Cardiology Flashcards
(209 cards)
1
Q
What is a ventricular septal defect (VSD)?
A
A congenital heart defect involving a hole in the interventricular septum, allowing left-to-right shunting of blood.
2
Q
What are the types of VSD based on location?
A
Perimembranous, muscular, inlet, and outlet (supracristal).
3
Q
What is the most common type of VSD?
A
Perimembranous VSD.
4
Q
What are clinical features of a moderate to large VSD?
A
Heart failure symptoms in infancy: tachypnea, poor feeding, failure to thrive, hepatomegaly, recurrent respiratory infections.
5
Q
What murmur is typically heard in VSD?
A
A pansystolic murmur best heard at the left lower sternal border.
6
Q
What are the ECG findings in moderate to large VSD?
A
Left ventricular hypertrophy (LVH), possibly right ventricular hypertrophy (RVH) in large shunts.
7
Q
What are the chest X-ray findings in significant VSD?
A
Cardiomegaly with increased pulmonary vascular markings.
8
Q
What are potential complications of untreated large VSD?
A
Pulmonary hypertension, Eisenmenger syndrome, failure to thrive, endocarditis.
9
Q
What is the medical management for a large VSD in infancy?
A
Diuretics, ACE inhibitors, and increased caloric support; surgical closure if not improving.
10
Q
When is surgical or device closure indicated in VSD?
A
Large VSD with signs of heart failure, failure to thrive, or pulmonary hypertension not responsive to medical management.
11
Q
What is an atrial septal defect (ASD)?
A
A congenital defect characterized by an abnormal opening in the atrial septum causing left-to-right shunt.
12
Q
What are the main types of ASD?
A
Ostium secundum (most common), ostium primum, sinus venosus, and coronary sinus defect.
13
Q
What is the most common type of ASD?
A
Ostium secundum, located at the fossa ovalis.
14
Q
What are the clinical features of ASD in children?
A
Often asymptomatic; may have recurrent respiratory infections, fatigue, or failure to thrive.
15
Q
What murmur is characteristic of ASD?
A
Wide fixed splitting of the second heart sound and a systolic ejection murmur at the left upper sternal border.
16
Q
What are the ECG findings in ASD?
A
Right axis deviation and incomplete right bundle branch block, especially in secundum ASD.
17
Q
What is the typical chest X-ray finding in ASD?
A
Enlarged right atrium and right ventricle, with increased pulmonary vascular markings.
18
Q
What complications may arise from an untreated ASD?
A
Pulmonary hypertension, right heart failure, atrial arrhythmias, paradoxical embolism.
19
Q
What is the management of small ASD?
A
Observation, as many secundum ASDs close spontaneously in early childhood.
20
Q
When is surgical or device closure indicated in ASD?
A
Moderate to large shunt with evidence of right heart dilation or paradoxical embolism.
21
Q
What is a patent ductus arteriosus (PDA)?
A
A persistent opening between the aorta and pulmonary artery after birth, resulting in left-to-right shunt.
22
Q
What factors contribute to persistence of the ductus arteriosus?
A
Prematurity, hypoxia, prostaglandin E1 exposure, congenital rubella infection.
23
Q
What are the clinical features of PDA?
A
Tachypnea, poor feeding, failure to thrive, bounding pulses, widened pulse pressure, and continuous ‘machinery’ murmur.
24
Q
Where is the PDA murmur best heard?
A
Left infraclavicular region; continuous and machine-like.
25
What are the ECG findings in PDA?
Left atrial and left ventricular hypertrophy in significant shunts.
26
What are chest X-ray findings in moderate to large PDA?
Cardiomegaly and increased pulmonary vascular markings.
27
What complications can arise from untreated PDA?
Heart failure, pulmonary hypertension, endarteritis, Eisenmenger syndrome.
28
How is PDA diagnosed?
Echocardiography with color Doppler confirming left-to-right ductal shunt.
29
What is the medical treatment for PDA in preterm infants?
NSAIDs like indomethacin or ibuprofen to promote ductal closure by inhibiting prostaglandins.
30
When is surgical or device closure indicated in PDA?
In moderate to large PDA causing symptoms or left heart volume overload not responding to medical therapy.
31
What is coarctation of the aorta (CoA)?
A congenital narrowing of the aortic lumen, usually near the ductus arteriosus (juxtaductal region).
32
What are the types of coarctation of the aorta?
Pre-ductal (infantile type) and post-ductal (adult type).
33
What are clinical features of severe CoA in neonates?
Poor feeding, tachypnea, weak femoral pulses, differential cyanosis (lower > upper extremities), and shock.
34
What physical finding is classic in older children with CoA?
Hypertension in upper limbs with diminished/absent femoral pulses and radio-femoral delay.
35
What murmur is associated with CoA?
A systolic murmur best heard over the back between the scapulae.
36
What are the ECG findings in CoA?
Left ventricular hypertrophy (LVH).
37
What are chest X-ray findings in CoA?
Rib notching (from collateral circulation) and the 'figure of 3' sign.
38
What diagnostic modality confirms CoA?
Echocardiography with Doppler; MRI/CT angiography for detailed anatomy.
39
What is the initial management in neonates with severe CoA?
Prostaglandin E1 to maintain ductal patency and stabilize systemic perfusion.
40
What are the definitive treatment options for CoA?
Surgical repair or balloon angioplasty with or without stenting.
41
What is Tetralogy of Fallot (TOF)?
A cyanotic congenital heart disease with four components: VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy.
42
What is the most common cyanotic congenital heart disease beyond infancy?
Tetralogy of Fallot (TOF).
43
What are clinical features of TOF?
Cyanosis, 'tet spells' (hypoxic spells), squatting after exertion, and poor weight gain.
44
What causes 'tet spells' in TOF?
Sudden increase in right-to-left shunting due to decreased systemic vascular resistance or increased obstruction.
45
How are 'tet spells' managed acutely?
Knee-chest position, oxygen, morphine, beta-blockers (e.g., propranolol), fluids, and phenylephrine.
46
What murmur is heard in TOF?
Harsh systolic ejection murmur at the left upper sternal border due to pulmonary stenosis.
47
What are ECG findings in TOF?
Right axis deviation and right ventricular hypertrophy (RVH).
48
What is the classic chest X-ray finding in TOF?
Boot-shaped heart (coeur en sabot) due to RVH and concave pulmonary segment.
49
What is the definitive diagnostic test for TOF?
Echocardiography confirms the four anatomical defects.
50
What is the treatment for TOF?
Surgical repair usually done in infancy with VSD closure and relief of RV outflow tract obstruction.
51
What is Transposition of the Great Arteries (TGA)?
A congenital heart defect where the aorta arises from the right ventricle and the pulmonary artery from the left ventricle, creating parallel circulations.
52
What type of shunt is required for survival in TGA?
Mixing of blood through an ASD, VSD, or PDA is essential for oxygenation.
53
What are the clinical features of TGA?
Severe cyanosis within hours of birth, tachypnea, no murmur unless associated defects exist.
54
What is the typical chest X-ray finding in TGA?
Egg-on-a-string appearance due to narrow mediastinum and enlarged cardiac silhouette.
55
What are the ECG findings in TGA?
Right ventricular hypertrophy (RVH) due to right ventricle functioning as systemic ventricle.
56
How is TGA diagnosed?
Echocardiography is the definitive diagnostic modality.
57
What is the initial emergency management of TGA?
Prostaglandin E1 to keep the ductus arteriosus open and balloon atrial septostomy (Rashkind procedure) to allow mixing.
58
What is the definitive surgical treatment for TGA?
Arterial switch operation (Jatene procedure) typically performed within the first 2 weeks of life.
59
Why is early diagnosis of TGA critical?
Because neonates deteriorate quickly without adequate mixing; early intervention is life-saving.
60
What factors improve survival in TGA?
Presence of a large VSD or PDA and early surgical correction.
61
What is tricuspid atresia?
A congenital heart defect where the tricuspid valve fails to develop, resulting in no direct connection between the right atrium and right ventricle.
62
What shunts are required for survival in tricuspid atresia?
An atrial septal defect (ASD) and either a ventricular septal defect (VSD) or patent ductus arteriosus (PDA) are required for blood flow and oxygenation.
63
What are the clinical features of tricuspid atresia?
Cyanosis, tachypnea, poor feeding, single second heart sound, and often a murmur if VSD or PDA is present.
64
What are the ECG findings in tricuspid atresia?
Left axis deviation and left ventricular hypertrophy (LVH).
65
What are chest X-ray findings in tricuspid atresia?
Decreased pulmonary vascular markings and a normal or mildly enlarged heart.
66
How is tricuspid atresia diagnosed?
Echocardiography confirms absence of the tricuspid valve and associated defects.
67
What is the initial management of tricuspid atresia in neonates?
Prostaglandin E1 to maintain PDA and balloon atrial septostomy if restrictive ASD is present.
68
What is the definitive treatment for tricuspid atresia?
Staged surgical palliation, including the Glenn shunt and Fontan procedure.
69
What is the purpose of the Fontan procedure?
To redirect systemic venous return directly to the pulmonary arteries, bypassing the right heart.
70
What complications are associated with Fontan circulation?
Protein-losing enteropathy, arrhythmias, thrombosis, and heart failure.
71
What is Total Anomalous Pulmonary Venous Return (TAPVR)?
A congenital defect where all pulmonary veins drain into the systemic venous circulation instead of the left atrium.
72
What are the types of TAPVR?
Supracardiac (most common), cardiac, infracardiac, and mixed.
73
What is required for survival in TAPVR?
An atrial septal defect (ASD) to allow oxygenated blood to reach systemic circulation.
74
What are clinical features of obstructed TAPVR?
Severe cyanosis, respiratory distress, pulmonary edema, and shock shortly after birth.
75
How does unobstructed TAPVR present?
Mild cyanosis, tachypnea, and failure to thrive in early infancy.
76
What murmur may be present in TAPVR?
A fixed split second heart sound; systolic ejection murmur at the upper left sternal border.
77
What is seen on chest X-ray in supracardiac TAPVR?
‘Snowman’ or ‘figure-of-eight’ sign due to dilated vertical vein and SVC.
78
What are ECG findings in TAPVR?
Right axis deviation and right ventricular hypertrophy (RVH).
79
How is TAPVR diagnosed?
Echocardiography is the diagnostic test of choice; CT or MRI angiography for further delineation.
80
What is the treatment for TAPVR?
Surgical correction by connecting pulmonary veins to the left atrium and closing the ASD.
81
What is truncus arteriosus?
A rare cyanotic congenital heart defect where a single arterial trunk arises from the heart, supplying the systemic, pulmonary, and coronary circulations.
82
What causes cyanosis in truncus arteriosus?
Mixing of oxygenated and deoxygenated blood through a large VSD, resulting in desaturated blood in systemic circulation.
83
What are the types of truncus arteriosus?
Types I–IV based on the origin and anatomy of pulmonary arteries (Collett and Edwards classification).
84
What are clinical features of truncus arteriosus?
Cyanosis, tachypnea, signs of congestive heart failure, poor feeding, and failure to thrive.
85
What murmur is heard in truncus arteriosus?
A loud single second heart sound with a systolic ejection murmur due to increased pulmonary blood flow.
86
What are ECG findings in truncus arteriosus?
Biventricular hypertrophy.
87
What does chest X-ray show in truncus arteriosus?
Cardiomegaly with increased pulmonary vascular markings.
88
How is truncus arteriosus diagnosed?
Echocardiography shows a single great vessel overriding a VSD with pulmonary arteries branching from it.
89
What is the definitive treatment for truncus arteriosus?
Surgical repair in the neonatal period with VSD closure and placement of a conduit to connect right ventricle to pulmonary arteries.
90
What are potential complications if truncus arteriosus is not treated?
Severe pulmonary hypertension and Eisenmenger syndrome, leading to irreversible damage and poor prognosis.
91
What is Ebstein anomaly?
A rare congenital heart defect characterized by apical displacement of the tricuspid valve leaflets into the right ventricle.
92
How does Ebstein anomaly affect heart function?
It causes 'atrialization' of part of the right ventricle, reducing effective right ventricular volume and often resulting in tricuspid regurgitation.
93
What are common clinical features of Ebstein anomaly?
Cyanosis, heart failure, hepatomegaly, fatigue, and arrhythmias such as supraventricular tachycardia.
94
What murmur is associated with Ebstein anomaly?
Holosystolic murmur of tricuspid regurgitation heard best at the lower left sternal border.
95
What ECG findings are seen in Ebstein anomaly?
Right atrial enlargement, prolonged PR interval, and sometimes Wolff-Parkinson-White (WPW) syndrome.
96
What does chest X-ray show in Ebstein anomaly?
Cardiomegaly with a box-shaped heart and decreased pulmonary vascular markings.
97
How is Ebstein anomaly diagnosed?
Echocardiography shows downward displacement of the tricuspid valve leaflets and tricuspid regurgitation.
98
What determines the severity of Ebstein anomaly?
Extent of valve displacement, degree of regurgitation, and size/function of the right ventricle.
99
What are treatment options for Ebstein anomaly?
Medical management of heart failure and arrhythmias, with surgical repair or valve replacement in severe cases.
100
What is the prognosis of Ebstein anomaly?
Varies widely; mild cases may be asymptomatic, while severe forms require surgery and carry higher risk of complications.
101
What is Kawasaki disease?
An acute, self-limited vasculitis of medium-sized arteries that primarily affects children under 5 years old.
102
What are the diagnostic criteria for classic Kawasaki disease?
Fever for ≥5 days plus 4 of 5: conjunctivitis, oral changes, rash, extremity changes, cervical lymphadenopathy.
103
What are the common oral findings in Kawasaki disease?
Strawberry tongue, cracked red lips, and erythema of the oral mucosa.
104
What skin changes are seen in Kawasaki disease?
Polymorphous rash and desquamation, especially on the fingers and toes during subacute phase.
105
What is the most serious complication of Kawasaki disease?
Coronary artery aneurysms.
106
What lab abnormalities support the diagnosis of Kawasaki disease?
Elevated ESR, CRP, thrombocytosis, leukocytosis, anemia, and sterile pyuria.
107
What is incomplete (atypical) Kawasaki disease?
When fewer than 4 of the principal features are present but lab and echo findings support the diagnosis.
108
What is the first-line treatment of Kawasaki disease?
IVIG (2 g/kg) and high-dose aspirin.
109
When should IVIG be given in Kawasaki disease?
Ideally within the first 10 days of illness to reduce the risk of coronary aneurysms.
110
What follow-up is required after Kawasaki disease?
Serial echocardiograms to monitor coronary arteries and long-term cardiology follow-up if aneurysms are present.
111
What is myocarditis?
Inflammation of the myocardium, often due to viral infection, resulting in cardiac dysfunction.
112
What are common causes of myocarditis in children?
Viruses (e.g., Coxsackie B, adenovirus, parvovirus B19), bacterial infections, autoimmune diseases, and toxins.
113
What are clinical features of myocarditis?
Fatigue, tachypnea, poor feeding, chest pain, palpitations, syncope, and signs of heart failure.
114
What signs on examination may suggest myocarditis?
Tachycardia disproportionate to fever, hepatomegaly, gallop rhythm, and hypotension.
115
What ECG findings may be seen in myocarditis?
ST-T changes, low voltage QRS, arrhythmias, or heart block.
116
What imaging is useful in myocarditis diagnosis?
Echocardiography (shows ventricular dysfunction); cardiac MRI for edema, inflammation, and fibrosis.
117
What blood tests support a diagnosis of myocarditis?
Elevated troponin, CK-MB, BNP/NT-proBNP, and inflammatory markers like ESR/CRP.
118
What is the role of endomyocardial biopsy in myocarditis?
Definitive diagnosis but reserved for unclear or severe cases due to invasiveness.
119
How is acute myocarditis managed?
Supportive care with diuretics, inotropes, afterload reduction, and treatment of arrhythmias or shock.
120
What are potential complications of myocarditis?
Dilated cardiomyopathy, arrhythmias, heart failure, and sudden cardiac death.
121
What is rheumatic fever?
An inflammatory disease that can develop after a group A streptococcal pharyngitis, affecting the heart, joints, skin, and brain.
122
What are the major Jones criteria for diagnosing rheumatic fever?
Carditis, polyarthritis, chorea, erythema marginatum, and subcutaneous nodules.
123
What are the minor Jones criteria?
Fever, arthralgia, elevated ESR/CRP, and prolonged PR interval on ECG.
124
What is required for the diagnosis of rheumatic fever (modified Jones criteria)?
Evidence of preceding strep infection + 2 major or 1 major and 2 minor criteria.
125
What are the manifestations of rheumatic carditis?
Pancarditis including endocarditis (mitral or aortic regurgitation), myocarditis, and pericarditis.
126
What joint findings are typical in rheumatic fever?
Migratory polyarthritis affecting large joints like knees, ankles, elbows, and wrists.
127
What is Sydenham chorea?
Involuntary, purposeless movements due to rheumatic involvement of the basal ganglia.
128
What labs support the diagnosis of rheumatic fever?
Positive throat culture or rapid antigen test for group A strep, elevated ASO titer, and inflammatory markers.
129
What is the treatment for acute rheumatic fever?
Benzathine penicillin, anti-inflammatory therapy (aspirin or corticosteroids), and supportive care for carditis or chorea.
130
What is secondary prophylaxis for rheumatic fever?
Monthly intramuscular benzathine penicillin G to prevent recurrence; duration depends on severity and cardiac involvement.
131
What is pericarditis?
Inflammation of the pericardial sac, which can be acute or chronic.
132
What are common causes of pericarditis in children?
Viral infections (e.g., coxsackievirus), bacterial infections (including TB), autoimmune diseases, and post-cardiac surgery.
133
What are classic clinical features of pericarditis?
Chest pain relieved by sitting forward, fever, tachycardia, and pericardial friction rub.
134
What are ECG findings in pericarditis?
Diffuse ST elevation and PR depression in multiple leads.
135
What may be seen on chest X-ray in pericardial effusion?
Enlarged cardiac silhouette if a large effusion is present.
136
What does echocardiography show in pericarditis?
Presence of pericardial effusion and signs of tamponade if severe.
137
What are signs of cardiac tamponade?
Hypotension, muffled heart sounds, jugular venous distension (Beck’s triad), and pulsus paradoxus.
138
How is acute pericarditis treated?
NSAIDs, colchicine, and treatment of underlying cause; corticosteroids in autoimmune cases.
139
What is the treatment for pericardial tamponade?
Urgent pericardiocentesis to drain the effusion.
140
What are complications of untreated pericarditis?
Cardiac tamponade, constrictive pericarditis, and recurrent pericardial inflammation.
141
What are the main types of pediatric cardiomyopathy?
Dilated, hypertrophic, and restrictive cardiomyopathy.
142
What is dilated cardiomyopathy (DCM)?
A condition characterized by dilation and impaired contraction of the left or both ventricles.
143
What are causes of dilated cardiomyopathy in children?
Viral myocarditis, genetic mutations, metabolic diseases, toxins, and chemotherapy (e.g., anthracyclines).
144
What are clinical features of dilated cardiomyopathy?
Heart failure symptoms such as tachypnea, poor feeding, hepatomegaly, and failure to thrive.
145
What is hypertrophic cardiomyopathy (HCM)?
Thickening of the myocardium, often asymmetric, that can cause outflow obstruction and arrhythmias.
146
What are causes of hypertrophic cardiomyopathy in children?
Genetic mutations (e.g., sarcomere proteins), Noonan syndrome, Friedreich ataxia, and metabolic disorders.
147
What are the symptoms and signs of hypertrophic cardiomyopathy?
Dyspnea, chest pain, syncope, sudden cardiac death, harsh systolic murmur that increases with Valsalva.
148
What is restrictive cardiomyopathy?
A rare form characterized by impaired ventricular filling with preserved systolic function.
149
What is the most sensitive diagnostic tool for cardiomyopathies?
Echocardiography, often followed by cardiac MRI for tissue characterization.
150
What are general treatment strategies for pediatric cardiomyopathies?
Medications (e.g., beta-blockers, ACE inhibitors), management of heart failure, anti-arrhythmic drugs, and possible heart transplant.
151
What are common types of arrhythmias in children?
Supraventricular tachycardia (SVT), ventricular tachycardia (VT), complete heart block, and long QT syndrome.
152
What is the most common symptomatic arrhythmia in children?
Supraventricular tachycardia (SVT).
153
How does SVT present in infants?
Poor feeding, irritability, pallor, and signs of heart failure; often with a heart rate >220 bpm.
154
What is the first-line treatment for stable SVT in children?
Vagal maneuvers such as ice to the face or Valsalva maneuver.
155
What drug is used for acute termination of SVT?
Adenosine IV push; rapid onset and short half-life.
156
What is the long-term management of recurrent SVT?
Beta-blockers, digoxin, or catheter ablation for definitive treatment.
157
What is complete (third-degree) heart block?
A condition where there is no conduction from the atria to the ventricles, resulting in AV dissociation.
158
What are causes of congenital complete heart block?
Maternal autoimmune diseases (e.g., SLE with anti-Ro/SSA or anti-La/SSB antibodies).
159
What is long QT syndrome?
A disorder of myocardial repolarization that prolongs the QT interval and predisposes to torsades de pointes and sudden death.
160
What is the treatment for long QT syndrome?
Beta-blockers, avoidance of QT-prolonging drugs, and ICD in high-risk cases.
161
What is Total Anomalous Pulmonary Venous Return (TAPVR)?
A congenital heart defect where all pulmonary veins drain into the systemic venous circulation instead of the left atrium.
162
What is the classic X-ray finding in TAPVR with obstruction?
Pulmonary edema and a small heart; in supracardiac type, a 'snowman' sign.
163
What is truncus arteriosus?
A congenital heart defect with a single arterial trunk arising from the heart supplying systemic, pulmonary, and coronary circulations.
164
What is the main feature of Ebstein anomaly?
Apical displacement of the tricuspid valve leaflets into the right ventricle, causing atrialization of part of the RV.
165
What is pulmonary atresia?
A congenital heart defect where the pulmonary valve does not form properly, preventing blood flow from RV to lungs.
166
What is the Norwood procedure used for?
Surgical palliation of hypoplastic left heart syndrome (HLHS) in neonates.
167
What is hypertrophic cardiomyopathy (HCM)?
A genetic disorder characterized by abnormal thickening of the heart muscle, often affecting the interventricular septum.
168
What is the most common cause of pediatric dilated cardiomyopathy?
Viral myocarditis (e.g., Coxsackie B virus).
169
What is restrictive cardiomyopathy?
A rare condition where the myocardium becomes rigid, leading to diastolic dysfunction with preserved systolic function.
170
What is Wolff-Parkinson-White (WPW) syndrome?
A condition with an accessory pathway (Bundle of Kent) causing pre-excitation and risk of supraventricular tachycardia.
171
What is the ECG finding in WPW syndrome?
Short PR interval, delta wave, and wide QRS complex.
172
What is long QT syndrome?
A genetic disorder characterized by prolonged QT interval and risk of torsades de pointes and sudden death.
173
What is the acute management of SVT in children?
Vagal maneuvers → Adenosine IV bolus → synchronized cardioversion if unstable.
174
What is the most feared complication of Kawasaki disease?
Coronary artery aneurysms.
175
What is the initial treatment of Kawasaki disease?
IVIG (2 g/kg) and high-dose aspirin.
176
What is MIS-C?
Multisystem Inflammatory Syndrome in Children: a post-COVID inflammatory condition mimicking Kawasaki disease but with more systemic involvement.
177
What are signs of congestive heart failure in infants?
Tachypnea, poor feeding, hepatomegaly, diaphoresis during feeds.
178
What drugs are commonly used in pediatric heart failure?
Diuretics, ACE inhibitors, beta-blockers (e.g., carvedilol), digoxin.
179
What is vasovagal syncope?
A common cause of fainting in children, triggered by emotional stress, prolonged standing, or heat exposure.
180
What is the most common secondary cause of pediatric hypertension?
Renal parenchymal disease.
181
What are common ECG findings in ASD?
Right axis deviation and incomplete RBBB.
182
What is the 'boot-shaped heart' on X-ray indicative of?
Tetralogy of Fallot.
183
When is surgical closure of a large VSD recommended?
Typically between 3 to 6 months of age if there is heart failure or failure to thrive despite medical therapy.
184
What is the optimal timing for surgical repair of Tetralogy of Fallot (TOF)?
Complete repair is typically done between 4 to 6 months of age or earlier if cyanotic spells occur.
185
When should an atrial septal defect (ASD) be closed?
Closure is recommended between 2 to 5 years of age if there is right heart volume overload or significant shunt (Qp:Qs >1.5).
186
When is patent ductus arteriosus (PDA) ligation or device closure performed?
Usually after 1 year of age for small, asymptomatic PDAs; earlier if symptomatic or large.
187
What is the timing of arterial switch operation for transposition of the great arteries (TGA)?
Should be performed within the first 2–3 weeks of life, ideally within the first week.
188
When is the Norwood procedure performed in hypoplastic left heart syndrome (HLHS)?
Within the first week of life (Stage I).
189
When is the bidirectional Glenn shunt typically done in HLHS?
At 4 to 6 months of age (Stage II).
190
When is the Fontan procedure performed in single ventricle physiology?
At 2 to 4 years of age (Stage III).
191
When is surgery for coarctation of the aorta usually performed?
Neonatal period if symptomatic; otherwise by 3 to 6 months of age.
192
What is the timing for TAPVR correction?
Emergency surgery in obstructed TAPVR; elective repair in non-obstructed cases during neonatal period.
193
What is infective endocarditis (IE)?
Infective endocarditis is an infection of the endocardial surface of the heart, typically involving the heart valves, characterized by vegetations composed of fibrin, platelets, microorganisms, and inflammatory cells.
194
What are the common causative organisms of infective endocarditis in pediatric patients?
Common pathogens include Staphylococcus aureus, Streptococcus viridans, Enterococcus, HACEK organisms (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella), and fungi such as Candida and Aspergillus in immunocompromised children.
195
What are the major risk factors for infective endocarditis in children?
Risk factors include congenital heart defects (especially cyanotic or unrepaired), prosthetic heart valves, previous history of endocarditis, indwelling central lines, and immunosuppression.
196
What are the typical clinical manifestations of infective endocarditis in children?
Common signs include persistent fever, fatigue, anorexia, new or changing heart murmur, petechiae, splenomegaly, embolic phenomena (stroke, hematuria), and classic signs like Janeway lesions, Osler nodes, and Roth spots.
197
What are the major criteria of the Modified Duke Criteria for diagnosing infective endocarditis?
1. Positive blood cultures for typical organisms from two separate cultures. 2. Echocardiographic evidence of endocardial involvement: vegetations, abscess, or new valvular regurgitation.
198
What are the minor criteria of the Modified Duke Criteria for infective endocarditis?
1. Predisposing cardiac condition or IV drug use. 2. Fever ≥38°C. 3. Vascular phenomena (e.g., Janeway lesions, emboli). 4. Immunologic phenomena (e.g., Osler nodes, glomerulonephritis). 5. Positive blood cultures not meeting major criteria.
199
How is a definite diagnosis of infective endocarditis established according to the Modified Duke Criteria?
Diagnosis is confirmed with 2 major criteria, or 1 major plus 3 minor, or 5 minor criteria.
200
What diagnostic investigations are essential for suspected pediatric infective endocarditis?
Three sets of blood cultures before antibiotics, echocardiography (TTE or TEE), CBC, ESR/CRP, renal function tests, urinalysis, chest X-ray, ECG, and sometimes serology or PCR for fastidious organisms.
201
Which echocardiographic modality is preferred in children with suspected endocarditis?
Transthoracic echocardiography (TTE) is preferred initially due to ease and safety; transesophageal echocardiography (TEE) offers better resolution and is used when TTE is non-diagnostic or in high-risk cases.
202
What is the standard treatment for infective endocarditis in pediatric patients?
High-dose intravenous antibiotics for 4–6 weeks based on culture sensitivity. Surgical intervention may be needed for complications like heart failure, large vegetations, embolic events, or valve dysfunction.
203
What is the initial empirical antibiotic therapy for native valve infective endocarditis in children?
Empirical therapy typically includes a combination of vancomycin and gentamicin to cover Staphylococcus aureus, Streptococcus spp., and Enterococcus spp.
204
What empirical antibiotics are recommended for prosthetic valve infective endocarditis in children?
Vancomycin + gentamicin + rifampin is commonly used to cover resistant organisms and biofilm-producing bacteria.
205
How long is antibiotic therapy typically administered for infective endocarditis in pediatrics?
Standard duration is 4–6 weeks of intravenous antibiotics, depending on the organism, site, and presence of prosthetic material.
206
What antibiotic regimen is used for Streptococcus viridans endocarditis in a child with a native valve and penicillin-sensitive strain?
Penicillin G or ceftriaxone for 4 weeks, with or without gentamicin for the first 2 weeks in selected cases.
207
How is methicillin-sensitive Staphylococcus aureus (MSSA) endocarditis treated in children?
Oxacillin or nafcillin is the preferred treatment for MSSA infective endocarditis. Cefazolin is an alternative in non-anaphylactic penicillin allergy.
208
What is the treatment for methicillin-resistant Staphylococcus aureus (MRSA) endocarditis in pediatric patients?
Vancomycin is the drug of choice. Daptomycin may be considered if vancomycin is not tolerated or ineffective.
209
When is surgical intervention indicated in infective endocarditis despite appropriate antibiotic therapy?
Indications include heart failure, persistent bacteremia, large vegetations (>10 mm), embolic complications, abscess formation, or prosthetic valve dysfunction.
