Dizziness while driving

DesertMedic66

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7 liters of NS? Looks like the iSTAT was before that...be interested to know what the lytes and abg were after that NaCl load.... Anyway, it's clear what the problem is...anyway...pre-hospital management is...fluid. and a finger stick BG.
The time stamp on the iSTAT was approx 15 minutes prior to landing. So I would imagine a decent amount of the NS was already infused by that time.

With the rales that are starting to develop and the suboptimal SpO2 should we keep going to fluids at this point?
 

E tank

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The time stamp on the iSTAT was approx 15 minutes prior to landing. So I would imagine a decent amount of the NS was already infused by that time.

With the rales that are starting to develop and the suboptimal SpO2 should we keep going to fluids at this point?
Something fishy about that. A hct of 48 after almost 7 L of NS? The sodium and chloride don't make sense either. There should be a significant dilutional effect on on those results that doesn't seem to be there. Have the receiving hospital labs?
 

Tigger

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7 liters of NS? Looks like the iSTAT was before that...be interested to know what the lytes and abg were after that NaCl load.... Anyway, it's clear what the problem is...anyway...pre-hospital management is...fluid. and a finger stick BG.
I think I would want to do something about that QRS width combined with his altered mentation, especially if this is an extend transport time.
 

StCEMT

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Did he have any improvement in mental status while there to be able to tolerate BiPAP? Not someone I particularly want to intubate yet with that SpO2 and pH. If so, BiPAP of 10/5 to start. Still want an ETT, but not before some prep work in this area. I'm confident in my intubation ability, but I know those numbers are not something I want to trifle with or get wrong.

If the ekg is the same, Calcium Gluconate 2g, Bicarb 50mEq, and Albuterol 10mg for the K. I don't like the ekg one bit.

I'd possibly go with the same treatments we do for CHF as well just to move fluid and optimize oxygenation before any intubation. Nitro drip short term to try and create some space for the fluid and Lasix to offload fluid.

Insulin drip at 9U/hr. Once labs start shifting, eventually adding a Potassium drip as well. As high as it is now though, I don't see a need for it yet. Monitor BGL to make sure it isn't dropping too quickly.

RSI plan would be VL with a bougie and backup airway ready as needed. Hopefully everything else would have provided more ideal intubating conditions. Etomidate and Roc 30/100. NC running at 15L during the pre-intubation and intubation phases.

Vent settings. AC/VC. Formula I have for minute ventilation in a patient like this says 21L. 8cc/kg tidal volume at a rate of 30 would give this. Reassess labs and EtCO2 to ensure settings are effective.
 

DesertMedic66

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I'm now thinking DKA (probably caused by underlying infection) that is causing hyperkalemia. If calcium and bicarb haven't been given yet, lets do so. Let's give him a lot of insulin and avoid intubating if at all possible. Physiologically a nightmare tube. Probably now has pulmonary edema from the 7 L of crystalloids (which is also not helping his acidosis). If I was in hospital with appropriate support staff, would really want to try BiPAP, despite the AMS, to try to support ventilations and avoid further desaturation which would necessitate a tube.

However, tough to tell if we can hold off on intubating this patient. Decreasing mentation plus (increasing) hypoxia is not great. If the clinical decision is made to intubate, premeditate with a couple of amps of bicarb couple of minutes prior to intubation attempt. Optimize for first pass success (good patient positioning, most experienced operator, VL +/- bougie or stylet, etc.). Upon passing the tube, very high RR and tidal volume (10 mL/kg) to try to prevent further acidosis and cardiopulmonary collapse.
This was along our lines of thinking also. We went with a total of 2,000mg calcium chloride, 100mEq bicarb, bolus of 9U insulin followed by infusion at 0.1u/kg/hr.

Due to how out of it he was and that he had several episodes of vomiting we felt intubating him was the better option. We were able to assist his ventilations with a BMV+PEEP and got his sats up to 96%. We went with with a standard 2mg/kg ketamine and 1mg/kg Roc. Intubation was a straight forward DL attempt with the C-Mac and bougie and passed on the first attempt. For vent settings we went with a Vt of 8mL/kg (630mL) and a rate of 30 for a Ve of 18.9L for our initial settings. We then ended up increasing the RR to maintain an EtCO2 in the 20mmHg range. We ended up having to bump the rate up to 36 for him to maintain an EtCO2 in the 20s.

Our initial BGL check just read "HI" on our meter. The hospital does not want to use anymore iSTAT cartridges so we are SOL with any updated labs.
 

DesertMedic66

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Something fishy about that. A hct of 48 after almost 7 L of NS? The sodium and chloride don't make sense either. There should be a significant dilutional effect on on those results that doesn't seem to be there. Have the receiving hospital labs?
The time stamp on the iSTAT print out was dated about 15 minutes prior to landing but with this specific hospital, who knows when they actually drew the sample. We are still attempting to do a follow up at the receiving but the PLN, Prehospital Liaison Nurse, is saying HIPAA laws are not letting them.....
 

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The time stamp on the iSTAT print out was dated about 15 minutes prior to landing but with this specific hospital, who knows when they actually drew the sample. We are still attempting to do a follow up at the receiving but the PLN, Prehospital Liaison Nurse, is saying HIPAA laws are not letting them.....
With that pH, might check the obits.
 

E tank

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I think I would want to do something about that QRS width combined with his altered mentation, especially if this is an extend transport time.
If you had iStat ability in the field, absolutely. I suppose you could intuit dka from a finger stick and physical exam and treat accordingly...
 

E tank

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This was along our lines of thinking also. We went with a total of 2,000mg calcium chloride, 100mEq bicarb, bolus of 9U insulin followed by infusion at 0.1u/kg/hr.

Due to how out of it he was and that he had several episodes of vomiting we felt intubating him was the better option. We were able to assist his ventilations with a BMV+PEEP and got his sats up to 96%. We went with with a standard 2mg/kg ketamine and 1mg/kg Roc. Intubation was a straight forward DL attempt with the C-Mac and bougie and passed on the first attempt. For vent settings we went with a Vt of 8mL/kg (630mL) and a rate of 30 for a Ve of 18.9L for our initial settings. We then ended up increasing the RR to maintain an EtCO2 in the 20mmHg range. We ended up having to bump the rate up to 36 for him to maintain an EtCO2 in the 20s.

Our initial BGL check just read "HI" on our meter. The hospital does not want to use anymore iSTAT cartridges so we are SOL with any updated labs.
No MM QB here so don't take it as such...but why the etCO2 so low? That a protocol or something? It's a metabolic acidosis.
 

DesertMedic66

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No MM QB here so don't take it as such...but why the etCO2 so low? That a protocol or something? It's a metabolic acidosis.
For us when we have a patient in metabolic acidosis we either attempt to match their pre-RSI EtCO2 levels or if we have blood gasses we will try to match the EtCO2 with the PCO2.

The thinking behind this is that if we adjust the patient to a normal EtCO2 we may cause the patient to become more acidotic. We are trying to compensate as much as we can for the metabolic acidosis by causing a respiratory alkalosis.
 

Tigger

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If you had iStat ability in the field, absolutely. I suppose you could intuit dka from a finger stick and physical exam and treat accordingly...
That EKG is almost pathognomonic for HyperK to me. That plus his symptoms (and even without the BGL), should be concerning enough to treat.
 

E tank

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For us when we have a patient in metabolic acidosis we either attempt to match their pre-RSI EtCO2 levels or if we have blood gasses we will try to match the EtCO2 with the PCO2.

The thinking behind this is that if we adjust the patient to a normal EtCO2 we may cause the patient to become more acidotic. We are trying to compensate as much as we can for the metabolic acidosis by causing a respiratory alkalosis.
Figured something like that...thanks...but the consequences of hypocarbia can't be discounted....in this guy...no big deal. He's 30 and bullet proof...but severe hypocarbia with attendant fall in cerebral blood flow in, for example, the elderly or someone with carotid artery disease shouldn't be ignored, IMHO. I'm in the end organ protection business and I understand field medicine is...well...field medicine. But folks are getting care in the field today that wasn't possible in the hospital a generation or so ago...
 
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