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Simple acid-base disturbances can be evaluated using the following strategy.
Combining this information, the following options are possible:
Acid-base disturbances are an important part of laboratory investigation of acutely ill patients. The common disturbances are acute respiratory acidosis or alkalosis and acute metabolic acidosis. Acute metabolic alkalosis is unusual. Mixed respiratory acidosis and metabolic acidosis is seen in the severely injured or infected patient.
Acute respiratory acidosis results from hypoventilation due to loss of respiratory drive, neuromuscular or chest wall disorders, or rapid, shallow breathing, which increases the fraction of dead-space ventilation. Acute respiratory alkalosis is caused by hyperventilation due to anxiety, central respiratory stimulation (e.g., in salicylate poisoning), or excessive artificial ventilation. Acute respiratory alkalosis usually accompanies acute metabolic acidosis, in which case the reduction in PCO2 from baseline (usually 40 mm Hg) is equal to the magnitude of the BD. For example, in a patient with lactic acidosis with a lactate concentration of 10 mEq/L, the BD should be -10, and the PCO2 should be 30 mm Hg. If the PCO2 is higher than expected, there is a problem with the respiratory apparatus. This is seen, for example, in a multitrauma patient who has massive blood loss, causing lactic acidosis, and a flail chest, causing respiratory acidosis.
Acute metabolic acidosis is caused by an alteration in the SID or ATOT . The SID is changed by an alteration in the relative quantity of strong anions to strong cations. This can be caused by anion gain, as occurs with lactic acidosis, renal acidosis, ketoacidosis, and hyperchloremic acidosis, or by cation loss, as occurs with severe diarrhea or renal tubular acidosis. Acidosis also results from increased free water relative to strong ions; dilutional acidosis, which occurs with excessive hypotonic fluid intake; certain poisonings, such as methanol, ethylene glycol, or isopropyl alcohol; hyperglycemia; or after mannitol administration.
To investigate acute metabolic acidosis in previously healthy patients, simple observational and mathematical tools such as the AG and BD are useful ( Table 41-4 ). The BD merely demonstrates the presence of an acid-base anomaly; the AG (= [Na+ + K+ ] − [Cl− + HCO3 − ]) separates acidosis due to hyperchloremia (e.g., renal tubular acidosis, excessive administration of normal saline) from that caused by UMAs and dilution. Many UMAs, such as lactate and ketones, are measurable. When a patient presents with acute metabolic upset caused by trauma, exsanguination, loss of consciousness, or tachypnea, a blood gas determination, electrolyte panel, serum osmolality level, and urinalysis should be obtained.
| 1. Is the acidosis caused by measured or unmeasured anions (e.g., chloride)? |
| Look at the blood chemistry: |
| Calculate the anion gap: Na + K - Cl = 10 to 12. |
| If the gap is normal, there is too much chloride present from excessive administration, excess loss of sodium (e.g., diarrhea, ileostomy), or renal tubular acidosis. |
| If the gap is wide (>16), other unmeasured anions are present, causing the acidosis. |
| Check the serum lactate level; if > 2, lactic acidosis is probably the cause: |
| If the high lactate level is explained by circulatory insufficiency (e.g., shock, hypovolemia, oliguria, under-resuscitation, anemia, carbon monoxide poisoning, seizures), this is type A lactic acidosis. |
| If not explained by circulatory insufficiency, consider the type B lactic acidosis (rare) causes, such as biguanides, fructose, sorbitol, nitroprusside, ethylene glycol, cancer, and liver disease. |
| Look at the creatinine and urine output: |
| If the patient is in acute renal failure, the identified molecules may be renal acids. |
| Assess the blood glucose and urinary ketone levels. |
| If the patient is hyperglycemic and ketotic, this condition is diabetic ketoacidosis. |
| If the patient is ketotic (unmeasured anion) and normoglycemic, this condition is alcoholic (check blood alcohol) or starvation ketosis. |
| Check for chronic alcohol abuse (e.g., high mean corpuscular volume, raised γ-glutamyl-transferase level on the liver panel). |
| 2. If all of the previous tests are negative, consider intoxication as a cause. |
| The toxicology laboratory can assess samples (particularly salicylates) and serum osmolality. Osmolality is calculated with the following formula: 2 (Na + K) + Glucose/18 + BUN/2.8. |
| Look for an unmeasured source of osmoles. If the gap between the measured and calculated serum osmolality is more than 12, consider an alcohol, particularly ethylene glycol, isopropyl alcohol, and methanol, as the cause. |
In cases of acute metabolic acidosis, three diagnoses should be immediately investigated: lactic acidemia (the serum lactate level should mirror the magnitude of the BD), ketoacidosis due to diabetes (the patient should be hyperglycemic and have positive urinary ketones), and acute renal failure, demonstrated by high serum urea and creatinine levels and a low total CO2 level. The latter condition is a diagnosis of exclusion. A low serum sodium concentration (>135 mEq/L) should alert the clinician to the possibility of a dilutional acidosis caused by alcohol poisoning. Alcohols such as ethanol, methanol, isopropyl alcohol, and ethylene glycol are osmotically active molecules that expand extracellular water; glucose and mannitol have the same effect but also promote diuresis because the molecules are small enough to be filtered by the kidney. Alcohol poisoning is suspected by the presence of an osmolar gap; a difference between the measured and calculated serum osmolality of greater than 12 mOsm demonstrates the presence of unmeasured osmoles. Toxicology laboratories can investigate for the presence of various toxic alcohols.
Acid-base disturbances are indicative of significant underlying pathology. Acute respiratory failure may be caused by a variety of pathologies, including neurologic injury (e.g., stroke, spinal cord injury, botulism, tetanus), toxic suppression of the respiratory center (e.g., opioids, barbiturates, benzodiazepines), neuromuscular disorders (e.g., Guillain-Barré syndrome, myasthenia gravis), abdominal hypertension, flail chest, hydro-hemo-pneumo-thorax, pulmonary edema, and pneumonia. Frequently, mechanical ventilation is required to reverse the acidosis.
Lactic acidosis is caused by increased glycolytic production of lactate. When hypoxemia or hypoperfusion is present, it is called type A lactic acidosis. When hypoxemia or hypoperfusion is absent, it is called type B lactic acidosis, which is associated with inborn errors of metabolism, some drugs such as biguanides, and toxins. Lactate is metabolized to carbon dioxide and water in the liver by means of the Cori cycle.
Diabetic ketoacidosis is characterized by ketosis and hyperglycemia. Ketone bodies are produced from β-hydroxylated fatty acids in states of starvation or insulin deficiency. They include acetate, acetoacetate, and β-hydroxybutyrate. The ketone bodies act as strong ions, causing metabolic acidosis. Patients with diabetic ketoacidosis have acidosis caused by ketones and lactate, as well as hypoperfusion. They are characteristically dehydrated because of hyperglycemia-induced diuresis.
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CASE 1 A 45-year-old man is admitted after a motor vehicle crash. He is bleeding, and his pulse is thready. His blood pressure is 90/50 mm Hg, heart rate is 120 beats/min, respiratory rate is 36, and temperature is 35°C. A serum chemistry panel and blood gas determinations are obtained. Consider the resulting data for the patient (in mEq/L unless otherwise stated): Na+ = 144, K+ = 4, Cl- = 110, total CO2 = 8, urea = 10, creatinine = 2.0, albumin = 4.0, lactate = 16.0, pH = 7.28, PCO2 = 24, HCO3 = 8, BE = -16, AG = 26, and corrected AG = 27.25. Does he have any acid-base disturbances?
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| Acidifying Processes | Magnitude | BDC | Alkalinizing Processes | Magnitude | BEC |
|---|---|---|---|---|---|
| Hyperchloremia | 120 mEq/L | -17 | Hypernatremia | 148 mEq/L | +2.4 |
| Lacticemia | 5 mEq/L | -5 | Hypoalbuminemia | 2.0 g/dL | +8.5 |
| Total |
|
-22 | Total |
|
+11.9 |
Using simple measures such as BDE to follow the resuscitation, the clinician might assume, based on the BD, that serum lactate was significantly higher that it was and that the patient is under-resuscitated. This is not so. The patient was resuscitated with normal saline.
Renal acidosis is caused by accumulation of strong ion products of metabolism excreted exclusively by the kidney. These include sulfate and formate. There also is accumulation of a weak acid, phosphate, which is caused by relative deficiency of vitamin D. Lactic acidosis is treated by volume resuscitation and source control. Diabetic ketoacidosis is treated with volume resuscitation and insulin. Renal acidosis is treated with dialysis.
The use of sodium bicarbonate boluses or infusions is controversial in treating metabolic acidosis. There is little evidence of benefit using this agent in lactic acidosis or ketoacidosis.[9] This situation is related not to the ability of sodium bicarbonate to reverse the acidosis, which it does by increasing the SID, but to the perception that the acidosis is the problem. Nevertheless, sodium bicarbonate (8.4%) is a hypertonic solution, which should have a plasma-expanding effect similar to that of hypertonic saline, albeit at the cost of increasing PaCO2 . This probably explains the perceived hemodynamic benefit in shock.[9] Sodium bicarbonate infusions, with the purpose of increasing the SID, have been used in patients awaiting dialysis to reduce symptoms and prevent hyperkalemia.
Methanol is metabolized to formaldehyde and formate by alcohol dehydrogenase. These are highly toxic compounds, causing blindness, cardiovascular instability, and death. Treatment strategies include the use of ethanol, which competes for binding to alcohol dehydrogenase, and fomepizole, which inhibits the enzyme. Ethylene glycol poisoning causes central nervous system depression, lactic acidosis, formation of calcium oxalate urinary crystals leading to hypocalcemia and renal failure, cardiovascular depression, and death. Treatment is with fomepizole, with or without hemodialysis.
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