Opoid crisis

The action of Opoid crisis on hypothalamic nuclei also may be involved in producing slight fall in the body temperature.

Modulation of pain through diencephalic areas like periaqueductal grey, thalamic center and hypothalamic areas is produced.

The mid-brain (Mesencephalon) basal nuclei, especially due to excitation of parasympathetic region of Edinger Westphal nucleus of the oculomotor nerve leads to activation of sphincter pupillae and miosis.

This activity is dose dependent and is described as a “classical sign” of  “opioid toxicity”—”Pinpoint pupil”.

The Opoid crisis action on brain and other important centers situated in this have very high concentration of opioid receptors especially µ2 receptors leading to following effects:

 Respiratory depression:  These drugs when dealing with opoid crisis produce dose-dependent respiratory depression, i.e., reduction in responsiveness of brainstem (pontine and medullary) respiratory centers to increases in carbon dioxide tension (Paco2). The death in opioid poisoning is almost always due to respiratory arrest.

The rate, tidal exchange and net minute volume are decreased. Initially there may be compensatory increase in tidal volume leading to deep, slow sighing type of respiration of 4—6 breaths/mm (apneustic breathing).

The peculiarity of this respiratory pattern in opoid crisis is, if the patient is forcibly kept conscious and stimulated, then the breathing will continue. If left alone, patient may become apnoeic and remains so.

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