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GALA Fin de Temporada 2022 Group

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Nolan Rivera
Nolan Rivera


The well-known correlation between the hydrophobicity of narcotic chemicals and the exposure concentration needed to produce an effect indicates that a lipid phase in the aquatic organism is the most likely target. The molar concentration in aquatic organisms at death is found to be approximately constant for different narcotic chemicals, varying from 2 to 8 mmol/kg organism. Because the proportion of lipid is known, the lethal in vivo membrane burden can be calculated to be 40 to 160 mmol/kg lipid. The exact mechanism underlying narcosis is still unknown. However, disturbance by narcotic chemicals in model membrane systems has been investigated, attention having been paid to disturbance of phospholipids and proteins, and of the interaction between the two groups. Model membrane burdens of different chemicals have been shown to be approximately constant for a particular effect. Different effects are found at different membrane concentrations. In the present review, the toxicity of narcotic chemicals to aquatic organisms is discussed, the possible mechanisms underlying narcosis are reviewed, and a comparison is made between membrane burdens that are lethal in vivo and membrane burdens that cause an effect in in vitro systems.


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Carbon dioxide (CO2) narcosis is a condition that develops when excessive CO2 is present in the bloodstream, leading to a depressed level of consciousness. This condition largely results from lung disease, hypoventilation, or environmental exposure. This activity reviews the evaluation and treatment of CO2 narcosis and highlights the role of the interprofessional healthcare team in improving care for patients with this condition.

Objectives:Outline the typical presentation of a patient with carbon dioxide narcosis.Describe the pathophysiology of carbon dioxide narcosis.Summarize the treatment and management options available for carbon dioxide narcosis.Explain the importance of improving care coordination amongst interprofessional team members to enhance care delivery for patients with carbon dioxide narcosis. Access free multiple choice questions on this topic.

Hypercapnia, a state of elevated serum carbon dioxide (CO2), can manifest as a broad spectrum of disease, the most severe of which is CO2 narcosis. The delineating feature of CO2 narcosis is a depressed level of consciousness. It is essential to recognize impending or current CO2 narcosis; if left untreated, it can result in coma or death. This article primarily focuses on CO2 narcosis, but it is crucial to appreciate that hypercapnia has multiple end-organ effects contributing to the patient's deterioration. Many etiologies contribute to hypercapnia; the most commonly encountered is chronic obstructive pulmonary disease (COPD). Treatment is focused on fixing the underlying cause and demands an interprofessional approach to optimize patient outcomes.

Overall, the driving mechanism of CO2 narcosis is acute hypercapnia. 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.[1]

The epidemiology of CO2 narcosis is difficult to ascertain due to all the possible disease entities contributing to it. Given that most hypercapnia cases result from lung diseases that increase dead space, one can make a generalized estimation. Approximately 5% of the US population is affected by COPD, and it appears to be more prevalent in women than men. Of this 5%, not all patients with COPD will develop CO2 narcosis. The prevalence of COPD increases as age increases but is more common over the age of 45.[2][3][4]

The current belief is that hypercapnia changes neurotransmitter levels involved with consciousness. There is a hypothesis that there are increased levels of glutamine and gamma-aminobutyric acid(GABA) and decreased glutamate levels.[5][6][7] Patient baseline PaCO2 is important to consider in the development of CO2 narcosis. Normal individuals do not experience alterations in consciousness until PaCO2 greater than75 mmHg. Patients with chronic hypercapnia may not experience alterations in consciousness until PaCO2 exceeds 90 mmHg.[8]

Cerebral 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. CO2 plays a fundamental role in the regulation of cerebral blood flow. 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. As PaCO2 levels rise, cerebral blood vessels dilate, and as PaCO2 levels drop, cerebral blood vessels constrict.[9] 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.

CO2 narcosis is classically considered in patients with a history of sedative use or chronic lung diseases that increase dead space, such as COPD. However, there is a wide range of etiologies that can contribute to CO2 narcosis. Identifying a risk factor or underlying disorder can help with its identification. Perhaps the patient is known to be a drug user or smokes tobacco. In the latter, be on the lookout for clubbing or wheezing. When evaluating the patient, look at the patient's body habitus. Evaluate for thoracic cage abnormalities or obesity. Inquire about a known history of neuromuscular disorders. If the patient just had surgery with anesthesia, consider that the patient was in a state of hypoventilation. An important point to note is that the patient does not need to be hypoxemic to be hypercapnic. If the patient is on supplemental oxygen and has an acceptable oxygen saturation due to hypoventilation, the patient may retain CO2. This situation can exist in COPD. Patients may be compensating with increased work of breathing, allowing them to have an acceptable PaO2, but as a consequence of the tachypnea, there is less time for exhalation, contributing to the hypercapnia. When the patient develops sufficient hypercapnia, the respiratory drive can decrease with subsequent hypoventilation and a decreased level of consciousness. Additionally, giving a hypoxic patient supplemental oxygen in COPD or another hypoventilation state can worsen the hypercapnia.[20][21]

The labs and studies obtained help build a complete picture of why the patient has CO2 narcosis. A complete blood count can be informative for the chronically hypoxic patient, as it can detect polycythemia. Serum chemistry can reveal an elevated bicarbonate level, reflecting the patient's body trying to compensate for the acidosis from chronic hypercapnia. ABG analysis is critical in the evaluation of CO2 narcosis. A PaCO2 greater than 45 mmHg is considered hypercapnia. Determining whether the patient's hypercapnia is acute or chronic depends on the accompanying pH. Acute hypercapnia typically has a pH of less than 7.35. Chronic hypercapnia has near-normal pH. A toxicology screen, including opiates and benzodiazepines, helps determine a possible cause. Thyroid function tests may reveal findings consistent with hypothyroidism. A chest X-ray should be performed on these patients to evaluate for hyperinflation, flattened diaphragms, thoracic cage abnormalities, or diaphragm abnormalities. CT imaging of the neck or brain should not be done routinely, only in select patients with a high degree of suspicion for a stroke, tumor, or traumatic dissection.[8]

As stated above, the initial patient encounter should always begin with evaluating the airway, breathing, and circulation. After addressing and securing these, the rest of the treatment can proceed. The goal of therapy is to determine the underlying cause and correct the hypercapnia. If the patient is having a COPD exacerbation, treat the patient with bronchodilators and steroids. In patients with suspected overdose, consider antidotes for reversal of sedative medications such as naloxone for opiate overdose. If the patient has significant pneumonia, it is necessary to include antibiotics in the treatment. If the patient has developed anaphylaxis that has threatened their airway, they need to be intubated and started on therapies including H1 and H2 blockers, corticosteroids, and epinephrine. If the patient already has a depressed level of consciousness, with poor respiratory effort or impending respiratory failure, they need to be intubated, followed by mechanical ventilation. Non-invasive ventilation is inappropriate for patients with CO2 narcosis due to the high risk of aspiration of gastric contents. These patients require admission to the ICU for close monitoring. A repeat ABG analysis is needed to monitor for improvement of PaCO2 while undergoing mechanical ventilation. If the patient has new-onset acute hypercapnia, the goal is a correction to normocapnia. If the patient has acute on chronic hypercapnia, the goal is back to the patient's baseline levels.[8] In the rare case that the individual had environmental exposure to high levels of carbon dioxide, the first step is to remove the individual from the environment and then treat accordingly, as stated above.

Patients that present with a depressed level of consciousness have a broad differential, and many etiologies need to be considered, such as toxins, sedative drugs, metabolic derangements, infections, and supratentorial or infratentorial abnormalities.[28] The clinician can differentiate CO2 narcosis by both a depressed level of consciousness and hypercapnia. The diagnosis of CO2 narcosis and ruling out other disease processes depends on the clinical presentation, lab findings, and imaging.

A complication that can occur when managing a patient with CO2 narcosis is overcorrecting the chronic hypercapnia in a patient with underlying COPD. Overcorrecting can result in alkalemia, reducing respiratory drive, and possibly induce seizures.[29] Mechanically ventilated patients can develop barotrauma, volutrauma, oxygen toxicity, ventilator-associated pneumonia, or auto-PEEP.[29][30] 041b061a72


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