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Paediatrics STG > Paediatric Cardiology > Flashcards

Paediatric Cardiology Flashcards

1
Q

Circulatory Changes at Birth

A

In utero: Left atrial pressure is low, right atrial pressure is higher as it receives systemic return from placental exchange, FO is open
At birth: First breaths leads to rapid reduction in pulmonary resistance and increase in pulmonary blood flow, right atrial pressure falls due to cessation of placental flow so foramen ovale flap closes
Ductus arteriosus closes within first few hours/days
Some congenital heart lesion cause babies to be duct-dependent, 1-2 days of age when duct closes or later condition will deteriorate

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2
Q

How do common congenital heart lesions present

A

Antenatal diagnosis

Detection with murmur, heart failure, shock and cyanosis

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3
Q

Causes of Left to Right Shunt

A

Ventricular Septal Defect
Patent Ductus Arteriosus
Atrial Septal Defect
Present with breathlessness

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4
Q

Causes of Right to Left Shunt

A

Tetralogy of Fallot
Transposition of the Great Arteries
Present with cyanosis

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5
Q

Causes of Mixing circulation

A

Complete Atrioventricular septal defect

Present with breathlessness and cyanosis

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6
Q

Causes of Obstruction in Well Child

A

Pulmonary Stenosis

Aortic Stenosis

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7
Q

Causes of obstruction in Unwell child

A

Coarctation

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8
Q

Aetiology of Congenital Heat Disease

A

Maternal Rubella: Peripheral Pulmonary Stenosis, PDA
SLE: Complete Heart Block
DM: Generally increased incidence of defects
Maternal Warfarin: Pulmonary stenosis, PDA
Foetal Alcohol Syndrome: ASD, VSD, TOF
Chromosomal:
Downs: ASD, VSD
Turner’s: AS, Coarc
DiGeorge: Aortic abnormalities, TOF,

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9
Q

What is the most common presentation of congenital heart disease

A

Most common presentation of Congenital Heart Disease; However clear majority of children
will have a normal heart = Innocent Murmur (almost 30% of children)

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10
Q

Features of innocent murmur

A 
Soft 
No radiation 
Praecordial only 
Systolic and short
Varies with posture
HS normal 
Usually maximal at lower left sternal edge
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11
Q

Features of significant murmur

A

Harsh
Can be heard elsewhere
Radiates
Other signs

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12
Q

What to do if significant murmur

A

Refer to paediatrician re: cardiology

CXR and ECG useful for diagnosis

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13
Q

Heart Failure in Paediatrics

A 
SOB (esp. SOBOE)
Poor feeding 
Sweating 
Recurrent chest infections
Poor weight gain
Tachypnoea
Tachycardia
Heart Murmurs and Gallops
Cardiomegaly 
Hepatomegaly 
Cool peripheries
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14
Q

Right Sided Heart Failure in Developed Countries

A

Ankle Oedema, sacral oedema and ascites

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15
Q

Causes of Heart Failure in Neonates

A

Often due to obstruction Hypoplastic Left Heart Syndrome
Critical Aortic Stenosis
Severe Coarctation
Interruption of aortic arch

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16
Q

Causes of Heart Failure in Infants

A

Obstruction due to high pulmonary blood flow
VSD
ASD
Large PDA

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17
Q

Causes of Heart Failure in Older Children

A 
Eisenmenger Syndrome (RHF)
Rheumatic Heart Disease
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18
Q

Eisenmenger Syndrome

A

Initial Left to right shunt
Pulmonary vascular resistance increases to compensate resulting in later development of right to left shunt
Typically presents in adolescence with cyanosis
Heart and lung transplant are only curative option

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19
Q

Types of Ventricular Septal Defect

A 
o Perimembraneous portion (Adjacent to Tricuspid Valve)
o Muscular (Surrounded by muscle)
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20
Q

Small VSD

A

Asymptomatic
• Loud Pansystolic Murmur (implies smaller defect); Quiet P2
• Normal ECG, CXR; Echo will identify precise anatomy of defect
• Pulmonary Hypertension is not present
• Many small VSDs close spontaneously; Murmur might disappear on follow up and Echo will be
normal; Prevention of Bacterial Endocarditis with good dental hygiene

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21
Q

Large VSD

A

– Same size, or bigger than Aortic Valve
• HF with Breathlessness, Faltering growth after 1 week and Recurrent Chest Infections
• Tachypnoea, Tachycardia, Hepatomegaly, Active Precordium, Soft PSM, or Silent (implies
large defect); Apical MDM due to increased Mitral Valve flow, Loud P2 due to increased
pulmonary arterial pressure
• ECG – V1 upright T wave indicated pulmonary HTN, Biventricular Hypertrophy by 2/12 age
• CXR – Cardiomegaly, Enlarged Pulmonary Arteries, Vascular Markings and Oedema
• Echo can identify anatomy, haemodynamic effect and Pulmonary HTN

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22
Q

Management of Large VSD

A
  • HF – Diuretics with Captopril (ACE Inhibitor), Additional calorie intake required
  • Pulmonary HTN can become irreversible in Eisenmenger Syndrome; Surgery early to prevent
  • Surgery 3 – 6/12 age to manage HF, Faltering Growth and prevent permanent lung damage
23
Q

Secundum ASD

A

Secundum is defect in centre of Atrial Septum involving Foramen Ovale

24
Q

Partial AVSD (Primum Defect)

A 
inter-Atrial
communication between bottom end of
Atrial Septum and AV valves, with
Abnormal AV valves, Tricuspid Mitral
Valve with leaky tendency
25
Q

Clinical Features of ASD

A

Asymptomatic, Recurrent Chest Infection and Wheeze, Arrhythmia for
fourth decade onwards; Signs: ESM on Upper Left Sternal Edge due to increased flow across
pulmonary valve from the L to R shunt, Fixed and widely split S2 (Often difficult to hear)
o Partial AVSD – Apical Pansystolic Murmur from AV regurgitation

26
Q

Management of Atrial Septal Defect

A

CXR – Cardiomegaly, Enlarged Pulmonary Arteries, Increased Pulmonary Vascular Markings
• ECG changes in Secundum – Partial RBBB, RAD
ECG changes in Partial AVSD
– Superior QRS Axis due to
defect where AV node is;
Displaced node conducts to
the nodes superiorly leading
to abnormal axis (AVF
negative)
• Echocardiogram will
delineate anatomy, mainstay of diagnostic investigation
• Children with significant ASD (large enough to cause RV dilatation) require treatment
• Secundum Defect – Cardiac Cath with Occlusion device; Surgery required for partial AVSD
o Typically, 3-5yrs age to prevent RHF and Arrhythmia in later life

27
Q

Patent Ductus Arteriosus

A

• In term infants, closes normally shortly after birth; Failure to close 1/12 after EDD due to defect in constrictor mechanism of duct
In preterm, presence of PDA not from congenital heart disease, but from prematurity

28
Q

Presentation of PDA

A

Continuous murmur beneath L clavicle; Continues into Diastole because Pulmonary pressures
lower than Aortic throughout entire cardiac cycle
• Increased Pulse Pressure leading to collapsing/Bounding pulse
• HF and Pulmonary HTN if large PDA defect

29
Q

Management of PDA

A

• CXR and ECG typically normal, but if large and symptomatic PDA, similar CXR and ECG to VSD
patients (Pulmonary HTN leads to upright T wave in V1, Cardiomegaly, etc)
• Duct is readily identified by Echo
• Closure recommended to abolish lifelong risk of Bacterial Endocarditis and Pul HTN
o Coil or Occlusion device by Cardiac Catheter at about 1yr
o Surgical ligation might be required

30
Q

How do right to left shunts present?

A

present with Cyanosis (Blue, Sats <94%, Collapse) usually within first
week of life; TOF or TGA

31
Q

How to diagnose cyanotic heart disease

A

• Hyperoxia Test – Infant placed in 100% oxygen for 10 minutes; if R Radial PaO2 (by gas) remains low (<15kPa), a diagnosis of cyanotic heart disease can be made if lung disease or pulmonary HTN of the newborn has been ruled out
o If PaO2 >20kPa, CHD can be ruled out

32
Q

Management of Cyanosed Neonate

A

• Airway, Breathing, Circulation; Artificial ventilation if necessary
• Prostaglandin infusion (5ng/kg/min) – Most infants with Cyanotic Heart Disease presenting in
first few days of life are duct-dependent
o SE: Apnoea, Jitteriness, Seizures, Flushing, Vasodilation, Hypotension

33
Q

Tetralogy of Fallot

A

Most common cyanotic congenital heart disease
Large VSF, Overriding Aorta (wrt Ventricular Septum),
Subpulmonary Stenosis leading to RVOT obstruction and resultant RVH due to obstruction

34
Q

Pathophysiology behind Tetralogy of Fallot

A

Superior aspect of ventricle diverts to the right when growing down to meet the inferior aspect so the two halves do not meet and as a result there is a VSD. The superior aspect of the septum creates a right ventricular outflow tract obstruction and pulls the aortic valve over creating an overarching aorta
VSD leads to high right ventricular pressures causing right ventricular hypertrophy

35
Q

Presentation of Tetralogy of Fallot

A 
Cyanosis 
Low oxygen saturations 
Murmur in post natal period 
Clubbing 
Harsh ESM left sternal edge due to pulmonary stenosis 
Soft second heart sound
36
Q

Investigation of TOF

A

CXR: Small Heart, Uptilted Apex (boot shape), Pulmonary artery bay sign, oligaemic lung fields due to reduced pulmonary blood flow
ECG: Older children-RVH-Upright T wave in V1 and absence of S wave
Echo
Catheterisation for detailed coronary anatomy

37
Q

Management of TOF

A

Initial medical management:
Very cyanosed infant: Pulmonary Shunt required, surgical placement of tube between subclavian and pulmonary artery (Modified Blalock) or RVOT Balloon Dilatation
There will be chronic pulmonary regurgitation as a result and is tolerated in childhood but will progress to RVF and is therefore repaired when features of this start to show
Surgery around 6months: VSD closure, relief of RVOT

38
Q

Hypercyanotic Spells

A

Rapid increase in Cyanosis associated with Irritability or Inconsolable crying because of Severe Hypoxia, Breathlessness and Pallor due to Tissue Acidosis
o Hypercyanotic spells might lead to MI, CVA, mortality

39
Q

Management of hypercyanotic spells

A

Self-limiting,
typically followed by a period of sleep
o If prolonged (>15 mins), prompt treatment required
o Sedation and Pain Relief (e.g. Morphine)
o Intravenous Propranolol (or another Alpha agonist) – Peripheral vasoconstrictor and relieving Subpulmonary muscular obstruction
o Intravenous fluids, Bicarbonates to correct acidosis
o Muscle Paralysis and Artificial Ventilation to reduce metabolic O2 requirement

40
Q

Transposition of the Great Arteries

A

Discordant ventricular-arterial connection; Aorta is coming from right ventricle and pulmonary artery is coming from left ventricle.
Condition not compatible with life unless blood is able to mix between circulations
o Achieved naturally through VSD, ASD and PDA and other therapy in short term

41
Q

Presentation of TGA

A

Profound, life-threatening cyanosis (typically, day 2 when PDA shunt closes leads to marked reduction in mixing); Cyanosis less severe and delayed presentation if other mixing anomalies
o S2 often loud and single; No murmur typically, but
can have Systolic Murmur from increased flow, or LVOT (Pulmonary outflow in TGA) stenosis

42
Q

Investigations in TGA

A
  • Narrow Upper Mediastinum; Egg-on-side Appearance due to AP relationship of great vessels, narrow vascular pedicle and RVH; Increased pulmonary vascular markings
  • ECG usually normal; Echo is essential for demonstrating abnormalities
43
Q

Management of TGA

A

In the sick cyanosed neonate, key is to improve mixing
o Maintaining PDA patency with Prostaglandin infusion is mandatory
o Balloon Atrial Septostomy – 20% of patients with TGA; Umbilical or Femoral Vein entry, onto Right Atrium and Foramen Ovale
• Definitive surgery – Arterial Switch, performed in first few days of life
o Pulmonary Artery and Aorta transected above valves and switched over; Coronary arteries transferred across to new Aorta

44
Q

Coarctation of the Aorta

A

Ductus tissue encircling Aorta just at point of insertion; Duct closure leads to Aorta constriction, causing severe obstruction
o Most common cause of collapse due to Left Outlet Obstruction

45
Q

Presentation of Aortic Coarctation

A

Neonates usually present with Acute Circulatory Collapse at 2-day age during duct closure
o Sick baby with severe HF
o Absent Femoral Pulses
o Severe Metabolic Acidosis

46
Q

Management of Aortic Coarctation

A

CXR might show Cardiomegaly from HF and shock; ECG typically normal
• Resuscitation (ABC), Prostaglandin infusion at earliest opportunity, referral made to cardiac centre for early surgical repair

47
Q

Causes of Ejection Systolic Murmurs

A

Aortic stenosis: Aortic area, carotid radiation
Pulmonary stenosis: Pulmonary area, radiation to back
ASD: Pulmonary area, split S2
ToF: Left Sternal Edge

48
Q

Causes of Pan Systolic Murmurs

A

VSD: Tricuspid Area
Mitral Regurgitation: Mitral area, radiation to axilla
Partial AVSD: Mitral area

49
Q

Causes of Continuous Murmurs

A

Venous hum: below clavicle, disappears when occluded
PDA: Below left clavicle, radiation to back
Coarctation: Loudest at left lower sternal edge

50
Q

Kawasaki’s Disease

A

Systemic vasculitis, unknown aetiology

• Typically, 6/12 to 4yrs, peaks 1yr; Uncommon (9 in 100,000); More common in Japanese and Black-Caribbean populations

51
Q

Diagnosis of Kawasaki

A

Clinical Diagnosis – Fever >5/7 difficult to control, plus 4/5 of:
o Conjunctivitis, Mucous Membrane changes (Pharyngeal injection, Red dry cracked lips, Strawberry Tongue), Cervical LNA, Polymorphic rash and Extremities changes (Red oedematous palms and soles followed by peeling of fingers and toes)
o Incomplete presentation can occur especially in infants; High index suspicion
•

52
Q

Investigation of Kawasaki

A

High Inflammatory markers, Platelet count
• Coronary arteries affected 1/3 of children within first 6/52 – Can lead to aneurysm, narrowing from Scar Formation, Ischaemia and Sudden Death
• Echo – Pericardial Effusion, Myocardial disease (Poor Contractility), Endocardial disease (Valve regurgitation) or Coronary Disease with Aneurysm (which can be >8mm diameter)
o Angio or MRA if coronary arteries abnormal

53
Q

Management of Kawasaki’s

A

IV Ig within first 10/7 lowers risk of Aneurysm; High-dose Aspirin to reduce risk of thrombosis; lower dose when fever breaks and continued until Echo at 6/52
• Second dose of IV Ig sometimes required if recurrent fever despite treatment
• Persistent inflammation and fever – Corticosteroids, Infliximab, Ciclosporin etc

Paediatrics STG (17 decks)

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