DKA Patient

firemedic31075

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Call came in at around 4am for unresponsive dibatic. I had run this address 2 times before this already for a women with high blood sugar so I already have an idea whats going on. We get there to find a 35 y/o female supine on floor unresponsive. boyfriend standing next to her saying just got home from work and found her. last seen 6pm previous day. I immediatly notice Kussmals resp. walking in. GCS-4. Pulse- weak and thready. skin- warm and moist. no gag reflex so put in an OPA began ventilating. Hx- diabetes (poorly controlled). Accucheck- "HI" means over 600. Pupils- fixed + dialated. Pulse- 110. B/P- 90/60. LS- clear + equal bilat. EKG- Sinus Tach. with wide QRS and tall peaked T waves. Respirations about 38. ETC02- 18. Pulse Ox. 95%. No IV possible so IO estab. and NS under pressure infuser started. Airway eventually controlled with Combitube after multiple failed intubation attempts....In ER pt. given insulin and Bicarb. and intubated using video laryngoscopy and accucheck- over 1000 didn’t hear what the PH was or too much else as dispatch was trying to put us on another call....Now I have a few questions. With having a metabolic acidosis why would the ETC02 read around 18? And with the pupils, why fixed and dilated? I've never seen that on a live person. EKG- I know her electrolytes are screwed up hence peaked T waves and such. I’m sure the wide QRS is related but why? what causes it to widen? And what are the chances of her recovering? I have not run too many of these patients so I have no clue.
 

mikeylikesit

Candy Striper
906
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Call came in at around 4am for unresponsive dibatic. I had run this address 2 times before this already for a women with high blood sugar so I already have an idea whats going on. We get there to find a 35 y/o female supine on floor unresponsive. boyfriend standing next to her saying just got home from work and found her. last seen 6pm previous day. I immediatly notice Kussmals resp. walking in. GCS-4. Pulse- weak and thready. skin- warm and moist. no gag reflex so put in an OPA began ventilating. Hx- diabetes (poorly controlled). Accucheck- "HI" means over 600. Pupils- fixed + dialated. Pulse- 110. B/P- 90/60. LS- clear + equal bilat. EKG- Sinus Tach. with wide QRS and tall peaked T waves. Respirations about 38. ETC02- 18. Pulse Ox. 95%. No IV possible so IO estab. and NS under pressure infuser started. Airway eventually controlled with Combitube after multiple failed intubation attempts....In ER pt. given insulin and Bicarb. and intubated using video laryngoscopy and accucheck- over 1000 didn’t hear what the PH was or too much else as dispatch was trying to put us on another call....Now I have a few questions. With having a metabolic acidosis why would the ETC02 read around 18? And with the pupils, why fixed and dilated? I've never seen that on a live person. EKG- I know her electrolytes are screwed up hence peaked T waves and such. I’m sure the wide QRS is related but why? what causes it to widen? And what are the chances of her recovering? I have not run too many of these patients so I have no clue.
QRS is widened due to an insufficiency in the K+ Ca+ pumps. Acidosis and electrolyte imbalances cause more hydrogen reversing the gradient and lowering the K+ levels thus affecting the depolarization of the ventricles and polarization of the atria. Fixed pupils that are dilated is due metabolic compensation measures i think...The mortality rate in DKA is high but if she was still breathing and her only arrhythmia was sinus tach and the fact that they got insulin to her presumably Rosilin it still would have taken a little time for her to come back don but she more than likely will survive. Being diabetic myself I have had DKA and it feels a lot worse than it looks. Hard to say in her situation though whether or not she made it but there is a high chance that she did. The Kusmauls respirations were her bodies attempt at metabolic compensation for the acidosis so she was fighting for her life unconsciously.
 

JPINFV

Gadfly
12,681
197
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With having a metabolic acidosis why would the ETC02 read around 18?

Ok, the way I think about this is that there are two components to acid-base balance. There's a metabolic component (hydrogen secretion, biological processes, etc) and a respiratory component (control of CO2 concentration). Simply put, a breakdown in one control mechanism results in the body using the other mechanism to compensate. For example, respiratory acidosis results in the kidneys secreting hydrogens. Metabolic alkadosis results in the body retaining CO2 to produce those protons.

The overall key component is CO2+H2O<->bicarbonate+proton. The body can control protons (excreted by the kidney) and CO2 (released through ventilation). Water is always going to be in excess and bicarbonate will be adjusted through the other processes.

Now the key chemistry concept is Le Chatelier's principle. Essentially, a reaction in equilibrium can be manipulated by adjusting any side of an equation. For example, the classic A+B<->C+D reaction. If you want to push that equation to the right, you could either remove C or D as it's formed, or dump a lot of A or B into the reaction. Similarly, CO2+H2O<->bicarbonate+proton can be pushed to the left by removing CO2 or dumping in bicarbonate (you can add protons to drive the reaction, but we want to lower the amount of protons).

Now, why does the patient have a low EtCO2? Because there's a limit to the amount a reaction can be driven by simply removing CO2 (bicarbonate becomes a limiting reagent) and the fact that they're breathing rapidly means less CO2 per breath which means lower EtCO2.
 

MSDeltaFlt

RRT/NRP
1,422
35
48
I think you're overthinking the metabolic acidosis and the EtCO2. The EtCO2 read 18 because of the the Kussmaul respirations at 38. Why was the EtCO2 so low? Simple. The metabolic acidosis.

The operative word in DKA in reference to acid base balance is "acidosis".

1. The bicarb bottomed out because of the DKA.
2. The body sensed this driving the resprations faster and deeper - Kussmaul Respirations.
3. The faster resp drop the PaCO2 (or EtCO2 in this case) to bring the pH back up because of the acidosis brought on by the DKA.

We live in a very narrow pH balance - somewhere around 7.4. Our bodies can only compensate so much for so long, then they stop compnsating. Major deviations from that can result in a GCS of 4 and on the floor... not unlike your pt.
 
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