Histotoxic Hypoxia

Histotoxic Hypoxia develops when body is getting enough oxygen, but it cannot use it sufficiently due to physiological problems at a cellular level.

Thus due to a disruption of oxidative phosphorylation enzymes activity, tissue cells are unable to use the oxygen effectively.

Excessive drinking of alcohol or narcotics, can also produce such physiological effect.

In other cases histotoxic hypoxia can be developed by a person exposed to poisoning chemicals or gases in poorly ventilated or insufficiently controlled areas.

In such cases hemoglobin’s abilities to bind, transport and release oxygen are inhibited by poisoning gas. The examples of such cause of histotoxic hypoxia are Carbon Monoxide Poisoning, Cyanide Poisoning, Poison Gas attack or other toxic chemicals.

The injuries caused by carbon monoxide (CO) traditionally have been viewed as due to a hypoxic stress mediated by an elevated carboxyhemoglobin (COHb) level. The two organ systems most susceptible to injury from CO are the cardiovascular and central nervous systems. Human and animal data indicate that major cardiac injury is due primarily to CO-induced hypoxic stress.

Representing only 2-3% of an adult’s body mass, the brain receives 20% of the cardiac output and accounts for about one fourth of overall resting oxygen consumption. The brain is one of the most oxygen-sensitive organs of the body, and it is not surprising that neurologic dysfunction is a prominent manifestation of hypoxia.²⁶⁰

Cerebral vascular resistance is prominently affected by acute hypoxia and increases when PaO₂ falls below 50-60 mm Hg. However, with continued hypoxia, adaptation occurs, and overall cerebral blood flow in hypoxemic patients with COPD is normal. The brain is very sensitive to changes in perfusion, and effects of hypoxia on the brain are more likely to be due to decreased perfusion than to hypoxemia.²⁶⁰

Photo courtesy of Kyle Kesselring

Methylene chloride is another toxic component presented in a solutioins like paint thinners. It is converted to CO by the cytochrome P-450 after it enters the liver. Endogenously created CO derived from methylene chloride has a much longer half life than exogenously inhaled CO, but the symptoms are similar. CO poisoning should be suspected in persons who exhibit toxicity after using paint thinning products in a closed environment.

Another increasingly more common source of CO is propane-powered motors such as those found in warehouse fork lifts and ndustrial floor buffers. Ideally, these propane engines should burn cleanly if properly maintained. However, a poorly maintained propane engine will emit nearly as much CO as an internal combustion (gasoline) engine.

Since 1960, the clinical use of HBO₂ for CO poisoning has occurred with increasing frequency. Over 2,500 CO-intoxicated patients were treated in North American hyperbaric chambers in 1992. However, this is only a small fraction of those poisoned with CO. Extrapolation of data from a 1994 survey across three western states projected that over 4,000 CO-poisoned patients are evaluated in emergency departments annually in the United States.

Hyperbaric oxygen (HBO₂) significantly increases the oxygen diffusion driving force, thus increasing oxygen availability to tissues. This helps to correct negative effects of histotoxic hypoxia and restore normal tissue oxygenation.

In reported series, clinical recovery among patients treated with HBO₂ appears to be improved beyond that expected with ambient pressure supplemental oxygen therapy. This has been observed both in terms of mortality and neurologic morbidity. This research found that the optimal benefit from HBO₂ occurs in those treated with the delay after exposure and that repeat treatments may yield a better outcome than just a single treatment in selected patients.¹²¹

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