CO8 Acid Base Flashcards

1
Q

Evaluation of Acid/Base Disturbances
- blood gas machine can tell us:

A
  1. blood gas analysis
  2. actual base excess

<><><><>

Arterial Blood Gas Analysis:

  1. Ventilation–O2&PCO2
  2. Actual blood pH
  3. Primary disturbance(s)
  4. Compensatory response
  5. Base Excess – bicarb
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2
Q

Evaluation of Acid/Base Disturbances
- biochem profile can tell us

A
  1. Total CO2
  2. Strong ions
  3. Anion Gap
  4. Strong Ion Gap (proteins)
  5. Strong Ion Difference
    <><><><>
    Biochemical Profile
    * Metabolicdisturbances – AG, SIG, SID
    – *TCO2
    – What can we fix?
    – Nothing about pH or compensatory response
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3
Q

TCO2 is a measurement of?
- on biochem profile, equivalent to what?

A

*TCO2 is a measurement of all CO2 dissolved in serum

> On the biochemical profile, because of the 20:1 ratio, we say that tCO2 = bicarb
<><><><>
cells excrete CO2 as metabolic byproduct, which goes into plasma
doesn’t like to be in plasma, so goes into RBC
quickly combines with water to form bicarb
bicarb likes to be dissolved in water

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4
Q

why look at acid base?

A
  • can tell where problem is ie. lungs, kidneys, GI
  • helps us determine how to fix it?
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5
Q

Blood Gas Analysis – Sample Collection

A
  • Arterial or venous > heparinized
    – pO2, pCO2, pH, electrolytes, lactate
    – Calculate HCO3- & base excess
    <><>
  • Cap syringe w. stopper – Mix well!
  • No air bubbles/clots
  • Analyze ASAP
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6
Q

can a compensatory A/B disorder response fix pH?

A
  • NEVER
    > can get close but. not perfect
    > never get overcompensation - if we see something like this, means mixed disturbance
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7
Q

2 ways we can get metabolic acidosis?
what compensation will we see?

A

i. Metabolic Acidosis: Loss of HCO3-
<><><><>

  1. Increased acid –titrates out HCO3-
    – Ketones, lactate, uremic acids, sulfate
    – Toxins (toxic metabolites of ethylene glycol, salicylates, ammonium chloride)
  2. Decreased base –loss of HCO3-
    – Diarrhea, ileus, ptyalism (ruminants), urinary loss

<><>
Compensation:
* Respiratory alkalosis = ↓ pCO2 = compensation
> animal increases ventilation to blow off respiratory acid

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8
Q

how do we get a respiratory acidosis? compensation?

A

Respiratory Acidosis: Gain of pCO2
<><><><>
Hypoventilation
– Anesthesia, abnormal muscle function, diffuse
pulmonary disease, altered CNS function
– ↑ pCO2 (hypercapnia)
<><>

Compensation:
- Metabolic alkalosis = ↑ HCO3- = compensation
> kidney recaptures more bicarb out of the lumen

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9
Q

2 ways we can get metabolic alkalosis? compensation?

A
  1. Decreased acid
    – Abomasum/rumen
    – Blocked pylorus
    – Vomit / reflux
    – Renal loss of H+
    – Ileus
    Sequestration or loss of HCl
  2. Increased base – administration of HCO3-
    <><>

Compensation:
* Respiratory acidosis = ↑ pCO2 = compensation
> animal does’t breathe as frequently or deeply, builds up respiratory acid

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10
Q

how do we get respiratory alkalosis? compensation?

A

Respiratory Alkalosis: Loss of pCO2
<><>

  • Hyperventilation, hypoxemia, hyperthermia, stimulation of medullary respiratory centre
  • ↓ pCO2 (hypocapnia)
    <><>
    Metabolic acidosis = ↓ HCO3- = compensation
    > kindey lets bicarb escape from the body
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11
Q

is compensation equivalent to a mixed acid base disturbance?

A

The compensatory response to a primary abnormality
is NOT a mixed disturbance
- mixed refers to an underlying abnormality in resp and metabolic pathways

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12
Q

TCO2 on the bioichem profile tells us what? what does it mean if it is high or low?

A

*TCO2 on the biochemical profile > measurement of all CO2 dissolved in serum

↓TCO2 = metabolic acidosis
↑TCO2 = metabolic alkalosis
> because it essentially represents bicarb, due to 20:1 ratio

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13
Q

what is included in the anion gap calculation? what does it tell us?
- remember what is shown to us on the biochem profile:

A
  • Biochemical profile: Na+ K+ Cl- HCO3-
    – i.e., strong ions and a weak anion
    – Cations: Ca2+ Mg 2+
    > Rarely markedly disordered
    – Anions that are not measured on the biochem profile: proteins, phosphate, sulfate, lactate, metabolites of
    ethylene glycol, salicylate
    <><>
    AG = (Na+ +K+)–(Cl- +HCO3-)
    <><>
    AG gives us an estimate of the contribution of unmeasured anions to Acid/Base status
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14
Q

Anion gap independent variables? dependent variables? what does this mean?

A

independent variables:
Change all by themselves = Na+ K+ Cl-
<><>
HCO3- is a dependent variable.
It changes because of changes in Cl- or UA

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15
Q

difference between anion gap reference values in clin path vs anesthesia? met acid vs alkalosis reference for anesthesia?

A
  • clin path has a long time to interpret data:
    > gives ranges of normal
    – 15-26 mmol/L SA
    – 13-22 mmol/L LA
    <><>
    Anesthesia has mere seconds to interpret data:
    – Metabolic acidosis >20 – Metabolic alkalosis <20
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16
Q

what does the strong ion gap tell us? reference number and what it tells us?

A
  • Adjusts Anion Gap for contribution of proteins
  • Determine unmeasured anions alone
  • SIG = AG – (Total Protein x 0.25)
    <><>
  • SIG>5 means unmeasured anions are present
    <><>
    e.g., animal has TP of 87 (high) and AG of 32 (high) – SIG=32-(87 x 0.25)
    = 32 - 20.5
    = 11.5
    > this could represent eg. ketones, lactate, uremic toxins, etc. depending on the underlying disease present
17
Q

how do strong ions affect A/B status?

A

Alkalemia:
- loss of Cl-, eg. from vomiting, cow with LDA, lab with gastric foreign body… they have sequestered chloride from the system so there is a loss of chloride
- increased Na+ or K+
> increased Na+ from dehydration
> increased potassium from hypoadrenocorticism (Addisons)
<><>
Acidemia:
- increased Cl-
- loss of Na+, K+, HCO3- > eg loss of bicarb in diarrhea, urine

18
Q

High Anion Gap Metabolic Acidosis
- caused by what? how is bicarb affected?

A

Caused by “gain of acid”:
a. Ketones
a. Lactic acid
> dehydration, diarrhea
b. Sulfates
b. Phosphates
b. Uremic acids
> acute kidney injury or end-stage kidney dz
c. EG metabolites
<><>
bicarb will be lower to fulfil electroneutrality
> bicarb low because it is mopping up all the excess H+ ions
(Cl-, Na+, K+ remain relatively normal)

19
Q

“Titrational Metabolic Acidosis” biochemical profile:

A
  • Decreased tCO2-
  • Normal Cl-
  • Increased K+
    > K+ comes into blood, H+ from blood moves into tissues (down its concentration gradient) > switcheroo
20
Q

Mixed Metabolic Acidosis & Alkalosis
- when do we see this?

A
  1. High GI obstruction & dehydration
  2. Vomiting & dehydration
    <><>
    * Decreased Cl- + increased AG (lactate)
    * tCO2 normal to increased
21
Q

Normal Anion Gap w. Loss of Chloride but No Dehydration
- when would we see this?

A

Loss/sequestration of Cl- rich fluid:
* Gastric vomiting – without dehydration
* High GI obstruction – without dehydration
* Sweating in horses
> decreased Cl-
> increased HCO3-
<><>
Bicarb has increased to make up for decreased Cl- in our AG calculation

22
Q

Normal Anion Gap w. Selective Loss of Bicarb
- when would we see this?

A

Caused by:
Selective loss of HCO3-
* Leading to Cl- retention
* ↑ Chloride = SID metabolic acidosis
* “Secretional Acidosis”
> diarrheaing out bicarb, peeing it out, losing it in drool