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Anesthesia > Blood gas analysis > Flashcards

Blood gas analysis Flashcards

1
Q

Arterial sampling

A

required to evaluate oxygenation

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2
Q

Venous sampling

A

Ok for acid-base evaluation
pH lower and PCO2 higher than arterial
Cannot evaluate oxygenation

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3
Q

Sampling

A

Rapid analysis and minimizing air contamination important

handheld analyzer common and convenient

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4
Q

Measured variables

A

pH
pCO2
PO2
lactate, electrolytes

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5
Q

Calculated variables

A

HCO3-
BE
SaO2

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6
Q

Acid-base physiology

A

acids are produced on a constant basis by metabolism
H+ from proteins and phospholipids
CO2 from carbohydrate and fat
H+ ions maintained within a narrow range to maintain enzyme function and cell structure
Dissolved CO2 is generally maintained within a narrow range by alveolar ventilation
pH is a logarithmic scale
-small changed in pH represent large changes in H concentration
pH = -log10[H+]

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7
Q

Acid

A

proton donor
CO2 is a potential acid
combines with H2O to form H2CO3 (carbonic acid)

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8
Q

Base

A

Proton acceptor

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9
Q

Severe acidemia

A

pH <7.2
decreased cardiac output
Decreased arterial blood pressure
Ventricular arrhythmias

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10
Q

Severe alkalemia

A

less clinical concern
Secondary to electrolyte changes
Hypokalemia=muscle weakness, arrhythmias
Hypocalcemia=decreased contractility, vasodilation

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11
Q

Buffer

A

Can accept or donate protons to minimize a change in pH
Bicarb (extracellular)
Proteins, phosphates (intracellular)
the bicarbonate-carbonic acid buffer system is used to monitor acid-base status in clinical practice

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12
Q

Henderson-hasselbach

A

pH is a function of the ratio between HCO3 and PCO2
as HCO3 inc, pH inc
as PCO2 inc, pH dec

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13
Q

Practical buffering-Response to a non-volatile acid:

A
  • immediate buffering by HCO3-

- inc in alveolar ventilation -> decreased CO2 = respiratory compensation

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14
Q

Practical buffering-Response to the volatile acid CO2:

A

Requires the kidneys

  • increased HCO3- reabsorption and H+ excretion
  • requires 2-5 days for maximum effect = metabolic compensation
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15
Q

Acid base disorders

A 
acidemia or alkalemia (defined by pH)
Acidosis or alkalosis (defined by changes in CO2 and/or HCO3-)
four primary disorders possible
-metabolic acidosis (low HCO3)
-metabolic alkalosis (high HCO3)
-respiratory acidosis (high CO2)
-respiratory alkalosis (low CO2)
Compensatory (secondary, adaptive) responses return the pH towards normal 
-overcompensation does not occur
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16
Q

Compensation

A

respiratory compensation for primary metabolic disturbances starts immediately- but anesthesia will blunt or eliminate this response
Metabolic compensation for primary respiratory disturbances occurs in two phases:
-immediate: small change in HCO3 due to titration of intracellular buffers
occurs during anesthesia
-2-5 days: large change in HCO3 due to renal changes in excretion and reabsorption
does not occur during anesthesia (takes too long)

17
Q

Mixed acid base disorder

A

simple disorder: primary disorder plus expected compensatory response
Mixed disorder: at least 2 separate abnormalities
-pH inconsistent with the change in PCO2 or HCO3-
-normal pH with abnormal PCO2 or HCO3-
-HCO3- and PCO2 changing in opposite direction

18
Q

Evaluate pH

A

normal: 7.35-7.45
Acidemia: pH <7.35
Alkalemia: pH >7.45

19
Q

Evaluate the respiratory component (PCO2)

A

normal: 40 +/- 5 mmHg
Respiratory acidosis >45
Respiratory alkalosis < 35
This is the partial pressure (mmHg) of CO2 in the blood
CO2 is a product of metabolism and is eliminated via alveolar ventilation
PCO2=CO2 production/alveolar ventilation
>45 = hypercapnia, hypoventilation
<35= hypocapnia, hyperventilation
this is not your blood gas diagnosis
Does not describe breathing pattern
PCO2 cannot be estimated from respiratory rate, effort, or tidal volume

20
Q

Evaluate the metabolic component (HCO3- and BE)

A

normal HCO3- = 24 +/- 4 mEq/L
Metabolic acidosis <20
Metabolic alkalosis >28

Normals are species-dependent
Herbivores are normally higher 
-sheep ~30 mEq/L
-Donkey ~28 mEq/L 
Cats are lower
21
Q

Metabolic component-base excess

A

Normal BE = 0 +/- 4mEq/L
Metabolic acidosis 4

Amount of strong acid or base required to titrate 1 L of blood to pH 7.40 at 37C with a constant PCO2 of 40 mmHg
Derived using pH and PCO2
A negative number is called a base deficit

22
Q

Anion gap

A

used to define a metabolic acidosis
Difference in major cations and major anions (Na+ + K+)- (Cl- + HCO3-)
Normal = 12-24 mEq/L (dogs)

Normal anion gap acidosis = high Cl-
Increased anion gap is d/t increase in unmeasured anions (Cl normal)
-lactic acidosis
-ketoacidosis
-toxins (alcohols, aspirin)
23
Q

Evaluate the PaO2

A 
Normal PaO2 (room air)= 90-110 mmHg 
Hypoxemia < 60 mmHg

PaO2 varies based upon the fraction of inspired oxygen (FiO2)
Room air FiO2= 0.21
100% O2= 1.0
A normal PaO2/FiO2 is >500

24
Q

Hypoxemia

A

refers specifically to low PaO2

25
Q

Hypoxia

A

low oxygen content in the tissues

26
Q

Hypoxia hypoxia

A

low PaO2 causing low blood content of oxygen

27
Q

Anemia hypoxia

A

low or abnormal hemoglobin causing low blood content of oxygen

28
Q

Circulatory hypoxia

A

poor perfusion (shock or local obstruction) causing poor oxygen delivery to tissues

29
Q

Histotoxic hypoxia

A

toxic substance causing tissues to be unable to use oxygen

30
Q

causes of hypoxemia

A

Hypoventilation (in generally only if breathing room air)
Diffusion impairment (rare)
Anatomic right to left shunt (PDA, tetralody)
Decreased FiO2 (delivery of a hypoxic mixture)
V/Q mismatch

31
Q

V/Q mismatch

A

ventilation/perfusion missmatch
Common clinical problem in vet med- esp under anesthesia
If breathing >21% O2 will lead to decreased PaO2:FiO2
Not necessarily hypoxemia unless severe

32
Q

Ventilation-perfusion mismatch

A

Could be perfusion without ventilation or ventilation without perfusion

33
Q

Perfusion without ventilation

A

No oxygen in alveolus
Atelectasis- common under anesthesia even in healthy animals
lung disease (pneumonia, pulmonary edema etc)

34
Q

Ventilation without perfusion

A

Rare in healthy animals
severe decrease in cardiac output (shock)
pulmonary thromboembolism

35
Q

Atelectasis

A

Lung collapse after induction to anesthesia due ot
weight and positioning (horses esp)
administration of 100% O2 (absorption atelectasis)
May persist for hours-days after anestehsia
Leads to V/Q mismatch due to perfusion without ventilation
Decreases PaO2: FiO2

36
Q

Lactate

A

Product of anaerobic glycolysis/metabolism
Normally produced at low levels by skin, RBC, brain, skeletal mm, and GI tract during rest
Liver can use lactate for gluconeogenesis
Tissue hypoxia –> lactate production by skeletal muscle and GI tract
-lactate increases when production exceeds clearance
Lactic acidosis results in an increased anion gap (it’s an unmeasured anion)

Normal <2mmol/L
Causes of lactic acidosis (>5)
-Type A: hypoxic
-Type B: nonhypoxic- toxins, DM, neoplasia, sepsis)
Hypoxic: increased O2 demand- decreased tissue perfusion (dec CO)
-shock, anesthetic complications
decreased arterial oxygen content
-hypoxemia, severe anemia
may inc with any shock- systemic hypoxia d/t poor perfusion
inc with specific pathologies causing ischemia, esp GI tract
-GDV, Colic
Lactate may be used as a prognostic indicator
-measurement at one time point less helpful
-trend is important (inc over time = poor prognosis)

Anesthesia (12 decks)

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