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Paediatrics > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the most common acyanotic congenital heart diseases?

A
  • Ventricular septal defects
  • Atrial septal defects
  • Patent ductus arteriosus
  • Coarctation of the aorta
  • Aortic valve stenosis
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2
Q

What is the most common congenital heart disease type?

A

Ventricular septal defects (accounts for ~30%)

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3
Q

What are the most common cyanotic congenital heart diseases?

A
  • Tetralogy of Fallot
  • Transposition of the great arteries
  • Tricuspid atresia
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4
Q

What is the difference between cyanotic and acyanotic heart diseases?

A
  • Cyanotic = heart defects that reduce the amount of oxygen delivered to the rest of the body
  • Acyanotic = heart defects where blood contains sufficient oxygen but is pumped throughout the body abnormally
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5
Q

What is a VSD?

A

Hole in the septum separating the ventricles of the heart

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6
Q

What is the murmur associated with VSDs?

A

Loud, harsh pansystolic murmur, loudest at the left lower sternal edge

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6
Q

What is the pathophysiology of VSDs?

A

Blood is shunted from the left to the right ventricle, this:
- Increases pressure on the right hand side of the heart
- Increases load delivered to the left side (more blood is pumped to the lungs and returned to the left side)

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7
Q

What is Eisenmenger’s syndrome?

A
  • Due to prolonged pulmonary hypertension from left to right shunt
  • Right ventricular hypertrophy and increased right ventricular pressure eventually exceeding the left ventricle and reversing the shunt
  • Results in cyanosis and clubbing
  • Indication for heart and lung transplant
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8
Q

How are VSDs classified?

A

Congenital and acquired (post MI impacting the septum)

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9
Q

What are congenital VSDs associated with?

A

Chromosomal disorders:
- Down’s syndrome
- Edward’s syndrome
- Patau syndrome
- Cri-du-chat syndrome

Congenital infections

Acquired causes
- Post-MI affecting the septum

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10
Q

When can VSDs be detected in utero?

A

During the routine 20 week scan

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11
Q

What are the post-natal presentations of VSDs?

A

Failure to thrive
Features of heart failure:
- Hepatomegaly
- Tachypnoea
- Tachycardia
- Pallor
Murmur

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12
Q

What are the complications of VSDs?

A
  • Aortic regurg (poorly supported right coronary cusp resulting in cusp prolapse)
  • Infective endocarditis
  • Eisenmenger’s syndrome
  • Right heart failure
  • Pulmonary hypertension
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13
Q

What would ECG demonstrate in VSD?

A
  • Left ventricular hypertrophy
  • P pulmonale
  • Biventricular hypertrophy
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14
Q

Which investigation is used to definitively diagnose VSDs?

A

Transthoracic echocardiogram

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15
Q

What is the management of VSDs?

A

Small VSDs that are asymptomatic usually close spontaneously and require simple monitoring

Moderate - large VSDs usually result in some degree of heart failure in the first few months:
- Nutritional support
- Medication for heart failure eg. diuretics
- Surgical closure of defect

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16
Q

Which is the most likely congenital heart defect to be found in adulthood?

A

Atrial septal defects

50% of patients are dead at 50 years

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17
Q

What are the three types of ASD?

A
  • Ostium secundum (defect in septum secundum)
  • Ostium primum (defect in septum primum)
  • Patent ductus arteriosus

Ostium secundum more common

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18
Q

What can play a role in ASD development?

A
  • Maternal alcohol consumption
  • Rubella infection during pregnancy
  • Maternal diabetes
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19
Q

What are the general features of ASDs?

A
  • Ejection systolic murmur, fixed splitting of S2
  • Embolism may pass from venous system to the left side of the heart causing a stroke
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20
Q

What are the features of ostium secundum ASD?

A
  • Associated with Holt-Oram syndrome (tri-phalangeal thumbs)
  • ECG: RBBB with RAD
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21
Q

What are the features of ostium primum?

A
  • Present earlier than ostium secundum defects
  • Associated with abnormal AV valves
  • ECG: RBBB with LAD, prolonged PR interval
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22
Q

How are ASDs usually detected?

A

Often an incidental finding of ejection systolic murmur, loudest lower-left sternal edge due to flow of blood through pulmonary valve

  • Patients can present as decompensated in heart failure
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23
Q

What is the management of ASDs?

A

Management depends on severity:
- Most managed conservatively
- Surgical closure may be necessary for larger defects (or those causing significant symptoms/ complications)
- Routine ECGs used for monitoring ASDs

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24
Q

What is patent ductus arteriosus?

A

Connection between the pulmonary trunk and descending aorta, generally classed as acyanotic lasting beyond the first four weeks after birth

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25
Q

When does the ductus arteriosus usually close?

A

With the first breaths due to increased pulmonary flow which enhances prostaglandins clearance

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26
Q

Which factors contribute to persistance of patent ductus arteriosus?

A
  • Prematurity
  • Genetic predispositions
  • Babies born at high altitude
  • Maternal rubella in the first trimester
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27
Q

What are the clinical features of patent ductus arteriosus?

A
  • Left subclavicular thrill
  • Continuous ‘machinery’ murmur
  • Large volume, bounding, collapsing pulse
  • Wide pulse pressure
  • Heaving apex beat
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28
Q

What is the definitive investigation for patent ductus arteriosus diagnosis?

A

Echocardiography

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29
Q

When is management of patent ductus arteriosus required?

A

If the infant presents with symptoms

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30
Q

What is the medical treatment of patent ductus arteriosus?

A

NSAIDs (indomethacin or ibuprofen)
- Inhibits prostaglandin synthesis
- Closes the connection in the majority of cases

(surgical ligation indicated in about 8% of cases)

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31
Q

When would prostaglandin E1 be given in patent ductus arteriosus?

A

If it’s associated with another congenital heart defect amenable to surgery, prostaglandin E1 is useful to keep the duct open until after surgical repair

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32
Q

When does tetralogy of fallot usually present?

A

1-2 months

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33
Q

What are the four characteristic findings of tetralogy of fallot (TOF)?

A
  • Overriding aorta (aortic opening directly in line with the VSD rather than the left ventricle)
  • VSD
  • Right ventricular outflow tract obstruction (caused by congenital valvular pathology, overriding aorta and RV hypertrophy contribute)
  • Right ventricular hypertrophy (due to increased outflow resistance from the pulmonary stenosis)
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34
Q

What determines the degree of cyanosis and clinical severity in TOF?

A

The severity of the right ventricular outflow tract obstruction

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35
Q

What factors have been implicated in increasing the risk of TOF?

A
  • Genetic factors
  • Maternal use of alcohol
  • Maternal use of drugs
  • Diabetes mellitus
  • Maternal age >40
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36
Q

What are the clinical features of TOF?

A
  • Episodic hypercyanotic ‘tet’ spells, due to near occlusion of the RV outflow tract leading to right to left shunt
  • Left to right shunt
  • Ejection systolic murmur (pulmonary stenosis, VSD usually doesn’t cause a murmur)
  • Right sided aortic arch (25% of patients)
  • Chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy
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37
Q

What are the features of tet spells?

A
  • Tachypnoea
  • Severe cyanosis that can result in loss of consciousness
  • Typically occur when the infant is upset, in pain or has a fever
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38
Q

What are the investigations for TOF?

A

1st line
- Echocardiography: confirms diganosis

Other
- Cardiac catheterization: may be needed to delineate coronary artery anatomy and assess degree of pulmonary vascular disease

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39
Q

What are the aims of treatment in TOF?

A
  • Correction of the right ventricular outflow tract obstruction
  • Closure of the ventricular septal defect
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40
Q

What is the management in an emergency situation like a tet spell?

A
  • Positioning the infant on their back and flexing the knees
  • Oxygen administration
  • Prophylactic use of propranolol is practised in some centres to reduce infundibular spasm
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41
Q

What are the anatomical changes in transposition of the great arteries (TGA)?

A
  • Pulmonary trunk leaves the left ventricle
  • Aorta leaves the right ventricle

A closed circuit is created meaning oxygenated blood leaving the lungs is never delivered to respiring tissues and deoxygenated blood from tissues is circulated around the body

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42
Q

What is the aetiology of TGA?

A
  • Normal heart development includes spiraling of the aortopulmonary septum
  • TGA spiraling fails to occur resulting in two parallel and separate circulations

Shunts remaining open after birth (foramen ovale, ductus arteriosus) increase the chance of survival

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43
Q

What is associated with a higher risk of TGA?

A

Maternal diabetes mellitus

44
Q

What are the clinical features of TGA?

A
  • Cyanosis at birth
  • Tachypnoea
  • Loud single S2
  • Prominent right ventricular impulse
  • Poor feeding
  • Low weight gain
  • Egg on side appearance on chest x-ray
45
Q

What is the management of TGA?

A
  • Maintenance of the shunts using prostaglandins (prostaglandin E1 infusion)
  • Definitive managment is an arterial switch operation performed within the first few weeks of life
  • Regular monitoring to ensure proper heart function and manage complications eg. arrhythmias or heart failure
46
Q

What is pulmonary/ tricuspid atresia?

A

Lack of formation of the tricuspid/ pulmonary valves meaning blood strongly regurgitates back into the right/ left atria and doesn’t travel to the lungs/ systemic circulation

47
Q

What increases the chance of survival in babies born with tricuspid/ pulmonary atresia?

A

Open shunts (ductus arteriosus/ foramen ovale/ ASDs)

48
Q

What is the management of tricuspid/ pulmonary atresia?

A
  • Prostaglandin infusion (prostaglandin E1) to maintain patency of the shunts
  • Surgical treatment called a modified Blalock-Taussig (BT) shunt
49
Q

What is Kawasaki disease?

A

A systemic vasculitis with unknown origin:
- Infectious mediated
- Autoimmune mediated
- Genetic predisposition

50
Q

Which vessels are most likely to be affected in Kawasaki?

A

Coronary arteries

51
Q

What is the pathophysiology of Kawasaki disease cardiac complications?

A

Endothelial cells are attacked and destroyed exposing the tunica media of blood vessels:
- Increases the formation of blood clots, reducing blood flow through the coronary arteries and leading to ischaemia and potentially MI
- Increases fibrin deposition, reducing vessel elasticity and therefore reducing vessel stretching under pressure leading to aneurysm formation
- Increases fibrin deposition which increases vessel thickening, reducing the lumen and therefore reducing blood flow to tissue resulting in ischaemia and potentially MI

52
Q

What are the symptoms of Kawasaki disease?

A

CRASH and burn
- Conjunctivities with limbus sparing
- Rash (starts polymorphous and desquamates)
- Adenitis (usually cervical)
- Strawberry tongue and dry lips
- Hands and feet swollen and covered in rash, red palms and soles which will eventually desquamate
- Burn - usually fever for > 5 days characteristically resistant to antipyretics

53
Q

What is Reye’s syndrome?

A

A complication of aspirin use in children:
- Encephalopathy
- Liver failure

54
Q

What are the investigations for Kawasaki disease?

A

Bedside
- ENT examination demonstrating strawberry tongue
- Urinalysis: mononuclear white blood cells and no bacteria

Bloods
- Anaemia
- Increased immature WBCs
- Increased CRP&ESR
- Increased liver enzymes
- Increased platelet count

Imaging
- Echocardiogram to check for coronary aneurysms and any damage to the cardiac muscle

55
Q

What is the management of Kawasaki’s?

A
  • High dose aspirin (80-100mg/kg) until the child is afebrile for 48-72 hours, maintenance dose (3-5mg/kg per day) for 6-8 weeks after disease onset
  • IVIG
  • Regular echocardiograms for ongoing surveillance of coronary artery aneurysms (recovery of acute episodes can take several weeks)
56
Q

What is the triad in shaken baby syndrome?

A
  • Retinal haemorrhages
  • Subdural haematoma (bridging cerebral veins are fragile in infants and can be torn when the baby is shaken)
  • Encephalopathy
57
Q

What is the most common cause of subarachnoid haemorrhage?

A

Traumatic

58
Q

What is the name of non-trauma caused SAH?

A

Spontaneous SAH

59
Q

What are the causes of spontaneous SAH?

A
  • Intracranial aneurysm (berry aneurysm) - 85% of cases
  • AV malformation
  • Pituitary apoplexy (bleeding in the pituitary that can leak into the subarachnoid space)
  • Mycotic (infective) aneurysms
60
Q

What conditions are berry aneurysms associated with?

A
  • Hypertension
  • Adult polycystic kidney disease
  • Ehlers-Danlos syndrome
  • Coarctation of the aorta
61
Q

What are the clinical features of SAH?

A
  • Headache (sudden onset, thunderclap, peaking within 1-5 minutes)
  • Nausea and vomiting
  • Meningism
  • Coma
  • Seizures
  • ST elevation may be seen on ECG (autonomic neural stimulation, elevated levels of circulating catecholamines)
62
Q

What is the first line investigation for SAH?

A

Non-contrast CT

63
Q

When would a lumbar puncture not be considered in suspected SAH?

A

If CT head done within 6 hours of symptom onset is normal, don’t do a LP and consider an alternative diagnosis

64
Q

What should be done if CT head is done more than 6 hours after symptom onset in SAH and is normal?

A
  • Lumbar puncture performed at least 12 hours following onset of symptoms
65
Q

Why should a lumbar puncture in suspected SAH only be performed 12 hours after the onset of symptoms?

A
  • Allows for the development of xanthochromia (breakdown of RBCs) which helps to distinguish true SAH from traumatic tap
  • LP will also show normal or raised opening pressure
66
Q

What should be done if the CT shows evidence of SAH?

A
  • Referral to neurosurgery made

Investigations to identify a causative pathology that needs treatment (if spontaneous):
- CT intracranial angiogram (aneurysm or AVM)
- +/- Digital subtraction angiogram

67
Q

What’s the management of aneurysmal SAH?

A

Supportive
- Bed rest
- Analgesia
- VTE prophylaxis
- Discontinuation of antithrombotics

Vasospasm is prevented using a course of oral nimodipine

Intracranial aneurysms require prompt intervention due to risk of rebleeding, within 24 hours
- Mostly treated with a coil by interventional neuroradiologists, minority require craniotomy and clipping

68
Q

What are the complications of SAH?

A
  • Re-bleeding
  • Hydrocephalus
  • Vasospasm
  • Hyponatraemia (most typically due to SIADH)
  • Seizures
69
Q

What are the important predictive factors for SAH?

A
  • Conscious level on admission
  • Age
  • Amount of blood visible on CT
70
Q

What is hydrocephalus?

A

A neurological disorder caused by excessive accumulation of CSF in the ventricular system of the brain increasing pressure on the parenchyma

71
Q

What are the causes of hydrocephalus in infants?

A
  • Congenital malformations
  • Haemorrhage

Affects 1-2/1000 live births

72
Q

How is hydrocephalus categorised?

A
  • Non-communicating
  • Communicating
73
Q

What is non-communicating hydrocephalus?

A

Obstruction in the ventricular system disrupting the flow of CSF, resulting from:
- Congenital malformations (stenosis of the aqueduct, Chiari malformation)
- Tumour or vascular malformation in the posterior fossa
- Intraventricular haemorrhage (premature infants at risk)

74
Q

What is communicating hydrocephalus?

A

CSF isn’t adequately reabsorbed due to damage to the arachnoid villi, resulting from:
- Meningitis
- Subarachnoid haemorrhage

75
Q

How does hydrocephalus present in infants?

A
  • Enlarged head circumference
  • Bulging anterior fontanelle
  • Distention of scalp veins
  • Sunsetting of the eyes (late sign where the upward gaze is limited due to raised ICP)
76
Q

What are the main investigations for infantile hydrocephalus?

A
  • Cranial ultrasound through the anterior fontanelle (first few months of life when the fontanelle is still open)
  • MRI or CT of the brain, assessing ventricular size and identifying underlying causes
77
Q

What is the management of hydrocephalus?

A
  • Ventriculoperitoneal shunt (diverts the excess CSF from the brain to the abdominal cavity where it can be reabsorbed)
  • Counselling about potential complications including signs of a blocked or infected shunt which require immediate medical attention
78
Q

Where should children with ASD be referred?

A

Paeds cardiologist

79
Q

When is closure of ASD deferred until?

A

2 years of age in asymptomatic patients

80
Q

What are the two approaches to ASD closure?

A

Transcatheter closure
- Ostium secundum (lower complication rates, shorter hospital stay)

Open heart surgery
- Primum ASD; direct repair

81
Q

What are the indications for closure in ASD?

A
  • Right heart enlargement
  • Symptomatic pulmonary over circulation
  • Evidence of left-to-right shunting (pulmonary:systemic blood flow >1:1.5)
82
Q

What is the gold standard investigation for aortic stenosis diagnosis?

A

Echocardiogram

83
Q

What is the follow up for aortic stenosis?

A
  • Paeds cardiology review
  • Echo
  • ECG
  • Exercise testing
84
Q

What are the management options for aortic stenosis?

A

Percutaneous balloon aortic valvuloplasty
- Commonly treatment of choice
- Aortic valve leaflets in children are easier than adults to dilate

Transcatheter aortic valve replacement or surgical valvotomy
- 2nd line

85
Q

What is the most common site for coarctation of the aorta?

A

Distal to the left subclavian artery, usually at the origin of the ductus arteriosus

86
Q

When does coarctation of the aorta present?

A

48 hours old when the ductus arteriosus closes

87
Q

Management of coarctation of the aorta?

A

Prostaglandin E1 infusion
- Maintain ductal patency

Surgical repair
- End-to-end anastomosis or arch reconstruction with patch placement or bypass graft

Older patients might need stent insertion or surgical resection

88
Q

What is the order of management for congenital cyanotic heart disease?

A
  1. Stabilise airway and breathing
  2. Circulation
  3. Maintain duct patency (presenting in 1st week of life = duct dependent), prostaglandin E1 infusion
  4. Check blood glucose regularly
89
Q

What is the airway management for congenital cyanotic heart disease?

A
  • Intubate if needed
  • Consider hyperoxia test: 10 mins 100% O2, if SpO2 persistently low likely congenital cyanotic heart disease
  • Supplemental O2 (sats 75-85%)
90
Q

Circulation management for congenital cyanotic heart disease?

A
  • 2 IV cannulae
  • 10ml/kg crystalloid bolus (max 30ml/kg)
  • Adrenaline if resistant hypotension
91
Q

What are the side effects of prostaglandin?

A
  • Apnoea
  • Hypoglycaemia
  • Seizures
  • Vasodilation
  • Hypotension
  • Fever
92
Q

What are the 6 aims of managing heart failure in a child?

A
  • Reduce preload
  • Enhance cardiac contractility
  • Reduce afterload
  • Improve O2 delivery
  • Enhance nutrition
  • Exercise and physical activity
93
Q

How is preload reduced in heart failure?

A
  • Diuretics (eg. furosemide)
  • (Rare) venous dilators (eg. nitroglycerin)
94
Q

How is cardiac contractility enhanced in heart failure?

A
  • IV agents (eg. dopamine)
  • Other: digoxin, dobutamine, adrenaline
95
Q

How is after load reduced in heart failure?

A
  • Oral ACE inhibitors
  • IV agents (eg. hydralazine, nitroprusside, alprostadil)
96
Q

How is oxygen delivery improved in heart failure?

A

Beta blockers

97
Q

How is nutrition enhanced in heart failure?

A

Intermittent/ continuous NG/ gastrostomy tube feeds needed

98
Q

Why is closure of PDA recommended?

A

Abolish risks of
- Bacterial endocarditis
- Pulmonary vascular disease

99
Q

Management PDA?

A

Cyanotic condition dependent on PDA:
- Prostaglandins (maintain patency)

Closure of duct:
- IV indomethacin (1st line)
- Prostacyclin synthetase inhibitor
- Ibuprofen (prem/ LBW)

100
Q

What is the management of PDA if pharmacological interventions are unsuccessful?

A
  • Surgical ligation
  • Percutaneous catheter device closure

Symptomatic, or heart failure treated earlier

101
Q

What is the definitive management of TOF?

A

Total surgical repair by open heart surgery
- Performed 4 months of age onwards
- Closing VSD and relieving right ventricular outflow tract obstruction

102
Q

What are the intermediary managements for TOF?

A
  • Prostaglandin E1 infusion
  • Blalock-Taussig shunt (artificial tube between subclavian and pulmonary artery)
103
Q

What is the management of tet spells?

A
  1. Knee to chest position
  2. Supplementray O2
  3. IV fluids
  4. Beta blockers (relax right ventricle and improve pulmonary flow)
  5. Morphine (decreased resp drive)
  6. Sodium bicarb (metabolic acidosis)
  7. Phenylephrine infusion (increase vascular resistance)
104
Q

What is the supportive management of TGA?

A
  • Maintain body temperature
  • Correct acidosis and hypoglycamia
  • Prostaglandin E1
  • Balloon atrial septostomy (creates a large ASD in the foramen ovale, bolus of heparin given before
105
Q

What is the definitive management of TGA?

A

Arterial switch (first two weeks of life)
- Cardiopulmonary bypass
- Coronary arteries also transferred to new aorta

106
Q

What is the first line treatment for VSD?

A

Observation

Whilst defect is present, good dental hygiene (prevent IE)

Prophylactic amoxicillin for patients at high risk of developing endocarditis

107
Q

What is the surgical correction for large VSDs?

A

Either:
- Transvenous catheter closure through femoral vein
- Open heart

Paediatrics (16 decks)

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