VII: Acid-Base Disorders Flashcards
Respiratory disorder due to
pCO2
Metabolic disorder due to
[HCO3-]
Metabolic acidosis HCO3- and pH
Low [HCO3-] and low pH
Compensation of metabolic acidosis (pCO2)
Hyperventilation to eliminate CO2 (decreased pCO2)
Kidney will compensate to increase HCO3- but it will take longer
Metabolic alkalosis
High [HCO3-] and high pH
Compensation for metabolic alkalosis
Hypoventilation to keep the CO2 (increase pCO2)
Kidney will secrete HCO3- to decrease its concentration in blood
Respiratory acidosis pCO2 and pH
High pCO2 and low pH
Compensation for respiratory acidosis
Synthesize more HCO3-
Cause of respiratory acidosis
Hypoventilation causing CO2 retention
Respiratory alkalosis
Low pCO2 and high pH
Compensation for respiratory alkalosis
Kidney will stop producing HCO3-
Cause of respiratory alkalosis
Hyperventilation causing CO2 loss
Mechanisms to maintaining blood pH in normal range
ICF and ECF buffers (HCO3-)
Respiratory compensation
Renal compensation
Use of anion gap of plasma
In diagnosis of acid-base disorders
Bases of anion gap
[cations] must equal [anions]
Na+ HCO3- and Cl-
So any unmeasured anions will make up for the “gap”
Calculation of plasma anion gap
[Na+] - ([HCO3-] - [Cl-])
Normal range of anion gap
8-12mEq/L
During metabolic acidosis, what happens to the anion gap
There is a loss of [HCO3-] and because the system has to be in equilibrium, there will be an unmeasured anion replacing the lost HCO3-
Anion gap increased during
Diabetic ketoacidosis
Lactic acidosis
If HCO3- replaced by Cl-
Hyperchloremic
Main cause of metabolic acidosis
Gain of non-volatile H+
Buffering of H+ excess by HCO3-
In ECF, HCO3- has decreased so there is buffering in ICF of H+ with organic anions or K+
Use of K+ to buffer can cause hyperkalemia
Respiratory compensation of metabolic acidosis
Hyperventilation to decrease pCO2
Consequence of hyperventilation in arterial pressure
Arterial pressure drops
Renal compensation in metabolic acidosis
Takes a few days
H+ is excreted as titrable NH4+
New HCO3- synthesized
Metabolic alkalosis loss of fixed acid
H+ loss from stomach
HCO3- is not stimulated so it stays in blood, HCO3- increase
Buffering in ECF and ICF in metabolic alkalosis
H+ leaves the cells so K+ enters = hypokalemia
Respiratory compensation in metabolic alkalosis
Hypoventilation = increased arterial pressure
To increase pCO2
Renal correction in metabolic alkalosis
HCO3- excreted in urine to decrease [HCO3-] in blood
What is complicated about HCO3- excretion during vomiting
There is ECF volume contraction which is causing reabsorbtion
During ECF depletion (a.k.a vomiting) what happend
Increase in HCO3- reabsorption
Increase in angiotensin II to increase Na+/H+ exchange and HCO3- reabsorption
Increase in aldosterone for H+ secretion, HCO3- reabsorption and K+ secretion
K+ seccretion during ECF contraction can cause
Hypokalemia
Main cause of repsiratory acidosis
Increase in pCO2 due to hypoventilation
Buffering in respiratory acidosis mainly by
RBC in ICF
Renal correction in respiratory acidosis
Increase in H+ excretion as NH4+
Increase in HCO3- synthesis
Main cause of respiratory alkalosis
Loss of CO2 from hyperventilation
Buffering in respiratory alkalosis
In ICF by RBC
CO2 out of cell to increase concentration
Renal compensation in respiratory alkalosis
Decrease in H+ excretion
Decrease in HCO3- synthesis
