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Pediatric Cardiac Emergencies Gavin Greenfield Peggy Thomsen
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► 4 year old female presents with fast breathing, “grunting”, cough x 5 days ► seen 2 days earlier and started on steroids and bronchodilators ► initial vitals: HR 150, BP 100/85, RR 36, T 37.5
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► 1 month old with irritability, poor feeding (fatigues), failure to thrive, fast breathing ► no fever or runny nose ► physical exam: HR 160, RR 60 with minimal respiratory distress, gallop rhythm, rales
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Infant Cardiac Disease Leading to ER Presentation ► Congenital ► Acquired Cardiomyopathy Myocarditis (usually with CHF) Dysrhythmias
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Congestive Heart Failure ► the physiologic state in which cardiac output is unable to meet tissue metabolic demands (Rosen) ► CO = HR x SV ► SV dependent upon preload, afterload, contractility
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CHF - Presentation ► infants: irritable, poor feeding (early fatigue), failure to thrive, respiratory symptoms ► always consider in patients with respiratory symptoms often misdiagnosed as respiratory illness / infection
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CHF - Etiology ► Increased Preload L to R shunts (VSD, PDA, AV fistula) severe anemia ► Increased Afterload HTN Congenital (aortic stenosis, coarctation of aorta) ► Decreased Contractility myocarditis, pericarditis with tamponade cardiomyopathy (dilated or hypertrophic) Kawasaki syndrome (early phase) metabolic: electrolyte, hypothyroid myocardial contusion toxins: dig, calcium channel blockers, beta blockers ► Dysrhythmia
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CHF - Etiology ► presents immediately at birth anemia, acidosis, hypoxia, hypoglycemia, hypocalcemia, sepsis ► presents at 1 day (congenital) PDA in premature infants ► presents in first month (congenital) HPLV, aortic stenosis, coarctation, VSD presents later ► presents later (acquired) myocarditis, cardiomyopathy (dilated or hypertrophic), SVT, severe anemia, rheumatic fever
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Myocarditis ► leading cause of dilated cardiomyopathy and one of the most common causes of CHF in children ► etiology: idiopathic, viral, bacterial, parasitic ► hallmark is CHF ► failure to respond to bronchodilators in wheezing child ► treatment includes inotropes, afterload reduction, diuretics, antibiotics, antivirals
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Pericarditis ► sharp stabbing precordial pain ► worse with supine and better leaning forward ► no sensory innervation of the pericardium pain referred from diaphragmatic and pleural irritation
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Etiology ► infectious viral bacterial TB fungal parasitic ► Connective tissue RA Rheumatic fever SLE ► Metabolic / Endocrine uremia hypothyroid ► Hematology / Oncology bleeding diathesis malignancy ► Trauma ► Iatrogenic
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Pericarditis ► usually a benign course ► virulent bacteria (H. flu, E. coli) can cause constrictive pericarditis and subsequent tamponade – may need urgent pericardiocentesis ► uncomplicated pericarditis usually responds to rest and anti-inflammatories
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Chest Pain ► 4% of children will have a cardiac origin ► remainder: MSK, pulmonic (asthma, bronchitis, pneumonia), GI ► Cardiac causes: myocarditis, pericarditis, structural abnormalities such as congenital heart disease or hypertrophic cardiomyopathy
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► 14 year old male collapses at school while in class ► non-responsive for one minute ► feels fine in the department ► Approach?
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Syncope ► 20-50% of adolescents experience at least one episode of syncope most cases benign ► Pathophysiology vascular orthostatic, hypovolemia neurally mediated hypoxia: PE, CNS depression from OD, CO cardiac
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Cardiac Syncope ► Dysrhythmias tachy brady ► Outflow obstruction ► Myocardial Dysfunction ► cardiac syncope often precedes future sudden cardiac death
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Sudden Cardiac Death ► includes those causes that directly relate to cardiovascular dysfunction ► one third of all sudden deaths
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Sudden Cardiac Death ► Etiology myocarditis cardiomyopathy (hypertrophic) cyanotic and noncyanotic congenital heart disease valvular heart disease congenital complete heart block WPW long QT syndrome Marfan syndrome coronary artery disease anomalous coronary arteries
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Risk Factors for Serious Cause of Syncope ► history of cardiac disease in patient ► FH of sudden death, cardiac disease, or deafness ► recurrent episodes ► recumbent episode ► exertional ► prolonged loss of consciousness ► associated chest pain or palpitations ► medications that can alter cardiac conduction
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What to look for in the Department: EKG ► Long QT syndrome congenital or acquired get paroxysmal v tach with torsades de pointes congenital long QT associated with hypertrophic cardiomyopathy long QT defined as corrected QT longer than 0.44 s T wave alternans sometimes present can have normal ECG in the department two clinical syndromes not associated with structural heart disease: Romano-Ward and Jervell-Lange-Nielsen
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Other dysrhythmias ► WPW and other SVT’s ► AV block usually acquired, rarely congenital ► Sick sinus syndrome
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Idiopathic Hypertrophic Cardiomyopathy ► aka IHSS ► both a fixed and dynamic subvalvular obstruction ► characterized by ventricular hypertrophy with principle involvement of the ventricular septum ► associated with long QT ► autosomal dominant ► often presents with exertional syncope ► 10 year mortality is 50% for children diagnosed by age 14
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Other structural cardiac diseases ► dilated cardiomyopathy usually secondary to myocarditis syncope and death secondary to ventricular dysrhythmias or severe myocardial dysfunction ► arrhythmogenic RV dysplasia ► congenital cyanotic and non-cyanotic heart disease ► valvular diseases aortic stenosis ► coronary artery anomalies exertional syncope or sudden death aberrant artery passes between aorta and pulmonary artery
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► 2 week old infant brought in by parents with difficulty breathing ► HR 180, BP 50/P, RR 80, T 37.5 ► history and physical ► investigations ► repeat vitals: HR 30, no BP, RR 12 ► “definitive treatment”:
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► 4 year old male presents with 2 weeks history of cough, fast breathing, fatigue, decreased exercise tolerance, “puffy eyes” ► On exam: tachypneic, moderate respiratory distress, O2 sats 92%, bilateral crackles
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► 6 month male presents with failure to thrive, fast breathing, blue lips ► On exam tachypnea but no respiratory distress, lips and extremities blue, oxygen saturations 70%
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Congenital Heart Disease ► Fetal to Neonatal Circulation
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Classification
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Congenital Heart Disease Classification ► pink (in failure) ► blue (no distress) ► gray (in shock)
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Anatomic Classification; 4 groups ► Right to Left Shunt Tetralogy of Fallot Transposition of the Great Arteries Tricuspid Atresia ► Left to Right Shunt ASD VSD PDA ► Stenotic Aortic valve stenosis Pulmonic valve stenosis Aortic coarctation ► Mixing Truncus Total Anomalous Pulmonary Venous Return Hypoplastic left heart syndrome
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CHD Classified as Cyanotic vs. Acyanotic ► Cyanotic (R to L shunt and mixing lesions) tetralogy of Fallot transposition of great vessels tricuspid atresia total anomalous pulmonary venous return truncus arteriosus hypoplastic left heart syndrome
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CHD Classified as Cyanotic vs. Acyanotic ► Acyanotic (L to R shunts, stenotic lesions) ASD VSD PDA aortic valve stenosis pulmonic valve stenosis aortic coarctation
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Cyanosis ► Classified as central or peripheral ► Central cyanosis (always abnormal) mucous membranes, trunk, extremities classified as cardiac (R to L shunt) or pulmonary ► Peripheral cyanosis (acrocyanosis) no involvement of mucous membranes involves hands, feet, circumoral area common in neonates from vasomotor instability CHF, PVD, shock, cold extremities
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Congenital Heart Disease ► History feeding difficulties tachypnea diaphoresis syncope cyanotic episodes failure to thrive
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Congenital Heart Disease ► Physical Examination colour: pink, blue, gray vitals: tachypnea, tachycardia, BP symptoms suggestive of infection palpation and auscultation of precordium chest auscultation survey for organomegaly pulses in all extremities
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Cyanotic Congenital Heart Disease ► R to L shunts ► mixing lesions
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Tetralogy of Fallot – the classic cyanotic lesion ► RV outflow obstruction ► RVH ► VSD ► overriding aorta ► CXR reveals boot shaped heart with decreased pulmonary blood flow
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► 2 month old female with known tetralogy of Fallot brought in with 24 hour history of vomiting and diarrhea ► On exam: moderate dehydration ► during IV attempts patient becomes irritable and cyanotic
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Treatment of Tet Spell ► quiet, calm environment ► knee-chest or squatting position increases afterload thus decreasing R to L shunting ► Oxygen ► Morphine to treat hyperpnea and decrease systemic catecholamines ► Phenylephrine increases afterload thereby decreasing R to L shunt ► Manual external aortic compression below level of renal arteries ► Propranolol to block beta receptors in infundibulum therefore lessening RV outflow obstruction
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Consider ► consider small volume challenge (5-10 cc/kg) to increase preload and reduce dynamic outflow obstruction ► ?NaHCO3 for correction of acidosis ► may need general anesthesia if severe and/or prolonged spell ► interim prophylactic treatment with propranolol while awaiting surgery
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Acyanotic Congenital Heart Disease ► L to R shunts ► stenotic lesions
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VSD Most common congenital lesion Large VSD’s may be silent and become symptomatic in first few weeks as pulmonary resistance SOB and diaphoresis w feeds Poor weight gain Systolic murmur CXR demonstrates CHF
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► 2 week old infant brought in by parents with difficulty breathing ► HR 180, BP 50/P, RR 80, T 37.5 ► history and physical ► investigations ► repeat vitals: HR 30, no BP, RR 12 ► “definitive treatment”:
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Differential Dx of Infant Shock ► infection (septic shock/ meningitis) bacterial: GBS, E. coli, S. aureus virus: enteroviruses, H. simplex ► metabolic: amino/organic acidopathies, urea cycle defect ► ‘hypoxic shock’: eg. RSV, C.N.S. depression ► heart disease: congenital or acquired
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LV Outflow Obstruction
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► Aortic coarctation ► Hypoplastic left heart syndrome ► Aortic stenosis (presents later) ► Rosen: “any neonate in shock that does not respond to fluids or pressors has LV outflow obstruction until proven otherwise” ► complete obstruction incompatible with life unless there is shunting
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Coarctation of the aorta Most often distal to L subclavian Can be diagnosed anytime Neonates present as acutely ill, gray shocky (from DA closure) Systolic murmur at the back Hepatomegaly Diminished femoral pulses BP difference b/t arms and legs CXR demonstrates CHF Treatment of CHF Prostaglandin E1
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Duct Dependant Lesions ► Duct needed to perfuse lungs or periphery ► Lungs Tetralogy of Fallot, transposition of great arteries, tricuspid or pulmonary atresia ► a patent ductus arteriosus results in preserved pulmonary blood flow ► Periphery Aortic coarctation (severe) and Hypoplastic left heart
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Treatment of acute decline in patients with ductal dependant lesions ► Open the closed duct ► Prostaglandin E1 0.1 ug/kg/min infusion ► reduce dosage as perfusion and colour return ► Rosen: “any infant in the first week of life with decreased perfusion, hypotension, or acidosis should be considered a candidate for PGE1 administration”
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What do you need to know about PGE ? ► it functions by dilating vascular smooth muscle, both systemically and in the pulmonary vascular bed ► it’s use in CHD pts’ is to maintain patency of the PDA, whether to maintain PBF or to maintain systemic blood flow past a
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Classification Review ► pink child in respiratory distress suggests acyanotic chd (L to R shunt, coarct, aortic stenosis) ► blue cyanotic child in little respiratory distress suggests R to L shunt or mixing lesions ► gray, shocky baby suggests outflow tract obstruction
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Bradyarrhythmias ► Etiology hypoxia, acidosis, hypoglycemia excess vagal stimulation (ex. intubation) ► Treatment Epinephrine Atropine if known vagally mediated or heart block
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Congenital Bradyarrhythmias ► complete AV block autoimmune injury to fetal conduction system secondary to maternal autoimmune disease atropine, isoproteronol, epinephrine may be tried temporarily prior to pacing
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Tachyarrhythmias ► Supraventricular Tachycardia re-entrant with accessory pathway (AV nodal or WPW) re-entrant without accessory pathway (re-entry occurs within sinus node or within atrium) ectopic ► nonspecific presentations in infants
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Murmurs ► Areas aortic: R 2 nd intercostal space pulmonic: L 2 nd intercostal space mitral: apex tricuspid and VSD: L lower sternal border ► Pathologic diastolic, holosystolic, late systolic, continuous
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Innocent Heart Murmurs ► History normal growth and development, normal exercise tolerance no history of cyanosis ► Physical Examination Grade II or less, localized varies with position (decreased with upright posture) normal precordium normal pulses ► Lab normal EKG, normal CXR
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3 innocent murmurs ► Still’s short ejection systolic murmur musical or vibratory quality heard best between apex and left sternal border ► physiologic pulmonary flow murmur harsh, located at pulmonic area ► peripheral arterial stenosis low-intensity systolic ejection murmur best heard in axilla and back
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► 8 year old male presents with fever, arthralgias ► mother mentions that he had a sore throat 3 weeks ago for a few days with spontaneous resolution ► a throat swab was done and positive for GAS but patient better so did not take the prescribed antibiotics
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Acute Rheumatic Fever ► school aged children ► associated with certain strains of Group A beta- hemolytic streptococcal infections ► the streptococcal organism stimulated antibody production to host tissues CT of heart, joints, CNS, subcutaneous tissues, skin ► carditis is an endomyocarditis with valvulitis involving mitral and aortic valves ► 2 to 6 weeks post streptococcal pharyngitis
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Jones Criteria ► Major carditis ► new or changing murmur ► cardiomegaly, CHF ► pericarditis migratory polyarthritis chorea erythema marginatum subcutaneous nodules ► Minor fever arthralgia history of previous ARF elevated ESR, CRP prolonged PR on EKG Rising titer of antistreptococcal antibodies
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Erythema Marginatum
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ER Treatment ► management of complicating features of carditis (CHF) significant carditis or CHF managed with glucocorticoids ► high-dose ASA 75-100 mg/kg/day ► pencillin ► long term management of rheumatic heart disease
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Pediatric EKG’s General Principles ► RV Dominance at birth; gradually changes to LV dominance ► axis up to +180 in normal newborn ► T waves negative in right precordial leads until adolescence (except they are upright in first week of life)
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