar

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91
Q

Cardiac Nuc med - how much stenosis do you need to see it?

A

50% with stress

90% if no stress

so it increases the sensitivity of the test

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92
Q

What drug to give in Cardiac Nuc med

A

Regadenson

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93
Q

Ragadenson does what?

A

Vasodilator

No bronchospasm

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94
Q

What use is dipyridamole in Cardiac nuc med?

A

inhibits the breakdown of adenosine

so adenosine builds up and causes vasidilation

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95
Q

List the left to right shunts

A

ASD
VSD
AVSD
PDA

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96
Q

how many adults have an unsealed formane ovale

A

25%

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97
Q

Tetrology of fallot consists of

A

he other components are pulmonary stenosis (valvular or infundibular), dextroposition of the aorta (the aortic root overrides the defect) and right ventricular hypertrophy.

and VDD

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98
Q

Types of atrial septal defects

A

secundum
primum
superior sinus venosus
inferior sinus venosus
coronary sinus defect
common atrium

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99
Q

ASd - secundum

A

Secundum: Defects within the oval fossa

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100
Q

ASD - primum

A

Partial atrioventricular defect - the defect lies low in the septum and is associated with abnormal development of one or both of the atrioventricular valves. This will be discussed under the section on AVSDs.

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101
Q

ASD - Superior sinus venosus

A

: The superior vena cava (SVC) terminates in such a way as to drain into both atria. Commonly, the pulmonary veins from the right upper lobe are also involved draining in an anomalous fashion to the SVC.

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102
Q

Inferior sinus venosus

ASD

A

IVC drain into both atria

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103
Q

ASD

Common atrium

A

confluence of one type of defect with another

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104
Q

size of a left to right shunt is realted to what

A

compliance of the ventricles

(not the size of the defect)

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105
Q

How to measure shunt flow on MRI

A

difference between aortic and pulmonary blood flow

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106
Q

how can invasive catheter monitor demsontrate shunting

A

measure oxygen level in the SVC and atrium. Atrium will have higher oxygen concerntration.

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107
Q

Associated abnormalities with ASD

A

partial anomalous pulmonary venous drainage,
pulmonary valve stenosis, mitral stenosis,
mitral valve prolapse,
VSD,
PDA and coarctation of the aorta.

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108
Q

which is better for right ventricle volumes - echo or MRI

A

MRI

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109
Q

Types of VSD

A

Perimembranous VSD - most common

Muscular ventricular septal defects

Doubly committed sub-arterila ventricular septal defects (between aortic and pulmonary valves)

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110
Q

What are goals of therapy for VSDs?

A

prevent infective endocarditis
preserve left sided heart function
close it if there is pulmonary htn, (Eisenmenger physiology)

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111
Q

Types of VSD at risk of infection

A

small

112
Q

if the pressure gradient across the VSD remains high what does this imply

A

pulmonary hypertension hasn’t happened yet

113
Q

What are the types of AVSD

A

Partial
Complete

114
Q

Partial AVSD

A

ostium primum ASD, common valve is divided into two orifices

115
Q

Complete AVSD - classified how

A

common valve guards a common orifice

116
Q

AVSD - CXR findings

A

massive pulmonary artery
small aorta

117
Q

Pulmonary artery calcification in a native vessel indicates

A

longstanding pulmonary arterial hypertension - consider PDA

118
Q

cardiomyopathy is what kind of process?

A

Idiopathic

119
Q

4 categories of cardiomyopathy

A

Hypertrophic cardiomyopathy
Restrictive cardiomyopathy (RCM)
Dilated cardiomyopathy (DCM)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)

120
Q

IS there a 5th category of cardiomyopathies?

Which conditions are in it?

A

Unclassfied category.

Left ventricular non-compaction and takotsubo cardiomyopathy

121
Q

Does HCM cause outflow obstruction?

A

no, this is an old consideration

122
Q

what part of the lv is affected by HCM

A

base

123
Q

Classical HCM affect the mitral valve leaflet in what way

A

classical HCM is systolic anterior motion of the anterior leaflet of the mitral valve

124
Q

What kind of gad sequence is used for reviewing scarring in MRI cardiac

A

late gad enhancement

125
Q

does myopathy scarring involve the subendocardium

A

no

126
Q

define restrictive cardiomyopathy

A

disease that restricts diastolic filling of ventricles

127
Q

restrictive cardiomypathies differential

A

amyloid
sarcoid
haemachromatosis

128
Q

What will restrictive cardiomypathies look like

A

The diastolic filling is stiff and non-compliant and there is often systolic dysfunction, particularly as the disease process progresses

129
Q

Echo vs MRI in reviewing for restrictive cardiomyopathy

A

benefit of MR is its ability to sometimes define an underlying cause by, for example, looking for evidence of mediastinal and hilar lymphadenopathy (sarcoid) or iron deposition in the myocardium with T2W imaging (haemochromatosis).

130
Q

Late gad enhancement in amyloid shows what?

A

enhances in thickened ventricular walls/atria/interatrial septum

white heart sign

131
Q

normal heart is what colour on late gad enhancement

A

black

132
Q

what is the definition of dilated cardiomyopathy?

A

Dilated cardiomyopathy is the term used to refer to ventricular dilatation of unknown cause and specifically there must be no evidence of underlying ischaemia.

Diagnosis of exclusion

133
Q

Arrhythmogenic right ventricular cardiomyopathy affects which venTricle most?

A

rIGHT

134
Q

Arrhythmogenic right ventricular cardiomyopathy

WHAT HAPPENS TO CAUSE IT?

A

DISORDER OF intercellular adhesion molecules between the myocytes

135
Q

infiltrating fat is typically of high signal on T1W images and the fibrous material can be seen on LGE imaging.

What condition is this ?

A

Arrhythmogenic right ventricular cardiomyopathy

136
Q

Left ventricular non compaction - what is it?

A

recently identified cardiomyopathy characterised by a very prominent pattern of trabeculation within the LV.

137
Q

What is Takotsubo Cardiomyopathy

A

isease of transient apical ballooning seen usually in post-menopausal female patients

Normally an overwhelming psychological event

due to sympathetic or catecholamine overdrive.

138
Q

Hypoplastic left heart syndrome anatomy at birth?

A

Pulmonary venous return is via a patent foramen ovale or atrial septal defect (ASD) to the right atrium (RA).

Cardiac output is supplied by the single right ventricle (RV) to the pulmonary arteries, and via the PDA to the aorta.

In the aorta, antegrade blood flow passes to the lower body, with retrograde blood flow to the head and neck vessels and coronary arteries (via the hypoplastic ascending aorta).

139
Q

Outcome for hypoplastic left heart syndrome?

A

without treatment death within 90 days

140
Q

hypoplastic left heat syndrome - treatment options

A

compassionate care
staged palliative surgery
cardiac transplantation

141
Q

hypoplastic left heart surgery in staged palliative surgery - three operations - what are they?

A

Norwood

Bi-dirctional glenn

Fontan

142
Q

hypoplastic left heart - bi-directional glenn - what is the main complication

A

branch pulmonary artery narowing from fibrosis/scarring or compression from other vascular structures

143
Q

What is a fontan operation ?

A

Cavopulmonary connection.

pulmonary venous return is now solely to the systemic right ventricle

144
Q

What is the main complication of the Fontan circulation?

A

dilatation of the right atrium and resultant atrial arrhythmias

145
Q

What is the issue in tetrology of fallot?

A

anterior displacement of the conal septum.

(the septum which divides pulmonary outflow tract (the infundibulum) from the left ventricle)

146
Q

4 hallmarks of Fallot

A

Pulmonary outflow tract stenosis

VSD
Over-riding aorta (over the VSD)

Right ventricular hypertrophy (as a consequence of high right heart pressures)

147
Q

commonest cause of right sided arch ?

A

Fallot tetraology

148
Q

Blalock-Taussig shunt (BT shunt)?

A

, anastomosing the subclavian artery down onto the pulmonary artery.

149
Q

An adult patient presents for cardiac MRI, having undergone correction of tetralogy of Fallot during childhood. Which structure is the most likely to be dilated?

A

RV

150
Q

Post MI risk in 1 month and 1 year of death

A

Post hospitalisation, the risk of death in the first month is 10-15%, with a further risk in the subsequent year of 10%.

151
Q

On angiograms - which type stenoses are the ones that will rupture and cause MI

A

the mild stenoses

152
Q

Describe the graph of lesion length and % stenosis for rest / excercise.

A

1mm length - 60% stenosis to cause excercise angina. 85% to cause unstable angina.

10mm - 30% stenosis to cause excercise angina, 60% to cause unstable angina.

Ie the longer the lesion the less narrowed it has to be to cause issues. Overall need at least 60% to cause unstable angina symptoms.

153
Q

inferior MI - commonest complication?

A

bradyarhthmia and complete heart block

154
Q

what kind of pacemakers are used for bradycardias post MI

A

dual lead

atrio and ventricular

155
Q

VF or Vt need what?

A

AICD

artifical implantable cardiac defibrillator

156
Q

The following are all seen in which part of the muscle and what phase?

End diastolic wall thinning
Wall motion abnormality
Absence of wall motion
Paradoxical wall motion

A

Systolic left ventricular wall motion abnormalities

157
Q

paradoxical motion (dyskinesis) - what is it ?

A

Mi causes thin muscle to balloon out rather than contract

158
Q

left ventricle pseudo aneurysm will form how long after an MI

A

3-5 days

159
Q

Rupture through the ventricular septum causing acute ventricular septal rupture occurs in

what kind of MI

A

both inferior and in anterior MI.

160
Q

Symptoms of cardiac failure tend to develop when over WHAT of the LV myocardial mass becomes damaged from an MI.

A

20-25%

161
Q

Right heart failure XR features

A

Chext x-ray: Prominent systemic veins – prominent azygos vein

162
Q

Left sided heart failure

normal LVF venous pressure?

A

8-12mmHg

163
Q

12-18 mmHg LVF chest xr sign

A

Blood flow is redirected to the upper lobes (erect)

164
Q

> 18 mmHg LVF chest xr sign

A

interstitial oedema

sub pleural effusions

loss of peribronchial definition

165
Q

> 25 mmHg LVF chest xr sign

A

alveolar oedema

alveolar shadwoing due to fluid in alveoli

166
Q

late post mi pericarditis is called what

A

dresslers syndrome

167
Q

There are three common causes of a single ventricle.

A

Tricuspid atresia
Double inlet left ventricle
Hypoplastic left heart syndrome

168
Q

What is a Blalock-Taussig Shunt

A

subclavian artery to the superior aspect of the pulmonary artery

169
Q

what is a fontan circulation ?

A

systemic venous shunts, ie IVC/SVC straight to the PA.

170
Q

Glen shunt is what?

A

When the IVC or SVC is put into the PA

171
Q

Which condition can only have a single ventricle repair?

A

Tricuspid and mitral atresia - failure of ventircle to develop.

Hypoplastic left heart syndrome

double inlet left ventricle.

172
Q

common complications of single ventrivle patients?

A

arrythmias
sinus node dysfunction

173
Q

You should be able to make a definite diagnosis for shunt stenosis using:

A

ECG-gated CT
Magnetic resonance imaging
Invasive angiography

174
Q

A PDA will allow some mixing and can be kept open by xxxx

A

prostacyclin

175
Q

moderator band exists in which ventricle

A

the right ventricle

176
Q

Congenitally Corrected Transposition of the Great Arteries

what is it?

A

TGa, but also have discordant atrium to ventricles.

IVC to left atrium, mitral valve, left ventricle, pulmonary artery

177
Q

examples of conditions that can give right ventricle dysfunction

A

COPD and myocardial dysfunction

178
Q

when is reflux of contrast into the IVC not an actual useful sign for PE

A

Tricupsid regurgiation

injection of contrast at greater than 3ml / second

179
Q

What can you do to improve the quality of the CTPA?

A

breathing from start of contrast adminsitration. Deep breaths. Long and gentle inspiration.

Avoid valsalva maneouver.

180
Q

CTPA what ratio should always be measured.

A

RV / LV

Should be less than 1

181
Q

Inspiratory CTPA - IVC should be what shape?

A

Ovoid.

Round measn hypertension.

182
Q

myoxomas most often found where

A

Left atrium

arise from the interatrial septum close to the fossa ovalis and are often based on a small pedicle

183
Q

On post-gadolinium images, myxomas mostly show enhancement which is

A

patchy and heterogeneous, but usually poor.

184
Q

second most common benign cardiac tumour

A

lipoma

185
Q

what percentage of caridac tumours are malignant?

where from?

A

25%

bronchus, breast and melanoma.

186
Q

Mets to the cardiac - appear how on MRI

A

f low signal on T1W images, except melanoma metastases, which are of high signal.

Metastases tend to demonstrate high signal on T2W imaging

enhance post gad

187
Q

main malignant cnacer of the heart is

A

Sarcomas

will invate wall and pericardium

188
Q

three main types of coartation of the aorta are

A

tubular hypoplasia

localised coarctation

interrupted arch

189
Q

Tubular hypoplasia of the aortic arch

A

presents in infancy and is often associated with other cardiac abnormalities.

The narrowed segment is of variable length and may be localised or involve the whole of the distal aortic arch

190
Q

Localised coarctation

A

focal narrowing near the site of attachment of the ligamentum arteriosum distal to the left subclavian artery

191
Q

Interrupted arch

A

his can occur beyond the left subclavian artery, between the left subclavian and left common carotid arteries or between the innominate and the left common carotid artery. In interrupted arch, the descending thoracic aorta is supplied from the pulmonary artery via a patent ductus arteriosus

192
Q

The first and second ribs do not show notching in Coarctation

A

because the intercostals arise from the thyrocervical trunk proximal to the coarctation.

193
Q

Associated cardiac abnormality for coarctation

A

bicuspid valve found in 85% of patients with CoA

but VSD, ASD, PDA also common

194
Q

Associated intracranial pathology for a patient with CoA

A

berry aneurysm and sub arachnoid haemorrhage

195
Q

coarctation is usually best seen on what view on echo?

A

Suprasternal notch

196
Q

Adults presenting later in life will have coarctation of the aorta where?

A

Localised narrowings distal to the sublcavian artery

197
Q

T or F

MRI can be safely used in patients with prosthetic aortic valves
A

T

All current valves are safe although there may be some artefact from the valve.

198
Q

T / F

MRI is contraindicated in patients with coronary artery stents

A

F

It is advisable to wait for 2 weeks after stent insertion, although even this may not be necessary.

199
Q

Intraaortic counterpulsation balloon pump is used for what?

A

treating postcardiotomy shock and as a bridge to either heart transplantation or implantation of a long-term device.

200
Q

for an aortic dissection, what information should be included in your report?

A

Type A / Type B involves only the aorta distal to left subclavia

Branch vessel involvement (particularly coronary and carotid)

Pericardial effusion (and whether its simple or haemorrhagic)

Signs of mediastinal blood or haemorrhagic pleural effusion (indicating a contained rupture)

Involvement of the aortic valve cusps

Lowermost extent of the dissection (important for putting the patient on bypass)

201
Q

An aortic dissection is secondary to a tear in the

A

intima of the vessel wall with subsequent extension through the media

202
Q

Why do 75% of aortic dissection happen in the ascending

A

greatest pressure here

203
Q

what causes Type B aortic dissection?

A

pre existing weakness in the wall

IMH or penetrating ulcer

204
Q

how can you differentiate between the true and false lumen of the aortic dissection?

A

Signs.
False lumen shearing is never v clean - irregularities / cobweb sign.

False lumen often elliptical shape

205
Q

in dissection what is an intramural haemaoms thought to be secondary to ?

A

a bleed in the media from vaso vasorum

206
Q

reflection between the four pulmonary veins is called the

A

oblique sinus

207
Q

reflection behind the ascending aorta is the

A

superior pericardial recess

208
Q

pericardium is abnormal if size greater than

A

4mm

209
Q

Pericardial cysts are

A

congenital outpouchings of the parietal pericardium.

210
Q

what does dipyramidamole do?

A

inhibit the breakdown of adneosine

211
Q

give some ddx for transudate or exudate cardiac effusoins

A

Congestive heart failure
Uraemia
Infectious (e.g. tuberculosis (TB))
Autoimmune (e.g. systemic lupus erythematosus (SLE))
Dressler’s syndrome (postoperative/post-infarction)
Neoplastic
Hypothyroidism
Sarcoid
Deep x-ray therapy (DXT)
Hypoalbuminaemia

212
Q

give some ddx for CHYLOUS cardiac effusoins

A

Thoracic duct obstruction
Yellow nail syndrome
Trauma
Neoplasm
Surgery

213
Q

igve some ddx for Haemorrhagic cardiac effusoins

A

Aortic dissection
trauma
cardiac rupture
aortic rupture
neoplasm

214
Q

pericardial effusion on cxr - what are the signs?

A

crisp border
cardiomegaly
rapid change in size
density change of effusion to cardiac muscle

215
Q

An effusion measuring >5 mm anterior to the RV is likely to be between ???

A

100 mls and 500 mls.

216
Q

Constrictive pericarditis results from

A

thickening of the pericardium
subsequent constriction of the ventricular chambers

impaired diastolic ventricular filling

217
Q

causes of constrictive pericarditis

A

Viral pericarditis
TB
Rheumatoid arthritis
SLE
Haemodialysis-treated renal failure
Mediastinal irradiation
Cardiac surgery

218
Q

what is the differential for constrictive pericardiitis?

A

Restrictive cardiomyopathy

thickened pericardium might be the only tell tale sign

219
Q

benign pericardial tumours

A

teratoma
fibroma
lioa
haeongioma
lymphangioma
hamartoma

220
Q

malignant primary tumours of pericardium

A

mesothelioma
lymphoma
teratoma
angiosarcoma
fibrosarcoma

221
Q

Which of the following features is most reliable in permitting a diagnosis of constrictive pericarditis?

Pericardial thickness up to 2 mm on CT
B. Septal flattening on real time cine MRI
C. Pericardial calcification identified on MRI
D. Atrial enlargement on CT
E. Rounding of the RV free wall on echo

A

b

222
Q

Aorta, signs of injury are what?

A

intimal flap
false aneurysm
mediastinal haematoma
change in aortic calibre

223
Q

how is an intimal falp different to a dissection?

A

Intimal flap is normally smaller

224
Q

traumatic aorta - location?

A

just beyond the left subclavian origin

225
Q

after an arotic ruputre where can the blood go?

A

mediastinum and haemothorax

226
Q

pristine aorta but haemorrhage around it? Why?

A

venous bleeding. self limiting

227
Q

minor injury causes massive damage for aortic injury

in which condition?

A

Elhoers Danlos

228
Q

traumatic intramural haematoma is normally caused by….

A

catheters

229
Q

A collar of adventitia surrounding the site of transection is called a

A

false aneurysm

230
Q

What are the features of a right atrium

A

receives the IVC
atrial appendage
fossa ovals upper margin limbus

231
Q

what is the main feature of a left atrium

A

narrow based finger like appendage

232
Q

main features of a right ventricel

A

moderator band
coarse trabeculations
tricupsid papillalry attachements, free wall and septum

muscular infundibulum below the outlet valve

233
Q

features of a left ventricle

A

fine trabeculations
two distinct papillary muscles

234
Q

what does situs normally mean?

A

viscero atrial situs.

liver ivc and right atrium are on right side

235
Q

another term of cardiac connections ?

A

concordant and discordant

236
Q

what is situs ambiguous

A

complex situation of both atria the same, eg two left atria

237
Q

bronchial situs is what

A

right bronchus is shorter and wider than the left

238
Q

Differentials for completely dense hemi thorax

A

Pleural fluid (serous, chyle, blood, pus)

Atelectasis

Diaphragmatic hernia
Consolidation (but rare for whole lung to be involved)

Contusion/haemorrhage

Chest wall mass/tumour (look for rib erosion)

Post pneumonectomy

Pulmonary aplasia/hypoplasia

Congenital cystic adenomatoid
malformation (CCAM), sequestration

Mediastinal masses (i.e. lymphoma, foregut cysts)

239
Q

The mediastinum:

Moves toward the opaque side: i.e. volume loss, usually due to XXX

A

collapse

240
Q

Mediastinum Is shifted away from the opaque side: i.e. mass effect, usually due to XXXX

A

pleural fluid

241
Q

segment collpase vs whole lung collapse by age

A

segment collapse more in older kids

whole lung in infants.

242
Q

whole lung collapse often caused by

A

mucus plugging

243
Q

trapped lung foreign body cases what appearance

A

Lucency of the affected lung portion

244
Q

cystic fibrosis causes what kind of collapse?

A

subsegmental

245
Q

paediatric air leaks - what are different typess?

A

Pneumothorax
Pneumomediastinum
Pneumopericardium
Pneumoperitoneum
Pulmonary interstitial emphysema

246
Q

most common causes of air leaks in children are

A

Foreign body aspiration

Neonatal disease including respiratory distress syndrome (RDS), meconium aspiration syndrome and complications of treatment, e.g. ventilator barotrauma

Asthma and bronchiolitis

247
Q

Causes of pneumo-mediastinum

A

raised intra alveolar pressure (cough vomit)

extension from pneumoperitoneum

rupture
Asthma
infection
trama

248
Q

Lung disease in neonates
Pneumothorax in this group is caused by:

A

Respiratory distress syndrome
Pulmonary interstitial emphysema
Meconium aspiration
Congenital bullous lesions

249
Q

Lung disease in children
Pneumothorax in this group is caused by:

A

Asthma
Bronchiolitis
Pulmonary infections, such as staphylococcal pneumonia, tuberculosis (TB), pertussis and pneumocystis carinii

250
Q

Diffuse lung diseases
Pneumothorax may occur in cases of:

A

Langerhans’ cell histiocytosis (LCH)
Marfan syndrome
Ehlers-Danlos syndrome
Tuberous sclerosis

251
Q

The following can mimic pneumothorax:

A

Skin folds- traced beyond the lung edge

A large cystic lesion
A cavity from staphylococcal pneumonia
A congenital lesion

252
Q

Risk factors for neonatal penumothorax

A

low birth weight and prematurity
espiratory distress syndrome, invasive and non-invasive ventilatory support

253
Q

angels wings signs is what ?

A

elevated thymus from anterior pneumomediastinum

254
Q

is pneumopericardium bengin

A

yes, normally

255
Q

signs of cystic fibrosis are usually obvious on the radiograph:

A

Upper lobe bronchiectasis
Mucoid impaction
Parahilar densities
Evidence of infection
Central lines

256
Q

how to define a lung nodule

A

The size of the nodule
The density of the nodule
Calcification
Cavitation
Feeding/draining vessels
Being well-defined or ill-defined

257
Q

Solitary lung opacity

Causes

A

Round pneumonia
Granuloma
Hamartoma
Fungus
Contusion, haemorrhage
Metastasis or lymphoma
Vascular lesion; arteriovenous malformation (AVM)
Round atelectasis
Vasculitis
Bronchogenic cyst
Pulmonary blastoma
Sequestration/congenital cystic adenomatoid
Adenoma
Hydatid
Pulmonary abscess/infarct

258
Q

Round pneumonia occurs because of

A

fee communication between adjacent air spaces via the pores of Kohn

259
Q

Round pneumonia organisms

A

Haemophilus influenzae
Streptococcus (pneumococcus)

260
Q

Round pneumonia differentials

A

Hamartoma
lymphoma
contusion
solitary met
granuloma
fungus

261
Q

which paeds malignancies love the lung for mets

A

Wilms nephroblastoma
sarcomas of soft tissue and bone

262
Q

osteosarcoma will usually have what in them

A

calcifications

263
Q

fungal nodules tend to exist where

A

small (<5mm)
peripheral and subpleural locations

264
Q

AVMs are associated with…

A

hereditary haemorrhagic telangiectasia

265
Q

Hamartomas contain variable amounts of

A

fat, epithelial tissue, fibrous tissue and cartilage.

on CT fat and calcification is considred diagnostic

266
Q

Drainage
Extralobar sequestrations usually drain into…

A

systemic veins (commonly the azygos and hemiazygos), whereas intralobar sequestrations usually drain into normal pulmonary veins.

267
Q

There are a large number of non-infective causes of pulmonary opacities which may undergo cavitation, including ……………

A

Wegener’s granulomatosis, pulmonary contusion, septic embolism and infarction.

268
Q

Pulmonary nodules

secondary features to look for

A

Pleural effusion
Mediastinal lymphadenopathy
Bone changes

269
Q

mass vs nodule

A

> 3cm

270
Q

multiple cavitating opacities nodules

A

Pyogenic abscess, TB, metastasis, fungus, vasculitis, infarction

271
Q

Multipkle pulmonary nodules

Calcification suggests:

A

Granuloma, TB, hamartoma, osteosarcoma metastasis

272
Q

Pulmonary masses
Ill-defined margins - causes

A

Infection, lymphoma, contusion, haemorrhage

273
Q

which bug orgnaism

is a common cause of multifocal opacities with a propensity to undergo cavitation and pneumatocoele formation.

A

Staphylococcal pneumonia

274
Q

multiple bilateral upper zone nodules less than 5 mm in diameter in both lungs

cause?

A

aspergillus

275
Q

hamartomas are solitary or multiple

A

solitary

AA ST2 (14 decks)

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