Respiratory and Circulatory Responses to Acute Carbon Monoxide Poisoning

A B S T R A C T The effects of carbon monoxide on ventilation were studied in unanesthetized goats. Responses to single breaths of 10-25% CO in 02, which rapidly raised carboxyhemoglobin (COHb) from 5 to 60%, were considered to reflect peripheral chemoreceptor-mediated reflexes whereas responses to continuous inhalation of 1% CO in 02, which slowly raised COHb from 0 to 60%, were considered to reflect both peripheral chemoreceptor and nonperipheral chemoreceptor mechanisms. In each of six goats, single breaths of CO failed to elicit any immediate ventilatory response.However, slow buildup of carboxyhemoglobinemia in the same animals always elicited ventilatory stimulation (from a mean of 7.43 to 16.02 liter/min, P < 0.001) beginning 5-6 min after onset of 1% CO in 02 inhalation when COHb saturation reached 50-60%. In eight studies of six animals HCOs-concentration fell (from 21.3 to 15.8 meq/liter; P <0.001) and lactate concentration rose (from 2.5 to 4.2 meq/liter; P < 0.05) in the cisternal cerebrospinal fluid during the CO-induced hyperpnea. Additional studies ruled out ventilatory stimulation from left heart failure or enhanced chemosensitivity to carbon dioxide. Although the delayed hyperpnea was associated with a hyperdynamic cardiovascular response to CO, blockade of these circulatory effects with propranolol (2 mg/kg) failed to abolish the delayed hyperpnea; however, the propranolol did unmask an element of ventilatory depression which preceded the hyperpnea. Conclusions were: (a) hyperventilation in response to CO inhalation is not mediated by the carotid bodies; (b) the delayed hyperpnea in response to CO inhalation is primarily due to braincerebrospinal fluid acidosis; (c) mobilization of body CO2 stores due to the circulatory response to CO may obscure an initial depression of ventilation by CO. INTRODUCTIONThe increase in ventilation caused by reduction in arterial 02 tension is well known and clearly ascribed

Section: Introductionmentioning

confidence: 58%

Mechanism of the ventilatory response to carbon monoxide.

Santiago¹,

Edelman²

1976

“…In addition activation of the sympathetic nervous system which occurs during hypoxia may greatly reduce carotid body flow during hypoxia (26). Secondly, there is general agreement that administration of carbon monoxide which preserves normal arterial oxygen tension but lowers oxygen content fails to stimulate ventilation (27)(28)(29). This has been strong evidence in support of the notion that the carotid body senses arterial oxygen tension rather than content.…”

Section: Methodsmentioning

confidence: 99%

Hypoxic ventilatory drive in normal man

Weil¹,

Byrne-Quinn²,

Sodal³

et al. 1970

381

174

A B S T R A C TFor purposes of quantitation these curves are approximated by a simple hyperbolic function, the parameters of which are evaluated by a least squares fit of the data. The parameter A denotes curve shape such that the higher the value of A, the greater the increase in ventilation for a given decrease in PAO2 and hence the greater the hypoxic drive. Curves are highly reproducible for each subject and curves from different subjects are similar. In 10 normal subjects at resting PAcO2, A = 180.2 +14.5 (SEM). When PACO, is adjusted to levels 5 mm Hg above and below control in six subjects A = 453.4 ±103 and 30.2 ±6.8 respectively. These latter values differed significantly from control (P < 0.05). These changes in curve shape provide a clear graphic description of interaction between hypercapnic and hypoxic ventilatory stimuli. At normal PACo2 the VE-PAO2 curve has an inflection zone located over the same P02 range as the inflection in the oxygenhemoglobin dissociation curve. This indicated that ventilation might be a linear function of arterial oxygen saturation or content. Studies in four subjects have

“…Adjustments in the oxygen unloading in the tissues up to this level of carboxyhemoglobinemia are accomplished not by changes in cardiac output, but by decreases in the venous oxygen tension (10,11). Both methemoglobinemia and carboxyhemoglobinemia shift the oxygen dissociation curve of the residual oxyhemoglobin to the left, and render the curve less sigmoid and more hyperbolic.…”

Section: Resultsmentioning

confidence: 99%

Effect of Methemoglobinemia on the Visual Threshold at Sea Level, at High Altitudes, and After Exercise

Bodansky¹,

Hendley²

1946

Experiments by one of us (1) have shown that methemoglobinemia exerts a protective effect in dogs against poisoning due to inhalation of HCN and CNCl. The possibility of applying these findings in man raised the question as to the extent to which methemoglobinemia would impair various physiological functions. Several groups of investigators (2 to 4) have found that a rise in the threshold of the dark adapted eye occurs during anoxia induced by low oxygen tensions, and have considered this visual test a very sensitive criterion of this type of anoxia. Accordingly, it was decided to determine whether the anoxia *due to methemoglobinemia would affect the visual threshold (a) at sea level, (b) at loWered oxygen tensions, and (c) after exercise. EXPERIMENTALMethemoglobinemia was induced by the ingestion of paminopropiophenone. This substance was shown by Van-denbelt, Pfeiffer, Kaiser and' Sibert (5) to be a potent methemoglobin-former in animals. Doses ranging from 1 to 2 mgm. per kgm. were dissolved in a minimal volume of propylene glycol, usually not more than 7 ml., and administered by mouth. Propylene glycol, without dissolved p-aminopropiophenone, was also given to a few individuals.The concentration of methemoglobin was determined by a slight modification of the method of Evelyn' and Malloy (6) and expressed as per cent of the total blood pigment. After ingestion of the p-aminopropiophenone in propylene glycol, the concentration of methomoglobin usually rose to a maximal value in about an hour. The concentration then remained fairly constant for about another hour when it began to decrease slowly. Measurements of the threshold were usually made during the period of constancy of the methemoglobin concentration, i.e. 1 to 2 hours after the ingestion of the drug. In the earlier experiments, a sufficient number of blood samples was taken so as to obtain a curve of the change in methemoglobin concentration, and to assure accurate estimation of the methemoglobin concentration at the time of measuring the dark adaptation.iLt. Colonel, M.C., A.U.S. Present address: Cornell University Medical College, New York City.The thresholds were measured with a Hecht-Shlaer adaptometer, Model 3. This instrument has a 30 blue test field which appears 7°below a red fixation point. The test field is exposed in flashes of 0.2 second, accurately controlled by a pendulum shutter. The subject is seated comfortably at the instrument and views the test field binocularly with the natural pupil. The device for controlling the shutter and exposing the field is easily accesible to the subject. The experimenter is seated directly across from the subject, at the other side of the instrument, where he can regulate and note the brightness of the test field. At a signal from the experimenter, the subject operates the shutter and informs the experimenter whether or not he has been able to discern the exposed field. The general principles and technique of dark adaptation measurements have been discussed by Hecht and Shlaer in describing their Mode...