Hypercapnia algorithm

[Bleepbloopblop]

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Does anyone know of an algorithm to help narrow in on the cause of hypercapnia? I'm having trouble organizing out which pulmonary diseases cause hypercapnia and why.

This is my line of reasoning but Im not sure if Im on the right track.

Minute ventilation = RR x (Vt - dead space); decreased Minute ventilation = increased CO2 retention = hypercapnia

Decreased RR = CNS depression/disorder and spinal cord dysfunction

Decreased Tidal volume = ? (not sure what would cause this) (Don't restrictive lung diseases have decreased tidal volume, yet increased RR, so no hypercapnia?)

Increased dead space = Diseases that increase V/Q ratio like PE and emphysema. (any other diseases im missing?) (and if this is true why do diseases like chronic bronchitis, asthma, and pulmonary edema, which have low V/Q ratios, cause hypercapnia?)

I know ARDS can cause hypercapnia but what category above would that fall under?
Apparently right to left shunts also cause hypercapnia... so now Im just confused.

 

[jdh71]

I never liked the way this was taught in medical school. I don't know if this is because it's mostly taught by nonclinians. The problem practically speaking is that it's not terribly predictable. And because the body compensates for slow chronic derangements in other ways there isn't some kind of definitely linear progression that you can count on. In my practice for every emphysema patient with an FEV1 <35%pred, most will have enough loss of pulmonary surface area to need oxygen but probably only around 5% are chronically hyprrcapnic. Why? Hell if I know for certain but the body retains the ability to dump out CO2 or produce less of it (weight loss) quite effectively.

Basically you see hypercapnia whenever you lose *effective* minute ventilation.

In the acute setting this is usually because of decreased breathing (RR). Overdose of respiratory depressing substances or medications. Also exacerbations of COPD and asthma where they can't get air in their lungs out. You will also see it acute worsened in anyone who has it chronically especially if they get a cardio or pulmonary acute complication (MI or pneumonia) for instance.

In the chronic setting you see it because you've lost the ability to compensate effectively with an increase in RR because the lungs suck. Destruction of pulmonary capillary beds in emphysema or inflammatory/fibrotic lung diseases. Or neuromuscular/chest wall diseases where the breath itself can't keep up even with an increase in RR because the volumes (or effective volumes) suck.

Obesity Hypoventilation Syndrome are folks who are just "too fat to breathe". It's probably more of a sleep disorder but the pathophys has never been explained to me in a way that makes a lot of sense to me but these folks just don't increase their RR like they should and probably (usually) will have an anatomical restriction on PFTs.

Those are where you are going to see hypercapnia clinically. PE causing it is more theoretical. If the PE is that big that patient is probably dead. Though a smaller PE in s chronic patient might be enough to push their CO2 higher. You see it in ARDS usually because we breath folks on the vent at low tidal volumes on purpose. We will compensate with an increase in RR. The fundamental problem in ARDS in hypoxia though. But if you've got enough lung damage to cause hypoxia there could be enough to cause ineffective CO2 exchange and hypercapnia too but you usually don't see it while patients can compensate.

Hope this helps a bit.