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Y2 MECHANISMS OF DISEASE > Acid Base Disorders > Flashcards

Acid Base Disorders Flashcards

1
Q

What is MetHb?

A

Haemoglobin that carries iron in the Fe3+ state rather than the Fe2+ state

it doesn’t have the same affinity for oxygen

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2
Q

What 6 areas are looked at when determining the acid-base status of a patient?

A
  1. gases - pCO2 and pO2
  2. metabolites - glucose and lactate
  3. electrolytes
  4. derived parameters
  5. pH
  6. co-oximetry
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3
Q

Which electrolytes are looked at when determining the acid-base status of a patient?

A
  1. sodium
  2. potassium
  3. chloride
  4. calcium
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4
Q

What are the derived parameters that are looked at when determining the acid-base status of a patient?

A
  1. base excess
  2. standard bicarbonate
  3. total CO2
  4. anion gap
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5
Q

What is meant by co-oximetry?

Which areas are looked at when determining the acid-base status of a patient?

A

the oxygen carrying state of haemoglobin

this looks at:

  1. total Hb
  2. O2 saturation
  3. OxyHb
  4. MetHb
  5. COHb
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6
Q

What are the 3 rules when taking samples for blood gas analysis?

A

Samples must be:

  1. well-mixed, heparinised whole blood with NO air bubbles
  2. analysed immediately
  3. NOT sent via pneumatic tube system
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7
Q

Why must there be no air bubbles in a blood gas sample?

A

the presence of air bubbles can affect pO2

this can cause an increase in pH and decrease in pCO2

(this is often clinically insignificant)

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8
Q

Why must samples for blood gas be analysed immediately?

A

there is a time-dependent decrease in pO2 and increase in pCO2

this is due to ongoing in vitro glycolysis

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9
Q

Why must samples for blood gas analysis not be sent via a pneumatic tube system?

A

pneumatic tube can cause any air present in the sample to mix rapidly

this changes the partial pressures of gases within

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10
Q

Which sample is being taken here?

A
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11
Q

What is the standard sample for blood gas analysis?

Why is it important to know which sample has been taken?

A

The standard sample is arterial blood (especially to look at pO2)

Different reference ranges apply for venous and arterial samples

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12
Q

What is the difference between metabolic and respiratory acidosis/alkalosis?

A

Metabolic:

primary disorder is caused by a non-respiratory element

Respiratory:

primary disorder is caused by altered respiration

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13
Q

What ionic changes are seen in metabolic acidosis/alkalosis?

A

Acidosis:

there is a decrease in bicarbonate

Alkalosis:

there is an increase in bicarbonate

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14
Q

What is the main change seen in respiratory acidosis/alkalosis?

A

acidosis:

there is an increase in pCO2

alkalosis:

there is a decrease in pCO2

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15
Q

What is meant by ‘compensatory mechanisms’?

What is their purpose and downfall?

A

Secondary changes in bicarbonate and pCO2 to correct for the primary disorder

They aim to restore a neutral pH, but full compensation rarely occurs

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16
Q

When may changes in bicarbonate concentration occur as a compensatory mechanism?

How fast is it?

A

changes in bicarbonate concentration occur through renal regeneration

this occurs to compensate for respiratory disorders

it is very slow

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17
Q

When may changes in pCO2 occur as a compensatory mechanism?

How fast is it?

A

changes in pCO2 occur through changes in respiratory rate

this occurs to compensate for metabolic disorders

it is very fast

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18
Q

What are the 2 criteria that would lead you to suspect a mixed disorder?

A
  1. pH is within the reference range but bicarbonate and pCO2 are not
  2. compensation falls outside the expected limits
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19
Q

WHat is the first step in assessing acid-base status?

What are the 2 categories?

A

What is the pH?

pH < 7.35 = acidaemia

pH > 7.45 = alkalaemia

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20
Q

What is the second step in assessing acid base status?

What is the easiest way to do this?

A

Is the primary disorder metabolic or respiratory?

The easiest way to do this is to check pCO2

(it should be 4.7-6 kPa)

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21
Q

What would lead you to suspect a respiratory or metabolic acidosis?

A

respiratory:

increase in pCO2

metabolic:

decrease or no change in pCO2

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22
Q

What would lead you to suspect a respiratory or metabolic alkalosis?

A

respiratory:

decrease in pCO2

metabolic:

increase or no change in pCO2

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23
Q

What is the third step in assessing acid-base balance?

What measurements are needed to work this out?

A

Is there any compensation?

You need BOTH pCO2 and bicarbonate measurements to work this out

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24
Q

How could you tell if respiratory or metabolic compensation is occurring?

A

Respiratory compensation occurs for metabolic disturbances

there are changes in CO2

Metabolic compensation occurs for respiratory disturbances

there are changes in HCO3-

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25
Q

What are the 2 measures of bicarbonate?

Which one is often used?

A
  1. main lab bicarbonate
  2. standard bicarbonate

main lab bicarbonate is most commonly used

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26
Q

What is a normal range for main lab bicarbonate?

How is it calculated?

A

it is sometimes called “total CO2” as it is an approximation of bicarbonate calculated, in part, from CO2

Normal range 22 - 29 mmol/L

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27
Q

What is the normal range for standard bicarbonate?

A

22 - 26 mmol/L

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28
Q

How is standard bicarbonate different to main lab bicarbonate?

A

standard bicarbonate removes the respiratory contribution

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29
Q

What does a normal and abnormal standard bicarbonate tell you about the status of an acid-base disorder?

A

normal standard bicarbonate:

the disorder is ALL respiratory

abnormal standard bicarbonate:

this disorder has a metabolic component

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30
Q

What is meant by base excess as a measurement?

What does it tell us?

A

it is the amount of acid or alkali needed to titrate blood pH to 7.40

it takes into account all buffers, not just bicarbonate

it tells us if there is a metabolic component to a disorder

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31
Q

What are the normal ranges for base excess?

A

- 2.3 to + 2.3 mmol/L

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32
Q

What does a negative and positive base excess show?

A

negative BE (< -2.3 mmol/L):

there is metabolic acidosis (a base deficit)

positive BE (> 2.3 mmol/L):

there is a metabolic alkalosis (a base excess)

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33
Q

What is anion gap as a measurement?

What is a normal range and why can’t it be zero?

A

the difference between the sum of measured anions and cations

normal range = 8 - 16 mmol/L

anion gap is not zero in healthy patients as not all anions are measured

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34
Q

What is the equation for calculating anion gap?

A

( [Na+] + [K+] ) - ( [Cl-] + [HCO3-] )

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35
Q

What does an increased anion gap show?

A

there are significant amounts of unmeasured anions present

e.g. ketones, lactate, salicylate, proteins etc.

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36
Q

How do the following features change in metabolic acidosis?

A
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37
Q

What are the 3 main signs and symptoms of metabolic acidosis?

A
  1. nausea, vomiting and anorexia
  2. subjective sense of dyspnoea caused by stimulation to the respiratory centre
  3. Kussmaul breathing
38
Q

What is Kussmaul breathing in severe acidosis?

A

a deep laboured breathing pattern

39
Q

What are the 4 causes of metabolic acidosis?

A
  1. increased acid formation
  2. decreased acid excretion
  3. loss of bicarbonate
  4. acid ingestion
40
Q

What are the 4 conditions that can lead to increased acid formation?

What is significant about these metabolic acidoses?

A

these are increased anion gap metabolic acidoses (plus uraemia)

  1. ketoacidosis
  2. lactic acidosis
  3. poisoning
  4. inherited organic acidoses
41
Q

What are the 3 types of ketoacidosis?

A
  1. diabetic ketoacidosis
  2. alcoholic ketoacidosis
  3. starvation
42
Q

What are the 2 types of lactic acidosis?

A
  1. type A - caused by tissue hypoxia
  2. type B - metabolic and toxic causes
43
Q

What types of poisoning can lead to increased acid formation in metabolic acidosis?

A
  1. salicylate poisoning
  2. toxic alcohols - e.g ethylene, glycol, methanol, ethanol
44
Q

What 2 conditions lead to decreased acid excretion?

A
  1. uraemia due to renal failure
  2. RTA type 1 (renal tubular acidosis)
45
Q

What conditions lead to loss of bicarbonate?

A

GI causes:

diarrhoea and fistulas

Renal causes:

RTA type 2 (proximal)

carbonic anhydrase inhibitors (e.g. acetazolamide)

46
Q

How is buffering involved in the physiological response to metabolic acidosis?

A
  • an acute increase in [H+] is resisted by bicarbonate buffering, causing decreased HCO3-
  • protein buffering is important in chronic acidosis
47
Q

What is the respiratory compensation involved in the physiological response to metabolic acidosis?

A
  • stimulation of the respiratory centre leads to hyperventilation
  • this blows off CO2
  • this process is self-limiting as it generates additional CO2
48
Q

How is renal compensation involved in the physiological response to metabolic acidosis?

A
  • urine H+ excretion is maximised
  • there is an increased rate of bicarbonate regeneration
49
Q

What is the main treatment for metabolic acidosis?

A

sodium bicarbonate

IV sodium bicarbonate:

this is only given if pH < 7.00

oral bicarbonate:

this is given in CKD and RTA types 1 and 2

50
Q
A
51
Q

What are the risks with giving sodium bicarbonate to treat metabolic acidosis?

A
  1. rapid correction impairs O2 delivery
  2. rebound alkalosis is possible
52
Q

How do the following features change in metabolic alkalosis?

A
53
Q

What is significant about the signs and symptoms of metabolic alkalosis?

A

they are usually related to an underlying disorder

54
Q

What condition may severe metabolic alkalosis lead to?

What are the symptoms and risk associated with this?

A

it increases protein binding of Ca2+, leading to hypocalcaemia

this causes headache, lethargy and neuromuscular excitability

sometimes with delirium, tetany and seizures

it lowers the threshold for arrhythmias

55
Q

What are the 3 main causes of metabolic alkalosis?

A
  1. administration of bicarbonate
  2. loss of H+ (usually through vomiting)
  3. potassium depletion
56
Q

Why can hypokalaemia cause a metabolic alkalosis, relating to the function of the kidneys?

A

excretion of H+ is favoured in order to spare K+ at aldosterone-controlled renal transporter

57
Q

Why can hypokalaemia cause a metabolic alkalosis, in relation to cells?

A

K+ ions are transported out of RBCs to increase plasma concentration

H+ ions move into the RBC to maintain electroneutrality

This leads to a decrease in plasma [H+]

58
Q

How are buffers involved in the physiological response to metabolic alkalosis?

A

there is release of H+ from buffers

59
Q

What is the respiratory compensation in the physiological response to metabolic alkalosis?

A

reduced respiratory rate in order to retain CO2

this is self-limiting, as an increase in pCO2 stimulates the respiratory centre

60
Q

Why is renal compensation in response to metabolic alkalosis difficult?

A

Decreased GFR leads to inappropriately high bicarbonate reabsorption

potassium deficiency contributes to persistence of alkalosis

61
Q

What are the stages involved in management of metabolic alkalosis?

A
  1. treat the underlying cause
  2. treat factors that sustain alkalosis
    e. g. replace potassium
62
Q

How are the following features changed in respiratory acidosis?

A
63
Q

What are the signs and symptoms of respiratory acidosis?

A
  1. they are usually related to an underlying disorder
  2. some patients complain of dyspnoea
64
Q

What are the 2 main causes of respiratory acidosis?

A
  1. defective control of respiration
  2. defective respiratory function
65
Q

What 3 main areas may lead to defective control of respiration?

A
  1. CNS depression
  2. CNS disease
  3. Neurological disease
66
Q

What typically causes CNS depression, leading to defective control of respiration?

A

anaesthetics and sedatives

narcotics and opiates

67
Q

What tends to cause CNS disease leading to defective control of respiration?

A
  1. trauma
  2. haemorrhage
  3. infarction
  4. tumour
  5. infection
68
Q

What neurological diseases lead to defective control of respiration?

A
  1. spinal cord lesions
  2. motor neurone disease
  3. Guillain-Barre
69
Q

What mechanical conditions can lead to defective respiratory function?

A
  1. myopathies
  2. pneumothorax
  3. pleural effusion
  4. inadequate mechanical ventilation
70
Q

What pulmonary diseases can lead to defective respiratory function?

A
  1. COPD, severe asthma, etc.
  2. impaired perfusion
71
Q

How is buffering involved in the physiological response to respiratory acidosis?

A

there is limited buffering by haemoglobin

72
Q

What is the respiratory compensation involved in the physiological response to respiratory acidosis?

A

an increase in pCO2 stimulates the respiratory centre, but disease prevents an adequate response

73
Q

What are the renal compensation mechanisms involved in the physiological response to respiratory acidosis?

A
  1. there is maximal bicarbonate reabsorption
  2. almost all phosphate is excreted as H2PO4- (rather than HPO42-)
  3. there is a marked increase in urinary NH4+
74
Q

What are the 3 steps involved in management of respiratory acidosis?

A
  1. treat underlying cause
  2. maintain adequate arterial pO2, but avoid loss of hypoxic stimulus to respiration
  3. avoid rapid correction of pCO2 as this increases risk of alkalosis
75
Q

How are the following features changed in respiratory alkalosis?

A
76
Q

What are the signs and symptoms of respiratory alkalosis?

A
  1. usually related to an underlying disorder
  2. more severe alkalosis leads to hypocalcaemia
77
Q

What are the 3 main causes of respiratory alkalosis?

A
  1. central
  2. pulmonary
  3. iatrogenic (excessive mechanical ventilation)
78
Q

What are examples of central causes of respiratory alkalosis?

A
  1. head injury
  2. stroke
  3. hyperventilation
  4. drugs (e.g. salicylates)
  5. sepsis (cytokines)
  6. chronic liver disease (toxins)
79
Q

What are pulmonary causes of respiratory alkalosis?

A
  1. pulmonary embolism
  2. pneumonia
  3. asthma
  4. pulmonary oedema
80
Q

How is buffering involved in the physiological response to respiratory alkalosis?

A

there is release of H+ from non-bicarbonate buffers

81
Q

How is respiratory compensation involved in the physiological response to respiratory alkalosis?

A

the inhibitory effect of decreased pCO2 is overwhelmed by the primary cause

82
Q

How is renal compensation involved in the physiological response to respiratory alkalosis?

A

there is decreased renal regeneration of bicarbonate

as CO2 is a substrate, this means it is preserved

83
Q

What are the stages involved in the management of respiratory alkalosis?

A
  1. treat the underlying cause
  2. rapid symptomatic relief by re-breathing
  3. sedation or prevention of hyperventilation by mechanical ventilation
84
Q

What is the difference between full and partial compensation?

A

full compensation:

occurs if compensation returns the pH to normal

partial compensation:

occurs when the pH has not returned to normal

over-compensation does not occur in any acid-base disorder

85
Q

What are the conditions and compensatory mechanisms in each of these disorders?

A
86
Q

what is meant by a mixed disorder?

what are the 2 types of mixed disorder?

A

two or more primary acid-base disorders presenting in the same patient

they can either be additive or counterbalancing

87
Q

What is involved in respiratory failure?

Is it an additive or counterbalancing mixed disorder?

A

additive

  • respiratory acidosis - increased pCO2
  • AND metabolic acidosis - increased lactic acid
88
Q

Is vomiting and CCF an additive or counterbalancing mixed disorder?

What is involved?

A

additive

  • metabolic alkalosis - loss of H+
  • AND respiratory alkalosis - increased respiratory rate
89
Q

Is salicylate poisoning an additive or counterbalancing mixed disorder?

What is involved?

A

counterbalancing

  • metabolic acidosis
  • AND respiratory alkalosis - increased respiratory rate
90
Q

Is vomiting and renal failure an example of an additive or counterbalancing mixed disorder?

A

counterbalancing

  • metabolic alkalosis - loss of H+
  • AND metabolic acidosis (decreased renal H+ excretion)

Y2 MECHANISMS OF DISEASE (36 decks)

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