Newsgroups: misc.emerg-services
Subject: Re: MD & Rn want to run it all.....
From: macridis_g@kosmos.wcc.govt.nz (Gerry Macridis)
Date: 15 Sep 1992 09:48:24 GMT
Reply-To: macridis_g@kosmos.wcc.govt.nz
Organization: Wellington City Council, Wgtn, NZ
NNTP-Posting-Host: kosmos.wcc.govt.nz

In article <01GODTXUW6YA9N47RG@ritvax.isc.rit.edu>, JAT8419@RITVAX.BITNET
(TRAUMA JUNKIE) writes:

>O.K. I checked NYS protocol for BLS servbices and it says treat a COPd pt. as
>you would any other...EXCEPT when the trouble is DIRECTLY related to the Pt's
>COPD disease... (i.e. an asthma pt. w/ atshmatic problems).
>        In these cases you are to keep the Pt. on the home care level of O2
>or if not taking home oxygen then give 2-4 LPm via N.C.
>
>        If the distress is great enought though and perfusion is not
>adaquate....


In response to the above comment on COPD and asthma, but mainly as a
relevant item of interest to add to this thread, I am reproducing the
following item which appeared on p. 89 of the June/July 1992 issue of
Frontline, the official journal of the Institute of Ambulance Officers
(New Zealand):

'{Q}

Tony Sutherland of Gore, Southland writes and asks:
   I am a volunteer Ambulance Officer and second year Comprehensive
Nursing Student at the Southland Polytechnic.
   Occasionally, I find conflict between what the Polytech teaches and
what I have learned at NAOTS in regard to asthma as it relates to Chronic
Obstructive Airways Disease (COAD).
   In the module of my nursing course covering this subject, asthma was
listed along with bronchitis and emphysema as being COAD.  My ambulance
training says that asthma is not COAD, although can have a chronic form,
but is acute, episodic and reversible; In only one of my text books is
asthma classified along with COADs.
   My main question relates to oxygen therapy, hypoxic drive and asthma.
If an asthmatic (a six year old for instance) is admitted to hospital
with an acute exacerbation of his/her asthma, will administration of
anything other than "low concentration, low flow" oxygen cause depression
of the respiratory centre leading to respiratory arrest?
   I understand that hypoxic drive respiratory stimulus only developed if
the body was exposed to high blood/CO2 levels for an extended period i.e.
months and years such as with emphysemic patients.  Because the asthmatic
has essentially 'normal' pCO2s, except during an exacerbation, hypoxic
drive would not develop.
   How fast does the respiratory stimulus change from high blood/CO2 as
in healthy people to that of low blood/O2 in the COAD patient?
   Are asthmatics subject to hypoxic drive just as emphysemics and
bronchitis are?
   I would appreciate your opinions on these questions.

{A}

   To answer these questions Frontline enlisted the help of Dr Andrew G.
Veale who is a specialist Physician and Consultant in Respiratory
Medicine and Diving and Hyperbaric Medicine.  Dr Veale lectures to the
Paramedic Course at NAOTS and works at the Mercy Specialist Centre and
Greenlane Hospital, Auckland.  Frontline is most grateful to Dr Veale for
his continuing support to Ambulance Officers education.
   "Thank you for asking me to comment on the questions raised by your
correspondent.  Asthma can be correctly listed along with bronchitis and
emphysema as obstructive airways disease, but is clearly different from
CHRONIC obstructive airways disease.  Your correspondent is perfectly
correct when he states that asthma is an acute episodic reversible
narrowing of small airways.
   It used to be taught that oxugen therapy should be "rationed" in
asthmatic patients because some asthmatics were hypercapnic (high CO2) as
well as hypoxic.  It was assumed that any hypercapnia was due to failure
of the respiratory control centre to respond to the high CO2 and that
hypoxic drive was the important factor.  This is incorrect as the
elevation in CO2 in an asthmatic patient simply reflects the inability to
achieve an adequate alveolar ventilation, ie it reflects the severity of
the attack of asthma, not a failure of respiratory drive.  All asthmatics
should be treated with high flow and therefore high inspired oxygen
concentrations and, certainly in the severe situation, 100%.  It is
possible to achieve adequate oxygenation even with extremely elevated CO2
levels in the setting of acute asthma.
   It is rather complicated to explain the physiology of ventilatory
control in a brief letter to the editor, but your correspondent is quite
correct that elevations of CO2 will initially change the pH of the CSF
fluid bathing the medulla oblongata, increasing the ventilatory drive. If
this ventilation is inadequate such that CO2 levels remain elevated, then
the kidneys compensate for this by retaining bicarbonate so that the
blood (and CSF) pH returns to the normal of 7.4-7.44.  Even at this level
there is significant increase in ventilatory drive if the CO2 should rise
further and hypoxic drive only takes over when pO2 falls to very low
levels, less than 60mmHg, in the setting of chronic elevation of CO2.
   In practical terms, any severely ill patient with respiratory
distress, aged less than 55 years, could appropriately be transported
with high FlO2s unless they were on a domiciliary oxygen programme or
were obviously oedematous and cyanosed.  Patients aged over 55 could
receive high FlO2s unless their clinical state when well was such that
their exercise was severely limited, or they were oedematous, or they
were on a domiciliary oxygen programme.
   From my comments, you will see that few patients in fact require
transport on very low FlO2s.
   Kind regards.
                                       A.G. Veale, Respiratory Physician'


-- 
Gerry Macridis,      /\/\     .... Email: macridis_g@kosmos.wcc.govt.nz
Private Box 3929,   ( oo )    :... Voice: +64 4 3899444
Wellington,           \/......:
New Zealand.                       Learn first aid; it saves lives.