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CO AND CN
Tox lecture 4
| Term | Definition |
|---|---|
| Fire Immediate Effects (4) | Mucosal Irritation (acids, soot) Oxygen consumption » Hypoxia Heat Stress Smoke density - limits visibility Chemical asphyxiants (CO.CN.metHgB) |
| Smoke Inhalation Combustion toxicology (7) | Carbon monoxide Cyanide - Hydrochloric acid - Phosgene - Acrolein - Nitrogen oxides - 80 % of fire related deaths are due to smoke inhalation |
| Carbon monoxide | - burning wood (Carbon) |
| Cyanide - | burning plastics, rubber, wool, silk (Nitrogen) |
| Hydrochloric acid - | burning chloride cmpds, thick smoke |
| Phosgene - | thermal degradation of PVC.delayed injury |
| Acrolein - | toxic aldehyde, deep lung/tissue penetration |
| Nitrogen oxides - | potential metHgB inducer |
| Smoke Inhalation Signs | Soot in airway Carbonaceous Sputum Hoarseness Altered LOC |
| CO Epidemiology | Leading case of death by poisoning in US |
| What are the Sources of CO | Incomplete Combustion Exhaust fumes: Automobiles -Sleeping in car with engine on -Pick-up truck camper shells Tractors and forklifts indoor Ice resurfacing Machines |
| Carbon Monoxide Detectors | Alarm limits: UL regs Sound at 85 decibels: -70 ppmfor 189 min -150 ppm for 50 min -400 ppm for 15 min -Resets in 6 minutes to realarm once silenced -And it will "ignore" 30 ppm for as long as 30 days & 70 ppm for 1 hour -IDLH = 1200 ppm |
| Pulse Oximetry | Measures saturation of hemoglobin Carboxyhemoglobin is "detected" by sensor as saturated hemoglobin New Product measures CoHgb and MetHgb by pulse ox |
| New Pulse oximeter | Measures by 7 wavelengths: • Oxy Hgb • CO Hgb • MetHgb |
| Carbon Monoxide: Systemic Asphyxiant | Does NOT displace 02 from air Binds to Hgb with 240 times affinity of O2 Changes Oxy-Hgb dissociation curve Decreases O2 release at tissue level Binds to Myoglobin with 40 times affinity of 02 Interferes with cytochrome oxidase a3 |
| Carboxyhemoglobin | Carbon monoxide (CO) binds competitively at oxygen (02) binding sites. CO impairs 02 transportation and delivery |
| CO Toxicology | Toxic effects similar to cyanide • Inhibits mitochondrial respiration • Oxygen cannot be utilized to generate ATP • Cells shift to anaerobic metabolism = LACTIC ACIDOSIS |
| Hyperbaric Oxygen | Decreases Half-life of CO-Hgb Increases dissolved 02 in blood 10 fold Accelerates Dissociation of CO from Cytochrome oxidase Prevents lipid peroxidation Prevents leukocyte mediated xanthine dehydrogenase free radical generation |
| Neurologic testing | Baseline neurologic exam and post dive • Statistical monitor Q 50 patients ( anticipated 200 patients to be enrolled) Neuropsychiatry battery at: 2 weeks 6 weeks 6 months 12 months |
| Interpreting CN Levels Numbers | CN 38 umol/L = 1 ug/L Potentially lethal 40 -100 umol/L Likely lethal > 100 umol/L Half-life is 1.2 hours. |
| Interpreting CN Levels Words | And levels decline in blood tube and stored blood. But levels are hard to get, so there is correlation with lactate levels > 10 mmol/L Or decreased pH But also elevated CO in fires |
| Cyanide Toxicology Absorption | Well-absorbed from inhalation and ingestion pathways of exposure Limited warning signs (inhalation) Fallacy of the "bitter almond" smell |
| Cyanide Toxicology Toxicodynamic effects | Toxicodynamic effects similar to sulfide, azide, & phosphine Inhibits mitochondrial respiration Oxygen is present, but cannot be utilized to generate ATP Cells shift to anaerobic metabolism |
| Cyanide: Effects Initially | Initially, non-specific Sense of doom, increased resp. rate |
| Cyanide: Effects Within minutes: | abnormal mental status, depressed cardiac output, bradycardia, sudden collapse, metabolic acidosis |
| Cyanide Effects: Oxygen and progression | Oxygen is present but cannot be utilized Oxygen saturation of arterial, venous blood is similar Rapidly progresses to shock, multi-system organ failure, death |
| Cyanide antidote kit | Three components: 1) Amyl nitrate pearls only until IV access established produces methemoglobinemia (MetHb)of~5% |
| Cyanide (Lilly) Antidote Kit (CAK) | Three Components Nitrites (inhaled = amyl nitrite) IV = sodium Nitrite Induces methemoglobinemia: (decreased oxygen carrying capacity) Redistributes CN- away from mitochondria Sodium thiosulfate -Converts cyanide to thiocyanate |
| Sodium thiosulfate | -Converts cyanide to thiocyanate |
| Nitrites | (inhaled = amyl nitrite) |
| IV = | Sodium Nitrite Induces methemoglobinemia: (decreased oxygen carrying capacity) Redistributes CN- away from mitochondria |
| Cyanide Antidote Kit Sodium Nitrite | ADULTS: 300 mg IV over 5 min. PEDS: 0.33 ml/kg Must reduce dose in anemia in both adults & peds Watch for hypotension !!! Blue skin discoloration Don't use for smoke inhalation |
| Cyanide Antidote Kit Sodium Thiosulfate | ADULTS: 12.5gmslV PEDS: 400 mg/kg IV Should be used alone for smoke inhalation or Nipride toxicity |
| Problems with Cyanide Kit | Less than 25 % of hospital stock it If stocked usually have only one Kit may have passed "expired" date Frequently amyl nitrite pedes missing Instructions missing |
| Hemoglobin | METHEMOGLOBIN: Hemoglobin's (Fe+2) is oxidized to (Fe+3) Oxygen (02) cannot bind to methemoglobin's Fe+3. ^ Water (H20) binds in oxygen's place. Methemoglobin cannot transport 02. |
| Therapeutic Methemoglobin Production for Cyanide Poisoning Fe | Amyl nitrite & sodium nitrite oxidize hemoglobin,'s Fe+2 to produce methhemoglobin's Fe+3, 02 cannot bind to methhemoglobin's, Fe+3 H20 binds in oxygen's place, |
| Therapeutic Methemoglobin Production for Cyanide Poisoning CN | CN preferentially binds to methhemoglobin,'s Fe+3 producing Cyanomethhemoglobin, CN" binds to methhemoglobin, rather than to cytochrome oxidase Cytochrome oxidase activity & aerobic metabolism resume |
| What about just Sodium Thiosulfate | Third component of CAK Does not induce MetHgb Crosses Blood brain barrier Induces enzyme RHODANESE to convert CN into sodium thiocyanate up to 3 times usual rate Thiocyanate is then eliminated by the liver |
| Sodium Thiosulfate | Not well studied alone Few animal models Most human uses are with full CAK or with Hydroxocobalamin Often used alone in suspected smoke inhalation in the US at 12.5 gms IV once |
| Sodium Thiosulfate Side effects | few, occ. Nausea, Vomiting, Pain at injection site |
| Nithiodote: | Two vial version of the classic Cyanide kit (2011) Sodium Nitrite 3 %: 300mg/10mL Do not exceed 5 ml/mi Sodium Thiosulfate: 12.5 grams/50 mL |
| Human Volunteer Studies HCB Doses | 2.5, 5.0, 7.5, 10.0 GMS |
| Human Volunteer Studies HCB Side Effects | Increased BP, in some cases substantial Highest post Rx 188 systolic /125 diastolic Resolved over 4 hours No associated ECG changes in healthy volunteers Red Skin Red Urine |
| Human Volunteer Studies HCB Red skin | 95 % at 5 gm dose 100 % at higher doses Duration 4 to 9 days |
| Human Volunteer Studies HCB Red urine | Duration 7 to 35 days |
| Hydroxocobalamin | Adult - 2.5 grams, repeat once if needed Pediatrics - 50 to 70 mg/kg Packaging 2.5 gm vials Reconstituted in 200 ml saline, give over 30 min. |
| Hydroxocobalamin - Adverse Effects | Increased Blood Pressure Orange or red discoloration of skin, urine and other body fluids Rare allergic reactions Interference with standard laboratory tests - Or, Mg, bilirubin, CPK and LFTs by colorometric tests May overread COHgb |
| Bottom Line Who do I treat pre-hospital | Only Paris Study had specific criteria HOB carries some risks of HTN BEST ADVICE: Persistent altered LOC after removal from fire and administration of 02 Soot in face/airway |
Created by:
pberriochoa
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