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Acid Base Disturbances Flashcards

1
Q

Why is expressing (H+) as blood (H+) better than expressing it as pH?

A

a rise in [H+] is reflected in an absolute increase in a concentration, rather than a fall in a log value.
it is the procedure adopted by the majority of clinical chemistry laboratories in the UK.

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2
Q

What is alkalaemia?

A

Blood (H+) below normal range of 36-44 nmol/L

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3
Q

What is acidaemia?

A

Blood (H+) above normal range of 36-44 nmol/L

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4
Q

What are the four types of acid-base disturbances?

A

Metabolic- associated with changes in plasma (HCO3-)
Respiratory- changes in Pco2
Classified as simple/ primary

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5
Q

What is primary disturbance?

A

original cause of the acid-base change

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6
Q

What is compensation/ secondary changes?

A

refers to the processes by which the body counteracts the primary disturbance.

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7
Q

What is complex/ mixed acid-base disturbances?

A

terms used to describe a situation in which the patient has more than one primary disorder

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8
Q

How can we deduce the effect of change in (HCO3-) on blood (H+) in terms of the bicarbonate system?

A

(H+)= 180 x Pco2/ (HCO3-)
If [HCO3-] decreases then [H+] increases - acidaemia.
If [HCO3-] increases this produces a decrease in [H+] - alkalaemia

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9
Q

How can we deduce the effect of change in (HCO3-) on blood (H+) in terms of buffering?

A

An increase in plasma [HCO3-] will push the equilibrium to the left, causing a decrease in [H+] - alkalaemia.
A decrease in plasma [HCO3-] will pull the equilibrium to the right, causing an increase in the [H+] - acidaemia.

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10
Q

What is the difference between acidaemia/alkalaemia and acidosis/alkalosis?

A

‘acidaemia’ means that plasma [H+] is above the normal range. ‘Acidosis’ means that there is a condition, such as hypoventilation or metabolic acid production, that will tend to increase [H+], so it may result in acidaemia - however if there is efficient compensation (see later), or some opposing condition that tends to reduce [H+], then you might not actually find acidaemia. Similarly with alkalosis and alkalaemia.
Thus acidosis and alkalosis refer to the CONDITIONS THAT TEND TO PRODUCE A DISTURBANCE in [H+]; acidaemia and alkalaemia refer to the disturbances themselves.

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11
Q

What are the causes of Metabolic Acidaemia?

A

Metabolic acidaemia can result from the loss of HCO3-, for example:

  1. in chronic diarrhoea (bile is alkaline, and HCO3- is also secreted directly into the intestine).
  2. when it is depleted by acting as a buffer during increased metabolic acid production (such as occurs in ketoacidaemia and lactic acidaemia).
  3. as a result of ingesting substances that are acidic, or are metabolised to acids.
    - In either case (2) or (3) plasma [HCO3-] falls as it combines with H+ and is converted to H2CO3, which is then removed via the lungs as CO2.
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12
Q

What are the causes of Metabolic Alkalaemia?

A

Metabolic alkalaemia can be caused by:

  • eating large amounts of sodium bicarbonate, such as indigestion remedies (“antacids”), or substances such as the salts of organic acids, which are metabolised to [HCO3-].
  • severe vomiting of the gastric content: HCl is lost from the stomach and consequently [H+] falls. This loss of acid must obviously result in alkalaemia.
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13
Q

How is gastric acid produced?

A

creation of such a large difference in [H+] requires energy. This is supplied in the form of ATP, by the many mitochondria in parietal cells, and it is used by the gastric ATPase, a proton pump that exchanges H+ for K+. (This enzyme is inhibited by omeprazole, a drug used in the treatment of gastric ulcers.)

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14
Q

What is the alkali tide?

A

The source of the H+ is carbonic acid, produced by the hydration of CO2 within the parietal cells. The other product is bicarbonate, which is transported into the plasma in exchange for chloride, so that plasma [HCO3-] rises when the parietal cells secrete HCl

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15
Q

How does vomiting therefore lead to alkalaemia?

A

If acid is pumped into one compartment – the stomach – then an equal amount of alkali is created, and enters the blood.
If the gastric contents are lost through vomiting, gastric acid secretion is stimulated, with a consequent increase in plasma [HCO3-]

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16
Q

How can we deduce the effect of change in (CO2) on blood (H+) in terms of Pco2?

A

(H+) = 180 x Pco2/(HCO3-)
an increase in [CO2] causes an increase in [H+] - acidaemia.
a decrease in [CO2] causes a decrease in [H+] - alkalaemia.

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17
Q

How can we deduce the effect of change in (CO2) on blood (H+) in terms of hyperventilation?

A

An excessive loss of CO2 due to hyperventilation will pull the equilibrium to the left, causing a decrease in [H+] - alkalaemia.
The accumulation of CO2 due to poor lung function (and consequently hypoventilation) will push the equilibrium to the right, causing an increase in [H+] - acidaemia

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18
Q

What is respiratory alkalaemia associated with?

A

hyperventilation, for example induced by anxiety

aspirin poisoning, through stimulation of respiratory centres by salicylate

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19
Q

What is respiratory acidaemia associated with?

A

Lung disease, resulting in hypoventilation

drugs such as anaesthetics or sleeping tablets, which depress the respiratory centre

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20
Q

How does shift in equilibrium affect H+ and HCO3-?

A

in the plasma, [HCO3–]&raquo_space;» [H+], so that small shifts in the equilibrium have a much greater relative effect on the concentration of protons than on the concentration of bicarbonate.

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21
Q

What is the electrical charge of plasma?

A

It is electrically neutral and so the number of positive charges must equal the number of negative charges
(cations=anions)

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22
Q

What are unmeasured ions?

A

The concentrations of the most abundant cations (K+, Na+) and anions (Cl-, HCO3-) are easy to measure in plasma, using ion-specific electrodes. However other ions are not measured routinely in most clinical chemistry laboratories

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23
Q

What are the principal unmeasured cations?

A

Ca2+ and Mg2+, the free concentrations of which are each around 1 mmol/L

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24
Q

What are the principle unmeasured anions?

A

sulphate, phosphate, lactate, ‘ketone bodies’ and also proteins such as albumin (which has a net negative charge at pH 7.4) – together their concentration is much greater than that of the unmeasured cations

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25
Q

How do we balance the charges on cations and anions mathematically?

A

[Na+] + [K+] + unmeasured cations = [Cl-] + [HCO3-] + unmeasured anions

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26
Q

What is the anion gap?

A

ANION GAP = ([Na+] + [K+]) - ([Cl-] + [HCO3-])
Thus the anion gap is only a gap in the measured concentrations - it is an index of the concentration of unmeasured anions in plasma.

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27
Q

How does the anion gap change with exercise?

A

The accumulating lactic acid produced by the muscles has been buffered by HCO3-, resulting in a decreased concentration of HCO3- in the plasma.
Lactate has accumulated in plasma and is now present as an unmeasured anion, increasing the anion gap.

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28
Q

What is the mnemonic for causes of metabolic acidaemia (hence increased anion gap)

A

MEG’S LARD

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29
Q

Describe the mnemonic

A 
Methanol
Ethylene Glycol
Salicylate
Lactic acidosis
Alcoholic ketoacidosis
Renal failure
Diabetic ketoacidosis
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30
Q

What are the main causes of an increased anion gap overall?

A
  • metabolism of alcohols (methanol, ethylene glycol)
  • salicylate (derived from aspirin)
  • lactic acidaemia (derived from anaerobic glycolysis in the muscles)
  • ketoacidaemia (which occurs in starvation, in type 1 diabetes and as a result of alcohol metabolism)
31
Q

Where are alcohols metabolised?

A

some extent in gastric and intestinal cells, but largely in the liver.

32
Q

Describe metabolism of alcohol

A

Initially they are oxidised to aldehydes by alcohol dehydrogenases, which are present in the stomach, intestine and liver (there are several isoenzymes).
Aldehydes are oxidized to carboxylic acids, by aldehyde dehydrogenases.

33
Q

Describe ethanol metabolism

A

-first oxidized to acetaldehyde (ethanal), which is oxidised to acetic (ethanoic) acid.
-acetic acid is converted to acetyl-CoA
acetyl-CoA can be converted to fatty acids, oxidized in the TCA cycle or converted to acetoacetic and 3-hydroxybutyric acids (‘ketone bodies’).

34
Q

When is ketone body formation favoured?

A

large amounts of ethanol are ingested, because ethanol oxidation raises the [NADH]/[NAD+] ratio in the liver, and this inhibits the TCA cycle, diverting the acetyl-CoA to ketones. This alcoholic ketoacidosis is often accompanied by lactic acidosis and hypoglycaemia, because gluconeogenesis is inhibited.

35
Q

Describe methanol metabolism

A

is oxidized to formaldehyde, which is further oxidised to formic acid: the toxicity of methanol is due to the formation of formaldehyde, which is very reactive. Formate can enter the ‘one carbon’ pool, by being attached to the coenzyme tetrahydrofolic acid, and is used in various biosynthetic reactions.
Methanol- methanol- methanoic acid

36
Q

How does methanol poisoning occur?

A

through the consumption of methylated spirit or of adulterated drinks; Its symptoms include renal failure and blindness

37
Q

Describe ethylene glycol metabolism

A

is oxidized to glyoxal, glycollic acid and finally oxalic acid

38
Q

What is ethylene glycol present in?

A

component of car radiator antifreeze: it has been used as a poison, and it is sometimes illegally added to wine to sweeten it. Its metabolites are very toxic, not least because oxalic acid binds Ca2+ and forms a precipitate of calcium oxalate in the kidneys.

39
Q

What are the symptoms of ethylene glycol poisoning?

A

intoxication, nausea, acidaemia and renal failure.

40
Q

How is poisoning by toxic alcohols treated?

A

infusion of ethanol, since this is the preferred substrate of alcohol dehydrogenase (it has a lower KM value than other alcohols, so competes with them for oxidation); instead of being metabolized the toxic alcohols are then excreted. Specific inhibitors of alcohol dehydrogenase, such as fomepizole, are also available and can be used in treatment, but they are expensive.

41
Q

What is lactic acid?

A

Lactic acid is the product of anaerobic glycolysis in muscle and a few other cell types, notably erythrocytes. It is mostly removed from plasma by the liver, which reconverts much of it to glucose (gluconeogenesis).

42
Q

When does lactic acid accumulate in the plasma?

A
  • during sudden intense exercise
  • if the oxygen supply to the muscles is compromised, for example by circulatory failure or carbon monoxide poisoning
  • if gluconeogenesis is inhibited (for example in hereditary fructose intolerance or alcohol intoxication)
43
Q

How does salicylate produce metabolic acidaemia?

A

Aspirin is hydrolysed to two acidic products: acetic acid (metabolised) and salicylic acid (conjugated by the liver and excreted)

44
Q

How does salicylate produce metabolic alkalaemia?

A

Salicylate stimulates the respiratory centres, causing an increase in ventilation and consequently a fall in PCO2 and [H+]

45
Q

How does salicylate result in mixed disturbance?

A

[H+] may be within the normal range, but with both [HCO3-] and PCO2 lower
Sometimes aspirin poisoning causes vomiting, so the acid-base disturbance becomes even more complexed

46
Q

What are the causes of ketoacidaemia?

A
  • Starvation
  • Type I (insulin dependent) diabetes mellitus (IDDM)
  • Alcohol abuse
47
Q

How does starvation lead to ketoacidaemia?

A

ketone body production is greatly increased during starvation, because triacylgylcerol breakdown is increased and the free fatty acids are converted by the liver to ‘ketone bodies’, which are used as fuel by the muscle and also brain. This is an important adaptation, which reduces the body’s requirement for glucose.

48
Q

How does IDDM cause ketoacidaemia?

A

most common cause of severe ketoacidaemia, because low insulin concentrations result in increased fat breakdown. Note that this is NOT a feature of type 2 diabetes.

49
Q

How does alcohol abuse lead to ketoacidaemia?

A

alcohol is ketogenic, and alcohol abuse tends to produce abnormally high levels of circulating ketones.
The ‘ketone bodies’ are acetoacetic acid and its reduction product, 3-hydroxybutyric acid: they are relatively strong acids, and are almost completely ionized in plasma - hence the acidaemia. Acetone is formed by the spontaneous decarboxylation of acetoacetate. It is not further metabolised but, being volatile and membrane-permeant, may be breathed out, and its characteristic smell is detectable on the breath in severe ketoacidaemia

50
Q

What are ketone bodies formed from?

A

acetyl-CoA, during the breakdown of fat, protein or alcohol. Acetyl-CoA is also formed from glucose, but during starvation, when ketone bodies are being produced, the liver is carrying out gluconeogenesis, not glycolysis.

51
Q

What does insulin normally inhibit?

A

lipolysis (breakdown of stored triacylglycerol)

52
Q

What occurs in IDDM?

A
  • the low level of insulin secretion results in uncontrolled lipolysis.
  • the fatty acids released from adipose tissue do not themselves produce acidaemia, as they are weak acids; they are quickly removed from circulation and their concentration in the plasma is never very high.
  • acetoacetic and 3-hydroxybutyric acids, the products of fatty acid oxidation in the liver, are relatively strong acids and their plasma concentration can become very high, creating a dangerous metabolic acidaemia.
53
Q

What is the difference in type 2 (non-insulin dependent) DM?

A

levels of circulating insulin are usually high enough to inhibit lipolysis, so ketoacidaemia is not seen.

54
Q

What are the symptoms of IDDM?

A
  • Weight loss, because of uncontrolled fat breakdown.
  • Polydypsia and polyuria - drinking and peeing a lot, if you prefer - because glucose and ketone bodies exceed their renal thresholds and appear in the urine, causing osmotic diuresis.
  • Hypokalaemia, because acetoacetic and 3-hydroxybutyric acids are mostly in their ionized forms in urine, so are accompanied by cations, Na+ and K+; the relative change in plasma concentration is greater for K+ than for Na+.
55
Q

What is the treatment for IDDM?

A

VIP treatment: volume (i.e. rehydration), insulin, potassium.

56
Q

How does renal failure cause acidaemia?

A

failure to excrete endogenous non-volatile acids (such as sulphuric). These accumulate in the plasma, resulting in decreased [HCO3-] and an increased anion gap

57
Q

How is toluene linked to acidaemia?

A

Toluene is a solvent used in many glues, and glue-sniffers can experience severe metabolic acidaemia because of the metabolism of toluene to benzoic acid and its glycine conjugate, which is called hippuric acid.

58
Q

How can we use data to interpret clinical acid-base disturbances?

A
  • the size and direction of the change in [H+] indicates the existence of alkalaemia or acidaemia.
  • an altered [CO2] indicates that the respiratory system is involved. Consideration of the direction of the change should indicate whether the respiratory system is malfunctioning, and is thus the cause of the disturbance, or whether it is attempting to correct the situation i.e. to compensate for a change in [HCO3–].
  • an altered [HCO3–] suggests a metabolic effect which, just as in the example above, may have caused the problem or may reflect compensatory activity by the renal system.
  • a raised anion gap indicates the presence of an unmeasured anion such as lactate or 3-hydrobutyrate. The accumulation of an unknown anion usually indicates that a strong acid has entered the plasma and has been buffered, thereby affecting the H+ balance.
59
Q

What is the body’s primary response to a primary acid-base disturbance?

A

try to restore the [H+] to its normal range, by altering either PCO2 (during a metabolic disturbance) or [HCO3–] (during a respiratory disturbance)

60
Q

What are the principles of compensation?

A

-Compensation alters the parameter that was not altered by the primary disturbance
-This parameter will change in the same direction as the parameter altered by the disturbance, so as to restore the value of the ratio PCO2 / [HCO3–], which is what defines [H+]
-Respiratory compensation (of metabolic disturbances) occurs rapidly, whereas the renal (metabolic) response to respiratory disturbances takes hours, even days to develop, because it involves the synthesis of proteins and their insertion into membranes
-Body cannot apply respiratory compensation to a respiratory disturbance, nor metabolic compensation to a metabolic disturbance
Compensation is easy to spot: if a parameter (PCO2 or [HCO3–]) has changed in a way that would oppose the observed change in [H+] in an acid-base disturbance, then this must be a compensatory response, not the primary disturbance.

61
Q

Describe respiratory compensation

A

This involves a change in the rate of respiration, in order to alter PCO2, following a metabolic disturbance: for example, metabolic acidaemia, which decreases [HCO3–], is compensated by an increased respiratory rate, so as to decrease PCO2 and thereby move [H+] back towards its normal range.

62
Q

How does a change in rate of respiration occur?

A

Receptors in the brain-stem sense changes in [H+] in the CSF: an increase in PCO2 produces an increase in [H+], leading to an increased rate of respiration and a consequent fall in PCO2, and vice versa. Note that the receptors do not sense CO2 directly, but detect the change in [H+] following a change in PCO2.

63
Q

Describe metabolic compensation

A

involves action by the kidney to change plasma [HCO3–]. This is brought about by altering the rate at which bicarbonate is filtered into the urine, and by the synthesis of ‘new’ bicarbonate; this is accompanied by increased excretion of NH4+.

64
Q

Why is metabolic compensation slow to develop?

A

Because these processes involve the up-regulation of genes encoding enzymes and transporters
compensation of acute respiratory disturbances is not seen

65
Q

What is the commonest type of metabolic compensation?

A

increase in plasma [HCO3–] in response to the increased PCO2 produced by chronic respiratory disease, such as COPD.

66
Q

What occurs in acute hypoxia?

A

(plasma PO2 < 10 kPa), the respiratory rate increases, on activation of receptors in the carotid body, which stimulate afferent nerves that signal to respiratory centres in the brainstem. The receptors do not sense PO2 directly, but respond to an increase in the plasma concentration of lactate, which is normally 1 - 5 mmol/L, and which rises in hypoxia.

67
Q

What occurs long-term in hypoxia?

A

PO2 is controlled by HIF-1 (hypoxia-induced factor), a protein complex that acts as a super-regulator of several hundred genes in many tissues. Oxygen-dependent hydroxylation of proline residues in HIF-1 leads to targeting of this protein for degradation, but in chronic hypoxia the concentration of HIF-1 increases, leading to increased angiogenesis, increased synthesis of erythropoietin and a shift toward anaerobic glycolysis for production of ATP.

68
Q

What is Standard bicarbonate?

A

[HCO3-], adjusted to what it would be if PCO2 had a normal value. i.e. 5.3 kPa. This eliminates any respiratory contribution to the bicarbonate concentration.

69
Q

What is Base Excess?

A

amount of acid required to titrate the blood to pH7.4, at 37° with PaCO2 = 5.3 kPa, and is calculated from the measured values of [H+], PCO2 and also [haemoglobin].

70
Q

What does Base Excess show?

A

metabolic component of any disturbance: a positive value indicates an excess of bicarbonate, i.e. metabolic alkalaemia, which arises from a loss of gastric HCl as a result of vomiting, from renal overproduction of bicarbonate or from compensation for respiratory acidaemia. A negative value of BE, i.e. a base deficit, indicates metabolic acidaemia.

71
Q

What happens if there is a base deficit?

A

(BE < -2 mmol/L), the anion gap can show whether this arises from addition of acid (i.e. buffering) or simple loss of bicarbonate. An elevated AG indicates an increase in unmeasured anions, as a result of addition of an acid to the plasma (for example, in ketoacidaemia or lactic acidaemia); a normal AG suggests loss of bicarbonate (for example through diarrhoea).

72
Q

What is interpreted using blood gas analysis?

A

total bicarbonate concentration is used to assess the metabolic component of acid-base status. For example, an [H+] >44 nmol/L, with a normal range PCO2 (4.8 - 6.0 kPa) and a bicarbonate below the normal range, [HCO3–] <21.0 mmol/L, suggests a simple metabolic acidaemia.

73
Q

What are the difficulties interpreting the metabolic component of the acid-base status?

A

when the PCO2 is not in the normal range. For example, an acute respiratory acidaemia, with a raised [H+] and raised PCO2, may result in a rise in [HCO3–], not from metabolic compensation, but as a consequence of the CO2/[HCO3–] equilibrium.
The metabolic component of acid-base status in a patient with an abnormal PCO2 can be obtained using an acid-base nomogram; but it is simpler to consider the two derived measurements, Standard Bicarbonate and Base Excess, which appear in data printouts and allow the metabolic component to be assessed independently of the PCO

Respiratory (41 decks)

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