Pediatric Cardiac Emergencies

Pediatric Cardiac Emergencies
Gavin Greenfield Peggy Thomsen

seen 2 days earlier and started on steroids and bronchodilators
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 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

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 feeding is infant’s exertion

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

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 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

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 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

CHF - Etiology Increased Preload Increased Afterload
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

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 Tintinalli

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 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

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

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

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 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

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 year old male collapses at school while in class
non-responsive for one minute feels fine in the department Approach?

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 Tintinalli

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

Sudden Cardiac Death includes those causes that directly relate to cardiovascular dysfunction one third of all sudden deaths Not all sudden death is cardiac (seizure, toxic ingestion, asthma)

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 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

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

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 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%

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

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 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

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

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”: 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

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

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%

Congenital Heart Disease
Fetal to Neonatal Circulation

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

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 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

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

CHD Classified as Cyanotic vs. Acyanotic
Acyanotic (L to R shunts, stenotic lesions) ASD VSD PDA aortic valve stenosis pulmonic valve stenosis aortic coarctation 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 delayed growth and development decreased exercise tolerance recurrent URTI’s CHF holosystolic murmur at LLSB with thrill 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 slender body build <10th percentile 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 surgical closure if necessary Patent Ductus Arteriosus 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

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 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

History feeding difficulties tachypnea diaphoresis syncope cyanotic episodes failure to thrive

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

Cyanotic Congenital Heart Disease
R to L shunts mixing lesions

Tetralogy of Fallot – the classic cyanotic lesion
RV outflow obstruction RVH VSD overriding aorta CXR reveals boot shaped heart with decreased pulmonary blood flow 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)

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

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

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 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

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 Lack of appropriate treatment will result in severe complications of hypoxia: seizures, lactic acidosis, deteriorating organ function and death

Acyanotic Congenital Heart Disease
L to R shunts stenotic lesions

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

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”:

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

LV Outflow Obstruction

LV Outflow Obstruction
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 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

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 98% just below origin of left subclavian artery, located at origin of ductus arteriosus associated bicuspid aortic valve in 70% Treatment of CHF Prostaglandin E1

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 duct dependent lesions include RV outflow tract stenosis or atresia, aortic coarctation

Treatment of acute decline in patients with ductal dependant lesions
Open the closed duct Prostaglandin E 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”

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 Dose 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

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

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

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

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 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 minutes procainamide 15 mg/kg over minutes lidocaine 1 mg/kg over 2-4 minutes followed by 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

Murmurs Areas Pathologic aortic: R 2nd intercostal space
pulmonic: L 2nd intercostal space mitral: apex tricuspid and VSD: L lower sternal border Pathologic diastolic, holosystolic, late systolic, continuous 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

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 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 low frequency, LSB 3-4 ICS or apex vibratory quality Differential Diagnosis subaortic stenosis, small VSD Pulmonary ejection LSB 2 and 3 ICS and transmits to pulmonary area rough and dissonant without the vibratory musical quality of the Still’s ASD, PS Peripheral pulmonic stenosis commonly heard in newborns and infants under 1 year SEM, LSB 2 ICS PDA, PS Supraclavicular arterial bruit low intensity, above clavicles AS, bicuspid aortic valve Aortic Systolic Murmur hypertrophic cardiomyopathy, fixed obstructions of LV outflow tract Always refer if suspect this murmur because of the differential diagnosis Continuous murmurs Venous hum low anterior part of neck, just lateral to sternocleidomastoid, continuous, R>L louder sitting up and with turning head away PDA Mammary Arterial Souffle most frequently occurs late in pregnancy and in lactating women but can occur in adolescence

3 innocent murmurs Still’s physiologic pulmonary flow murmur
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

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

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

Jones Criteria Major Minor carditis migratory polyarthritis chorea
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 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)

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

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)

Pediatric Cardiac Emergencies

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