I want more Hx. Use of ETOH, cigs, recreational drugs? Allergies? Meds? Other medical Hx? What about labs? CBC, ABG?

Sepsis jumps out to me too, but ned to know more. Clubbing fingers is odd.

Does the pt have an elevated temp?

And yes, what are his labs? Lactate level, WBC count… etc

Clubbing… Is the SaO2 a reliable reading? Is the pulseOx tracking? What do his lungs sound like? Do we need an ABG?

I enjoy a mystery

oh yeah… a 12 lead too!

Clubbing is a clinical sign of prolonged respiratory disease.

Hospice

Yes, but I meant odd in this case. usually seen in those a lot older than 18yrs lol

Any history of surgical repair, maybe with a technique that admixes venous and arterial blood? Dig more into hx and see if he had Tetralogy of Fallot.

If so, Dispo:
Call up a children's hospital and have them start dropping quarters in the ECMO machine?


Not sure I'd jump right to an aggressive fluid bolus if he's having possible RV failure. That could wind up quickly on the road to milrinone and pressor support. Maybe a short-acting vasoconstrictor (i.e. phenylephrine) could be enlightening. It could tighten up arterial tone, slow heart rate, and also preferentially move more blood to the pulmonary system if he has a right to left shunt. At T4 para level, he could also have autonomic dysreflexia superimposed on suspected sepsis and cardiopulmonary abnormalities. You said no murmur, but that doesn't rule out possible septic pulmonary embolism. He's got a source of infection, immobility, and abnormal pulmonary vasculature.

Just spitballing here, as there could be a lot going on, and I'd want to lay eyes on the kid. If he's not protecting his airway or is fatiguing from work of breathing, then think about airway control. Move the clothes from his neck to see if he has a trach stoma.

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I believe Azygos is correct. I would not attempt a fluid bolus challenge due to the possibility of potential right/left ventricular failure. How about initiating a dopamine drip beginning at 5mcg/kg/min and see what we get?

Also, what does he normally sat at?

Cyanotic heart defects have way too many eponyms for me to remember without consulting a reference.  My reasoning behind the short duration phenylephrine was to emulate the "sqaut" that some kids learn to do with their tet spells. It briefly increases the SVR and reverses some of the right to left shunt.

I'm not doing the central line. You do the central line. "Asps. Very dangerous. You go first."


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Direct agonists like phenylephrine, norepi, etc. don't rely on intact spinal cord innervation. A spinal anesthetic gives a partial sympathectomy, and that's one of the ways of counteracting it. Conversely, indirect agonists like do require some portion of innervation. Ephedrine still can work to some extent with BP in the absence of spinal function, but still requires endogenous catecholamines to be present at the postsynaptic receptors.

In this case, the heart rate was already high. The tachycardia from ephedrine, norepi, or dopamine could potentially be counterproductive. Now, if you had told me that the guy had a heart transplant too, we'd be talking about the denervation and unresponsiveness to vagal maneuvers/atropine/glycopyrrolate. In his case, a T4 injury may be high enough to impair his cardiac accelerator nerves. He could still get a heart rate increase, albeit more gradually, from circulating catecholamines.