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Congenital Heart Disease, Cyanotic, Emergency Medicine


Basics


Description


  • Aberrant embryonic development results in mixing of deoxygenated and oxygenated blood returning to systemic circulation by 2 mechanisms:
    • Right-to-left intracardiac shunt
    • Anatomic defects of the aortic root
  • Subtypes: 5 T's, 2 E's, single ventricle:
    • Tetralogy of Fallot (TOF):
      • Ventricular septal defect (VSD)
      • Right ventricular (RV) outflow obstruction
      • Overriding aorta
      • RV hypertrophy (RVH)
    • Transposition of the great arteries (TGA):
      • Aorta arises from RV and pulmonary artery from left ventricle (LV)
    • Tricuspid atresia:
      • No outlet from right atrium to RV
      • Obligatory atrial level connection
    • Truncus arteriosus:
      • Single arterial trunk for systemic, pulmonic, and carotid circulations
    • Total anomalous pulmonary venous return (TAPVR):
      • Pulmonary veins drain into systemic venous circulation
      • Supracardiac, cardiac, infracardiac, or mixed
    • Ebstein anomaly of tricuspid valve:
      • Abnormal and displaced tricuspid valve divides RV resulting in poor RV function
    • Eisenmenger syndrome:
      • Complication in longstanding acyanotic heart disease with L→R shunts
      • Pulmonary vascular resistance reaches suprasystemic levels; R→L shunt
    • Single ventricle physiology:
      • Total mixing of systemic and venous return

Etiology


For most forms, cause is unknown �

Diagnosis


  • Most common initial ED presentations of cyanotic congenital heart disease (CHD):
    • Cyanosis
    • CHF
    • Circulatory collapse
  • Physiologic stress triggers cyanosis in older patients with CHD:
    • Cardiac shunt obstruction
    • Pulmonary disease
    • Decreased systemic vascular resistance
    • Fever
    • Dehydration

Signs and Symptoms


  • Central cyanosis:
    • Visible in lips, nail beds, mucosa
    • Increases with cry or agitation
    • Minimal change with 100% O2
  • CHF:
    • Rales, gallop, hepatomegaly, scalp edema
  • Hypercyanotic spells or "Tet spells"�:
    • Restless and hyperpneic then increased cyanosis then syncope
    • Follows reductions in already compromised pulmonary blood flow:
      • Wakening, feeding, vigorous cry, exercise
  • Older child may compensate by squatting.
  • Temporary reduction or absence of systolic ejection murmur during spell

History
  • Family history of CHD:
    • If parent or sibling: Increased risk of CHD
    • If 2 relatives: Risk of CHD triples
  • Prenatal history:
    • Exposure to teratogens
    • Abnormal fetal ultrasound
  • TOF:
    • Often asymptomatic at birth; symptoms develop as RV infundibulum hypertrophies
    • Severe RV outflow obstruction; neonatal cyanosis (duct-dependent lesion)
    • Cyanosis during crying or feeding (Tet spells) in toddlers
    • Older, uncorrected patients:
      • Dyspnea on exertion and growth delay
  • Tricuspid atresia:
    • Usually cyanotic from birth
    • Feeding difficulties
    • Older patients show dyspnea on exertion and easy fatigability
  • Ebstein anomaly:
    • Teens may present with dysrhythmias.
  • TGA:
    • Presents in 1st hr to days of life
  • TAPVR:
    • Neonatal presentation; severely ill:
      • Cyanosis
      • Does not improve with mechanical ventilation
    • Infantile presentation; heart failure:
      • Mild cyanosis
    • If no obstruction to pulmonary venous return:
      • Asymptomatic or mild cyanosis
      • Frequent pneumonias
      • Growth problems
  • Truncus arteriosus:
    • Mild cyanosis in newborn
    • Heart failure in older infants

Physical Exam
  • TOF:
    • Loud systolic murmur left sternal border (LSB)
    • Systolic thrill in 50%
    • +/- Continuous murmur of PDA
    • Loud, single 2nd heart sound (S2)
    • RV prominence/bulge
    • Older, uncorrected patients:
      • Dusky, blue skin
      • Clubbing of digits
      • Retinal engorgement
  • Tricuspid atresia:
    • Tachypnea
    • Regurgitant murmur from VSD at LSB
    • +/- continuous PDA murmur
    • Single S2
    • Prominent LV impulse
  • Ebstein anomaly:
    • Holosystolic murmur of tricuspid regurgitation
    • Many have diastolic murmur
    • Gallop
  • TGA:
    • Single, loud S2
    • Severe hypoxemia
  • TAPVR:
    • Neonatal; severe tachypnea and cyanosis
    • Infantile; heart failure:
      • Tachycardia
      • Systolic ejection murmur at LSB
      • Mid-diastolic murmur at lower LSB
      • Gallop
      • Fixed, split S2
      • Hepatomegaly
  • Truncus arteriosus:
    • Newborn:
      • Mild cyanosis
      • Regurgitant systolic murmur at LSB
      • Single S2
  • Older infants; heart failure:
    • Hyperdynamic precordium
    • Bounding pulses
    • Wide pulse pressure
    • Loud, single S2
    • Systolic ejection murmur and thrill
    • Mid-diastolic murmur

Essential Workup


  • Oxygen saturation
  • ABG
  • CBC, glucose
  • Sepsis evaluation
  • CXR to assess pulmonary blood flow
  • EKG to assess for hypertrophy and QRS axis
  • Cardiology consult and ECG

Diagnosis Tests & Interpretation


Lab
  • Decreased room air oxygen saturation
  • Hyperoxia test:
    • ABG in room air and after several minutes 100% oxygen:
      • PaO2 >150 in O2; no intracardiac shunt
      • PaO2 <100 in O2; highly suspicious of cyanotic CHD
  • CBC: Erythrocytosis with chronic cyanosis

Imaging
  • CXR:
    • Decreased pulmonary blood flow:
      • TOF (enlarged RV)
      • Tricuspid atresia (enlarged LV)
      • Single ventricle physiology
    • Increased pulmonary flow:
      • Transposition of the great vessels (large RV)
      • TAPVR (large RV)
      • Truncus arteriosus (large LV and RV)
    • Classic CXR descriptions:
      • Boot-shaped heart: TOF; large and upturned RV looks like toe of boot
      • Egg on a string: TGA; narrow mediastinum, great vessels anterior/posterior position
      • Snowman sign: Supracardiac TAPVR; upper portion formed by pulmonary veins

Diagnostic Procedures/Surgery
EKG: �
  • TOF:
    • Right axis deviation (RAD)
    • RVH
  • TAPVR:
    • RAD
    • RVH and right atrial enlargement (RAE)
  • Transposition of the great vessels:
    • RAD
    • RVH
  • Tricuspid atresia:
    • Superior axis
    • LVH, RAE, LAE
  • Truncus arteriosus:
    • RVH, LVH
  • Ebstein anomaly:
    • Right bundle branch block
    • Often Wolff-Parkinson-White

Differential Diagnosis


  • Pulmonary:
    • Pneumothorax/hemothorax
    • Bronchopulmonary dysplasia
    • Congenital lung hypoplasia/dysplasia
    • Pulmonary hemorrhage
    • Pulmonary embolus
    • Pulmonary HTN
    • Diaphragmatic hernia
    • Foreign body/anatomic obstruction
  • Cardiac:
    • Cyanotic CHD
    • CHF
    • Cardiogenic shock
  • Infectious:
    • Pneumonia, bronchiolitis
    • Sepsis
  • Neurologic:
    • Seizure
    • Neuromuscular disease
    • Drug-induced respiratory depression
  • Other:
    • Polycythemia
    • Methemoglobinemia
    • Dehydration
    • Hypoglycemia

Treatment


Initial Stabilization/Therapy


  • Maintain warmth (cold ↑ O2 consumption).
  • Treat hypoglycemia and acidosis.
  • Maintain oxygenation.
  • Establish IV access.
  • Prepare for endotracheal intubation.

  • High oxygen tensions promote ductal closure.
  • Place air filters on all IV lines to avoid paradoxical emboli through R→L shunt.

Ed Treatment/Procedures


  • Administer prostaglandin E1 (PGE1) to dilate or reopen the ductus arteriosus:
    • Continuous IV infusion 0.05-0.1 μg/kg/min
    • Complications include apnea, bradycardia, hypotension, and seizures:
      • Generally intubate prior to transport
    • Not effective for obstructed TAPVR:
      • May require ECMO awaiting surgery
    • Overall benefits far outweigh potential risks
  • Evaluate and treat alternate causes of cyanosis:
    • Septic workup and empiric antibiotics
    • Fluid resuscitate (increments of 10 mL/kg)
    • Maintain normoglycemia
  • Patients with Tet spells:
    • Provide a calming environment.
    • Place child in knee-chest position.
    • Supplemental O2 if not agitating to patient
    • IV or IM morphine
    • For severe cases not responding to above:
      • IV bicarbonate to treat severe acidosis
      • IV phenylephrine to ↑systemic vascular resistance and reduce R→L shunt
      • IV propranolol for β-adrenergic blockade
  • Cyanosis in the older patient with known CHD:
    • 10-20 mL/kg NS IV if dehydration likely
    • Supplemental O2 if suspicious for pulmonary diseases
    • Antipyretics for fever
    • Antibiotics for pneumonia/infectious process
  • Circulatory collapse from CHD:
    • Fluid resuscitation
    • Inotropes: Dobutamine, dopamine, milrinone
    • Aggressive treatment of acidosis

Medication


  • Acetaminophen: 15 mg/kg PO or PR
  • Ampicillin: 50 mg/kg IV
  • Dobutamine: 5-20 μg/kg/min IV
  • Dopamine: 5-20 μg/kg/min IV
  • Gentamicin: 4 mg/kg/d IV or 2.5 mg/kg/dose
  • Ibuprofen: 10 mg/kg PO (>6 mo)
  • Milrinone: 0.25-1 μg/kg/min
  • Morphine sulfate: 0.1 mg/kg SC, IM, or IV
  • Phenylephrine: 0.5-5 μg/kg/min IV
  • Propranolol: 0.1 mg/kg IV
  • PGE1: 0.05-0.1 μg/kg/min
  • Sodium bicarbonate: 1-2 mEq/kg IV

Follow-Up


Disposition


Admission Criteria
  • All newborns with suspected CHD:
    • Admit to pediatric ICU.
  • CHD with acute worsening of cyanosis or CHF
  • CHD with symptomatic pneumonia or respiratory syncytial virus

Discharge Criteria
  • Determine in consult with cardiologist
  • Patients who respond to minimal intervention (i.e., TOF patients treated noninvasively)
  • Ensure close follow-up.

Issues for Referral
  • Primary care physician to coordinate care
  • Cardiologist for diagnosis, medical management, and ongoing monitoring
  • Cardiothoracic evaluation for surgery

Follow-Up Recommendations


  • Plan for follow-up should be determined in consult with the pediatric cardiologist.
  • Clear instructions for return visits, as any physiologic stress may worsen condition.

Pearls and Pitfalls


  • Visual appearance of cyanosis requires >3-5 mg/dL deoxygenated hemoglobin.
  • Duct-dependent lesions:
    • Present at 2-3 wk of age
    • Sudden cyanosis or cardiovascular collapse
    • Treat with PGE1:
      • Beware apnea and hypotension

Additional Reading


  • Apitz �C, Webb �GD, Redington �AN. Tetralogy of Fallot. Lancet.  2009;374:1462-1471.
  • Bonow �RO, Mann �DL, Zipes �DP, et al., eds. Congenital heart disease. Braunwalds Heart Disease. 98th ed. Philadelphia, PA: Saunders Elsevier; 2012:1411-1467.
  • Dolbec �K, Mick �N. Congenital heart disease. Emerg Med Clin North Am.  2011;29:811-827.
  • Fleisher �GR, Ludwig �S, Bachur �RG, et al., eds. Cardiac emergencies. Textbook of Pediatric Emergency Medicine. 6th ed. Philadelphia, PA: Lippincott Williams, & Wilkins, 2010:690-701.
  • Yee �L. Cardiac emergencies in the first year of life. Emerg Med Clin North Am.  2007;25:981-1008.

Codes


ICD9


  • 745.2 Tetralogy of fallot
  • 745.4 Ventricular septal defect
  • 746.89 Other specified congenital anomalies of heart
  • 747.21 Anomalies of aortic arch
  • 429.3 Cardiomegaly
  • 745.10 Complete transposition of great vessels

ICD10


  • Q21.0 Ventricular septal defect
  • Q21.3 Tetralogy of Fallot
  • Q24.8 Other specified congenital malformations of heart
  • Q25.4 Other congenital malformations of aorta
  • I51.7 Cardiomegaly
  • Q20.3 Discordant ventriculoarterial connection

SNOMED


  • 12770006 cyanotic congenital heart disease (disorder)
  • 86299006 Tetralogy of Fallot (disorder)
  • 30288003 Ventricular septal defect (disorder)
  • 253530007 right ventricular outflow tract obstruction (disorder)
  • 204296002 Discordant ventriculoarterial connection
  • 63934006 Overriding aorta (disorder)
  • 89792004 right ventricular hypertrophy (disorder)
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