pinkport.blogg.se - Carbon monoxide poisoning symptoms dead

PaO2 should be normal, SpO2 only accurate if measured (not calculated from PaO2).HbCO (elevated levels are significant, but low levels do not rule out exposure).solvents and paint removers (metabolised to CO in liver).

Symptoms are usually non-specific but can include headache, personality changes, poor concentration, dementia, psychosis, Parkinsonism, ataxia, peripheral neuropathy and hearing loss.

compared with acute exposures, they typically involve a lower dose of carbon monoxide for a long period, which increases the risk of developing neurological complications.

may have similar effects to acute poisoning, but often with a gradual, insidious onset, and symptoms may fluctuate with varying levels of exposure to CO over time.

RESP: dyspnea, tachypnea, chest pain, palpitation.

CVS: Dysrhythmias, Ischaemia, hyper or hypotension (exacerbated in patients with anaemia or underlying cardiovascular disease).

CNS: Headahce, nausea, dizziness, confusion, mini mental status examination errors, incorrdination, ataxia, seizures and finally coma.

hyperventilation, increased cardiac output)

elimination is affected by the factors as absorption (see above) and is likely faster in many CO poisoned patients due to compensatory measures (e.g.

~ 23 minutes with hyperbaric oxygen (2 atmospheres).~ 40–80 minutes with administration of 100% oxygen.This half-life decreases with oxygen administration.The biological half-life of CO in a sedentary healthy adult is 4–5 hours.CO is eliminated unchanged from the lungs in an exponential manner.Tobacco smokers have higher baseline concentrations of COHb (3 to 10%) and therefore will reach toxic concentrations earlier in any exposure.Uptake (and elimination) of CO is increased by:.Clinical effects occur within 2 hours of exposure at concentrations as low as 0.01% (100 ppm).COHb concentration in blood is a function of the CO concentration in inspired air and the time of exposure.Thus on presentation there is little correlation between prior symptoms and signs and the measured COHb% However, the COHb% changes rapidly and variably, but generally to a greater extent in the severely poisoned. 70 – 80% (circulatory and ventilatory failure, cardiac arrest, death).50 – 60% (coma, convulsions, Cheyne-Stokes breathing, arrhythmias, ECG changes).30 – 40% (headache, tachycardia, confusion, weakness, nausea, vomiting, collapse).10 – 20% (nil or vague nondescript symptoms).Typical clinical symptoms and signs relative to COHb (Normal = 0.5%): These mechanisms are probably responsible for delayed neurological sequelae.Carbon monoxide also triggers endothelial oxidative injury, lipid peroxidation and an inflammatory cascade.CO also binds to intracellular cytochromes, impairing aerobic metabolism.This can result in tissue hypoxia and ischaemic injury. Binding therefore renders haemoglobin oxygen carrying capacity and delivery to the tissues. Carbon monoxide has ~210 times the affinity for haemoglobin than oxygen.intermittent headaches), and a high index of suspicion is required in at-risk groups (e.g. Chronic CO poisoning may have an insidious presentation (e.g.Prevalance varies with geography and demographics, and may be high in some groups.Exposure is most commonly from suicide attempts using car exhaust, and accidental exposures from incomplete combustion in charcoal burners, faulty heaters, fires, and industrial accidents.Carbon monoxide (CO) is a colourless, odourless gas produced by incomplete combustion of carbonaceous material.