Quantitative Approach Acid Base. Hopper et al. 2008. JVECC Flashcards
Explain the difference between conventional and quantitative acid base analysis.
Conventional analysis assesses whether there is a respiratory/metabolic acidosis/alkalosis but does not assess what the underlying cause for the metabolic disturbance is.
How long does respiratory compensation take to start and to reach its max effect?
respiratory compensation starts immediately but needs several hours to reach maximum effect
How long does metabolic compensation take to start and when does it reach its max effect?
takes hours to start and is complete within days (2-5 days)
How do you identify whether a secondary change is compensatory or presents a mixed acid base disorder?
calculate expected compensation, if outside of this range expect mixed acid base disorder
What is the expected change in pCO2 for a given change in HCO3-
BE x 0.7 = expected change up/down in pCO2
What is the expected metabolic compensation to an acute respiratory acidosis?
increasing HCO3 of 0.15 mEq/L per 1 mm Hg increase of PaCO2
What is the expected metabolic compensation to a chronic respiratory acidosis?
increase of HCO3 of 0.35 mEq/L per 1 mm Hg increase in PaCO2
What is the expected metabolic compensation to an acute respiratory alkalosis?
decrease in HCO3 of 0.25 mEq/L per 1 mm Hg decrease in PaCO2
What is the expected metabolic compensation to a chronic respiratory alkalosis?
decrease in HCO3- of 0.55 mEq/L per 1 mm Hg decrease in PaCO2
Why could the HCO3- be unreliable to assess metabolic status?
HCO3- will change with
* pCO2 values
* temperature
* Hemoglobin
Describe Standard Base Excess (SBE)
reflects the titratable strong acid or base needed to restore plasma pH of 1L EC fluid to pH of 7.4
* at PCO2 of 40 mm Hg
* at temperature of 37C
* with fully oxygenated hemoglobin
How does SBE of cats compare to dogs
slightly more negative in cats
What is the Anion Gap equation?
AG = (Na + K) - (HCO3- + CL)
Why does the accumulation of acids - other than Cl - cause a high anion gap?
accumulation of acids will decrease HCO3- in tha AG equation –> will be more positive/higher
Why does hyperchloremic metabolic acidosis not cause a high AG?
HCO3- will decrease however, Cl increases –> AG does not become higher
What is the major unmeasured anion in health?
albumin
hypoalbuminemia could obscure an otherwise elevated AG
According to the Stewart Approach, what are the 3 independent determinants of acid-base balance?
- pCO2
- difference between strong cations and anions
- total weak acids (Atot)
What is the simplified equation for SID?
SID = Na+ - Cl- = OH - H+
What does apropte ion mean and what are 2 examples?
Na and Cl are aprote ions, which means they can neither donate or accept H+, and therefore per se do not cause a direct change in pH
What are the 5 parameters evaluated in the Fencl-Stewart approach of acid base abnormalities?
1) free water effect
2) changes in Cl concentration
3) albumin effect
4) lactate effect
5) phosphate effect
UA=(1+2+3+4+5)
How do you calculate the free water effect on acid base status (in dogs and cats)
Dogs = 0.25 (NaPatient - NaNormal)
Cat = 0.22 (NaPatient - NaNormal
How do you calculate the corrected Chloride and chloride effect on the acid base status
corrected Cl = ClPatient x (normal Na/Patient Na
chloride effect = normal Cl - corrected Cl
How do you calculate the phosphate effect on the acid base status?
mg/dL P
phosphate effect = 0.58 (normal P - measured P)
How do you calculate the albumin effect on the acid base status?
g/dL
albumin effect = 3.7 (3.1 - measured albumin)
How do you calculate the lactate effect on the acid base status?
lactate effect = - 1 x lactate
How do you calculate the unmeasured anion effect?
UA = standardized base excess - sum of effects in frencl stewart approach
How does hyponatremia or hypernatremia affect the acid base status? How are those conditions called?
excess of free water (hyponatremia) –> dilutional acidosis
deficit of free water (hypernatremia) –> contraction alkalosis
Explain how hypochloremia or hyperchloremia can indicate alkalosis or acidosis
Cl and HCO3- are reciprocally linked in many processes within the body, e.g., gastric acid secretion, intestinal bicarbonate secretion, renal acid-base handling, transcellular ion exchange
–> when Cl ion is excreted, a bicarbonate ion is retained and vice versa
can use Cl as an estimate –> increased Cl associated with decrease in bicarbonate and vise versa
Explain how lactic acidosis leads to acidosis
lactate is produced during anaerobic metabolism –> pyruvate not incorporated in the Kreb’s cycle –> pyruvate converted to lactate instead to regenerate NAD –> allowing for ongoing glycolysis
happens concurrent with equimolar production of H+ as consequence of hydrolysis of ATP (for every mole lactate produced, 1 mole of H+ is produced)
Name examples of causes for hyperlactatemia that are not or little associated with acidosis
- cytokine mediated increases in glucose metabolism
- hyperventilation
- beta-adrenergic receptor agonists
- contaminaton of blood sample with lactated Ringer’s solution