Especially from dry ice
Afterdamp is CO2 release after mine explosion of firedamp
In mines, called firedamp
Blackdamp is 87%N2 and 13% CO2
Phosgene (smells like fresh cut hay)
NCPE, consider steroids if bronchospasm. Can give proventil/saline nebs.
If acid, use Bicarb in 1:3 dilution c saline
Carbon Monoxide (CO) Poisoning
from incomplete combustion.
Modern cars do not produce though propane burners like tractors, mowers do
Home heating sources
230-260 times the affinity of oxygen for Hb
Carboxyhemoglobin does not carry O2, shifts O2 disassoc curve to left limiting Hb O2 release to tissue, Binds to myglobin limiting muscle O2, Blocks oxidative phosphorylation
Causes NO release which can cause peripheral vasodilation, can knock a pt out
Levels do not correlate c toxicity. Normal 1-2%, smokers 5-10%
>25% should get hyperbaric, >10-15% in pregnant women, >15 in CAD
Room air ½ is 2-7 hrs, O2 90 min, Hyperbaric 23 minutes
Need cooximetry to detect, normal pulse ox is 100%
PaO2 is normal
“Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure (Chest 2000; 117:801-808)
They calculated the COHb t1/2 as 74 mins 25 mins with a range of 26 – 148 minutes. There were a number of other articles suggesting that the half-life of carboxyhemoglobin could be affected by additional factors such as the duration of CO exposure and the inspired PO2, and that two exponential decay curves could be utilized in calculating the rate of decrease in the serum COHb over time. However, even after taking all those factors into consideration – it should be possible to “guesstimate” that the serum COHb level should decrease to < 5% within < 6 hours of continuous 100% oxygen therapy irrespective of the initial serum COHb level (or duration of CO exposure). I cannot understand the rationale for 72 hours of 100% oxygen therapy, and how it could produce different clinical effects than ~ 6 hours of 100% oxygen therapy.
The best review article that I have read on carbon monoxide posioning is by Lindell Weaver in Critical Care Clinics Volume 15 Number 2 April 1999 “Carbon monoxide poisoning”.
He reviews the literature and he states “With inhalation of 100% O2 , elimination of COHb is increased, although the elimination half-life varies across studies. Pace et al  found the elimination COHb half-life with 100% normobaric O2 inhalation to be 47 minutes in men and 36 minutes in women. Peterson and Stewart  found the elimination half-life of CO-exposed men breathing 100% normobaric O2 to be approximately 80 minutes. In patients who have CO poisoning, Myers et al  found the elimination half-life to be 131 minutes with a range of 27 to 462 minutes. In another study of CO-poisoned patients, Peirce and Bensky  found the COHb half-life to be 126 minutes (1 SD = 246 minutes). We have found the elimination half-life of patients breathing O2 by nonrebreathing face mask or by endotracheal tube to be 72 ± 26 minutes (1 SD), with a range of 26 to 146 minutes ( N=93). .”
3 Hyperbaric treatments with 100% O2 vs. One placebo on 100% and 2 on room air? Hyperbaric was better (NEJM 347 (14), 2002)
Randomized, double blind, High flow O2 with once daily HBO or placebo: no difference between groups (191 pts) (Med J Australia 170;203, 1999
and f/u editorial discussing the major flaws in the Weaver study: Scheinkestel, C.D., et al, Emerg Med Australasia 16:151, 2004)
The oxygen saturation gap refers to the gap between oxygen saturation as measured by pulse oximetry and the actual arterial oxygen hemoglobin saturation. Some refer to it as the difference between the oxygen saturation calculated from routine blood gas analysis and the oxygen saturation measured by pulse oximetry. Others use this term for the difference between the calculated oxygen saturation from a standard blood gas machine and the measured value from a co-oximeter. An oxygen saturation gap is present when there is more than a 5% difference. Toxins that are associated with an elevated oxygen saturation gap include carbon monoxide, methemoglobinemia, and hydrogen sulfide ( and ). Cyanohemoglobin does not result in this finding (3). Although cyanide poisoning may result from smoke inhalation, it is not associated with an oxygen saturation gap, but rather with an elevated serum lactate and a severe metabolic acidosis. (JEM Sept 2007)
Two randomized trials ? any benefit outside special circumstances (Inten Care Med 2011;37(3):486)
In paint strippers and wax removers
Metabolized in the liver to CO
Methylene chloride, a solvent found in paint remover and aerosol propellants, is a source of significant toxicity after inhalation exposure due tp carbon monoxide (Emerg Med Clin N Am, Vol. 22, pg. 987).
Methemoglobinemia (Met HB)
Oxidation of iron in Hb from ferrous 2+ to ferric 3+. This form can not bind to O2 and impairs release of remaining normal Hb by shifting curve to left.
All sorts of drugs and toxins, eg. Nitro. Nitrites (poppers) or as genetic defect in RBCs
Benzocaine (or any of the local anesthetics except cocaine), Amyl Nitite, Dapsone, Well water (from nitrites), nitrite salts, Pyridium
Infants can get it from dehydration and diarrhea, adults from sepsis.
Symptomatic above 20%, lethal above 70%
Profound cyanosis, will see with MetHb >1.5 g/dl in contrast to normal Hb which requires 5 g/dl of deoxygenated form.
In infants, must also be differentiated from cyanotic heart disease. Heart disease has low PO2 while MetHb has high PaO2 despite cyanosis
Pulse ox readings stay at 85% while calculated blood gas sat will be normal.
PaO2 is normal (Sat Gap-on o2, high PO2, low pulse ox Sat)
Place venous blood on piece of paper, in normals, should turn bright red after 15 min, MetHb wont.
Methylene blue 1 to 2 mg/kg over 5 minutes (Do not give if G6PD (can give in low doses)) Serves as electron carrier for reduction of MetHb. You will see transient drop in Sats from the blue color of the drug.
½ life of MetHb is 1-3 hours. HBO if no other option.
Give AC if ingestion.
1.5 g of MetHb to get Cyanosis
Methylene blue (MB), given intravenously in a dose of 1 to 2 mg/kg over five minutes provides an artificial electron acceptor for the reduction of methemoglobin via the NADPH-dependent pathway (show figure 2). The response is usually rapid; the dose may be repeated in one hour, but is frequently not necessary. Caution should be exercised to avoid overdosage as large (>7 mg/kg) cumulative doses of MB can cause dyspnea, chest pain, and hemolysis [36,37] . Since co-oximetry detects MB as methemoglobin, this technique cannot be used to follow the response of methemoglobin levels to treatment with MB.
don’t give meth blue to methb if g6pd, do exchange transfusion instead
Dapsone is one of the few agents that can cause recurrent methemoglobinemia; one of the treatments is actually cimetidine, since it inhibits the P450 system and prevents dapsones toxic metabolite from being produced as quickly.
bedside test using a scanner to analyze hue (Ann Emerg Med 2010;55(2):184)
which is usually more mild, but doesnt respond to the methylene blue.
Moves disassociation curve to right so less dangerous
Common drugs: Reglan, Dapsone, local anesthetics, phenacetin, and antimalarial drugs or any drug which causes MetHb
Can have Met-Sulf-Hb in which case sulfur bound to Hb goes from ferrous to ferric state, this will have partial response to meth blue. Sulf-Hb is a biological dead end, no treatment except supportive care.
If from dapsone, give cimetidine 1200 mg/day to decrease metabolism of dapsone which can last in body for weeks
.5 G of SulfHb to get cyanosis
Methemoglobinemia has been linked to the use of nitrates and nitrites, nitroglycerin, dapsone, and local anesthetics, such as lidocaine and benzocaine.2 Both methemoglobinemia and sulfhemoglobinemia have occurred with the use of phenazopyridine and sulfonamides (i.e., TMX/SMX).3 Our patient was using TMX/SMX for chronic urinary tract infections, but the peculiar aspect of this case was the long duration of exposure to the medication. She had taken it for the past 9 months, with clinical manifestations only in the past month.
Clinical presentations of both diseases manifest as cyanosis and shortness of breath. In regard to methemoglobinemia, if the percentage level is under 10% there can be shortness of breath; between 10 and 20%, headache, ataxia, and weakness can occur; from 20% to 40% seizures and arrhythmia can occur; and levels above 70% are incompatible with life.1
The diagnosis can be suggested by the pulse oximetry level and the ABG, but caution in the evaluation of these measures must be exercised. The pulse oximetry reading is usually low in both disease states and plateaus around 85%; however, in a patient with a significantly elevated sulfhemoglobin level, the pulse oximetry can be falsely elevated.4 In addition, an ABG measures dissolved hemoglobin and not bound hemoglobin, which can falsely elevate the reading.5 Cooximetry is needed to measure the abnormal hemoglobin levels. Most cooximetry machines utilize four different spectral absorbance levels for oxyhemoglobin, deoxyhemoglobin, methemoglobin, and carboxyhemoglobin. However, both methemoglobin and sulfhemoglobin utilize similar absorbance levels (methemoglobin uses 570 and 620 nm, sulfhemoglobin uses 520 and 626 nm), which accounts for an elevated methemoglobin level in a patient with sulfhemoglobinemia.6 If suspicious of sulfhemoglobinemia, cyanide can be added to the sample. Cyanide will bind the methemoglobin and block the interference, thus allowing sulfhemoglobin alone to be recognized by the cooximeter. In addition, newer cooximetry machines can now independently measure a sulfhemoglobin level.
Treatment for both diseases is supportive and includes the removal of the offending agent. However, methemoglobinemia responds to methylene blue, while sulfhemoglobin does not. The dose is commonly 12 mg/kg IV infused over 5 minutes and can be redosed as needed. Response to methylene blue usually occurs within 1 hour. A patient who has a enzyme glucose-6-phosphate dehydrogenase deficiency will not be able to respond to methylene blue due to the inability to produce nicotinamide adenine dinucleotide phosphate-oxidase and therefore the fails to oxygenate the ferric molecule. Gastric decontamination with activated charcoal could be considered if the ingestion is within a reasonable time range; however, most presentations are distant from the time of ingestion. Finally, blood or exchange transfusions can be utilized to enhance the naturally occurring red cell turnover that must occur to remove the agent completely. (Acad Emerg Med 2008;15(4))
Decreased difference between PaO2 and PvO2, Lactate>10
HA, Coma, seizures
Myocardial Ischemia, Dysrhythmias, Eventual hypotension and bradycardia
Tachypnea then bradypnea, pulm edema
Abd pn and emesis
Bind to Cytochrome 450 and blocks oxidative phosphorylation
Binds to O2 site on other enzymes
Lilly Cyanide Kit
Amyl Nitrite: Inhaled for 30 sec, results in MetHb levels of ~5%
Sodium Nitrite (10%): IV form. .33 cc/kg in kids, 10 cc adults. Gives MetHb ~7-14% (shooting for 20-30%)
Sodium Thiosulfate: provides sulfur for rxn #2
MetHb will combine with Cyanide first, so if given and then no MetHb measured, then cyanide was definitely present and you should give more. Also tears cyanide off of cytochromes. Then the enzyme rhodanese transfers cyanide from cyanmethemoglobin to thiosulfate forming thiocyanate which is harmless and excreted into the urine.
Can give thiosulfate portion to all fire inhalations (CN+CO), but not the nitrites as you do not want to form MetHb as that + COHb is deadly.
Hydroxocobalamin (Pre-Vit B12)-binds cyanide to form cyanocobalamin
For many years the only antidotal therapy available in the U.S. was the Cyanide Antidote Kit. This threecomponent
kit contains amyl nitrite, sodium nitrite, and sodium thiosulfate. While effective, the Cyanide Antidote
Kit also has many drawbacks. The nitrites induce methemoglobinemia which can be deadly in patients
with concurrent carbon monoxide poisoning. Additionally, the nitrites are potent vasodilators which cause hypotension
and reflex tachycardia. There are case reports of pediatric fatalities from dosing errors which resulted
in profound methemoglobinemia and hypotension. This has led some healthcare providers to disregard
the nitrites altogether and use only sodium thiosulfate, although it has a slow onset of action
The FDA approved hydroxocobalamin for use as a cyanide antidote in December 2006 and it has recently become
available for widespread distribution. It is marketed by Dey, L.P. as Cyanokit
®. Hydroxocobalamin chelates
cyanide and forms cyanocobalamin (a form of vitamin B
12) which is excreted in the urine. The kit contains
two 2.5 g vials of hydroxocobalamin as a lyophilized powder. Each vial should be reconstituted with 100
mL of normal saline. Dosing for adults is 5 g administered as an IV infusion over 15 minutes. A second 5 g
dose can be given if an incomplete clinical response is observed. Pediatric patients should receive 70 mg/kg
as an initial dose. Due to its red color, hydroxocobalamin causes self-limiting skin reddening and chromaturia
in most patients that may last up to a week. Hydroxocobalamin also causes a transient, relative hypertension
which resolves within 4 hours. Allergic reactions are possible, including pustular rash and face swelling. These
effects can effectively be treated with antihistamines and steroids. Cyanokit
® is a safe and effective alternative
to the Cyanide Antidote Kit and has the potential to become the mainstay of therapy for cyanide poisoning
victims. Call the Maryland Poison Center for assistance in diagnosing and managing all poisonings, including
cyanide. (Maryland Poison Center)
Stroma-free MetHb-free methemoglobin without an RBC
Short term high dose therapy or longer term normal dose
Increased cyanide if bottle not protected well from light
Add thiosulfate to nitroprusside solution 10 cc of 25% thiosulfate for each 100 mg of nitroprusside
Cyanide Treatment should be undertaken immediately if cyanide poisoning is suggested by a compatible history, rapidly progressive coma, central apnea, and severe lactic acidosis with decreased arteriovenous oxygen extraction. Immediate treatment should ensue even in the presence of concomitant carbon monoxide poisoning, which may partially explain the constellation of symptoms. The treatment of cyanide poisoning remains based largely upon the work of Chen and colleagues at Eli Lilly in the early 1930s . They tested a number of compounds singly and in combination and found that both sodium nitrite and sodium thiosulfate used singly could reverse the toxicity of approximately four times the lethal cyanide dose in dogs. When the two drugs were used in combination, 21 times the lethal dose of cyanide could be detoxified in dogs. The “Lilly kit” or cyanide antidote kit, consists of amyl nitrite for inhalation followed by intravenous sodium nitrite and then intravenous sodium thiosulfate. It is the only licensed antidote for cyanide poisoning in the United States . The ingredients of the kit work as follows: The nitrites exert their effect by oxidizing hemoglobin to methemoglobin. Cyanide is attracted to the ferric ion with sufficient affinity to detach it from cytochrome a-a3 and form a ferricyanide complex . The onset of action of the nitrites is rapid, but the induction of methemoglobinemia decreases the oxygen-carrying capacity of blood and may therefore be harmful in patients with anemia or significant carboxyhemoglobinemia . Sodium thiosulfate works by a different and complementary mechanism. It donates its sulfane sulfur atom in a reaction catalyzed by the enzyme rhodanese to convert cyanide to the much less toxic thiocyanate ion, which is then excreted in the urine . In cases where cyanide toxicity is suspected and significant carboxyhemoglobinemia has been ruled out, one should proceed with both nitrite and thiosulfate therapy. If carboxyhemoglobinemia is significant or unknown, thiosulfate can be given alone or nitrites can be given cautiously, aiming to keep the sum of methemoglobin and carboxyhemoglobin below 40 percent [10,34]. Additional antidotes to cyanide poisoning appear to be effective:
appears to be a safe and effective alternative antidote and does not impair oxygen-carrying capacity. Its effect results from its ability to react with cyanide to form cyanocobalamin. Despite extensive European experience with the drug, it is available in the United States only in a dilute form for vitamin B12 supplementation; the use of this preparation for the treatment of cyanide toxicity requires infusion of a volume of approximate 5 liters [49,50]. Similarly, there is a large British experience with the chelating agent dicobalt edetate, but it carries the risk of cobalt toxicity if it is administered in the absence of cyanide. This medication is not licensed for clinical use in the United States
Presence of OHCob in blood intereferes with CO, MetHb measurements by co-oximetry (Ann Emerg Med 2007;49:802)
if lactate > 10 think cyanide in smoke inhalation. (NEJM 1991;325:1761)
Sour Gas from decaying organic material or sulfur springs
Dizziness, Tremor, HA, Coma. Smell might disappear as overwhelms nasal mucousa, High concentrations can cause knock-down effect (transient LOC)
Give the nitrite portions of the kit
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