Arterial blood gas

An ABG is probably one of the most important and heavily utilized tests in the ICU. It provides information about the patient's respiratory status (oxygenation and ventilation), acid base status, and often times even provides a rapid assessment of hemoglobin and electrolyte levels. An ABG can be withdrawn from any artery and should be analyzed immediately (or immersed in iced water) to provide accurate information before leukocyte and reticulocyte metabolism ensue. The normal values for ABGs from a healthy young adult are:

Acidemia occurs when the hydrogen ion concentration in the blood rises above the normal range and alkalemia when it falls below it. Acidosis and alkalosis are the processes which lead to acidemia and alkalemia, respectively. Arterial hypox-emia occurs when the PaO2 is <8 kPa (60 mmHg) and arterial hypercapnia when the PaCO2 is >6.7 kPa (50 mmHg).

Actual bicarbonate is calculated from the Henderson-Hasselbach equation. Standard bicarbonate is the value obtained after correction of the PCO2 to 5.3kPa (40 mmHg). This correction is performed in order to remove any respiratory component. The base deficit is the amount of base needed to return the pH to 7.4.

Interpretation of the blood gases should be performed systematically. First, the arterial pH indicates whether the patient is acidemic or alkalemic. Next the PCO2 and the standard bicarbonate are inspected. PCO2 will be elevated in a respiratory acidosis and will be decreased in a respiratory alkalosis. Standard bicarbonate is low when there is metabolic acidosis and is elevated when there is metabolic alkalosis. The primary acid base disturbance will generally be accompanied by a compensatory response. For example, if a primary respiratory acidosis occurs, the body responds by increasing bicarbonate re-absorption and metabolic alkalosis results. However, not uncommonly in severely ill patients, compensatory mechanisms may be weak and there may be more than one reason for an acidosis. For example, a patient who has a cardiac arrest may have both a metabolic and respiratory acidosis, the metabolic acidosis occurring as a result of the absence of perfusion and the respiratory acidosis from the absence of respiration.

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