Lactate

Question 1

Lactate Normal

Answer 1

Normal = 0.5-2.5 mmol/L dogs and cats

Question 2

Formation of Lactate

Answer 2

Anion/conjugate base of lactic acid: lactic acid = strong acid, fully dissociates at physiologic pH which releases its hydrogen = acidosis
o
Produced in cytosol from pyruvate by lactate dehydrogenase (LDH) during normal glycolysis
 LDH reaction bidirectional, drive toward lactate production – 10:1 lactate:pyruvate

Most of lactate released into blood from lactate producing tissues crosses cell membranes via monocarboxylic acid transporters, enters plasma/RBCs

Question 3

How much of blood lactate carried by RBCs?

Answer 3

30%

Question 4

Lactate - Following Production/Release into Blood Stream

Answer 4

Once blood reaches low lactate producing tissue (liver > kidney) lactate taken up via diffusion (down concentration gradient)
 L lactate used in liver > kidney for gluconeogenesis, other cells for energy production
 Oxidized via tricarboxylic acid cycle after conversation back to pyruvate

Question 5

Lactate Half Life in Healthy Animals?

Answer 5

20-60’

Question 6

Lactate Shuttle

Answer 6

movement btw production cell, metabolized cell

Question 7

Main Sources of lactate production in physiological circumstances

Answer 7

SkM (50%), intestine RBCS, brain, skin

Question 8

Lactate means?

Answer 8

• Representation of global tissues – disproportionately overweighs large tissue masses
  o May not be sensitive acute measure of oxygen deficiency in tissues with low mass, high O2 demand (brain, kidney)

Question 9

Which form of lactate is routinely measured?

Answer 9

L - Lactate

Question 10

D Lactate

Answer 10

cattle especially, other ruminants, dogs with parvo, cats with DM/GI dz
 Produced by bacteria, can be absorbed into circulation – encephalopathy (floppy kid syndrome)
 Not detected by routine analyzers
 Suspected in non dehydrated animals with neurologic clinical signs, high anion gap metabolic acidosis that cannot be explained by L lactate results or other acids

Question 11

Type A Lactic Acidosis

Answer 11

TISSUE HYPOXIDA

Question 12

MOA Type A LA

Answer 12

 DT decreased aerobic glycolysis from tissue hypoxia
 Accumulation of pyruvate in cytosol, converted to lactate
 If local normally functioning cells cannot take up excess lactate produced by hypoxic cells, excess lactate enters circulation

Question 13

Type B LA

Answer 13

No Tissue Hypoxia

Question 14

MOA Type B Lactic Acidosis

Answer 14

Inability of the mitochondria to process pyruvate

DT increased aerobic glycolysis, defects in ability of mitochondria to take up pyruvate (eg thiamine deficiency), decreased consumption of lactate by tissues (eg liver failure)
 NE, EPI: direct stimulation of glycolysis, activation of m Na/K ATPase
 Increased metabolism, inflammatory cytokine stimulation

Question 15

MOA Type B Lactic Acidosis, B1

Answer 15

increases in lactate due to underlying diseases
* Cancer
* DM especially with DKA
* Sepsis: liver becomes lactate producer versus consumer, vascular changes in microcirculation and endothelial dysfunction - regional tissue hypoxia, abnormal mitochondrial respiration
* Stimulation of SNS by catecholamines via stimulation of glycolysis

Question 16

MOA Type B Lactic Acidosis, B2

Answer 16

increases in lactate due to drugs
* Impairment of mitochondrial function, liver function or stimulation of SNS
* Acetaminophen, glucocorticoids, beta 2 adrenergic receptors etc.

Question 17

MOA Type B Lactic Acidosis, B3

Answer 17

Congenital inborn errors of metabolism
* mitochondrial dysfunction or glycolytic pathway

Question 18

Clinical Indication for Lactate Measurement/Monitoring

Answer 18

o Patients at risk for increased lactate
o Shock
o Thromboembolism
o GDV
o Excessive muscular activity – e.g. seizures
o Substantial traumatic event – e.g. hit by car
o Primary hypoxemia
o Significant/prolonged hypotension