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43 Cards in this Set
- Front
- Back
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What is a simple asphyxiant?
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An inert gas that displaces oxygen causing hypoxia
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What hypoxic symptoms are expected with a fall in FiO2?
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15% - autonomic dysfunction (dyspnea, tachycardia, tachypnea) and cerebral hypoxia (ataxia, dizziness, confusion)
10% - cerebral edema 6% - death |
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What is the most common history of asphyxiant exposure?
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Complaints consistent with asphyxiation and rapid resolution upon removal from the exposure
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How is asphyxiation treated?
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Removal from exposure
Supportive care Supplemental oxygen Observation if symptomatic or have comorbidities |
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How do pulmonary irritants cause damage?
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They dissolve in the lungs and irritate the mucosa by producing acid/alkali/free radicals
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Where do highly water-soluble gases have their effects?
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The upper airways and mucous membranes
See lacrimation, nasal burning, cough, laryngeal edema, laryngo/bronchospasm and ALI. |
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Where do poorly water-soluble gases have their effects?
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The alveoli.
They do not irritate the mucous membranes and have no immediate symptoms so they are able to work their way further down with pulmonary injury in 2-24 hours. ARDS can develop in 24-36 hours. |
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How is hoarseness and strider managed?
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Direct visualization of the larynx and airway stabilization if necessary.
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How is bronchospasm managed?
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It usually responds well to inhaled beta-adrenergic agents.
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How is chlorine/hydrogen chloride gas exposure treated?
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Nebulized 2% sodium bicarbonate.
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What experimental treatments may be used for pulmonary irritants?
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Exogenous surfactant and nitric oxide
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How does smoke inhalation cause injury?
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1 - Direct thermal damage from steam/soot
2 - Irritant toxins produced by the fire and deposited in the lungs (work similar to irritant gases) |
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What are the clinical features of significant smoke inhalation?
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-Singed nasal hairs and soot
-Cough or stridor from laryngeal injury -Bronchospasm -Airway inflammation -Positive CO/CN levels |
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How can lower airway injury be assessed?
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-Hyperinflated lungs
-Abnormal CO diffusion on PFT's -Abnormal clearance of radiolabeled gas |
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How can debris be cleared from the distal airways?
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Bronchoscopy with bronchoalveolar lavage
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What does hydrogen cyanide smell like?
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Bitter almonds
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Where is hydrogen cyanide used?
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Jewelry and photographig industries
Apricot pits |
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Where is hydrogen sulfide produced
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Petroleum refineries
Sewage storage |
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What does hydrogen sulfide smell like?
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Rotten eggs
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How does hydrogen cyanide cause toxicity?
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Binds complex IV of the electron transport chain preventing oxidative phosphorylation
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How does hydrogen sulfide cause toxicity?
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Pulmonary irritant
Blocks the electron transport chain preventing oxidative phosphorylation BUT does so only transiently. Brief exposure can be treated by getting the person away from the exposure. |
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What are the clinical features of hydrogen cyanide/sulfide poisoning?
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Tissue hypoxia (heart and CNS first) causing coma, seizures, dysrhythmias
Metabolic acidosis (lactate) Sulfide resolves quickly, cyanide does not |
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What is abnormal about the VBG in hydrogen cyanide/sulfide poisoning?
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The pO2 is relatively high reflecting the lack of oxygen utilization by the body
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What laboratory values are helpful in hydrogen cyanide/sulfide poisoning?
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Profound lactic acidosis (>10)
Co-oximetry It can be difficult to distinguish CN and CO poisoning on history/exam and they often copresent |
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How can cyanide poisoning be treated?
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Classic cyanide kit: sodium thiosulfate, amyl nitrite, sodium nitrite
New treatment - Hydroxocobalamin |
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How does the classic cyanide kit work?
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Use sodium nitrite if you have IV access, amyl if you do not. Sodium thiosulfate should be initial therapy.
Amyl (inhaled) and sodium nitrite (IV) form methemoglobin which combines with CN to form cyanomethemoglobin. This is converted to thiocyanate that can be renally excreted. Sodium thiocyanate gives sulfur to cyanomethemoglobin/free cyanide to form thiocyanate. |
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When should the nitrite components of the classic cyanide kit NOT be used? Why?
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In patients that also have CO poisoning because compromised hemoglobin capacity will be compromised further.
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What is the most common side effect of nitrite therapy?
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Hypotension!
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How does hydroxocobalamin work?
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It binds cyanide with cobalt to form vitamin B12.
Can cause red discoloration of the patient's skin. |
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How does hydroxocobalamin effect laboratory tests?
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The red color interferes with spectrophotometric testss for things like lactate and carboxyhemoglobin. Get blood work first.
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How is hydrogen sulfide exposure treated?
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Remove the patient from the exposure and use standard resuscitative techniques. Consider nitrite use in prolonged exposure. Thiosulfate and HBO do not work.
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What is the role of hyperbaric oxygen treatment in cyanide poisoning?
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There is no evidence that it will help. Consider if chamber is accessible and cocommitent CO poisoning. Can give entire cyanide kit in hyperbaric chamber (don't need to worry about O2 carrying capacity)
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How is carbon monoxide produced?
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Incomplete combustion of virtually any carbon-containing product.
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How does CO cause toxicity?
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1 - Combines with Hb to form carboxyhemoglobin which cannot carry oxygen
2 - inhibits the final cytochrome complex (4) in oxidative phosphorylation |
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What are the clinical features of CO toxicity?
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CNS - headache, altered mental status, seizures, coma
Metabolic - acidosis (lactate) GI - N/V |
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What is the classic skin color in patients with CO poisoning?
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"Cherry-red skin"
However, this is a postmortem finding. It is not seen in living patients. |
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What are risk factors for delayed neurological sequelae from CO poisoning?
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Age
Loss of consciousness |
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What delayed neurologic sequelae are associated with CO poisoning?
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Psych/Cognitive - apathy, memory deficits
Neurologic - focal deficits/seizures |
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Does the COHb level correlate with toxicity?
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No. Due to the "soaking phenomenom" - high tissue levels with low blood levels.
Prolonged, low levels can kill Brief, high levels can be tolerated |
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How is COHb interpreted by most pulse oximeters?
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As oxyhemoglobin.
The level can not be relied upon in this context. |
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How is CO poisoning treated?
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High-flow oxygen - increased pO2 decreases the half-life of CO (5h on RA to 1h on 100%)
HBOT - further reduces the half life (to 30m) and can sustain life even in the absence of Hb but would only be helpful if Hb was REALLY high! |
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Does HBOT have a clinical benefit in CO poisoning?
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Perhaps for reducing delayed neurologic sequelae. However, this is controversial. The studies are not very good.
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When should HBOT be considered for CO poisoning?
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Patients with neurologic abnormalities or cardiovascular instability
Some institutions use an absolute level of 25-40% Pregnant (relative hypoxia of fetus) should get special consideration (?15%) |
