Sie sind auf Seite 1von 43

A 2-day-old baby had been discharged home the day after

delivery following a normal routine examination.

He suddenly collapsed at home after 3 days
at hospital.; He was pale, with grey lips.
The right brachial pulse could just be felt, the femoral pulses
were impalpable and his liver was significantly enlarged.
Blood gases showed severe metabolic acidosis.
The differential diagnosis?
 Sepsis
 Congenital heart disease
• Inherited disorder of metabolism.
It is important to realize then that any infant ≤ 6
weeks who presents in shock or profoundly cyanotic
might be secondary to closure of the ductus arteriosus
in conjunction with a right or left sided obstructive
cardiac lesion
Left-sided obstructive lesions Right-sided obstructive lesions

 HLHS  severe tetralogy of Fallot

 critical aortic stenosis  pulmonary atresia with intact
ventricular septum
 coarctation of the aorta
 Interruption of the aortic arch
as the PDA closes
 pulmonary overcirculation develops
and systemic hypoperfusion
 circulatory collapse and shock

Type A Type B Type C
 basic resuscitative measures (ABC’s) should be initiated
 Prostaglandin infusion
 Oxygen therapy can either help or hurt the patient and should be used judiciously
Starting dose: 0.1 mcg/kg/min
 Administration
 1 ml ampul of 500 micrograms (0.5 mg).
 Use one of the following methods to prepare a solution for infusion.
 Dilute one ampul in 500 ml D5W or D10W = 1 mcg/ml (0.001 mg/ml) solution.
To give 0.05 mcg/kg/min. = 3.0 ml/kg/hr
 [weight (kg) ÷ 10] = # mg PGE1 in 100 ml IVF @ 3 ml/hr = 0.05 mcg/kg/min
 Dilute one vial in 100 ml of D5W or D10W = 5 mcg/ml solution. To give 0.05 mcg/kg/min. =
0.6 ml/kg/hr
 Side effect :
 apnea (12%), fever (14%), and flushing (10%)
 1 wk 2 wk 3wk 4wk 5wk

PGE dependent CHF

 Cyanotic if PDA for Pulmonary Flow

 Shock if PDA for circulatory Flow
 Severe coarctation of the aorta
was diagnosed on echo.
 He had developed shock from a left heart outflow
tract obstruction once
the arterial duct had closed.
 2 month old female from rural area moved to Buraydah last week ,
 brought to ER with history of vomiting and diarrhea
for 1 days
 On exam: non-dysmorphic infant female, moderate dehydration,
 CVS: Prominent pulsation at subxiphoid ;normal S1, single S2 with Harsh
systolic murmur noted at the left mid-upper sternal border, with radiation to
back and axilla,
 Abd: Liver edge palpable below RCM
 While discussing the most likely diagnosis with the parents, you are urgently
called back to the examination room by the nurse that while the infant was
crying, her color became blue (“she’s never done this before”) and became
irritable …
The pulse oximeter is reading a HR of 170 and an oximetry reading of less
than 70%. Upon auscultation, you note the murmur is diminished in intensity.
 importation and management plan ?
“Tet spell”,
paroxysmal hyperpnea “ rapid and deep respiration”
 Etiology uncertain
 “Infundibular spasm”
 Decrease in systemic vascular resistance

 Goal of therapy is to increase pulmonary blood flow

A) Tricuspid atresia with pulmonary stenosis.
B) Transposition of Great arteries with pulmonary stenosis
C) Single ventricle physiology with PS or pulmonary atresia
 quiet, calm environment
 knee-chest or squatting position
 increases afterload thus decreasing R to L shunting
 Oxygen
 Phenylephrine Hydrochloride
 ↑ SVR – increases afterload thereby decreasing R to L shunt
 10 ug/kg initial followed by infusion
 Morphine
 to treat hyperpnea and decrease systemic catecholamines
 Depresses respiratory center→ Decreases Systemic Venous Return
 start with 0.1 mg/kg IM then start IV once have access
 Propranolol
 to block beta receptors in infundibulum therefore lessening RV outflow obstruction
 0.05 mg/kg IV
 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
 Ketamine, works well.
 ↑ SVR
 sedates the infant.

 prophylactic treatment
 propranolol while awaiting surgery

5 -10
 6 month old male, with history of URTI last 4 days , present with runny nose and
fast breathing.
O/E Punky, mild tachypnea & mild wheezy chest other Physical examination are
Received 2 dose of 3%NaCl neb and Dx as bronchiolitis and discharge on Saline nose
 2 days later mother return to ER the infant was irritabole , poor feeding (fatigues)and
fast breathing •
 failure to respond to 3 doses of bronchodilators on other hospital, where diagnosed as
 physical exam: Temp 36.1 HR 160, RR 60, BP 80/40 with minimal respiratory
distress, CVS ; gallop rhythm, CHEST :wheeze with rales ; Abd :soft and lax with
palpable liver
 your action plan ?
 ICU admission
 Diuretics ( preload reduction )
 includes inotropes
 afterload reduction
 positive pressure ventilation
 medication

 IVIG, steroid, immuno-suppresion are controversial

 Increased Preload
 L to R shunts (VSD, PDA, AV fistula)
 severe anemia

 Increased Afterload
 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 , adriamycin (doxorubicin hydrochloride)
 Dysrhythmia
 history of sweating and shortness of breath during feeding is associated with
cardiac disease in infancy
 thorough cardiac exam:
 Listen for soft murmurs and gallop
 Feel for hepatosplenomegaly
 Feel the distal pulses — infants with asthma/reactive airways disease are typically well
 A 9 years old boy with Hx of frequent episode of palpitation, reach to ED via red
crescent, that he suddenly feel unwell with several episode of vomiting during
Break time at the school , the doctor noted that he is pale ,
 Vital sign : HR 300, RR 35 , BP 96/ 65 , SpO2 96%& CRT <2 sce
 ECG done show
 Goal: identify unstable patients, differentiate from sinus
tachycardia, and terminate the rhythm
 Vagal maneuvers in stable patients
 Adenosine if IV access readily available
 Stop conduction through AV node
 Helps to define p waves if unsure of etiology
 0.1 mg/kg (max 6 mg), repeat 0.2 mg/kg ( max 12 mg) in line closest to
central circulation
 Need continuous ECG and BP monitoring

 Synchronized cardioversion
 Amiodarone, Procainamide if above unsuccessful
 Transesophageal atrial pacing can also be performed
 Upto 13% of pediatric arrhythmias
 Incidence of 0.1 – 0.4%
 Most frequent age presentation:
 1st 3 months of life,
 2nd peaks 8-10 y/o and in adolescence

 Rates of SVT vary with age

 Neonate > 220bpm
 Older children: avg rate is 210 bpm ( 180-250)
Rapid, regular, usually narrow QRS rhythm, originating above the
P waves difficult to define, but 1:1 with QRS
Important to differentiate from sinus tachycardia
 Need post conversion EKG – identify those with WPW
syndrome ( 25 % pts with SVT)
 echo – identify structural problems
 Radiofrequency catheter ablation
 Frontline treatment
 Very effective
 Cutoff points usually are 5 y.o. and 15 kg, unless severe SVT

 Medications
 Digoxin and beta blockers as first line
 Flecainide, sotalol, amiodarone
 A flutter, A fib, ectopic atrial tachycardia, junctional tachycardias
 Not commonly seen in pediatric patients
 Adenosine does not terminate these rhythms, originate above AV node
 Treatments: procainamide, amiodarone, cardioversion, or ablation
 DDX:


 Idiopathic,
 drug toxicity,
 cardiomyopathy,
 myocarditis,
 cardiac tumors
 metabolic abnormalities
 Very thorough history – cardiomyopathy, toxins, family hx of sudden cardiac death
 Lab – electrolyte
 Ekg to r/o –
 Brugada syndrome,
 long Q-T, arrhythmogenic
 right ventricular cardiomyopathy,
 electrolyte abnormalities
 structural heart disease
 ischemia

 Cardiology consult
 Echo
 Admission for observation
Congenital heart disease and associated
Congenital heart disease Associated arrhythmia

Tetralogy of Fallot Atrial tachycardia

Double outlet right ventricle Ventricular tachycardia
Sinus node dysfunction
Transposition of the great arteries Ventricular arrhythmias
Atrioventricular block
Ebstein's anomaly Supraventricular tachycardia
Ventricular septal defect repair Heart block
Ventricular arrhythmias
Atrialseptal defect Atrial tachycardia
Atrial septal defect repair Sinus node dysfunction
 Must common pediatric cardiac emergence in clouded
 Recognition of cardiogenic shock in neonate and key management
 Approach to cyanotic spell .
 CHF management at level of ER
 Common Arrhythmias seen at level of ER.
 Major CHD discussed
 Aisha Frazier,1,2 Elizabeth A Hunt,1,3 and Kathryn Holmes1,2 Pediatric cardiac
emergencies: Children are not small adults,
 EHRA/AEPC CONSENSUS STATEMENT “Pharmacological and non-
pharmacological therapy for arrhythmias in the pediatric population: EHRA and
AEPC-Arrhythmia Working Group joint consensus statement” JULY 12, 2013