Anaesthesia, blood gases etc Flashcards

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1
Q

Define acidaemia/alkalaemia and acidosis/alkalosis? And difference between the primary disturbance and compensatory response?

A

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)

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2
Q

What are the 4 types of primary acid-base disturbances? What are the compensatory responses to each of these?

A

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

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3
Q

pH equation?

A

pH = -log10[H+]

Small changes in pH represents large [H+] changes

Inversely related - the lower the pH, the more H+ ions

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4
Q

What is pH affected by and what is it controlled by?

A

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

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5
Q

Why is pH so tightly controlled?

A

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

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6
Q

Why is bicarbonate such an important buffer?

A

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

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7
Q

What is the bicarbonate/H+ equation to remember for blood gases?

A

CO2 + H20 <—> H2CO3 <—> H+ + HCO3-

Moves left or right to keep equilibrium

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8
Q

If the immediately available chemical buffers become overwhelmed when controlling pH, what is the secondary mechanism? How quick is it?

A

The respiratory system, by manipulating CO2

Acts over minutes to hours

E.g. blowing off CO2 to correct acidosis

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9
Q

What is the third mechanism for controlling pH? How quick is it? How does it do it?

A

Kidneys
Precise control
Longer term action (hours to days)
Generates buffers from PCT cell metabolism
Conserve/excrete bicarbonate
Conserve/excrete acids

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10
Q

What is the normal arterial pH range in horses? At what point would death occur?

A

Death if <6.8 or > 7.8

Preferred range in arterial range: 7.35 - 7.45

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11
Q

What is the normal PaCO2 in horses?

A

35-45mmHg

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12
Q

What are the 3 ways CO2 is carried in blood?

A

As bicarbonate (85%)
Carbamino compounds (10%)
Dissolved CO2 (5%)

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13
Q

Why can bicarbonate be confusing when analysing blood gases with mixed disturbances?

A

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

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14
Q

Normal arterial HCO3- range?

A

21-28mmol/L

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15
Q

What are the two HCO3- measurements often recorded by blood gas machines?

A

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)

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16
Q

What is base excess?

A

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

17
Q

Which systems do pH, PCO2, bicarb and base excess tell us about?

A

pH - overall reflection of both resp and metabolic
PCO2 - respiratory only
Bicarb - resp and metabolic
Base excess - metabolic only

18
Q

What are the 2 ways base excess may appear on results?

A

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)

19
Q

Reference range for base excess in horses?

A

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

20
Q

What causes normal variation of base excess?

A

Diet
Species (obligate carnivores tend to be more naturally acidic so have a lower negative range, herbivores more alkaline)

21
Q

What can be done to correct an excessively negative base excess (metabolic acidosis)?

A

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’

22
Q

Most common cause of metabolic acidosis in hirses?

A

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)

23
Q

Equation for adminstering bicarbonate for correcting metabolic acidosis?

A

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

24
Q

Why do you have to be careful when deciding whether to administer bicarbonate to treat metabolic acidosis? When should you not adminster it?

A

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)

25
Q

What do you need to be able to properly interpret a PO2 value?

A

Needs to be arterial
Need to know the FiO2 (0.21 for room air, 0.9 or 1 if GA)
(Barometric pressure)

26
Q

Why is PO2 important?

A

Drives oxygen binding to Hb

27
Q

Explain the O2 Hb dissociation curve and the main points on it for horses?

A

P50 = oxygen tension in plasma at which 50% of the Hb will be bound to O2

90/60 = if have an oxygen tension of 60mmol/L,there will be around 90% oxygen saturation of Hb

Venous point = normal venous oxygen tension (45mmol/L), which should have around 75% oxygen saturation of Hb

Arterial point = normal arterial oxygen tension (100mmol), which should have around 97% oxygen saturation of Hb

Curve is sigmoidal in shape
After the 90/60 point, the curve starts dropping quicker (i.e. increasing past 60mmol/L up to 100 only increases the oxygen saturation from 90% to 100%, whilst if drop below 60 the oxygen saturation quickly dramatically drops)

28
Q

Which factors can shift the Hb O2 dissociation curve to the left or right? What is this effect called?

A

To the left (ie. improved oxygen saturation):
- Decreased temperature
- Increased pH
- Decreased CO2 or 2,3 DPG
The above is true in the lungs where CO2 is being eliminated, pH is higher, lower temp from breathing in ambient air - maximises O2 binding to Hb

To the right (ie. reduced oxygen saturation):
- Increased temperature
- Decreased pH
- Increased CO2 or 2,3 DPG
The above is true in the tissues, where CO2 is being produced and so the pH is lower, and oxygen is needed to offload from Hb

= The Bohr effect

29
Q

How to determine if the PO2 is adequate? Calculate for room air and GA.

A

Use the alveolar gas equation and compare to measured value

PAO2 = FiO2 (PB - PH2O) - (PACO2/RQ)

PAO2 = alveolar oxygen tension
FiO2 = fractional inspired O2 (e.g. 0.21 in room air)
PB = barometric pressure
PH20 = saturated water vapour pressure
PACO2 = alveolar CO2 tension - generally substitute PaCO2 in here as don’t have PACO2 value
RQ = respiratory quotient (CO2 produced/O2 consumed): in horses value debated, 0.8 in people, may use 1 in horse)

E.g. breathing room air at sea level assuming normal ventilation:
PAO2 = 0.21(760-47) - (40/0.8) = 100
So PaO2 should therefore = 90-100mgHg (allow a little leeway as nothing is perfect in a biological system)

Breathing 100% O2 at sea level assuming normal ventilation (GA):
PAO2 = 1.0(760-47) - (40/0.8) = 663mmHg
So if PaO2 <550mmHg indicates impaired oxygenation

So if on 100% oxygen and measure PaO2 as 90mmHg, although would be a close to normal value on room air, it indicates pretty impaired lung function under GA

30
Q
A