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🚨 This summary is more comprehensive than the previous version, almost 1.5 times larger, but contains more explanations and is more comprehensive.

• 2.1 update: Added the missed Nephrology part </aside>

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🔊 Podcast Style Review (Experimental Feature)

Pediatrics Final Summary Key Points.m4a

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👨‍💻 Made by: Ibrahim Al-Khatib

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• NOTE: Highlighted in bold are the important key info!
• Check the table of contents below for easier navigation
• Good luck 🍀 </aside>

1. Cardiology

I. Congenital Heart Defects (CHD) & Acquired Conditions

• Patent Ductus Arteriosus (PDA)
  • Large PDA Findings:
    • Blood pressure example: 100/45 mmHg (wide pulse pressure).
    • Bounding pulses.
    • Displaced apical impulse.
    • Left axis deviation on ECG.
    • Cardiomegaly on CXR.
    • Continuous murmur at the left upper sternal border/left subclavicular area.
    • Not typically associated with right atrial dilatation on CXR.
  • Physiology: Leads to wide pulse pressure and prominent (bounding) peripheral pulses due to continuous runoff of blood from aorta to pulmonary artery.
  • Management (when PDA is vital): For cyanotic CHDs dependent on PDA for pulmonary or systemic blood flow, administer Prostaglandin E1 (PGE1) to keep the ductus arteriosus open.
• Ventricular Septal Defect (VSD)
  • Large VSD Presentation:
    • Symptoms: Progressive tachypnea, poor feeding, failure to thrive, cool extremities, intercostal retractions.
    • Auscultation: Holosystolic murmur on the left sternal border (due to VSD flow), loud second heart sound (P2 component due to pulmonary hypertension).
    • Pathophysiology:
      • Intercostal retractions are due to pulmonary vascular congestion.
      • Liver enlargement can occur due to congestive heart failure.
    • ECG/CXR: Left atrial dilatation on ECG, cardiomegaly on CXR.
    • Symptoms typically start after 4-8 weeks with dyspnea.
  • Small VSD: Often presents with a loud, high-pitch pansystolic murmur heard best at the apex or lower left sternal border; the murmur becoming louder can indicate the VSD is getting smaller.
  • Failure to gain weight can be due to increased metabolic demand and poor feeding.
  • Not typically associated with wide pulse pressure (unlike PDA).
• Atrial Septal Defect (ASD)
  • Clinical Features:
    • Often asymptomatic.
    • Auscultation: Soft mid-systolic ejection murmur (grade 2/6) at the left upper sternal border (pulmonic area) or left second intercostal space, with wide and fixed splitting of the second heart sound (S2).
    • Gallop rhythm is not a typical finding of ASD.
  • Complications (Large Secundum ASD):
    • Dilatation of the right atrium (RA) and right ventricle (RV).
    • Risk of tachyarrhythmias (e.g., atrial fibrillation) in adulthood.
    • Risk of paradoxical emboli, increasing with age.
    • Risk of Eisenmenger syndrome is rare and occurs late in uncorrected large defects.
    • Large defects often require closure even if asymptomatic.
  • CXR: May show enlarged RA and increased pulmonary markings.
  • Not associated with left ventricular dilatation (causes RV volume overload).
• Tetralogy of Fallot (TOF)
  • Components:
    1. Ventricular Septal Defect (VSD)
    2. Pulmonary Stenosis (PS) (determines severity of cyanosis)
    3. Overriding Aorta
    4. Right Ventricular Hypertrophy (RVH)
  • Clinical Presentation:
    • Cyanosis: Varies with severity of PS; classically presents around 3-9 months.
    • Murmur: Loud, long, harsh systolic ejection murmur at the left sternal border (due to RV outflow tract obstruction/PS).
    • Right ventricular heave due to RVH.
    • Pulses are typically normal.
    • Cyanotic spells (“Tet spells”): Attacks of increased cyanosis, often precipitated by crying, feeding, or defecation.
  • CXR: Boot-shaped heart with decreased pulmonary vascular markings.
  • Factors Worsening Cyanosis: Exercise, fever, dehydration, travel to high altitude (due to decreased SVR or increased PVR).
  • Factors Improving Cyanosis: Squatting (increases SVR, promoting pulmonary blood flow).
  • Generally not associated with cardiomegaly on CXR unless other complications.
• Transposition of Great Arteries (TGA)
  • Presentation: Early and severe cyanosis in a newborn, often without a significant murmur unless associated defects (e.g., VSD, PDA) are present.
  • CXR: Classic finding is an “egg-on-a-string” appearance (narrow mediastinum with ovoid cardiac silhouette).
  • Survival: Often dependent on mixing at atrial level (PFO/ASD) or ductal level (PDA).
• Aortic Stenosis (AS)
  • Murmur: Systolic ejection murmur, typically loudest at the right upper sternal border, radiating to the suprasternal notch and carotid arteries.
• Coarctation of Aorta (CoA)
  • Clinical Features:
    • Hypertension in upper extremities.
    • Radio-femoral pulse delay and weaker/absent femoral pulses.
    • Displaced apical impulse, LVH on ECG.
    • Systolic murmur often heard best in the inter-scapular area (back).
  • CXR:
    • Rib notching (due to collateral circulation via intercostal arteries) in older children.
    • Cardiomegaly.
    • Not typically associated with a wide mediastinum.
• Tricuspid Atresia
  • Presentation: Cyanotic CHD.
  • ECG: Characteristic finding is left axis deviation (due to hypoplastic RV and relatively larger LV).
  • Physical Exam: May have a holosystolic murmur if VSD is present. No right ventricular heave (RV is hypoplastic); left ventricle is often enlarged.
• Hypoplastic Left Heart Syndrome (HLHS)
  • Survival is dependent on a patent ductus arteriosus for systemic circulation and a PFO for shunting.
• Truncus Arteriosus
• Total Anomalous Pulmonary Venous Return (TAPVR)
• Pulmonary Atresia with Intact Ventricular Septum

II. Cardiovascular Physiology & General Principles