Blood gas analysis Flashcards
Arterial sampling
required to evaluate oxygenation
Venous sampling
Ok for acid-base evaluation
pH lower and PCO2 higher than arterial
Cannot evaluate oxygenation
Sampling
Rapid analysis and minimizing air contamination important
handheld analyzer common and convenient
Measured variables
pH
pCO2
PO2
lactate, electrolytes
Calculated variables
HCO3-
BE
SaO2
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+]
Acid
proton donor
CO2 is a potential acid
combines with H2O to form H2CO3 (carbonic acid)
Base
Proton acceptor
Severe acidemia
pH <7.2
decreased cardiac output
Decreased arterial blood pressure
Ventricular arrhythmias
Severe alkalemia
less clinical concern
Secondary to electrolyte changes
Hypokalemia=muscle weakness, arrhythmias
Hypocalcemia=decreased contractility, vasodilation
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
Henderson-hasselbach
pH is a function of the ratio between HCO3 and PCO2
as HCO3 inc, pH inc
as PCO2 inc, pH dec
Practical buffering-Response to a non-volatile acid:
- immediate buffering by HCO3-
- inc in alveolar ventilation -> decreased CO2 = respiratory compensation
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
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
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)
