Blood Gas and Acid-Base Analysis

Question 1

What is the method for acid-base interpretation? (what steps)

Answer 1

1. Look at the pH. Identify if there is an alkalaemia (high pH) or acidaemia (low pH)
2. Assess the respiratory contribution to the pH (Use the CO2 to determine if there is a respiratory acidosis or alkalosis)
3. Assess the metabolic contribution to the pH (Use HCO3- and BE to determine if there is a metabolic acidosis or alkalosis)
4. Determine the primary process (Which process is varying in the same direction as the change in pH?)
5. Is there a secondary process and is it compensatory or a mixed disorder? (Is the magnitude appropriate for compensation alone? Is the timeline appropriate for compensation? Do the measurements correspond to the clinical status of the patient?)
6. Assess the anion gap and narrow down possible causes of the acid-base disorder
7. Summarise the findings in a concise statement (EXP: Acidaemia due to a primary metabolic acidosis with appropriate compensatory respiratory alkalosis)

Question 2

Normal pH range for a dog?

Answer 2

7.35-7.45

Question 3

What buffer systems are there?

Answer 3

1. Extracellular buffers – bicarbonate buffer system (HCO3 binds H+)
2. Intracellular buffers – proteins and phosphates (bind H+)
3. Respiratory system – as per the carbonic anhydrase equation excess H+ will result in production of CO2 and H2O then excess CO2 can be removed via ventilation
4. Renal system - excretes hyrdrogen H+ ions - regulates reabsorption of HCO3-.

Question 4

How long does it take for the renal system to ramp up?

Answer 4

3-5 days

Question 5

What can acidaemia lead to?

Answer 5

Impedance of cardiac output and contractility
Blunted response to catecholamines
Insulin antagonism
Compensatory hyperkalaemia (and its associated effects)

Question 6

What can Alkalaemia lead to?

Answer 6

• muscle spasms
• stuporous mentation
• Shifts O2 dissociated curve to the left – increases the affinity of Hb for oxygen and reduces unloading in the tissues
• hypocalcaemia
• Hypokalaemia – potassium moves into cells in exchange for H+
  Altered function of enzymes and maintenance of cell structures that require H+ ions

Question 7

Normal Base Excess range in cat and dogs?

Answer 7

Normal range for dogs is -4 to 4 and cats is -6 to 5 mEq/L.

Question 8

Normal PCO2?

Answer 8

35-45 mmHg

Question 9

Respiratory acidosis - what causes can there be?

Answer 9

Drugs that depress respiratory centre or cause relaxation of thoracic muscles e.g. sedation or anaesthesia

Neuronal/neuromuscular/muscular disease e.g. tick paralysis, botulism, snake envenomation, peripheral neuropathies, cervical spinal injury, myopathies, myasthenia gravis

Upper airway obstruction

Restrictive extrapulmonary disease - diaphragmatic hernia, pneumothorax, pleural effusions, rib fractures (pain)

Severe pulmonary disease e.g. pneumonia, asthma, pulmonary oedema

Question 10

When can increased PCO2 be life threatening?

Answer 10

> 60 mmHg,
May or may not be associated with hypoxaemia (low blood oxygen)

Question 11

What can cause decreased PCO2?

Answer 11

Fear, pain, stress, anxiety

Hyperthermia

Neurological causes affecting the respiratory centre – head trauma, neoplasia

Secondary problem – response to metabolic acidosis

Question 12

Possible causes for metabolic acidosis?

Answer 12

Lactic acidosis (shock or poor perfusion)

Renal failure - reduced ability to excrete H+ and increased loss of HCO3-

Diabetic ketoacidosis

Intestinal losses - loss of HCO3- through vomiting and diarrhoea

Question 13

Possible causes for metabolic alkalosis?

Answer 13

Gastric and intestinal obstructive processes -
* loss of H+ and chloride ions via vomiting
* sequestration and reduced reabsorption of H+ and Chloride ions in the small intestine

Hypovolaemia or dehydration in the face of hypochloraemia (low chloride) - results in reabsorption of sodium and water by the kidney (along with HCO3- instead of chloride to maintain electroneutrality)

Severe hypokalaemia (low potassium)
* K+ moves out of the cell to compensate for low serum levels - the serum concentrations increase with K+ in exchange for H+ ions causing an alkalosis
* Causes a shift of H+ into cells in proximal tubules results in an intracellular acidosis - this then promotes excretion of H+ in ammonium in the urine
* Causes H+ excretion in the proximal and distal tubules which results in further reabsorption of HCO3- and net acid excretion

Renal insufficiency

Diuretic therapy - results in free water loss (without HCO3- loss) so get a relative increased HCO3- concentration (total HCO3- hasn’t changed)

Question 14

How can you determine which process is the primary disorder?

Answer 14

The primary disorder will be in the same direction as the pH change (away from 7.4).

This includes changes that are within the normal range - if the pH is trending towards acidaemia the process that is an acidosis will be the primary disorder.

Question 15

How do you determine if there is a compensatory or secondary disorder?

Answer 15

Compensatory mechanisms will never return the pH to normal or overcompensate

The body will normally create the opposite disorder and attempt to correct the pH – a compensatory response
* Respiratory compensation is fast, taking minutes to hours
* Metabolic compensation takes 2-5 days. Assess whether the time frame of disease is appropriate for a compensatory response to occur.

Assess whether the apparent compensatory response is adequate by comparing it to the expected or required compensation. This requires calculation.

Question 16

Assess the anion gap - what parts are in it? (formula)

Answer 16

Anion Gap = ([Na+] + [K+]) - ([Cl-] + [HCO3-])

Question 17

What can affect the anion gap so we can’t trust it?

Answer 17

Because a significant portion of the anion gap is plasma protein, patients with hypoproteinaemia may have falsely low anion gaps. This can make interpretations from the anion gap unreliable.

Question 18

Normal anion gap for cats and dogs?

Answer 18

A normal anion gap in a dog is 8-21mEq/L, and for a cat is 12-16mEq/L

Question 19

Metabolic acidosis patients will have low HCO3 because of?

Answer 19

In a patient with metabolic acidosis (decreased pH) there will be a low HCO3- either because of

i) a loss of HCO3- 

ii) a gain of acid.

Question 20

What three causes of metabolic acidosis when it’s loss of HCO3?

Answer 20

Loss of HCO3- - if the lowered HCO3- is matched by an increase in Cl- and the anion gap is normal - this is a Hyperchloraemic Metabolic Acidosis

Primary causes - e.g. dilutional acidosis - with aggressive high chloride fluids (NaCl 0.9%) - the HCO3- will decrease due to increased chloride in order to maintain electroneutrality

Secondary causes - Chloride Cl- concentration increases due to losses of HCO3- (e.g. in diarrhoea or from kidney losses) in order to maintain electroneutrality

Hypoadrenocorticism.

Question 21

metabolic acidosis - not increased Cl while increased AG - what does that mean?

Answer 21

If the lowered HCO3- is not matched by an increase in Cl- the anion gap increases, and there is a gain in acid – this is a high or increased anion gap metabolic acidosis.

Question 22

MUDPILES - what does it mean?

Answer 22

high or increased anion gap metabolic acidosis - seen by lowered HCO3- that is not matched by an increase in Cl- the anion gap increases, and there is a gain in acid

MUDPILES:
M – methanol toxicity
U – uraemic acids
D – diabetic ketoacidosis
P – paracetamol, propylene glycol and paraldehyde toxicity
I – infection
L – lactic acidosis
E – ethylene glycol toxicity, ethanol toxicity
S – Salicylic acid poisoning (aspirin)

Question 23

What is lactic acid?

Answer 23

Lactic acid is a strong acid that, at physiological pH (in the body) ionizes to lactate and H+ ions.

Question 24

Hyperlactatemia and what equimolar effect does it has on BE?

Answer 24

Hyperlactatemia is the term used to describe elevated lactate.

If the lactate is associated with an acidaemia (negative BE), it can be called lactic acidosis.

Lactate has an equimolar effect on BE, that is if lactate is elevated by 5mmol/L, BEecf can be expected to decrease by 5 mmol/L (if the BE change is due to the same process as the hyperlactatemia).

If the change in base excess is greater than that which can be attributed to the change in lactate consider other causes of acidosis e.g. ketones.

Question 25

Plasma lactate concentrations are used as a?

Answer 25

MARKER of poor perfusion.

Question 26

Type A hyperlactataemia - why and causes?

Answer 26

(most common form) - due to tissue hypoxia

Hypoperfusion – shock states including cardiogenic shock

Increased muscle activity - seizures

Severe hypoxaemia / severe anaemia

Carbon monoxide poisoning

Local hypoperfusion e.g. GDV, FATE cats

Question 27

Type B hyperlactataemia - why and causes?

Answer 27

no tissue hypoxia

Diabetes mellitus, due to reduced intracellular glucose available for energy metabolism

Severe liver disease (the liver is one of the most efficient organs for lactate metabolism)

Neoplasia and sepsis (due to a hypermetabolic state)

Toxins e.g. acetaminophen

Congenital defects of mitochondria

Question 28

pH balance and electroneutrality - what does that mean?

Answer 28

Remember that in addition to maintaining pH balance the body also maintains electroneutrality – positive ions = negative ions.

When H+ is excreted in the kidneys – K+ is often retained and vice versa

When HCO3- is excreted in the kidneys – Cl- is retained and vice versa

Question 29

How does one calculate the bicarbonate deficit? How do you give it and when do you stop the giving?

Answer 29

Calculate the bicarbonate deficit = base deficit x 0.3 x BW (kg)

Give ¼ to 1/3 of dose over 20-30 minutes IV, then the rest over the next 6 – 12 hours.

Monitor serum HCO3- levels regularly and stop CRI when bicarbonate levels approach 12 mEq/L

Question 30

Normal PaO2 on room air is? And how high can it reach?

Answer 30

Normal PaO2 on room air is 80 - 100mmHg.

Although PaO2 can reach much higher levels (up to 500mmHg when breathing 100% FiO2), there is no significant benefit to oxygen transport because Hb is 100% saturated.

PaO2 greater than normal physiological levels may be associated with increased oxidant injury to cells and in severe cases, oxygen toxicity.

Question 31

At what level is PaO2 classified as hypoxaemia?

Answer 31

A PaO2 below 80mmHg is consistent with hypoxaemia and indicates requirement for oxygen supplementation

Question 32

SP02 - When does it reach severe hypoxaemia?

Answer 32

A PaO2 of 60mmHg identifies severe hypoxaemia and the need for immediate intervention. If the patient is already receiving oxygen supplementation, and FiO2 cannot be further increased, mechanical ventilation is recommended.

Question 33

What does Low V/Q mean? Causes?

Answer 33

Abnormal ventilation but normal perfusion

Pneumonia
Asthma
Pulmonary oedema
Inflammation
Pulmonary neoplasia

Question 34

What does High V/Q mean? Causes?

Answer 34

Normal ventilation but poor perfusion

Pulmonary thromboembolism
Shunts

Question 35

What does Diffusion impairment mean and causes?

Answer 35

Increased distance between the gas exchange surfaces and the pulmonary capillaries

Not a common cause of hypoxaemia in dogs and cats

Chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis

Question 36

There are 2 main ways to assess oxygenating performance of the lungs: A-a gradient? Normal value? When is it most useful?

Answer 36

A-a gradient - the difference between partial pressure of oxygen in the alveoli (PAO2) and arterial partial pressure of oxygen (PaO2). A normal A-a gradient is about 5-10mmHg.

The A-a gradient is most useful when a patient is breathing room air because it accounts for CO2 (hypoventilation)

Question 37

There are 2 main ways to assess oxygenating performance of the lungs: P:F ratio? Normal value? When is it most useful? What values are considered dysfunction?

Answer 37

P:F ratio – this is the ratio of PaO2 to FiO2 (fractionally inspired oxygen)

In normal animals the P:F ratio should be 300-500

A healthy animal breathing room air with 21% oxygen (has FiO2 of 0.21) should have a PaO2 of 100mHg

Therefore P:F ratio is 100:0.21 or approximately 500:1

The ratio remains useful in patients receiving supplemental oxygen - a healthy animal breathing 100% oxygen (FiO2 = 100% 1) and will have PaO2 of 500mHg : P:F ratio 500:1 (ratio of 500)

A ratio of less than 300 is consistent with moderate lung dysfunction

A P:F of less than 200 is consistent with severe lung dysfunction and part of the diagnostic criteria for acute respiratory distress syndrome (ARDS).

Question 38

Ventilation - assessed by looking at?

Answer 38

Ventilation is assessed by looking at PCO2.

Question 39

High PCO2 indicates what and causes.

Answer 39

High PCO2 indicates hypoventilation or an inability to ‘blow off’ the CO2 produced by cells. This can contribute to respiratory acidosis and mortality.

Neuromuscular disease – snake envenomation, tick paralysis, botulism,

Thoracic wall disease – rib fracture, pain, deformities

Pleural disease – pleural effusion

A PCO2 > 60mmHg requires intervention – usually a reason to consider mechanical ventilation

Question 40

120 rule - what is it?

Answer 40

The 120 rule helps to determine if ventilation is adequate

The PaO2 + PaCO2 should be >120. If it is less than 120, there is problem with ventilation or oxygenation (based on a patient breathing room air at sea level)