1. Lethal Exposures: CO Assessment Technologies For Civilians and Firefighters
Mike McEvoy, PhD, RN, CCRN, REMT-P
EMS Coordinator – Saratoga County, New York
FireEMS Editor – Fire Engineering Magazine
This presentation will discuss the dangers of CO poisoning and the need for rapid detection.

2. Disclosures
I am on the speakers bureaus for Masimo Corporation and Dey, LLP.
I am the Fire/EMS technical editor for Fire Engineering magazine.
I do not intend to discuss any unlabeled or unapproved uses of drugs or products.

3. Learning Objectives CO exposure, incidence, sources
Pathophysiology, clinical effects, sequelae
Diagnostic challenges, treatment issues
Fire Service role in CO assessment and treatment

4. Carbon Monoxide (CO) Gas: Colorless Odorless Tasteless Nonirritating
Physical Properties:
Vapor Density = 0.97
LEL/UEL = 12.5 – 74%
IDLH = 1200 ppm
Physical properties of note: Vapor Density is just about equal to that of the ambient air. This means that rather than rising to the highest point (lighter than air) or sinking to the low lying areas, CO acts like the ambient air and travels through the entire occupancy, following natural air flow. This translates to poisonous gasses presenting themselves across the occupancy, rather than lingering near the offending source, and exposure should never be ruled out because the occupants’ report that they were not near fuel fired appliances. The flammability range, expressed as the range between the Upper Explosive Limits (UEL) and the Lower Explosive Limits (LEL) is rather wide, therefore efforts to control ignition sources should be undertaken. The Immediately Dangerous to Life and Health is expressed as the IDLH in parts per million. While this number may seem a bit on the high side, EMS providers should take caution as they typically do not respond with self-contained breathing apparatus (SCBA) and atmospheric levels in an enclosed environment can climb rather quickly. The bond length is pm.

5. Endogenous Sources of CO
Normal heme catabolism (breakdown):
Only biochemical reaction in the body known to produce CO
Hemolytic anemia
Sepsis

6. Common Sources
Incomplete combustion of any carbon-based material will produce carbon monoxide. Most commons sources are:
Automobiles, trucks, buses, boats
Gas heaters and furnaces
Small gasoline engines
Portable / space heaters
Portable gas-powered generators
Barbecues / fireplaces
Structure / wildland fires
Cigarette smoke
Methylene chloride (paint stripper) - liver converts to CO
IMPORTANT POINTS
Common sources are all around us.
Everyone is at risk.
Space heaters and generators after natural disasters can be a serious problem.
The most common carbon monoxide exposures are from furnaces, generators, and automobiles. After natural disasters or during prolonged periods of power interruptions, including construction projects, winter storms, and floods, the use of these devices is quite common, all leading to the potential of excessive ambient CO that progressively binds to hemoglobin to exert its primary toxic influence.

7. CO Exposure 0.06-0.5 1-30 2-16 100 400-500 100,000 Exposure (ppm)
Source
Exposure (ppm)
Fresh Air
Urban Air
1-30
Smoke-filled Room
2-16
Cooking on Gas Stove
100
Smoking a Cigarette
Automobile Exhaust
100,000
Environmental exposure typically <0.001% (10 ppm).
Higher in urban areas.
Sources:
Volcanic gasses
Bush fires
Human pollution

8. Severity of Intoxication: Morbidity Associated with COHb and Duration
Highlighted Area demonstrates current OSHA Standard for CO:
[500ppm/30 minutes]
Consider 500 ppm/60-90 minutes….
IMPORTANT POINTS
Toxicity is a combination of level and time of exposure.
Low levels of CO for a prolonged time period can be lethal.
OSHA Standard is 500 ppm for 30 minutes, but 500 ppm for 90 minutes is lethal
CO Poisoning is progressive. Poisoning continues over time, and worsens, even if the baseline levels of ambient CO are unchanged. Identify from the graphic above and demonstrate this. Even if the patient is exposed to a level considered by OSHA to be at the upper limit of allowable tolerance for environmental CO levels in parts per million (ppm), if the level remains constant and the exposure continues, COHb accumulates in the blood. If you breath even 500ppm long enough, it will reliably kill you.
Spend time understanding this slide. If your audience understands the slide, they will leave the lecture with a healthy ‘respect’ for the insidious and highly toxic nature of this odorless, colorless silent killer.

9. Case Study: Even Low Exposure Levels Can Lead to Death
52 yo male
Prominent attorney in Salt Lake City found dead in his home after failing to show up for work
Had complained to co-workers of nausea and other flu-like symptoms for several days
Upon discovery of his body, elevated levels of CO were discovered in the home—but levels were relatively low, only 130 PPM
Faulty boiler discovered
IMPORTANT POINTS
The level in this man’s home was only 130 ppm.
Long term exposure to even 130 ppm can be lethal.
A man passed away from CO poisoning after being exposed to an environmental level of on 130ppm for several days.
The levels were not extremely high but because his exposure was overnight it proved to be lethal. Here breathing only 130ppm will kill you.
Even 130 Parts Per Million Over a Prolonged Period Can Kill You!

10. Carbon Monoxide Poisoning
Leading cause of poisoning deaths in industrialized countries:
50,000 emergency room visits in the US annually 1
At least 3,800 deaths in the US annually 2
1,400-3,000 accidental deaths in the US annually 3,4
Even a single exposure has the potential to induce long-term cardiac and neurocognitive/psychiatric sequelae:
Brain damage at 12 months after exposure is significant 5
Myocardial Injury is a common consequence of CO poisoning and can identify patients at a higher risk for premature death 6
IMPORTANT POINTS
While CO poisoning is the leading cause of poisoning deaths in the industrialized world, just surviving CO poisoning may not be enough.
Significant brain damage can occur.
Significant heart damage can occur.
CO poisoning is a very large problem, especially in the winter. A recent study indicates that the 40,000 ED visits annually in the US for CO poisoning may only represent 50% of the actual number. Also take into account all of the patients that do not consider a trip to the ER and may suffer long term damage from intermittent sub-clinical exposure. While most understand that CO is a poison, most believe that if the initial insult is resolved and treated that the clinical problem is completely resolved. Most do not appreciate and understand the long term effects on brain function and heart damage (neurological and cardiac sequelae). This must be stressed here and supported by the references from the peer-reviewed literature.
1 Hampson NB, Weaver LK. Carbon Monoxide poisoning: A new incidence for an old disease. Undersea and Hyperbaric Medicine 2007;34(3):
2 Mott JA, Wolfe MI, Alverson CJ, MacDonald SC, Bailey CR, Ball LB, Moorman JE, Somers JH, Mannino DM, Redd SC. National Vehicle Emissions policies and practices and declining US carbon monoxide-related mortality. JAMA 2002;288:
3 Hampson NB, Stock AL. Storm-Related Carbon Monoxide Poisoning: Lessons Learned from Recent Epidemics. Undersea Hyperb Med 2006;33(4):
4 Cobb N, Etzel RA, Unintentional Carbon monoxide-related deaths in the United States, 1979 through JAMA 1991;266(5):659.
5 Weaver LK, et al. N Engl J Med, 2002;347(14):
6 Henry CR, et al. JAMA ;295(4):

11. Unintentional Poisoning Deaths – US, 1999-2004
Drugs
CO and other gases
Alcohol
Organic solvents & halogenated hydrocarbons
Pesticides
MMWR, 9 Feb 2007 / 56 (05);93-96

12. Incidence Increased accidental CO deaths:
Patient > 65 years of age.
Male
Ethanol intoxication.
Accidental deaths peak in winter:
Use of heating systems.
Closed windows.
Significant increase seen following disasters:
Related to utility loss.

13. Case Study
26 yo female visits PMD c/o severe headaches unrelieved by repeated doses of Excedrin® - has been home alone, 2 children visiting with ex-husband
Neuro exam WNL, no other findings. Dx sinusitis. Tx Amoxil and T3’s
Next day: h/a worse, now vomiting, calls EMS, transport to ED
MD evaluates, no specific findings. Tx IV fluids, antiemetic, analgesic, head CT (neg). Given phenergan Rx, f/u with PMD
Arrives home by taxi, ex-husband waiting to return children

14. Case Study continued…
Next morning, same headache. Children difficult to awaken, once awake both have trouble walking, stumble and fall.
EMS summoned, FD also dispatched. CO metering finds 1,200 to 1,600 ppm from bedroom space heater. Dead kitten found in children’s room. All three transported.
Mom 29% COHb – sent for HBO, home 48 hours later. 4 yo son 14%, 2 yo daughter 17% - both admitted to regional children’s hospital for 24 hours observation.
Mom with permanent neurological deficit, children no sequelae.
Litigation considered against PMD, ED, and EMS.

15. Carbon Monoxide

16. Carbon Monoxide Firefighter Injuries – 2006 (United States):
Total injuries = 83,400
Smoke or Gas Inhalation = 2,825 (3.4%)
Burns & Smoke Inhalation = 730 (0.9%)
- NFPA Survey of Fire Depts for U.S. Fire Experience, 2006.

17. Station Nightclub Fire - RI
Feb 2003 band pyrotechnics ignite polyurethane foam lining stage walls
440 people, 100 deaths

18. 90 seconds – CO, CN, O2 incompatible with life
Simulation of platform area
60 seconds - flashover
90 seconds – CO, CN, O2 incompatible with life

19. NIST Simulation

20. Show me the money…Is this real?
104 CCU admissions UAP: 3 CO toxic, 5 others minor exposure (> smoker). Balzan et al, Postgrad Med J, 1994;70:
307 acute neuro admits: 3 CO toxic (all from group of 29 w/ decr. LOC absent focal s/s). Balzan et al, Postgrad Med J, 1996;72:470-3.
168 acute neuro admits: 5 CO toxic (2 from group w/ seizures) Heckerling et al, Clin Toxicol, 1990;28:29-44.
48 h/a pts: 7 COHb > 10% (14.6%, all unrelated to smoking) Heckerling et al, Am J Emer Med, 1987;5:201-4.
146 h/a pts: 4 COHb > 10% (3%, all unrelated to smoking) Heckerling et al, Ann Intern Med, 1987;107:174-6.
Up to 10% of UAP, ACS, seizure, and h/a admits have CO poisoning
Marty Balzan (St. Luke’s – Malta Island off Coast of Greece)
Paul Heckerling (U Illinois)

21. Attempts to Develop a Model
Heckerling et al apply criteria to validate a predictor model for identifying CO poisoned pts. In ED.
61 patients tested, model only detects 3 of 4 pts with  COHb Heckerling et al, Am J Med 1988;84:251-6.
753 acute admits med-surg, neuro, psych: 2 w/ minor COHb  Heckerling et al, Am J Emerg Med 1990;8:301-4.
Conclusion: Widespread ED screening expensive, unproductive unless quick and cheap screening tool became available.
Paul Heckerling – U Illinois (Chicago)

22. Pathophysiology CO displaces O2 from hemoglobin binding sites (4)
CO prevents O2 from binding
(carboxyhemoglobin)
COHb increases O2 affinity, interfering with normal release
CO binds to hemoglobin, producing carboxyhemoglobin (COHb) - the traditional belief is that carbon monoxide toxicity arises from the formation of carboxyhemoglobin, which decreases the oxygen-carrying capacity of the blood. This inhibits the transport, delivery, and utilization of oxygen. Because hemoglobin is a tetramer with four oxygen binding sites, binding of CO at one of these sites also increases the oxygen affinity of the remaining 3 sites, which interferes with normal release of oxygen. This causes hemoglobin to retain oxygen that would otherwise be delivered to the tissue.

23. Messy Pathophysiology
Cytochrome c is a small, wtaer soluble, heme containing protein. In the process of oxidative phosphorylation in the mitochondria, the heme moiety of cytochrome c serves to transport electrons from complex III to complex IV (the forth and final protein in the electron transport chain). It receives an electron from each of four cytochrome c molecules, and transfers them to one oxygen molecule, converting molecular oxygen to two molecules of water. In the process, it translocates four protons, helping to establish a chemiosmotic potential that the ATP synthase then uses to synthesize ATP. Cyanide, sulfide, azide and carbon monoxide all bind to Cytochrome c Oxidase, thus inhibiting the protein from functioning which results in chemical suffocation of cells (referred to most recently as “cytopathic hypoxia”). NOTE: CO does not bind to cytochrome oxidase with the same affinity as oxygen, so it likely requires significant intracellular hypoxia before binding. This binding interferes with aerobic metabolism and efficient adenosine triphosphate (ATP) synthesis. Cells respond by switching to anaerobic metabolism, causing anoxia, lactic acidosis, and eventual cell death. Another note: cytochrome c plays another very important role in cellular biology: apoptosis (programmed cell death) is triggered by release of cytochrome c from the mitochondrion into the cytosol. Once released, cytochrome c binds to another protein called apoptosis-activating factor-1. This event triggers oligomerization of apoptosis-activating fator-1, binding of atp, and eventually, formation of a protein complex called the apoptosome which ultimately lead to activation of a series of proteolytic enzymes known as caspases, culminating in death of the cell.
Complex IV of Electron Transport Chain – binds cytochrome c oxidase
CO does NOT bind with same affinity as O2 (requires significant hypoxia)
Delayed effect ATP synthesis produces lactic acidosis

24. Pathophysiology CO limits oxygen transport Inhibits oxygen transfer
Greater affinity (>210 x) for hemoglobin
Inhibits oxygen transfer
Interferes with normal unloading to tissues
Binds with myoglobin (muscle)
Interferes with heart and skeletal muscle fxn
Binds to cytochrome oxidases
Induces anerobic metabolism (cellular & tissue)
Increases nitric oxide (NO) formation
Accelerates free radical formation
CO causes endothelial cell and platelet release of nitric oxide, and the formation of oxygen free radicals including peroxynitrite. In the brain, this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis. The end result is lipid peroxidation (degradation of unsaturated fatty acids), which causes delayed reversible demyelinization of white matter in the central nervous system, and can lead to edema and focal areas of necrosis within the brain.
This brain damage occurs mainly during the recovery period and results in cognitive defects (especially affecting memory and learning) and movement disorders. The movement disorders are related to a predilection of CO to damage the basal ganglia. These delayed neurological effects may develop over days following the initial acute poisoning.
IMPORTANT POINTS
CO results in more than just hypoxia
CO also acts as an intracellular poison.

25. Pathophysiology - Effects
Hypoxia
Cellular, cardiac and cerebral
Intracellular toxicity
Cardiac and skeletal muscle dysfunction
Inflammatory response
Secondary to hypoxia
Vasodilation
Induced by NO release (hypotension)
Free radical formation
Endothelial and oxidative cerebral damage
IMPORTANT POINTS
CO results in more than just hypoxia
CO also acts as an intracellular poison.
Pathophysiology review of CO. Carbon Monoxide poisoning does induce hypoxemia by robbing the tissues of needed oxygen, but it also has toxic influences that have long term effects on the nervous system and the heart. Emphasize the long term health effects and the potential for heart and brain damage.

26. Clinical Effects
Immediate threat to life AND long term health effects:
Neurologic: Headaches, dizziness, confusion, permanent neurocognitive and/or neuropsychiatric sequelae.
Cardiac: Chest pain, arrhythmias (immediate mortality), long term cardiac sequelae includes decreased EF% and increased odds ratio early cardiovascular death.
Metabolic: respiratory alkalosis, hyperventilation, metabolic acidosis in severe cases (marker for severity).
Pulmonary: pulmonary edema in percent of acute exposures.
Severe hypoxemia with potential for multiple organ failure, brain damage and death
IMPORTANT POINTS
Death is a real possibility from CO exposure
The brain is at risk for permanent damage.
The heart is at risk for permanent damage.
Multiple Organ Failure-the outcome is likely to be lethal without immediate treatment
The clinical effects are much more severe with the brain and heart, 2 organs that have a high oxygen demand to function properly. Long term brain damage or heart damage are of critical concern to patients and clinicians.
Neurologic-long term neurocognitive and neuropsychiatric sequelae are reported even after moderate to severe single exposures.
Cardiac-decreased oxygen delivery to and decreased oxygen utilization by the myocardium. Patients may also be hypotensive or present with tachycardia. Most deaths from CO poisoning result from ventricular dysrhythmias. Long-term cardiac sequelae are reported even after moderate to severe single exposures, increasing the odds ratio of premature cardiac death.
Metabolic-respiratory alkalosis and hyperventilation is possible in mild cases.
Pulmonary-pulmonary edema may be due to a direct effect on the alveolar membrane, left ventricular failure, aspiration or neurogenic causes.

27. Neurologic Effect Delayed Neurologic Syndrome
Experienced by 11-30% of patients with CO Poisoning (DNS)
Long-Term/Chronic Sequelae
Cognitive and personality changes, dementia, seizures, psychosis, amnesia, parkinsonism, depression, short-term memory loss, incontinence.
Harper A et. al, Age and Ageing. 2004;33(2): Kao LW et. al, Emerg Med Clin North Am Weaver LK, et al. N Engl J Med, 2002;347(14):
IMPORTANT POINTS
A large number of patients experience brain damage.
This problem can be long-term or even permanent.
The effects of CO exposure are not confined to the period immediately after exposure. Persistent or delayed effects have been reported. In particular, the syndrome of delayed neurologic effects may manifest in a myriad of forms. The sequelae may appear even in patients where the neurologic impairment is not initially recognized. There is no way to predict which patients will suffer such sequelae. In general, those with more severe initial symptoms are at the highest risk. Most mild cases resolve in about 2 months, although patients with severe exposure may never make a full recovery from DNS.
Abelsohn A, CMAJ 2002:166 (13):

28. Case Studies: Neurological Sequelae
51 yo female Physical Therapist
Iditarod racer stopped to change wet socks in a tent
Experienced nausea, then lost consciousness
Inhaled CO from a faulty propane heater for 3 hours
Prolonged recovery, IQ fell from 140 to 76, had to relearn reading & writing
IMPORTANT POINTS
1) Severe brain damage is a real problem
2) Lives can be permanently changed.
In the above case studies, both patients had total disruptions of their lives with permanent effects. Not only a healthcare tragedy, but a significant cost burden to healthcare system and social programs designed to provide support for patients with permanent disability secondary to the poisoning by CO.
32 yo female & 35 yo male Attorneys
CO from inadequately ventilated furnace
Both unable to function as attorneys

29. Cardiac Effect
“Myocardial injury occurs frequently in patients hospitalized for moderate to severe CO poisoning and is a significant predictor of mortality”
Odds ratio’s from recent study demonstrate that a patient has a 3 times higher likelihood of cardiac death (within a 7 year follow-up period) from even one moderate to severe toxic CO exposure, when compared to a control group
IMPORTANT POINTS
Heart damage can result from CO poisoning.
CO poisoning increases by 3 fold a victim’s risk of death from a heart attack.
A link between COT and MI has been presented in JAMA Jan This is a significant predictor of mortality.
Myocardial Injury and Long-Term Mortality Following Moderate to Severe Carbon Monoxide Poisoning. Henry CR, Satran D, Lindgren B, Adkinson C, Nicholson C, Henry TD. JAMA ;295(4):

30. Cardiac Effect
19 year study 8,333 Swedish males ÷ smokers, non-smokers, never smokers.
Never smokers split into quartiles:
0.13 – 0.49% COHb
0.50 – 0.57%
0.58 – 0.66%
0.67 – 5.47%
Relative risk CV event 3.7, death 2.2 highest to lowest quartiles
Incidence CV disease & death in non-smokers related to COHb%
Bo Hedblad – Lund University- Sweden
A link between COT and MI has been presented in JAMA Jan This is a significant predictor of mortality.
COHb% as a marker of cardiovascular risk in never smokers: Results from a population-based cohort study. Hedblad BO, Engstrom G, Janzon E, Berglund G, Janzon L. Scand J Pub Health ;34:

31. High Risk Groups Patients at High Risk for Negative Outcomes Children
Elderly
Adults with cardiac disease
Patients with decreased O2 carrying capacity (Anemia)
Patients with chronic respiratory insufficiency
Pregnant women, with emphasis on fetal damage and death
Cerebral palsy
Limb and cranial deformities
Mental disabilities
IMPORTANT POINTS
Several groups are at increased risk to damage from CO poisoning
Patients that have reduced hypoxia tolerance are at risk.
Fetal damage is especially dangerous.
A subset of patients exist that do not have sufficient cardiopulmonary reserves to be able to handle the problems of hypoxia caused by CO poisoning. This condition may severely damage those that are already close to hypoxia. It may be enough to cause permanent damage.

32. Fetal Damage
Theoretical effect of different treatments on maternal and fetal COHb levels over time
IMPORTANT POINTS
Fetuses are especially at risk for damage from CO poisoning.
Even if the mother is removed from the CO toxic environment the fetal levels will continue to rise.
Hyperbaric oxygen is the only way to rapidly reduce the fetal levels.
Fetal uptake is delayed but fetal COHb levels will exceed maternal levels if the mother is not rescued from the CO environment. If only normobaric treatment is used the fetal levels will continue to rise. The only way to rapidly reduce the fetal level is with prompt hyperbaric therapy.
Rucker J, Fisher J, Carbon Monoxide Poisoning, Chapter 63 Longo LD: The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant. Am J Obstet Gynecol 1977;129:

33. Clinical Manifestations
Signs and Symptoms
SpCO%
Clinical Manifestations
<5%
None
5-10%
Mild headache, tire easily
11-20%
Moderate headache, exertional SOB
21-30%
Throbbing headache, mild nausea, dizziness, fatigue, slightly impaired judgment
31-40%
Severe headache, vomiting, vertigo, altered judgment
41-50%
Confusion, syncope, tachycardia
51-60%
Seizures, unconsciousness
IMPORTANT POINTS
CO poisoning can present just like the flu.
It is very difficult to correctly diagnose.
There is a wide variation in patient symptoms.
There are 2 main types of CO poisoning, acute and chronic. Acute is caused by short term exposure to very high levels of CO, and these patients are more likely to present with more serious symptoms. These would include: confusion, syncope, coma, seizure and cardiopulmonary problems. Chronic exposure is generally associated with less severe symptoms. Low level exposure can exacerbate angina and chronic obstructive pulmonary disease. Patients with coronary artery disease have an increased risk for ischemia and myocardial infarction even at low CO levels. To make this situation even more problematic, it may present just like the flu, making the correct diagnosis extremely difficult.
Carbon Monoxide Poisoning Presents Like the Flu!

34. Haunted Houses or CO Poisoning?
Wilmer W. “Mr. and Mrs. H.” Amer J Opthamology. 1921
Purchased new home, c/o headaches & fatigue. Heard bells and footsteps during nights with sightings of mysterious figures.
Investigation revealed prior owners had similar experiences.
Furnace chimney found blocked, venting CO into home.
In one famous case, carbon monoxide poisoning was clearly identified as the cause of an alleged haunting. Dr. William Wilmer, an ophthalmologist, described the experiences of one of his patients in a 1921 article published in the American Journal of Ophthalmology. "Mr. and Mrs. H." moved into a new home, but soon began to complain of headaches and fatigue. They began to hear bells and footsteps during the night, accompanied by strange physical sensations and sightings of mysterious figures. When they began to investigate the symptoms, they discovered the previous residents of the house had similar experiences. An examination of their furnace found it to be severely damaged, resulting in incomplete combustion and forcing most of the fumes (including carbon monoxide) into the house rather than up the chimney.

35. CO Poisoning: The Great Imitator
IMPORTANT POINTS
Emergency departments can miss the diagnosis up to half of the time.
Just because the patient makes it to the hospital does not mean they will be accurately diagnosed.
This shows just how much of a problem the emergency department has in correctly diagnosing this problem. This is a serious concern for a condition that requires prompt recognition and treatment.
30-50 % of CO-exposed patients presenting to Emergency Departments are misdiagnosed
Barker MD, et al. J Pediatr. 1988;1:233-43
Barret L, et al. Clin Toxicol. 1985;23:309-13
Grace TW, et al. JAMA. 1981;246:

36. Diagnostic Problem Vague symptoms Food poisoning Viral illness
Migraines
Drug abuse
ACS
Current diagnostic method is invasive, slow, and costly
If the proper diagnosis is not made the patient is often inadvertently returned to the toxic environment
IMPORTANT POINTS
Symptoms are vague.
Current diagnostic techniques are invasive and require time.
If the proper diagnosis is missed the patient may return to the dangerous environment and die.
The combination of a vague and ambiguous symptomatology, together with the recognized inconveniences of the Lab CO-Oximetry test (costly, slow, requires a blood sample), inaccurate diagnosis are not uncommon.

37. Limitations of Pulse Oximetry
Conventional pulse oximetry can not distinguish between COHb, and O2Hb
From Conventional Pulse Oximeter
SpCO-SpO2 Gap:
The fractional difference between actual SaO2 and display of SpO (2 wavelength oximetry) in presence of carboxyhemoglobin
IMPORTANT POINTS
The arterial oxygen saturation (SpO2) from conventional two-wavelength pulse oximetry is inaccurate (often significantly inaccurate) in the presence of CO poisoning.
Two-wavelength pulse oximeters actually count carboxyhemoglobin as oxyhemoglobin
The reported functional value often lends a false sense of security that the patients oxygenation status is good, as SpO2 may read normal even when significant COHb is poisoning the patient.
A standard 2 wavelength oximeter adds to the problem. They only read 2 parameters, which result in a ratio of the oxyhemoglobin to the hemoglobin that is available for binding . This is called the Functional value and does not decrease
to any significant degree, as shown by the graph above, even when exposed to high levels of CO. In this experiment a dog is exposed to CO and the pulse oximeter only decreases slightly to 90% when the actual oxyhemoglobin saturation is 30%. This actual saturation value is called the fractional saturation. Fractional saturation is not subjected to this false reading and would have read 30% in this situation.
From invasive CO-Oximeter Blood Sample
[Blood]
Barker SJ, Tremper KK. The Effect of Carbon Monoxide Inhalation on Pulse Oximetry and Transcutaneous PO2. Anesthesiology 1987; 66:

38. National Academy of Clinical Biochemistry:
COHb Recommendations
“We recommend that clinicians routinely provide POCT of HbCO by CO-oximetry to screen patients with flu-like symptoms or headache in the emergency department for occult CO poisoning, particularly in communities where combustion is used for heating during the heating season. We found at least fair evidence that POCT of HbCO by CO-oximetry will lead to a correct and timely diagnosis of CO poisoning in patients who otherwise would have been missed”
(Weight of Evidence = Fair; Net Benefit = Substantial; Recommendation = B)
IMPORTANT POINTS
Since CO poisoning is so difficult to detect, the National Academy of Clinical Biochemistry recommends measuring COHb levels on all patients that present with flu-like symptoms or headache.
POCT means point of care testing.

39. Blood Sampling for COHb
A-COHb = V-COHb
Touger et al, Ann Emerg Med, 1995;25:481-3.
61 suspected CO poisoning Bronx Municipal Hospital ED, simultaneous A and V sampling COHb. Correlation r value 0.99 (95% CI, 0.99 to 0.99), r2 value 0.98.
CONCLUSION: “Arterial and venous COHb levels only rarely differ by more than 1% to 2%.”
Mike Touger and John Bronx Municipal Hosp

40. Laboratory CO-oximetry
CO-oximetry capability found in 50% of hospital laboratories
Standard ABG cannot differentiate carboxy from oxyhemoglobin
Invasive—need compelling reason to order, repeated tests to monitor tx
Variable time to analysis (can take from minutes to hours to get results)
Golden Standard—for measurement and/or detection of COHb (± 2%)
IMPORTANT POINTS
Unless they have very compelling reasons physicians will avoid ordering a CO test because it requires a blood draw.
CO-oximeters are not in all hospitals.
The time it takes to obtain a result varies widely.
In the hospital, the only way to measure the COHb level is to use a CO-Oximeter. This may or may not be part of the hospital blood gas routine. It may require a specific order for this measurement to be carried out. If a standard blood gas is drawn, then the saturation level that is obtained will be calculated from the plasma level that will not account for the high COHb. Also, a study that was conducted by N Hampson et al. in the Pacific NW found that less that half of the hospitals in WA, AK, ID, MT had CO-Oximeters. The time to in-hospital analysis ranged from 1-60 minutes with a mean of 10 minutes. The off-site measurements ranged from 20-10,080 minutes with an average time of 15 hours. Clearly, if you are trying to diagnose and treat quickly the off-site measurement is not acceptable. In addition, a blood gas provides a single point in time measurement, so trending is very difficult unless the patient has an artline or serial blood gases are drawn. Even with all of that, they would still be discontinuous measurements and would only approximate continuous trending.

41. Challenges to Detecting CO Poisoning
Endogenous CO – we all have some level of COHb
Kinetics CO uptake and excretion very complex, toxicity mechanism unclear
Pollution: atmospheric vs. smoking
Symptoms ambiguous, flu-like
COHb levels poorly correlate with clinical condition
Testing limitations: Lab CO-Oximetry, pulse oximetry, no biochemical marker
Paucity of research
IMPORTANT POINTS
Making the correct diagnosis is complicated.
CO symptoms vary widely.
Regardless of the means of detection used in the ED, there are several factors that make assessing the severity of CO poisoning difficult. The length of time since exposure is a problem because the half life (the time for the level of CO to decrease by 50%) is about 4-6 hours on room air. If the patient is given oxygen during the transport, this half life can be reduced to about an hour. It will then be difficult for the treating physician to know when the level peaked and may have reduced the severity of the symptoms by the time the patient is seen.
Also, COHb levels may not fully correlate with the clinical condition because the COHb level is not an absolute index of oxygen delivery to the tissues. In other words, patients with moderate levels may not appear worse than patients with lower levels. Lab oximeters and pulse oximeters both have limitations.

42. Exhaled CO Meters
Estimation COHb from alveolar CO concentration first described in (Sjostrand T. Acta Physiol Scand 16:201-7)
Predominantly used to monitor smoking cessation
Compact, portable, well validated
Requires 20 second breath holding, measures ETCO in PPM
Present accuracy + 2 PPM, COHb obtained from Haldane Equation (essentially = PPM ÷ 6)

43. Exhaled CO Meters Fast, economical, portable CPT Code (94250)
Requires 20 second breath hold (awake, alert patient)
Disposable mouthpieces
Regular gas calibration
Despite widespread availability since 1970’s utilization very low

44. Noninvasive Pulse CO-Oximetry
FDA approved January 2006
Compact, portable, well validated
CPT Code (82375 SpCO, SpMet)
Continuous carboxyhemoglobin measurement
Present accuracy + 3 % COHb
Also measures oxyhemoglobin (SpO2), methemoglobin (SpMet), perfusion index (PI), approval for hemoglobin (Hgb) pending.
No calibration needed

45. Pulse CO-Oximetry Fast, economical
Can be used on any patient (including unconscious)
No disposables
No calibration necessary
Use wider than exhaled devices after only 20 months in marketplace

46. How Noninvasive Pulse CO-Oximetry Works
IMPORTANT POINTS
Conventional pulse oximeters use two wavelengths of light to
Masimo Rainbow SET uses multiple (7+) wavelengths of light
Additional wavelengths combined with sophisticated adaptive filters and signal processing algorithms working in parallel make this breakthrough possible
Conventional pulse oximetry technologies use only two wavelengths of light and lack the sensitivity to determine dyshemoglobin levels—as a result they overestimate SpO2 saturation in the presence of dyshemoglobins.
Masimo Rainbow SET Rainbow Pulse CO-Oximetry Technology uses multiple (7+) wavelengths of light housed in a single, simple-to-apply sensor and sophisticated signal processing technologies including parallel engines and adaptive filters to accurately determine the dyshemoglobins SpCO and SpMet, as well as SpO2, PI, PVI and pulse rate.
By taking advantage of the different extinction coefficients for each of the analytes and adding additional signal processing capability, multiple dyshemoglobin measurements are now possible
Masimo Rainbow SET Pulse CO-Oximeters are capable of reading the correct saturation in seconds, and no blood gas is required to measure for Carbon monoxide poisoning.
Oxygenated Hb and reduced Hb absorb different amounts of Red (RD) and Infrared (IR) Light
(Two-wavelength oximeters cannot measure dyshemoglobins)

47. FDA Validation Masimo Rainbow SET Compared to Reference Methodology
IMPORTANT POINTS
Masimo SET with Rainbow Technology was FDA cleared as a substantial equivalent to invasive CO-Oximetry
This device performed very well and was approved by the FDA with accuracy of + 3% from 0-40% when compared to invasive blood CO-oximetry.
This is the data that was submitted to the FDA of the CO capability for the Pulse CO-Oximeter. The predicate device used for the comparison of noninvasive Pulse CO-Oximetry was laboratory CO-Oximetry with the attendant blood draws and analysis. The accuracy was determined to be + 3% from 0-40% at 1 SD. 452 samples were obtained from 160 patients. These patients represented a variety of ages, weights, skin colors, and genders. The Rad-57 is one of the Masimo devices that uses Pulse CO-Oximetry to measure Carboxyhemoglobin.
Red

48. 5,000 Patient Brown University Study
Partridge and Jay (Rhode Island Hospital, Brown University Medical School), assessed carbon monoxide (CO) levels of nearly 5,000 ED patients
9 unsuspected cases of CO Toxicity (COT) were discovered. 13 false positives, 0 false negatives
Extrapolated to all US hospitals, this would equal 50,000 cases of unsuspected COT annually
They concluded “unsuspected COT may be identified using noninvasive COHb screening and the prevalence of COT may be higher than previously recognized”
IMPORTANT POINTS
This device can be used practically in a clinical setting on large numbers of patients.
9 cases were found that would have been missed.
There were no false negative which means that all patients with CO poisoning were detected.
A retrospective chart review over 39 days by Dr. Greg Jay et al. at the ER of Rhode Island Hospital in Providence. He was the first to use a Pulse CO-Oximeter in a study of patient’s CO levels. The device (Rad-57) was placed on a pole and used in the triage area. About 72% of the patients that visited his ER had their CO level measured. False positive means that the patient’s level read high and it was not actually high. These patients may have received oxygen and possibly had blood gasses unnecessarily. In these situations it is always important to try to minimize the false positives. But out of 5,000 patients to only have 13 false positives is certainly acceptable. In this situation a false negative means that patients would not have been treated that had high levels of CO. The fact that there were no false negative is very impressive. These is the potential of discovering up to 50,000 patients in the US with unsuspected COT (Carbon Monoxide Toxicity).
Non-Invasive Carboxyhemoglobin Monitoring: Screening Emergency Department Patients for Carbon Monoxide Exposure. Partridge R, Chee KJ, Suner S, Sucov A, Jay G. Department of Emergency Medicine, Rhode Island Hospital, Brown Medical School, Providence, RI.

49. Pulse CO-Oximeter Treatment Algorithm
No further medical evaluation
of SpCO needed
0 - 3%
Transport on 100% oxygen
for ED evaluation.
Consider transport to hospital
with hyperbaric chamber.
Yes
for ED evaluation
SpCO > 12%
of SpCO needed.
Determine source of CO
if nonsmoker. No
Symptoms of
CO exposure? *
SpCO < 12%
Loss of consciousness or
neurological impairment
or SpCO > 25%?
> 3%
Measure SpCO
IMPORTANT POINTS
This treatment algorithm was created by Drs. Neil Hampson and Lin Weaver, two of the foremost authorities on CO poisoning
Combines immediate feedback from pulse Co-Oximeter with symptoms and history to arrive at the most appropriate decisions regarding treatment
Can be used by first responders to determine which victims should be transported and where they should be transported to
This a recommended treatment algorithm introduced by Dr. Hampson and Dr. Weaver using non-invasive SpCO measurements. Note that treatment decisions are made at non-invasive CO levels of 3,12 and 25%. If the SpCO level is 3-12%, the elevation could be due to smoking. If the patient is experiencing certain symptoms*(headache, nausea, vomiting), then they should receive 100% oxygen and further treatment, if required. If the level is 3-12% and the patient is asymptomatic, then no treatment is required, but the source of the CO should be identified. Unless the source is identified, the patient may be placed back in the dangerous environment.
Hampson NB, Weaver LK JEMS 2006

50. Triage & Treatment Algorithm1

51. Categorizing Symptoms
Headache:
None
Mild
Moderate
Throbbing
Severe
LOC:
Alert
Slight confusion
Very confused
Syncope or unconscious
Seizures
SOB:
Exertional
At rest
GI:
Mild nausea
Nausea
Vomited or vomiting

52. Treating CO Poisoning - Oxygen
Oxygen is the cornerstone of treatment for CO poisoning as it accelerates the dissociation of CO from heme proteins

53. Treatment of CO Poisoning
Chemical Half-life of Carbon Monoxide bound to Hemoglobin
4 hours on room air
45 minutes on 100% oxygen
22 minutes on 100% in Hyperbaric Chamber at 2-4 atmospheres
IMPORTANT POINTS
In order to minimize damage to the brain, heart and other organs, it is critical that CO levels be reduced as quickly as possible
Hyperbaric chambers can significantly reduce the CO level much faster than other options.
First responders need to know quickly if patients should be transported to a hyperbaric chamber.
Half-life is defined as the amount of time that it takes to reduce a specific level by 50%. In practice, to reduce a CO level of 20% to less than 2% could take 20 hours on room air. This means that rapid implementation of treatment is critical. Carboxyhemoglobin will reverse on its own if the patient is removed from the source, but generally the time involved is too long to truly be considered an effective treatment. By adding oxygen or even hyperbaric oxygen treatment, the half-life can be reduced dramatically. This is a picture of a 10 person hyperbaric chamber in Salt Lake City, UT at LDS Hospital.

54. Hyperbaric Oxygen Treatment
Rate of cognitive sequelae was nearly twice as high when hyperbaric treatment was not used
Methods
Random assignment of symptomatic patients with CO poisoning into one of two groups
Group 1: 3 hyperbaric oxygen treatments in a 24 hour period
Group 2: 1 normobaric oxygen treatment and two normobaric room air treatments
Results
Group 1: 25% sequelae at 6 weeks, 18 % at 12 months
Group 2: 46% sequelae at 6 weeks, 33% at 12 months
IMPORTANT POINTS
A large number of patients experience brain damage from CO poisoning.
Hyperbaric treatments can reduce these problems dramatically.
Dr Weaver looked at 2 different treatment methods and had statistically significant outcomes by using hyperbaric oxygen rather than normobaric oxygen. The irony was that he did not expect this outcome.
Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliot GC, Clemmer TP, Orme JF, Thomas FO, Morris AH. N Engl J Med, 2002;347(14):
Introduction
Unfavorable cognitive sequelae (problems with memory, attention, concentration, affect) can occur immediately after carbon monoxide (CO) poisoning exposure and persist. While cognitive sequelae can also be delayed, they generally occur within 20 days after CO poisoning. Cognitive sequelae lasting one month or more appear to occur in 25-50% of the patients with loss of consciousness or with carboxyhemoglobin (COHb) levels greater than 25%. While normal treatment for CO poisoning is 100% normobaric oxygen, hyperbaric oxygen is often recommended for patients with acute CO poisoning. Advantages of treatment with hyperbaric oxygen include increased dissolved oxygen in the blood and accelerated elimination of carbon monoxide. Potential benefits of hyperbaric oxygen treatment include prevention of liquid perioxidation in the brain, and preservation of ATP levels in the tissues exposed to elevated CO. This double-blind, randomized trial evaluates the effect of hyperbaric oxygen treatment on such cognitive sequelae.
Methods
Random assignment of symptomatic patients with acute CO poisoning in equal proportions to three hyperbaric chamber sessions in a 24 hour period: either three (3) hyperbaric oxygen treatments or one normobaric oxygen treatment plus two sessions of exposure to normobaric room air. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and at two weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae 6 weeks after CO poisoning.
Results
Cognitive sequelae at 6 weeks and at 12 months were less frequent in the hyperbaric oxygen group than in the normobaric oxygen group.
Incidence of Cognitive Sequelae: after CO Exposure Hyperbaric O2 (n=76) Normobaric O2 Group (n=76) 6 Weeks 25% 46.1% 6 Months 21.1% 38.2% 12 Months18.4% 32.9% Symptoms at 6 weeks (difficulties - memory, attention, concentration) 30% 47%
Authors Discussion and Conclusions:
“Three hyperbaric oxygen treatments within a 24 hour period appeared to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning. Hyperbaric oxygen therapy reduced the frequency of cognitive sequelae by 46% as assessed 6 weeks after acute, symptomatic carbon monoxide poisoning.” The patients had nearly normal carboxyhemoglobin concentrations just before the first chamber session, a finding that suggests the presence of therapeutic mechanisms accorded by the use of hyperbaric medicine that are independent of elevated carboxyhemoglobin levels at the time of therapy.
Weaver LK et al, Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning, N Engl J Med 2002;347(14) :

55. CO Alarms 61,100 CO incidents in 2005
Increase 9% each year (= 77,597 in 2008)
Peak December & January and 6-10 PM
92% residential
Source: NIFRS

56. UL 2034: listings for CO alarms
Revised 1992, 1995, 1998
Presently:
30 PPM for 30 days
70 PPM for 1 – 4 hours
150 PPM for 10 – 50 minutes
400 PPM for 4 – 15 minutes (6 min reset > 70 PPM)
Non-alarm status CO2 < 5,000 PPM
Non-alarm limits for methane, butane, heptane, ethyl acetate and isopropyl alcohol
- NFPA 720

57. CO Symptoms Based on Concentration
PPM
Symptoms 30
No adverse effects w/ 8 hours
200
Mild h/a after 2-3 hours
400
H/a and nausea after 1-2 hours
800
H/a, nausea, dizzy 45 min, collapse 2 hours
1,000
LOC after 1 hour
1,600
H/a, nausea, dizzy after 20 min
3,200
H/a, nausea, dizzy 5-10 min, collapse 30 min
6,400
H/a, nausea, dizzy 1-2 min, collapse/death min
12,800
Collapse, danger death 1-2 min
Source NFPA 720

58. Firefighter Rehab
Greatest short surge physiologic demands of any profession.
10% firefighter time spent on fireground
50% of deaths & 66% of injuries occur on scene.

59. Firefighter Rehab – NFPA 1584
National Fire Protection Association “Standard on the Rehabilitation Process for Members During Emergency Operations and Training Exercises”
Originally issued in 2003, revision effective December 31, 2007.
Every fire department responsible for developing and implementing rehab SOGs

60. NFPA 1584 - Overview Ongoing education on when & how to rehab.
Provide supplies, shelter, equipment, and medical expertise to firefighters where and when needed.
Create a safety net for members unable to recognize when fatigued.

61. Medical Monitoring in Rehab
Vital signs per local protocol
Options suggested:
Temperature
Pulse
Respiration
Blood pressure
Pulse oximetry
CO assessment (pulse CO-oximetry)

62. CO Assessment Every patient, every time.
All occupants at CO alarm calls.
Firefighters.

64. Conclusions We’re missing Carbon Monoxide poisonings
Leads poisoning deaths worldwide, harms at low levels
Commonly misdiagnosed (medical and fire personnel)
Screen every patient every time
Screen people as well as buildings at CO calls
Assess firefighters (rehab, routinely, research)

65. Thank You