Arterial blood gas analysis is an effective way to determine the acid-base status of blood. Correct interpretation not only allows efficient acid-base status determination, but it also will determine whether the cause is respiratory or metabolic.
Normally, the body will attempt to compensate for an acid-base abnormality. That is, the kidneys adjust bicarbonate reabsorption when respiratory disorders exist, and the respiratory system attempts to compensate for metabolic disorders. The following equations will determine the expected change in PaCO2 when a metabolic disorder is present:
For metabolic acidosis:
For metabolic alkalosis:
If the actual PaCO2 is different than the above calculated value for a given ABG with a metabolic disorder, then there is also an associated respiratory disorder present. If the actual PaCO2 is greater than the calculated value, then there is an associated respiratory acidosis. If the actual PaCO2 is less than the calculated value, then there is an associated respiratory alkalosis.
Acidosis may result from hypoventilation (respiratory) or from an underlying metabolic disorder. There are two types of metabolic acidosis, a high anion gap acidosis and a non-gap (normal anion gap) acidosis. Non-gap acidosis is associated with renal tubular acidosis (RTA), chronic renal insufficiency, and diarrhea. Vomiting may also be associated with a non-gap acidosis if the vomitus originates from an intestinal site because it would then be very alkalotic. A high gap acidosis is secondary to ingestion of toxic levels of certain substances (ethanol, methanol, aspirin, paraldehyde and ethylene glycol), chronic renal failure, diabetic ketoacidosis, and lactic acidosis.
Lactate is produced during glucose metabolism at a rate of 1mEq/kg/hour. The normal serum level is 2 mEq/L but may increase to 4 mEq/L in response to strenuous exercise. Common causes of lactic acidosis include sepsis, hypoxia, cardiogenic shock, thiamine deficiency, D-lactic acidosis, seizure activity, and the administration of certain medications to include epinephrine and nitroprusside. D-lactic acidosis should be suspected in patients who present with acute neurologic dysfunction, a high-gap acidosis, an intact colon and a past surgical history significant for resection of the small intestine. The diagnosis is confirmed by measuring the D-lactate level. Acute treatment entails carbohydrate restriction, intravenous rehydration, and the administration of poorly absorbed oral antibiotics (clindamycin, tetracycline, vancomycin or neomycin). Long term therapy entails a low carbohydrate diet, measures to guard against thiamine deficiency, and possible long term antibiotic therapy.
In chronic renal failure, acidemia may occur early in the course of the disease or it may not present until the GFR falls to less than 20 ml/min. The acidosis that develops early has a different pathologic cause than the later-developing acidosis. Mild hyperchloremic acidosis is a non-gap acidosis that occurs early in the course of renal disease. The later-occurring acidosis is the result of impaired renal ammonia production, which results in insufficient urinary hydrogen ion buffering.
Symptoms of acidosis result from depression of the central nervous system and include altered mental status, or in severe cases, coma. Metabolic acidosis is associated with hyperventilation. Respiratory acidosis is associated with hypoventilation; however, hypoventilation is usually the cause, not a symptom, of respiratory acidosis.
Metabolic alkalosis is a common abnormality. Determination of a random urinary chloride helps determine the etiology. A low urinary chloride (<15 mEq/L) is consistent with a chloride responsive alkalosis whereas a high urinary chloride (>15 mEq/L) is consistent with a chloride resistant alkalosis. If the blood pressure is elevated with a chloride resistant alkalosis, then the differential diagnosis includes primary hyperaldosteronism, Cushings syndrome, adrenogenital syndrome, renal artery stenosis, or licorice ingestion (licorice containing glycyrrhizic acid). A chloride-resistant alkalosis not associated with hypertension is often secondary to hypomagnesemia or hypokalemia. A chloride-responsive alkalosis is usually associated with volume contraction. Common etiologies include diuretic use (excluding carbonic anhydrase inhibitors as they induce urinary bicarbonate wasting), vomiting, nasogastric suctioning, volume contraction, and post hypercapnia.
The first step in determining the underlying etiology of a respiratory alkalosis is to calculate the alveolar-arterial (A-a) oxygen gradient. The normal value is 20 or less, but this increases to 30 in the elderly older than 60 years of age. The differential diagnosis for a respiratory alkalosis with a normal A-a gradient includes sepsis, hyperventilation, encephalopathy, and liver disease (cirrhosis). When there is a respiratory alkalosis with an elevated A-a gradient, the differential diagnosis includes congestive heart failure, asthma, pneumonia, pneumothorax, and pulmonary emboli.
Symptoms of alkalosis result from overexcitability of the central nervous system. Symptoms include tetany, which usually starts in the musculature of the forearms and spreads to the face and eventually the entire body.
Treatment for an acid-base disorder is to determine and correct the underlying causative agent. Oral sodium bicarbonate is effective at neutralizing excess acid. Intravenous sodium lactate or sodium gluconate may also be effective. Controversy surrounds the use of intravenous sodium bicarbonate as therapy for acidosis as some believe that this causes a paradoxical worsening of the acidosis. Oral therapy for alkalosis entails ammonium chloride or lysine monohydrochloride. The ammonium portion of ammonium chloride undergoes hepatic conversion into urea, and this reaction produces hydrochloric acid.
Hypoxia refers to a measured PaO2 that is lower than the expected PaO2. The PaO2 varies depending on the age of the patient, and the expected PaO2 value may be calculated from the following equation using age as the only variable:
The cause of hypoxia should be determined so that appropriate therapy may be administered. The first step in determining the cause is to calculate the A-a gradient. Hypoxia associated with a normal A-a gradient may be secondary to either hypoventilation or a decreased FI02. Hypoxia with an elevated A-a gradient is due to either ventilation-perfusion mismatching (pulmonary emboli, pneumonia), intracardiac or intrapulmonary shunting of blood (cardiac septal defects or pulmonary arteriovenous malformations) or diffusion abnormalities (emphysema, interstitial lung disease). The workup should be dictated by the suspected etiology; however, pulmonary angiography (pulmonary emboli or intrapulmonary shunts), echocardiography (intracardiac shunts), and chest computed tomography (interstitial disease) often provide a thorough evaluation.
Platypnea-orthodeoxia syndrome refers to tachypnea and decreased O2 saturations (measured by pulse oximetry) upon moving to a standing position. Values are normal while seated or supine. Right to left shunting of blood is the underlying cause. This condition may be seen with hepatic cirrhosis, pulmonary arterio-venous malformations, chronic pulmonary embolism, intracardiac shunting and postpneumonectomy.