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Phase 3a - Paediactrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the most common form of heart defect?

A

Ventricular Septal Defect

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2
Q

Pathophysiology of VSD

A

A congenital hole in the septum between the ventricles. Blood typically flows from left-right through the hole as there is increased pressure in the left ventricles therefore they remain acyanotic If severe, can cause pulmonary HTN as there is extra blood flow in the pulmonary vessels If this continues, pressure in the right heart may become higher than the left causing a right to left shunt: cyanosis - this is Eisenmenger’s syndrome

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3
Q

VSD causes a ____ to ____ shunt.

A

Causes a left to right shunt

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4
Q

Associated conditions with VSD

A

Down’s and Turner’s Syndrome

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5
Q

Moderate VSD can cause

A

Enlarged atria and ventricles can lead to pulmonary HTN and congestive heart failure

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6
Q

Severe VSD can cause

A

Severe pulmonary HTN and early onset heart failure

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7
Q

Risk factors for VSD

A
  • Premature birth - Certain genetic conditions such as Down’s syndrome, Edward’s, Patau - Family history of congenital heart defects
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8
Q

Symptoms of VSD

A

Often can by symptomless but can have: Poor feeding
- Tachypnoea
- Dyspnoea
- Failure to thrive

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9
Q

Signs of VSD

A

Pansystolic murmur at the lower left sternal border + High resp rate / SOB

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10
Q

3 forms of investigations for VSD

A

Echo + ECG + Chest X-ray

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11
Q

Which Ix is used to confirm dx of VSD?

A

Echo

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12
Q

What might you see on X-ray for VSD?

A

Cardiomegaly

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13
Q

Initally you monitor the VSD - why?

A

Small VSDs often close spontaneously

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14
Q

Treatment of VSD

A

Diuretics + ACEi+ Surgical Repair (for large VSDs)

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15
Q

Tx: Diuretics - what for?

A

to relieve pulmonary congestion

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16
Q

Tx: ACEi - what for?

A

to reduce systemic pressure

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17
Q

Name 3 complications of VSD

A

Eisenmengers - Endocarditis - Heart failure

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18
Q

What is Eisenmenger’s Syndrome?

A

-Left to right shunt causes pulmonary HTN -Right sided heart pressure now exceeds left sided heart pressure leading to an irreversible cyanotic shunt -Management is heart+lung transplant

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19
Q

Define Atrial Septal Defect (ASD)

A

Defect in the septum between the 2 atria causing a left to right shunt due to the higher pressure in the left atria

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20
Q

Pathophysiology of ASD

A

A congenital hole in the septum between the atria. This causes a left to right shunt due to higher pressure in the left atria compared to the right and so blood is still oxygenated and so there is no cyanosis However, over time this can cause strain on the right heart leading to right heart failure and pulmonary HTN This can again lead to Eisenmenger’s syndrome

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21
Q

Aetiology of ASD

A

Maternal smoking in 1st trimester - Family History of CHD - Maternal diabetes - Maternal rubella

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22
Q

Symptoms of ASD

A

Tachypnoea - Poor weight gain - Recurrent chest infections

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23
Q

Signs of VSD

A

Soft, systolic ejection murmur heard in 2nd intercostal space - Wide, fixed split S2 sound

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24
Q

Ix for ASD

A

ECG + Echo

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25
Q

Managment of ASD

A

If small, can be managed conservatively and will close within 12 months of birth - Surgical closure, usually if ASD >1cm

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26
Q

Name 4 complications of ASD

A

Stroke from DVT - Atrial fibrillation - Pulmonary HTN - Eisenmenger’s syndrome

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27
Q

What is the most common cyanotic congenital heart disease?

A

Tetralogy of Fallot

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28
Q

What 4 conditions are in the tetralogy of fallot

A
  • Overriding aorta - Large VSD - Pulmonary stenosis - Right ventricular hypertrophy
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29
Q

Epidemiology of Tetralogy of Fallot

A

More common in males - Rubella - Increased age of the mother (>40)

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30
Q

Pathophysiology of Tetralogy of Fallot

A

-VSD means blood will flow between the ventricles -Overriding aorta essentially means the aortic valve is placed more to the right than normal which means when the right ventricle contracts, some of the blood enters the aorta rather than all going into the pulmonary artery -Pulmonary stenosis means there is greater resistance against the flow of blood which pushes it through the VSD and into the aorta i.e. shunts from right to left causing cyanosis -Increased strain of the right heart causes right ventricular hypertrophy -These 4 features cause a right to left shunt meaning blood bypasses the lungs and does not become oxygenated this causes cyanosis

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31
Q

Risk Factors for Tetralogy of Fallot

A

-Rubella infection -Increased maternal age -Alcohol consumption in pregnancy -Diabetic mother

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32
Q

Mild Tetralogy of Fallot

A

: asymptomatic but as heart grows, develops cyanosis aged 1-3 year

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33
Q

Moderate Tetralogy of Fallot

A

Cyanosis and respiratory distress in the first few months of life

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34
Q

Extreme Tetralogy of Fallot

A

Often detected on antenatal scan, present with cyanosis in first few hours of life

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35
Q

Symptoms of Tetralogy of Fallot

A

Irritability, Poor feeding, Poor weight gain

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36
Q

Signs of Tetralogy of Fallot

A

Cyanosis, Clubbing, Ejection systolic murmur in pulmonary region (caused by pulmonary stenosis), Tet spells

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37
Q

Ix for Tetralogy of Fallot

A

CXR, MRI/Cardiac Catheter, Echo

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38
Q

Finding on CXR for Tetralogy of Fallot

A

Boot shaped heart

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39
Q

Tx for Tetralogy of Fallot

A

Prostaglandin infusion PGE1 to maintain ductus arteriosus - Beta blockers - Morphine to reduce respiratory drive - Surgical: repair under bypass 3 months - 4 years but needs ICU post op

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40
Q

Complications of Tetralogy of Fallot

A

Pulmonary regurgitation - Lifelong follow up

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41
Q

Transposition of the great arteries

A

Aorta rises from right ventricle and pulmonary artery from left ventricle

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42
Q

Epidemiology of Transposition of the great arteries

A

More common in males - Mum>40 - Rubella - Maternal diabetes - Alcohol consumption

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43
Q

Pathophysiology of Transposition of the great arteries

A

-The aorta and the pulmonary artery is essentially switched meaning right ventricle pumps blood into the aorta and left ventricle pumps blood into the pulmonary artery -During pregnancy, this does not affect development however upon birth, this is life threatening as the baby will be cyanosed -Survival depends on the presence of a PDA, VSD or ASD to allow blood to mix

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44
Q

Symptoms of Transposition of the great arteries

A

Sometimes PD/VSD can make symptoms however within a few weeks they will develop respiratory distress, poor feeding etc

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45
Q

Signs of Transposition of the great arteries

A

Cyanosis in the first 24 hours of life, Right ventricular heave, Loud S2 heart sound, Systolic murmur if VSD present

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46
Q

Ix/Dx for Transposition of the great arteries

A

Low SATS, Echo, CXR, Metabolic acidosis

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47
Q

Findings on CXR for Transposition of the great arteries

A

‘egg on a string’ due to narrowed mediastinum and cardiomegaly

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48
Q

Tx of Transposition of the great arteries

A

PGE1 infusion to ensure PDA and mixing of blood + Surgical correction before 4 weeks ;-Prostaglandin infusion to maintain PDA and mixing of blood -Definitive management is surgical correction

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49
Q

Patent ductus arteriosus

A

Persistent connection between the aorta and pulmonary artery - Normal in utero but usually closes within first 10-15 minutes of life - Left to right shunt. -Failure of the closure of the ductus arteriosus after birth -Initially acyanotic, if uncorrected can develop in lower extremity cyanosis

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50
Q

Pathophysiology of PDA

A

A persistent connection between the aorta and the pulmonary artery causing a left to right shunt. Normally, this closes within the first few weeks of life however sometimes this can fail to close

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51
Q

Risk factors of Patent ductus arteriosus

A

Female - Prematurity - Maternal rubella

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52
Q

Symptoms of Patent ductus arteriosus

A

Respiratory distress - Apnoea - Tachypnoea - Tachycardia

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53
Q

Signs of Patent ductus arteriosus

A

Continuous machinery murmur at the left sternal edge

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54
Q

Ix for Patent ductus arteriosus

A
  • Echo - ECG/CXR
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55
Q

Management of Patent ductus arteriosus

A

Cardiac catheterisation to close around 1 years old or sooner in more severe cases - Premature infants: Indomethacin or Ibuprofen inhibits prostaglandin and stimulates closure

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56
Q

Why would a stroke be more likely in patients with atrial septal defects?

A

It is worth remembering atrial septal defects as a cause of stroke in patients with a DVT. Normally when patients have a DVT and this becomes an embolus, the clot travels to the right side of the heart, enters the lungs and becomes a pulmonary embolism. In patients with an ASD the clot is able to travel from the right atrium to the left atrium across the ASD. This means the clot can travel to the left ventricle, aorta and up to the brain, causing a large stroke.

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57
Q

Pulmonary Stenosis is associated with ___

A

Noonan’s Syndrome

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58
Q

Which conditions are Acyanotic Heart Diseases?

A

VSD, PDA, ASD, Pulmonary Stenosis, Aortic Stenosis

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59
Q

Which conditions are Cyanotic Heart Diseases?

A

TGA + Tricuspid Atresia

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60
Q

Tricuspid Atresia

A

-Complete absence of the tricuspid valve.-Hypoplastic/absent RV. -The heart doesn’t finish developing.

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61
Q

Symptoms of Tricuspid Atresia

A

-Progressive cyanosis. -Poor feeding.

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62
Q

Signs of Tricuspid Atresia

A

Holosystolic murmur

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63
Q

Ix for Tricuspid Atresia

A

Antenatal scan + foetal Echo + CXR + ECG

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64
Q

Definitive Ix for Tricuspid Atresia

A

Echocardiogram

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65
Q

Inital management for Tricuspid Atresia

A

IV Prostaglandin E1

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66
Q

Surgical Management of Tricuspid Atresia

A

1.Blalock-Taussing Shunt.2.Glenn Shunt or Hemi-Fontan Procedure. 3.Fontan Procedure.

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67
Q

What is paediatric heart failure?

A

Paediatric heart failure occurs when the heart cannot pump enough blood to meet the metabolic demands of the body, leading to symptoms such as poor growth, fatigue, and respiratory distress.

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68
Q

Paediatric heart failure occurs when the heart cannot pump enough blood to meet the ________ demands of the body

A

Metabolic

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69
Q

What are the common causes of heart failure in children?

A

Structural abnormalities: Congenital heart defects (e.g., VSD, ASD, PDA, coarctation of the aorta).
Cardiomyopathy: Dilated or hypertrophic cardiomyopathy.
Myocarditis: Viral infections causing inflammation of the heart.
Arrhythmias: Tachycardia or bradycardia.
High-output failure: Severe anaemia or sepsis.

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70
Q

Common structural causes of paediatric heart failure include congenital heart defects such as ________ or atrial septal defect (ASD).

A

Ventricular septal defect (VSD)

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71
Q

What are the signs and symptoms of heart failure in infants?

A

Poor feeding.
Failure to thrive or weight loss.
Tachypnoea and respiratory distress.
Sweating, especially during feeds.
Irritability and lethargy.

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72
Q

Signs of heart failure in infants include ________ to thrive, tachypnoea, and sweating during feeds

A

Failure

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73
Q

What are the signs and symptoms of heart failure in older children?

A

Fatigue.
Exercise intolerance.
Breathlessness on exertion.
Peripheral oedema.
Hepatomegaly.

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74
Q

In older children, heart failure may present with ________ intolerance and peripheral oedema.

A

Exercise

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75
Q

What clinical signs indicate heart failure in paediatric patients?

A

Tachycardia and tachypnoea.
Gallop rhythm (S3 or S4).
Hepatomegaly.
Peripheral oedema.
Raised jugular venous pressure (JVP) in older children.

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76
Q

Hepatomegaly and a ________ rhythm (S3 or S4) are clinical signs of paediatric heart failure.

A

Gallop

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77
Q

What investigations are performed to diagnose heart failure in children?

A

Blood tests: Full blood count, electrolytes, BNP.
Chest X-ray: Cardiomegaly, pulmonary congestion.
ECG: Signs of hypertrophy, arrhythmias.
Echocardiogram: Structural abnormalities, ventricular function.
MRI: Detailed cardiac imaging if required.

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78
Q

A ________ is the gold standard for assessing structural abnormalities and ventricular function in paediatric heart failure.

A

Echocardiogram

79
Q

What are the general management principles for paediatric heart failure?

A

Treat the underlying cause: Correct congenital defects or treat infections.
Optimise preload: Diuretics (e.g., furosemide).
Reduce afterload: ACE inhibitors (e.g., captopril).
Improve contractility: Inotropes (e.g., dobutamine in acute settings).
Nutritional support: High-calorie feeds in infants.

80
Q

________ inhibitors (e.g., captopril) are used to reduce afterload in paediatric heart failure.

A

ACE

81
Q

How is acute decompensated heart failure managed in children?

A

Oxygen therapy for respiratory distress.
Intravenous diuretics (e.g., furosemide).
Inotropes for severe cases.
Correction of metabolic derangements (e.g., acidosis, electrolyte imbalances).

82
Q

In acute decompensated heart failure, ________ diuretics such as furosemide are administered.

A

Intravenous

83
Q

What medications are commonly used in chronic paediatric heart failure?

A

Diuretics: Furosemide, spironolactone.
ACE inhibitors: Captopril, enalapril.
Beta-blockers: Carvedilol.
Digoxin: Improves contractility in selected cases.

84
Q

________ (e.g., digoxin) is used to improve cardiac contractility in paediatric heart failure.

A

Inotropes

85
Q

What are the complications of untreated heart failure in children?

A

Growth failure.
Recurrent respiratory infections.
Pulmonary hypertension.
Multiorgan failure in severe cases.

86
Q

Untreated paediatric heart failure can lead to ________ failure and pulmonary hypertension.

A

Multiorgan

87
Q

What is the prognosis for paediatric heart failure?

A

The prognosis depends on the underlying cause. Congenital heart defects corrected early may lead to good outcomes, whereas cardiomyopathies may have a poorer prognosis.

88
Q

The prognosis for paediatric heart failure depends on the underlying ________.

A

Cause

89
Q

What is cyanotic heart disease?

A

Cyanotic heart disease refers to congenital heart defects that cause a right-to-left shunt of blood, leading to reduced oxygenation and cyanosis.

90
Q

Cyanotic heart disease involves a ________-to-left shunt, causing reduced oxygenation of blood.

A

Right

91
Q

What are the main types of cyanotic heart disease?

A

Tetralogy of Fallot (TOF).
Transposition of the Great Arteries (TGA).
Tricuspid Atresia.
Total Anomalous Pulmonary Venous Return (TAPVR).
Hypoplastic Left Heart Syndrome (HLHS).

92
Q

Examples of cyanotic heart disease include Tetralogy of ________ and Transposition of the Great Arteries.

A

Fallot

93
Q

What are the hallmark features of Tetralogy of Fallot (TOF)?

A

Ventricular Septal Defect (VSD).
Pulmonary stenosis.
Overriding aorta.
Right ventricular hypertrophy.

94
Q

The four components of Tetralogy of Fallot include VSD, pulmonary stenosis, overriding aorta, and ________ ventricular hypertrophy.

A

Right

95
Q

What is the characteristic finding in Transposition of the Great Arteries (TGA)?

A

The aorta arises from the right ventricle, and the pulmonary artery arises from the left ventricle, causing parallel circulations.

96
Q

In Transposition of the Great Arteries, the ________ arises from the right ventricle, and the pulmonary artery arises from the left ventricle.

A

Aorta

97
Q

What are the clinical features of cyanotic heart disease?

A

Cyanosis (blue discoloration of skin and mucosa).
Clubbing of fingers and toes (chronic cases).
Respiratory distress.
Failure to thrive.
Fatigue and irritability.
“Tet spells” in Tetralogy of Fallot.

98
Q

Cyanotic heart disease may present with cyanosis, ________ of the fingers, and failure to thrive.

A

Clubbing

99
Q

What is a “Tet spell”?

A

A “Tet spell” refers to a sudden episode of severe cyanosis due to a decrease in pulmonary blood flow, often triggered by crying or feeding in children with Tetralogy of Fallot.

100
Q

A “Tet spell” is a sudden episode of severe ________ due to decreased pulmonary blood flow in Tetralogy of Fallot.

A

Cyanosis

101
Q

What investigations are used to diagnose cyanotic heart disease?

A

Pulse oximetry: Detects hypoxia.
Chest X-ray: Identifies heart size and lung vascularity.
Echocardiogram: Confirms structural abnormalities.
ECG: Detects ventricular hypertrophy or arrhythmias.
Blood gases: Shows hypoxaemia.

102
Q

________ is the primary imaging tool used to confirm structural abnormalities in cyanotic heart disease.

A

Echocardiogram

103
Q

What are the management principles for cyanotic heart disease?

A

Stabilisation: Oxygen, prostaglandin E1 infusion to keep ductus arteriosus open in duct-dependent lesions.
Surgical repair: Definitive treatment (e.g., corrective surgery for TOF or arterial switch for TGA).
Medical management: Diuretics, digoxin, ACE inhibitors for heart failure symptoms.

104
Q

Prostaglandin E1 is used in cyanotic heart disease to keep the ________ arteriosus open.

A

Ductus

105
Q

What is the purpose of prostaglandin E1 infusion in cyanotic heart disease?

A

Prostaglandin E1 keeps the ductus arteriosus open, ensuring blood flow to the lungs in duct-dependent lesions.

106
Q

Prostaglandin E1 is particularly useful in ________-dependent cyanotic heart lesions.

A

Duct.

107
Q

How is a “Tet spell” managed acutely?

A

Calm the child to reduce oxygen demand.
Place the child in a knee-chest position to increase systemic vascular resistance.
Administer oxygen.
Morphine may be used to reduce agitation.
Beta-blockers (e.g., propranolol) to reduce right ventricular outflow obstruction.

108
Q

The knee-______ position is used during a Tet spell to increase systemic vascular resistance.

A

Chest

109
Q

What are the long-term complications of cyanotic heart disease?

A

Polycythaemia due to chronic hypoxia.
Stroke or embolism.
Developmental delay.
Arrhythmias.
Heart failure.

110
Q

Chronic ________ in cyanotic heart disease can lead to polycythaemia and stroke.

A

Hypoxia

111
Q

What surgical interventions are used for Tetralogy of Fallot?

A

Palliative procedure: Blalock-Taussig shunt to increase pulmonary blood flow.
Definitive repair: Closure of the VSD and relief of pulmonary stenosis.

112
Q

The ________-Taussig shunt is a palliative procedure for Tetralogy of Fallot to improve pulmonary blood flow.

A

Blalock

113
Q

What is the prognosis for cyanotic heart disease after surgical repair?

A

The prognosis varies depending on the specific defect but is generally good after successful surgical repair. Regular follow-up is required for potential complications like arrhythmias or heart failure.

114
Q

The prognosis for cyanotic heart disease is generally good after successful ________ repair.

A

Surgical

115
Q

What is rheumatic fever?

A

Rheumatic fever is an autoimmune inflammatory condition that develops as a complication of untreated or inadequately treated group A Streptococcus (GAS) throat infection.

116
Q

Rheumatic fever is a complication of untreated ________ __ Streptococcus throat infection.

A

Group A

117
Q

What is the pathophysiology of rheumatic fever?

A

Rheumatic fever occurs due to molecular mimicry, where antibodies against GAS antigens cross-react with host tissues, leading to inflammation in the heart, joints, skin, and central nervous system.

118
Q

The pathophysiology of rheumatic fever involves molecular ________, where antibodies cross-react with host tissues.

A

Mimicry

119
Q

What are the major manifestations of rheumatic fever as per the Jones criteria?

A

Carditis.
Polyarthritis.
Chorea.
Erythema marginatum.
Subcutaneous nodules.

120
Q

Major criteria for rheumatic fever include carditis, polyarthritis, chorea, ________ marginatum, and subcutaneous nodules.

A

Erythema

121
Q

What are the minor manifestations of rheumatic fever as per the Jones criteria?

A

Fever.
Arthralgia.
Elevated inflammatory markers (CRP/ESR).
Prolonged PR interval on ECG.

122
Q

Minor criteria for rheumatic fever include fever, arthralgia, elevated inflammatory markers, and prolonged ________ interval.

A

PR

123
Q

What is the modified Jones criteria for diagnosing rheumatic fever?

A

Evidence of recent GAS infection plus:

Two major criteria, or
One major and two minor criteria.

124
Q

The Jones criteria for rheumatic fever requires evidence of recent ________ __ Streptococcus infection.

A

Group A

125
Q

What laboratory evidence supports a recent GAS infection in rheumatic fever?

A

Positive throat culture for GAS.
Positive rapid antigen detection test for GAS.
Elevated anti-streptolysin O (ASO) or anti-DNase B titers.

126
Q

Elevated anti-________ O or anti-DNase B titers indicate a recent GAS infection.

A

Streptolysin

127
Q

What are the cardiac complications associated with rheumatic fever?

A

Rheumatic heart disease.
Mitral valve regurgitation or stenosis.
Aortic valve regurgitation or stenosis.
Heart failure.

128
Q

The most commonly affected valve in rheumatic fever is the ________ valve.

A

Mitral

129
Q

What is Sydenham’s chorea, and how does it present?

A

Sydenham’s chorea is a neurological manifestation of rheumatic fever, presenting with involuntary, rapid, and irregular movements, emotional lability, and muscle weakness.

130
Q

________ chorea is a neurological manifestation of rheumatic fever with involuntary movements and emotional lability.

A

Sydenham’s

131
Q

What is erythema marginatum, and how does it appear?

A

Erythema marginatum is a skin rash associated with rheumatic fever, characterized by pink, non-itchy, serpiginous macules that often appear on the trunk and limbs.

132
Q

Erythema marginatum is a ________ rash associated with rheumatic fever that appears on the trunk and limbs.

A

Serpiginous

133
Q

How is rheumatic fever treated?

A

Antibiotics: Penicillin to eradicate GAS infection.
Anti-inflammatory treatment: Aspirin or corticosteroids for inflammation.
Symptomatic management: Anticonvulsants for chorea, diuretics for heart failure.
Secondary prophylaxis: Long-term penicillin to prevent recurrence.

134
Q

________ is the first-line antibiotic for treating rheumatic fever.

A

Penicillin

135
Q

What is the purpose of secondary prophylaxis in rheumatic fever?

A

To prevent recurrence of GAS infections and subsequent rheumatic fever episodes.

136
Q

Secondary prophylaxis for rheumatic fever typically involves long-term ________ antibiotics.

A

Penicillin

137
Q

What are the recommended durations for secondary prophylaxis in rheumatic fever?

A

5 years or until age 21 for mild cases without carditis.
10 years or until age 21 for cases with carditis but no residual heart disease.
Lifelong for cases with rheumatic heart disease.

138
Q

Secondary prophylaxis is lifelong in patients with residual ________ heart disease.

A

Rheumatic

139
Q

How can rheumatic fever be prevented?

A

Early treatment of GAS pharyngitis with antibiotics.
Public health measures to reduce GAS transmission.
Education on recognizing and treating sore throats promptly.

140
Q

Early treatment of ________ pharyngitis with antibiotics can prevent rheumatic fever.

A

GAS

141
Q

What inflammatory markers are elevated in rheumatic fever?

A

C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).

142
Q

Elevated CRP and ________ are common inflammatory markers in rheumatic fever.

A

ESR

143
Q

What is the definition of arrhythmia?

A

Arrhythmia refers to any abnormality in the rate, rhythm, or conduction of the heart’s electrical activity.

144
Q

Arrhythmia is an abnormality in the ________, ________, or ________ of the heart’s electrical activity.

A

Rate, rhythm, conduction

145
Q

What are the common types of arrhythmias in children?

A

Supraventricular tachycardia (SVT).
Ventricular tachycardia (VT).
Bradyarrhythmias (e.g., sinus bradycardia, heart block).
Premature atrial or ventricular contractions.
Long QT syndrome.

146
Q

Common arrhythmias in children include SVT, VT, bradyarrhythmias, premature contractions, and ________ QT syndrome

A

Long

147
Q

What is the most common arrhythmia in children?

A

Supraventricular tachycardia (SVT).

148
Q

The most common arrhythmia in children is ________.

A

Supraventricular tachycardia (SVT)

149
Q

What are the causes of arrhythmias in children?

A

Congenital heart defects.
Post-surgical complications (e.g., after cardiac surgery).
Structural heart disease (e.g., cardiomyopathy).
Electrolyte imbalances.
Genetic conditions (e.g., Long QT syndrome, Wolff-Parkinson-White syndrome).
Myocarditis.
Drug toxicity.

150
Q

Congenital heart defects, electrolyte imbalances, and ________ QT syndrome are common causes of arrhythmias in children.

A

Long

151
Q

What are the clinical features of arrhythmias in children?

A

Palpitations.
Syncope or dizziness.
Poor feeding in infants.
Fatigue or exercise intolerance.
Chest pain.
Symptoms of heart failure (e.g., breathlessness, peripheral edema).

152
Q

Clinical features of arrhythmias include palpitations, syncope, poor ________, and fatigue.

A

Feeding

153
Q

What are the characteristic features of supraventricular tachycardia (SVT) in children?

A

Sudden onset of rapid heart rate.
Heart rate often >200 bpm in infants.
Poor feeding or irritability in infants.
Palpitations or chest discomfort in older children.

154
Q

In SVT, the heart rate in infants is often >______ bpm.

A

200

155
Q

How is an arrhythmia diagnosed in children?

A

History and clinical examination.
Electrocardiogram (ECG) to identify rhythm abnormalities.
Holter monitoring for intermittent arrhythmias.
Echocardiography to assess structural abnormalities.
Blood tests (e.g., electrolytes, thyroid function).

156
Q

An ECG is essential to diagnose ________ in children.

A

Arrhythmias

157
Q

What is the initial management of SVT in a hemodynamically stable child?

A

Vagal maneuvers (e.g., carotid sinus massage, cold stimulus to the face).
Adenosine if vagal maneuvers fail.

158
Q

Initial management of SVT involves ________ maneuvers followed by adenosine if needed.

A

Vagal

159
Q

What is the treatment for SVT in an unstable child?

A

Synchronized cardioversion.

160
Q

The treatment for SVT in an unstable child is synchronized ________.

A

Cardioversion

161
Q

What is the long-term management of recurrent SVT in children?

A

Antiarrhythmic medications (e.g., beta-blockers).
Radiofrequency ablation for refractory cases.

162
Q

_______ ablation is used for refractory cases of SVT in children.

A

Radiofrequency

163
Q

What are the ECG findings in ventricular tachycardia (VT)?

A

Wide QRS complexes.
Rapid ventricular rate.
AV dissociation may be present.

164
Q

Ventricular tachycardia on ECG shows ________ QRS complexes and a rapid ventricular rate.

A

Wide.

165
Q

What is the acute management of ventricular tachycardia in children?

A

Hemodynamically stable: Amiodarone or procainamide.
Hemodynamically unstable: Synchronized cardioversion.

166
Q

In stable ventricular tachycardia, ________ or procainamide is used for treatment.

A

amiodarone

167
Q

What are the features of Long QT syndrome?

A

Prolonged QT interval on ECG.
Risk of ventricular arrhythmias (e.g., Torsades de Pointes).
Symptoms: Palpitations, syncope, sudden cardiac death.

168
Q

Long QT syndrome increases the risk of ________ arrhythmias such as Torsades de Pointes.

A

Ventricular

169
Q

What are the common triggers for arrhythmias in children with Long QT syndrome?

A

Exercise.
Emotional stress.
Certain medications (e.g., macrolides, antipsychotics).

170
Q

Common triggers for arrhythmias in Long QT syndrome include exercise, emotional stress, and certain ________.

A

Medications

171
Q

What is the treatment for Long QT syndrome?

A

Avoid triggers and medications that prolong the QT interval.
Beta-blockers to reduce arrhythmia risk.
Implantable cardioverter-defibrillator (ICD) for high-risk cases.

172
Q

Beta-blockers and ________ cardioverter-defibrillators are treatments for Long QT syndrome.

A

Implantable

173
Q

What is infective endocarditis?

A

Infective endocarditis is an infection of the endocardium, usually involving the heart valves, caused by bacteria, fungi, or other pathogens.

174
Q

Infective endocarditis is an infection of the ________, typically affecting the heart ________.

A

Endocardium; valves

175
Q

What are the common risk factors for infective endocarditis in children?

A

Congenital heart disease (e.g., ventricular septal defect, coarctation of the aorta).
Prosthetic heart valves.
Previous infective endocarditis.
Indwelling central lines or catheters.
Poor dental hygiene or recent dental procedures.
Immunosuppression.

176
Q

Risk factors for infective endocarditis include congenital heart disease, prosthetic ________, and poor dental ________.

A

Valves; hygiene

177
Q

What are the most common causative organisms of infective endocarditis in children?

A

Streptococcus viridans (most common in dental cases).
Staphylococcus aureus (common in healthcare-associated infections).
Enterococcus species.
Fungi (e.g., Candida species) in immunocompromised patients.

178
Q

The most common causative organism of infective endocarditis following dental procedures is ________.

A

Streptococcus viridans

179
Q

What are the classic clinical features of infective endocarditis in children?

A

Fever (most common symptom).
Malaise and fatigue.
Heart murmur (new or changing).
Petechiae or splinter hemorrhages.
Janeway lesions (non-tender macules on palms/soles).
Osler nodes (tender nodules on fingers/toes).
Roth spots (retinal hemorrhages).
Signs of heart failure in severe cases.

180
Q

Non-tender macules on the palms and soles, known as ________ lesions, are associated with infective endocarditis.

A

Janeway

181
Q

What are Osler nodes, and how are they different from Janeway lesions?

A

Osler nodes: Tender nodules on the fingers and toes caused by immune complex deposition.
Janeway lesions: Non-tender macules on the palms and soles caused by septic emboli.

182
Q

_______ nodes are tender nodules on the fingers or toes in infective endocarditis, while ________ lesions are non-tender macules on the palms or soles.

A

Osler; Janeway

183
Q

What are the complications of infective endocarditis?

A

Heart failure (due to valvular damage).
Systemic embolism (e.g., stroke, renal infarction).
Mycotic aneurysms.
Abscess formation (e.g., cardiac, systemic).
Persistent bacteremia or sepsis.

184
Q

Complications of infective endocarditis include heart failure, systemic ________, and mycotic ________.

A

Embolism; aneurysms

185
Q

What investigations are essential for diagnosing infective endocarditis?

A

Blood cultures (3 sets, taken before antibiotics).
Echocardiography (transthoracic or transesophageal).
Full blood count (shows leukocytosis, anemia).
C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).
Urinalysis (for microscopic hematuria).

186
Q

The gold standard diagnostic test for infective endocarditis is ________, with at least 3 sets taken before starting antibiotics.

A

Blood cultures

187
Q

What are the modified Duke criteria for diagnosing infective endocarditis?

A

Major criteria:
Positive blood cultures for typical organisms.
Evidence of endocardial involvement on echocardiography.
Minor criteria:
Fever >38°C.
Predisposing heart condition or IV drug use.
Vascular phenomena (e.g., emboli, Janeway lesions).
Immunologic phenomena (e.g., Osler nodes, Roth spots).

188
Q

Major criteria for infective endocarditis diagnosis include positive blood cultures and evidence of ________ involvement.

A

Endocardial

189
Q

What is the initial empirical antibiotic treatment for infective endocarditis in children?

A

Empirical treatment typically includes:

Vancomycin and gentamicin for broad coverage.
Adjust based on blood culture results.

190
Q

Initial empirical treatment for infective endocarditis includes vancomycin and ________.

A

Gentamycin

191
Q

What is the duration of antibiotic therapy for infective endocarditis?

A

Typically 4-6 weeks of intravenous antibiotics, depending on the organism and presence of complications.

192
Q

The duration of antibiotic therapy for infective endocarditis is usually ________ to ________ weeks.

A

4; 6

193
Q

What measures can prevent infective endocarditis in at-risk children?

A

Antibiotic prophylaxis before certain dental and surgical procedures.
Good dental hygiene.
Regular follow-up for children with congenital heart disease or prosthetic valves.

194
Q

Preventive measures for infective endocarditis include good ________ hygiene and antibiotic ________ before high-risk procedures.

A

Dental; prophylaxis

Phase 3a - Paediactrics (17 decks)

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