Cardiac Emergencies.ppt


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  • further history: recent URI – no further fever or runny nose, PMHx negative, FH negative for asthma further physical examination: moderate respiratory distress, circumoral cyanosis, diffuse expiratory wheezes and crackles, cool extremities, delayed cap refill, liver edge palpated 3 cm below right costal margin treatment: no response to bronchodilator, condition worsens with fluid bolus CXR: large cardiac silhouette and pulmonary edema
  • feeding is infant’s exertion
  • neonatal myocardium is stiff and unable to increase contractility – must increase HR to get increased CO. With increased hr’s get decreased diastolic filling – therefore infants have a reduced cardiac reserve – limited ability to handle pressure or volume overloads
  • typical physical exam and CXR findings symptoms and signs of increased pulmonary venous pressure and respiratory infection overlap -fever, runny nose, stridor, vomiting suggest infection -dyspnea during feeding, slow feeding, tachypnea, dyspnea suggest elevated pulmonary venous pressures Feeding is how infants exert themselves – symptoms during feeding are equivalent to SOBOE
  • Tintinalli
  • viral causes include: coxsackie, echovirus, mumps, influenza, varicella, Epstein-Barr, HIV bacterial causes include: corynebacterium, Lyme disease, E. coli, Haemophilus influenzae other clues to myocarditis include fever, muscle tenderness, exposure to known toxins or etiologic agents
  • pericaridocentesis with an 18G over the needle catheter is indicated in the emerg dept. if an infant with large heart becomes rapidly unstable with loss of pulse
  • Tintinalli
  • 25% of children suffering sudden death have history of syncope (percentage may be higher in those patients with a sudden cardiac death) History syncope during exertion increased likelihood of serious etiology FH of structural heart disease, dysrhythmias, sudden death Physical when trying to rule this out pay particular attention to the CV exam: palpation of cardiac impulse, auscultation of heart, evaluation of peripheral pulses; orthostatic measurements
  • Not all sudden death is cardiac (seizure, toxic ingestion, asthma)
  • most common cause of sudden cardiac death in athletes is hypertrophic cardiomyopathy and aberrant coronary arteries - can also have all the other causes commotio cordis
  • Romano-Ward: autosomal dominant condition not associated with deafness Jervell-Lange-Nielsen – autosomal recessive disease associated with deafness mortality from untreated congenital long QT syndrome is 50%
  • Secondary hypertrophic cardiomyopathy can occur from AS, aortic coarctation, etc. weakness, fatigue, dyspnea on effort, palpitations, angina pectoris, dizziness, and syncope risk of sudden death even in asymptomatic children electrocardiogram shows left ventricular hypertrophy with or without ST segment depression and T-wave inversion
  • lethargic, blue lips bilateral crackles weak radials, no femorals, delayed cap refill normal pregnancy poor feeding began 5 days ago chest x-ray: large heart, pulmonary edema code the patient Prostaglandin E
  • changes from low to normal pulmonary blood flow oxygenated blood goes from placenta to ivc via ductus venosus. Then to LA to LV to ascending aorta – supplies cerebral circulation venous blood from head and neck enters SVC, RA, RV, through ductus arteriosus into descending aorta to placenta via umbilical arteries and to caudal fetus at birth with first few breaths pulmonary arterioles dilate with drastic decrease in pulmonary vascular resistance and increase in blood circulating through the lungs systemic BP rises with elimination of placental circulation foramen ovale and ductus arteriosus close
  • Heart Murmurs Systolic PDA VSD MR TR Fixed Split S2 ASD R to L shunt – decreased pulmonary vasculature on CXR L to R shunt – increased pulmonary vasculature on CXR  
  • ASD: widely fixed split second heart sound and pulmonic flow murmur as pulmonary vascular resistance decreases with ASD and VSD get increased L to R shunts L to R shunting causes increased pulmonary blood flow…overload…CHF Left to Right Shunts   References U of T 1997 MCCQE Review Notes   Ventricular Septal Defect   Epidemiology most common (30-50%) of all patients with CHD   Small VSD Presentation often asymptomatic Physical Exam early systolic to holosystolic, best heard at LLSB Lab EKG Normal   Moderate to large VSD Presentation delayed growth and development decreased exercise tolerance recurrent URTI’s CHF Physical Exam holosystolic murmur at LLSB with thrill Lab EKG LVH, LAH, RVH CXR increased pulmonary vasculature, cardiomegaly, signs of CHF Management 50% close and 25% get smaller treat CHF with digoxin and diuretics antibiotic prophylaxis against infective endocarditis surgical closure if CHF, failure to thrive, recurrent infections, pulmonary vascular disease   Complications pulmonary hypertension infective endocarditis infundibular hypertrophy   Atrial Septal Defect Three types Ostium primum common in Down’s Ostium secundum most common type Sinus venosus defect located at entry of SVC into RA Presentation often asymptomatic slender body build <10th percentile Physical Exam Grade II-III/VI pulmonic outflow murmur that may be absent in infants widely fixed split S2 hyperdynamic RV RA dilatation, RV hypertrophy Associations 20% of patients with ostium secundum or sinus venosus have mitral valve prolapse Natural History 80-100% closure rate if <8mm if remains patent, CHF and pulmonary hypertension develop in adults Management surgical closure if necessary   Patent Ductus Arteriosus Epidemiology 5-10% of all CHD more common in premature (33% of infants less than 1750 g) duct dependent lesions include RV outflow tract stenosis or atresia, aortic coarctation
  • central cyanosis produced as a result of arterial unsaturation, the aortic blood carrying reduced hemoglobin peripheral cyanosis produced as a result of an excessive amount of reduced hemoglobin in the venous blood, caused by extensive oxygen extraction at the capillary level cardiac cyanosis not improved much by oxygen, pulmonary cyanosis is typically minimal respiratory distress in patients with cardiac cause of their cyanosis
  • RV outflow obstruction; fixed component at level of pulmonary valve, dynamic component at infundibular level; infundibular tissue has relatively more beta receptors resulting in increased obstruction with increased catecholamines RVH; results from RV having to pump against systemic circulation (secondary to over-riding aorta) VSD; free flowing Over-riding aorta (over-rides ventricular septum)
  • shunt becomes more R to L because of increased catecholamines with resulting increased dynamic outflow obstruction shunt worsens with worsening hypoxia and resulting lactic acidosis (secondary to decreased systemic vascular resistance) increased R to L shunt results in increased cyanosis
  • morphine: start with 0.1 mg/kg IM then start IV once have access Propranolol 0.05 mg/kg IV can also consider esmolol 0.5 to 1.0 mg/kg IV both followed by continuous infusions Phenylephrine: 10 ug/kg initial followed by infusion
  • Lack of appropriate treatment will result in severe complications of hypoxia: seizures, lactic acidosis, deteriorating organ function and death
  • remember the pink baby in CHF, the blue baby, and the gray baby in shock the gray baby in shock tends to present earlier and with a profound sudden deterioration clinical picture may be confused with sepsis
  • 98% just below origin of left subclavian artery, located at origin of ductus arteriosus associated bicuspid aortic valve in 70%
  • duct dependent lesions include RV outflow tract stenosis or atresia, aortic coarctation
  • Dose 0.05-0.1 mcg/kg/min as an infusion needs a secure I.V. line side effects include apnea, hypotension, seizures, fever many authors claim running of PGE is indication for intubation
  • re-entrant with accessory pathway – 85% are orthrodromic conduction (anterograde down AV node) more rapid rate > 220 suggests SVT (versus sinus tach) lethargy, poor feeding, heart failure heart rate bang on regular in svt while may get some degree of variability if sinus treatment: adenosine 0.1 mg/kg then double dose and repeat synchronized cardioversion VT stable amiodarone 5 mg/kg over 20-60 minutes procainamide 15 mg/kg over 30-60 minutes lidocaine 1 mg/kg over 2-4 minutes followed by 20-50 ug/kg/min unstable cardioversion 2-4 J/kg (start at 2 and then subsequent shocks at 4) if greater than 8 yo or greater than 50 kg use adult doses of electricity
  • Innocent Heart Murmurs   References U of T 1997 MCCQE Review Notes Pelech, The Cardiac Murmur, When to Refer? Pediatric Clinics of North America, Volume 45, Number 1, February 1998   Epidemiology Heart murmurs very common in children only 0.8 % have congenital heart disease  
  • Physical Exam Palpation normal precordium normal peripheral pulses no radial or brachial / femoral delay Systemic venous status assessed with liver margin   no difference in upper and lower limb BP   Auscultation ejection systolic short duration low intensity, grade III/VI or less crescendo-decrescendo varies with position, usually best heard when supine, decreased with upright posture and Valsalva vibratory in quality (not harsh) otherwise normal history, physical exam and appearance   Lab (only if worried) consider EKG (but must be interpreted by pediatric cardiologist) consider Echo but if feel this is necessary than probably should have Pediatric cardiology referral anyway   5 Innocent Heart Murmurs Systolic Still’s murmur (vibratory systolic) History most typically audible between ages 2-6, may be present as early as infancy or as late as adolescence Physical Exam low frequency, LSB 3-4 ICS or apex vibratory quality Differential Diagnosis subaortic stenosis, small VSD   Pulmonary ejection Physical Exam LSB 2 and 3 ICS and transmits to pulmonary area rough and dissonant without the vibratory musical quality of the Still’s Differential Diagnosis ASD, PS   Peripheral pulmonic stenosis History commonly heard in newborns and infants under 1 year Physical Exam SEM, LSB 2 ICS Differential Diagnosis PDA, PS   Supraclavicular arterial bruit Physical Exam low intensity, above clavicles Differential Diagnosis AS, bicuspid aortic valve   Aortic Systolic Murmur Differential Diagnosis hypertrophic cardiomyopathy, fixed obstructions of LV outflow tract Always refer if suspect this murmur because of the differential diagnosis   Continuous murmurs Venous hum Physical Exam low anterior part of neck, just lateral to sternocleidomastoid, continuous, R>L louder sitting up and with turning head away Differential Diagnosis PDA   Mammary Arterial Souffle most frequently occurs late in pregnancy and in lactating women but can occur in adolescence
  • chorea – the ceaseless occurrence of a wide variety of rapid, highly complex, jerky, dyskinetic movements that appear to be well coordinated but are performed involuntarily Need 2 major or 1 major and 2 minor for diagnosis (plus evidence of antecedent streptococcal infection)
  • Cardiac Emergencies.ppt

    1. 1. Pediatric Cardiac Emergencies Gavin Greenfield Peggy Thomsen
    2. 2. <ul><li>4 year old female presents with fast breathing, “grunting”, cough x 5 days </li></ul><ul><li>seen 2 days earlier and started on steroids and bronchodilators </li></ul><ul><li>initial vitals: HR 150, BP 100/85, RR 36, T 37.5 </li></ul>
    3. 3. <ul><li>1 month old with irritability, poor feeding (fatigues), failure to thrive, fast breathing </li></ul><ul><li>no fever or runny nose </li></ul><ul><li>physical exam: HR 160, RR 60 with minimal respiratory distress, gallop rhythm, rales </li></ul>
    4. 4. Infant Cardiac Disease Leading to ER Presentation <ul><li>Congenital </li></ul><ul><li>Acquired </li></ul><ul><ul><li>Cardiomyopathy </li></ul></ul><ul><ul><li>Myocarditis (usually with CHF) </li></ul></ul><ul><ul><li>Dysrhythmias </li></ul></ul>
    5. 5. Congestive Heart Failure <ul><li>the physiologic state in which cardiac output is unable to meet tissue metabolic demands (Rosen) </li></ul><ul><li>CO = HR x SV </li></ul><ul><li>SV dependent upon preload, afterload, contractility </li></ul>
    6. 6. CHF - Presentation <ul><li>infants: irritable, poor feeding (early fatigue), failure to thrive, respiratory symptoms </li></ul><ul><li>always consider in patients with respiratory symptoms </li></ul><ul><ul><li>often misdiagnosed as respiratory illness / infection </li></ul></ul>
    7. 7. CHF - Etiology <ul><li>Increased Preload </li></ul><ul><ul><li>L to R shunts (VSD, PDA, AV fistula) </li></ul></ul><ul><ul><li>severe anemia </li></ul></ul><ul><li>Increased Afterload </li></ul><ul><ul><li>HTN </li></ul></ul><ul><ul><li>Congenital (aortic stenosis, coarctation of aorta) </li></ul></ul><ul><li>Decreased Contractility </li></ul><ul><ul><li>myocarditis, pericarditis with tamponade </li></ul></ul><ul><ul><li>cardiomyopathy (dilated or hypertrophic) </li></ul></ul><ul><ul><li>Kawasaki syndrome (early phase) </li></ul></ul><ul><ul><li>metabolic: electrolyte, hypothyroid </li></ul></ul><ul><ul><li>myocardial contusion </li></ul></ul><ul><ul><li>toxins: dig, calcium channel blockers, beta blockers </li></ul></ul><ul><li>Dysrhythmia </li></ul>
    8. 8. CHF - Etiology <ul><li>presents immediately at birth </li></ul><ul><ul><li>anemia, acidosis, hypoxia, hypoglycemia, hypocalcemia, sepsis </li></ul></ul><ul><li>presents at 1 day (congenital) </li></ul><ul><ul><li>PDA in premature infants </li></ul></ul><ul><li>presents in first month (congenital) </li></ul><ul><ul><li>HPLV, aortic stenosis, coarctation, VSD presents later </li></ul></ul><ul><li>presents later (acquired) </li></ul><ul><ul><li>myocarditis, cardiomyopathy (dilated or hypertrophic), SVT, severe anemia, rheumatic fever </li></ul></ul>
    9. 9. Myocarditis <ul><li>leading cause of dilated cardiomyopathy and one of the most common causes of CHF in children </li></ul><ul><li>etiology: idiopathic, viral, bacterial, parasitic </li></ul><ul><li>hallmark is CHF </li></ul><ul><li>failure to respond to bronchodilators in wheezing child </li></ul><ul><li>treatment includes inotropes, afterload reduction, diuretics, antibiotics, antivirals </li></ul>
    10. 10. Pericarditis <ul><li>sharp stabbing precordial pain </li></ul><ul><li>worse with supine and better leaning forward </li></ul><ul><li>no sensory innervation of the pericardium </li></ul><ul><ul><li>pain referred from diaphragmatic and pleural irritation </li></ul></ul>
    11. 11. Etiology <ul><li>infectious </li></ul><ul><ul><li>viral </li></ul></ul><ul><ul><li>bacterial </li></ul></ul><ul><ul><li>TB </li></ul></ul><ul><ul><li>fungal </li></ul></ul><ul><ul><li>parasitic </li></ul></ul><ul><li>Connective tissue </li></ul><ul><ul><li>RA </li></ul></ul><ul><ul><li>Rheumatic fever </li></ul></ul><ul><ul><li>SLE </li></ul></ul><ul><li>Metabolic / Endocrine </li></ul><ul><ul><li>uremia </li></ul></ul><ul><ul><li>hypothyroid </li></ul></ul><ul><li>Hematology / Oncology </li></ul><ul><ul><li>bleeding diathesis </li></ul></ul><ul><ul><li>malignancy </li></ul></ul><ul><li>Trauma </li></ul><ul><li>Iatrogenic </li></ul>
    12. 12. Pericarditis <ul><li>usually a benign course </li></ul><ul><li>virulent bacteria (H. flu, E. coli) can cause constrictive pericarditis and subsequent tamponade – may need urgent pericardiocentesis </li></ul><ul><li>uncomplicated pericarditis usually responds to rest and anti-inflammatories </li></ul>
    13. 13. Chest Pain <ul><li>4% of children will have a cardiac origin </li></ul><ul><li>remainder: MSK, pulmonic (asthma, bronchitis, pneumonia), GI </li></ul><ul><li>Cardiac causes: myocarditis, pericarditis, structural abnormalities such as congenital heart disease or hypertrophic cardiomyopathy </li></ul>
    14. 14. <ul><li>14 year old male collapses at school while in class </li></ul><ul><li>non-responsive for one minute </li></ul><ul><li>feels fine in the department </li></ul><ul><li>Approach? </li></ul>
    15. 16. Syncope <ul><li>20-50% of adolescents experience at least one episode of syncope </li></ul><ul><ul><li>most cases benign </li></ul></ul><ul><li>Pathophysiology </li></ul><ul><ul><li>vascular </li></ul></ul><ul><ul><li>orthostatic, hypovolemia </li></ul></ul><ul><ul><li>neurally mediated </li></ul></ul><ul><ul><li>hypoxia: PE, CNS depression from OD, CO </li></ul></ul><ul><ul><li>cardiac </li></ul></ul>
    16. 17. Cardiac Syncope <ul><li>Dysrhythmias </li></ul><ul><ul><li>tachy </li></ul></ul><ul><ul><li>brady </li></ul></ul><ul><li>Outflow obstruction </li></ul><ul><li>Myocardial Dysfunction </li></ul><ul><li>cardiac syncope often precedes future sudden cardiac death </li></ul>
    17. 18. Sudden Cardiac Death <ul><li>includes those causes that directly relate to cardiovascular dysfunction </li></ul><ul><li>one third of all sudden deaths </li></ul>
    18. 19. Sudden Cardiac Death <ul><li>Etiology </li></ul><ul><ul><li>myocarditis </li></ul></ul><ul><ul><li>cardiomyopathy (hypertrophic) </li></ul></ul><ul><ul><li>cyanotic and noncyanotic congenital heart disease </li></ul></ul><ul><ul><li>valvular heart disease </li></ul></ul><ul><ul><li>congenital complete heart block </li></ul></ul><ul><ul><li>WPW </li></ul></ul><ul><ul><li>long QT syndrome </li></ul></ul><ul><ul><li>Marfan syndrome </li></ul></ul><ul><ul><li>coronary artery disease </li></ul></ul><ul><ul><li>anomalous coronary arteries </li></ul></ul>
    19. 20. Risk Factors for Serious Cause of Syncope <ul><li>history of cardiac disease in patient </li></ul><ul><li>FH of sudden death, cardiac disease, or deafness </li></ul><ul><li>recurrent episodes </li></ul><ul><li>recumbent episode </li></ul><ul><li>exertional </li></ul><ul><li>prolonged loss of consciousness </li></ul><ul><li>associated chest pain or palpitations </li></ul><ul><li>medications that can alter cardiac conduction </li></ul>
    20. 21. What to look for in the Department: EKG <ul><li>Long QT syndrome </li></ul><ul><ul><li>congenital or acquired </li></ul></ul><ul><ul><li>get paroxysmal v tach with torsades de pointes </li></ul></ul><ul><ul><li>congenital long QT associated with hypertrophic cardiomyopathy </li></ul></ul><ul><ul><li>long QT defined as corrected QT longer than 0.44 s </li></ul></ul><ul><ul><li>T wave alternans sometimes present </li></ul></ul><ul><ul><li>can have normal ECG in the department </li></ul></ul><ul><ul><li>two clinical syndromes not associated with structural heart disease: Romano-Ward and Jervell-Lange-Nielsen </li></ul></ul>
    21. 22. Other dysrhythmias <ul><li>WPW and other SVT’s </li></ul><ul><li>AV block </li></ul><ul><ul><li>usually acquired, rarely congenital </li></ul></ul><ul><li>Sick sinus syndrome </li></ul>
    22. 23. Idiopathic Hypertrophic Cardiomyopathy <ul><li>aka IHSS </li></ul><ul><li>both a fixed and dynamic subvalvular obstruction </li></ul><ul><li>characterized by ventricular hypertrophy with principle involvement of the ventricular septum </li></ul><ul><li>associated with long QT </li></ul><ul><li>autosomal dominant </li></ul><ul><li>often presents with exertional syncope </li></ul><ul><li>10 year mortality is 50% for children diagnosed by age 14 </li></ul>
    23. 24. Other structural cardiac diseases <ul><li>dilated cardiomyopathy </li></ul><ul><ul><li>usually secondary to myocarditis </li></ul></ul><ul><ul><li>syncope and death secondary to ventricular dysrhythmias or severe myocardial dysfunction </li></ul></ul><ul><li>arrhythmogenic RV dysplasia </li></ul><ul><li>congenital cyanotic and non-cyanotic heart disease </li></ul><ul><li>valvular diseases </li></ul><ul><ul><li>aortic stenosis </li></ul></ul><ul><li>coronary artery anomalies </li></ul><ul><ul><li>exertional syncope or sudden death </li></ul></ul><ul><ul><li>aberrant artery passes between aorta and pulmonary artery </li></ul></ul>
    24. 25. <ul><li>2 week old infant brought in by parents with difficulty breathing </li></ul><ul><li>HR 180, BP 50/P, RR 80, T 37.5 </li></ul><ul><li>history and physical </li></ul><ul><li>investigations </li></ul><ul><li>repeat vitals: HR 30, no BP, RR 12 </li></ul><ul><li>“ definitive treatment”: </li></ul>
    25. 26. <ul><li>4 year old male presents with 2 weeks history of cough, fast breathing, fatigue, decreased exercise tolerance, “puffy eyes” </li></ul><ul><li>On exam: tachypneic, moderate respiratory distress, O2 sats 92%, bilateral crackles </li></ul>
    26. 27. <ul><li>6 month male presents with failure to thrive, fast breathing, blue lips </li></ul><ul><li>On exam tachypnea but no respiratory distress, lips and extremities blue, oxygen saturations 70% </li></ul>
    27. 28. Congenital Heart Disease <ul><li>Fetal to Neonatal Circulation </li></ul>
    28. 30. Anatomic Classification; 4 groups <ul><li>Right to Left Shunt </li></ul><ul><ul><li>Tetralogy of Fallot </li></ul></ul><ul><ul><li>Transposition of the Great Arteries </li></ul></ul><ul><ul><li>Tricuspid Atresia </li></ul></ul><ul><li>Left to Right Shunt </li></ul><ul><ul><li>ASD </li></ul></ul><ul><ul><li>VSD </li></ul></ul><ul><ul><li>PDA </li></ul></ul><ul><li>Stenotic </li></ul><ul><ul><li>Aortic valve stenosis </li></ul></ul><ul><ul><li>Pulmonic valve stenosis </li></ul></ul><ul><ul><li>Aortic coarctation   </li></ul></ul><ul><li>Mixing </li></ul><ul><ul><li>Truncus </li></ul></ul><ul><ul><li>Total Anomalous Pulmonary Venous Return </li></ul></ul><ul><ul><li>Hypoplastic left heart syndrome </li></ul></ul>
    29. 31. CHD Classified as Cyanotic vs. Acyanotic <ul><li>Cyanotic (R to L shunt and mixing lesions) </li></ul><ul><ul><li>tetralogy of Fallot </li></ul></ul><ul><ul><li>transposition of great vessels </li></ul></ul><ul><ul><li>tricuspid atresia </li></ul></ul><ul><ul><li>total anomalous pulmonary venous return </li></ul></ul><ul><ul><li>truncus arteriosus </li></ul></ul><ul><ul><li>hypoplastic left heart syndrome </li></ul></ul>
    30. 32. CHD Classified as Cyanotic vs. Acyanotic <ul><li>Acyanotic (L to R shunts, stenotic lesions) </li></ul><ul><ul><li>ASD </li></ul></ul><ul><ul><li>VSD </li></ul></ul><ul><ul><li>PDA </li></ul></ul><ul><ul><li>aortic valve stenosis </li></ul></ul><ul><ul><li>pulmonic valve stenosis </li></ul></ul><ul><ul><li>aortic coarctation </li></ul></ul>
    31. 33. Cyanosis <ul><li>Classified as central or peripheral </li></ul><ul><li>Central cyanosis (always abnormal) </li></ul><ul><ul><li>mucous membranes, trunk, extremities </li></ul></ul><ul><ul><li>classified as cardiac (R to L shunt) or pulmonary </li></ul></ul><ul><li>Peripheral cyanosis (acrocyanosis) </li></ul><ul><ul><li>no involvement of mucous membranes </li></ul></ul><ul><ul><li>involves hands, feet, circumoral area </li></ul></ul><ul><ul><li>common in neonates from vasomotor instability </li></ul></ul><ul><ul><li>CHF, PVD, shock, cold extremities </li></ul></ul>
    32. 34. Congenital Heart Disease <ul><li>History </li></ul><ul><ul><li>feeding difficulties </li></ul></ul><ul><ul><li>tachypnea </li></ul></ul><ul><ul><li>diaphoresis </li></ul></ul><ul><ul><li>syncope </li></ul></ul><ul><ul><li>cyanotic episodes </li></ul></ul><ul><ul><li>failure to thrive </li></ul></ul>
    33. 35. Congenital Heart Disease <ul><li>Physical Examination </li></ul><ul><ul><li>colour: pink, blue, gray </li></ul></ul><ul><ul><li>vitals: tachypnea, tachycardia, BP </li></ul></ul><ul><ul><li>symptoms suggestive of infection </li></ul></ul><ul><ul><li>palpation and auscultation of precordium </li></ul></ul><ul><ul><li>chest auscultation </li></ul></ul><ul><ul><li>survey for organomegaly </li></ul></ul><ul><ul><li>pulses in all extremities </li></ul></ul>
    34. 36. Cyanotic Congenital Heart Disease <ul><li>R to L shunts </li></ul><ul><li>mixing lesions </li></ul>
    35. 37. Tetralogy of Fallot – the classic cyanotic lesion <ul><li>RV outflow obstruction </li></ul><ul><li>RVH </li></ul><ul><li>VSD </li></ul><ul><li>overriding aorta </li></ul><ul><li>CXR reveals boot shaped heart with decreased pulmonary blood flow </li></ul>
    36. 39. <ul><li>2 month old female with known tetralogy of Fallot brought in with 24 hour history of vomiting and diarrhea </li></ul><ul><li>On exam: moderate dehydration </li></ul><ul><li>during IV attempts patient becomes irritable and cyanotic </li></ul>
    37. 41. Treatment of Tet Spell <ul><li>quiet, calm environment </li></ul><ul><li>knee-chest or squatting position </li></ul><ul><ul><li>increases afterload thus decreasing R to L shunting </li></ul></ul><ul><li>Oxygen </li></ul><ul><li>Morphine </li></ul><ul><ul><li>to treat hyperpnea and decrease systemic catecholamines </li></ul></ul><ul><li>Phenylephrine </li></ul><ul><ul><li>increases afterload thereby decreasing R to L shunt </li></ul></ul><ul><li>Manual external aortic compression below level of renal arteries </li></ul><ul><li>Propranolol </li></ul><ul><ul><li>to block beta receptors in infundibulum therefore lessening RV outflow obstruction </li></ul></ul>
    38. 42. Consider <ul><li>consider small volume challenge (5-10 cc/kg) to increase preload and reduce dynamic outflow obstruction </li></ul><ul><li>?NaHCO3 for correction of acidosis </li></ul><ul><li>may need general anesthesia if severe and/or prolonged spell </li></ul><ul><li>interim prophylactic treatment with propranolol while awaiting surgery </li></ul>
    39. 43. Acyanotic Congenital Heart Disease <ul><li>L to R shunts </li></ul><ul><li>stenotic lesions </li></ul>
    40. 44. VSD <ul><li>Most common congenital lesion </li></ul><ul><li>Large VSD’s may be silent and become symptomatic in first few weeks as pulmonary resistance  </li></ul><ul><li>SOB and diaphoresis w feeds </li></ul><ul><li>Poor weight gain </li></ul><ul><li>Systolic murmur </li></ul><ul><li>CXR demonstrates CHF </li></ul>
    41. 45. <ul><li>2 week old infant brought in by parents with difficulty breathing </li></ul><ul><li>HR 180, BP 50/P, RR 80, T 37.5 </li></ul><ul><li>history and physical </li></ul><ul><li>investigations </li></ul><ul><li>repeat vitals: HR 30, no BP, RR 12 </li></ul><ul><li>“ definitive treatment”: </li></ul>
    42. 46. Differential Dx of Infant Shock <ul><li>infection (septic shock/ meningitis) </li></ul><ul><ul><li>bacterial: GBS, E. coli, S. aureus </li></ul></ul><ul><ul><li>virus: enteroviruses, H. simplex </li></ul></ul><ul><li>metabolic: amino/organic acidopathies, urea cycle defect </li></ul><ul><li>‘ hypoxic shock’: eg. RSV, C.N.S. depression </li></ul><ul><li>heart disease: congenital or acquired </li></ul>
    43. 47. LV Outflow Obstruction
    44. 48. LV Outflow Obstruction <ul><li>Aortic coarctation </li></ul><ul><li>Hypoplastic left heart syndrome </li></ul><ul><li>Aortic stenosis (presents later) </li></ul><ul><li>Rosen: “any neonate in shock that does not respond to fluids or pressors has LV outflow obstruction until proven otherwise” </li></ul><ul><li>complete obstruction incompatible with life unless there is shunting </li></ul>
    45. 49. Coarctation of the aorta <ul><li>Most often distal to L subclavian </li></ul><ul><li>Can be diagnosed anytime </li></ul><ul><li>Neonates present as acutely ill, gray shocky (from DA closure) </li></ul><ul><li>Systolic murmur at the back </li></ul><ul><li>Hepatomegaly </li></ul><ul><li>Diminished femoral pulses </li></ul><ul><li>BP difference b/t arms and legs </li></ul><ul><li>CXR demonstrates CHF </li></ul><ul><li>Treatment of CHF </li></ul><ul><li>Prostaglandin E1 </li></ul>
    46. 50. Duct Dependant Lesions <ul><li>Duct needed to perfuse lungs or periphery </li></ul><ul><li>Lungs </li></ul><ul><ul><li>Tetralogy of Fallot, transposition of great arteries, tricuspid or pulmonary atresia </li></ul></ul><ul><ul><ul><li>a patent ductus arteriosus results in preserved pulmonary blood flow </li></ul></ul></ul><ul><li>Periphery </li></ul><ul><ul><li>Aortic coarctation (severe) and Hypoplastic left heart </li></ul></ul>
    47. 51. Treatment of acute decline in patients with ductal dependant lesions <ul><li>Open the closed duct </li></ul><ul><li>Prostaglandin E1 0.1 ug/kg/min infusion </li></ul><ul><li>reduce dosage as perfusion and colour return </li></ul><ul><li>Rosen: “any infant in the first week of life with decreased perfusion, hypotension, or acidosis should be considered a candidate for PGE1 administration” </li></ul>
    48. 52. What do you need to know about PGE ? <ul><li>it functions by dilating vascular smooth muscle, both systemically and in the pulmonary vascular bed </li></ul><ul><li>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 </li></ul>
    49. 53. Classification Review <ul><li>pink child in respiratory distress suggests acyanotic chd (L to R shunt, coarct, aortic stenosis) </li></ul><ul><li>blue cyanotic child in little respiratory distress suggests R to L shunt or mixing lesions </li></ul><ul><li>gray, shocky baby suggests outflow tract obstruction </li></ul>
    50. 54. Bradyarrhythmias <ul><li>Etiology </li></ul><ul><ul><li>hypoxia, acidosis, hypoglycemia </li></ul></ul><ul><ul><li>excess vagal stimulation (ex. intubation) </li></ul></ul><ul><li>  </li></ul><ul><li>Treatment </li></ul><ul><ul><li>Epinephrine </li></ul></ul><ul><ul><li>Atropine if known vagally mediated or heart block </li></ul></ul>
    51. 55. Congenital Bradyarrhythmias <ul><li>complete AV block </li></ul><ul><ul><li>autoimmune injury to fetal conduction system secondary to maternal autoimmune disease </li></ul></ul><ul><ul><li>atropine, isoproteronol, epinephrine may be tried temporarily prior to pacing </li></ul></ul>
    52. 56. Tachyarrhythmias <ul><li>Supraventricular Tachycardia </li></ul><ul><ul><li>re-entrant with accessory pathway (AV nodal or WPW) </li></ul></ul><ul><ul><li>re-entrant without accessory pathway (re-entry occurs within sinus node or within atrium) </li></ul></ul><ul><ul><li>ectopic </li></ul></ul><ul><li>nonspecific presentations in infants </li></ul>
    53. 57. Murmurs <ul><li>Areas </li></ul><ul><ul><li>aortic: R 2 nd intercostal space </li></ul></ul><ul><ul><li>pulmonic: L 2 nd intercostal space </li></ul></ul><ul><ul><li>mitral: apex </li></ul></ul><ul><ul><li>tricuspid and VSD: L lower sternal border </li></ul></ul><ul><li>Pathologic </li></ul><ul><ul><li>diastolic, holosystolic, late systolic, continuous </li></ul></ul>
    54. 58. Innocent Heart Murmurs <ul><li>History </li></ul><ul><ul><li>normal growth and development, normal exercise tolerance </li></ul></ul><ul><ul><li>no history of cyanosis </li></ul></ul><ul><li>Physical Examination </li></ul><ul><ul><li>Grade II or less, localized </li></ul></ul><ul><ul><li>varies with position (decreased with upright posture) </li></ul></ul><ul><ul><li>normal precordium </li></ul></ul><ul><ul><li>normal pulses </li></ul></ul><ul><li>Lab </li></ul><ul><ul><li>normal EKG, normal CXR </li></ul></ul>
    55. 59. 3 innocent murmurs <ul><li>Still’s </li></ul><ul><ul><li>short ejection systolic murmur </li></ul></ul><ul><ul><li>musical or vibratory quality </li></ul></ul><ul><ul><li>heard best between apex and left sternal border </li></ul></ul><ul><li>physiologic pulmonary flow murmur </li></ul><ul><ul><li>harsh, located at pulmonic area </li></ul></ul><ul><li>peripheral arterial stenosis </li></ul><ul><ul><li>low-intensity systolic ejection murmur best heard in axilla and back </li></ul></ul>
    56. 60. <ul><li>8 year old male presents with fever, arthralgias </li></ul><ul><li>mother mentions that he had a sore throat 3 weeks ago for a few days with spontaneous resolution </li></ul><ul><li>a throat swab was done and positive for GAS but patient better so did not take the prescribed antibiotics </li></ul>
    57. 61. Acute Rheumatic Fever <ul><li>school aged children </li></ul><ul><li>associated with certain strains of Group A beta-hemolytic streptococcal infections </li></ul><ul><li>the streptococcal organism stimulated antibody production to host tissues </li></ul><ul><ul><li>CT of heart, joints, CNS, subcutaneous tissues, skin </li></ul></ul><ul><li>carditis is an endomyocarditis with valvulitis involving mitral and aortic valves </li></ul><ul><li>2 to 6 weeks post streptococcal pharyngitis </li></ul>
    58. 62. Jones Criteria <ul><li>Major </li></ul><ul><ul><li>carditis </li></ul></ul><ul><ul><ul><li>new or changing murmur </li></ul></ul></ul><ul><ul><ul><li>cardiomegaly, CHF </li></ul></ul></ul><ul><ul><ul><li>pericarditis </li></ul></ul></ul><ul><ul><li>migratory polyarthritis </li></ul></ul><ul><ul><li>chorea </li></ul></ul><ul><ul><li>erythema marginatum </li></ul></ul><ul><ul><li>subcutaneous nodules </li></ul></ul><ul><li>Minor </li></ul><ul><ul><li>fever </li></ul></ul><ul><ul><li>arthralgia </li></ul></ul><ul><ul><li>history of previous ARF </li></ul></ul><ul><ul><li>elevated ESR, CRP </li></ul></ul><ul><ul><li>prolonged PR on EKG </li></ul></ul><ul><ul><li>Rising titer of antistreptococcal antibodies </li></ul></ul>
    59. 63. ER Treatment <ul><li>management of complicating features of carditis (CHF) </li></ul><ul><ul><li>significant carditis or CHF managed with glucocorticoids </li></ul></ul><ul><li>high-dose ASA 75-100 mg/kg/day </li></ul><ul><li>pencillin </li></ul><ul><li>long term management of rheumatic heart disease </li></ul>
    60. 64. Pediatric EKG’s General Principles <ul><li>RV Dominance at birth; gradually changes to LV dominance </li></ul><ul><li>axis up to +180 in normal newborn </li></ul><ul><li>T waves negative in right precordial leads until adolescence (except they are upright in first week of life) </li></ul>