Hyperventilation in Carbon-monoxide Poisoning

Leathart, G. L.

doi:10.1136/bmj.2.5303.511

BMJ

1962

DOI: 10.1136/bmj.2.5303.511

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Hyperventilation in Carbon-monoxide Poisoning

G. L. Leathart¹

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1968

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Cited by 4 publications

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“…However, it is not a recommended therapeutic option for CO poisoning (14). The use of hyperventilation in treating CO poisoning is constrained by concerns about the hypocapnia-induced reduction of O 2 delivery to the brain owing to both a decrease in cerebral blood flow (15) and a shift of the oxyhemoglobin dissociation curve further to the left.…”

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confidence: 99%

Isocapnic Hyperpnea Accelerates Carbon Monoxide Elimination

Fisher

Rucker

Sommer

et al. 1999

Am J Respir Crit Care Med

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A major impediment to the use of hyperpnea in the treatment of CO poisoning is the development of hypocapnia or discomfort of CO2 inhalation. We examined the effect of nonrebreathing isocapnic hyperpnea on the rate of decrease of carboxyhemoglobin levels (COHb) in five pentobarbital-anesthetized ventilated dogs first exposed to CO and then ventilated with room air at normocapnia (control). They were then ventilated with 100% O2 at control ventilation, and at six times control ventilation without hypocapnia ("isocapnic hyperpnea") for at least 42 min at each ventilator setting. We measured blood gases and COHb. At control ventilation, the half-time for elimination of COHb (t1/2) was 212 +/- 17 min (mean +/- SD) on room air and 42 +/- 3 min on 100% O2. The t1/2 decreased to 18 +/- 2 min (p < 0.0005) during isocapnic hyperpnea. In two similarly prepared dogs treated with hyperbaric O2, the t1/2 were 20 and 28 min. We conclude that isocapnic hyperpnea more than doubles the rate of COHb elimination induced by normal ventilation with 100% O2. Isocapnic hyperpnea could improve the efficacy of the standard treatment of CO poisoning, 100% O2 at atmospheric or increased pressures.

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mentioning

confidence: 99%

Isocapnic Hyperpnea Accelerates Carbon Monoxide Elimination

Fisher

Rucker

Sommer

et al. 1999

Am J Respir Crit Care Med

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Effect of perfluorochemical (PFC) emulsion on acute carbon monoxide poisoning in rats

Yokoyama

1978

The Japanese Journal of Surgery

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The effect of perfluorochemical (PFC) emulsion (25 w/v per cent of PFC concentration) on carbon monoxide poisoning was studied in rats exposed to 97 per cent O2 and three per cent CO. There was no significant difference in conversion rate of hemoglobin to carboxyhemoglobin (COHb) between PFC emulsion and saline groups. However, after re-exposure to pure oxygen, PFC emulsion group circulation reconverted to oxyhemoglobin (OXYHb) at a significantly faster rate than circulation in the control group. Survival time of rats was considerably affected by infusion of PFC emulsion and prolonged in proportion to increased injection dosage. Significant elevations in plasma glucose, lactate and aldolase levels and lactate/pyruvate ratio were found in the saline group and these levels remained well within normal range in the PFC emulsion group. These results indicate that PFC emulsion can function as an oxygen carrier in the presence of carbon monoxide and can deliver sufficient oxygen to peripheral tissues.

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Treatment of carbon monoxide poisoning by mechanical ventilation: Case report

Townsend¹,

Stetson

1968

Can. Anaes. Soc. J.

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StacmE is among the ten leading causes of death in industrialized countries. During 1965 there were 22,000 reported suicides in the United States (statistics compiled by the Center for Studies of Suicide Prevention). There is no way of estimating the incidence of unreported suicides, or of the number of survivors after attempted suicide. One of the more frequent modes of suicide is carbon monoxide inhalation. As an accidental cause of death, carbon monoxide poisoning ranks second only to alcohol, x This, combined with the increasing incidence of non-accidental carbon monoxide poisoning, has made the acute management of these cases a pertinent problem in modern medicine. As an example of the extent of the "disease," in the period 1950 to 1955, carbon monoxide poisoning represented 2.1 per cent of eases investigated by the Los Angeles county coroner's oflqce (875 of 41,615). 2 Mann, in 1958, found 1,156 cases of carbon monoxide poisoning out of a total of 18,513 suicides) In the state of Indiana, in 1965, there were 80 suicides by carbon monoxide inhalation and 47 accidental poisonings. 4 Carbon monoxide has been termed the perfect asphyxiant. Haemoglobin combines with carbon monoxide 200-300 times as readily as it does with oxygen and dissociates from it 250 times as slowlyP The poisonous effects of carbon monoxide are derived from its double action in the production of asphyxia. First, any excess in inspired air reduces the percentage of oxygen inhaled. Second, it forms a stable compound with haemoglobin, and the carboxy-haemoglobin interferes with dissociation of any oxyhaemoglobin which remains in the erythrocytes. (Consequently, the tissue damage done by carbon monoxide poisoning results from histotoxie anoxia secondary to anoxemia.) Removal of carbon nonoxide is also hindered by the insufficient supply of oxyhaernoglobin to act as a catalyst in the liberation of carbon monoxide. The prominent neurological sequelae of carbon monoxide poisoning result from damage to the basal ganglia; most commonly the globus pallidus, and sometimes the head of the caudate nucleus and putamen. There is a softening and necrosis of the basal ganglia as well as damage to the reticular zone of the substantia nigra and the deeper layers of Purkinje cells of the cerebellum. If the patient survives into the chronic stage in which residuals of carbon monoxide are seen, three patterns are evident. The patient may survive for several months and then succumb after a progressive downhill course (progres

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Hyperventilation in Carbon-monoxide Poisoning

Cited by 4 publications

References 7 publications

Isocapnic Hyperpnea Accelerates Carbon Monoxide Elimination

Isocapnic Hyperpnea Accelerates Carbon Monoxide Elimination

Effect of perfluorochemical (PFC) emulsion on acute carbon monoxide poisoning in rats

Treatment of carbon monoxide poisoning by mechanical ventilation: Case report

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