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Increased anions from toxic ingestion
12%
12/100
Decreased minute ventilation
5%
5/100
Decreased oxygen delivery to tissues
63%
63/100
Increased metabolic rate
2%
2/100
Decreased ability for the tissues to use oxygen
17%
17/100
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Type A lactic acidosis results from decreased oxygen delivery to tissues due to hypoxia or hypoperfusion. Increased lactic acid levels cause an anion-gap metabolic acidosis. Type A lactic acidosis can be seen in carbon monoxide (CO) poisoning that results from smoke inhalation. CO binds to hemoglobin (Hb) with an affinity more than 200 times that of oxygen. CO displaces oxygen from Hb, thereby decreasing the number of binding sites available for oxygen, which decreases the oxygen content of the blood. CO binding to Hb also shifts the oxyhemoglobin dissociation curve to the left, thereby decreasing the unloading of oxygen to tissues. The result is increased anaerobic metabolism, increased lactic acid production, and anion-gap metabolic acidosis. In addition the content of oxygen in the blood (CaO2) = (Hgb x 1.34 x SaO2) + (0.0031 x PaO2). You will notice in this equation that the CaO2 is determined primarily by the amount of hemoglobin and the saturation of hemoglobin, not the partial pressure of oxygen dissolved in the blood. In CO poisoning the amount of O2 dissolved in the blood (PaO2) is normal however O2 cannot bind to the hemoglobin (CO is binding with higher affinity), which is the major transporter of oxygen and rationale for the acidemia seen in this patient with a high PaO2. Kales reviews the diagnosis and management of CO poisoning. The presentation of CO poisoning may include neurologic symptoms such as headache and dizziness, as well as systemic symptoms such as nausea. Tachycardia and tachypnea are seen with more severe cases. When CO intoxication is a potential diagnosis, patients should be treated empirically with 100% O2 immediately and CO blood levels drawn to confirm. Blood levels greater than 10-15% indicate likely CO poisoning. Andersen et al. review the various causes of lactic acidosis. Elevated lactate can be caused by a variety of conditions including shock, sepsis, cardiac arrest, trauma, seizure, ischemia, diabetic ketoacidosis, thiamine deficiency, malignancy, liver dysfunction, genetic disorders, toxins, and medications. When approaching the patient with an elevated lactate level, the multiple etiologies must be considered. Illustration A depicts the effects of various metabolic changes on the oxyhemoglobin dissociation curve. Illustration B summarizes pathophysiologic classifications of lactic acidosis. Incorrect Answers: Answer 1: Ethylene glycol poisoning results in increased production of oxalic acid and glycolic acid. However, this patient's presentation is more concerning for CO poisoning. Answer 2: While reduced ventilation may cause a respiratory acidosis, the primary disturbance is low bicarbonate due to metabolic acidosis. Answer 4: Increased metabolic rate can cause lactic acidosis and occurs following seizures. Answer 5: Oxygen utilization is decreased in CO poisoning due to inhibition of cytochrome c oxidase by CO. However, this is not the major cause of acidosis in CO poisoning.
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