Interpretation of arterial blood gases

Published on 13/02/2015 by admin

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Interpretation of arterial blood gases

Bradly J. Narr, MD and Steven G. Peters, MD

The clinical utility of arterial blood gas (ABG) measurements includes assessment of oxygenation (arterial O2 tension [PaO2]), ventilation (arterial CO2 tension [PaCO2]), and acid-base status (pH). The bicarbonate (HCO3) value in an ABG measurement is calculated from the CO2 tension and pH, as opposed to the bicarbonate value on an electrolyte panel, which is actually measured. Modern blood gas machines also have a means to measure hemoglobin concentration and a co-oximeter to measure hemoglobin O2 saturation. These measurements allow quantitative assessment of the functions of the cardiorespiratory system. Recognition of abnormal measurements permits specific diagnostic and therapeutic interventions in the operating room, postanesthesia care unit, and intensive care unit. Specific clinical situations for which ABG analysis can guide patient care include management of hypoxia or hypercarbia, weaning from mechanical ventilation, use of permissive hypercapnia as a component of lung-protective ventilation strategies, and diagnosis and management of acid-base disorders.

Acid-base disturbances

Intracellular pH is tightly regulated; several buffering systems minimize the changes in pH that are associated with the addition of acid or base. In humans, the major extracellular buffer pair is bicarbonate/carbonic acid. The Henderson-Hasselbalch equation describes the effect of the dissociation of carbonic acid to hydrogen ion and bicarbonate:

< ?xml:namespace prefix = "mml" />pH =pK+logHCO3H2CO3

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Using 6.1 as the pK for carbonic acid, and expressing the concentration of carbonic acid as dissolved CO2 (0.03 × PCO2), the pH determined by the Henderson-Hasselbalch equation becomes:

pH=6.1+log(HCO3)0.03×PaCO2

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The physiologic response to an acid-base disturbance is threefold. Initially, the acid or base is buffered immediately in that body-fluid compartment. In plasma and interstitial fluid, bicarbonate is the major buffer, with proteins and phosphate compounds contributing to a lesser extent. In erythrocytes, hemoglobin is the major buffer, with bicarbonate contributing approximately 30% and phosphate 10% of the buffering capacity. Secondary and tertiary compensation for the underlying acid-base abnormality occurs via the lungs and kidneys. Elimination of CO2 by hyperventilation is the initial compensatory mechanism for metabolic acidemia. The kidneys eliminate organic acids and [H+] as ammonium ions and reabsorb bicarbonate from tubular fluids, with formation of titratable acid. Ultimately, however, to restore true homeostasis, the underlying pathophysiologic process must be corrected (e.g., administration of fluids and insulin for diabetic ketoacidosis or antibiotics for pneumonia in a patient with chronic obstructive lung disease).

Acid-base abnormalities are the result of pathophysiologic processes and are not unique disease entities. The differential diagnosis of any specific acid-base pattern begins with obtaining the patient’s history and performing a physical examination. Common conditions and disease states associated with acid-base disturbances include metabolic acidosis (septic or cardiogenic shock, renal failure, diabetic ketoacidosis), metabolic alkalosis (diuretics, nasogastric suction, vomiting), respiratory acidosis (narcosis, neuromuscular blockade or profound weakness of respiratory muscles, chronic obstructive pulmonary disease), and respiratory alkalosis (hyperventilation).