Chapter 048. Acidosis and Alkalosis (Part 1)

Harrisons Internal Medicine Chapter 48. Acidosis and AlkalosisNormal Acid-Base HomeostasisSystemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (PaCO2) by the central nervous system and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation:Under most circumstances, CO2 production and excretion are matched, and the usual steady-state PaCO2 is maintained...
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Chapter 048. Acidosis and Alkalosis (Part 1) Chapter 048. Acidosis and Alkalosis (Part 1) Harrisons Internal Medicine > Chapter 48. Acidosis and Alkalosis Normal Acid-Base Homeostasis Systemic arterial pH is maintained between 7.35 and 7.45 by extracellularand intracellular chemical buffering together with respiratory and renal regulatorymechanisms. The control of arterial CO2 tension (PaCO2) by the central nervoussystem and respiratory systems and the control of the plasma bicarbonate by thekidneys stabilize the arterial pH by excretion or retention of acid or alkali. Themetabolic and respiratory components that regulate systemic pH are described bythe Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, andthe usual steady-state PaCO2 is maintained at 40 mmHg. Underexcretion of CO2produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless,production and excretion are again matched at a new steady-state PaCO2.Therefore, the PaCO2 is regulated primarily by neural respiratory factors (Chap.258) and is not subject to regulation by the rate of CO 2 production. Hypercapnia isusually the result of hypoventilation rather than of increased CO 2 production.Increases or decreases in PaCO2 represent derangements of neural respiratorycontrol or are due to compensatory changes in response to a primary alteration inthe plasma [HCO3–]. The kidneys regulate plasma [HCO3–] through three main processes: (1)reabsorption of filtered HCO3–, (2) formation of titratable acid, and (3) excretionof NH4+ in the urine. The kidney filters ~4000 mmol of HCO3– per day. Toreabsorb the filtered load of HCO3–, the renal tubules must therefore secrete 4000mmol of hydrogen ions. Between 80 and 90% of HCO3– is reabsorbed in theproximal tubule. The distal nephron reabsorbs the remainder and secretes protons,as generated from metabolism, to defend systemic pH. While this quantity ofprotons, 40–60 mmol/d, is small, it must be secreted to prevent chronic positive H+balance and metabolic acidosis. This quantity of secreted protons is represented inthe urine as titratable acid and NH4+. Metabolic acidosis in the face of normalrenal function increases NH4+ production and excretion. NH4+ production andexcretion are impaired in chronic renal failure, hyperkalemia, and renal tubularacidosis. In sum, these regulatory responses, including chemical buffering, theregulation of PaCO2 by the respiratory system, and the regulation of [HCO3–] by thekidneys, act in concert to maintain a systemic arterial pH between 7.35 and 7.45. Diagnosis of General Types of Disturbances The most common clinical disturbances are simple acid-base disorders, i.e.,metabolic acidosis or alkalosis or respiratory acidosis or alkalosis. Sincecompensation is not complete, the pH is abnormal in simple disturbances. Morecomplicated clinical situations can give rise to mixed acid-base disturbances. Simple Acid-Base Disorders Primary respiratory disturbances (primary changes in PaCO2) invokecompensatory metabolic responses (secondary changes in [HCO 3–]), and primarymetabolic disturbances elicit predictable compensatory respiratory responses.Physiologic compensation can be predicted from the relationships displayed inTable 48-1. Metabolic acidosis due to an increase in endogenous acids (e.g.,ketoacidosis) lowers extracellular fluid [HCO 3–] and decreases extracellular pH.This stimulates the medullary chemoreceptors to increase ventilation and to returnthe ratio of [HCO3–] to PaCO2, and thus pH, toward normal, although not to normal.The degree of respiratory compensation expected in a simple form of metabolicacidosis can be predicted from the relationship: Pa CO2 = (1.5 x [HCO3–]) + 8 ± 2,i.e., the PaCO2 is expected to decrease 1.25 mmHg for each mmol per liter decreasein [HCO3–]. Thus, a patient with metabolic acidosis and [HCO3–] of 12 mmol/Lwould be expected to have a Pa CO2 between 24 and 28 mmHg. Values for Pa CO228 mmHg define a mixed disturbance (metabolic acidosis and respiratoryalkalosis or metabolic alkalosis and respiratory acidosis, respectively). Anotherway to judge the appropriateness of the response in [HCO 3–] or PaCO2 is to use anacid-base nomogram (Fig. 48-1). While the shaded areas of the nomogram showthe 95% confidence limits for normal compensation in simple disturbances,finding acid-base values within the shaded area does not necessarily rule out amixed disturbance. Imposition of one disorder over another may result in valueslying within the area of a third. Thus, the nomogram, while convenient, is not asubstitute for the equations in Table 48-1.