06-03-23 - Clinical aspects of Acid-Base control Flashcards

1
Q

Learning outcomes

A
  • To be able to apply a simple stepwise method to the clinical interpretation of arterial blood gas results
  • To discuss metabolic causes of acid base abnormalities
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2
Q

What is 1kPa equal to?

When is the body producing acid?

What are 3 ways the pH is maintained?

What are 2 ways acid is excreted from the body?

A
  • 1kPa = 7.5mmHg
  • The body is constantly producing acid – volatile acid from CO2 and non-volatile acid usually from the metabolism of proteins
  • 3 ways the pH is maintained:
    1) Proteins
    2) Haemoglobin
    3) Carbonic acid / bicarbonate
  • 2 ways acid is excreted from the body:
    1) Lungs – excretes CO2 which would form volatile acid
    2) Kidneys – excretes non-volatile acids
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3
Q

What are 3 cases when acid-base disturbances occur?

A
  • 3 cases when acid-base disturbances occur:
    1) There is a problem with ventilation
    2) There is a problem with renal function
    3) Overwhelming acid or base load the body can’t handle
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4
Q

Describe the normal arterial and venous values for (in picture):
* pH
* PO2
* PCO2
* Bicarbonate (standard)

A
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5
Q

What is the equation for acid base balance (in picture).

How is standard bicarbonate calculated?

What does standard bicarbonate reflect?

A
  • Equation for acid base balance (in picture)
  • Standard bicarbonate is calculated from the actual bicarbonate but assuming 370C and a paCO2 of 5.3kPa
  • Standard bicarbonate reflects the metabolic component of acid base balance
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6
Q

How is base excess calculated?

What is the definition of base excess?

What is its normal range?

When does it become more negative?

A
  • Base excess Is the value calculated from blood pH & pCO2
  • Base excess is defined as Defined as the amount of acid required to restore a litre of blood to its normal pH at a PCO2 of 5.3.
  • Normal range -2 - +2mmol/L
  • It becomes more negative in the case of metabolic acidosis, as bicarbonate is use to buffer the excess acid
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7
Q

What are the 4 steps to analysing ABGs?

A
  • 4 steps to analysing ABGs:

1) Assess pO2 & oxygenation

2) Assess pH, acidaemia or alkalaemia?

3) Determine the primary problem (think about the patient)

4) Is compensation occurring?

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8
Q

Step 1: assess pO2 & oxygenation.

What is P/F ratio? What is FiO2?

What is the P/F ratio for patients that are:
1) Healthy
2) Acute lung with injury
3) ARDS

What do we have to consider about the patient?

What is the Oxygen saturation (SpO2) target ratio for someone with Type 2 respiratory failure?

A
  • Step 1: assess pO2 & oxygenation
  • PaO2 / FiO2 ratio is known as the P/F ratio (kpa divided by inspired fraction of oxygen)
  • FiO2 is the % of air breathed that is oxygen e.g normal air is 20% oxygen, so FiO2 = 0.2
  • P/F ratio for patients that are:
    1) Healthy - >50 (PaO2 about 12, and FiO2 about 0.2, so P/F around 60)
    2) Acute lung with injury - <40
    3) ARDS <26.7
  • We have to consider the situation the patient is in e.g breathing an oxygen mask at 30% will change the FiO2 to 30% therefor altering the P/F ration
  • Those with type 2 respiratory failure (hypoxic and hypercapnic) have an oxygen saturation (SpO2) target of 88-92%
  • They are running off hypoxic drive, so we have to be cautious of this when giving oxygen, as they can become over oxygenated
  • The most common cause of type 2 respiratory failure is COPD
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9
Q

Step 4: Is compensation happening?

What is compensation?

How is pH linked to HCO3- and PCO2?

What will the body never do?

When is there respiratory compensation?

How can we tell if compensation is occurring?

A
  • Step 4: Is compensation happening?
  • Compensation is the altering in function of the respiratory or renal system to change the secondary variable in an attempt to minimise an acid – base imbalance
  • pH correlates with HCO3/pCO2
  • The body will never overcompensate
  • In metabolic problems the compensation is respiratory
  • If pCO2 and bicarb are moving in the same direction compensation is likely to be occurring.
  • If they are moving in different directions suspect a mixed disorder
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10
Q

What is the anion gap?

How is it calculated?

What is the formula for it?

What are the typical values for each of the anions and cations in the formula?

When are these ions measured?

A
  • The anion gap Is the sum of routinely measured cations in venous blood minus routinely measured anions
  • This is calculated from venous blood
  • Formula for anion gap - ([Na+] + [K+])- ([Cl- ] +[HCO3 - ])
  • Some equations dont have potassium, as it tends to be small
  • Typical values for each of the anions and cations in the formula:
  • Anions:
    1) Chloride - 104
    2) Bicarbonate - 24
  • Cations:
    1) K+ - 4.5
    2) Na+ - 140
  • These ions are routinely measure in routine urinary electrolytes
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11
Q

What is a normal value for anion gap?

Why do we use anion gap?

What can an increase in anion gap indicate?

A
  • Normal anion gap = 16
  • We use the anion gap as it helps differentiate the cause of a metabolic acidaemia
  • An increased anion gap signals the presence of a metabolic acidaemia – metabolic acidaemias increase the anion gap
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12
Q

How are metabolic problems often caused?

How will it change the anion gap?

What are 3 events that can lead to an overwhelming acid load?

A
  • Metabolic problems commonly occur from an overwhelming acid load
  • This will lead to an increased anion gap
  • 3 events that can lead to an overwhelming acid load:
    1) Bodies own production (endogenous)
    2) Ingestion (exogenous source)
    3) Failure of excretion/ regeneration bicarb by the kidneys
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13
Q

What conditions will lead to excess acid production in the body?

How will this affect the anion gap?

What will this result in?

A
  • Any condition causing hypoperfusion will lead to excess acid production in the body (increased anion gap)
  • These conditions include:

1) Of the whole body: shock (cardiogenic, septic, hypovolaemic, anaphylactic)

2) Or part of the body: femoral artery embolism
* In atrial fibrillation, there can be formation of thrombi which can move around the body and potentially cause stroke or ischaemia distal to the embolism

  • These will result in increased anaerobic metabolism with subsequent increased production of lactic acid, leading to lactic acidaemia
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14
Q

What is lactic acid a product of?

What happens to lactate in a healthy person?

What does this process require?

When will production of lactate increase?

A
  • Lactic acid is a product of anaerobic metabolism
  • In health lactate is metabolised in liver and overall, there is no NET production of acid
  • This process needs oxygen
  • Production of lactate increases when O2 delivery falls and consumption of lactate by the liver falls
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15
Q

What are 3 other causes of lactic acidaemia?

When is lactate level a cause for concern?

A
  • 3 other causes of lactic acidaemia:
    1) Severe acute hypoxia
    2) Severe convulsions (respiratory arrest)
    3) Strenuous exercise (dehydration)
  • Lactate >2mmol/L is a marker of concern – have to think is there any reason the patient might be in shock?
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16
Q

How does a normal ionogram differ with the addition of lactic acid?

A
  • How a normal ionogram differs with the addition of lactic acid:
  • Bicarbonate falls, as it has been used to buffer H+ ions
  • There is also an addition of lactate in the unmeasured anions
17
Q

What is another situation in which the body will increase production of acid?

How will this affect the anion gap?

What are 3 conditions this can occur in?

What will this lead to?

What can be a sign of ketoacidosis?

How can we test for ketones?

Describe the interpretation of ketones (in picture)?

A
  • The body can increase production of acid in Situations of ↓ insulin & ↑ glucagon
  • This will lead to an increased anion gap
  • 3 conditions this can occur in:
    1) Uncontrolled diabetes mellitus (severe, lifethreatening)
    2) Alcoholic ketoacidosis (common clinically)
    3) Starvation ketoacidosis (mild)
  • In these cases, it will lead to ketoacidosis
  • A sign of ketoacidosis is when a patients breath smells like nail polish
  • There is a point of care testing kit for ketones
  • Interpretation of ketones (in picture)
18
Q

How can we monitor the response to treatment in ketoacidosis?

What blood vessels should be used for this?

Why is this?

What is the venous blood range we look for (in photo)?

A
  • The method of choice for monitoring response to ketoacidosis treatment is bedside measurement of capillary blood ketones
  • Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers
  • This is because it is less painful, easier and, carries less risk
  • Venous blood range we look for (in photo)
19
Q

What can cause an exogenous acid load?

How does this affect the anion gap?

What 2 ingested substances can cause an increase in exogenous acid load?

A
  • An exogenous acid load can be caused by accidental / deliberate ingestion
  • This will lead to an increased anion gap
  • 2 ingested substances that can cause an increased exogenous acid load:

1) Methanol (industrial solvent, windscreen wash)

2) Ethylene glycol (anti-freeze)

  • These substances are not acids in their own right, but are metabolised to acid by the liver
20
Q

What are 2 renal functions regarding bicarbonate?

What are 2 renal causes of metabolic acidosis?

How do they each affect the anion gap?

A
  • 2 renal functions regarding bicarbonate:
    1) Reabsorbs filtered bicarbonate
    2) Regenerates bicarbonate consumed by buffering
  • 2 renal causes of metabolic acidosis:
    1) Renal failure both acute and chronic (↑ anion gap)
    2) Renal tubular acidosis (normal anion gap)
  • Renal metabolic acidosis can have a variable ion gap
21
Q

What are 2 causes of normal anion gap metabolic acidosis?

How common is normal anion gap metabolic acidosis?

A
  • 2 causes of normal anion gap metabolic acidosis:
    1) Diarrhoea
    2) Renal tubular acidosis
  • Normal anion gap metabolic acidosis is less common
22
Q

What is the anion gap like in Gastrointestinal causes of metabolic acidosis?

Describe the 5 steps in the development of Gastrointestinal metabolic acidosis.

How does this affect the normal ionogram?

A
  • Gastrointestinal causes of metabolic acidosis lead to a normal anion gap
  • 5 steps in the development of Gastrointestinal metabolic acidosis:

1) Much of gut below pylorus secretes bicarbonate into gut lumen

2) For every bicarb ion into gut a H+ ion enters ECF

3) In diarrhoea, this process increases

4) This volume depletion can lead to the renin/angiotensin/aldosterone axis being stimulated, which leads to the retaining of chloride

5) This will result in metabolic acidaemia

  • In the ionogram, this will lead to chloride being retained while bicarbonate falls
  • There are no additional unmeasured anions (in picture)
23
Q

What are 3 similar pathologies to gastrointestinal metabolic acidosis?

A
  • 3 similar pathologies to gastrointestinal metabolic acidosis:
    1) Laxative abuse
    2) Ileostomy
    3) Colostomy
24
Q

What is the compensation for metabolic problems?

What corrections can also occur?

In what 2 situations will slow metabolic correction occur?

When will this criterion not be met?

A
  • The compensation for metabolic problems is respiratory
  • There is also slow metabolic (renal) correction
  • The kidneys will secrete more acid (therefore also make NEW bicarbonate) – plasma H+ decreases (pH rises) and plasma bicarbonate rises to normal
  • Slow metabolic (renal) correction only occurs if:
    1) The metabolic acidaemia is of non-renal origin
    2) The kidneys are functioning effectively.
  • This criterion will often not be met in lactic acidaemia or shock, as the kidneys are functioning sub-optimally
25
Q

What needs to happen to compensate for metabolic acidosis?

What is minute ventilation?

How will this respiratory compensation affect the breathing of the patient?

How long can maximal compensation take?

What is respiratory compensation limited by?

What can minute volume increase to?

A
  • To compensate for metabolic acidosis, pCO2 must fall, therefore minute volume must increase
  • Minute ventilation is the volume of gas inhaled (inhaled minute volume) or exhaled (exhaled minute volume) from a person’s lungs per minute
  • This respiratory compensation leads to Kussmaul respiration a - laboured deep, rapid pattern of breathing
  • Maximal compensation can take up to 24hrs
  • Respiratory compensation is limited by the work involved in breathing
  • We can increase minute volume up to about 30l/min but it is difficult to maintain (depends on how fit you are)
26
Q

How common is metabolic alkalosis? Why is this?

What 2 processes have to happen for metabolic alkalosis to occur?

A
  • Metabolic alkalosis (alkalaemia is the Least common of the acid base disturbances
  • This is because the kidney is very good at excreting excess bicarbonate
  • 2 processes that have to happen for metabolic alkalosis to occur:
    1) An initiating process
    2) A maintaining process
27
Q

What is the most common initiating process for metabolic alkalaemia?

What can this be due to?

What is another initiating factor?

How common is this?

A
  • The most common initiating process for metabolic alkalaemia is the lost of H+ ions:

1) From the gut (above the pylorus)
* This can be due to pyloric stenosis, which is more common in male infants and has an incidence of 1:1000

2) From the kidney
* Due to furosemide & thiazide

  • Another initiating factor for metabolic alkalaemia is the gain of exogenous alkali
  • This is much less common, and may be caused by a massive blood transfusion
28
Q

How is metabolic alkalosis maintained?

What are 3 processes that can maintain metabolic alkalosis?

A
  • Metabolic alkalosis can be maintained if there is a process that impairs the kidneys ability to excrete bicarbonate
  • 3 processes that can maintain metabolic alkalosis:
    1) Hypokalaemia
    2) Aldosterone Excess
    3) Volume & chloride depletion group
  • It’s all you HAV to remember
29
Q

Describe the 5 steps in the development of hypokalaemia in metabolic alkalaemia from pyloric stenosis

A
  • 5 steps in the development of hypokalaemia in metabolic alkalaemia from pyloric stenosis:

1) In health parietal cell secrete H+ into lumen of the stomach. The bicarb is secreted into the ECF

2) Gastric fluid also contains Na+ , water & K+ (5-10 mmol/l)
* Due to the vomiting in pyloric stenosis, this leads to loss of all of these substances and an excess of bicarbonate

3) Initially excess bicarb is spilled in the urine but accompanied by a cation

4) Worsening volume depletion from vomiting results in aldosterone secretion (RAAS)

5) Sodium & water retained exacerbating hypokalaemia
* This is because the potassium has to act as the cation to accompany excess bicarbonate in the event of sodium retention

30
Q

Describe the maintenance of metabolic alkalosis flow chart

A
31
Q

How is metabolic alkalosis compensated for?

What must happen for this to occur?

A
  • pH correlates to HCO3/pCO2
  • To compensate fir metabolic alkalosis, pCO2 must increase, therefore minute volume must fall
  • It is difficult to predict the extent of this
32
Q

Why we must consider clinical context scenario

A
33
Q

Summary

A
  • Summary:
  • Remember the structured approach to interpretation of ABGs
  • Always consider the clinical context
  • Think about the anion gap