Cardiology Flashcards
1
Q
- How is coarctation of the aorta diagnosed?
A
Diagnosis: Echocardiography
- CXR: Rib notching (older children), ‘figure 3 sign’
- Confirmed by CT/MRI angiography
2
Q
- What are the treatment options for coarctation of the aorta?
A
Treatment: Prostaglandin E1 to keep duct open (neonates), balloon angioplasty or surgical repair
3
Q
- What are the physical examination findings in coarctation of the aorta?
A
Exam: BP differential (upper > lower limbs), weak/delayed femoral pulses, systolic murmur left infrascapular area
4
Q
- What are the clinical features of coarctation of the aorta in infants?
A
Features: CHF, poor feeding, tachypnea, weak lower limb pulses, shock in ductal-dependent cases
5
Q
- What is coarctation of the aorta and its typical location?
A
Coarctation: Narrowing of the aorta, usually just distal to the origin of the left subclavian artery (juxtaductal region)
6
Q
- How is PDA treated in preterm infants?
A
Treatment: Indomethacin or ibuprofen (prostaglandin inhibitors)
- Effective in preterm infants
7
Q
- What are the clinical signs of a significant PDA?
A
Signs: Continuous ‘machinery’ murmur at left infraclavicular area, bounding pulses, wide pulse pressure
8
Q
- What is the pathophysiology of patent ductus arteriosus (PDA)?
A
PDA: Persistent communication between aorta and pulmonary artery
- Causes left-to-right shunt → pulmonary overcirculation
9
Q
- When is closure of an ASD indicated?
A
Indications: Significant left-to-right shunt (Qp:Qs >1.5), RV volume overload, paradoxical embolism
10
Q
- What are the auscultatory findings in ASD?
A
Auscultation: Wide fixed splitting of S2, systolic ejection murmur at pulmonary area (↑ flow across pulmonary valve)
11
Q
- What are the clinical features of ASD in children?
A
Features: Often asymptomatic in childhood
- Large ASD: Fatigue, exercise intolerance, frequent respiratory infections
12
Q
- When is surgical or catheter closure of PDA indicated?
A
Indications: Persistent PDA beyond infancy, symptomatic, large left-to-right shunt, pulmonary hypertension
13
Q
- What is the management approach for asymptomatic VSD in a growing child?
A
Observation: If small VSD, good weight gain, no PAH—regular follow-up; many close spontaneously in early years
14
Q
- What is interrupted aortic arch and how does it present in neonates?
A
Interrupted aortic arch: Complete discontinuity of aortic arch; presents with shock, acidosis, absent femoral pulses
- Associated with 22q11 deletion
15
Q
- What is the pathophysiology of pulmonary overcirculation in left-to-right shunts?
A
Left-to-right shunt increases pulmonary blood flow → pulmonary hypertension, volume overload, risk of Eisenmenger syndrome
16
Q
- What is an aortopulmonary window and how is it differentiated from PDA?
A
Aortopulmonary window: Rare connection between ascending aorta and pulmonary artery
- Presents like PDA but with central pulmonary overcirculation on imaging
17
Q
- What are the indications for surgical closure of a VSD?
A
Indications: Large VSD with heart failure, failure to thrive despite medications, pulmonary hypertension
18
Q
- How is a VSD diagnosed and what are the key auscultation findings?
A
Diagnosis: Echo confirms size and shunt
- Auscultation: Harsh holosystolic murmur at lower left sternal border
19
Q
- What are the types of atrial septal defects (ASDs) and which is most common?
A
Types: Ostium secundum (most common), ostium primum, sinus venosus, coronary sinus type
20
Q
- What are the clinical features of a ventricular septal defect (VSD)?
A
Features: Poor feeding, failure to thrive, tachypnea, recurrent respiratory infections
- Small VSDs may be asymptomatic
21
Q
- How is WPW diagnosed and treated?
A
Diagnosis: Short PR, delta wave, wide QRS on ECG
- Treatment: Avoid AV blockers in AFib; ablation if symptomatic
22
Q
- What is Wolff-Parkinson-White (WPW) syndrome?
A
WPW: Pre-excitation syndrome with accessory pathway
- Risk of tachyarrhythmia or sudden death
23
Q
- What are the long-term management options for recurrent SVT?
A
Long-term: Beta-blockers or digoxin, catheter ablation if refractory or older child
24
Q
- What is the emergency management of SVT in unstable patients?
A
Emergency (unstable): Synchronized cardioversion (0.5–1 J/kg)
25
84. What is the acute management of SVT in stable pediatric patients?
Acute: Vagal maneuvers (ice to face, Valsalva), IV adenosine if vagal fails
26
83. How is SVT diagnosed on ECG?
ECG: Narrow QRS tachycardia, absent/retrograde P waves, regular rhythm
27
95. What is torsades de pointes and how is it treated?
Torsades: Polymorphic VT in setting of prolonged QT
- Treat with IV magnesium, pacing, isoproterenol
28
81. What are the common pediatric arrhythmias?
Common arrhythmias: SVT (most common), WPW, atrial flutter, AV block, VT, bradycardia in neonates
29
109. What is the evaluation for syncope in pediatric patients?
Evaluation: History (position, exertion), ECG, tilt-table, echo if cardiac suspicion
- Rule out arrhythmia or structural disease
30
92. What are the clinical features of long QT syndrome?
Features: Syncope, palpitations, seizures, sudden death—often during exertion or emotion
31
93. How is long QT syndrome managed in children?
Management: Beta-blockers (propranolol, nadolol), ICD for high-risk cases, avoid QT-prolonging drugs
32
89. What are the causes of bradycardia in children?
Causes: Hypoxia, increased ICP, heart block, congenital defects, hypothyroidism, drug toxicity
33
110. What are the common ECG changes in pediatric long QT subtypes (LQT1–3)?
LQT1: Broad T waves, LQT2: Notched T waves, LQT3: Long isoelectric ST
- Guide therapy (e.g., beta-blockers vs pacing)
34
82. What is supraventricular tachycardia (SVT) and how does it present in infants?
SVT: Presents with poor feeding, tachypnea, irritability, pallor, HR >220 bpm in infants
35
91. What are the ECG findings in long QT syndrome?
ECG: Prolonged QT interval (QTc > 460 ms in boys, > 480 ms in girls), abnormal T waves, may see PVCs
36
105. How do rhabdomyomas affect pediatric cardiac function?
Rhabdomyomas: May cause arrhythmias, obstruction, heart failure
- Often regress spontaneously
37
104. What are the most common primary cardiac tumors in children?
Most common: Rhabdomyomas (associated with tuberous sclerosis), fibromas, myxomas
- Often detected on fetal or neonatal echo
38
68. What is dilated cardiomyopathy and its presentation in children?
DCM: LV dilation and systolic dysfunction
- Presents with CHF symptoms, tachypnea, hepatomegaly, poor growth
39
76. What is restrictive cardiomyopathy and how does it present?
RCM: Stiff myocardium with impaired filling and normal systolic function
- Presents with hepatomegaly, ascites, JVD, edema
40
69. What are the causes of dilated cardiomyopathy in pediatrics?
Causes: Idiopathic, post-myocarditis, metabolic diseases, neuromuscular disorders, chemotherapy
41
70. What are the treatment options for dilated cardiomyopathy in children?
Treatment: Diuretics, ACE inhibitors, beta-blockers, digoxin
- Severe cases: ICD, cardiac transplant
42
71. What is hypertrophic cardiomyopathy (HCM) and how is it inherited?
HCM: Genetic condition (autosomal dominant) with asymmetric septal hypertrophy
- Commonly mutations in sarcomeric proteins
43
72. What are the symptoms of hypertrophic cardiomyopathy in children?
Symptoms: Exertional chest pain, syncope, palpitations, dyspnea, sudden death in adolescents/athletes
44
80. What is the definitive treatment for end-stage cardiomyopathy?
Definitive: Cardiac transplant
45
79. What are the ECG features in restrictive cardiomyopathy?
ECG: Low voltage QRS, ST-T abnormalities, atrial enlargement, conduction blocks
46
78. How is restrictive cardiomyopathy diagnosed?
Diagnosis: Echo shows biatrial enlargement, normal EF, restrictive filling pattern
- Cardiac MRI, biopsy may help
47
77. What are the common causes of restrictive cardiomyopathy in children?
Causes: Infiltrative (amyloidosis), storage disorders (hemochromatosis, Fabry), idiopathic, post-radiation
48
57. What are the differences between cyanotic and acyanotic congenital heart diseases?
Cyanotic: Right-to-left shunt (↓O2) → TOF, TGA, TAPVC, truncus
- Acyanotic: Left-to-right shunt or obstructive lesions
49
39. What are the ECG findings in Ebstein anomaly?
ECG: Tall P waves, right atrial enlargement, RBBB, WPW syndrome (in some cases)
50
111. What is the embryologic basis of truncus arteriosus?
Truncus: Failure of truncal septation → single arterial trunk from both ventricles
- Related to neural crest cell defects
51
5. What is the embryological basis of tetralogy of Fallot?
TOF: Abnormal anterior and cephalad deviation of infundibular septum
52
6. What are the four components of tetralogy of Fallot?
1. VSD
2. Pulmonary stenosis
3. Overriding aorta
4. Right ventricular hypertrophy
53
7. What is the presentation of tetralogy of Fallot in infants?
Presentation: Cyanosis, murmur, hypoxic spells (tet spells), boot-shaped heart on CXR
54
9. How is tetralogy of Fallot repaired surgically?
Surgical repair: VSD closure and relief of RV outflow obstruction (patch or resection)
55
10. What is the long-term complication after TOF repair?
Long-term: Pulmonary regurgitation, right ventricular dilation, arrhythmias
56
26. What is transposition of the great arteries (TGA)?
TGA: Aorta arises from RV and pulmonary artery from LV → parallel circulations
- Cyanotic heart disease
57
27. How does TGA present in neonates?
Presentation: Cyanosis within hours of birth, no murmur, single S2, minimal response to oxygen
58
28. What is the initial management of TGA?
Initial: Prostaglandin E1 to maintain PDA
- Balloon atrial septostomy to improve mixing
59
29. What definitive surgical correction is done for TGA?
Definitive: Arterial switch operation (Jatene procedure) in first weeks of life
60
31. What is total anomalous pulmonary venous connection (TAPVC)?
TAPVC: All pulmonary veins drain into systemic venous circulation instead of left atrium
- Requires ASD for survival
61
30. What is truncus arteriosus and how does it present?
Truncus arteriosus: Single arterial trunk from heart
- Presents with cyanosis, CHF, bounding pulses, wide pulse pressure
62
33. How does obstructed TAPVC present in neonates?
Obstructed TAPVC: Severe cyanosis, respiratory distress, shock-like picture, pulmonary edema
63
34. What is the management of TAPVC?
Management: Prostaglandin E1 for PDA, emergency surgery to connect pulmonary veins to left atrium
64
35. What is the pathophysiology of hypoplastic left heart syndrome (HLHS)?
HLHS: Underdevelopment of LV, mitral/aortic atresia or stenosis
- Systemic circulation depends on PDA
65
38. What is the clinical presentation of Ebstein anomaly?
Ebstein: Apical displacement of tricuspid valve → atrialized RV
- Cyanosis, RHF, arrhythmias
66
40. What is the treatment approach for Ebstein anomaly?
Treatment: Mild cases—observe
- Severe—surgical repair or tricuspid valve replacement
67
42. What is the most common cyanotic heart disease in the neonatal period?
Most common: Transposition of the great arteries (TGA)
68
32. What are the types of TAPVC?
Types: Supracardiac (most common), cardiac, infracardiac (often obstructed), mixed
69
108. What are the cardiac features of systemic lupus erythematosus (SLE) in children?
SLE: Can cause pericarditis, myocarditis, Libman-Sacks endocarditis, conduction defects
70
90. How is congenital complete heart block diagnosed and managed?
Diagnosis: Bradycardia, AV dissociation on ECG
- Management: Observation (asymptomatic), pacemaker (symptomatic or low rate)
71
114. What is the role of cardiac catheterization in pediatric CHD?
Cardiac catheterization: Defines anatomy, measures pressures/shunts, used for interventions (e.g., device closure, ballooning)
72
116. What is Noonan syndrome and its cardiovascular manifestations?
Noonan: AD disorder with dysmorphic features, short stature, pulmonic stenosis (dysplastic), hypertrophic cardiomyopathy
73
117. What is the role of genetic testing in congenital heart disease?
Genetic testing: Useful in syndromic CHD (e.g., 22q11 deletion, Noonan, Williams)
- Aids in counseling, prognosis
74
118. What are the cardiac manifestations of Marfan syndrome?
Marfan: Aortic root dilation (risk of dissection), mitral valve prolapse, aortic regurgitation
- Monitor with echo
75
94. What are the causes of acquired prolonged QT interval in pediatrics?
Causes: Medications (macrolides, antipsychotics), electrolyte disturbances (hypo-K, Mg, Ca), congenital LQTS
76
113. What is the double outlet right ventricle (DORV) and how does it present?
DORV: Both great arteries arise from RV; must be associated with VSD
- Presentation depends on VSD and pulmonary flow
77
1. What is the most common congenital heart defect overall?
Most common: Ventricular septal defect (VSD)
78
120. What is the Ross procedure and when is it used?
Ross procedure: Pulmonary autograft to replace diseased aortic valve in children
- Grows with child, avoids anticoagulation
79
74. What is the risk of sudden cardiac death in HCM and how is it assessed?
Risk: Based on family history, syncope, wall thickness, VT, abnormal BP response
- Risk stratification for ICD placement
80
75. How is HCM managed in pediatric patients?
Management: Beta-blockers, calcium channel blockers, activity restriction, ICD for high-risk
- Surgery (myectomy) if obstruction
81
43. What congenital heart defect is associated with 22q11 deletion syndrome?
22q11 deletion: Associated with truncus arteriosus, interrupted aortic arch, VSD, tetralogy of Fallot
82
41. What is the clinical significance of a single second heart sound (S2)?
Single S2: Indicates absent or inaudible pulmonary or aortic component
- Seen in TGA, truncus arteriosus, severe pulmonary stenosis
83
37. What is the initial and definitive management of HLHS?
Initial: Prostaglandin E1 to maintain ductal flow
- Definitive: Staged Norwood-Glenn-Fontan procedures or heart transplant
84
61. What are the common causes of chest pain in children?
Causes: Musculoskeletal (costochondritis), precordial catch syndrome, asthma, reflux, anxiety, rare cardiac causes
85
19. What are the features of Eisenmenger syndrome?
Features: Reversal of shunt due to pulmonary hypertension
- Cyanosis, clubbing, polycythemia, RV failure
86
8. What are 'tet spells' and how are they managed?
Tet spells: Cyanotic episodes due to infundibular spasm
- Managed with knee-chest position, O2, morphine, beta-blockers
87
73. What are the echocardiographic features of HCM?
Echo: Asymmetric septal hypertrophy, systolic anterior motion (SAM) of mitral valve, small LV cavity, preserved EF
88
20. Which congenital heart lesions commonly lead to Eisenmenger syndrome if untreated?
Common causes: Large VSD, PDA, AV canal defects, ASD (late)
- All involve significant left-to-right shunting initially
89
56. How is CHF managed in infants?
Management: Diuretics (furosemide), ACE inhibitors (captopril), digoxin, nutritional support
- Surgery if defect persists
90
55. What are the clinical signs of congestive heart failure (CHF) in infants?
Signs: Tachypnea, poor feeding, hepatomegaly, diaphoresis, failure to thrive
91
54. What is the most common cause of heart failure in the first year of life?
Most common cause: Large left-to-right shunt (e.g., VSD, AVSD, PDA)
92
98. What is the treatment of Kawasaki disease?
Treatment: IVIG + aspirin
- Start within 10 days of illness onset to reduce coronary complications
93
103. What are coronary artery anomalies and their clinical importance?
Coronary anomalies: May cause myocardial ischemia or sudden cardiac death (esp. anomalous origin from opposite sinus)
94
100. What are coronary artery aneurysms and when do they occur in children?
Aneurysms: Coronary artery dilation due to vasculitis
- Occur in ~25% untreated Kawasaki cases
95
97. What are the diagnostic criteria for Kawasaki disease?
Criteria: Fever ≥5 days + 4 of: conjunctivitis, oral changes, rash, extremity changes, cervical lymphadenopathy
96
99. What is the role of echocardiography in Kawasaki disease?
Echocardiography: Assesses coronary artery dilation/aneurysms
- Baseline and follow-up at 2 and 6 weeks
97
96. What is Kawasaki disease and what cardiac complication is it associated with?
Kawasaki: Medium vessel vasculitis in children <5 yrs
- Cardiac risk: Coronary artery aneurysms
98
67. How is myocarditis diagnosed?
Diagnosis: Elevated troponin/CK-MB, ECG changes, echocardiogram (↓ EF), cardiac MRI, endomyocardial biopsy (rare)
99
66. What are the clinical manifestations of myocarditis in children?
Manifestations: Fatigue, dyspnea, chest pain, arrhythmias, signs of heart failure
100
65. What are the causes of myocarditis in pediatrics?
Causes: Viral (Coxsackie, adenovirus), bacterial, autoimmune (Kawasaki), toxins, post-viral inflammation
101
64. How is pericardial tamponade managed in children?
Management: Emergency pericardiocentesis, supportive care, treat underlying cause
102
63. What are the clinical features of pericardial tamponade?
Features: Beck’s triad (hypotension, muffled heart sounds, JVD), tachycardia, pulsus paradoxus
103
62. How is pericarditis diagnosed in pediatric patients?
Diagnosis: Chest pain, pericardial rub, ECG (diffuse ST elevation), effusion on echocardiogram
104
60. What are contraindications to prostaglandin E1 therapy?
Contraindications: Severe apnea without ventilatory support, caution in prematurity or pulmonary overcirculation
105
58. What are hyperoxia test findings in congenital heart disease?
Hyperoxia test: PaO2 fails to rise >150 mmHg in cyanotic CHD
- Helps differentiate from pulmonary causes
106
59. What is the role of prostaglandin E1 in congenital heart disease?
PGE1: Maintains ductal patency in duct-dependent lesions (e.g., HLHS, TGA, coarctation)
107
119. What are common side effects of prostaglandin E1 therapy in neonates?
PGE1 side effects: Apnea (most common), fever, hypotension, flushing
- Requires respiratory support in some cases
108
36. How does HLHS present in neonates?
Presentation: Cyanosis, shock as ductus closes, weak pulses, no murmur, RV heave
109
106. What are the cardiac manifestations of acute rheumatic fever?
Rheumatic fever: Causes pancarditis (endocarditis, myocarditis, pericarditis)
- Mitral regurgitation is most common lesion
110
107. What is the Jones criteria for diagnosing rheumatic fever?
Jones Criteria: Major (carditis, polyarthritis, chorea, rash, nodules) + Minor (fever, arthralgia, ↑ESR/CRP, prolonged PR)
111
52. What are the causes of mitral regurgitation in pediatrics?
Causes: Rheumatic heart disease, endocarditis, MVP, AV canal defects, connective tissue disorders (e.g., Marfan)
112
45. What is supravalvular aortic stenosis and what syndrome is it associated with?
Supravalvular aortic stenosis: Narrowing above aortic valve
- Associated with Williams syndrome (elfin face, hypercalcemia)
113
46. What are the clinical features of pulmonary stenosis?
Pulmonary stenosis: Asymptomatic or exertional dyspnea, fatigue, RV heave, systolic murmur at upper left sternal border
114
48. What are the indications for balloon valvuloplasty in pulmonary stenosis?
Indications: Gradient >50 mmHg, RV pressure >75% systemic, symptoms
- Preferred over surgery in isolated cases
115
49. What is the presentation of mitral valve prolapse in children?
MVP: Usually asymptomatic
- May cause chest pain, palpitations, or anxiety in adolescents
116
50. What are the auscultatory findings of mitral valve prolapse?
Auscultation: Mid-systolic click followed by late systolic murmur best heard at apex
117
51. What are the features of mitral regurgitation in children?
Features: Holosystolic murmur at apex, radiates to axilla
- May cause fatigue, dyspnea, poor growth if severe
118
53. What is the murmur of tricuspid regurgitation?
TR murmur: Holosystolic murmur at lower left sternal border, may increase with inspiration (Carvallo’s sign)
119
44. What is the murmur of aortic stenosis in children?
Aortic stenosis murmur: Harsh systolic ejection murmur at right upper sternal border
- Radiates to neck
120
47. What are the ECG findings in severe pulmonary stenosis?
ECG: Right axis deviation, RV hypertrophy, peaked P waves in severe cases
