Giving patients with hypercapnia supplemental bicarbonate will worsen their condition if not adequately ventilating. This buffer equation is in constant flux. CO2 combines with H20 to form H2CO3, which dissociates into H+ and HCO3. Hypercapnia commonly causes respiratory acidosis. In patients with CO2 narcosis, the smooth muscle will relax, causing dilation of cerebral blood vessels, increasing cerebral blood flow, potentially causing increased intracranial pressure. As PaCO2 levels rise, cerebral blood vessels dilate, and as PaCO2 levels drop, cerebral blood vessels constrict. The belief is that changes in PaCO2 drive changes in the pH of the cerebral spinal fluid, causing relaxation or contraction of the smooth muscle. CO2 plays a fundamental role in the regulation of cerebral blood flow. Ĭerebral autoregulation is a process in which the brain works to maintain a constant and steady supply of nutrients and oxygen despite changes in cerebral perfusion pressure. Patients with chronic hypercapnia may not experience alterations in consciousness until PaCO2 exceeds 90 mmHg. Normal individuals do not experience alterations in consciousness until PaCO2 greater than75 mmHg. Patient baseline PaCO2 is important to consider in the development of CO2 narcosis. There is a hypothesis that there are increased levels of glutamine and gamma-aminobutyric acid(GABA) and decreased glutamate levels.

The current belief is that hypercapnia changes neurotransmitter levels involved with consciousness. It is more likely that this group only partially contributes to hypercapnia and is not commonly the primary cause but can occur in conditions that increase metabolic rate, sepsis, thyrotoxicosis, or fever.Įnvironmental exposure to areas rich in carbon dioxide, such as volcanoes or geothermal activity, puts patients at risk for carbon dioxide poisoning.Īnother unique situation to consider is oxygen-induced hypercapnia, which presents in some patients with COPD when given supplemental oxygen. The third group is anything that increases CO2 production. A large pulmonary embolism can also cause significant dead space. This condition can be due to pulmonary capillary compression (positive pressure ventilation) or the destruction of pulmonary capillaries (pulmonary vasculitides, COPD, asthma, interstitial lung disease). The second group is anything that increases physiologic dead space (part of the lung that does not participate in gas exchange) this is ventilation without perfusion. Deformity of the thoracic cage can impact tidal volumes, therefore decreasing minute ventilation. Notable etiologies include Guillain-Barre, myasthenia gravis, amyotrophic lateral sclerosis, myositis, multiple sclerosis, phrenic nerve injury, tetanus, botulism, organophosphates, and ciguatera. Decreased respiratory neuromuscular function can decrease minute ventilation. Although the medulla functions to control the respiratory drive, many peripheral nerves and respiratory muscles are needed to perform respirations. Notable etiologies include overdose of sedative medications (narcotics, benzodiazepines, tricyclic antidepressants, etc.), stroke, and hypothermia.

Anything that affects the central respiratory center can affect the minute ventilation. The central respiratory center in the medulla takes feedback from multiple inputs and integrates them into a respiratory drive, which functions to control our minute ventilation. The first group is anything that causes decreased minute ventilation (respiratory rate x tidal volume). The etiology can be extensive, but it can be helpful to divide the potential causes into three groups: decreased minute ventilation, increased physiologic dead space, increased carbon dioxide production. Overall, the driving mechanism of CO2 narcosis is acute hypercapnia.

Carbon dioxide poisoning