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Respiratory System > Acid-Base regulation > Flashcards

Acid-Base regulation Flashcards

1
Q

Recall typical values for blood gases once it is pumped into the arteries

A

PaO2 >10kPa
SaO2 >95%
PaCO2- 4.7-6.4kPa

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2
Q

Recall typical values for blood gases in the veins

A

5.3 kPa
~75%
6.1 kPa

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3
Q

Which other factor is important in the acid-base equilibrium

A

Temperature

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4
Q

Define alkalaemia

A

Refers to high-than-normal pH of blood

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5
Q

Define acidaemia

A

Refers to lower-than-normal pH of blood

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6
Q

Define alkalosis

A

Describes circumstances that will decrease [H+] and increase pH

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7
Q

Define acidosis

A

Describes circumstances that will increase [H+] and decrease pH

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8
Q

How can you easily distinguish between -osis and -aemia

A
  • osis- what causes the change in pH

- aemia- conc in blood at that time

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9
Q

What is measured in the arterial blood gas test

A

PO2 – the partial pressure of oxygen: How much oxygen is dissolved in the arterial blood.
PCO2 – the partial pressure of carbon dioxide: How much CO2 is dissolved in the arterial blood.
pH – the ‘power of hydrogen’: Describes the [H+] of the blood.
HCO3- - plasma bicarbonate: Describes how much bicarbonate is dissolved in the arterial blood.
BE – base excess: Describes the concentration of bases compared to the ‘expected concentration’. An exact match is zero.

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10
Q

What is meant by an acid

A

An acid is any molecule that has a loosely bound H+ ion that it can donate
H+ ions are also called protons (because an H atom with a +1 valency has no electrons or neutrons)
PARADOX: A greater concentration of H+ ions refers to a lower pH (discussed next)

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11
Q

Why is it important that the acidity of the blood is tightly regulated

A

The acidity of the blood must be tightly regulated, marked changes will alter the 3D structure of proteins (enzymes, hormones, protein channels)
Ultimately, this is achieved by the actions of buffers of the respiratory and renal systems.

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12
Q

What is meant by a base

A

A base is an anionic (negatively charged ion) molecule capable of reversibly binding protons (to reduce the amount that are ‘free’)
H+A- H+ and A-

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13
Q

What is the equation for the acid-base equilibrium

A

H2O + CO2 H2CO3 H+ + HCO3-
changes in CO2, HCO3- will have an effect on pH.
CO2 regulated by ventilation
HCO3- regulated by kidneys

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14
Q

What did the pitts and swan experiment show

A

The Pitts and Swan experiment discovered the buffering capacity of the blood when they injected 14 molar acids into a dog and found it
The blood has an ENORMOUS buffering capacity that can react almost IMMEDIATELY to imbalances
s blood pH barely changed at all.

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15
Q

What are the concentrations of H+, Na+ and K+ in the ECF

A 
H+ = 0.00000004 Eq/L
Na+ = 140 Eq/L  and  K+ =  4 Eq/L
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16
Q

Describe the work of Sorenson

A

Sørensen scaled the data using a log10 transformation
This was great as it made numbers much more manageable, although negative . This was easily fixed by applying a minus sign to the equation
The inverse function of log is (10x), using this we can calculate [H+] from pH

-log10[H+] = 7.4
[H+] = 10-pH
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17
Q

What are the sources of acid

A

Respiratory- CO2
Metabolic- HCL from stomach, lactic acid, phosphate, sulphate, bicarbonate
Respiratory acids have a much larger effect on the pH of the blood.
Small amounts from diet too

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18
Q

What is the Henderson equation

A

To calculate the dissociation constant (Ka)

K = [H+][HCO3-]/[CO2][H2O]

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19
Q

What is the Henderson-hasselbach equation

A

pH = pK + log10([HCO3-]/[CO2])

combination of Henderson and Sorenson equations

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20
Q

Using Sørensen’s equation and your gas transport notes, calculate the change in [H+] between arterial blood and venous blood. What is it as a percentage?

A

a. pHarterial = 7.4, pHvenous = 7.36. This 0.04 change in pH is equivalent to a 10% increase in acidity.

21
Q

Using the notes from the gas transport lecture, estimate the volume of respiratory acid (i.e. CO2) produced in a typical adult over a 24-hour period.

A

a. CO2 total flux is 200mlCO2min-1 so in a day that is 200x60x24 = 288Lday-1 of respiratory acid.

22
Q

Calculate the pH of an arterial blood gas sample if the [H+] is 48 nmol/L.

A

a. pH = -log10[H+] = -log10(48 x 10-9) = 7.32.

23
Q

Outline a systematic approach for analysing arterial blood gases

A 
Is a low blood pH acidosis or acidaemia?
[H+] only? You’d better convert!
Is the PaCO2 normal, high or low?
This is assessing the respiratory component
Is the BE excess high or low?
This is assessing the metabolic component
Is the patient hypoxaemic?
No, mildly, moderately or severely?
24
Q

What are the guidelines for hypoxaemia

A 
Basic guidelines for PaO2
>10 kPa is normal
8-10 kPa is mild hypoxaemia
6-8 is moderate hypoxaemia
<6 kPa is severe hypoxaemia

Different values for different locations

25
Q

What are the values for pH in different locations of the body

A 
Intracellular fluid: 7.0. 
Extracellular fluid: 7.4. 
Arterial blood: 7.4. 
Venous blood: 7.36. 
Stomach: 2.4.
26
Q

Summarise compensatory mechanisms

A

Changes in ventilation can stimulate a RAPID compensatory response to change CO2 elimination and therefore alter pH
Changes in HCO3- and H+ retention/secretion in the kidneys can stimulate a SLOW compensatory response to increase/decrease pH

An acidosis will need an alkalosis to correct
An alkalosis will need an acidosis to correct

27
Q

What are the causes of respiratory acidosis

A

Hypoventilation
V/Q mismatch
An increase in PCO2 will increase an increase in hydrogen ion concentration. Plasma bicarbonate ion cocn will increase to compensate.

28
Q

Describe the renal compensations for respiratory acidosis

A

Increased filtration of hydrogen ions in the kidneys
increased HCO3- reabsorption and production
Raises the pH back towards normal

29
Q

List some conditions linked to respiratory acidosis

A 
Asthma 
COPD
Blocked airway (tumour or foreign body)
Spontaneous lung collapse, brain lesion
Injury to the chest wall.
Drugs that reduce ventilation include: morphine, barbituarates and general anaesthetics.
30
Q

Describe respiratory alkalosis

A

Decrease in PCO2
Hyperventilation- hypoxic drive in pneumonia, diffuse interstitial lung diseases, high altitude, mechanical ventilation, brainstem damage, hysteria, drugs (aspirin) and infections causing fever

31
Q

Describe the renal compensation for respiratory alkalosis

A

Reduced hydrogen ion filtration in the glomeruli
Reducing HCO3- reabsorption and production
Renal compensation reduces pH towards normal.

32
Q

Describe metabolic acidosis

A

Excess hydrogen, which reduces the bicarbonate conc (think to the equilibrium).
Respiration is unaffected therefore PCO2 is initially normal.

Exogenous acid loading (aspirin overdose)
Endogenous acid production (ketogenesis in diabetes)
Loss of HCO3- from kidneys or gut (diahhroea)
Renal failure- metabolic production of H+ ions, the kidney may not be able to excrete the excess hydrogen ions immediately.

33
Q

Describe respiratory compensation for metabolic acidosis

A

Decrease in pH is detected by peripheral chemoreceptors- increasing ventilation and lowering PCO2.
This shifts the equilibrium to the left, reducing H+ conc and bicarbonate
Raising pH towards normal.

34
Q

Can respiratory compensation fully correct metabolic acidosis

A

No. There is a limit to how far PCO2 can fall with hyperventilation. Correction can only be carried out by removing the excess H+ from the body or restoring the lost bicarbonate.

35
Q

Describe metabolic alkalosis.

A

Increase in bicarbonate or fall in hydrogen concentration (removing H+ will shift the equilibrium to the right, increasing the conc of bicarbonate).
Initially PCO2 is normal

Causes;
vomiting (hcl loss from stomach)
ingestion of alkaline substances
potassium depletion (diuretic, excess aldosterone)

36
Q

Describe respiratory compensation for metabolic alkalosis

A

increase in pH is detected by peripheral chemoreceptors. This causes a decrease in ventilation- increasing PCO2.
Equilibrium is shifted to the right
pH returns to normal.

37
Q

Can respiratory compensation fully correct metabolic alkalosis

A

No
Full correction can only be carried out by removing the problem of either reduced hydrogen ion conc or increased bicarbonate conc. This is done by reducing renal hydrogen ion secretion.
more bicarbonate is excreted because more is filtered at the glomerulus and less is reabsorbed in combination with hydrogen ions.

38
Q

What is meant by base excess

A
  1. The ABG analyser calculates hypothetical [HCO3-] based on PCO2 and assumes no metabolic or renal disturbance.
  2. The machine then ELIMINATES the changes in [HCO3-] due to PCO2 so that any change in [HCO3-] is due to metabolic acid base disturbance or a change in renal excretion of acid.
39
Q

What can change base excess

A

A rise in base excess is due to an increase in renal excretion of acid, ingestion/administration of a base or loss of acid from vomiting. The result is a metabolic alkalosis. A fall in base excess is due to the overproduction of metabolic acids, the ingestion of acid, a reduction/failure of acid excretion by the kidney or excessive loss of alkali from intestines with diarrhoea. The result is a metabolic acidosis.

40
Q

Describe the chronic and acute phases of respiratory acidosis

A

Partial Compensation: will have lower pH, high PCO2 and high base excess
Acute phase: CO2 moves into erythrocytes, combines with H2O in presence of carbonic anhydrase to form bicarbonate, which moves out of cell by AE1 transporter; increased bicarbonate leads to raised base excess, shifting equilibrium backwards to carbonic acid and reducing [H+]
Chronic phase: increases bicarbonate reabsorption in kidneys to stabilise pH
Full Compensation: will normalise pH with large PCO2 and base excess

41
Q

Describe the chronic and acute phases of respiratory alkalosis

A

Partial Compensation: will have higher pH, low PCO2 and low base excess
Acute phase: none
Chronic phase: reduces bicarbonate from nephrons and increases secretion in collecting duct, causing more carbonic acid dissociation, reducing base excess
Full compensation: will normalise pH with low PCO2 and base excess

42
Q

Summarise the partial and full compensations for metabolic acidosis

A

Partial compensation: will have a lower pH, low PCO2 and low base excess; occurs by increasing ventilation rate to increase diffusion gradient and reduce PCO2, causing shift to left on equilibrium, forming carbonic acid, and then CO2
Full compensation: will normalise pH with low PCO2 and base excess

43
Q

Summarise the partial and full compensations for metabolic alkalosis

A

Partial compensation: will have high pH, high PCO2 and high base excess; reducing ventilation rate to increase arterial PCO2 drives equation to right to increase protons and bicarbonate
Full compensation: will normalise pH with high PCO2 and base excess

44
Q

Outline an interpretation procedure

A

Type of imbalance?
Acidosis (or acidaemia) / Alkalosis (or alkalaemia) / Normal
Aetiology of imbalance?
Respiratory (acidosis or alkalaemia) / Metabolic (acidosis or alkalosis) / Mixed (respiratory and metabolic) / Normal
Any homeostatic compensation?
Uncompensated / Partially compensated / Fully compensated
Oxygenation?
Hypoxaemia / Normoxaemia / Hyperoxaemia

45
Q

List the normal values

A

[Hb] 130 to 170 g/L

pH            7.35 to 7.45 
PCO2       4.7 to 6.4 kPa (35 - 48 mm Hg)
PO2          >10 kPa (>80 mmHg)     
HCO3-       22-26 mEq/L
Base excess       -2 to +2 mmol/L or mEq/L  (This variable is calculated)
Standard BE   BE for 5 g/dL [Hb]
46
Q

What should you look at when assessing acidosis

A

f acidosis has been established:

  1. Assess the PaCO2:
    a. Elevated = respiratory acidosis.
    b. Low = metabolic acidosis.
  2. Assess the BE:
    a. Low:
    i. With low PaCO2 = partially compensated metabolic acidosis.
    ii. With normal PaCO2 = uncompensated metabolic acidosis.
    iii. With high PaCO2 = uncompensated mixed acidosis.
    b. Normal:
    i. With low PaCO2 = N/A to this lecture.
    ii. With high PaCO2 (this is usually associated) = uncompensated respiratory acidosis.
    c. High:
    i. With low PaCO2 = N/A to this lecture.
    ii. With high PaCO2 (this is usually associated) = partially compensated respiratory acidosis.
47
Q

What should you look at when assessing alkalosis

A

Assess the PaCO2:

a. Elevated or normal = metabolic alkalosis.
b. Low = respiratory alkalosis.
2. Assess the BE:
a. Low:
i. With low PaCO2 (this is usually associated) = partially compensated respiratory acidosis.
ii. With high/normal PaCO2 = N/A to this lecture.
b. Normal:
i. With low PaCO2 (this is usually associated) = uncompensated respiratory alkalosis.
ii. With high/normal PaCO2 = N/A to this lecture.
c. High:
i. With low PaCO2 = uncompensated mixed alkalosis.
ii. With normal PaCO2 = uncompensated metabolic alkalosis.
iii. With high PaCO2 = partially compensated metabolic alkalosis.

48
Q

What can explain a normal pH

A
  1. Assess the PaCO2 AND BE together:
    a. Both within range = patient is normal.
    b. Both low – one of either:
    i. Fully compensated respiratory alkalosis.
    ii. Fully compensated metabolic acidosis.
    c. Both high – one of either:
    i. Fully compensated respiratory acidosis.
    ii. Fully compensated metabolic alkalosis.

Respiratory System (23 decks)

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