Blood Gas and Acid-Base Analysis Flashcards
(40 cards)
What is the method for acid-base interpretation? (what steps)
- Look at the pH. Identify if there is an alkalaemia (high pH) or acidaemia (low pH)
- Assess the respiratory contribution to the pH (Use the CO2 to determine if there is a respiratory acidosis or alkalosis)
- Assess the metabolic contribution to the pH (Use HCO3- and BE to determine if there is a metabolic acidosis or alkalosis)
- Determine the primary process (Which process is varying in the same direction as the change in pH?)
- 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?)
- Assess the anion gap and narrow down possible causes of the acid-base disorder
- Summarise the findings in a concise statement (EXP: Acidaemia due to a primary metabolic acidosis with appropriate compensatory respiratory alkalosis)
Normal pH range for a dog?
7.35-7.45
What buffer systems are there?
- Extracellular buffers – bicarbonate buffer system (HCO3 binds H+)
- Intracellular buffers – proteins and phosphates (bind H+)
- 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
- Renal system - excretes hyrdrogen H+ ions - regulates reabsorption of HCO3-.
How long does it take for the renal system to ramp up?
3-5 days
What can acidaemia lead to?
Impedance of cardiac output and contractility
Blunted response to catecholamines
Insulin antagonism
Compensatory hyperkalaemia (and its associated effects)
What can Alkalaemia lead to?
- 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
Normal Base Excess range in cat and dogs?
Normal range for dogs is -4 to 4 and cats is -6 to 5 mEq/L.
Normal PCO2?
35-45 mmHg
Respiratory acidosis - what causes can there be?
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
When can increased PCO2 be life threatening?
> 60 mmHg,
May or may not be associated with hypoxaemia (low blood oxygen)
What can cause decreased PCO2?
Fear, pain, stress, anxiety
Hyperthermia
Neurological causes affecting the respiratory centre – head trauma, neoplasia
Secondary problem – response to metabolic acidosis
Possible causes for metabolic acidosis?
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
Possible causes for metabolic alkalosis?
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)
How can you determine which process is the primary disorder?
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.
How do you determine if there is a compensatory or secondary disorder?
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.
Assess the anion gap - what parts are in it? (formula)
Anion Gap = ([Na+] + [K+]) - ([Cl-] + [HCO3-])
What can affect the anion gap so we can’t trust it?
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.
Normal anion gap for cats and dogs?
A normal anion gap in a dog is 8-21mEq/L, and for a cat is 12-16mEq/L
Metabolic acidosis patients will have low HCO3 because of?
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.
What three causes of metabolic acidosis when it’s loss of HCO3?
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.
metabolic acidosis - not increased Cl while increased AG - what does that mean?
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.
MUDPILES - what does it mean?
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)
What is lactic acid?
Lactic acid is a strong acid that, at physiological pH (in the body) ionizes to lactate and H+ ions.
Hyperlactatemia and what equimolar effect does it has on BE?
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.
