ABG Flashcards
Factors that increase O2 off-loading
Rightward shift:
Decreased pH < 7.4 (Bohr Effect)
Increased PCO2 > 40 Torr
Increased temperature
Increased 2,3-DPG
Factors that decrease O2 off-loading
Increased pH
Decreased PCO2
Decreased Temperature
Decreased 2,3-DPG
Calculate O2 delivery to tissues as a function of CO and arterial O2 content
DO2 = Q x (SaO2 x 1.39[Hb]) + (0.003 x PaO2)
Calculate O2 consumption from CO and the difference in O2 saturation between arterial and venous blood
VO2 = Q x (SaO2 - SVO2) x 1.39[Hb]
Hypoxemia - Cut off values
PaO2 < 80 Torr at sea level
PaO2 < 65 torr in Denver
5 causes of hypoxemia
Low ambient PO2 in inspired air (altitude) Reduced ventilation Diffusion limitations V/Q mismatch Shunt
3 ways CO2 is carried in the blood
Freely dissolved CO2 (~1.2mM at typical PCO2 of 40Torr)
HCO3- (~24mM)
Carbamino compounds - CO2 bound to Hb (1.2mM)
Haldane effect
Deoxygenated Hb binds CO2 better than oxygenated Hb; therefore, there is enhanced carriage of CO2 by Hb in venous blood
Henderseon-Hasselbach Equation for Bicarbonate
pH = 6.1 + log ([HCO3-] / 0.03 x PCO2)
Normal arterial blood gas values for pH, PaCO2, and [HCO3-]
pH = 7.4 (7.38 - 7.43)
PaCO2 = 40 Torr
[HCO3-] = 24mM
Respiratory acidosis
Increased PaCO2 leading to decreased pH
Caused by hypoventilation
Compensation via conservation of bicarbonate in the kidney; bicarbonate buffers by “absorbing” extra protons
Respiratory alkalosis
Decreased PaCO2 leading to increased pH
Caused by excessive ventilation in relation to CO2 production
Compensation via increased excretion of bicarbonate by the kidney
Anion gap metabolic acidosis
Low pH due to the presence of additional, unmeasured acids in the blood (AG > 14)
Caused by: MUDPILES
Methanol Uremia Diabetic Ketoacidosis (and other causes of ketoacidosis: starvation, alcoholism) Propylene glycol Isoniazid Lactate Ethylene Glycol Salicylates
Non-gap metabolic acidosis
Low pH without the presence of additional, unmeasured acids in the blood; AG within normal range of 12 +/- 2
Caused by loss of HCO3- due to GI loss or renal loss, or by giving large quantities of saline
Compensation of metabolic acidosis
Increased ventilation to “blow off” CO2
Expected pCO2 = 1.5[HCO3-] + 8 +/- 2 (Winter’s Formula)
if the pCO2 measured on ABG is within this range, then the compensation is considered complete; if pCO2 is higher than expected then compensation is incomplete
Metabolic alkalosis
Increased pH caused by an increase in base such as HCO3- or a decrease in acid other than CO2
Acid loss during vomiting
Ingestion of antacids or baking soda
Hypovolemia causing re-absorption of bicarbonate in the kidney (contraction alkalosis)
Compensation involves decreased ventilation to increase PaCO2; however, the brain will not allow hypoventilation to the point of hypoxemia and so compensation is usually incomplete
Compensation rule - acute respiratory disturbances
An acute change in PaCO2 of 10 Torr yields a pH change of 0.08 units
This is the uncompensated situation
Compensation rule - chronic respiratory disturbances
A change in PaCO2 of 1 Torr yields a compensatory change in [HCO3-] of 0.4 in the same direction
This is the compensated situation
Metabolic disturbances - compensation rule
A decrease in [HCO3-] of 1mEq results in a decrease in PaCO2 of 1.3 Torr
An increase in [HCO3-] of 1mEq results in an increase in PaCO2 of 0.7 Torr
Calculate the anion gap
AG = [Na+] - ([Cl-] + [HCO3-]) = 12 +/- 2