Blood gas analysis Flashcards by Rebecca Murphy

Arterial sampling

required to evaluate oxygenation

How well did you know this?

Not at all

Perfectly

Venous sampling

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

How well did you know this?

Not at all

Perfectly

Sampling

Rapid analysis and minimizing air contamination important

handheld analyzer common and convenient

How well did you know this?

Not at all

Perfectly

Measured variables

pH
pCO2
PO2
lactate, electrolytes

How well did you know this?

Not at all

Perfectly

Calculated variables

HCO3-
BE
SaO2

How well did you know this?

Not at all

Perfectly

Acid-base physiology

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+]

How well did you know this?

Not at all

Perfectly

Acid

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

How well did you know this?

Not at all

Perfectly

Base

Proton acceptor

How well did you know this?

Not at all

Perfectly

Severe acidemia

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

How well did you know this?

Not at all

Perfectly

Severe alkalemia

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

How well did you know this?

Not at all

Perfectly

Buffer

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

How well did you know this?

Not at all

Perfectly

Henderson-hasselbach

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

How well did you know this?

Not at all

Perfectly

Practical buffering-Response to a non-volatile acid:

immediate buffering by HCO3-

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

How well did you know this?

Not at all

Perfectly

Practical buffering-Response to the volatile acid CO2:

Requires the kidneys

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

How well did you know this?

Not at all

Perfectly

Acid base disorders

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

How well did you know this?

Not at all

Perfectly

Compensation

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)

Mixed acid base disorder

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

Evaluate pH

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

Evaluate the respiratory component (PCO2)

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

Evaluate the metabolic component (HCO3- and BE)

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

Metabolic component-base excess

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

Anion gap

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)

Evaluate the PaO2

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

Hypoxemia

refers specifically to low PaO2

Hypoxia

low oxygen content in the tissues

Hypoxia hypoxia

low PaO2 causing low blood content of oxygen

Anemia hypoxia

low or abnormal hemoglobin causing low blood content of oxygen

Circulatory hypoxia

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

Histotoxic hypoxia

toxic substance causing tissues to be unable to use oxygen

causes of hypoxemia

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

V/Q mismatch

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

Ventilation-perfusion mismatch

Could be perfusion without ventilation or ventilation without perfusion

Perfusion without ventilation

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

Ventilation without perfusion

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

Atelectasis

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

Lactate

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)