Clearwater Fire and Rescue and a transport service ambulance are dispatched to a local pediatrician’s office at 6 a.m. for a baby with trouble breathing. Upon arrival, the responders hear audible grunting as they walk down the hallway toward the patient’s exam room. There they find a 2.5-kg, 34-day-old male infant in obvious respiratory distress.
The pediatrician says the parents brought the child in because he’d been having trouble breathing since around midnight. The child was a normal, full-term, vaginal delivery with no medical history until this point.
The nurse in the room is providing supplemental O2 via blow-by and getting an oxygen saturation of 79%. There’s no pulse rate on their oximeter.
A primary survey of the child shows he’s grunting to breathe, and using accessory muscles with nasal flaring and belly breathing. The child is mottled in color with a capillary refill time of about six seconds. He’s afebrile and without any obvious respiratory secretions. Lung sounds are clear bilaterally and no stridor is noted in the airway.
Paramedics carry the patient to the ambulance for rapid transport to the pediatric receiving facility approximately 20 minutes away. General supportive care is initiated, including ECG, pulse oximetry, capillary blood glucose and oxygen via non-rebreather mask at 15 Lpm.
Vital signs show a pulse rate of 280 bpm, absent brachial pulse and a pulse oximetry reading of 80% on high-flow O2. ECG shows a supraventricular tachycardia (SVT) with a sustained rate of 280 bpm with no ectopy noted.
Due to the extremely small size of the patient and the large size of the ECG electrodes, providers are unable to perform a 12-lead. An attempt at an IV is also made, but is unsuccessful. Vagal maneuvers are attempted by soaking a piece of gauze in cold water and briefly placing it on the child’s face without any success in slowing the rate.
Cardioversion was discussed but the pediatric defib pads are found to be too large and wrap all the way around the child’s body. During this time the child’s breathing becomes extremely erratic and has to be assisted during long periods of apnea via bag-valve mask (BVM). An IV is established on a second attempt and a rapid fluid bolus of 40 cc given.
With still no break in the SVT, a dose of adenosine is given at 0.1 mg/kg. The SVT persists and, prior to giving a second dose, the ambulance arrives at the hospital. At time of transfer to the ED the patient’s color has improved significantly, pulse ox readings are in the low 90s and a brachial pulse is now palpable.
On arrival in the ED, the child is quickly assessed by nursing staff as well as a pediatric emergency physician. The child is placed on a monitor and determined to still be in an SVT. The physician pushes two more doses of adenosine at 0.1 mg/kg with no effect noted in the rhythm. A third dose is administered at 0.2 mg/kg that finally breaks the SVT into a normal sinus rhythm.
The child is admitted to the pediatric ICU and found to be suffering from Wolff-Parkinson-White (WPW) syndrome upon further evaluation. He’s placed on beta-blockers with no recurrent issues of SVT. The child is eventually discharged and his parents instructed to follow up with cardiology with the potential for future ablation.
SVT is a rapid tachycardia that occurs above the bundle of His. It can occur in as many as one in 250 children, though is often misdiagnosed due to multiple possible presentations.
For an infant, any sustained narrow complex tachycardia greater than 220 bpm can be considered an SVT.1 The SVT must be rapidly treated to prevent hemodynamic instability—the initial treatment of choice is application of an ice pack to the child’s face to increase vagal tone. If this is unsuccessful then adenosine should be administered at a dose of 0.1 mg/kg rapid IV push. If the patient hasn’t returned to sinus rhythm after 1–2 minutes, the dose should be increased in increments of 0.05–0.1 mg/kg to not exceed 0.3 mg/kg.2
WPW syndrome is caused when an aberrant accessory pathway is formed and causes a pre-excitation of the ventricles. This condition is uncommon and is noted by its delta wave on the ECG. This wave can’t be seen when the heart is in an SVT rhythm and can only be diagnosed once slowed. An electrophysiological study is the gold standard for ultimate diagnosis of this syndrome and further treatment would be determined by a pediatric cardiologist.1
Although pediatric hemodynamic instability is often respiratory in nature, providers must never overlook the possibility of a cardiac component. The ECG monitor should be applied rapidly in the beginning of the assessment to observe for any abnormal rhythms that may need interventions.
IV access may be difficult in unstable infants, so intraosseous access should be considered if vascular access is needed. In regard to respiratory insufficiency in infants, it must be noted that the use of a BVM to assist should be done with careful attention paid to the amount of air being bagged into the infant’s lungs.
Over-ventilation can cause serious damage to a young infant and impair oxygen intake because of a pneumothorax or gastric inflation. Providers should check the sizing of their system’s pediatric equipment; as noted in this case, the ECG leads and defib pads were too large for the tiny infant’s body and would’ve made defibrillation difficult
When giving adenosine to adult or pediatric patients, a three-way stopcock is recommended to ensure the medicine is pushed into the access point as rapidly as possible due to its short duration in the body.
This case was one that would put many EMS personnel out of their comfort zones. The presentation of an unstable child is enough to have some providers put on their blinders and focus solely on the respiratory causes and overlook the cardiac.
This child had been unstable most of the evening and by the time EMS was summoned was in severe need of treatment.
The diagnosis of WPW in the field is almost impossible, especially when there is no history with the patient. Quick recognition of the infant’s symptoms and analysis of the ECG allowed the paramedics to deliver the correct treatment for the arrhythmia while ensuring the respiratory issues weren’t overlooked. The rapid treatment and transport were a significant part of why this patient had a positive final outcome.
1. Biondi E. Focus on diagnosis: Cardiac arrhythmias in children. Pediatr Rev. 2010;31(9):375–379.
2. Tingelstad J. Consultation with the specialist: Cardiac dysrhythmias. Pediatr Rev. 2001;22(3):91–94.