Blood Gas Analysis Flashcards
Compare venous and arterial sampling
Arterial blood gases are preferred when assessing respiratory status, but venous samples also yield useful information regarding metabolic status.
Venous blood tends to have a slightly lower pH and higher partial pressure of carbon dioxide (pCO2) than arterial blood
Peripheral venous samples will not be representative in low flow states and arterial samples may not always be representative of changes occurring in peripheral tissues.
What is the most commonly used sample site for blood gas analysis?
Dorsal pedal
How quickly should you analyse a sample?
Ideally immediately, but definitely within 12 mins as then there starts to be changes
What are the main causes of hypoxaemia?
Hypoventilation Venous admixture -Shunt (eg, right to left shunt) -Ventilation/perfusion (V/Q) mismatch -Diffusion impairment (of little significance small animals) Low inspired oxygen concentration
Outline V/Q mismatch
most common cause of hypoxaemia.
Impairment of normal oxygen and carbon dioxide transfer results from a mismatch in ventilation and blood flow in various regions of the lung.
Pulmonary parenchymal diseases such as pulmonary oedema, pneumonia, pulmonary contusion and pulmonary neoplasia will all lead to hypoxaemia secondary to V/Q mismatch
How does hypoventilation cause hypoxamia?
occurs secondary to either a decreased sensitivity to raising carbon dioxide concentrations in the blood (eg, during anaesthesia or with cerebral impairment) or secondary to a physical/mechanical obstruction to airflow.
this obstruction may result from laryngeal paralysis, brachycephalic obstructive airway syndrome, collapsing trachea, or a foreign body or mass associated with the upper airway
How can you determine the effect of hypoventilation on a patient’s hypoxaemia?
an alveolar-arterial gradient (A-a gradient) can be calculated
This is obtained by subtracting the arterial PaO2 from the so-called ‘ideal’ alveolar PaO2 that the lung would have if there were no V/Q mismatch (a healthy lung).
How does a shunt lead to deoxygenated blood?
results in deoxygenated venous blood bypassing the lungs and mixing with oxygenated arterial blood.
This results in an arterial sample that has a lower oxygen content than normal arterial blood and can occur secondary to multiple congenital cardiac anomalies including a right to left shunting patent ductus arteriosus (most start as left to right) and tetralogy of Fallot
What are the major cations and anions in ECF?
The major cations within the extracellular fluid are potassium (K+), sodium (Na+), calcium and magnesium.
The major anions are bicarbonate (HCO3−), chloride (Cl−), plasma proteins, organic acid anions, phosphate and sulfate
What is the anion gap?
the difference between unmeasured cations and unmeasured anions. In reality, electroneutrality is maintained and there is no gap, just unmeasured anions
An anion gap exists because not all electrolytes are routinely measured
Anion gap = (Na + K) - (Cl + HCO3)
What do you look at to assess the acid base status of a patient
Assess the pH and the PCO2
Check HCO3- and BE
How do you assess and interpret the pH for blood gases?
Is it acidaemic (pH less than 7.35)?
If yes, there must be a metabolic acidosis, a respiratory acidosis, or both
Is it alkalaemic (pH greater than 7.45)?
If yes, there must be a metabolic alkalosis, a respiratory alkalosis, or both
Is the pH within normal range (7.35–7.45)?
There is no acid-base disorder
There is an acid-base disorder with complete compensation
There are two opposing acid-base disorders (mixed)
How do you assess PCO2?
Is PCO2 increased (greater than 45 mmHg)?
Primary respiratory acidosis or
Compensatory response to a metabolic alkalosis
Is PCO2 decreased (less than 30 mmHg)?
Primary respiratory alkalosis
Compensatory response to a metabolic acidosis
How do you examine BE and HCO3-?
Is HCO3− increased (greater than 24 mmol/l) or BE positive?
There is a primary metabolic alkalosis
Is HCO3− decreased (less than 18 mmol/l) or BE negative?
There is a primary metabolic acidosis
How do you examine the oxygenation status of a patient (arterial samples only)
Examine the PaO2
Calculate the A-a gradient
How do you examine the PaO2?
Should be five times the inspired oxygen concentration (FiO2).
For example, on room air (21 per cent O2) PaO2 would be expected to be around 100 mmHg
If PaO2 greater than 90 mmHg then this is normal
If PaO2 = 75–90 mmHg, mild hypoxia
If PaO2 less than 75 mmHg, severe hypoxia
What is the alveolar arterial oxygen gradient?
The alveolar arterial oxygen gradient gives an estimate of the effectiveness of gas transfer and should generally only be interpreted on room air. It reflects the difference between the amount of oxygen in the alveoli and arterial blood.
Reference ranges: less than 20 mmHg on room air
less than 100 mmHg on 100 per cent oxygen
Outline the assessment of the anion gap
The normal range for the anion gap is between 12 to 24 mmol/l.
Increases in the anion gap are much more common than decreases and can be used to help the clinician identify the cause of a metabolic acidosis.
In healthy animals, albumin is the major unmeasured anion, but in disease states a limited number of endogenous and exogenous anions can contribute to an increase in the anion gap.
Endogenous anions include uraemic acids (such as phosphates and sulfates), ketoacids and lactic acid. Exogenous anions are produced in ethylene glycol toxicity (glycolic acid) and aspirin toxicity (salicylate). An elevated anion gap therefore helps the clinician create a relatively small list of differentials to explain the changes seen on blood gas analysis. A decreased anion gap is uncommon but can occur in hypoalbuminaemic patients.
What is metabolic acidosis?
a reduction in blood pH and a reduction in bicarbonate. It can be divided into hyperchloraemic (normal anion gap) and normochloraemic (high anion gap) metabolic acidose
BE
What is metabolic alkalosis?
increased blood pH (greater than 7.45) and an increase in bicarbonate. The most common cause of metabolic alkalosis is gastric or proximal duodenal vomiting where fluid rich in hydrogen ions is expelled in the vomit. Less common causes include diuretic therapy, primary hyperaldosteronism and hyperadrenocorticism
What is respiratory acidosis?
increased PaCO2 and a reduction in pH. This usually reflects hypoventilation and reduced alveolar gas exchange. Possible causes include pulmonary and airway disease, restrictive extrapulmonary disorders (eg, pleural effusion, flail chest, pneumothorax) and respiratory centre depression (intracranial disease or anaesthesia), or neuromuscular disease e.g. botulism, tetanus, MG
Respiratory acidosis also occurs as a compensatory mechanism for metabolic alkalosis.
What is respiratory alkalosis?
decreased PaCO2 and an increase in pH. This usually reflects hyperventilation and can be caused by pain, fear or early pulmonary disease, and can also be iatrogenic in origin (mechanical ventilation). Respiratory alkalosis may also occur as a compensatory mechanism for metabolic acidosis.
Compare respiratory and metabolic compensation
In cases with primary metabolic acidosis, the expected compensatory response is via the respiratory system with loss of carbon dioxide (hyperventilation); this is a rapid response that occurs within minutes to hours. Where a primary respiratory disturbance is present, metabolic compensation occurs via the kidneys; this is a more gradual response, which can take several days to complete.
What can cause a hyperchloraemic metabolic acidosis (normal anion gap)?
Severe diarrhoea (gastrointestinal losses) Renal tubular acidosis Dietary acidification
What can cause a normochloraemic metabolic acidosis? (high anion gap)
Renal failure Diabetes ketoacidosis Lactic acidosis Ethylene glycol toxicity Aspirin toxicity
What are the causes of metabolic acidosis in cats and dogs?
Gain of acid
Lactate (most commonly from hypoperfusion)
Ketones (b-hydroxybutyrate)
Renal failure (build up of phosphates and sulphates)
Intoxication (eg, ethylene glycol, aspirin)
Loss of bicarbonate
From the kidney (renal disease or addisons)
From the gastrointestinal tract (more of a problem in large animals)
What is pH a measure of
= log [1/H+]
What is a buffer?
A compound that accepts or donates H+
Bicarb is the main on in the ECF
What is the main equation for H+ in the body?
H20 + CO2 -> H2CO3 -> H+ + HCO3-
What would you expect for a high AG metabolic acidosis?
low bicarb
What would you expect for a normal AG metabolic acidosis?
suggests Cl has gone up
How should the respiratory system compensate a metabolic acidosis?
CO2 should drop 0.7mmol/l for every 1mmol drop in HCO3
Maximal 12-24 hours
How does the renal system compensate a metabolic acidosis?
Kidneys excrete acid NH3 -> NH4+ NH4+ excretion enhanced Cl- excreted along with NH4 HC03 regenerate and re absorbed
How can anion gap be used to diagnose the type of metabolic acidosis?
High AG - means increased unmeasured anions
Normochloraemia
e.g. lactic acidosis, uraemia, DKA, EG toxicity
Normal AG - means high Cl-, low HC03
D+
Rapid saline administration
Addisons
How would you treat metabolic acidosis?
Tx underlying cause
Administer NaHCO3 when pH <7.15 and volume resuscitated
What types of metabolic alkalosis
Can be Cl- responsive or resistant
How does Cl responsive alkalosis occur?
Development phase:
Loss of HCl from gastric fluid
Therefore increase in HCO3 in ECF
Increased HCO3 goes to kidneys to be excreted
Renal excretion of HCO3 leads to increased Na and H2O excretion
Maintenance phase:
ECF volume depletion (RAAS system activated, Na and H2O retention, K+ excreted)
Cl still low, more marked now due to Na retention
Why is hypo K+ an issue with metabolic alkalosis?
Low K+ causes H+ movement intracellularly in exchange for K+ moving out
Therefore low K+ will make low H+ worse as kidneys may lose more H+ to retain K+
What is the respiratory system compensation for metabolic alkalosis?
CO2 increases by 0.7mmol/l for every 1mmol/l rise in HCO3
Max compensation by 12-24 hours
How do you treat metabolic alkolosis?
Cl responsive
when from gastric fluid loss - 0.9%NaCl
Variable K+ supplementation needed
When from diuretic tx (therefore unlikely to want to do fluids) - oral supplementation
Cl unresponsive
Only from cushings or primary hyperaldosteronism
Tx underlying disease
What is the metabolic compensation for respiratory acidosis?
Acute - HCO3 increases by 1.5mmol/l for every 10mmHg rise in CO2
Chronic (2-3d) - HCO3 increases by 3.5 mmol/l for every 10mmHg increase in PCO2
Chronic caused by renal retention of HCO3, this takes time to kick in
How do you treat respiratory acidosis?
Underlying disease - aim to increase alveolar ventilation
give 02
Only give NaHCO3 when pH <7.1 and no response tio improved alveolar ventilation
Start IPPV if PaCO2 >60mmHg + pH <7.1
What are the causes of respiratory alkalosis?
Hypoxaemia - stimulation of the respiratory centre by peripheral chemoreceptors
Pulmonary disease - stimulation of stretch/ nociceptors
Independent of hypoxia
Centrally mediated - sepsis, drugs, exercise, central neurologic disease
Outline metabolic compensation for respiratory alkalosis
Acute:
HCO3 drops by 2.5 for every 10mmHg decline in PCO2
Chronic - HCO3 drops by 5.5 for every 10 mmHg decline in pCO2
How do you treat respiratory alkalosis?
Only tx underlying disease
Hypocapnia of limited clinical significance
