Dispatched to 16 y/o F Unknown

[firemanemt]

you are all thinking what im think also. but the one thing that has got me questioning is if she was having that much of a difficulty breathing then why isnt somebody getting hold of the childs parents and asking them if she has any known allergies or if she is on any inhalers that the school nurse is not aware of.

[AZCEP]

How would that information change the management of the situation at hand?

WPW with a rapid response, tenuous stability at the moment following cardioversion, 5 minute transport to a receiving facility. Unless we make an unscheduled turn someplace, and the patient's condition worsens, there is no reason to be chasing down details that will not change our situation.

[p3medic]

I wouldn't get too hung up on the respiratory aspect of this call, her respiratory distress is secondary to her tachycardia, not the other way around, fix her rate, you fix her breathing. The "asthma" hx is something to note, but this is not her problem today.

[VentMedic]

I wouldn't get too hung up on the respiratory aspect of this call, her respiratory distress is secondary to her tachycardia, not the other way around, fix her rate, you fix her breathing. The "asthma" hx is something to note, but this is not her problem today.

WPW can go undiagnosed for years in children. They will go in an out of it many times before it is picked up. If a breathing problem such as asthma precipitated this rhythm, then you can have real problems.

In this scenario the girl made the mistake of telling a school nurse she was having problems breathing who promptly stuck her head into a paper bag.

[p3medic]

In the given senario she has clear breath sounds and an etco2 of 45mmHg, and a good waveform, this is not bronchospasm, this is dypnea secondary to exteme tachycardia. Clearly she hasn't been dx with WPW until now. Her 12ld is diagnostic, and theres no room to really argue that point, IMHO.

[sledogg1]

Asthma and wide complex tachy are 2 no no's for adenosine...............sytomatic go to repeat cardiversion if not lido is the way to go, but lido is a no no for WPW as well.

[sledogg1]

History

The symptoms of lidocaine toxicity tend to follow a predictable progression. The toxicity begins with numbness of the tongue, lightheadedness, and visual disturbances and progresses to muscle twitching, unconsciousness, and seizures, then coma, respiratory arrest, and cardiovascular depression.

CNS toxicity: When the lidocaine dose is increased from 1 mg/kg to 1.5 mg/kg, the risk of CNS toxicity increases from 10% to 80%. Symptoms include the following:

Lightheadedness, dizziness

Visual disturbance

Headache

Perioral tingling, numbness or tingling of tongue

Sedation

Impaired concentration

Dysarthria

Tinnitus

Metallic taste

Muscular twitching, tremors

With progression of toxicity, the patient may experience tonic-clonic seizures and, eventually, unconsciousness and coma. Seizures generally do not occur with lidocaine levels of less than 10 mcg/mL.

Cardiovascular: Excessive lidocaine concentration can cause cardiovascular toxicity, although this is less common than CNS toxicity. Lidocaine is somewhat less cardiotoxic than lipophilic local anesthetics such as bupivacaine. Risk of cardiac toxicity is greatest in those patients with underlying cardiac conduction problems or after myocardial infarction. Potential cardiovascular effects include the following:

Negative inotropic effects

Effects on vascular tone (with low doses having vasoconstrictive effects and higher doses causing relaxation of vascular smooth muscle)

Effects on cardiac conduction (including widened PR interval, widened QRS duration, sinus tachycardia, sinus arrest, and partial or complete atrioventricular dissociation. Cardiac arrest has been reported after intraurethral administration of lidocaine.)

Cardiac toxicity is potentiated by acidosis, hypercapnia, and hypoxia, which worsen cardiac suppression and increase the chance of arrhythmia. This is important to consider since seizure makes this metabolic picture more likely.

Plasma lidocaine levels of less than 5 mcg/mL are unlikely to have cardiovascular toxicities. Levels of 5-10 mcg/mL can cause hypotension by inducing both cardiac suppression and vascular smooth muscle relaxation. Levels of more than 30 mcg/mL are associated with cardiovascular collapse.

Lidocaine should be avoided in persons with Wolff-Parkinson-White syndrome.

CNS symptoms may be masked in patients premedicated with anticonvulsants such as benzodiazepines or barbiturates. The first sign of toxicity in these premedicated patients may be cardiovascular system (CVS) depression.

When blood levels are high enough to block inhibitory and excitatory pathways, convulsions cease and the patient experiences respiratory depression or arrest and cardiovascular depression.

Large bolus injections may increase peak anesthetic levels to the point where the CNS and CVS are simultaneously affected.

Causes

[ERDoc]

I think it is safe to assume that this genius nurse didn't even check a pulse.

[zzyzx]

Although I"m only 5 minutes from the hospital, I would cardiovert her again. Asking the hospital what to do may be bad advice because this is not a situation where you have someone in a stable wide-complex tachycardia of unknown type. If I really knew that it was WPW, then I would cardiovert her again. From what I've read about WPW, it is much more dangerous than other causes of SVT and must be treated more aggressively because even in a young person it can quickly progress into ventricular fibrillation.

[zzyzx]

Do you guys clearly see delta waves here? I'm not too familiar with them---I understand that they are complexes with slurred or notched R waves.