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cardiology > cyanotic lesions > Flashcards

cyanotic lesions Flashcards

1
Q

what are the five congenital cyanotic cardiac lesions?

A 
truncus arteriosus 
transposition of the great arteries (TGA) 
tricuspid atresia
tetralogy of fallot
total anomalous pulmonary venous return
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2
Q

truncus arteriosus

  • what
  • a/w what acyanotic lesion ALWAYS
  • how does HF occur
A

separate aorta and pulmonary artery don’t form
ALWAYS a/w VSD
more blood in pulmonary circ

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3
Q

transposition of the great arteries

  • what
  • a/w what acyanotic lesions
A

the spiral don’t form right, so aorta attached to RV and pulmonary attached to LV
forms 2 separate systems: 1) deoxy blood through right heart and aorta to body 2) oxy blood to and from lungs
only way to survive is a PDA/PFO
50% have a VSD too

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4
Q

tetralogy of fallot

  • what
  • a/w what acyanotic lesion
  • murmur
A
  • right POV - from infundibular septum displacement narrowing the right outflow tract:
    RVH, pulmonary stenosis, overriding aorta, VSD
  • pulmonary stenosis so LUSE ejection systolid +/- VSD, so holosystolic murmur at LLSE
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5
Q

TAPVR

  • what
  • a/w what acyanotic lesion
  • murmur
A
  • pulmonary veins drain into right heart instead, so everyone gets mixed ox blood
  • ASD/PDA - as they allow blood to get to body
  • ASD, so ejection systolic at LUSE
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6
Q

tricuspid atresia

  • what
  • a/w what acyanotic lesions
  • murmur
A
  • tricuspid don’t form right > no blood in RV
  • incompatible with life unless has ASD and VSD. will get right ventricular atrophy
  • ASD, so ejection systolic at LUSE
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7
Q

when do the cyanotic lesions present?

A

birth to first few weeks of life

BUT ToF related to pulmonary stenosis severity, so if mild, could present later!

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8
Q

what is Eisenmenger’s syndrome?

A

initial left to right shunt
then get pulmonary HTN
so eventually RHP > LHP … then get reversal into a R>L shunt
e.g. ToF

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9
Q

pathogenesis of neonatal cyanosis - four ways

A

1) O2 can’t diffuse across alveolar membrane e.g. oedema
2) blood can’t get to lungs - R to L shunt, intrapulmonary shunt
3) lungs not ventilated - airway / pulmonary / neurological
4) V/Q mismatch - e.g. PTX, parenchymal disease

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10
Q

neonatal causes of early vs mid systolic click

A

Early systolic click
Semilunar valve stenosis
Bicuspid aortic valve
Truncus arteriosus

Mid systolic click
MVP
Ebstein’s anomaly

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11
Q

CXR findings:

  • boot shaped
  • egg on string
  • snow man sign
A
  • boot shaped = TOF
  • egg on string = TGA
  • snow man sign = TAPVR
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12
Q

what is the hyperoxia test, and what kind of results suggest cardiac vs pulmonary cause?

A

Hyperoxia test = after 10 minutes of breathing 100% O2, take right arm, preductal (radial artery) ABG

  1. PaO2 <70 mmHg – occur in most cyanotic defects
  2. PaO2 >150 mmHg – suggests cyanosis NOT due to CHD
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13
Q

which of the congenital cyanotic lesions cause increased vs decreased pulmonary blood flow? so what do they present with?

A

Increased BPF = truncus arteriosus, TAPVR, TGA
- Present with heart failure

Reduced PBF = TOF, TA, Ebstein’s
- Present with cyanosis

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14
Q

di george a/w which congenital cyanotic lesions?

A

TOF

truncus arteriosus

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15
Q

extra-cardiac complications of cyanosis

A
  1. polycythaemia
  2. iron deficiency
  3. clubbing
  4. clots
  5. cerebral abscess
  6. thrombocytopaenia
  7. hyperuricaemia
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16
Q

explain tet spells

A

feeding/exercising/crying for whatever reason causes SVR drop > inc systemic flow vs pulmonary flow > less O2 > breath more > inc VR > cycle&raquo_space; can cause death

decreased intensity of murmur
worse cyanosis

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17
Q

surgical complications of TOF repair

A
  1. Bleeding
  2. Pulmonary valve regurgitation
  3. CCF – more common in setting of transannular patch
  4. RBBB (due to R ventriculotomy)
  5. Complete heart block < 1%
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18
Q

what are some things to use to manage tet spells?

A
  • squatting: traps blood in the legs, decreasing systemic venous return and increasing SVR
  • morphine - reduces the hyperpnoea
  • vasoconstrictors
  • beta blockers!!
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19
Q

Key risk of tetralogy of fallot?

A

arryhthmia!

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20
Q

what is the most extreme TOF variant? % of TOF cases?

A

15-20% - TOF with pulmonary atresia + VSD

21
Q

TOF with pulmonary atresia:

  • whats the problem
  • how do they present
A
  • no flow through pulmonary artery: complete R to L shunt
  • lungs get blood from either a PDA (so obviously use prostin) or collaterals. Need ASD / PFO to get blood from RA to LA
  • present cyanotic from birth with either no murmur, a faint continuous murmur from collaterals, or a click from enlarged aortic root
22
Q

ECG findings tricuspid atresia

A

RAH
LVH
** superior QRS axis and LAD **

23
Q

what kind of Mx is critical for pulmonary atresia?

A

PGE2 to keep PDA open

24
Q

ebstein anomaly most associated with what maternal thing?

A

maternal lithium use

25
Q

ebstein anomaly - what’s the abnormality

A

portion of tricuspid in the RV
portion of RV IN the RA (atrialised RV)

ALL will have ASD/PFO

26
Q

ebstein anomaly - consequences

A

RV is shit
can have RVOT from TR
so you get no pulmonary flow (unless have PDA)
a/w WPW

27
Q

ebstein anomaly

  • murmur
  • rhythm
  • ecg
A
  • CLASSIC triple or quadruple rhythm – widely split S, split S1, S3 and S4
  • soft holosystolic TR murmur at LLSE
28
Q

murmur of TGA

A

usually silent
if has VSD
- pansystolic murmur LLSE
- PS/LVOT soft mid systolic murmur - can have holosystolic murmur

29
Q

type of ventricular hypertrophy with D-TGA

A

RVH after few days of life

BVH if have large VSD/PDA as these can cause LVH

30
Q

surgery to fix D-TGA

A

arterial switch

LV needs to have good enough pressure to support the system

31
Q

L-TGA - describe the anatomy

A

ventricles and and AV valves are switched:

i. Systemic venous blood > RA > mitral valve > LV > PA
ii. Oxygenated blood > LA > tricuspid valve > RV > aorta
iii. Coronary arteries have mirror image distribution

32
Q

long term complications of L-TGA

A

tricuspid gets saggy and TR with RV failure bc of high pressures they weren’t anatomically supposed to have to withstand

33
Q

classification of TAPVR subtypes, and consequences on presentation

A

supracardiac 50% - mildly obstructive only
infracardiac 20% - obstructive lesion from tortuous course, often through liver
cardiac 20% - different presentation to other types; 6wk with FTT
mixed 10%

34
Q

what is the biggest determinant of clinical presentation for TAPVR?

A

whether or not there’s obstruction to pulmonary venous drainage

No obstruction:

  • mild cyanosis + FTT.
  • widely split S2 (high RV volume). pulmonary stenosis ES @ LUSE. mid diastolic LLSE from inc tricuspid flow
  • snowman sign on CXR

Obstruction

  • cyanosis and resp distress in neonatal
  • …cardiac signs usually minimal
  • RAD + RVH
35
Q

PBF and PVR effects in truncus arteriosus

A

high PVR e.g. at birth > lower PBF > cyanosis more obvious

then lower PVR > high PBF > development of heart failure

36
Q

double inlet ventricle

  • also known as what?
  • what is the defect?
A 
double inlet ventricle = single ventricle = unilateral heart 
both atriums connect to one ventricle 
most common = connect to left ventricle, L-TGA i.e. aorta with RV and pulmonary artery with LV, but the valves dont switch - mitral still with aorta and pulmonary artery still has TV
37
Q

what kind of procedures are needed for a double inlet ventricle?

A

initial palliative - type will depend on presence of pulmonary stenosis

  • -> PS = BT shunt from aorta to pulmonary artery to improve PBF
  • -> no PS = can band PA to reduce PBF or again PA-to-aorta anastamosis to improve PBF

second stage palliative
definitive is fontan at 18-24mo

38
Q

Most common cause of death from cardiac defects in the first month of life is…?

A

HLHS

39
Q

syndromes HLHS associated with?

A

Turner, Trisomy 18, Jacobsen’s syndrome

40
Q

key pathologies of HLHS, and associated abnormalities (4)

A

Key characteristics

i. Hypoplasia of the LV – completely nonfunctional
ii. Atresia or critical stenosis of the aortic or mitral valves
iii. Hypoplasia of the ascending aorta and aortic arch

Associated features

i. ASD/foramen ovale (15%)
ii. VSD (10%)
iii. Coarctation (75%)
iv. High prevalence of associated CNS abnormalities (30%)

41
Q

what anomaly is a requirement for survival in HLHS?

A

ASD/PFO and PDA - if not the pressure is way too high in the LA, and there’s also nothing coming out of the left ventricle

42
Q

major findings of a HLHS in terms of Ix

A

metabolic acidosis
RVH on ECG
CXR pulmonary oedema

43
Q

management of HLHS

A
  1. PROSTIN
  2. correct acidosis
  3. surgical
44
Q

surgical management of HLHS

A

staged:
- norwood a birth - connect PA and aorta so one outlet from RV, so at least body can get blood. connect PA and branch of aorta so lungs still get blood
- BCPC
- definite Fontan at 3-4yo

45
Q

indications for a fontan procedure

A

single ventricle physiology

a. Dominant RV
i. HLHS (mitral/aortic atresia)

b. Dominant LV
i. Double inlet left ventricle (DILV) = single ventricle
ii. Pulmonary atresia with intact ventricular septum (PAIVS)
iii. Tricuspid atresia

46
Q

ideal saturations post fontan, and why

A

between 70-80% Qp:Qs = 1
if its too high, then pulmonary flow too high, and systemic low
single ventricle pathologies don’t have the ability to incease CO well

47
Q

how do you know when to move from stage I to II of the fontan?

A

sats dropping - child has outgrown their shunt

48
Q

describe the BCPC

A

bi-directional cavo-pulmonary shunt = Glenn. SVC attached to pulmonary artery, so the heart doesn’t have to pump blood into the heart anymore

49
Q

what happens in the stage III fontan?

A

SVC remains attached to PA as per stage II
then IVC attached to PA via conduit
fenestration can be made between conduit and atrium

cardiology (6 decks)

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