Acid-Base and Electrolyte Disorders



Acid-Base and Electrolyte Disorders





1-A. Acid-Base Nomogram






FIGURE 1-1. Redrawn from Shapiro JI, Kaehny WD. Pathogenesis and management of metabolic acidosis and alkalosis. In: Schrier RW, ed. Renal and electrolyte disorders. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2003:122.



1-B. Metabolic Acidosis


Increased Anion Gap

Renal failure, acute or chronic

Ketoacidosis



  • Diabetic


  • Alcoholic


  • Starvation

Lactic acidosis (see 1-E)

Toxins



  • Aspirin


  • Methanol


  • Ethylene glycol


  • Toluene

Massive rhabdomyolysis

Inborn errors of metabolism (e.g., maple syrup urine disease, methylmalonic aciduria)


Normal Anion Gap

Gastrointestinal loss



  • Diarrhea


  • Ileal loop, ureterosigmoidostomy


  • Small bowel or pancreatic fistula or drainage


  • Ion-exchange resins (e.g., cholestyramine)


  • Calcium or magnesium chloride ingestion

Renal loss



  • Renal tubular acidosis (see 5-F)


  • Hypoaldosteronism


  • Potassium-sparing diuretics


  • Carbonic anhydrase inhibitors

Recovery phase of ketoacidosis

Rapid expansion of extracellular fluid volume with bicarbonate-free fluid (e.g., dilutional acidosis)



References

1. Shapiro JI, Kaehny WD. Pathogenesis and management of metabolic acidosis and alkalosis, p. 115. See Bibliography, 1.

2. Rose BD, p. 578. See Bibliography, 2.


1-C. Respiratory Acidosis


Neuromuscular Causes

Ingestion or overdose (e.g., tranquilizers, sedatives, anesthetics, anticholinesterases)


Cerebral, brainstem, or high spinal cord injury or infarct

Primary neuromuscular disease



  • Guillain-Barré syndrome


  • Myasthenia gravis


  • Amyotrophic lateral sclerosis


  • Poliomyelitis


  • Botulism


  • Tetanus

Myopathy involving respiratory muscles, especially:



  • Muscular dystrophy


  • Hypokalemic myopathy


  • Familial periodic paralysis

Primary hypoventilation

Sleep apnea syndrome

Diaphragmatic paralysis


Airway Obstruction

Upper airway



  • Laryngeal edema or spasm


  • Tracheal edema, stenosis


  • Obstructive sleep apnea

Lower airway



  • Mechanical



    • Foreign body


    • Aspirated fluid (e.g., vomitus)


    • Neoplasm


  • Bronchospasm



    • Acute


    • Chronic (e.g., chronic obstructive pulmonary disease)


Cardiopulmonary-Thoracic Causes

Cardiac arrest

Severe pneumonia

Severe pulmonary edema

Respiratory distress syndrome (infant or adult)

Restrictive lung disease (e.g., interstitial fibrosis)

Massive pulmonary embolism

Pneumothorax, hemothorax

Chest trauma

Kyphoscoliosis

Smoke inhalation

Inadequate mechanical ventilation




References

1. Rose BD, p. 647. See Bibliography, 2.

2. Kaehny WD. Pathogenesis and management of respiratory and mixed acid-base disorders, p. 154. See Bibliography, 1.


1-D. Anion Gap


Increased

Without acidosis



  • Administration of sodium salts of organic compounds (e.g., citrate, lactate, acetate)


  • High-dose penicillin or carbenicillin


  • Respiratory or metabolic alkalosis


  • Dehydration

With acidosis



  • Renal failure, acute or chronic


  • Ketoacidosis



    • Diabetic


    • Starvation


    • Alcoholic


  • Lactic acidosis (see 1-E)


  • Toxins



    • Aspirin


    • Methanol


    • Ethylene glycol


    • Toluene


  • Inborn errors of metabolism (e.g., maple syrup urine disease, methylmalonic aciduria)


Decreased

Hypoalbuminemia

Hypernatremia, severe

Dilution of extracellular fluid

Multiple myeloma

Hyperviscosity

Bromide ingestion

Hypercalcemia, hypermagnesemia (severe)

Lithium toxicity



References

1. Rose BD, p. 578. See Bibliography, 2.

2. Emmett M, Narins RG. Clinical use of the anion gap. Medicine. 1977;56:38.



1-E. Lactic Acidosis


Associated with Impaired Tissue Oxygenation

Shock (e.g., hypovolemic, cardiogenic, septic)

Hypoxemia, respiratory failure

Anemia, severe


Occurring in Absence of Apparent Hypoxemia or Circulatory Insufficiency

Diabetes, uncontrolled

Hepatic failure

Renal failure

Malignancy, especially leukemia or lymphoma

Drugs, toxins



  • Metformin


  • Methanol


  • Salicylates


  • Human immunodeficiency virus (HIV) nucleoside reversetranscriptase inhibitors (e.g., stavudine, zidovudine)


  • Iron


  • Strychnine


  • Ethanol


  • Cyanide


  • Carbon monoxide

Seizures

Excessive muscular activity (e.g., excessive exercise)

Alkalosis, respiratory or metabolic

D-Lactic acidosis (secondary to intestinal bacterial overgrowth)

Congenital enzyme deficiency (e.g., glycogen storage disease)



References

1. Shapiro JI, Kaehny WD. Pathogenesis and management of metabolic acidosis and alkalosis, p. 115. See Bibliography, 1.

2. Rose BD, p. 578. See Bibliography, 2.

3. Kreisberg RA. Lactate homeostasis and lactic acidosis. Ann Intern Med. 1980;92:227.


1-F. Metabolic Alkalosis


Chloride-Responsive (Urine Cl− <10 mEq/L)

Vomiting, nasogastric suction

Gastric drainage or fistula


Diuretics

Posthypercapnic state

Villous adenoma of colon

Congenital chloride diarrhea

Cystic fibrosis


Chloride-Resistant (Urine Cl− >20 mEq/L)

Primary aldosteronism

Secondary aldosteronism



  • Congestive heart failure


  • Cirrhosis and ascites


  • Malignant hypertension


  • Adrenocorticotropic hormone (ACTH) or glucocorticoid excess (Cushing disease, Cushing syndrome, ectopic ACTH production)


  • Bartter syndrome


  • Gitelman syndrome


  • Renin-secreting tumor (e.g., hemangiopericytoma)

Licorice ingestion

Excessive use of chewing tobacco

Severe potassium depletion

Congenital adrenal hyperplasia

Liddle syndrome


Miscellaneous

Administration of alkali or alkalinizing agents, especially in the presence of renal insufficiency:



  • Alkalinizing agents (e.g., citrate, lactate)


  • Antacids (milk-alkali syndrome)


  • Massive transfusion of blood or plasma substitute

Nonparathyroid hypercalcemia (e.g., bone metastases, multiple myeloma)

Nonreabsorbable anionic antibiotics, large doses (e.g., penicillin, carbenicillin)

Glucose ingestion after starvation



References

1. Shapiro JI, Kaehny WD. Pathogenesis and management of metabolic acidosis and alkalosis, p. 115. See Bibliography, 1.

2. Rose BD, p. 551. See Bibliography, 2.



1-G. Respiratory Alkalosis


Central Causes

Voluntary hyperventilation

Anxiety, pain

Hypoxia

Fever

Salicylate toxicity

Head trauma

Brain tumor

Central nervous system infection

Cerebrovascular accident

Pregnancy

Recovery phase of metabolic acidosis


Cardiopulmonary Causes

Congestive heart failure

Pneumonia

Pulmonary embolism

Interstitial lung disease

Adult respiratory distress syndrome

High altitude


Other

Hepatic insufficiency

Sepsis (especially gram-negative)

Drugs



  • Progesterone, medroxyprogesterone


  • Xanthines (e.g., aminophylline)


  • Catecholamines (massive amounts)


  • Nicotine

Mechanical ventilation

Heat exposure (e.g., heatstroke)



References

1. Rose BD, p. 673. See Bibliography, 2.

2. Kaehny WD. Pathogenesis and management of respiratory and mixed acid-base disorders, p. 154. See Bibliography, 1.

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Jun 19, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on Acid-Base and Electrolyte Disorders

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