The presence of cyanosis suggests the possibility of hypoxemia, and pulse oximetry analysis is readily available to assist the physician in the early diagnosis of hypoxemia and provide continuous oxygen saturation measurements. However, an exception occurs when the hemoglobin is in a state in which it is unable to bind to oxygen (i.e., methemoglobin or carboxyhemoglobin). In such situations, pulse oximetry analysis not only overestimates the oxygen saturation but also reflects a diminished response to any supplemental oxygen. ABG analysis with co-oximetry is still the gold standard in the assessment of any patient with suspected cyanosis. In central cyanosis, the oxygen saturation of the ABGs is decreased due to the underlying hypoxia. In peripheral cyanosis, assuming normal cardiopulmonary and hemoglobin status, the oxygen saturation should be normal. If methemoglobinemia or carboxyhemoglobinemia is suspected, the ABG analysis will show a normal PaO2 (reflecting a normal amount of dissolved oxygen in the plasma), a normal calculated oxygen saturation (from the normal Pa o2), and a decrease in measured oxygen saturation (due to decreased number of oxygen binding sites).

Few tests are as vulnerable to errors introduced by improper sampling, handling, and storage as are ABG analyses. The technical difficulties with obtaining an arterial sample via percutaneous puncture accounts for much of the high preanalytic error rate for isolated ABG samples obtained in the emergency department, compared to a low error rate for samples obtained from an indwelling arterial catheter.

Special attention should be given to the following sources of preanalytic error with ABG samples:

1. Heparin is the anticoagulant of choice, and one make sure that the syringe is flushed with heparin and then emptied thoroughly. This will allow adequate anticoagulation of a 2- to 4-mL blood sample with assurance that the results will not be altered by the anticoagulant. Excessive heparin affects the pH, P co2, and Po2 as well as the hemoglobin determination.

2. Air bubbles that mix with the blood sample will result in gas equilibration, significantly lowering the P co2 values with an increase in pH and Po2. Any sample obtained with more than minor air bubbles should be discarded.

3. Reducing the temperature of the blood by placing the sample immediately in an ice slush will significantly deter changes in the P co2 and pH for a period of several hours. If the sample is not iced immediately, changes can be significant. As a general rule, arterial blood samples should be analyzed within 10 min or cooled immediately. Failure to properly cool the sample is a common source of preanalytic error.

Hypoxemia, anemia, and polycythemia can be diagnosed by means of hemoglobin and ABG determination. The red cyanosis of polycythemia vera occurs because the increase in the number of red blood cells and the hemoglobin concentration results in sludging of blood flow in cutaneous capillaries and venules. Similarly, cyanosis is enhanced in chronic hypoxemia accompanied by polycythemia.

If the Pao2 and the hemoglobin concentration are normal, the cyanosis may be due to abnormal skin pigmentation or abnormal hemoglobin. The term pseudocyanosis is used to describe a blue, gray, or purple cutaneous discoloration that may mimic cyanosis. Pseudocyanosis can be caused by heavy metals [e.g., iron (hemochromatosis), gold, silver, lead, or arsenic] or drugs (e.g., phenothiazines, minocycline, amiodarone, or chloroquine). Chrysiasis is a specific type of pseudocyanosis that is characterized by a gray, blue, or purple pigmentation of areas exposed to light. It is a rare dose-dependent complication of gold treatment that tends to cause permanent discoloration of the skin. Another example of pseudocyanosis is argyria, which is a slate blue-to-gray coloration of the skin resulting from either chronic ingestion or chronic local application of silver salts or colloidal silver. In pseudocyanosis the skin does not blanch with pressure, in contrast to true cyanotic skin, which does blanch. Carboxyhemoglobinemia does not cause cyanosis. Occasionally, however, carboxyhemoglobinemia does produce a cherry-red flush of the skin, retina, or mucous membranes.

Cyanosis can be caused by methemoglobinemia and sulfhemoglobinemia. Most cases are due to chemicals or medications. Although a wide range of drugs can produce methemoglobinemia, benzocaine, nitrates, and nitrites are the most common agents implicated in drug-induced methemoglobinemia. Sulfhemoglobinemia most commonly results from either phenacetin or acetanilid (Bromo Seltzer). Industrial aniline compounds may produce either sulfhemoglobinemia or methemoglobinemia.

The incidence of acquired methemoglobinemia secondary to industrial exposure to aniline dyes and aromatic amino and nitro compounds has decreased with improvement in occupational health standards. Hereditary methemoglobinemia is a rare genetic disorder affecting the enzyme NADH-methemoglobin reductase, resulting in structural alterations of the hemoglobin molecule. This enzyme is the major pathway responsible for converting methemoglobin to its reduced state. This pathway plays a clinically significant role in the treatment of methemoglobinemia because it is the pathway by which the antidote, methylene blue, is able to enhance the reduction of methemoglobin. Patients with NADH-methemoglobin reductase deficiency appear cyanotic but are usually compensated and asymptomatic.

Methemoglobinemia produces visible cyanosis with as little as 1.5 g of methemoglobin per 100 mL of blood. Since methemoglobin is incapable of binding with oxygen, the symptoms of methemoglobinemia are secondary to hypoxia, and the severity is related to the quantity of methemoglobin present, the rapidity of onset, and the patient's cardiopulmonary system. Cyanotic patients without cardiovascular or pulmonary disease should be suspected of having methemoglobinemia, especially if cyanosis is not relieved by oxygen administration. An additional clue is that venous blood will appear chocolate brown. Spectrophotometric analysis is required for identification of the pigment and its quantity.

Sulfhemoglobin is inert as an oxygen carrier and can produce deep cyanosis at a level of less than 0.5 g of sulfhemoglobin per 100 mL of blood. Unlike methemoglobinemia, sulfhemoglobinemia is irreversible. Treatment is directed toward symptomatic and supportive care as well as the identification and removal of suspected agents.

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