More clinical case talk.

[fakin' the funk]

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CO2 won't hurt the pt. Think about your ICU rotation. Remember permissive hypercapnea?

I just wanna point out that "permissive hypercapnia" and "hypoventilation is OK" are not the same thing.

Permissive hypercapnia refers to patients with SEVERE lung injury who are, to a degree, failing conventional ventilation. The patient with ARDS who is on "max" ventilation like with RR > 30, FiO2 1.0, PEEP > 15 etc. In THIS patient, the priorities are
1) pseudophysiologic oxygenation: SpO2 88-92%, PaO2 > 55
2) Plateau pressures < 30cmH2O
3) TV = 4-6ml/kg IBW
If, in order to achieve those 3 goals, you have to "permit" hypercapnia, then by all means do so. The acidemia is well tolerated for the most part from a metabolic and cardiovascular standpoint; typically you see some decrease in SVR with acidemia.

 

[fakin' the funk]

So,what distinguished this case from MH?

Lack of rigidity
Lack of metabolic acidosis

 

[deleted162650]

In Yao & Artusio they claim the lethal dose for a CO2 embolism is approx 7x greater than the lethal dose for an air embolism. I didn't dig deep enough to find where they are drawing that conclusion from though.

 

[BuzzPhreed]

In Yao & Artusio they claim the lethal dose for a CO2 embolism is approx 7x greater than the lethal dose for an air embolism. I didn't dig deep enough to find where they are drawing that conclusion from though.

Umm... forget about the acidosis and just think about basic partial pressures, sahib.

 

[deleted162650]

Buzz,

I never thought or implied that acidosis was a contributing factor in the case of CO2 embolism. I'm sure the circulatory collapse would take you out first. One can infer all they want from partial pressures and diffusion coefficients etc, but I think without an actual study (preferably in animals) where you intentionally cause gas embolisms of various sizes it's pretty much just speculation as to just how much is gonna be fatal.

 

[BuzzPhreed]

Buzz,

I never thought or implied that acidosis was a contributing factor in the case of CO2 embolism. I'm sure the circulatory collapse would take you out first. One can infer all they want from partial pressures and diffusion coefficients etc, but I think without an actual study (preferably in animals) where you intentionally cause gas embolisms of various sizes it's pretty much just speculation as to just how much is gonna be fatal.

Suffocation.

If your PCO2 is too high - even if they can otherwise tolerate the "embolism" - there are only two organs that can rid it from the body: the lungs and the kidney. Forget the kidney. Too slow.

You cannot possibly ventilate someone fast enough if their PCO2 is 280 mmHg -- even at 100% FiO2 -- to adequate oxygenate at the alveolus. Think about what's happening at that level. That threshold may be even lower in some people.

Forget about acidosis. Forget about the narcotizing effect on the brainstem. This is what happens: suffocation.

Your only hope in that situation is to immediately take them to a hyperbaric oxygen chamber and dive them.

 

[fakin' the funk]

You cannot possibly ventilate someone fast enough if their PCO2 is 280 mmHg -- even at 100% FiO2 -- to adequate oxygenate at the alveolus. Think about what's happening at that level. That threshold may be even lower in some people.

Um...we're being nitpicky here, but if you do the alveolar gas equation you will indeed find that you can oxygenate just fine with a PaCO2 of 280mmHg, for example.

And to prove it...

Paediatr Anaesth. 2004 Jul;14(7):596-603.
Hypercapnia: what is the limit in paediatric patients? A case of near-fatal asthma successfully treated by multipharmacological approach.
Mazzeo AT1, Spada A, Praticò C, Lucanto T, Santamaria LB.
Author information

Abstract
We describe a case of prolonged severe hypercapnia with respiratory acidosis occurring during an episode of near-fatal asthma in an 8-year-old boy, followed by complete recovery. After admission to the intensive care unit, despite treatment with maximal conventional bronchodilatative therapy, the clinical picture deteriorated with evident signs of respiratory muscle fatigue. The child was sedated, intubated and mechanically ventilated. Magnesium sulphate, ketamine and sevoflurane were gradually introduced together with deep sedation, curarization and continuous bronchodilatative therapy. Ten hours after admission, arterial pCO2 reached 39 kPa (293 mmHg), pH was 6.77 and pO2 8.6 kPa (65 mmHg). Chest radiograph showed severe neck subcutaneous emphysema, with signs of mediastinal emphysema. No episode of haemodynamic instability was seen despite severe prolonged hypercapnia lasting more than 14 h. Oxygenation was maintained and successful recovery followed without neurological or cardiovascular sequelae. This case shows the cardiovascular and neurological tolerance of a prolonged period of supercarbia in a paediatric patient. The most important lesson to be learned is the extreme importance of maintaining adequate tissue perfusion and oxygenation during an asthma attack. The second lesson is that when conventional bronchodilators fail, the intensivist may resort to the use of drugs such as ketamine, magnesium sulphate and inhalation anaesthesia. In this context deep sedation and curarization are important not only to improve oxygenation, but also to reduce cerebral metabolic requirements.

 

[BuzzPhreed]

Oh, so we're including kids with their nice little compliant chest walls and virgin lungs... and a ****load of adjuncts. 😉 😀

Yes, you can achieve this: 1 torr (740 mmHG) = water vapor (40 mmHg) + PCO2 (280 mmHg) + 100% O2 (420 mmHg)

But, come on...

The washout in an adult lung... I hope you have a very fast ventilator.

I'm sticking with my primary response. Or, Yao & Artusio better come up with a better explanation.

 

[risnwb]

Below is a link to a case report from anesthesiology describing a massive grain aspiration in a 16 year old male. If you look at the chart with the abgs his PCO2 gets to > 500! And his Pa02 is still 76. Pretty crazy he survived...

http://mobile.journals.lww.com/anes...ewer.aspx?year=1997&issue=10000&article=00039

 

[BuzzPhreed]

What's the highest PCO2 you've ever seen clinically yourself? Me personally: 155 mmHg. And the patient was in deep doo-doo. And, even then, the PO2 was only in the 60's range on 100% FiO2. Died within 24 hours of admission.

It's very hard to kill a young person.

 

[deleted162650]

In the apneic oxygenation study by Frumin et al in the 50's 1 subject reached a pCO2 of 250mmHg after 53min of apnea. The subject suffered a few PVC's followed by a short run of v-tach which spontaneously converted back to NSR and was otherwise fine.

 

[fakin' the funk]

The washout in an adult lung... I hope you have a very fast ventilator.

Don't really know what you mean by "washout," or what the differences between adult and pediatric lungs have to do with anything. As I recall, the discussion was about the mechanism of death or cardiopulmonary dysfunction in CO2 embolism. I think we have all concluded that the mechanism is probably a mechanical obstruction in the pulmonary circulation leading to R heart failure and in turn cardiac/circulatory arrest, since none of us really believes that that degree of respiratory acidosis would be the sole cause of cardiac/circulatory arrest. Cheers.

 

[Random Anesthesiologist]

Do you have a hyperbaric O2 chamber? We have a case of CO2 embolism treated with one.