Derangements of Acid-Base Homeostasis:
Respiratory acidosis-– How?–Rise in CO2 production (fever, sepsis), or failure of ventilation (CNS causes, muscle weakness, increased dead space) For each 10 mmHg pCO2, pH falls by 0.08 units Renal compensation-hydrogen ion secretion and ammonium secretion increase predicted [HCO3]=(pCO2-40)x0.3 + 24
Respiratory alkalosis How?-result of hyperventilation or decreased CO2 production Causes of hyperventilation in the ICU: iatrogenic, sepsis, pain, acidemia, CNS, liver, pulmonary disease Causes of decreased CO2 production: sedation/paralysis, hypothermia, low carbohydrate diet, brain death delta[H+] = 0.008x delta PCO2, or for fall PCO2 of 10mmHg, pH rises by 0.08 units. Compensation: renal excretion bicarbonate ion, titratable acid excretion decreases Predicted [HCO3]=(40-PCO2)x0.17 + 40
Metabolic Acidosis
Renal (non anion-gap) :Renal Tubular Acidosis (RTA) proximal (type II)–HCO3^15, difficult to treat distal (type I)–less severe, can be more easily treated. Renal Failure: Complete renal failure: cant regenerate bicarb, cant excrete unmeasured anions. Bone buffers to [HCO3]=14 Acute increase in acid during critical illness can be life-threatening (previously compensated acidosis can become clinically important in the face of acute illness).
GI Bicarbonate losses (non anion-gap): Pancreatic, bile, small intestinal fluid high in HCO3. Usually renal compensation occurs, except in the case of severe dehydration, very excessive loss (ie, cholera), or renal failure.
Other (anion gap): Lactic acidosis ketoaciosis congenital metabolic defects: organic acidemias, CHO metabolism defects (MCAD) Exogenous: ethylene glycol, methanol, TPN amino acids
Compensation for metabolic acidosis: Central chemoreceptors cause increased VA (alveolar minute ventilation)–increased ventilation, hence decreased pCO2. Predicted pCO2=1.5x[HCO3]+8 +/- 2.
Metabolic Alkalosis: Initiation phase–excessive HCO3 production (net gain of HCO3 or net loss of H+) excess renal production: mineralacorticoid excess, steroids stimulate distal nephron acidification (H ions excreted, HCO3 produced) + – vomiting/NG suction–loss of Cl- and volume–secondary hyperaldosteronism and renal acidification, plus attempt to retain volume and Na leads to Na/H+ exchange and increased HCO3 resporbtion. (H+, Cl loss, mineralacorticoids, volume contraction all contribute) Bicarbonate, acetate, lactate, citrate administration.
