ABG's Flashcards

1
Q

How is bicarbonate gained and lost from the body?

A

Gained from net renal bicarbonate regeneration

Lost from buffering of endogenously produced acid.

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2
Q

Where is most of the H+ excreted?

A

99.9% is excreted in the urine.

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3
Q

How much H+ do we have normally?

A

35- 45 nanomol/L

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4
Q

How much bicarbonate do we normally have?

A

22 - 26 mmol/L

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5
Q

What is the equation for H+ buffering by bicarbonate?

A
H+ + HCO3-   
Gives
H2CO3   
Giving
CO2 + H2O
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6
Q

What 4 H+ buffer systems exist in the body and what is the most important one?

A

Bicarbonate, Hb, phosphate and ammonia.

Most important is bicarbonate.

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7
Q

What is the chemical formula for carbonic acid?

A

H2CO3

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8
Q

How is carbonic acid removed from the body?

A

As CO2 from the lungs.

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9
Q

What limits H+ being removed as CO2?

A

Bicarbonate levels.

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10
Q

What happens to the H+ equation when we have too much H+?

What results does this have on the body?

A

The equation will be pushed to the right.

The body will increases the respiratory rate to blow off the CO2.

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11
Q

how does DKA cause excess H+?

What do we often see patients with DKA doing?

A

The rising H+ is caused by ketone bodies.

DKA patients usually do big breaths to try and blow it off.

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12
Q

What happens to bicarbonate when there is too much H+?

A

The levels will fall as the excess is trying to mop up the H+.

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13
Q

What happens to the H+ equation when there is too much CO2 in the body?
What does the body do to attempt to fix this?

A

It is pushed to the left.

Excreted more H+ in the urine.

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14
Q

What is acidaemia?

A

Increased H+ in the blood

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15
Q

What is alkalaemia?

A

Decreased H+ in the blood

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16
Q

What is acidosis?

A

Process tending to cause increased H+

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17
Q

What is alkalosis?

A

Process tending to cause decreased H+

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18
Q

Why is the differentiation between acidosis and acidaemia important?

A

The two processes could be happening at the same time. E.g. A tourniquet could cause acidosis but not overall acidaemia.

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19
Q

What do we call the respiratory component?

A

PCO2

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20
Q

What do we call the metabolic component?

A

HCO3-

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21
Q

What causes respiratory acidosis?

A

Raised H+ due to raised PCO2.

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22
Q

What causes respiratory alkalosis?

A

Decreased H+ due to decreased PCO2.

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23
Q

What causes metabolic acidosis?

A

Increased H+ due to decreased HCO3-.

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24
Q

What causes metabolic alkalosis?

A

Decreased H+ due to increased HCO3-.

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25
Q

What physiological mechanism is respiratory acidosis caused by?
What are a few possible causes?

A

Alveolar hypoventilation due to COPD, airway obstruction, Stoke and cardiac arrest etc.

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26
Q

What is the physiological mechanism behind respiratory alkalosis?
What are some causes of respiratory alkalosis?

A

Alveolar hyperventilation.

Can be early acute asthma attack, PE, pneumonia, Hysterical over breathing, mechanical over ventilation and raised ICP.

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27
Q

What happens in metabolic compensation of respiratory acidosis?

A

The kidneys excrete more H+

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28
Q

What mechanism causes metabolic acidosis and what are a few causes?

A

Excess production of H+ ions.

Could be DKA, renal failure, circulatory shock or loss of HCO3-

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29
Q

What mechanism causes metabolic alkalosis and what are a few causes?

A

Excess HCO3 ions.

Loss of H+ in vomiting, diuretics K+ loss and excess HCO3 reabsorption, excess alkali ingestion or potassium deficiency.

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30
Q

How do we gain and lose CO2 in the body?

A

Gained from tissue metabolism

Lost from lungs.

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31
Q

What is the normal level of PaO2 on air?

A

> 10

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32
Q

What is our normal pH?

A

7.35 - 7.45

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33
Q

What is the normal PaCO2?

A

4.7 - 6.0 kPa

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34
Q

What is the normal base excess?

A

+/- 2

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35
Q

When we see high PCO2 what should we think?

A

Respiratory acidosis

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36
Q

When we see low PCO2 what should we think?

A

Respiratory alkalosis

37
Q

When we see high Bicarb what should we think?

A

Metabolic alkalosis

38
Q

When we see low bicarb what should we think?

A

Metabolic acidosis

39
Q

What two buffers are used in metabolic compensation of respiratory acidosis?

A

Phosphate and ammonia.

40
Q

What happens during renal excretion of H+ and what does this mean for bicarb?

A

CO2 diffuses into the cell.
It goes through the equation and is turned to carbonic acid and then H+ and bicarb.
1 H+ is realised into the urine and the bicarb is returned to the blood.
This means one bicarb is gained for each H+ lost.
This is why in long term conditions like COPD bicarb may be through the roof when H+ is normal.

41
Q

If there is a primary respiratory acidosis what is the compensatory measure?

A

Increased HCO3

42
Q

If there is a primary respiratory alkalosis what is the compensatory measure?

A

Decreased HCO3

43
Q

If there is a primary metabolic acidosis what is the compensatory measure?

A

Decreased PCO2

44
Q

If there is a primary metabolic alkalosis what is the compensatory measure?

A

Increased PCO2.

45
Q

Is it possible to overcompensate physiologically?

A

No

46
Q

Which artery are ABGs most commonly taken from?

A

Radial artery.

47
Q

What is the normal level of HB?

A

Over 120

48
Q

What are four different types of tissue hypoxia?

What causes them?

A

Anaemic hypoxia from lack of Hb.
Perfusional hypoxia from low cardiac output.
Toxic hypoxia from failure of release of O2 at the tissue level e.g. In cyanide poisoning.
Hypoxaemia hypoxia from low PO2 and low SaO2 from respiratory insufficiency.

49
Q

What is a visible indication of cyanide poisoning and why?

A

Bright red venous blood.

Caused by haemoglobinaemia as the O2 doesn’t release.

50
Q

What patients should we ply with O2?

A

Very sick patients e.g. Cardiac arrest, trauma, sepsis and anaphylaxis.

51
Q

What patients should we give controlled O2?

A

COPD, skeletal abnormalities preventing lung expansion, obesity, neurological compromise etc.

52
Q

What is pickwicks syndrome?

A

Obesity related hypoventilation syndrome.

53
Q

What patients should we never give CO2?

A

Suspected poisoning patients. Some poisons are activated by O2.

54
Q

What saturation do we want for COPD patients?

A

88-92

55
Q

What is the most abundant buffer?

A

Hb

56
Q

What kind of compensation is rapid?

A

Respiratory

57
Q

What kind of compensation is slow?

A

Metabolic

58
Q

What kind of alkalosis is uncommon on its own?

A

Respiratory.

59
Q

Is respiratory acidosis with metabolic compensation common?

What are some causes?

A

Yes.

Chronic type 2 respiratory failure e.g. COPD

60
Q

Is metabolic alkalosis with respiratory compensation common?

What are some causes?

A

No

Can be caused by vomiting or severe hypokalaemia.

61
Q

Is metabolic acidosis with respiratory compensation common?

What are some causes?

A

Yes

Caused by sepsis, DKA and lactate etc.

62
Q

Is respiratory alkalosis with metabolic compensation common?

What are some causes?

A

No it’s rare.

Can be caused by chronic hyperventilatory states.

63
Q

What is uncompensated respiratory acidosis caused by in terms of respiratory failure?

A

Acute type 2 respiratory failure.

64
Q

What is compensated respiratory acidosis in terms of respiratory failure?

A

Chronic type 2 respiratory failure.

65
Q

What is decompensated respiratory acidosis caused by in terms of respiratory failure?

A

Acute on chronic type 2 respiratory failure.

66
Q

What can ingestion of aspirin and NSAIDs result in and why?

A

Acidosis as they are both acidic.

67
Q

What should PaO2 normally be in relation to FiO2?

A

About 10% less.

68
Q

What is type 1 respiratory failure? What causes it?

A

Reduced PaO2 and PCO2. Alveolar hyperventilation.

69
Q

What is type 2 respiratory failure?

A

Decreased PaO2 and raised PCO2 from alveolar hypoventilation.

70
Q

What is the anion gap?

A

The difference between the positive ions in the blood and the negative ions.

71
Q

What kinds of acidosis can we have in relation to anion gap?

A

High or low anion gap acidosis.

72
Q

What can be the causes of a high anion gap?

A
A MUD PILES
Alcohol
Methanol
Uraemia
DKA
Paraquat
Infection
Lactic acid
Ethylene glycol
Salicylates
73
Q

What do alcohol and methanol dissociate into?

A

Weak acids

74
Q

What can methanol cause?

A

Blindness.

75
Q

Why can uraemia cause a high anion gap?

A

Failure to excrete H+ and retain bicarb.

76
Q

What is paraquat?

A

A very nasty poison that is banned in the UK.

77
Q

Why do diabetics get polyuria?

A

Glucose is highly osmotic.

It passes into the kidney and sucks in water.

78
Q

What does tissue produce when it dies?

A

Lactic acid.

79
Q

What is ethylene glycol?

A

Antifreeze a potent acid.

80
Q

What respiratory symptom does aspirin overdose cause and how does the body compensate?

A

Fast respiratory rate as it is acidic. This causes respiratory acidosis and then metabolic alkalosis.

81
Q

What does the base excess mean?

A

The amount of strong acid needed to bring the pH back to 7.4 when CO2 is corrected to 5.3.

A big positive base excess means we need to add more acid.
A big negative base excess means we need to add more alkali.

82
Q

What are blue bloaters?

A

Chronic bronchitis patients

83
Q

What are pink puffers?

A

Emphysema patients.

84
Q

What happens to ventilation, respiratory drive and blood gasses in an early asthma attack?
What O2 do we give them?

A

Alveolar hyperventilation with decreased respiratory drive.
Decreased PaO2 and PaCO2.
Give high concentration O2 (60%)

85
Q

What happens to ventilation, respiratory drive and blood gasses in a late asthma attack?
What O2 do we give them?

A

Alveolar hypoventilation, decreased respiratory drive.
Gives decreased PaO2 and increased PaCO2.
Give high flow O2 (60%) and May need mechanical ventilation.

86
Q

What happens to ventilation, respiratory drive and blood gasses in a acute exacerbation of COPD?
What O2 do we give them?

A

Chronic alveolar hypoventilation with decreased respiratory drive.
Switch from hypercapnia to hypoxic drive.
Initially use low concentration O2 initially to avoid suppressing possible hypoxic drive.

87
Q

What cause hypoventilation in the late stages of asthma attacks?

A

Fatigue.

88
Q

If there is evidence of type 2 respiratory failure or evidence of increasing PaCO2, despite treatment in an asthma patient what should we do?

A

Call an anaesthetist as they may require mechanical ventilation.

89
Q

Why do we always use high flow O2 in acute asthma patients, even if the PaCO2 is high?

A

The patient is still relying on hypercapnia drive.