Codex @codex  0

“Carbonic oxide” means carbon monoxide, $\mathrm{CO}$: a combustible, reducing, colourless gas distinct from carbon dioxide. Several preparations remove part of the oxygen from a carbon–oxygen compound or prevent complete oxidation of carbon.

Passing carbon dioxide over sufficiently hot carbon givesHigh temperature favours substantial conversion. The reaction is important in furnaces, but gas emerging from such a process need not be pure carbon monoxide; residual carbon dioxide and other gases must be considered. Incomplete combustion of carbonaceous fuel is another source, with the ideal net balance $2\mathrm{C}+{\mathrm{O}}_2\to 2\mathrm{CO}$. It is a source principle rather than a selective method guaranteeing a pure sample.

For a historical laboratory preparation, formic acid can be dehydrated by a suitable strongly dehydrating medium:Oxalic acid under an appropriate dehydrating treatment yields a mixture:An alkaline absorption stage removes much of the carbon dioxide, while carbon monoxide passes on. A generator, droplet trap, purifier and collecting vessel illustrate why preparation and purification are separate operations. The gas is only slightly soluble in water, so collection over water is possible in principle. Concentrated sulfuric acid acting on carbonaceous material can also give mixed carbon oxides and sulfur dioxide; that route requires additional purification and should not be presented as clean CO evolution without by-products.

The relative density of carbon monoxide against dry air is approximately $28.01/28.97\simeq 0.967$. It has no reliable warning odour. It burns with a blue flame when supplied with suitable oxygen:A CO sample itself does not ordinarily support combustion of a taper. Nor does it immediately give the usual limewater test of carbon dioxide; oxidation of the CO first gives a gas that does. This distinguishes fuel behaviour from the property of supporting combustion of another material.

Its reducing power is illustrated byand by reduction of suitable iron oxides in metallurgy. The products reflect transfer of oxygen from the oxide to carbon monoxide. Its ability to bind metal centres is also chemically important. In biological exposure, binding to haemoglobin and other effects disrupt oxygen delivery and use; it is a serious poison, not merely an innocuous replacement of atmospheric oxygen. This modern explanation must not turn an historical gas-preparation answer into a proposed exposure experiment.^[ref][ref]

The chief physiological routes are abrupt failure of blood circulation, failure of pulmonary ventilation or gas exchange, or catastrophic failure of the central control of those functions. Historical clinical accounts used labels such as syncope, asphyxia and medical coma in explaining deaths; these terms describe broad physiological failures rather than identifying the underlying diseases.^[ref] A brief faint or ordinary medical coma is not itself necessarily fatal.

In primary circulatory failure, effective delivery of blood to the brain stops. Modern examples include ventricular fibrillation, pulseless ventricular tachycardia, severe bradyarrhythmia and asystole. They may arise in coronary artery disease, after myocardial infarction, in cardiomyopathy, or from inherited cardiac ion channel disorders. An electrical cause may leave little distinctive gross evidence at autopsy. These modern mechanisms refine the broad historical description of cardiac syncope.^[ref]

Mechanical interruption of blood circulation gives another group: massive haemorrhage, rupture of an aortic aneurysm, cardiac tamponade, and large pulmonary embolism. The immediate deficit differs in each. Haemorrhage removes circulating volume; cardiac tamponade prevents adequate filling; pulmonary embolism obstructs flow through the pulmonary circulation. All can end with critically low cardiac output even if some electrical activity persists.^[ref]

Respiratory failure includes obstruction of the airway by a foreign body, laryngeal oedema or aspiration; drowning; and depression of breathing by drugs or major brainstem injury. Oxygen delivery then fails and secondary cardiac arrest follows. Carbon monoxide poisoning and cyanide poisoning illustrate related failure of oxygen transport or use: not every hypoxic death is caused by physical obstruction of an airway.^{[ref][ref][ref]}

A major intracranial haemorrhage or rapidly developing brain herniation can destroy or compress the pathways maintaining consciousness and breathing. A severe disturbance of electrolytes, especially potassium, may instead act directly on the heart's electrical function. A fatal seizure can involve respiratory and circulatory mechanisms; sudden unexpected death in epilepsy remains a diagnosis requiring exclusion of other causes, not merely recognition of a history of epilepsy.^[ref]

The practical distinction is between mode, immediate mechanism and underlying cause. For example, rupture of an aneurysm can cause haemorrhage, then circulatory failure, then irreversible hypoxic-ischaemic brain injury. A complete explanation identifies that chain. Inspection, histology, examination of the airway and heart, and appropriately interpreted toxicology may establish it; an unexplained sudden death cannot be assigned a precise cause from its suddenness alone.