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Pediatric Cardiac Emergencies Gavin Greenfield Peggy Thomsen.

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1 Pediatric Cardiac Emergencies Gavin Greenfield Peggy Thomsen

2 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

3 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

4 Infant Cardiac Disease Leading to ER Presentation Congenital Acquired –Cardiomyopathy –Myocarditis (usually with CHF) –Dysrhythmias

5 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

6 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

7 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

8 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

9 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

10 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

11 Etiology infectious –viral –bacterial –TB –fungal –parasitic Connective tissue –RA –Rheumatic fever –SLE Metabolic / Endocrine –uremia –hypothyroid Hematology / Oncology –bleeding diathesis –malignancy Trauma Iatrogenic

12 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

13 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

14 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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16 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

17 Cardiac Syncope Dysrhythmias –tachy –brady Outflow obstruction Myocardial Dysfunction cardiac syncope often precedes future sudden cardiac death

18 Sudden Cardiac Death includes those causes that directly relate to cardiovascular dysfunction one third of all sudden deaths

19 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

20 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

21 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

22 Other dysrhythmias WPW and other SVT’s AV block –usually acquired, rarely congenital Sick sinus syndrome

23 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

24 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

25 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”:

26 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

27 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%

28 Congenital Heart Disease Fetal to Neonatal Circulation

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30 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

31 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

32 CHD Classified as Cyanotic vs. Acyanotic Acyanotic (L to R shunts, stenotic lesions) –ASD –VSD –PDA –aortic valve stenosis –pulmonic valve stenosis –aortic coarctation

33 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

34 Congenital Heart Disease History –feeding difficulties –tachypnea –diaphoresis –syncope –cyanotic episodes –failure to thrive

35 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

36 Cyanotic Congenital Heart Disease R to L shunts mixing lesions

37 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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39 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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41 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

42 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

43 Acyanotic Congenital Heart Disease L to R shunts stenotic lesions

44 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

45 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”:

46 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

47 LV Outflow Obstruction

48 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

49 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

50 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

51 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”

52 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

53 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

54 Bradyarrhythmias Etiology –hypoxia, acidosis, hypoglycemia –excess vagal stimulation (ex. intubation) Treatment –Epinephrine –Atropine if known vagally mediated or heart block

55 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

56 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

57 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

58 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

59 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

60 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

61 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

62 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

63 ER Treatment management of complicating features of carditis (CHF) –significant carditis or CHF managed with glucocorticoids high-dose ASA mg/kg/day pencillin long term management of rheumatic heart disease

64 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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