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Paediatric Cardiology > Congenital Heart Disease > Flashcards

Congenital Heart Disease Flashcards

1
Q

What are the examination features of ASD?

A

Recurrent chest infections
Arrhythmia as an adult (4th decade onwards)

  • Ejection systolic murmur
  • Upper left sternal edge
  • Fixed and widely split S2
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2
Q

What are the investigation findings in ASD?

A

ECG

  • Superior QRS (negative in AVF)
  • Right axis deviation
  • RBBB (may be normal in kids)

CXR

  • Cardiomegaly
  • Enlarged pulmonary arteries
  • Increased pulmonary vascular markings
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3
Q

RBBB findings

A

Broad QRS > 120 ms
RSR’ pattern in V1-3 (‘M-shaped’ QRS complex)
Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

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4
Q

Name the left to right shunts (Breathless)

A

ASD
VSD
PDA (as systemic pressures always > pulmonary in systole and diastole), Pulse pressure increased, collapsing or bounding pulse

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5
Q

What makes VSD large or small?

A

Relation to size of aortic valve diameter

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6
Q

Examination findings in small VSD

A

Pansystolic murmur at lower left sternal edge
Soft S2

Smaller VSD = Louder murmur

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7
Q

Investigation findings in small VSD

A

Normal CXR, ECG

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8
Q

Management small VSD

A

Watch and wait
Usually close spontaneously
Maintain good dental hygiene

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9
Q

Treatments of ASD/ AVSD

A

ASD significant enough to cause RV dilation will need closing with cardiac catheter and occlusion device

Partial AVSD will need surgical correction
Usually 3-5 years of age
Prevents arrhythmias/ failure later in life

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10
Q

Large VSD examination findings

A

Heart failure with breathlessness and faltering growth
Recurrent chest infections

Active percordium
Soft pansystolic mumur or no murmur
Apical mid-diastolic murmur
Loud P2 (soft P2 in small VSD)

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11
Q

Large VSD investigation findings

A

CXR - cardiomegaly, pulmonary oedema, increased vascular markings

ECG - bi-ventricular hypertrophy by 2 months

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12
Q

Large VSD management

A

Diuretics and Captopril to manage failure
Dietetics - increase calories

Surgery at 3-6 months of age

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13
Q

What are the signs of bi-ventricular hypertrophy on ECG and in which condition would you expect to see it?

A

Katz-Wachtel phenomenon: Tall diphasic QRS complexes (>50 mm in height) in the mid-precordial leads (leads V2, V3 or V4) typically associated with Biventricular Hypertrophy.

Seen in large VSD

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14
Q

What is the MOA and SE of Captopril?

A

ACE inhibitor
Suppresses RAAS
Reduced effect aldosterone
(Normally salt and water retention, loss of K)
(ACE - salt/ water loss, retention of K - hyperK)

SE - dry cough, GI upset, pruritis, taste impairment, hypotension

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15
Q

Name the right to left shunts (Blue)

A

Tetralogy of Fallot
Transposition of the great arteries

Presents with cyanosis in first week of life

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16
Q

What are the side effects of prostaglandin infusions?

A

Apnoea, jitteriness, seizures, flushing, vasodilation, hypotension

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17
Q

Explain and draw the clinical features of Tetralogy of Fallot

A
  1. Large VSD
  2. Overriding aorta
  3. (Sub) Pulmonary stenosis (infundibular septum) causing RVO
  4. Resulting RVH
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18
Q

Presentation of ToF

A

Antenatally diagnosed often
Murmur in first 2 months of life
May be cyanotic at this point, but tends to develop later
Tet spells (Hypercyanotic spells)

19
Q

What are the findings in ToF?

A

ECG may be normal, progressing to RVH

CXR
Boot shaped heart (uptilting of apex) due to RVH
Pulmonary artery bay (earlier finding as no RVH yet)

20
Q

Management of ToF

A

Will need surgical correction, usually 6 months

  • Closure of VSD
  • Correction right outflow tract obstruction

If very cyanosed, may need holding procedure

  • balloon dilatation of right outflow tract
  • Modified Blalock Taussig shunt

*shunt between right subclavian artery and pulmonary artery - increases pulmonary blood flow.

21
Q

Management of Tet spell

A 
Squatting
Increases SVR/ Afterload...
Increasing LA/ LV pressures..
Reverses R-L to L-R shunt...
Less cyanosis, increased pulmonary flow

OR

  1. Morphine (venodilatation - reduced preload)
  2. Propranolol - increases peripheral arterial resistance and reduced the pulmonary stenosis/ infundibular spasm
  3. IV fluid bolus
  4. Bicarbonate for acidosis/ I&V to reduce metabolic demand
22
Q

Explain TGA

A

Closed circulations

  • Aorta connected to the RV
  • Pulmonary artery connected to LV

Deoxygenated blood goes to body
Oxygenated blood to lungs

Requires mixing to be compatible with life

  • ASD
  • VSD
  • PDA
23
Q

Presentation of TGA

A

Cyanosis is predominant

  • Usually day 2 when ducts close
  • Usually no murmur, single S2
  • May have systolic flow murmur
24
Q

Investigation findings in TGA

A

CXR
Egg on the side
Narrow mediastinum
Increased pulmonary vascular markings

ECG
Usually normal

25
Q

Management of TGA

A

Need to improve mixing!

  • Maintain PDA
  • Balloon atrial septostomy

Definitive

  • Arterial switch in first few days of life
  • Coronary arteries to be reconnected to new aorta
26
Q

What are the common mixing defects?

Blue AND breathless

A 
Complete AVSD
Complex CHD (may be cyanotic/ failure dominant)
- Tricuspid atresia*** most common 
- Double inlet left ventricle
- Mitral atresia
- Truncus arteriosus 
- Common arterial trunk
27
Q

Draw and explain the features of AVSD

A

Large 5 leaflet common AV valve

Lower atrial and upper ventricular wall defect

28
Q

Clinical features of AVSD?

A 
Presents with cyanosis, heart failure 2-3 weeks of life
Pulmonary hypertension
Always superior axis on ECG
No murmur 
Most often seen in T21
29
Q

Management of AVSD?

A

Medically manage heart failure

Surgical correction at 3-6 months of age

30
Q

Draw and explain tricuspid atresia

A

Issue - nonfunctional and small right ventricle. No tricuspid valve. Flow from RA is through an ASD, then VSD to reach the pulmonary artery.

  • May have low flow to pulmonary artery - BT shunt
  • May have high flow to pulmonary artery - PA banding
31
Q

Describe the palliation of tricuspid atresia

A

Issue - small non-functioning right ventricle
relies on ASD/VSD
Left ventricle basically has to pump mixed blood to systemic circulation AND pulmonary circulation

Initially may have Blalock-Taussig shunt

  • Subclavian and pulmonary artery
  • basically bigger PDA
  • Increases pulmonary flow

Then may have

  1. Glenn/ Hemi-fontan (6 months)
    - Connects the SVC to the pulmonary artery
  2. Fontan (3-5 years of age)
    - Connects the IVC to the pulmonary artery

End effect - preload pressures drive all of the venous return to the pulmonary circulation passively

LEAVING the left ventricle to deal with the systemic circulation

32
Q

What are the outflow tract obstructions in a well child?

A

These are murmurs in well children therefore usually have no symptoms. They are:

Aortic stenosis
Pulmonary stenosis
Adults type coarctation of the aorta

33
Q

Clinical features and management of AS

A

Usually well child

If severe - reduced exercise tolerance, syncope, chest pain on exertion

If critical - would be duct dependent and present as neonate

OE: Slow rising pulse, ejection systolic murmur at upper right sternal edge, Apical ejection click, soft A2
THRILL ALWAYS PRESENT

ECG: May have LVH

OFTEN associated with Coarctation, other valve stenosis - should always be checked.

Management depends on symptoms:

  • Balloon valvotomy (safer children, dangerous neos)
  • Aortic valve replacement is definitive
34
Q

Clinical features and management of PS

A

Most asymptomatic
May be duct dependent if critical

OE: Ejection systolic murmur at left upper sternal edge
Thrill may be present. Ejection click. May have heave.

ECG may show RVH

Managed by balloon dilatation when the pressure across the pulmonary valve becomes critical - about >64 mmHg

35
Q

What are the outflow tract obstructions in the sick infant?

A

Coarctation of the aorta - most common
Interrupted aortic arch
Hypoplastic left heart
Critical AS

36
Q

Presentation and management of coarctation

A

Sick, collapsed neonate (but well at birth)
Duct dependent
Day 2-3 of life

Absent femorals
Severe metabolic acidosis

CXR - cardimegally
ECG - normal

Prostaglandin to maintain duct. Surgical repair.

37
Q

Presentation and management of hypoplastic left heart syndrome

A

Sickest of all collapsed neonates
Usually diagnosed antenatally

All of left heart is small

  • nonfunctional left ventricle
  • small or atretic mitral valve
  • aortic valve atresia
  • usually associated with coarctation

Sick. Metabolic acidosis. No pulses.

Management with prostaglandin
Surgical correction - Norwood

38
Q

Describe the Norwood procedure and in which condition would it be indicated?

A

Hypoplastic Left Heart syndrome

Step 1: The Norwood procedure

  • Aorta diverted from LV to RV
  • Pulmonary artery detached, now pulmonary flow is through a BT shunt attached to the subclavian artery
  • RV is driving both pulmonary and systemic mixed flow

Step 2: Glenn shunt, or semi-fontan

  • SVC is diverted directly to the pulmonary artery
  • BT shunt removed

Step 3: Fontan

  • IVC is diverted directly to the pulmonary artery via a conduit. Pulmonary flow is now driven by venous return and preload pressures
39
Q

Presentation and management of interrupted aortic arch

A 
Presents as collapsed/ sick neonate
Only right brachial pulse palpable
Metabolic acidosis
Duct dependent
VSD usually present

Associated with DiGeorge syndrome

40
Q

Cardiac defects and genetics of Williams syndrome?

A

Deletion in chromosome 7

Supravalvular aortic stenosis
Peripheral pulmonary artery stenosis

41
Q

Cardiac defects and genetics of DiGeorge?

A

22q11.2

Truncus arteriosus
Tetralogy of Fallot
Aortic arch abnormalities

42
Q

Cardiac defects and genetics of Noonans?

A

PTPN11

Pulmonary stenosis
Hypertrophic cardiomyopathy

43
Q

Genetics and cardiac defects of Turners?

A

45XO

Aortic valve stenosis
Coarctation of the aorta

Paediatric Cardiology (1 decks)

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