Article Dexmedetomidine: A Comprehensive Review of Pharmacology, Cli...

The efficacy of dexmedetomidine in managing pain and sedation has been studied extensively, and several clinical trials and meta-analyses have compared its efficacy to traditional opioids and sedatives. Here's a summary of the evidence:

Overall, the evidence suggests that dexmedetomidine is a valuable alternative to traditional opioids and sedatives for managing pain and sedation in various clinical settings. Its unique pharmacological profile, including sedative, analgesic, and anxiolytic properties, makes it particularly well-suited for use in critically ill patients and those requiring sedation with minimal respiratory depression. However, individual patient factors and clinical context should always be considered when selecting the most appropriate sedative and analgesic regimen.

I am a board-certified American anesthesiologist. There is near-universal confusion among anesthesiologists, other medical specialists, and patients about the differences between and among anesthetic inhalation agents, sedative/hypnotic agents, and genuine analgesic agents, so that all these types of drugs are commonly used interchangeably to control pain. Unfortunately, this is slipshod practice that can cause unnecessary harm to patients. Some definitions are in order.

Nociception is nervous signals generated by nervous sensors in the skin and internal organs that detect tissue distortion and disruption. These are called “nociceptors.”

Consciousness is nervous activity generated by the cerebral cortex that works closely with memory mechanisms to combine all forms of nervous sensory information into a cohesive perception of the surrounding environment.

Pain is the interpretation of nociception by consciousness, much like sound is the interpretation of auditory nervous signals from the ear by consciousness.

Sedative/hypnotic agents including anesthetic inhalation agents, benzodiazepines, barbiturates, beverage alcohol, Propofol and Precedex all progressively inhibit consciousness in a dose-related manner. They can abolish the ability of consciousness to perceive pain long before they eliminate environmental awareness and the ability to speak coherently. Ether is an excellent example of this. It has a high solubility coefficient so that it takes effect slowly, so that a surgical patient’s consciousness can be partially obtunded to the point that he can no longer interpret nociception as pain, but still remains awake and able to carry a conversation, even when his leg is being amputated.

The gate theory of Melzac and Wall explains the danger of using anesthesia alone to control surgical stress, or using sedative/hypnotic agents to control pain. Consciousness generates corticofugal (descending) inhibitory signals from the cerebral cortex to the spinal cord to continuously inhibit and regulate spinal cord pathways that convey nociception signals to BOTH the brain AND sympathetic ganglia in the chest and abdomen. Using sedative/hypnotic/anesthetic agents to suppress consciousness abolishes fear, anxiety, and the ability to perceive the perception of nociception as pain BUT they simultaneously suppress the corticofugal inhibitory signals that regulate spinal cord nociception. As a result, they indirectly EXAGGERATE SYMPATHETIC NERVOUS ACTIVITY THAT INCREASES MICROVASCULAR FLOW RESISTANCE IN ORGANS AND TISSUES, AND UNDERMINES TISSUE PERFUSION AND OXYGENATION. They are also inherently toxic, and they cause toxic depression of respiratory drive and organ function.

Narcotics inhibit spinal cord nociception pathways to prevent nociception from reaching either the brain or sympathetic ganglia. They have virtually no toxicity, but they obtund respiratory chemoreceptors and depress respiratory drive until accumulating body reserves of carbon dioxide accumulate and stimulate respiratory chemoreceptors to counteract the respiratory depressant effects of the narcotics. Thus narcotics are extremely safe if they are administered in small divided doses that allow accumulation of body reserves of carbon dioxide.

Local analgesics such as lidocaine can block nociceptors and nociception pathways in peripheral sensory nerves and the spinal cord.

NSAID agents inhibit nociceptors directly, but they are extremely toxic.

Carbon dioxide is the primary regulator of the capillary gate mechanism. It directly releases nitric oxide from the vascular endothelium to cause “Nitrergic neurogenic vasodilation” that reduces microvascular flow resistance and increases tissue perfusion. Hypercarbia simultaneously exaggerates the release of oxygen from hemoglobin to elevate cellular oxygen delivery.

Mechanical hyperventilation is extremely dangerous and confers no benefits. It depletes CO2 body reserves, dangerously undermines respiratory drive, cardiac output, tissue perfusion, and tissue oxygenation. It is incompatible with beneficial narcotics.

Narcotics and hypercarbia go together like love and marriage. The hypercarbia counteracts the respiratory depression caused by narcotics, and simultaneously promotes cardiac output, tissue perfusion, and tissue oxygenation. Narcotics inhibit harmful sympathetic nervous hyperactivity that exaggerates microvascular flow resistance and inhibits tissue perfusion.

Read my attached paper that reviews the pathophysiology of carbon dioxide and the criminal history of the anesthesiology profession that has caused a deadly hoax that has derailed and reversed medical progress. Even better, explore my website www.stressmechanism.com where you can download relevant papers free of charge.