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MBCHB3 RBF > Lecture 22-24: Acid:Base Part Two > Flashcards

Lecture 22-24: Acid:Base Part Two Flashcards

1
Q

Where is a blood gas measurement taken from, whats measured and whats calculated?

A

Arterial or venous

Measured: pH, pCO2, pO2

Calculated: HCO3, base excess

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2
Q

What is the risks of an arterial puncture?

A

Painful, occasional severe complications such as thrombosis or haemorrhage

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3
Q

When is it ok to use a venous puncture?

A
  • In patients with reasonable perfusion, pH, HCO3 and base excess are almost identical in venous and arterial (Oxygen and CO2 are v. different obviously)

Perfectly ok when:
- pO2 is not needed AND severe circulatory failure is not present

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4
Q

Give some examples of conditions when you might use a venous puncture?

A
  • Diabetic ketoacidosis
  • Renal tubular acidosis
  • Poisoning cases etc
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5
Q

What are some potential artefacts/errors in blood gases and what do they do to the results?

A

Air in blood-gas syringe
- Falsely low pCO2 = apparent resp. alkalosis

Delayed separation of plasma from RBCs
- RBCs produce lactic acid, leading to an apparent lactic acidosis

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6
Q

What is a 3 step approach to interpreting simple acid:base data?

A
  1. Is it an acidosis or an alkalosis? (look at pH)
  2. Is the primary disturbance resp. or metabolic? (Look at the pCO2, HCO3 and base excess)
  3. Is it compensated or not? (Look at the non-primary component)
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7
Q

Describe step 1/4 in the detailed approach to interpreting acid/base data?

A
  1. What is the primary diagnosis?
    - Acidaemia/alkalaemia first, then; primary acidosis or alkalosis (look at pH)
    - Is the primary disturbance resp. or metabolic? Look at the pCO2, HCO3 and base excess
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8
Q

Describe step 2/4 in the detailed approach to interpreting acid/base data?

A
  1. Does the compensation seem appropriate?
    - Use an acid-base map (or a rule of thumb) - inappropriate compensation implies a mixed disorder
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9
Q

Describe step 3/4 in the detailed approach to interpreting acid/base data?

A
  1. Calculate the anion gap (esp. in metabolic acidosis).
    - An increased anion gap implies metabolic acidosis (High Anion Gap Metabolic Acidosis HGAMA)
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10
Q

Describe step 4/4 in the detailed approach to interpreting acid/base data?

A

Use other tools depending on the condition:
a) Urine anion gap or ammonium (normal anion gap metabolic acidosis; NAGMA)
b) Urine chloride (metabolic alkalosis)
c) Delta gap* (mixed disorder diagnosis)
d) Serum osmol gap* (Useful in HAGMA due to some types of poisoning)

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11
Q

If the arterial puncture results are outside the light blue what does this imply?* insert picture

A

If results are outside compensation ranges (light blue) this implies more than one (i.e mixed) disorder

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12
Q

What is the rule of thumb for primary change and expected compensatory response in a metabolic acidosis?

A

Primary change: Decreased HCO3

ECR: 1.6kPa DECREASE in pCO2 for every 10mmol/L decrease in HCO3

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13
Q

What is the rule of thumb for primary change and expected compensatory response in a metabolic alkalosis?

A

Primary change: Increased HCO3

ECR: 0.93kPa INCREEASE in pCO2 for every 10mmol/L increase in HCO3

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14
Q

What is the rule of thumb for primary change and expected compensatory response in an ACUTE respiratory acidosis?

A

Increased pCO2

Acute: 1mmol/L increase in HCO3 for every 1.3kPa increase in pCO2

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15
Q

What is the rule of thumb for primary change and expected compensatory response in an CHRONIC respiratory acidosis?

A

Increased pCO2

Chronic: 3.5mmol/L increase in HCO3 for every 1.3kPa increase in pCO2

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16
Q

What is the rule of thumb for primary change and expected compensatory response in an ACUTE respiratory alkalosis?

A

Decrease pCO2

2mmol/L reduction in HCO3 for every 1.3 kPa decrease in pCO2

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17
Q

What is the rule of thumb for primary change and expected compensatory response in an CHRONIC respiratory alkalosis?

A

Decrease pCO2

4mmol/L reduction in HCO3 for every 1.3 kPa decrease in pCO2

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18
Q

What is base excess?

A

Non-carbonic acid removed in metabolic alkalosis and added in metabolic acidosis can be quantified by base excess and base deficit respectively.

i.t is the amount of acid or base needed to return pH to 7.4

19
Q

What is BE calculated from, what does it reflect and whats its normal value?

A

BE is calculated from: pH, pCO2, Hb

It reflects all buffers in plasma (not only HCO3)

Normal BE = 0 (-2 +2)

20
Q

What does a positive and negative BE reflect?

A

BE is positive in metabolic alkalosis

BE is negative in metabolic acidosis

21
Q

What causes respiratory acidosis?

A

Due to failure of pulmonary ventilation

22
Q

What are some common causes of respiratory acidosis?

A
  1. Lungs with impaired gas diffusion i.e obstructive lung disease, pulmonary fibrosis
  2. CNS disease i.e spinal cord injury
  3. Chest wall disorders
  4. Peripheral nerve and muscle disorders
  5. Drugs causing resp. depression via CNS i.e opiates
23
Q

What is the pattern of an acute resp. acidosis?

A
  • Initial rise in pCO2 and drop in pH
  • Small rise in HCO3 (buffering)
24
Q

What is the pattern of a chronic resp. acidosis?

A
  • Progressive rise in HCO3 from renal compensation (pCO2 stays same)
  • Return of pH towards normal (chronic resp. conditions only ones to do this)
25
Q

What causes resp. alkalosis?

A

Sustained hyperventilation leading to reduced pCO2

26
Q

What can cause a resp. alkalosis?

A
  • Anxiety states
  • Drug related stimulation of resp. centers
  • High altitude
  • Liver disease
27
Q

What is the pattern of an acute resp. alkalosis?

A

Initial drop in pCO2 and rise in pH

  • Small fall in HCO3 (buffering)
28
Q

What is the pattern of a chronic resp. alkalosis?

A
  • Progressive fall in HCO3 from renal compensation (pCO2 stays the same)
  • Return of pH towards normal (chronic resp. conditions only ones to do this)
29
Q

How are metabolic acidosis and alkalosis defined? and what causes this?

A

Accumulation or loss of non-volatile acid from the body

No distinction of acute or chronic because lungs compensate within hours.

30
Q

How is the metabolic acidosis further defined?

A

Further distinguished based on effect on plasma paramteres: THE ANION GAP

Normal anion gap and high anion gap metabolic acidosis

31
Q

What is the cause of a metabolic acidosis with NAGMA?

A
  • Acid added as HCL mineral acid or
  • Primary loss of HCO3 from the ECF
32
Q

What has happened in a HAGMA?

A

Addition to plasma of a new organic acid anion

33
Q

What is the anion gap and hows does it work?

A

Anion gap is calculated

Normal AG reflects mainly protein anions

Increased anion gap reflects presence of unmeasured anions i.e lactate

AG is ONLY useful in metabolic acidosis

34
Q

What can cause a HAGMA and NAGMA?

A

HAGMA: Diabetic ketoacidosis

NAGMA: GI based HCO3 loss i.e diarrhoae or renal base loss of HCO3 i.e PT acidosis

35
Q

Describe the approach for determining a metabolic acidosis:

A
  1. Confirm metabolic acidosis
    -> Low pH with a low HCO3
  2. Check serum anion gap
    High = Anion gap acidosis
    Normal = Non-anion gap acidosis
  3. If NAGMA check urine anion gap
    - Positive UAG or low urine ammonium = failure of renal acidification
    - negative UAG = non-renal cause
36
Q

NAGMA, why is the chloride high?

A

When HCO3 is low, extra Cl needs to be reabsorbed to maintain electroneutrality with NA reabsoprtion

37
Q

How does potassium link with acid base disturbances?

A

Acidosis Hyperkalemia
Alkalosis Hypokalemia

38
Q

Why is Potassium linked with acid base disturbances?

A

1) Relates to shift of H+ into and out of cells. (To balance each other) i.e H in (acid) = K out (hyper)

2) H+ and K+ compete with each other for secretion

39
Q

What are the exceptions to
Acidosis Hyperkalemia
Alkalosis Hypokalemia
??

A
  1. Diarrhoea (HCO3 and K loss)
  2. Renal tubular acidosis (PT and DT both associated with hypokalemia)
40
Q

What do the kidneys try and do in a metabolic alkalosis? and how can a chloride responsive alkalosis interfere?

A

In Metabolic alkalosis Kidneys attempt to increase HCO3 loss

BUT if hypovolaemia with Cl depletion is present (as occurs in some metabolic alkalosis): (a secondary hyperaldosteronism will most likely have developed)

  • Dec. vol drives HCO3 reabsorption to preserve Na
  • Aldosterone stimulates distal acid secretion, losing more HCO3 and K
  • Hypokalemia further stimulates distal acid secretion

Net effect:
- Kidneys cannot correct alkalosis until ECF volume and Cl is replaced i.e with normal saline, K often needs replacing too.

41
Q

What are the causes of chloride responsive metabolic alkalosis

A
  • Vomiting or gastric drainage (loss of H+ and Cl)
  • Diuretic induced (loss of H+ and Cl)
  • Recovery from chronic hypercapnia
42
Q

What are some causes of chloride resistant metabolic alkalosis?

A
  • Mineralcorticoid excess (primary aldosteronism)
  • Severe hypokalemia
  • Antacids

i.e no loss of Cl

43
Q

Why is Cl depletion perhaps common in acidosis? what might impair compensation?

A

Cl is exchanged for HCO3.

When Na/K reabsorbed need balancing ions to maintain electroneutrality

Thus a deficit in one means increased reabsorption of the other. Diuretics -> Loss of NaCl, volume depleted i.e aldo inc. or low Cl intake. Can all pose a risk.

= Affects HCO3 reabsorbption

44
Q

How can K depletion be linked to acid base dysfunction?

A

Rare but important

Hyperaldosteronism:

Directly: Inc. ENAC and ROMK / HATPase

Increased Na reabsorption = increased H secretion.

-» HCO3 reabsoprtion matches H loss = Alkalosis. because H loss and HCO3 gain. Also risk of low K status.

MBCHB3 RBF (39 decks)

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