‫البقرة آية ‪32‬‬

 CO is an odorless, colorless and

tasteless gas that results from
incomplete combustion of fuels (i.e.,
gas heaters coal, wood, gasoline).

 CO has been called the silent killer

and has been the cause of
approximately 5,000 deaths annually
in USA., with 2 to 5 times that
requiring treatment.
 Even with treatment the devastating
sequalle that can accompany CO
poisoning can be life changing.
 These include chorea, rigidity,
dementia, myoclonus, impaired
sensory function, seizures, and gait
dysfunction.
 There can also be permanent cardiac
damage due to the hypoxia involved
in the poisoning process .
 .Physical Aspects of CO
 CO. in human body will be present
in combination with
• Hemoglobin (85-90%)
• Myoglobin (10-15%)

This is governed by Haldain’s law

COHb/OHb = K x PCo / PO k=240

COMb/OMb = K x PCo / PO K=40

 .Biochemical effects of CO
CO. Leads to
inhibition of
OXYGEN

Transport Availability Utilization

 Oxygen Transport

COHb Oxygen
saturation of the hemoglobin in the
lungs due to decrease in the
available sites to be chemically
combined with and saturated by
Oxygen Leading to
Decrease in PaO2
 Oxygen Availability
Binding of CO. with one hemoglobin
molecule leads to Allosteric modification
in the remaining heme groups leading
to shift of oxygen dissociation curve to
the left resulting in decreased oxygen
availability to tissues.
This explains why tissue hypoxia is far
greater than that would expected from
loss of oxygen carrying capacity of
hemoglobin.
 Oxygen Utilization
 CO. combats with oxygen for the
reduced form of cytochrome oxidase a3
which is the terminal enzyme of the
cellular respiratory chain leading to
cellular hypoxia.
 This explains the particular affection of
organs with high metabolic rates such
as heart and brain.
Fortunately the reduced cytochrome
oxidase a3 prefers O2 to CO by a factor
of 9:1
 :In conclusion CO. Leads to
1. Decrease the amount of chemically
transported o2 from the lungs to
the blood.
2. Decrease the availability of the
chemically transported o2 from the
blood to the tissue cells.
3. Decrease the cellular utilization of
o2 reaching to the tissue cells.
 Delayed CO neurotoxicity
 The suggested mechanism of
delayed CO-mediated neurotoxicity is
a demyelinating process caused by
brain lipid peroxidation and leukocyte
mediated inflammatory changes
 Clinical Manifestations
 Normal carboxyhemoglobin (HbCO) levels
are 0% to 3% for non-smokers and
3% to 8% for smokers.
 Levels of 10% to 20% causes headaches,
nausea, vomiting and dyspnea.
 Levels of 30% to 40% causes
• confusion, altered mentation, ataxia blurred
vision, weakness
• dyspnea, tachypnea with tachycardia,
• and abnormal neuropsychiatric testing .
 Greater than 40% causes
• chest pain, palpitations, severe
drowsiness, disorientation with
• dysrhythmias, signs of ischemia on ECG,
hypotension, syncope, lactic acidosis,
• seizures, pulmonary edema, coma
 up to 20% of patients with
moderate poisoning will develop the
recurrent symptom syndrome
manifested by memory and/or
cognitive impairments. The average
time to onset is 7 days with the
range of asymptomatic interval
between 1 and 40 days.
 Most of these patients recover with
treatment.
 Unfortunately, a sub-group develop a
more severe syndrome defined as
the delayed neuropsychiatric
syndrome.
 Unlike the recurrent symptom
syndrome, approximately 50% of
these patients do not recover.
 Clinical rational for use of
HBOT in CO. poisoning
 HBOT help speed up the CO washout by
providing high O2 concentrations at
increased atmospheric pressures
The half-life of CO is
• 320 minutes on room air
• 90 minutes on 100% face mask
• 60 minutes by cuffed endotracheal tube
• 23 minutes HBO at 3 ATA
 Clinical rational for use of
HBOT in CO. poisoning
 Increase the amount of transported
physically dissolved O2 from the
lungs to the blood.
 Increase the availability of O2 from
the blood to the tissue cells.
 HBO also accelerates the dissociation
of carboxycytochrome oxidase a3 .
 Clinical rational for use of
HBOT in CO. poisoning

 Also, HBO is suggested to prevent

brain lipid peroxidation and leukocyte
mediated inflammatory changes ;
these are believed to be the etiology
of the neurological sequelae.
 Decision making
 Every case should be considered
individually.

 The following guidelines are

offered to assist decision making.
 Accepted indications for HBOT
 COHb > 40%
 COHb > 25%<40% plus any of the
following:
*history of cardiovascular disease,
*history cerebrovascular disease,
*age > 60 yrs, age < 2 yrs,
*Hgb < 10 gm%
*exposure duration > 2 hours
 COHb < 25% plus any of the following:
1. History of loss of consciousness
2. Serious toxicity including lethargy,
confusion, disorientation on arrival to
medical facility,
3. History of seizures, focal neurologic
deficit.
4. Ischemic chest pain, new dysrhythmias,
ECG changes, or hypotension
 COHb >15% with
Pregnancy, or signs of fetal distress with
any level of COHb.
 Symptoms that do not resolve
after 6 hours of continuous 100%
normobaric oxygen.

 Recurrent symptoms up to
3 weeks after original treatment
with normobaric oxygen.
 Protocol
1. 100% oxygen by non-rebreather mask
until beginning of HBO
2. 100% oxygen at 2.4 ATA x 90 minutes
could be repeated every 12 or 8 hours
until patient becomes asymptomatic and
COHb < 3%
3. Intermittent 100% oxygen by non-
rebreather mask after & between sessions.
4. Admit or D/C as appropriate.
5. F/U Neurology 1 month.
 Other treatment modalities may include
• CPR
• Haemodynamic support
• Cardiac monitoring
• Mannitol (1-2G/kg) to help decrease the
cerebral edema accompanying the CO
poisoning.
• Steroids.
 Randomized Study
 Dr. Lindell K. Weaver and his colleagues
compared high-pressure oxygen treatment
to normally pressurized oxygen in2002.

 A total of 152 patients experiencing acute

carbon monoxide poisoning received either
three sessions of high-pressure oxygen or
three sessions of oxygen and air
administered at atmospheric pressures, all
within a 24-hour period.
 Weaver and his team found that
only 25% of patients who received
the high-pressure oxygen treatment
experienced neurological problems 6
weeks later, relative to 46% of those
whose treatment was administered
at atmospheric pressure .
 Weaver explained that the benefit of
high-pressure oxygen therapy lies in
its dosing, with high-pressure
treatment administering a more
effective doses of oxygen than
normally pressurized treatment.
(The New England Journal of Medicine 2002;347:1054-1055 )
 Randomized Study
 Thom et al.in1995 prospectively studied
patients with mild to moderate CO
poisoning who presented within 6 hours of
the onset of symptoms.
The incidence of delayed neurological
sequelae was significantly greater in the
group treated with NBO 7 of 30 (23%)
than HBO, 0 of 30.
 They confirmed that delayed
neuropsychiatric sequelae are not
yet predicable by clinical or
neuropsychiatric testing and
suggest that HBO may abort the
neurotoxicity of CO poisoning.
(Thom SR, et al. Ann Emerg Med 1995;25:474-480.)
 According to the above
considerations, it can be
presumed that
HBO should be an essential
part in the CO poisoning
therapeutic
armamentarium.
THANK
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