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Advanced Principles of Anesthesia > Week 9 - Blood Gas Analysis > Flashcards

Week 9 - Blood Gas Analysis Flashcards

1
Q

Why do we care about acid-base balance in anesthesia?

A

A physiologic acid-base balance optimizes enzyme function, myocardial contractility, and saturation of hemoglobin with oxygen

*increase in carbon dioxide forces pH to drop, which causes the affinity of Hbg to oxygen to decrease

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2
Q

What is the carbonic acid-bicarbonate buffer equation?

A

Equation

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3
Q

What role does the kidneys play in acid-base balance?

A

Proton secretion (H+) and HCO3 filtration

  • if PCO2 rises, proton secretion becomes dominant and the kidney excretes acid, raising blood pH
  • if HCO3 rises, HCO3 filtration increases and the kidney excretes alkali, reducing blood pH

*adjusts H+ ion secretion and HCO3 filtration in response to elevated CO2 or HCO3

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4
Q

What are the normal arterial blood gas values for the following on room air?

  • pH
  • PCO2
  • HCO3
  • PO2
A

pH 7.35-7.4
PCO2 35-45 mmHg
HCO3 22-28 mEq/L
PO2 80-100 mmHg

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5
Q

What are the normal venous blood gas values for the following on room air?

  • pH
  • PCO2
  • HCO3
  • PO2
A

pH 7.30 - 7.40
PCO2 42-48 mmHg
HCO3 24-30 mEq/L
PO2 35-45 mmHg

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6
Q

Fill in the chart

A
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7
Q

How does the body compensate for acidemia and alkalemia?

A
  • Metabolic Acidosis –> Respiratory compensation (CO2 <40)
  • Respiratory Acidosis –> Renal compensation (HCO3 >24)
  • Metabolic Alkalosis –> Respiratory compensation (PCO2 >40)
  • Respiratory Alkalosis –> Renal compensation (HCO3 <24)
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8
Q

How long does it take for acid-base compensation to occur?

A

Respiratory compensation is almost immediate

Metabolic compensation takes 6-12 hrs to appear, several days to maximize

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9
Q

What is acute respiratory acidosis? What can cause this in anesthesia?

A

Increase in CO2

  • Hypoventilation (pressure control ventilation)
  • Increased CO2 production (MH, sepsis, shivering, prolonged seizure, thyroid storm)
  • Rebreathing (exhausted or missing CO2 absorber, incompetent one way valves)
  • Laparoscopic insufflation
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10
Q

How do you treat respiratory acidosis?

A
  • Most cases, increase ventilation (bronchodilation, reversal of narcosis or sedation)
  • Decrease CO2 production (dantrolene, tx shivering)
  • In chronic respiratory acidosis (return to baseline PCO2, respiratory drive may be dependent upon low PaO2)
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11
Q

What is chronic respiratory acidosis?

A

Elevated PCO2 with near normal pH

Shift to right of respiratory response curve

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12
Q

What is the cause of respiratory alkalosis?

A
  • Usually due to over-ventilation and usually easily remedied by decreasing total minute ventilation
  • If spontaneous, maybe be caused by increased breathing due to pain, anxiety, drugs, CNS disease, fever etc…
  • Decreases stimulus to breathe
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13
Q

What is metabolic acidosis? What is typical compensation?

A
  • Accumulation of any acids in the body

- Normal physiologic compensation is to increase respiratory rate – if mechanically ventilated we need to compensate

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14
Q

How is metabolic acidosis diagnosed?

A

Differential Diagnosis = Anion Gap

-provides info as to whether the acidosis is due to increased acid accumulation or bicarbonate loss

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15
Q

What is the anion gap?

A

Difference between major measured cations (Na+) and anions (Cl- + HCO3-)
-there are always more unmeasured anions (albumin…) than cations (K+, Ca++..)

Normal Gap is 7-14

Anion Gap = [Na] - [Cl + HCO3]

*any process that increases unmeasured anions or decreases unmeasured cations will increase the gap (and vice versa)

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16
Q

What is metabolic acidosis with an increased gap characterized by?

A

An increase in relatively strong nonvolatile acids

  • these acids dissociate into H+ and their respective anions
  • the H+ consumes HCO3 to produce CO2, whereas their anions (conjugate bases) accumulate and take the place of HCO3 in extracellular fluid
17
Q

What is typical causes of high anion gap acidosis?

A

Lactic acidosis

Ketoacidosis

*acid present that dissociates with H+ which consumes bicarb

18
Q

What are causes of intra-op high anion gap lactic acidosis?

A

Tissue Hypoperfusion

Hypoxemia

19
Q

What are the causes of intra-op high anion gap non-lactic acidosis?

A

Ketoacidosis – diabetes, ethanol, starvation

Uremia
Salicylates
Ethylene glycol
Methanol
Paraldehyde
Isoniazid
20
Q

What is intraop development of metabolic acidosis frequently attributed to?

A

Hypovolemia

Tissue Hyoperfusion

Lactic Acidosis

21
Q

How do you treat lactic acidosis?

A
  • Increase oxygenation
  • Controlled respiration, keep PaCO2 in low 30s
  • Fluid resuscitation
  • Circulatory support, maintain BP and CO!
  • Bicarb (only for severe acidosis <7.1) – doesn’t treat problem, only temp measure and may cause intracellular acidosis, must increase RR to compensate for CO2
22
Q

What are causes of normal anion (hyperchloremic) gap acidosis?

A
  • GI loss of bicarb (diarrhea – pancreatic, small bowel, biliary fluids are all rich in bicarb)
  • Renal wasting of bicarb (renal tubular acidosis)
  • Dilutional hyperchloremic acidosis (rapid volume expansion with 0.9% NS results in excessive chloride and impaired bicarb reabsorption)
23
Q

What is the equation to determine the bicarb deficit in mEq?

A

Deficit in mEq = Base Deficit x 0.3 x bodyweight (kg)

24
Q

Define base excess

A

The amount of strong acid or base that has to be added to a sample of blood to produce a pH of 7.4

-reflects the non respiratory contribution to acid-base balance (the metabolic component)

25
Q

What are the base deficit categories?

A

Normal: -2 to 2
Mild: -5 to -3
Moderate: -9 to -6
Severe: < -10

26
Q

What is metabolic alkalosis and its causes?

A

Gain of bicarbonate or loss of hydrogen

  • loss of H+ from stomach (vomiting) or kidney (diuretic therapy)
  • Alkali administration (citrate in blood products, TPN, giving bicarb)
  • hypovolemia leading to decreased chloride which increased bicarb reabsorption with sodium

*may be compensatory from over-ventilation

27
Q

What is the 1 for 10 rule for ACUTE Respiratory Acidosis?

A

HCO3 will increase by 1 mmol/L for every 10 mmHg elevation in pCO2 above 40 mmHg

Expected HCO3 = 24 + {(Actual pCO2 - 40) / 10}

  • ex. pt with acute respiratory acidosis (pCO2 60mmHg) has an actual HCO3 of 31 mmol/L.. the expected HCO3 for this acute elevation of pCO2 is 24+2 = 26 mmol/L
  • the actual measured value is higher than this indicating that a metabolic alkalosis must also be present
28
Q

What is the 4 for 10 rule for CHRONIC respiratory acidosis?

A

HCO3 will increase by 4 mmol/L for every 10 mmHg elevation in pCO2 above 40 mmHg

Expected HCO3 = 24 + 4 {(Actual pCO2 - 40) / 10}

  • pt with chronic respiratory acidosis (pCO2 60) has an actual HCO3 of 31.. the expected HCO3 for this chronic elevation is 24 + 8 = 32
  • the actual measured value is extremely close to this so renal compensation is maximal and there is no evidence indicating a second acid-base disorder
29
Q

What is the compensation formula for metabolic acidosis?

A

pCO2 = 1.5 [HCO3] + 8

30
Q

What is the compensation formula for metabolic alkalosis?

A

pCO2 = 0.9 [HCO3] +16

31
Q

What is the compensation formula for respiratory acidosis?

A

For every 10 change in pCO2, pH decreases by:

  1. 08 in acute resp acidosis
  2. 03 in chronic resp acidosis
32
Q

What is the compensation formula for respiratory alkalosis?

A

For every 10 change in pCO2, pH increases by:

  1. 08 in acute respiratory alkalosis
  2. 03 in chronic respiratory alkalosis
33
Q

What is the step by step approach to interpreting blood gas?

A
  1. Look at pH
  2. What is the process? look at pCO2 and HCO3 to distinguish the initial change from the compensatory response
  3. Calculate the anion gap (Na - (Cl + HCO3))
  4. Is compensation adequate? calculate estimated pCO2 (1.5 x HCO3 + 8 +/- 2)

Advanced Principles of Anesthesia (31 decks)

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