Chapter 4. Fluids, Electrolytes, and Acid-Base Disorders

When altered, fluids and electrolytes should be corrected in the following order: (a) volume; (b) pH; (c) potassium, calcium, and magnesium; and (d) sodium and chloride. Reestablishment of tissue perfusion often equilibrates the fluid-electrolyte and acid-base balances. Because the osmolarity of normal saline (NS) matches that of serum, it is an excellent fluid for volume replacement. Hypotonic fluids such as 5% dextrose in water (D5W) should never be used to replace volume. Lactated Ringer solution is commonly used for surgical patients or trauma patients; however, only NS can be given in the same line with blood components. D5½NS, with or without potassium, is given as a maintenance fluid. The more concentrated dextrose solutions, D10W or D20W, are used for patients with compromised ability to mobilize glucose stores, such as patients with hepatic failure, or as part of total parental nutrition solutions.

Volume loss and dehydration can be inferred by the patient history. Historical features include: vomiting, diarrhea, fever, adverse working conditions, decreased fluid intake, chronic disease, altered level of consciousness, and reduced urine output. Tachycardia and hypotension are late signs of dehydration. On physical examination, one may find dry mucosa, shrunken tongue (excellent indicator), and decreased skin turgor. In infants and children, sunken fontanelles, decreased capillary refill, lack of tears, and decreased wet diapers are typical signs and symptoms of dehydration. Lethargy and coma are more ominous signs and may indicate a significant comorbid condition. Laboratory values are not reliable indicators of fluid status. Plasma and urine osmolarity are perhaps the most reliable measures of dehydration. Blood urea nitrogen (BUN), creatinine, hematocrit, and other chemistries are insensitive.

Volume overload is a purely clinical diagnosis and presents with edema (central or peripheral), respiratory distress (pulmonary edema), and jugular venous distention (in congestive heart failure). The significant risk factors for volume overload are renal, cardiovascular, and liver diseases. Blood pressure does not necessarily correlate with volume status alone; patients with volume overload can present with hypotension or hypertension.

• Adult: D5½NS at 75 to 125 mL/h + 20 mEq/L potassium chloride for an average adult (approximately 70 kilograms).
• Children: D5½NS or D10½NS, 100 mL/kilogram/d for the first 10 kilograms of body weight, 50 mL/kilogram/d for the second 10 kilograms, and 20 mL/kilogram/d for every kilograms thereafter. (See Chapter 81 for further discussion of pediatric fluid management.)

If the clinical picture and the laboratory data conflict, repeat the lab test prior to initiating therapy. Correcting a single abnormality may not be the only intervention needed because most electrolytes exist in equilibrium with others. Abnormalities should be corrected at the same rate they develop; however, slower correction is usually safe unless the condition warrants rapid or early intervention (eg, hypoglycemia or hyperkalemia). Evaluation of electrolyte disorders frequently requires a comparison of the measured and calculated osmolarities (number of particles per liter of solution). To calculate osmolarity, measured serum values in mEq/L are used:

osmolarity (mOsm/L) = 2 [Na+] + (glucose/18) + (BUN/2.8) + (ETOH/4.6)

Hyponatremia ([Na+] < 135 mEq/L)

Clinical Features

The clinical manifestations of hyponatremia occur when the [Na+] drops below 120 mEq/L; they include nausea, weakness, headache, agitation, hallucinations, cramps, confusion, lethargy, and seizures.

Diagnosis and Differential

Evaluate volume status and measured and calculated serum osmolarities. True hyponatremia presents with reduced osmolarity and is further differentiated based on volume status and urine [Na+]. This state results from primary water gain, [Na+] loss greater then that of water, or alteration in the distribution of water. Factitious hyponatremia (false low measurement of the serum sodium) is due to hyperglycemia, hyperproteinemia, hyperlipidemia, and other osmotically active solutes and is associated with a normal to high osmolarity. The syndrome of inappropriate antidiuretic hormone, characterized by hyponatremia, inappropriately elevated urine osmolality despite low serum osmolarity, elevated urine sodium, and clinical euvolemia, is a diagnosis of exclusion. Causes of hyponatremia are listed in Table 4-1.

Emergency Department Care and Disposition

1. Correct existing volume or perfusion deficits with NS.

2. In euvolemic or hypervolemic patients, restrict fluids (500 to 1500 mL of water daily)

3. In severe hyponatremia ([Na+] <120 mEq/L) that has developed rapidly with central nervous system (CNS) changes such as coma or seizures, give hypertonic saline, 3% NS (513 mEq/L), at 25 to 100 mL/h. The [Na+] should not be corrected faster than 0.5 mEq/L/h in chronic hyponatremia or 1.0 mEq/L/h in acute hyponatremia. The [Na+] correction should not exceed 12 mEq/L/day.

4. The sodium dose can be calculated as follows: weight (kilograms) × 0.6 × (desired [Na+] - measured [Na+]) = sodium deficit (mEq).

5. Complications of rapid correction include congestive heart failure (CHF) and central pontine myelinolysis.

Hypernatremia ([Na+] > 150 mEq/L)

Clinical Features

An osmolarity increase of 2% stimulates thirst to prevent hypernatremia. Symptoms of hypernatremia are usually noticeable at a serum osmolarity > 350 or [Na+] > 158 mEq/L. Initial symptoms include irritability, tremulousness, and ataxia. Lethargy, coma, and seizures may be seen with osmolarities above 400. Morbidity and mortality are highest in infants and the elderly who may be unable to respond to increased thirst.

Diagnosis and Differential

Hypernatremia is most commonly caused by a decrease in total body water due to decreased intake or excessive loss. It is less often due to an increase in total body [Na+]. Common causes are GI loss, hyperpyrexia, and excessive sweating. An important etiology of hypernatremia is diabetes insipidus (DI), which results in the loss of hypotonic urine. Central DI (no antidiuretic hormone secreted) results from CNS disease, surgery, or trauma. Nephrogenic DI (unresponsive to antidiuretic hormone) results from congenital disease, drugs, hypercalcemia, hypokalemia, or renal disease. The causes of hypernatremia are listed in Table 4-2.

Emergency Department Care and Disposition

1. Correct existing volume or perfusion deficits with NS or Lactated Ringer solution. Free water deficits are corrected with ½NS. Avoid lowering the [Na+] more than 10 mEq/L/day.

2. Each liter of water deficit causes the [Na+] to increase 3 to 5 mEq/L. Use the formula to calculate the free water deficit: water deficit (L) = (measured [Na+]/desired [Na+]) − 1.

3. If no urine output is observed after NS or lactated Ringer solution rehydration, rapidly switch to ½ NS: unload the body of the extra sodium by using a diuretic (eg, furosemide 20 to 40 milligrams IV).

4. Central diabetes insipidus DI is treated with desmopressin with careful monitoring of electrolytes, urine osmolarity, and specific gravity. Consult a specialist.

5. In children with a serum sodium level higher than 180 mEq/L, consider peritoneal dialysis using high-glucose, low-[Na+] dialysate in consultation with a pediatric nephrologist (see Chapter 81 for further discussion).

Hypokalemia ([K+] < 3.5 mEq/L)

Clinical Features

The signs and symptoms of hypokalemia usually occur at levels below 2.5 mEq/L and affect the following body systems: the CNS (weakness, cramps, hyporeflexia, paresthesias), gastrointestinal system (ileus), cardiovascular system (dysrhythmias, worsening of digoxin toxicity, hypotension or hypertension, U waves, ST-segment depression, and prolonged QT interval), and renal system (metabolic alkalosis and increased ammonia production); glucose intolerance also can develop.

Diagnosis and Differential

Causes can be grouped by decreased [K+] intake, increased [K+] excretion, or transcellular shift. The most common cause is the use of loop diuretics. Table 4-3 lists the causes.

Emergency Department Care and Disposition

1. A 20 mEq/dose [K+] will raise the [K+] by 0.25 mEq/L.

2. In stable patients, oral replacement is preferred (safe and rapid); a 20 to 40 mEq [K+] dose is used.

3. In unstable patients, IV Potassium chloride (KCl in doses of 10 to 20 mEq/h may be given). Add no more than 40 mEq of KCl to each liter of IV fluid. Infusion rates should not exceed 40 mEq/hr. Doses greater than 20 mEq/h should be given through a central line. Patients should be monitored continuously for dysrhythmias.

Hyperkalemia ([K+] > 5.5 mEq/L)

Clinical Features

The most concerning and serious manifestations of hyperkalemia are the cardiac effects. At levels of 6.5 to 7.5 mEq/L, the electrocardiogram (ECG) shows peaked T waves (precordial leads) and prolonged PR and short QT intervals. At levels of 7.5 to 8.0 mEq/L, the QRS widens and the P wave flattens. At levels above 8 mEq/L, a sine-wave pattern, ventricular fibrillation, and heart blocks occur. Neuromuscular symptoms include weakness and paralysis. Gastrointestinal symptoms include vomiting, colic, and diarrhea.

Diagnosis and Differential

Beware of pseudohyperkalemia, which is caused by hemolysis after blood draws. Renal failure with oliguria is the most common cause of true hyperkalemia. Appropriate tests for management include an ECG, electrolytes, calcium, magnesium, arterial blood gases (check for acidosis), urine analysis, and a digoxin level in appropriate patients. Causes of hyperkalemia are listed in Table 4-4.

Emergency Department Care and Disposition

1. Symptomatic patients are treated in a stepwise approach: stabilize the cardiac membrane with CaCl2 or Ca-gluconate; shift [K+] into the cell using glucose and insulin and/or bicarbonate and/or albuterol; enhance [K+] excretion by using sodium polystyrene sulfonate (Kayexalate), diuretics, or dialysis in severe cases.

2. For levels over 7.0 mEq/L or if there are any ECG changes, give: IV calcium chloride (10%) 5 to10 mL or IV calcium gluconate (10%) 10 to 20 mL. In children, give calcium gluconate (10%) 0.5 mL/kilogram.

3. The presence of digoxin toxicity with hyperkalemia is an indication for digoxin immune Fab therapy (see Chapter 108). Avoid using calcium.

4. In acidotic patients, consider giving 50 to 100 mEq of sodium bicarbonate slow IV. In children 1 to 2 mEq/kilogram is given slow IV.

5. Give 50 mL (25 grams) of D50W with 10 to 20 units regular insulin IV push (5 to 10 units in dialysis patients). In children, give 0.5 to 1 gram/kilogram of glucose as D10W plus insulin 0.1 units/kilogram.

6. Diuresis is maintained with furosemide 20 to 40 milligrams IV.

7. Kayexalate (PO or rectal [PR]) 1 gram binds 1 mEq [K+]. Administer Kayexalate 15 to 30g PO with sorbitol or 30 to 50 grams PR with sorbitol. Sorbitol is used because Kayexalate is constipating. Kayexalate can exacerbate CHF. In children, give Kayexalate 1gram/kilogram PO or PR.

8. In patients with acute renal failure, consult a nephrologist for emergent dialysis.

9. Albuterol 5 to 10 milligrams by nebulization may also be used to lower [K+].

10. Kayexalate and insulin/glucose therapies last several hours; all other therapies (except hemodialysis) have transient effects. Frequent monitoring of [K+] should occur.

Hypocalcemia ([Ca2+] < 8.5 mEq/L or Ionized Level < 2.0 mEq/L)

Clinical Features

The signs and symptoms of hypocalcemia are usually seen with ionized [Ca2+] levels below 1.5 mEq/L. Symptoms include paresthesias, increased deep tendon reflexes (DTRs), cramps, weakness, confusion, and seizures. Patients also may demonstrate the Chvostek sign (twitch of the corner of mouth on tapping with finger over cranial nerve VII at the zygoma) or the Trousseau sign (more reliable; carpal spasm when the blood pressure cuff is left inflated at a pressure above the systolic blood pressure for longer than 3 min). Alkalosis decreases the ionized [Ca2+] fraction (physiologically active form) without changing the total calcium level. Low [Ca2+] decreases myocardial contractility, so patients may present with CHF or prolonged QT intervals on the ECG.

Diagnosis and Differential

Causes include: shock, sepsis, fat embolism, renal failure, pancreatitis, drugs (usually cimetidine), hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, hypomagnesemia, and fluoride poisoning.

Emergency Department Care and Disposition

1. If asymptomatic, use calcium gluconate tablets 1 to 4 grams/d PO divided every 6 hours with or without vitamin D (calcitriol 0.2 micrograms two times a day). Milk is not a good substitute.

2. In symptomatic patients or those with severe hypocalcemia, give calcium gluconate, or calcium chloride, 10 mL 10% solution IV slowly over 10 min.

3. Replace magnesium in conjunction with [Ca2+].

Hypercalcemia ([Ca2+] > 10.5 mEq/L or Ionized [Ca2+] > 2.7 mEq/L)

Several factors affect the serum calcium level: parathyroid hormone increases calcium and decreases phosphate; calcitonin and vitamin D metabolites decrease calcium. Decreased [H+] causes a decrease in ionized [Ca2+]. A decrease in albumin causes a decrease in [Ca2+] but not in the ionized portion.

Clinical Features

Clinical signs and symptoms develop at levels above 12 milligrams/dL. Patients often have profound volume depletion; concomitant electrolyte abnormalities are frequent. A mnemonic to aid recall of common hypercalcemia symptoms is stones (renal calculi), bones (osteolysis), psychic moans (lethargy, weakness, fatigue, and confusion), and abdominal groans (abdominal pain, constipation, polyuria, and polydipsia). ECG changes include depressed ST segments, widened T waves, shortened QT intervals, and heart blocks.

Diagnosis and Differential

Most cases of hypercalcemia are due to hyperparathyroidism or malignancy. A mnemonic to aid recall of the common causes is PAM P. SCHMIDT:parathyroid hormone, Addison disease, multiple myeloma, Paget disease, sarcoidosis, cancer, hyperthyroidism, milk-alkali syndrome, immobilization, excess vitamin D, and thiazides.

Emergency Department Care and Disposition

1. Initiate treatment in patients with severe symptoms, [Ca2+] above 14 milligrams/dL, or significant dehydration. Restore fluid deficits, enhance calcium elimination, and decrease osteoclastic activity.

2. Correct fluid deficits with NS; several liters may be required. Correct concomitant electrolyte abnormalities cautiously.

3. Loop diuretics inhibit the renal resorption of [Ca2+], but worsen dehydration and other electrolyte abnormalities. They are no longer recommended for malignancy-related hypercalcemia. In isolated cases, furosemide (10 to 40 milligrams IV) may be administered after fluid deficits are corrected, with careful attention to avoid dehydration. Thiazide diuretics should not be used.

4. Drugs that inhibit osteoclastic activity include the bisphosphonates, calcitonin, and glucocorticoids. Recommendations for initiating therapy in the ED are lacking; consultation with a specialist is advised.

Hypomagnesemia

Clinical Findings

[Mg2+], [K+], and [PO4−] move together intra- and extracellularly. Hypomagnesemia presents with CNS symptoms (depression, vertigo, ataxia, seizures, increased DTR, or tetany) or cardiac symptoms (arrhythmias, prolonged PR, QRS and QT, or worsening of digitalis effects). Also seen are anemia, hypotension, hypothermia, and dysphagia.

Diagnosis and Differential

In adults, the most common cause is alcoholism, followed by poor nutrition, cirrhosis, pancreatitis, correction of diabetic ketoacidosis (DKA), excessive gastrointestinal losses, and renal wasting (especially diurectic use). Severe [Mg2+] depletion can occur before significant laboratory changes are seen.

Emergency Department Care and Disposition

1. Correct volume deficits and other electrolyte abnormalities. Oral [Mg2+] replacement is sufficient for most patients.

2. In patients with severe symptoms and normal renal function, administer 2 grams magnesium sulfate IV over an hour, followed by 6 grams over the first 24 hours. Continuous cardiac monitoring and frequent DTR checks are recommended.

Hypermagnesemia

Clinical Findings

Signs and symptoms manifest progressively: nausea and somnolence occur first, followed by muscle weakness and loss of DTRs. Respiratory depression, hypotension, heart block, and cardiac arrest occur at progressively higher magnesium levels.

Diagnosis and Differential

Hypermagnesemia is rare. Common causes are renal failure with concomitant ingestion of [Mg2+]-containing preparations (antacids) and lithium ingestion. Serum levels are diagnostic. Hyperkalemia, hypercalcemia, and hyperphosphatemia often present concurrently.

Emergency Department Care and Disposition

1. In many patients, stopping [Mg2+] intake is sufficient. More aggressive therapy includes rehydration with NS.

2. In severely symptomatic patients, give 5 mL (10% solution) of calcium chloride IV to antagonize the effects of magnesium.

Initial Assessment

Clinical Features

Several conditions should alert the clinician to possible acid-base disorders: history of renal, endocrine, or psychiatric disorders (drug ingestion); or signs of acute disease: tachypnea, cyanosis, Kussmaul respiration, respiratory failure, shock, changes in mental status, vomiting, diarrhea, or other acute fluid losses.

Acidosis is due to gain of acid or loss of alkali; causes may be metabolic (fall in serum [HCO3−]) or respiratory (rise in PCO2). Alkalosis is due to loss of acid or addition of base and is metabolic (rise in serum [HCO3−]) or respiratory (fall in PCO2). The lungs and kidneys primarily maintain the acid–base regulation. Metabolic disorders prompt an immediate compensatory change in ventilation, thereby venting CO2 in cases of metabolic acidosis or retaining it in cases of metabolic alkalosis. The effect of the kidneys in response to metabolic disorders is to excrete the hydrogen ion (with chloride) and recuperate [HCO3−], a process that requires hours to days. The compensatory mechanisms of the lungs and kidneys will return the pH toward, but not to, normal.

Diagnosis and Differential

Diagnosis and differential must begin with defining the nature of the acid-base disorder (with the stepwise approach below) and then determining the most likely etiology from the differential listings in each section that follows. In a mixed disorder, the pH, PCO2, and [HCO3−] may be normal, and the only clue to a metabolic acidosis is a widened anion gap (AG, see step 4 below).

Stepwise Method of Acid-Base Clinical Problem Solving

Use the patient's pre-illness values as a baseline if available; otherwise, a pH of 7.4, [HCO3] of 24 mEq/L, and PCO2 of 40 mm Hg can be considered normal.

1. Examine the pH for acidemia (pH < 7.4) or alkalemia (pH > 7.4).

2. Establish the primary mechanism by evaluating the [HCO3−] and PCO2.

   • Metabolic acidosis: pH < 7.4 and [HCO3−] < 24 meQ/L
   • Metabolic alkalosis: pH > 7.4 and [HCO3−] > 24 meQ/L
   • Respiratory acidosis: pH < 7.4 and PCO2 > 40 mm Hg
   • Respiratory alkalosis: pH > 7.4 and PCO2 < 40 mm Hg

3. Calculate the AG: [Na+] − ([Cl−] + [HCO3−]) = approximately 10 to 12 mEq/L is normal.

   • If the AG is increased compared with the known previous value or greater than 15, then an anion gap metabolic acidosis is present.
   • If the AG is unchanged and a metabolic acidosis is present (low [HCO3−]), then a normal anion gap (or hyperchloremic) acidosis is present.

4. For anion gap metabolic acidosis, evaluate for a concomitant hidden metabolic process: each 1 mEq/L decrease in [HCO3−] results in a 1 mEq/L increase in AG. Compare the Δ Gap (= present gap −12) to the Δ [HCO3−] (= 24 − present [HCO3−]).

   • Δ Gap = Δ [HCO3−]: pure anion gap metabolic acidosis
   • Δ Gap > Δ [HCO3−]: concomitant metabolic alkalosis is likely present
   • Δ Gap < Δ [HCO3−]: concomitant non-AG acidosis is likely present

5. Estimate the compensatory response for the primary process. If the compensatory response is not as expected, then the compensatory mechanism requires more time for complete mobilization or a secondary acid-base disturbance exists.

   • Metabolic acidosis: expected PCO2 = (1.5 × [HCO3−] + 8) ± 2. A simpler observation is the PCO2 decreases by 1 mm Hg for every 1 mEq/dL decrease in [HCO3−]. This process takes 12 to 24 hrs.
   • Metabolic alkalosis: expected PCO2 = 0.9 [HCO3−] + 16.
   • For either of above formulas, if:
     • Current PCO2 = expected PCO2: normal respiratory compensation
     • Current PCO2 < expected PCO2: possible concomitant respiratory alkalosis
     • Current PCO2 > expected PCO2: possible concomitant respiratory acidosis
   • Respiratory acidosis: clinically judge whether the process is acute (< 72 hrs) or chronic (> 72 hrs). The [HCO3−] increases 1mEq/L (acute) or 4 mEq/L (chronic) for every 10 mm Hg increase in PCO2.
   • Respiratory alkalosis: clinically judge whether the process is acute (72 hrs) or chronic (> 72 hrs). The [HCO3−] decreases 2mEq/L (acute) or 5 mEq/L (chronic) for every 10 mm Hg decrease in PCO2.
   • For either of above formulas, if:
     • Current [HCO3−] = expected [HCO3−]: normal metabolic compensation.
     • Current [HCO3−] < expected [HCO3−]: possible concomitant metabolic acidosis.
     • Current [HCO3−] > expected [HCO3−]: possible concomitant metabolic alkalosis.

6. See the sections below for determining the etiology and management.

Metabolic Acidosis

Metabolic acidosis should be divided into an increased and normal AG acidosis. The term anion gap is misleading because the serum has no gap between total positive and negative ions; however, the unmeasured anions exceed the unmeasured cations.

Clinical Features

No matter the etiology, acidosis can cause nausea and vomiting, abdominal pain, change in sensorium, and tachypnea, sometimes a Kussmaul respiratory pattern. Acidosis causes many negative physiologic effects that result in hypoxia. Patients may present with nonspecific complaints or shock.

Diagnosis and Differential

Causes of metabolic acidosis can be divided into 2 main groups: (a) those associated with increased production of organic acids (Table 4-5); and (b) those associated with a loss of [HCO3−], failure to excrete [H+], or addition of [H+] (Table 4-6).

Causes of anion gap metabolic acidosis include renal failure, lactic acidosis, ketoacidosis, and toxins. A mnemonic to aid the recall of the causes of increased AG metabolic acidosis is: A MUD PILES: alcohol, methanol, uremia, DKA, paraldehyde, iron and isoniazid, lactic acidosis, ethylene glycol, salicylates, and starvation. Caution should be used when applying the A MUD PILES mnemonic because the presence of alcohol in the patient's blood does not rule out a more serious cause of acidosis. Iron and isoniazid exert their effects on the AG due to lactic acidosis. Causes of normal anion gap acidosis include GI or renal loss of [HCO3−]. A mnemonic that can aid the recall of normal AG metabolic acidosis is USED CARP:ureterostomy, small bowel fistulas, extra chloride, diarrhea, carbonic anhydrase inhibitors, adrenal insufficiency, renal tubular acidosis, and pancreatic fistula.

Emergency Department Care and Disposition

1. Address the underlying cause to restore tissue perfusion and oxygenation.

2. Administer fluids, oxygen, and ventilation as needed.

3. For specific etiologies, consult the appropriate chapters in this handbook for further guidance.

Indications for bicarbonate therapy are listed in Table 4-7. Give 0.5 mEq/kilogram bicarbonate for each mEq/L desired rise in [HCO3−]. The goal is to restore adequate buffer capacity ([HCO3−] > 8 mEq/dL) or achieve clinical improvement in shock or dysrhythmias. Seventy-five mEq of sodium bicarbonate in 500 mL D5W produces a nearly isotonic solution for infusion.

Metabolic Alkalosis

Metabolic alkalosis is classified as [Cl−] sensitive or [Cl−] insensitive. The two most common causes of metabolic alkalosis are excessive diuresis (with loss of potassium, hydrogen ion, and chloride) and excessive loss of gastric secretions (with loss of hydrogen ion and chloride).

Clinical Features

Symptoms of the underlying disorder (usually fluid loss) dominate the clinical presentation, but general symptoms of metabolic alkalosis include muscular irritability, tachydysrhythmia, and impaired oxygen delivery. In most cases, there is also an associated hypokalemia and hypochloremia.

Patients with [Cl−] sensitive causes present with hypovolemia secondary to vomiting, diarrhea, or diuretic therapy. Patient with [Cl−] insensitive causes present with normo- to hyper-volemia associated with excess mineralocorticoid activity (renin-secreting tumors, adrenal hyperplasia, hyperaldosteronism, Cushing syndrome).

Emergency Department Care and Disposition

1. Administer NS to treat dehydration.

2. Monitor electrolytes.

Respiratory Acidosis

Clinical Features

Respiratory acidosis secondary to hypoventilation may be life threatening. The clinical picture usually is dominated by the underlying disorder. Typically, respiratory acidosis depresses the mental function, which may progressively slow the respiratory rate. Patients may be confused, somnolent, and, eventually, unconscious. Pulse oximetry may be misleading, making arterial blood gases essential for the diagnosis.

The differential diagnosis includes drug overdose, CNS disease, chest wall disease, pleural or lung disease, and trauma.

Emergency Department Care and Disposition

1. The treatment is to improve ventilation. Depressed mental status is an indication for intubation. An exception to this is opiate intoxication where rapid administration of naloxone may improve ventilation.

2. Treat the underlying disorder.

Respiratory Alkalosis

Clinical Features

Hyperventilation syndrome is a problematic diagnosis for the emergency physician because many life-threatening disorders present with tachypnea and anxiety: asthma, pulmonary embolism, diabetic ketoacidosis, and others. Symptoms of respiratory alkalosis often are dominated by the primary disorder promoting the hyperventilation. Symptoms of hyperventilation include dizziness, carpal-pedal spasm, and, frequently, a chest pain described as tightness.

The diagnosis of hyperventilation due to anxiety is a diagnosis of exclusion. Arterial blood gases can be used to rule out acidosis and hypoxia. Causes of respiratory alkalosis include CNS tumor or stroke, infection or fever, hypoxia, lung disease, hyperthyroidism, toxins (eg, sympathomimetics or aspirin), liver disease, pregnancy, and anemia.

Emergency Department Care and Disposition

1. Treat the underlying cause.

2. Rule out life threatening causes of hyperventilation before diagnosing anxiety. Anxiolytics may be helpful, such as lorazepam 1 to 2 milligrams IV or PO.

3. Rebreathing into a paper bag can cause hypoxia; it is not recommended.