From: ashes.mukherjee [mailto:[log in to unmask]]
Sent: Wednesday, December 20, 2000 2:40 PM
To: [log in to unmask]
> It is very important to check what the HCO3 is on the gas as those with
chronic retention will have a raised HCO3 as part of their
compensation.These patients may be treated with more caution rather than
giving everybody oxygen.
Maybe. But this oversimplifies a bit. HCO3 is calculated (CO2 / hydrogen
ions, multiplied by a constant), not measured, and is affected both by the
metabolic 'compensation' and the CO2 tension. Bicarb also rises (by about a
third as much in acute respiratory acidosis). As basic advice to new SHOs,
looking at bicarb may be worthwhile. Otherwise (if you really want a number
to look at), calculate the metabolic component whether acidosis or alkalosis
by the CO2: hydrogen ions ratio (a lot easier to do if you use SI units
rather than pH). Do this a few times and its a lot easier than you think
(honest, it really is).
Also, good point about the LVF. Trouble is, in early stages, before the
lactic acidosis sets in, they will still have a metabolic alkalosis (as I
think you were implying).
> I agree with giving high flow oxygen in those who need it and then monitor
the effect by repeating gases. In the ward though where monitoring is less
intensive I would suggest more caution with high % oxygen unless it has been
demonstrated that the patient is not retaining CO2.
Yes, but if a patient is hypoxic or sick (Sats under 90%, resp rate over 24,
severe dyspnoea, abnormal respiratory pattern, respiratory dyssynergy etc),
less intensive monitoring is inappropriate. The big risk to the patient is
hypoxia; hypercarbia is a debatable (in terms of seriousness of effects),
but probably considerably lesser risk. If you can't monitor the patient well
enough to see if they're getting hypercarbic, you probably can't monitor
them well enough to see if they're hypoxic (although, I suppose, at a pinch,
you could put them on a sats monitor with a loud alarm and strict
instructions to move them to a higher dependency area if sats drop below 90%
or signal quality drops off).
Do not confuse withholding a life saving treatment (possibly with the
potential for severe, if reversible side effects in a minority of patients)
with caution. That's like being 'cautious' by driving at 120 to cut the risk
of someone rear ending you.
Another point I'd make about oxygen is the humanitarian one. It does partly
improve the symptoms of dyspnoea. Anything that can do that for my patients
would need pretty good evidence that is dangerous (rather than just no,
poor, or contradictory evidence) for me to withhold it. (Similar argument on
doxapram, by the way- it worsens symptoms, but of no proven benefit).
Sorry to be pedantic with someone with whom I am mostly in agreement, but I
feel it's important to remember:
1. Hypoxic patients need oxygen regardless of whether they are CO2
2. Even among CO2 retainers, a minority (if any) lose their hypoxic drive if
3. Even within this theoretical minority, it seems pretty unlikely that they
will lose their hypoxic drive while they are hypoxic (sats <85 - 90%)
regardless of Fi O2.
4. Raised CO2 is pretty safe in a lot of CO2 retainers- I've certainly seen
patients with tensions well over 10 kPa without obtundation of conscious
level or evidence of myocardial depression- check the patient not the gases.
(And if they've got an O2 of 6 and a CO2 of 12, don't rush to the conclusion
that hypercarbia is the problem and turn off the oxygen...)
5. If you're fiddling about and find that to get acceptable sats, you need
to raise the pCO2 to levels with unacceptable side effects, NIPPV is good
(Cochrane review, Crit Care Med 25 (10), 1685-1692).
6. Respiratory depression is a clinical diagnosis- gases will tell you about
ventilation, but not respiratory drive.
Apologies if I'm teaching my granny to suck eggs.