Carbon monoxide poisoning occurs when excessive levels of carbon monoxide are breathed in from incomplete combustion. Sources include fires, malfunctioning heating systems, vehicles operating in enclosed spaces, and methylene chloride. CO binds to hemoglobin, preventing oxygen transport and causing tissue hypoxia. Symptoms range from headache and nausea at lower levels to coma and death at higher levels. Treatment involves high-flow oxygen therapy and possibly hyperbaric oxygen for those at high risk of complications.

1. CARBON
MONOXIDE
POISONING
Dr. DAMINENI RAVI TEJA
EMERGENCY MEDICINE

2. INTRODUCTION
● Carbon Monoxide poisoning occurs after breathing in excessive levels of carbon monoxide
● It is released into the environment by the incomplete combustion of carbonaceous
materials

3. EPIDEMIOLOGY
● Carbon Monoxide may be responsible for 50% of all fatal poisonings
● Carbon Monoxide poisoning victims dies before reaching the hospital ,of those
hospitalised, approximately 2% die, 10%recovery partially , and 23% to 47% suffer
delayed neurologic sequelae

4. SOURCES OF EXPOSURE
CO is produced from incomplete combustion of fuels. Potential sources of CO include:
● Smoke inhalation from fires
● Poorly functioning heating systems
● Improperly vented fuel-burning devices
● Motor vehicles operating in poorly ventilated areas
● Open air exposure to motorboat exhaust
● Underground electrical cable fires that produce large amounts of CO, which can seep into
adjacent buildings and homes
● Inhaled or ingested methylene chloride

5. PATHOPHYSIOLOGY
● Normal physiologic CO levels (as carboxyhemoglobin) from this process are approximately
1% in healthy nonsmokers.
● Physiologic production can be increased in hemolysis or sepsis.
● CO toxicity causes profound tissue hypoxia and activation of inflammatory mediators that
may lead to permanent injury of the heart, the CNS and less commonly, the peripheral
nervous system

6. CO enters the body via lungs
Direct interactions damages the lung parenchyma
In the body CO is delivered by Hb
CO causes capillary leakage of macromolecules from the lungs and systemic vasculature
This can occur in humans who have been exposed to relatively low concentration

7. As Carboxyhemoglobin(COHgb) levels rises
Cerebral blood vessels dilate, and both coronary blood flow and capillary density increases
If exposure continues, central respiratory depression develops which may result from cerebral hypoxia
Cardiac effects VENTRICULAR arrhythmias occur
Ventricular arrhythmias are implicated as the cause of death most often in CO poisoning

8. There is evidence that myocardial impairment begins at the relatively low level of COHgb of
20%
The overall cause of death for CO poisoning is combined hypoxia and ischemia during the acute
events

9. Tissue hypoxia
● Approx 85% of CO is bound to HB
● Rest dissolve in plasma or bound intracellularly
often to myoglobin
● CO shift the oxyhemoglobin dissociation curve to
left,imparin 02 release to tissues
● Half life of COHb on RA ranges b/w 249-320 min
● On 100% 02 AP ½ life is about 74-80 min
● ½ life of METHYLENE CHLORIDE exposure >
8 hrs due to metabolic production
OXYGEN TENSION 150 mm Hg
HbO2
%
sat
0
100%

10. Mitochondrial inhibition
CO binds as ferrous heme A3
disabling oxidative phosphorylation
(more under the hypoxic conditions)
● Decreases adenosine triphosphate production
● production of free radicals
● compromising tissues with the highest metabolic demand(brain & heart)
● generating lactic acidosis

11. CO activates
By displacing NO reacts with superoxide
Platelets
Peroxynitrite
Compromise mitochondrial functions
Platelets activation
To yield
further
stimulates
Inflammatory and platelets effects

12. the combined effect
Neutrophil to degenerate
Myeloperoxidase further degranulation
stimulates
releases
amplifying
&
Platelet activation

13. Proinflammatory mediators
catalyze
Lipid peroxidation of myelin proteins of nerves tissues
triggering
&
microglia (primarily of the CNS)
Cells are more sensitive to this neurotoxic effect
lymphocytes

14. Demonstrate GLOBUS PALLIDUS lesion Evident in CT/MRI
Platelet activation
endothelial injury &
cell apoptosis combine
to yield several types of
cardiac injury or dysfunction

15. CARBOXYHEMOGLOBIN MEASUREMENT
● Co-oximetry, which measures total hemoglobin as well as oxyhemoglobin, methemoglobin,
and COHb saturation, is the only accurate measurement tool.
● venous blood gas with co-oximetry is sufficient in most cases.

16. TOXICODYNAMICS
● Carbon monoxide has ~210 times the affinity for haemoglobin than oxygen.
● Binding Therefore renders haemoglobin oxygen carrying capacity and delivery to the
tissues.
● This can result in tissue hypoxia and ischaemic injury.

17. ● CO also binds to intracellular cytochromes, impairing aerobic metabolism
● Carbon monoxide also triggers endothelial oxidative injury, lipid peroxidation and an
inflammatory cascade
● These mechanisms are probably responsible for delayed neurological sequelae

18. Typical clinical symptoms and signs relative to COHb
● <10% (nil, commonly found in smokers)
● 10 – 20% (nil or vague nondescript symptoms)
● 30 – 40% (headache, tachycardia, confusion, weakness, nausea, vomiting, collapse)
● 50 – 60% (coma, convulsions,Cheyne-Stokes breathing, arrhythmias, ECG changes)
● 70 – 80% (circulatory and ventilatory failure, cardiac arrest, death)

19. TOXICOKINETICS
● Absorption:
● COHb concentration in blood is a function of the CO concentration in inspired air and the
time of exposure
● Clinical effects occur within 2 hours of exposure at concentrations as low as 0.01% (100
ppm)

20. ● Uptake (and elimination) of CO is increased by:
● Decreased barometric pressure
● increased activity
● increased rate of ventilation
● high metabolic rate
● Anaemia
● Tobacco smokers have higher baseline concentrations of COHb (3 to 10%) and therefore
will reach toxic concentrations earlier in any exposure

21. ● Distribution:
● Rapidly binds available haemoglobin

22. ● Metabolism:
● <1% of the absorbed CO is metabolised endogenously to carbon dioxide

23. Elimination:
● CO is eliminated unchanged from the lungs in an exponential manner
● The biological half-life of CO in a sedentary healthy adult is 4–5 hours

24. ● This half-life decreases with oxygen administration
● ~ 40–80 minutes with administration of 100% oxygen
● ~ 23 minutes with hyperbaric oxygen (2 atmospheres)
● elimination is affected by the factors as absorption and is likely faster in many CO
poisoned patients due to compensatory measures (e.g. hyperventilation,increased cardiac
output)

25. ACUTE POISONING
● CNS:Headache,nausea,dizziness,confu
sion,AMS,ataxia,seizures and finally
comma
● CVS: Dysrhythmias,Ischaemia,hyper
or hypotension
● GI:Abdominal Pain,
Nausea+Vomiting, Diarrhoea
● RS: Dyspnea,Tachycardia,Chest Pain,
Palpitation
CHRONIC POISONING
● Headache
● Personality changes
● Poor Concentration
● Dementia, Psychosis
● Parkinsonism
● Ataxia
● Peripheral Neuropathy and
● Hearing loss
CLINICAL FEATURES

26. INVESTIGATIONS
ABG:
● HbCO (elevated levels are significant, but low levels do not rule out exposure)
● lactate (tissue hypoxia)
● PaO2 should be normal, SpO2 only accurate if measured (not calculated from PaO2)
● MetHb (exclude)
ECG:
● sinus tachycardia, ischaemic changes
Urinalysis
● positive for albumin and glucose in chronic intoxication

28. IMAGING
Radiographic features:
● Changes tend to be bilateral with the
globus pallidus most commonly
affected.
CT:
● Classically seen as low attenuation in
the globus pallidus region. Other
features include diffuse
hypoattenuation in cerebral white
matter.

29. LABORATORY
● CBC (mild leukocytosis)
● BSL (hyperglycaemia)
● UEC (hypokalaemia, acute renal failure from myoglobinuria)
● CK (rhabdomyolysis)
● LFT derangement (ischaemia)
● ethanol level (polypharmacy OD)
● cyanide level (industrial fire, cyanide exposure)

30. TREATMENT
LOW-RISK FEATURES
● If CO poisoning is suspected, start
100% oxygen immediately.
● Identify risks for possible referral for
hyperbaric oxygen treatment
HIGH-RISK FEATURES
● HBO2 [hyperbaric oxygen] therapy or
high-flow normobaric therapy for
acute CO-poisoned patients

32. ● role is uncertain
● 3 atmospheres will decrease the half life of carboxyHb from 6 hours to ~ 24 minutes
often considered for therapy if:
● All pregnant patients
● Significant LOC
● Signs of ischaemia
● Significant neurological deficit
● Metabolic acidosis

33. contra-indications:
● chest trauma
● other major comorbidity or acute instability (e.g. serious drug overdose, severe burns)
● uncooperative patient

34. complications:
● decompression sickness
● rupture of tympanic membranes
● damaged sinuses
● oxygen toxicity
● problems due to lack of monitoring

35. DISPOSITION
● Those without any high-risk features of CO intoxication may be discharged from the ED
after symptom resolution and normalization
● If there is a suspected source of environmental CO, other potentially exposed persons
should be contacted and evaluated in the ED
● Patients with accidental or inadvertent CO exposure should be referred for cognitive
follow-up in 4 to 6 weeks

36. ● Intentional CO poisoning requires emergency psychiatric consultation in the ED and
eventual follow-up for cognitive dysfunction
● For those with high-risk features of CO intoxication, prior to referral or transport for
hyperbaric oxygen, secure the airway, stabilize vital signs, continue 100% oxygen, and
identify and treat trauma or acute surgical or medical issues.

37. SPECIAL SITUATIONS
● Delayed Neurological Sequelae(OR Encephalopathy)
● Occur 4 days to 5 weeks after CO exposure
● Reported neurologic effects include cognitive impairments and affective disorders
● The precise neuropathology is not known
● Hyperbaric oxygen has been used anecdotally with success for the treatment of delayed
neurologic sequelae of CO

38. INFANTS, PREGNANT WOMEN, AND THE ELDERLY
● Infants may be more susceptible to the effects of CO due to the persistence of fetal
hemoglobin for the first 6 months of life, as well as higher metabolic rates.
● The indications for referral of children for hyperbaric oxygen therapy are similar to those
for adults
● Pregnant women should be considered for admitting at a hyperbaric center at CO levels of
15% to 20% because fetal morbidity has been demonstrated at lower levels than usual due
to the high affinity of CO for fetal hemoglobin.

39. ● The elderly, particularly those with serious comorbid disease, are also at higher risk from
CO poisoning.
● In patients with known coronary artery disease, even low levels of COHb (4% to 6%) can
cause ECG changes and myocardial ischemia
● Some elderly may also be at risk due to use of alternative heating sources, particularly
during the winter

41. THANK YOU