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intravenously (see 38), is administered to all such patients if no obvious cause for respiratory depression is present In all forms of respiratory acidosis, treatment is directed at the underlying disorder to improve ventilation
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Epstein SK et al Respiratory acidosis Respir Care 2001 Apr;46 (4):366 83 [PMID: 11262556] Madias NE et al Cross-talk between two organs: how the kidney responds to disruption of acid base balance by the lung Nephron Physiol 2003;93(3):61 6 [PMID: 12660492]
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B Saline-Unresponsive Metabolic Alkalosis
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Therapy for saline-unresponsive metabolic alkalosis includes surgical removal of a mineralocorticoid-producing tumor and blockage of aldosterone effect with an ACE inhibitor or with spironolactone Metabolic alkalosis in primary aldosteronism can be treated only with potassium repletion
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Khanna A et al Metabolic alkalosis J Nephrol 2006 Mar Apr;19(Suppl 9):S86 96 [PMID: 16736446]
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RESPIRATORY ALKALOSIS (HYPOCAPNIA)
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Respiratory alkalosis, or hypocapnia, occurs when hyperventilation reduces the PCO2, which increases the pH The most common cause of respiratory alkalosis is hyperventilation syndrome (Table 21 17), but bacterial septicemia and cirrhosis are other common causes Symptoms in acute respiratory alkalosis are related to decreased cerebral blood flow induced by the disorder Pregnancy is another cause of chronic respiratory alkalosis, probably from progesterone stimulation of the respiratory center, producing an average PCO2 of 30 mm Hg Determination of appropriate compensatory changes in the HCO3 is useful to sort out the presence of an associated metabolic disorder (see above under Mixed Acid Base Disorders)
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Respiratory acidosis results from decreased alveolar ventilation and subsequent hypercapnia Pulmonary as well as nonpulmonary disorders can cause hypoventilation The clinician must be mindful of readily reversible causes of respiratory acidosis, especially opioid-induced central nervous system depression Acute respiratory failure is associated with severe acidosis and only a small increase in the plasma bicarbonate After 6 12 hours, the primary increase in PCO2 evokes a renal compensatory response to generate more HCO3 , which tends to ameliorate the respiratory acidosis This usually takes several days to complete Chronic respiratory acidosis is generally seen in patients with underlying lung disease, such as chronic obstructive pulmonary disease 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
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Table 21 17 Causes of respiratory alkalosis
Hypoxia Decreased inspired oxygen tension High altitude Ventilation/perfusion inequality Hypotension Severe anemia CNS-mediated disorders Voluntary hyperventilation Anxiety-hyperventilation syndrome Neurologic disease Cerebrovascular accident (infarction, hemorrhage) Infection Trauma Tumor Pharmacologic and hormonal stimulation Salicylates Nicotine Xanthines Pregnancy (progesterone) Hepatic failure Gram-negative septicemia Recovery from metabolic acidosis Heat exposure Pulmonary disease Interstitial lung disease Pneumonia Pulmonary embolism Pulmonary edema Mechanical overventilation Adapted, with permission, from Gennari FJ Respiratory acidosis and alkalosis In: Maxwell and Kleeman s Clinical Disorders of Fluid and Electrolyte Metabolism, 5th ed Narins RG (editor) McGraw-Hill, 1994
Clinical Findings
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
Treatment
Because opioid drug overdose is an important reversible cause of acute respiratory acidosis, naloxone, 004 2 mg
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Table 21 18 Replacement guidelines for sweat and gastrointestinal fluid losses
Average Electrolyte Composition Na+ (mEq/L) Sweat Gastric secretions Pancreatic juice Bile Duodenal fluid Ileal fluid Colonic diarrhea
Replacement Guidelines per Liter Lost 09% Saline (mL) 045% Saline (mL) 500 300 D5W (mL) 500 700 600 400 1000 600 1000 400 KCl (mEq/L) 5 20 5 5 15 10 10 2 amps 05 amp 025 amp 1 amp 1 amp 75% NaHCO3 (45 mEq HCO3 /amp)
K+ (mEq/L) 5 10 5 5 15 10 10
Cl (mEq/L) 50 10 35 100 100 60 85
HCO3 (mEq/L)
30 50 20 130 145 60 100 1401
115 25 10 60 60 600
In the absence of diarrhea, colonic fluid Na levels are low (40 mEq/L)
As in respiratory acidosis, the changes in HCO3 values are greater if the respiratory alkalosis is chronic (Table 21 13) Although serum HCO3 is frequently below 15 mEq/L in metabolic acidosis, it is unusual to see such a low level in respiratory alkalosis, and its presence would imply a superimposed (noncompensatory) metabolic acidosis
Foster GT et al Respiratory alkalosis Respir Care 2001 Apr; 46(4):384 91 [PMID: 11262557] Laffey JG et al Hypocapnia N Engl J Med 2002 Jul 4;347(1):43 53 [PMID: 12097540]
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