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1.2 Asthma > ABGs > Flashcards

ABGs Flashcards

1
Q

At what PaO2 is a patients on air considered to be hypoxaemic?

A

<10 kPa

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2
Q

At what PaO2 is a patients on air considered to be severely hypoxaemic and in respiratory failure?

A

<8 kPa

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3
Q

Define Type 1 respiratory failure

A

hypoxaemia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa)

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4
Q

Define Type 2 respiratory failure

A

hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa)

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5
Q

What causes type 1 respiratory failure

A

It occurs as a result of ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue

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6
Q

What is the result of V/Q mismatch

A

PaO2 falls and PaCO2 rises

The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa) with normocapnia (PaCO2 < 6.0 kPa).¹

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7
Q

What are the scenarios that can result in V/Q mismatch (not specific conditions)

A

Reduced ventilation and normal perfusion

Reduced perfusion with normal ventilation

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8
Q

Give 2 examples of conditions that can cause reduced ventilation and normal perfusion

A

pulmonary oedema, bronchoconstriction

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9
Q

Give an example of a condition that can cause reduced perfusion with normal ventilation

A

pulmonary embolism

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10
Q

What is type 2 respiratory failure

A

hypoxaemia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa)

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11
Q

What scenario causes type 2 respiratory failure (not specific medical conditions)

A

Alveolar hypoventilation, which prevents the patient from being able to adequately oxygenate and eliminate CO2 from their blood

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12
Q

Give unto 4 conditions or situations that can cause type 2 respiratory failure

A

Increased resistance as a result of airway obstruction (e.g. COPD).
Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures, obesity).
Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease).
Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates).

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13
Q

Why is it important to closely monitor blood pH

A

Seemingly small abnormalities in pH have very significant and wide-spanning effects on the physiology of the human body

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14
Q

What is the normal range for blood pH

A

pH 7.35 – 7.45

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15
Q

Broadly speaking, what are the 2 causes for change in blood pH

A

metabolic or respiratory

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16
Q

There is an imbalance of what molecule in respiratory acidosis

A

CO2

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17
Q

There is an imbalance of what molecule in metabolic acidosis

A

HCO3-

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18
Q

What is the role of CO2 and HCO3- in maintaining blood pH

A

They work as buffers to keep the pH within a set range and when there is an abnormality in either of these the pH will be outside of the normal range

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19
Q

Why is it important to look at CO2

A

Looking at the level of CO2 quickly helps rule in or out the respiratory system as the cause for the derangement in pH.

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20
Q

What is the 3 step carbonic acid equation

A

CO2 + H2O <=> H2CO3 <=> HCO3- + H+

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21
Q

What do we mean by compensation

A

The idea that the body can try and adjust other buffers to keep the pH within the normal range

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22
Q

What does it suggest if CO2 is high and pH is low

A

Likely a respiratory acidosis because the increased CO2 has combined with water to produce increased carbonic acid

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23
Q

What does it suggest if CO2 is abnormal but fits with the pH eg high CO2 and low pH

A

Suggests respiratory acidosis because the increased carbonic acid would cause a drop in pH

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24
Q

What does it suggest if CO2 is abnormal but does not fit with the pH eg low CO2 and low pH

A

Suggest metabolic cause

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25
Q

What is the result of a increase in HCO3-

A

pH is increased as there are less free H+ ions (alkalosis)

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26
Q

What is the result of a decrease in HCO3-

A

pH is decreased as there are more free H+ ions (acidosis)

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27
Q

When assessing HCO3- what 3 questions should we ask ourselves

A

Is the HCO3– normal or abnormal?
If abnormal, does this abnormality fit with the current pH (e.g. ↓HCO3– and acidosis)?
If the abnormality doesn’t make sense as the cause for the deranged pH, it suggests the cause is more likely respiratory (which you should have already known from your assessment of CO2).

28
Q

When assessing PaCO2 what 3 questions should we ask ourselves

A

Is the CO2 normal or abnormal?
If abnormal, does this abnormality fit with the current pH (e.g. if the CO2 is high, it would make sense that the pH was low, suggesting this was more likely a respiratory acidosis)?
If the abnormality in CO2 doesn’t make sense as the cause of the pH abnormality (e.g. normal or ↓ CO2 and ↓ pH), it would suggest that the underlying cause for the pH abnormality is metabolic.

29
Q

What is the base excess

A

the amount of acid required to restore a litre of blood to its normal pH

30
Q

What does a high base excess suggest (> +2mmol/L)

A

indicates that there is a higher than normal amount of HCO3– in the blood, which may be due to a primary metabolic alkalosis or a compensated respiratory acidosis.

31
Q

What does a low base excess suggest (< -2mmol/L)

A

indicates that there is a lower than normal amount of HCO3– in the blood, suggesting either a primary metabolic acidosis or a compensated respiratory alkalosis.

32
Q

How can respiratory acidosis/alkalosis (changes in CO2) be compensated for

A

They can be metabolically compensated by increasing or decreasing the levels of HCO3

33
Q

How can Metabolic acidosis/alkalosis (changes in HCO3-) be compensated for

A

They can be compensated by the respiratory system retaining or blowing off CO2

34
Q

What is the time frame for respiratory compensation

A

Can occur quickly by either increasing or decreasing alveolar ventilation

35
Q

What is the time frame for metabolic compensation

A

Metabolic compensation for a respiratory disorder, however, takes at least a few days to occur as it requires the kidneys to either reduce HCO3– production (to decrease pH) or increase HCO3– production (to increase pH).

36
Q

What is the significance of the time delay before metabolic compensation occurs

A

If you see evidence of metabolic compensation for a respiratory disorder (e.g. increased HCO3-/base excess in a patient with COPD and CO2 retention) you can assume that the respiratory derangement has been ongoing for at least a few days, if not more.

37
Q

What is the significance of over-compensation

A

‘Over-compensation’ should never occur and, therefore, if you see something that resembles this you should consider other pathologies driving the change (e.g. a mixed acid/base disorder).

38
Q

What is mixed acidosis

A

respiratory and metabolic acidosis

In these circumstances, the CO2 and HCO3– will be moving in opposite directions

There are at least 2 primary drivers of the acidosis

39
Q

How is mixed acidosis treated

A

Treatment is directed towards correcting each primary acid-base disturbance.

40
Q

What causes respiratory acidosis

A

inadequate alveolar ventilation leading to CO2 retention

41
Q

What are the characteristics of a respiratory acidosis on an ABG

A

↓ pH

↑ CO2

42
Q

Give up to 5 causes of respiratory acidosis

A

Respiratory depression (e.g. opiates)
Guillain-Barre: paralysis leads to an inability to adequately ventilate
Asthma
Chronic obstructive pulmonary disease (COPD)
Iatrogenic (incorrect mechanical ventilation settings)

43
Q

What causes respiratory alkalosis

A

excessive alveolar ventilation

44
Q

What are the characteristics of a respiratory alkalosis on an ABG

A

↑ pH

↓ CO2

45
Q

Give up to 5 causes of respiratory alkalosis

A

Anxiety (i.e. panic attack)
Pain: causing an increased respiratory rate.
Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate.
Pulmonary embolism
Pneumothorax
Iatrogenic (e.g. excessive mechanical ventilation)

46
Q

What causes metabolic acidosis

A

Increased acid production or acid ingestion.

Decreased acid excretion or rate of gastrointestinal and renal HCO3– loss.

47
Q

What are the characteristics of a metabolic acidosis on an ABG

A

↓ pH
↓ HCO3-
↓ BE

48
Q

What is an anion gap

A

A derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions

49
Q

What is an anion gap used for

A

To work out if the metabolic acidosis is due to increased acid production or ingestion vs decreased acid excretion or loss of HCO3

50
Q

What is a normal anion gap

A

4 to 12 mmol/L

51
Q

What is the formula for calculating the anion gap

A

Anion gap = Na+ – (Cl- + HCO3-)

52
Q

What does an increased AG suggest

A

increased acid production or ingestion

53
Q

What does a decreased AG suggest

A

decreased acid excretion or loss of HCO3–

54
Q

What can cause increased AGs

A 
Diabetic ketoacidosis (↑ production)
Lactic acidosis (↑ production)
Aspirin overdose (ingestion of acid)
55
Q

What can cause decreased AGs

A

Gastrointestinal loss of HCO3– (e.g. diarrhoea, ileostomy, proximal colostomy)
Renal tubular acidosis (retaining H+)
Addison’s disease (retaining H+)

56
Q

In 2 situations can metabolic alkalosis occur (not specific medical conditions)

A

A decreased hydrogen ion concentration, leading to increased bicarbonate
or
A direct result of increased bicarbonate concentrations.

57
Q

What would a metabolic alkalosis show on an ABG

A

↑ pH
↑ HCO3-
↑ BE

58
Q

What conditions can cause metabolic alkalosis

A

Gastrointestinal loss of H+ ions (e.g. vomiting, diarrhoea)
Renal loss of H+ ions (e.g. loop and thiazide diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome)
Iatrogenic (e.g. addition of excess alkali such as milk-alkali syndrome)

59
Q

What would a mixed respiratory and metabolic acidosis show on an ABG

A

↓ pH
↑CO2
↓HCO3–

60
Q

What medical conditions can cause mixed respiratory and metabolic acidosis

A

Cardiac arrest

Multi-organ failure

61
Q

What would a mixed respiratory and metabolic alkalosis show on an ABG

A

↑ pH
↓ CO2
↑ HCO3–

62
Q

What medical conditions can cause mixed respiratory and metabolic alkalosis

A

Liver cirrhosis in addition to diuretic use
Hyperemesis gravidarum
Excessive ventilation in COPD

63
Q

How would profuse vomiting present on ABG results

A

They have lost significant amounts of hydrochloric acid (HCL). This results in a net loss of H+ ions, meaning less H+ to bind to HCO3- and therefore more free HCO3- in the system. As a result of vomiting the patient is also volume depleted which encourages the release of aldosterone which in turn increase HCO3- reabsorption by the kidneys, further increasing the amount of free HCO3- in the serum, ultimately resulting in metabolic alkalosis.

64
Q

Which of the following is a possible cause of type 2 reparatory failure-

PE
MND
pulmonary oedema

A

MND

65
Q

Why does MND cause type 2 respiratory failure even though it involves reduced with ventilation with adequate perfusion a.k.a the definition of type 1 respiratory failure.

A

Because it is a case of hypoventilation rather than V/Q mismatch. The body is not able to increase breathing rate so doesn’t blow off excess CO2. so ABG would show high CO2 where’s a type 1 rest failure would show normal or decreased CO2 with low O2.

66
Q

How does hyperventilation lead to perioral and peripheral paresthesia

A

Hypocalcaemia

As blood plasma becomes more alkalotic, the concentration of freely ionised calcium, the biologically active component of blood calcium, decreases (hypocalcaemia).

Because a portion of both hydrogen ions and calcium are bound to serum albumin, when blood becomes alkalotic, the bound hydrogen ions dissociate from albumin, freeing up the albumin to bind with more calcium and thereby decreasing the freely ionized portion of total serum calcium leading to hypocalcaemia.

This hypocalcaemia related to alkalosis is responsible for the paraesthesia often seen with hyperventilation.

1.2 Asthma (1 decks)

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