Download Pediatric Cardiac Emergencies

Pediatric Cardiac
Emergencies
Gavin Greenfield
Peggy Thomsen
►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
►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
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
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
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
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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
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
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
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►
viral
bacterial
TB
fungal
parasitic
►
 uremia
 hypothyroid
►
Hematology / Oncology
 bleeding diathesis
 malignancy
Connective tissue
 RA
 Rheumatic fever
 SLE
Metabolic / Endocrine
►
►
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
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
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vascular
orthostatic, hypovolemia
neurally mediated
hypoxia: PE, CNS depression from OD, CO
cardiac
Cardiac Syncope
► Dysrhythmias
 tachy
 brady
► Outflow
obstruction
► Myocardial Dysfunction
► cardiac
syncope often precedes future
sudden cardiac death
Sudden Cardiac Death
► includes
those causes that directly relate to
cardiovascular dysfunction
► one third of all sudden deaths
Sudden Cardiac Death
► Etiology
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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
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
Other dysrhythmias
► WPW
and other SVT’s
► AV block
 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
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”:
►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
Classification
Congenital Heart Disease
Classification
► pink
(in failure)
► blue (no distress)
► gray (in shock)
Anatomic Classification; 4 groups
►
Right to Left Shunt
►
 Tetralogy of Fallot
 Transposition of
the Great Arteries
 Tricuspid Atresia
►
 Aortic valve
stenosis
 Pulmonic valve
stenosis
 Aortic
coarctation
Left to Right Shunt
 ASD
 VSD
 PDA
Stenotic
►
Mixing
 Truncus
 Total Anomalous
Pulmonary Venous
CHD Classified as Cyanotic vs.
Acyanotic
► Cyanotic
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(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
lesions)
(L to R shunts, stenotic
 ASD
 VSD
 PDA
 aortic valve stenosis
 pulmonic valve stenosis
 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
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cyanosis (acrocyanosis)
no involvement of mucous membranes
involves hands, feet, circumoral area
common in neonates from vasomotor instability
CHF, PVD, shock, cold extremities
Congenital Heart Disease
► History
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feeding difficulties
tachypnea
diaphoresis
syncope
cyanotic episodes
failure to thrive
Congenital Heart Disease
► Physical
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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
►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
Treatment of Tet Spell
►
►
quiet, calm environment
knee-chest or squatting position
 increases afterload thus decreasing R to L shunting
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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
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
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
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
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
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”
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
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
 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
Murmurs
► Areas
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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
► History
 normal growth and development, normal exercise
tolerance
 no history of cyanosis
► Physical
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Examination
Grade II or less, localized
varies with position (decreased with upright posture)
normal precordium
normal pulses
► Lab
 normal EKG, normal CXR
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
►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 betahemolytic 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
 carditis
► new
or changing murmur
► cardiomegaly, CHF
► pericarditis
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migratory polyarthritis
chorea
erythema marginatum
subcutaneous nodules
► Minor
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fever
arthralgia
history of previous ARF
elevated ESR, CRP
prolonged PR on EKG
Rising titer of
antistreptococcal
antibodies
Erythema Marginatum
ER Treatment
► management
carditis (CHF)
of complicating features of
 significant carditis or CHF managed with
glucocorticoids
► high-dose
ASA 75-100 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)