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The syringe used for taking blood arterial blood gas determinations should be coated with 1 mL of heparin (1000 units/mL) as an anticoagulant, but excessive heparin artificially lowers the PCO2 and HCO3– derived from that sample. If precise measurements of oxygenation are not needed or if oxygen saturation obtained from the pulse oximeter is adequate, venous blood gases generally provide useful information for assessment of acid-base balance and can be used interchangeably with arterial blood gases since the arteriovenous differences in pH and PCO2 are small and relatively constant. Venous blood pH is usually 0.03–0.04 units lower than that of arterial blood, and venous blood PCO2 is 7 or 8 mm Hg higher. Calculated HCO3– concentration in venous blood is at most 2 meq/L higher than that of arterial blood. An important exception to the rule of interchangeability between arterial and venous blood gases for determination of acid-base balance is during cardiopulmonary arrest. In this setting, arterial pH may be 7.41 and venous pH 7.15, and arterial blood PCO2 can be 32 mm Hg with a venous blood PCO2 of 74 mm Hg.
There are two types of acid-base disorders: respiratory and metabolic. Primary respiratory disorders affect blood acidity by causing changes in PCO2, and primary metabolic disorders are caused by disturbances in the HCO3– concentration. The primary disturbances are usually accompanied by compensatory changes, but these changes do not fully compensate for the primary acid-base disorders even if the disorders are chronic. Therefore, if the pH is less than 7.40, the primary process is acidosis (either respiratory or metabolic). If the pH is higher than 7.40, the primary process is either respiratory or metabolic alkalosis. The presence of one disorder with its appropriate compensatory change is a simple disorder.
The presence of more than one simple disorder (not compensatory) is a mixed disorder. Double or triple disorders can coexist but not quadruple ones, since simultaneous respiratory acidosis and alkalosis are not possible.
Clinicians frequently find it difficult to decide if a mixed disorder is present. One useful scheme is to determine if the degree of compensation for the primary disorder is appropriate. In respiratory disorders, if the magnitude of compensation in HCO3– level differs from that which is predicted, the patient has a mixed disorder. Therefore, superimposed metabolic acidosis will decrease HCO3– to lower than the predicted level, and a metabolic alkalosis will increase HCO3– over the predicted value. For example, a patient with chronic respiratory acidosis and PCO2 of 60 mm Hg should have a HCO3– of 31 meq/L (assuming that normal HCO3– is 24 meq/L). If the HCO3– is 25 meq/L, a superimposed metabolic acidosis exists, and if the HCO3– is 45 meq/L, there is a superimposed metabolic alkalosis.
Chronic respiratory acidosis is generally seen in patients with underlying lung disease, such as chronic obstructive disease. In chronic respiratory acidosis, the serum bicarbonate level should increase by 3.5 meq/L for each increment of 10 mm Hg PCO2. Urinary excretion of acid in the form of NH4+ and Cl– ions results in the characteristic hypochloremia of chronic respiratory acidosis. When chronic respiratory acidosis is corrected suddenly, especially in patients who receive mechanical ventilation, there is a 2- to 3-day lag in renal bicarbonate excretion, resulting in posthypercapnic metabolic alkalosis.
A. Symptoms and Signs: With acute onset, there is somnolence and confusion, and myoclonus with asterixis may be seen. Coma from CO2 narcosis ensues. Severe hypercapnia increases cerebral blood flow and cerebrospinal fluid pressure. Signs of increased intracranial pressure (papilledema, pseudotumor cerebri) may be seen.
B. Laboratory Findings: Arterial pH is low, and PCO2 is increased. Serum HCO3– is elevated, but not enough to completely compensate for the hypercapnia. If the disorder is chronic, hypochloremia is seen.
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