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MD3001 > Blood Gas Analysis > Flashcards

Blood Gas Analysis Flashcards

1
Q

State the scale of kPa to mmHg. Which of kPa or mmHg should you use ?

A

1kPa = 7.5mmHg

kPa

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2
Q

Identify the main volatile and non-volatile acids in the body.

A

Volatile: carbonic acid (H2CO3)

Non-volatile: lactic acid, phosphoric acid, sulfuric acid

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3
Q

How are non-volatile acids produced ?

A

Through the breakdown of proteins

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4
Q

What are the main buffers in the body ? What is the function of buffers ?

A

♦ Proteins
♦ Haemoglobin
♦ Carbonic acid / bicarbonate
Keep pH within tight range.

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5
Q

Why is it important to maintain pH within a tight range ?

A

Because enzymes work sub-optimally above or below optimal pH.

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6
Q

What are the main ways of excreting acid ?

A

Lungs (by exhaling CO2)

Kidneys (by excreting acids in urine)

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7
Q

What would happen to the buffer system if an acid overload occur ?

A

Since buffers have limited capacity, an overload would result in more acidic pH. However, the body can get rid of volatile acids (through lungs) and non-volatile acids (through kidneys), to prevent this happening.

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8
Q

Where are blood gases usually taken from ?

A

From radial artery, but it can be any palpable artery.

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9
Q

Briefly explain the process of taking blood gases.

A

Local anaesthetic used first because procedure painful.
Then, puncture performed at the distal part of the limb.
Sample then kept cool until analysed.

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10
Q

What are the main components of the blood gases analysis results.

A

pH
pCO2
PO2
Bicarbonate

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11
Q

Define standard bicarbonate.

A

Concentration of bicarbonate in the plasma from blood which is equilibrated with a normal PaCO2 (40 mmHg, i.e. 5.3kPa) and a normal pO2 (over 100 mmHg) at a normal temperature (37°C).

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12
Q

How do we calculate standard bicarbonate ?

A

Obtained by solving the Henderson-Hasselbalch equation to get a bicarbonate value when the pH is known and PaCO2 is 40mmHg.

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13
Q

State the equation for the bicarbonate buffer system.

A

H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3-

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14
Q

What is the impact of respiratory failure on blood gases ?

A

Increased CO2 (cannot blow it off) and thus increased bicarbonate (since equation shifts to the bicarbonate)

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15
Q

What happens if, the calculation of standard bicarbonate by the machine in hospital is for a patient with respiratory failure (i.e. not normal pCO2 5.3 kPa) ?

A

High pCO2 will result in high bicarbonate because of equilibrium. Machine would standardise it (i.e. would say what bicarbonate would be if pCO2 was 5.3 kPa).

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16
Q

Which of the components of the bicarbonate buffer system reflects the metabolic component of acid base balance ?

A

Bicarbonate

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17
Q

Which of the components of the bicarbonate buffer system reflects the respiratory component of acid base balance ?

A

CO2

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18
Q

Once the patient (e.g. with accident induced pneumothorax) is in and inspection has been performed, what are ways to gather more clues about their condition ?

A
  • History
  • Examination
  • What are they breathing
  • Urea and Electrolytes
  • Haemoglobin
  • Glucose (i.e. diabetic ?)
  • Arterial blood gases
  • CXR

Then, look at arterial blood gas results

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19
Q

What are the main chronological steps in analysing arterial blood gas results ?

A

Step 1: Assess oxygenation (i.e. look at PO2)
Step 2: Assess pH
Step 3: Determine the primary problem
Step 4: Is compensation occurring?

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20
Q

Why is it necessary to assess oxygenation first and foremost in a blood gas analysis ?

A

Because hypoxia would kill the patient before anything else

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21
Q

What are the main ways to assess oxygenation ?

A
  • Looking at pO2 (more precise than other two)
  • Sometimes, arterial blood gas results are not even necessary, obvious central cyanosis
  • Pulse oximetry can also be used
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22
Q

What are potential issues with oxygenation ?

A

Hypoxia

Oxygenation too high

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23
Q

What is high oxygenation a risk factor for ?

A

♪ Retinopathy in neonates
♪ Hypercapnic respiratory failure in acute exacerbations of COPD
♪ Increased mortality survivors of cardiac arrest
♪ Increased mortality intensive care patients
♪ Increased mortality in acute severe asthma
♪ Increase free radical generation
♪ Lung toxicity-
a) increased oxygenation means less nitrogen, which normally holds alveoli open. With too much oxygen, collapse of alveoli occurs due to atelectasis.
b) high oxygen irritates mucous membrane
♪ Also: Ocular toxicity, myocardial damage

24
Q

Why is high oxygen a risk factor for hypercapnic respiratory failure in acute exacerbations of COPD ?

A

Because in patients with high pCO2 (e.g. COPD), respiration driven by hypoxia
so if given additional O2, danger of suppressed respiration further

25
Q

What is the target oxygenation for type II respiratory failure ?

A

88% to 92%

26
Q

What is the target oxygenation for patients in intensive care/survivors of cardiac arrest/acute severe asthmatic patients.

A

96%

27
Q

Describe the British Thoracic Society guidelines on oxygen use.

A

♠ Oxygen is a treatment for hypoxia not dyspnoea.
♠ In an unstable medical emergency give high conc of oxygen then titrate to target once stable
♠ Targets 94-96% (normally)
88-92% (type 2 resp failure)

28
Q

Identify therapeutic uses of high inspired concentrations of oxygen.

A

1) Pneumothorax (major portion of air in pleural cavity is nitrogen, so when given 100% oxygen, nitrogen will move from area of high to low concentration so will speed up decrease in size of pneumothorax )
2) Carbon monoxide poisoning (trying to increase oxygen dissolved in bloodstream and push CO out of haemoglobin)

29
Q

Define and describe the main features of the alveolar-arterial oxygen gradient.

A

Measure of the difference between the alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen. It is used in diagnosing the source of hypoxemia.

  • Oxygen in arterial blood can never exceed what you’re breathing in
  • Oxygen partial pressure keeps falling as it progresses in the airway (through humidification, mixing with expired gas, alveolar ventilation and oxygen consumption, then it gets into arterial blood at 12-13 kPa, then venous mixing and V/Q mismatch cause a further decrease in oxygen partial P)

If it falls too much, hypoxemia

30
Q

Distinguish between hypoxia and hypoxemia.

A 
Hypoxia = diminished availability of oxygen to the body tissues (e.g. viewed through central cyanosis)
Hypoxemia = abnormally low arterial oxygen tension (PaO2) in the blood (i.e. problem with oxygenation)

Hypoxemia usually results in hypoxia (unless patient given supplemental oxygen), but hypoxia can be due to other issues (e.g. due to low arterial oxygen tension due to high altitude or hypoventilation, resulting in low pO2)

31
Q

Identify the main causes of hypoxemia.

A

-Locations of high altitudes, where oxygen in the air is lower
-Lung conditions such as asthma, emphysema, and bronchitis
-Inflammation or scarring of the lung tissue (as in pulmonary fibrosis or ageing)
Since all of these lead to mismatch between ventilation and perfusion (high perfusion, low ventilation) leading to low pO2.

32
Q

What is a “normal” alveolar-arterial gradient ? How is this useful ?

A

Normal Alveolar –arterial (A-a) gradient is less than 3kPa

Clinically not useful, because we cannot measure alveolar P

33
Q

Given that we cannot calculate alveolar-arterial gradient (since we cannot measure alveolar P) to compare with the normal value of 3 kPa, what are other ways to check hypoxemia (i.e. oxygenation) ?

A

♣ Can expect the arterial pO2 to be approximately 2/3 FiO2

♣ PaO2 / FiO2 ratio (AKA P/F ratio i.e. kPa divided by inspired fraction of oxygen)
P/F ratio > 50 = healthy
P/F ratio < 40 = acute lung injury
P/F ratio <26.7 = ARDS

34
Q

As part of step 2 (assess pH) what are possible abnormalities ?

A
  • pH <7.35 acidaemia
  • pH >7.45 alkalaemia
  • normal pH with mixed acid base abnormality
35
Q

Distinguish between acidaemia and acidosis, and between alkalaemia and alkalosis.

A

Acidosis is process driving pH towards acidemia
Acidemia means it has exceeded normal range

and vice versa

36
Q 
Interpret the following arterial blood gas results. 
• pH 7.20
• pO2 28.7kPa
•pCO2 11kPa  
• HCO3- (standard) 25mmol/l
A
  • pH 7.20↓ - Acidemia
  • pO2 28.7kPa - no hyoxia
  • pCO2 11kPa ↑
  • HCO3- (standard) 25mmol/l - normal

Since the pH and pCO2 are changing in opposite directions this suggests a respiratory problem.

37
Q

What is a normal pO2 ?

A

> 10.5 kPa

38
Q

What is a normal pCO2 ? a normal standard HCO3 ?

A

4.5–6.0 kPa

22 to 28 mEq/L

39
Q

Based on arterial blood gas results, how can we know whether the problem is respiratory or metabolic ?

A

If the pH and pCO2 are changing in opposite directions this suggests a respiratory problem

If the pCO2 and pH are changing in the same direction, the primary problem is probably metabolic

40
Q

Define compensation in the context of blood acid base balance.

A

Altering of function of the respiratory or renal system in an attempt to correct an acid – base imbalance.

41
Q

Write an equation which demonstrates how the body compensate (i.e. how do we know that bicarbonate will increase with an increase in CO2 (or vice versa)).

A

pH α (HCO3/pCO2)
Since pH must be maintained in a tight range, an increase in either of the components will result in an increase of the other (compensation).

42
Q

Does the body ever overcompensate ?

A

No, the body never overcompensates.

43
Q

Which organ is responsible for compensation in respiratory imbalances ? in metabolic imbalances ?

A

Primary respiratory problem, renal compensation

Primary metabolic problem, respiratory compensation

44
Q 
A few minutes/hours after the following initial arterial blood gas results,
• pH 7.20
• pO2 28.7kPa
• pCO2 11kPa  
• HCO3- (standard) 25mmol/l 
arterial blood gases were done again and these were the results:
• pH 7.20
• pO2 28.7kPa
• pCO2 11kPa  
• HCO3- (standard) 25mmol/l

How can you explain this ?

A

Since this is primarily a respiratory problem, renal compensation should take place but it take hours to days to take full effect so none of the blood gases have really changed.

45
Q

How can one determine if compensation is occurring ?

A

♠ If pCO2 and HCO3- move in the same direction compensation is possibly occurring (since pH ∞ bicarbonate/pCO2)

♠ If both values move in opposite directions more than 1 pathology must be present (i.e. mixed acid base abnormality)

46
Q

What would you anticipate in terms of arterial blood gas results from the following patient ?
Smoker, COPD, centrally cyanosed

A
  • Low pO2 (central cyanosis) (in this case both hypoxic and hypoxemic since centrally cyanosed but also low pO2)
  • High PCO2 (COPD)
47
Q 
Interpret the following arterial blood gas results. 
• pH 7.32
• pO2 6kPa
• pCO2 10.6kPa
• HCO3(standard)37mmol/l
A

Slight acidemia (respiratory since pH and pCO2 moving in opposite directions)
Low pO2
High PCO2
High HCO3

Type II respiratory failure (because high PCO2 and low pO2)

48
Q

What is the management for a patient with type II respiratory failure ?

A

88 to 92% Oxygen

49
Q

Compare the likely blood gas results between a patient with acute respiratory acidemia due to opioid overdose and a patient with chronic respiratory failure.

A
  • Both will have acidemia (lower pH).
  • Acute patient will have normal pO2 (or even elevated pO2 if supplemental oxygen given to him) whereas the chronic patient will have low pO2 due to COPD (i.e. hypoxemia and probably hypoxia if not given supplemental oxygen straight awayà.
  • Both will have elevated pCO2 levels, but in the case of the chronic patient renal compensation will have occurred bringing HCO3 higher with it, which will have enabled pH to be closer to normal range (so acidemia less marked in chronic patient). In the acute patient compensation will not have happened yet, meaning HCO3 values are likely to be normal whereas pH is likely to be further away from normal.
50
Q

Identify the main causes of hyperventilation.

A
  • Acute severe asthma
  • Pulmonary embolism
  • Pulmonary oedema
  • Anxiety attack

through hypoxia, stimulated lung mechanoreceptors/chemoreceptors, stimulation of respiratory centre.

51
Q

What is the main consequence of hyperventilation wrt acid base balance ?

A

Respiratory alkalaemia (low pCO2)

52
Q

What arterial blood gas results would you expect from a hyperventilating patient ?

A

pO2 - normal
pCO2 - low, can’t get rid of CO2 through ventilation)
HCO3(std) - normal, has not compensated yet
pH -alkalemia due to low pCO2

53
Q

What are possible consequences of high altitude on acid-base balance ?

A

Atmospheric pO2 lower than at sea level.
This results in hypoxemia (which usually leads to hypoxia), which induces hyperventilation. This leads to chronically low pCO2 (i.e. chronic respiratory alkalosis). Compensation occurs by renal excretion of bicarbonate, to maintain pH as close to normal as possible.

54
Q

Calculate atmospheric pO2 at the top of the Andes (where atmospheric P = 50 kPa).

A

50 kPa x 0.20 (proportion of oxygen in the air) = 10 kPa

Atmospheric pO2 = 10kPa

55
Q

True or False: Arterial pO2 can never exceed atmospheric pO2.

A

True

MD3001 (75 decks)

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