Pulmonary Embolism ABG Question

[Photonic]

Sorry in advanced if this is a stupid question. I've been trying to figure out why a PE is considered respiratory alkalosis. I thought it would be a metabolic acidosis with respiratory compensation. Isn't the mechanism for a pulmonary embolism:

PE -> decrease PO2 -> lactic acid generation(metabolic acidosis) -> tachypnea (respiratory compensation)

I would appreciate any help on what I am missing. This has really been nagging at me today.

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[FindMeOnTheLinks]

In PE the V/Q defect causes high PaCO2 and low PaO2. In an effort to correct the blood gases, there is increased respiratory drive which causes a tachypnea. It is very easy to blow off PaCO2, so the the PaCO2 is actually decreased as a result of the tachypnea. This causes a respiratory alkalosis.

 

[Photonic]

In PE the V/Q defect causes high PaCO2 and low PaO2. In an effort to correct the blood gases, there is increased respiratory drive which causes a tachypnea. It is very easy to blow off PaCO2, so the the PaCO2 is actually decreased as a result of the tachypnea. This causes a respiratory alkalosis.

Thanks for the response. My next question then would be why would someone with a PE stay in a state of alkalosis? If there is not a metabolic component, then shouldn't the person become bradypneic in response to the low PaCO2 which would then cause a respiratory acidosis?

 

[Photonic]

Thanks for the response. My next question then would be why would someone with a PE stay in a state of alkalosis? If there is not a metabolic component, then shouldn't the person become bradypneic in response to the low PaCO2 which would then cause a respiratory acidosis?

I think I figured what I was having a problem with. If I'm right, someone with a PE will stay hyperventilating and in a state of alkalosis due to the decrease PaO2 sensed in the carotid/aortic bodies. I didn't think the carotid/aortic bodies would play a role since they respond to both PaO2 and PaCO2, but they actually don't respond to decreases in PaCO2. Does that sound right?

 

[FindMeOnTheLinks]

I think I figured what I was having a problem with. If I'm right, someone with a PE will stay hyperventilating and in a state of alkalosis due to the decrease PaO2 sensed in the carotid/aortic bodies. I didn't think the carotid/aortic bodies would play a role since they respond to both PaO2 and PaCO2, but they actually don't respond to decreases in PaCO2. Does that sound right?

Bingo. Good work

 

[cellsaver]

Thanks for the response. My next question then would be why would someone with a PE stay in a state of alkalosis? If there is not a metabolic component, then shouldn't the person become bradypneic in response to the low PaCO2 which would then cause a respiratory acidosis?

There are several resources that can answer your question. Try these:

Lectures in Pulmonary Pathophysiology @ UC Davis SOM by the brilliant Dr John West, MD, PhD.
Select the video lectures dealing with Vascular Diseases. Dr West teaches out of his excellent textbook, which you can read in a couple of hours. by reading his text, you will understand what you are missing in the above question. By the way, you asked an excellent question. good for you for digging deeper and seeking understanding.

Pulmonary Pathophysiology: The Essentials (PULMONARY PATHOPHYSIOLOGY (WEST))Eighth Edition
There is a newer edition. I used the 8th edition and I'm certain the 9th will have better diagrams.

Respiratory Physiology: The Essentials (Respiratory Physiology: The Essentials (West)) Ninth Edition
There is also a newer edition for the "Essentials" text. Get that one instead. I used the 9th edition along with his free videos on his website at UC Davis SOM. Dr West writes in a way that is easily understood.


Lastly, Linda Costanzo does a great job, as always, in explaining concepts on a basic level. Buy her Physiology text (not the BRS version), and take a highlighter to it.

Physiology: with STUDENT CONSULT Online Access, 4e (Costanzo Physiology) 4th Edition
There is also a newer edition to Costanzo's text. buy that one instead. I used the 4th edition years ago.

You will come away feeling confident in your understanding of physiology in general, but also re: your question. I am including a screen shot of PE from her text

Have fun with this. By the time you get around to Step 1, you should own the material and crush it because you put forward the hard work....a trait few embrace today, and it shows...like in the responses you got

The attached images/text are from Costanzo's textbook

, Chapter 7, pages 319 & 327.

1. Loss of CO2. Hyperventilation causes an excessive loss of CO2 and a decrease in PCO2. The decreased PCO2 is the primary disturbance in respiratory alkalosis and, as predicted by the Henderson-Hasselbalch equation, causes an increase in pH (pH = 6.1 + log HCO3/CO2). The decreased PCO2, by mass action, also causes a decreased concentration of HCO3.

2. Buffering. Buffering occurs exclusively in ICF, particularly in red blood cells. In this case, CO2 leaves the cells and intracellular pH increases.

3. Respiratory compensation. As with respiratory acidosis, there is no respiratory compensation for respiratory alkalosis because respiration is the cause of the disorder.​

4. Renal compensation. Renal compensation for respiratory alkalosis consists of decreased excretion of H+ as titratable acid and NH4+ and decreased synthesis and reabsorption of new HCO3−. Decreased reabsorption of HCO3− decreases the HCO3 − concentration even further than did the effect of mass action alone. ​