Anaesthesia, blood gases etc (CCA week 9) Flashcards
Define acidaemia/alkalaemia and acidosis/alkalosis? And difference between the primary disturbance and compensatory response?
Acidaemia/alkalaemia = altered blood pH resulting it it becoming more acidic or alkaline
Acidosis/alkalosis = the process tending to result in a change in pH, may be metabolic or respiratory in origin
Primary disturbance = the problem which initiated the change in pH (4 types)
Compensatory response = physiological response aimed at preserving homeostasis (animal tries to adapt to the change)
What are the 4 types of primary acid-base disturbances? What are the compensatory responses to each of these?
Respiratory acidosis: Increased PCO2, increased [H+], decreased pH
- Compensatory response = increase HCO3- (renal response to conserve bicarbonate and secrete more acid)
Respiratory alkalosis: Decreased PCO2, decreased [H+], increased pH
- Compensatory response = decrease HCO3- (renal increased excretion of bicarbonate)
Metabolic acidosis: Decreased HCO3-, increased [H+], decreased pH
- Compensatory response = decrease PCO2 (body blows off CO2)
Metabolic alkalosis: Increased HCO3-, decreased [H+], increased pH
- Compensatory response = increase PCO2 (but this not actually seen so often as would involve animal reducing ventilation which has other deleterious consequences)
Magnitude of response is variable and if have a mix of primary metabolic and respiratory involvement can make interpretation of results difficult
Can have a single primary change with associated compensatory response
Or can have mixed disturbances, which may be:
- Additive: respiratory acidosis + metabolic acidosis
- Offsetting: metabolic acidosis + respiratory alkalosis
Overcompensation never occurs
pH equation?
pH = -log10[H+]
Small changes in pH represents large [H+] changes
Inversely related - the lower the pH, the more H+ ions
What is pH affected by and what is it controlled by?
Affected by:
- respiratory system
- metabolism
- exogenous substances
Controlled by buffering:
1. Immediate: Chemical buffers that are capable of binding H+ ions and are able to act immediately (weak acids and their conjugate base): HCO3-, H2PO4-, NH3/NH4+, proteins, haemoglobin, also H+/K+ exchange
2. Medium term: Resp system
3. Long term: Kidneys
Why is pH so tightly controlled?
Enzymatic pathways rely on it as function optimally at specific temperatures and pH
If stray too far out of normal range, disrupts basic cellular processes
Why is bicarbonate such an important buffer?
It is the most abundant ECF buffer
Open buffer system - the chemical amount of it can be changed as needed, rather than just having a finite amount of it
What is the bicarbonate/H+ equation to remember for blood gases?
CO2 + H20 <—> H2CO3 <—> H+ + HCO3-
Moves left or right to keep equilibrium
If the immediately available chemical buffers become overwhelmed when controlling pH, what is the secondary mechanism? How quick is it?
The respiratory system, by manipulating CO2
Acts over minutes to hours
E.g. blowing off CO2 to correct acidosis
What is the third mechanism for controlling pH? How quick is it? How does it do it?
Kidneys
Precise control
Longer term action (hours to days)
Generates buffers from PCT cell metabolism
Conserve/excrete bicarbonate
Conserve/excrete acids
What is the normal arterial pH range in horses? At what point would death occur?
Death if <6.8 or > 7.8
Preferred range in arterial range: 7.35 - 7.45
What is the normal PaCO2 in horses?
35-45mmHg
What are the 3 ways CO2 is carried in blood?
As bicarbonate (85%)
Carbamino compounds (10%)
Dissolved CO2 (5%)
Why can bicarbonate be confusing when analysing blood gases with mixed disturbances?
Influenced by both respiratory and metabolic systems
So what you might expect to see with a primary respiratory disturbance may then be offset by the kidneys compensating
Normal arterial HCO3- range?
21-28mmol/L
What are the two HCO3- measurements often recorded by blood gas machines?
Standard bicarbonate = concentration of bicarb in fully oxygenated whole blood after equilibrium with CO2 at 40mmHg at 37C; reflects metabolic component (ie if this sample had a normal PCO2, this is what the bicarb would be)
Actual bicarbonate = uncorrected bicarb concentration in sample; reflects respiratory and metabolic components (tend to use this when analysing results as does not rely on machine’s calculations)
What is base excess?
The mmol of acid or alkali required to restore pH of 1L of blood to 7.4 after correcting pCO2 to 40mmHg
Indicates metabolic component of disturbance by ruling out respiratory influence
Incorporates influence of HCO3-, H2PO4-, plasma proteins, Hb etc
Which systems do pH, PCO2, bicarb and base excess tell us about?
pH - overall reflection of both resp and metabolic
PCO2 - respiratory only
Bicarb - resp and metabolic
Base excess - metabolic only
What are the 2 ways base excess may appear on results?
Actual BE(B) = buffering capacity of whole blood
BE(ecf) = buffering capacity of ECF (tend to use this for correcting acid-base balance in patients)
Reference range for base excess in horses?
Debateable
-1 to +5 mmol/L ish (but may go up to +9 in some normal horses)
-ve value indicates metabolic acidosis
+ve value indicates metabolic alkalosis
What causes normal variation of base excess?
Diet
Species (obligate carnivores tend to be more naturally acidic so have a lower negative range, herbivores more alkaline)
What can be done to correct an excessively negative base excess (metabolic acidosis)?
Appropriate fluid therapy - restore O2 delivery to tissues (if due to generalised poor peripheral perfusion –> anaerobic metabolism e.g. if hypovolaemic)
Surgery - remove devitalised tissue (e.g. if intestinal strangulation causing localised lack of perfusion)
Bicarbonate administration to provide additional buffering capacity
‘Nice textbooks with flowcharts for rationale for treating these’
Most common cause of metabolic acidosis in hirses?
Metabolic lactic acidosis, from anaerobic metabolism, due to failure of oxygen delivery to tissues (e.g. strangulated intestine, or more diffuse tissues if hypovolaemia/fluid deficits leading to reduced perfusion)
Equation for adminstering bicarbonate for correcting metabolic acidosis?
Adults: mmol of bicarbonate = base excess x 0.3 x bodyweight
Neonates: mmol of bicarbonate = base excess x 0.45 x bodyweight
0.45 in neonates because larger extracellular fluid amount
Usually administer half first, then reassess the situation
Why do you have to be careful when deciding whether to administer bicarbonate to treat metabolic acidosis? When should you not adminster it?
Not a benign thing to do as by adding more bicarb will stimulate horse to produce more CO2 which is a problem if horse is unable to blow off this additional CO2 e.g. if collapsed/recumbent, and so can actually worsen the acidosis
DO NOT administer bicarbonate if concurrent respiratory acidosis is present e.g. collapsed/recumbent/GA without mechanical ventilation available (need to be able to eliminate the extra CO2)
