Chapter 32 - Disorders of Acid-Base Balance

• an acid is a molecule that can release H+
• a base is an ion or molecule that can accept or combine with an H+
• physiological pH is 7.35 to 7.45
• protein function, cell membranes, and biochemical reactions all rely on the regulation of specific H+ concentration gradients
• metabolic acids are by-products of metabolic processes
• volatile acids are in equilibrium with CO2 and leaves the body via the lungs
• nonvolatile acids are fixed acids that are buffered by body proteins or extracellular buffers and are eliminated via the kidney
• nonvolatile acids are formed from the metabolism of dietary proteins
• sources of base for nonvolatile acids include the metabolism of aspartate, glutamate, and organic anions (citrate, lactate, and acetate)
• avid nonvolatile acid production typically exceeds base production
• the pH of ECF must be maintained within 7.35 to 7.45 for optimal functioning of body cells
• pH is determined by the ratio of the bicarbonate base to the volatile carbonic acid (normally 20:1)
• the concentration of metabolic acids and bicarbonate base is regulated by the kidney
• the concentration of CO2 is regulated by the respiratory system
• extracellular and intracellular system buffer changes in pH that occur due to metabolic production of volatile and nonvolatile acids
• buffer systems trade a strong acid/base for a weak acid/base to prevent a change in pH
• a buffering system consists of mixtures of an acids and its conjugate base or vice versa
• the 3 major buffer systems are: bicarbonate, proteins, and transcellular H+/K+ exchange
• the lungs use the bicarbonate buffer system which causes increased/decreased ventilation
• ventilation is regulated by chemoreceptors
• the lungs have the fasted pH regulating mechanism
• the lungs have an incomplete return of pH to normal but rapid action allows time for the kidneys to respond
• the kidneys eliminate H+ and both reabsorb and generate bicarbonate
• most of the pH regulation in the kidneys takes place in the proximal tubule
• the kidneys regulate pH by phosphate and ammonia buffer systems which involve the buffering or acidic urine to limit damage to urinary tract structures
• lab tests that are used in assessing acid-base balance include: ABGs, pH, CO2 content, bicarbonate levels, base excess or deficit, and anion gap
• the anion gap measures the difference between the negatively charged and positively charged electrolytes in the blood
• if the anion gap is too high, blood is more acidic than normal
• if the anion gap is too low, blood isn't acidic enough
• differences in metabolic and respiratory acid-base disorders arise from the site of causation
• in metabolic acid-base disorders, there is an alteration in plasma bicarbonate due to changes in ECF acid-alkali levels
• metabolic acidosis could result from renal bicarbonate wasting
• in respiratory acid-base disorders, there is an alteration in PCO2 due to changes in alveolar ventilation rates
• respiratory acidosis results from impaired CO2 aliminations
• manifestations of metabolic and respiratory acid-base disorders arise either from the employment of compensatory mechanisms or from decreased cellular functioning due to conformational changes in protein structures
• the primary disturbance in metabolic acidosis is a decrease in bicarbonate
• causes of metabolic acidosis:

  • excessive production (or ingestion) of metabolic acids (e.g., lactic acidosis, ketoacidosis, salicylate toxicity)
  • inability of the kidneys to excrete metabolic acids
  • bicarbonate loss (renal or interstitial)
  • increased plasma chloride concentrations (anion gap)
• respiratory compensation in metabolic acidosis is hyperventilation to decrease PCO2
• renal compensation in metabolic acidosis is increased H+ secretion and increased bicarbonate reabsorption (if no renal disease)
• treatment for metabolic acidosis:

  • correct root cause
  • restore fluid and electrolyte loss
  • improve oxygen delivery to overcome lactic acidosis
  • use of NaHCO3 under limited circumstances