Acid-Base Disorders Flashcards
what causes change in pH
-HCO3- concentration change
-Pco2 concentration change
-depending on which is changed -> either metabolic (HCO3-) or respiratory (Pco2)
metabolic acidosis disorder
-HCO3- decrease -> pH decrease
-caused by increase production of fixed acids (ketoacids or lactic acid), ingestion of fixed acids (salicylic acid), inability of kidneys to excrete fixed acids
-OR from a loss of HCO3- via kidneys or GI
-compensation: hyperventilation -> decreased Pco2
things that cause metabolic acidosis
-MUDPILES
-Methanol
-Uraemia
-Diabetic ketoacidosis
-Propylene glycol
-Isoniazid *- med
-Lactic acidosis
-Ethylene glycol
-Salicylates *- aspirin - med
-anion gap will be high
metabolic alkalosis
-increase in HCO3- -> increase pH
-caused by loss of fixed H+ from GI or kidney OR gain of HCO3- or ECF volume contraction (via diuretics)
-ex. vomiting
-compensation: hypoventilation -> increase Pco2
metabolic alkalosis: vomiting
-HCl lost from stomach
-gastric parietal cells produce H+ and HCO3-
-H+ enters stomach with Cl for digestion and HCO3- enters blood
-normally, H+ moves down and triggers pancreas to secrete HCO3- into GI tract -> however H+ never makes it down during vomiting -> HCO3- secretion is not stimulated and it stays in the blood -> increase HCO3- concentration -> increase pH
respiratory acidosis
-caused by hypoventilation
-CO2 retention
-increased Pco2
-decreased pH
-causes of CO2 retention- inhibition of medullary respiratory center (drugs), paralysis of respiratory muscles, obstruction (sleep apnea), gas exchange failure**
-renal compensation: increase reabsorption of new HCO3-
acute vs chronic respiratory acidosis
-in acute renal compensation has not occurred yet -> pH is low
-in chronic -> renal compensation is occurring -> increases HCO3- and normalizes HCO3-/CO2 ratio and pH
respiratory alkalosis
-caused by hyperventilation
-CO2 loss
-decreased Pco2
-increased pH
-caused by: stimulation of medullary respiratory center (hyperventilation), hypoxemia (high altitude), mechanical ventilation***
-renal compensation: decreased reabsorption of HCO3-
buffering of acid-base disturbance
-first line of defense- buffering in ECF and ICF
-compensatory response:
-respiratory and renal
acute vs chronic respiratory alkalosis
-acute -> renal compensation has not occurred yet -> pH is high
-chronic -> renal compensation is occurring -> further decreases blood HCO3- -> normalizes HCO3-/CO2 and pH
metabolic disorder compensation
-HCO3- disturbance
-respiratory -> adjust Pco2
-ex. metabolic acidosis -> DECREASE in HCO3- -> hyperventilation -> DECREASE Pco2
respiratory disorder compensation
-disturbance of CO2
-renal compensation -> adjust HCO3- concentration
-ex. respiratory acidosis -> INCREASED Pco2 -> renal compensation -> INCREASE HCO3-
anion gap of plasma
-dx of acid-base disorders
-cations and anion must be equal
-we usually measure Na, HCO3- and Cl in plasma
-Na (cation) concentration > HCO3- and Cl- (anions) concentration
-there is an anion gap
-bc there must be electroneutrality there must be unmeasured anions that make up for the difference -> plasma proteins, phosphate, citrate, sulfate
-anion gap WNL- 8-16
-especially usefull in fx of metabolic acidosis -> associated with decrease in plasma HCO3- concentration
-anion gap = Na - (HCO3- + Cl-)
metabolic acidosis with an increased anion gap
-associated with decrease in plasma HCO3- concentration -> anion gap
-organic anion (unmeasured anions) is accumulated (ketoacid, lactate, formate, salicylate) which offsets the HCO3- (decreases it)
-ex. diabetic ketoacidosis, lactic acidosis, salicylate poisoning, methanol poisoning, ethylene glycol poisoning, chronic renal failure
metabolic acidosis with normal anion gap
-ex. diarrhea and RTA
-no anion gap
-decrease in HCO3- offset by increase in Cl- concentration (which is a measured anion)
