In this video, we'll talk about the workup of a respiratory alkalosis.

Let's go.

Respiratory alkalosis equals hyperventilation.

Note that hyperventilation does not equal respiratory alkalosis per se.

A little side step: what's the difference between tachypnea and hyperventilation?

Well, tachypnea is solely an increased respiratory rate.

Hyperventilation is defined as a lowered carbon dioxide level.

This is accomplished by breathing fast and deep.

Tachypnea could therefore lead to hyperventilation but it doesn't have to.

Breathing fast and shallow increases dead space ventilation, and will not cause hyperventilation

or low CO2 levels.

Now back to hyperventilation.

Remember that you're blowing out your asses, ehh acids.

You're blowing out your acids.

And you're doing this by breathing fast and deep and thus lowering pCO2.

In the Henderson-Hasselbalch equation, lowering pCO2 shifts the equation to the left and therefore

also lowers hydrogen, increasing pH.

So, if your blood is already acidic, if you're blowing out your acids, your pH will be normal.

This is the case in compensated metabolic acidosis.

If your pH is however normal to start out with, if you're blowing out your acids, you'll

become more alkaline.

This is respiratory alkalosis.

An example:

pH is 7.51, this is an alkalosis.

pCO2 is 3.7 kilopascal or 28 mmHg.

pCO2 is low, so this explains my alkalosis.

It's therefore a respiratory alkalosis.

Bicarb is 23.5, which does not explain pH so we were correct.

Now why would a patient do this?

There are two main reasons.

You've learned that our respiratory center is triggered by high CO2 levels, right?

Well, thankfully, if you're hypoxic, your body will also try to breathe faster and deeper.

So the first main reason for respiratory alkalosis is hypoxia.

We call this hypoxic drive.

If this is the case, you'll need to do a workup on hypoxia.

Common causes are pneumonia, pulmonary embolism and congestive heart failure.

I might do a video on shunting in the future if that's something you're interested in.

Let me know!

The second cause is pretty straight forward.

Can you think of a couple of reasons why people would breathe faster and deeper (that isn't

hypoxia or acidosis)?

Pain is an extremely common cause.

Also agitation (common in sympathomimetic drug use, like amphetamines), fear or fever.

We call these causes either stimulated respiratory drive or non-hypoxic drive.

Some people hyperventilate for no apparent reason.

This is called primary hyperventilation syndrome.

They also fall into this category, and they typically experience hyperventilation symptoms

like dizziness and tingling of the lips.

Did you know that these patients could have elevated lactate levels?

This caused by the alkalosis, and it is benign.

So how do you distinguish the two?

Please don't deprive your patient of his or her oxygen.

If your patient needs oxygen, it's pretty obvious there's some sort of hypoxic drive.

In this workup, however, an arterial blood gas is preferred over a venous blood sample

for obvious reasons.

If pO2 is low to lower limit of normal, think hypoxic drive.

If pO2 is high to upper limit of normal, think non-hypoxic drive.

So why is this important?

Respiratory alkalosis could be the expression of underlying hypoxia, which definitely deserves

a workup and proper treatment of its own.

Or it could be the expression of underlying pain, fear or agitation, which also deserves

your attention and treatment.

Also, in respiratory alkalosis beware of transcellular shifts of electrolytes like potassium.

For more information on that, watch my video on hypokalemia.

That's all for respiratory alkalosis.

Pretty easy, right?

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I'll see you next time.