1. Loss or sequstriation of HCl

2. Metabolic Acidosis w/ Ketones or Lactate

Buffer for H+

Dependent on SODIUM - H+ ANTIPORT (proximal tubule)

Dependent on H+ pump (Distal nephron)

Metabolic Alkalosis (Increase HCO3)

·      Takes up to 3-5 days to develop

·      Tubular epithelial cells stimulated to secrete H+ ion  à HCO3 generation 

1. Increased production of H+ ions 

(Ketoacidosis, Lactic Acidosis, Toxins)

2. Decreased excretion of H+ ions by Kidneys 

Renal Failure (dec. functional mass)

Urinary tract Obstruction 

Uropertioneum

Hypoadrenocorticism (b/c aldosterone stimulates renal H+ sercretion)

Besides increased H+ production and renal dz can also have loss 

1. Loss of pancreatic HCO3 rich fliuds

2. Proximal renal tublar acidosis. (tubules lose abiliy to retain HCO3)

All anions other than Cl and HCO3-

Health - Albumin, Globulins, Phosp, Sulfates

Dz = Lactate, KEtone bodies 

All other cations besides Na+ and K+

Health - Ca++ and Mg++

1. Metabolic Acidosis 

2. Recognizing Mixed Metabolic Acid/Alkalosis 

3. Decrease in UC (Cations)

1. Inc Production of Lactate 

2. Decreased removal of lactate 

1. Kidney /Liver overwhelmed by Lactate

2. In Vitro  -RBC break down glucose

3. In VIVO - Tissue hypoxia --> Anaerobic glycolysis 

4. Grain Overload. --> changes bacterial population and increases lactate

 Diabetes Mellitus

·      Cant utilize Glucose à so they utilize fat

§  Starvation/Prolonged Anorexia

·      Start to use fat

§  Endurance racing

·      Fat stores for energy

§  Freshening in Cows

·      High demands

·       

Responds QUICKLY (minutes)

will increase or dec CO2 levels 

Urea

Glucose 

§  Shifts freely across membranes

§  Ex: UREA

§  Doesn’t freely shift across the membrane

§  Will cause Water to shift in attempt to equalize [solute]

§  Ex. Glucose and Na+  - Both contribute to osmolality 

·      ADH release and renal resorption of water

·      é thirst 

WHen there is an increase in the EFFECTIVE osmolality

Na and Glucose Increases can cause 

Increase in Urea Would NOT cause ADH release 

Most animals show Metabolic Acidosis 

Cattle are different --> They show Metabolic Alkalosis with renal failure 

in Carotid and Aortic Body 

respond to H+ ions AND Hypoxemia 

Takes DAYS to respond

responds by altering H+ and Bicarb levels 

éH+     êpH    êHCO3

Respiratory compensation: Hyperventilation to blow off CO2 (inc excretion)

Renal Compensation(if kidneys not affected): Increase H+ excretion and inc HCO3 resorption 

Useful for Metabolic Acidosis 

Suggests an Acid Gain  (Inc H+ production or Dec. H+ Secretion)

Because if AG is normal it suggests HCO3 loss not H+ gain 

Suggests that the Metabolic Acidosis is caused by 

1. Increased production of H+ Ion 

2. Decreased secretion of H+ ions 

Lactic Acidosis, Ketoacidosis, renal acids

Same as Bicarb but a little higher 

HCO3 + dissolved CO2 

Amount of Acid needed to bring pH to 7. 4 

Calculated assuming normal CO2

(independent of resp effects)

Metabolic Acidosis 

need to remove acid 

Metabolic Alkalosis 

add acid 

get from arterial Blood gas

tells you NOTHING about oxygen carrying capacity 

Looks at respiratory function 

A) Anorexia***
B) In vitro hemolysis

C) Metabolic acidosis
D) Anuric renal failure
E) Hypoadrenocorticism

A) Diarrhea 
B) Dehydration

C) Ketoacidosis
Feedback: Loss of ketones in urine result in decreased chloride resportion
D) Diabetes insipidus 
E) Hypoadrenocorticism

A) Urea
b) Lactate**

C) Sodium
D) Glucose
E) Chloride
Feedback: Increased Cl typically means that there will not be increased unmeasured anions which is what makes up the anion gap.

A) Urea
B)Lactate

C) Sodium
D) Albumin
E) Bicarbonate

Sodium and Glucose can  EFFECTIVE osmole 

Urea effects osmolality but not EFFECTIVE osmole