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Poisoning by belladonna characteristically combines delirium with dry secretions and dilated pupils; poisoning by hydrocyanic acid can cause very rapid collapse with failure of breathing. The two patterns are distinctive descriptions, not infallible diagnoses from one symptom.

With belladonna, expect dryness of the mouth and throat, difficulty swallowing, blurred vision and mydriasis. The skin may become hot, dry and flushed; the pulse is often rapid. Restlessness, confusion, visual hallucinations and agitated delirium may be prominent: the person may talk incoherently or pick at imaginary objects. Reduced intestinal activity and urinary retention can accompany the dryness. Severe poisoning can proceed to seizures, depressed consciousness, coma and circulatory failure. This is now understood chiefly as an antimuscarinic poisoning syndrome produced by alkaloids including atropine, which oppose the action of acetylcholine at muscarinic receptors.^[ref]

Hydrocyanic acid is hydrogen cyanide, historically also called prussic acid. Depending on the route and amount, early complaints may include dizziness, headache, anxiety, nausea, weakness and a sense of suffocation. Rapid breathing may give way to slow or failing breathing, followed by seizures, coma, circulatory collapse and death. A sufficiently large exposure may be so rapid that an elaborate sequence of preliminary symptoms is not observed. There is no single obligatory interval from exposure to collapse.^[ref]

In modern terms, cyanide impairs cellular use of oxygen, including inhibition of cytochrome c oxidase in cellular respiration. An apparently oxygenated colour therefore cannot exclude serious poisoning. A bitter-almond odour is an unreliable clue: it may be absent or not perceived, and no examiner should intentionally smell a suspect sample. The historical term “narcotic poison” does not mean that either belladonna or hydrogen cyanide acts like an opioid. The receptor and cellular explanations above are present scientific interpretations, rather than molecular explanations available in 1864.^[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.