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Yr 2 - EMS > Acid-Base Homeostasis > Flashcards

Acid-Base Homeostasis Flashcards

1
Q

Why is acid-base homeostasis important?

A

H+ ions are present everywhere in the body –> maintenance of appropriate conc is critical to normal function

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2
Q

How can changes in [H+] affect proteins?

A

Changes can affect the surface charge and physical conformation of proteins, changing their function Can lead to denatured proteins.

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3
Q

How can [H+] affect oxidative phosphorylation?

A

The gradient of [H+] between the inner and outer mitochondrial membrane drives oxidative phosphorylation

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4
Q

Acid-base homeostasis (in a nutshell).

  • How are H+ ions inputted into the body?
  • What is the purpose of buffers?
  • What are the 2 ways that H+ are removed from the body?
A
  • Metabolism
  • Maintenance of normal [H+]
  • Lungs and kidneys
    • Lungs: excretion of CO2 in expired air
    • Kidneys: Excretion of H+ in urine
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5
Q

Describe how H+ ions are removed by the lungs

A

When CO2 is dissolved in an aqueous solution, it forms carbonic acid (H2CO3)

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6
Q

What is plasma [H+] typically kept at?

A

40nmol/L

N.B. H+ ions are produced in mmol quantities, yet must be kept at nmol concentrations.

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7
Q

How are H+ ions kept at nmol quantities?

A
  • Excretion of H+ in kidneys
  • Excretion of CO2 in lungs
  • Buffers
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8
Q

Where does acid in our bodies come from?

A
  • Glucose
  • Triglycerides
  • Amino acid metabolism
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9
Q

How can glucose produce acids?

A

Incomplete metabolism:

  • Intermediary anaerobic process
  • Glucose –> 2 lactate + 2 H+
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10
Q

Where does glucose metabolism mainly take place?

A

In skeletal muscle and RBCs

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11
Q

How can triglycerides produce acid?

A

Incomplete metabolism –> ketogenesis

  • Triglycerides –> free fatty acids + H+
  • Free fatty acids –> ketones + H+
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12
Q

What is ketogenesis?

A

Ketogenesis is a metabolic pathway that produces ketone bodies, which provide an alternative form of energy for the body.

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13
Q

Where are ketones produced?

A

They are made in the liver from the breakdown of fats. Ketones are formed when there is not enough sugar or glucose to supply the body’s fuel needs.

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14
Q

Where are free fatty acids produced?

A

In adipose tissue

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15
Q

How can amino acid metabolism produce acids?

A

Ureagenesis:

  • Metabolism of neutral amino acids results in the generation of H+
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16
Q

What is ureagenesis?

A

Formation of urea, usually referring to the metabolism of amino acids to urea.

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17
Q

Are acids H+ donors or acceptors? Bases?

A
  • Acids are H+ donors:
    • HCl –> H+ + Cl-
  • Bases are H+ acceptors
    • OH- + H+ –> H2O
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18
Q

Example of an acid + base reaction

A

HCl(aq) + NaOH(aq) –> NaCl(aq) + H2O(l)

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19
Q

What is pH?

A

Negative logarithm of the hydrogen ion concentration (mol/L)

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20
Q

Why is pH used rather than [H+]?

A

pH scale was devised to cope with the wide range of H+ concentrations encountered in chemistry (taking logarithms makes it more manageable).

Use of H+ rather than pH is becoming more prevalent in medicine, as it is a direct reflection of acid-base status.

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21
Q

If [H+] > 45 nmol/L (pH <7.35), what does this mean about the patient?

A

They are acidaemic (low blood pH)

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22
Q

If [H+] <35 nmol/L (pH >7.45), what does this mean about the patient?

A

The patient is alkalaemic

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23
Q

What is acidaemia? How does it differ from acidosis?

A

Acidaemia: low blood pH

Acidosis: abnormal process or condition that lowers arterial pH

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24
Q

What are the reference ranges for [H+]?

A

35-45 nmol/L

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25
Q

What is the reference range for pH?

A

7.35 - 7.45

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26
Q

What is Ka?

A

Acid dissociation constant: the higher the Ka, the greater the dissociation, and the stronger the acid

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27
Q

What is pKa?

A
  • The negative logarithm of Ka
  • The pKa is the pH at which a buffer exists in equal proportions with its acid and conjugated base
  • The lower the pKa, the greater the dissociation, and the stronger the acid
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28
Q

What is the equation for pKa?

A
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29
Q

What is the Henderson-Hasselbach equation?

A

Explains how acids and bases contribute to pH (and therefore [H+])

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30
Q

In this reaction, how is CO2 acting as an acid? How is HCO3- acting as a base?

A
  • CO2 acting as acid:
    • When dissolved in plasma, CO2 becomes an acid (carbonic acid; H2CO3), which readily dissociates to release H+
  • HCO3- acting as base:
    • HCO3- accepts a proton to form carbonic acid, which is converted to CO2 for excretion in the lungs
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31
Q

What does blood pH depend on regarding CO2 and HCO3-?

A

Blood pH depends not on absolute amounts of CO2 or HCO3-, but on the ratio of the two

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32
Q

Substituting HCO3- and CO2 into the Henderson-Hasselbalch equation:

  • What does pCO2 stand for?
  • What does a stand for?
  • What is the result?
A
  • pCO2: partial pressure of CO2 (kPa)
  • a: solubility constant (0.225 for CO2)
  • Result: pH is proportional to [HCO3-] / pCO2
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33
Q

What does bicarbonate buffering in the blood have a pKa of?

A

6.1

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34
Q

What is the definition of a buffer?

A

A buffer is a solution which resists change in pH when an acid or base is added.

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35
Q

What is the purpose of buffers?

A

Ensures H+ ions are transported and excreted safely without affecting physiological processes.

The body has a limited capacity to buffer changes in [H+].

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36
Q

What are the main buffers in the body?

A
  • Bicarbonate
  • Haemoglobin
  • Phosphate
  • Ammonia
  • Proteins
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37
Q

How does bicarbonate act as a buffer? Why can it not buffer CO2?

A
  • Mopping up H+ ions
  • Cannot buffer CO2 because of the equation
    • Buffering by bicarbonate would only result in the production of more CO2
  • Equilibration of CO2 therefore requires non-bicarbonate buffers (e.g. Hb)
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38
Q

What is the principal non-bicarbonate buffer?

A

Haemoglobin

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39
Q

How does Hb act as a buffer?

A

Important for buffering CO2:

  • Reduction of CO2
  • Production of HCO3-
  • Also reduce Hb to HHb (deoxyhaemoglobin)
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40
Q

Mechanism of Hb acting as a buffer:

A
  • CO2 in plasma diffuses into red cell
    • Combines with water under the action of carbonic anydrase –> forms H2CO3
  • H2CO3 readily dissociates to release H+ and HCO3- ions
    • HCO3- diffuses out into plasma
      • Replaced by Cl- from plasma that diffuses into red cell (chloride shift)
    • H+ reduces Hb to form HHb
      • Byproduct of this is O2 which diffuses out into plasma
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41
Q

How does phosphate act as a buffer?

A
  • Monohydrogen phosphate and dihydrogen phosphate form a buffer pair
    • Concentrations of these anions are too low in plasma to make an appreciable difference
    • Important buffer in urine, where phosphate is present at a much higher concentration
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42
Q

Where is phosphate an important buffer?

A

Urine

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43
Q

How does ammonia act as a buffer?

A
  • Ammonia and ammonium ions form a buffer pair
  • Vast majority of ammonia in the body is already in ammonium (NH4+) form, limiting its buffering capacity, but some sources still claim that NH3 is an important buffer in urine
  • More important role of urinary ammonium excretion is providing a route for ammonium disposal that does not result in the generation of H+ (unlike urea synthesis)
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44
Q

What form is the vast majority of ammonia in the body in? How does this affect its buffering capacity?

A

NH4+ form - limiting its buffering capacity, but some sources still claim that NH3 is an important buffer in urine

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45
Q

What is the important role of urinary ammonium excretion?

A

Provides a route for ammonium disposal that does not result in the generation of H+ (unlike urea synthesis)

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46
Q

How do proteins act as buffers?

A

Proteins contain weakly acidic and basic groups due to their amino acid composition, and can therefore accept and donate H+ ions to some extent.

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47
Q

What is the predominant plasma protein?

A

Albumin –> is also the main protein buffer

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48
Q

How does albumin act as a buffer?

A

It has a net negative charge, so can “mop up” H+ ions

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49
Q

Can bone proteins play a role in buffering?

A

Yes

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50
Q

Explanation of albumin buffer:

A
  • In patient with no acid-base disorder:
    • Albumin molecule with negative charges around it
      • Some bound H+ ions to those charges
  • In patient with acidosis ([H+] increased):
    • Extra H+ ions bound to albumin, reducing the plasma conc of H+ ions
  • In patient with alkalosis ([H+] decreased):
    • Bound H+ ions to albumin are released into plasma
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51
Q

What are the main functions in the lungs?

A

Transfer of O2 from inspired gas into blood and removal of CO2 from the blood to the expired gas

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52
Q

What are respiratory control mechanisms extremely sensitive to?

A

pCO2 –> the rate of elimination is equal to the rate of production, so that blood pCO2 remains constant

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53
Q

Regarding the oxyhaemoglobin dissociation curve, what is on the x and y axis?

A

x axis: pO2 (kPa)

y axis: saturation of Hb (%)

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54
Q

What type of curve is the Oxyhaemoglobin dissociation curve?

A

Sigmoid

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55
Q

Why is the Oxyhaemoglobin dissociation curve sigmoid?

A

pO2 can decrease significantly before saturation is affected

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56
Q

Oxyhaemoglobin dissociation curve shifts to the left/right affect what?

A

Curve shifts to right or left if specific variables change, affecting the affinity of Hb for O2 and the amount of O2 released to the tissues

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57
Q

What is the effect when the Oxyhaemoglobin dissociation curve shifts to the right? What causes the Oxyhaemoglobin dissociation curve to shift to the right?

A
  • A shift to the right results in Hb having a reduced affinity for O2 so more O2 is available to tissues
  • Shift caused by:
    • Body temperature increasing
    • Increased in 2,3-DPG (patient is hypoxic or anaemic)
    • [H+] increases (Bohr effect)
    • CO2 increases
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58
Q

What is the Bohr effect?

A

Increases in the pCO2 of blood or decreases in blood pH result in a lower affinity of Hb for O2.

Occurs because the higher [H+] causes an alteration in amino acid residues on Hb - this stabilises deoxyhaemoglobin in a state that has a lower affinity for oxygen.

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59
Q

What is 2,3-DPG?

A
  • An increase in the concentration of 2,3-DPG decreases oxygen affinity of Hb –> therefore increases O2 available to tissues
  • An increase in the red cell 2,3-DPG is found in response to hypoxia or anaemia and a decrease of 2,3-DPG is caused by acidosis
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60
Q

What causes the Oxyhaemoglobin dissociation curve to shift to the left? What is the result of this?

A
  • Results in Hb having a higher affinity for O2 so less O2 is available to tissues
  • Curve shifts to left when:
    • Body temperature decreases
    • Decreases in 2,3 DPG
    • Decreases in CO2
    • Decreases in H+
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61
Q

When does a sharp fall in Hb saturation occur?

A

Below pO2 of 8 kPa

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62
Q

Describe how the acid-base balance is kept in the kidneys

A
  • Excretion of H+ ions (distal tubule)
  • Reabsorption of bicarbonate (proximal tubule)
  • Regeneration of bicarbonate (distal tubule)
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63
Q

Describe the composition of urine created by the kidneys

A

Creates acidic urine containing almost no bicarbonate

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64
Q

What area of the kidney does:

  • Excretion of H+ ions
  • Reabsorption of bicarb
  • Regeneration of bicarb

occur?

A
  • Distal tubule
  • Proximal tubule
  • Distal tubule
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65
Q

Why can bicarb not be directly reabsorbed across luminal membranes? What does it rely on instead?

A

Luminal membranes are impermeable to it. Instead, relies on ability of CO2 to diffuse.

66
Q

Describe the mechanism of renal bicarb reabsorption:

A
  1. H2CO3 generated in tubular cell from CO2 and H2O under action of carbonic anhydrase –> H2CO3 formed and dissociates into H+ and HCO3- (2)
  2. HCO3- formed in the cell then pumped into the plasma (along with Na+ for charge balance) (3)
  3. H+ ions formed in the cell then secreted into glomerular filtrate in exchange for Na+ (4)
  4. Secreted H+ ions combine with HCO3- ions in filtrate to form H2CO3 and then CO2 (1). The CO2 diffuses into the tubular cell, providing a substrate for the continued formation of H2CO3 (2)
67
Q

Describe the mechanism of renal H+ excretion and HCO3- regeneration

A
  1. H2CO3 generated from CO2 and H2O under action of carbonic anhydrase –> dissociates into H+ and HCO3- (6)
  2. H+ actively secreted into glomerular filtrate in exchange for Na+ (4), where H+ ions are excreted as dihydrogen phosphate (H2PO4-) (1)
  3. HCO3- and Na+ ions pumped into plasma
  4. Additionally, ammonia is transported into the urine where it forms NH4+, providing a route for ammonia excretion that does not generate H+
68
Q

What is the continued formation of H+ in renal tubular cells accompanied by? How does this maintain buffering capacity?

A

Stoichiometric generation of bicarbonate –> excretion of H+ results in bicarbonate regeneration –> maintains buffering capacity

69
Q

What are mineralocorticoids?

A
  • A class of corticosteroids, which in turn are a class of steroid hormones
  • Produced in the adrenal cortex
  • Influence salt and water balances (electrolyte balance and fluid balance)
  • The primary mineralocorticoid is aldosterone.
70
Q

What is excreted/reabsorbed in the distal tubule? What is the under the control of?

A
  • Excretion of potassium and hydrogen ions in the distal tubule, with concomitant reabsorption of sodium ions
  • Under the control of aldosterone
71
Q

How does aldosterone affect sodium reabsorption and potassium/H+ excretion?

A

Increased aldosterone leads to increased sodium reabsorption and potassium/hydrogen ion excretion

72
Q

How does this liver affect acid-base?

A
  • CO2 production from complete oxidation of carbohydrates and fats
  • Metabolism of lactate, ketones and amino acids (consumption of H+)
  • Metabolism of NH4+ to urea via urea cycle (producer of H+)
  • Production of plasma proteins (e.g. albumin) (buffering)
73
Q

What is the most common acid-base disturbances in liver failure?

A

Respiratory and metabolic alkalosis

74
Q

What is hyperammonaemia?

A

A metabolic condition characterised by the raised levels of ammonia

75
Q

How can liver failure lead to hyperammonaemia?

A
  • Liver is unable to perform urea cycle, which normally converts toxic ammonia to urea for excretion in urine
  • Ammonia stimulates the respiratory centre, causing the patient to hyperventilate and blow off CO2
    • Leads to increase in blood pH –> respiratory alkalosis
  • Metabolic alkalosis can also arise as a result of reduced production of H+ (due to liver failure)
76
Q

Why must samples for blood gas analysis be heparinised?

A

Anticoagulant

77
Q

Why must samples for blood gas analysis be well mixed with no air bubbles?

A

Air bubbles can affect pO2 –> can increase pH and decrease pCO2

78
Q

Why must samples for blood gas analysis be analysed immediately?

A

In-vitro glycolysis can cause a time-dependent decrease in pO2 and increase in pCO2

79
Q

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

A

Rapid deceleration of sample can affect pO2 and pCO2 if air bubbles present

80
Q

Is a standard blood sample venous or arterial?

A

Arterial (particulary if interest in pO2)

N.B. Different reference ranges apply for venous and arterial samples

81
Q

What is the principal feature of respiratory acidosis/alkalosis?

A

Primary disorder caused by altered respiration:

  • Acidosis: increased pCO2
    • Lungs not getting rid of enough CO2
  • Alkalosis: decreased pCO2
    • Lungs getting rid of too much CO2 e.g. hyperventilation
82
Q

What is the principal feature of metabolic acidosis/alkalosis?

A

Primary disorder caused by non-respiratory element

  • Acidosis: decreased HCO3-
    • Bicarb being used up buffering the extra H+ ions
  • Alkalosis: increased HCO3-
83
Q

How do we classify acid-base disorders?

A
  1. What is the pH?
    1. pH <7.35 acidosis
    2. pH >7.45 alkalosis
  2. Is the primary disorder respiratory or metabolic?
  3. Is there any compensation?
84
Q

How can you tell if the primary disorder respiratory or metabolic?

A

Easiest way to determine this is to look at the pCO2 [4.7 -6.0 kPa]:

  • If pH <7.35 (acidosis):
    • If increased pCO2 –> respiratory acidosis
    • If normal (or decreased pCO2 if compensation) –> metabolic acidosis
  • If pH >7.35 (alkalosis):
    • If decreased pCO2 –> respiratory alkalosis
    • If normal (or increased pCO2 if compensation) –> metabolic alkalosis
85
Q

What is compensation?

A

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

  • Changes in bicarbonate concentration (renal regeneration) can occur to compensate for respiratory disorders (slow)
  • Changes in pCO2 (respiratory rate) can occur to compensate for metabolic disorders (fast)
86
Q

What is the aim of compensation?

A

Compensatory mechanisms aim to restore a neutral pH (but full compensation rarely occurs, and over-compensation never occurs)

87
Q

Compensation for acidosis/alkalosis:

88
Q

Summary table for acid-base disorders

89
Q

What are the 2 measurements of bicarb?

A
  • Bicarb (main lab)
  • Bicarb (standard)
90
Q

What is bicarb (main lab) measurement?

A
  • 22-29 mmol/L
  • Approximation of bicarbonate, calculated in part from CO2
  • Sometimes called “total CO2”
91
Q

What is bicarb (standard) measurement?

A
  • 22-26 mmol/L
  • Removes respiratory contribution so an abnormal standard bicarbonate tells us that there is a metabolic component to the disorder
  • Uses Henderson-Hasselbalch equation to calculate bicarbonate from pH and “corrected” pCO2 (i.e. “normal” pCO2)
92
Q

What would a normal standard bicarb result indicate?

A

Purely respiratory disorder

93
Q

What would an abnormal standard bicarb tell you?

A

There is a metabolic component

94
Q

What is base excess (BE)? What does it tell you?

A
  • Amount of acid or alkali needed to titrate blood pH to 7.40 (takes into account all buffers, not just bicarb)
  • Tells us if there is a metabolic component to the disorder
95
Q

What would a normal base excess tell you about the disorder?

A

Purely respiratory disorder

96
Q

What would a negative BE (<-2.3 mmol/L) tell you?

A

Metabolic acidosis (i.e. a base deficit)

97
Q

What would a positive BE tell you (>2.3 mmol/L)?

A

Metabolic alkalosis (i.e. a base excess)

98
Q

What is an anion gap?

A

The anion gap is the difference between certain measured cations (positively charged ions) and the measured anions (negatively charged ions) in serum, plasma, or urine.

99
Q

What would an increased anion gap indicate?

A

Indicates that there are significant amounts of “unmeasured” anions present (e.g. ketones, lactate, salicylate, proteins, and many more)

Can be useful in determining the cause of a metabolic acidosis

100
Q

Why is the anion gap not zero in healthy patients?

A

As not all anions are measured and included in the calculation

101
Q

How is pH, [H+], pCO2, HCO3- and pO2 affected in metabolic acidosis?

A
  • pH decreased
  • [H+] increased
  • pCO2 N/decreased
  • HCO3- decreased
  • pO2 increased
102
Q

What are the signs and symptoms of metabolic acidosis?

A
  • Nausea, vomiting and anorexia frequently present
  • Subjective sense of dyspnoea caused by stimulation of the respiratory centre
  • Deep laboured breathing pattern, known as Kussmaul breathing, in severe acidosis
  • Other symptoms caused by underlying disorder
103
Q

What are the 4 main causes of metabolic acidosis?

A
  1. Increased acid formation
  2. Acid ingestion
  3. Decreased acid excretion
  4. Loss of bicarb
104
Q

What are the causing of increased acid formation?

A
  • Ketoacidosis
    • Diabetic (DKA)
    • Alcoholic (AKA)
    • Starvation
  • Lactic acidosis
    • Type A (tissue hypoxia)
    • Type B (metabolic and toxic causes)
  • Poisoning
    • Salicylate
    • Toxic alcohols (e.g. ethylene glycol, methanol, ethanol)
  • Inherited organic acidoses
105
Q

What are the causes of decreased acid excretion?

A
  • Uraemia (renal failure)
  • RTA type 1 (distal)
106
Q

What can cause a loss of bicarb?

A
  • GI: diarrhoea / fistula
  • Renal:
    • RTA type 2 (proximal)
    • Carbonic anhydrase inhibitors (e.g. acetazolamide)
107
Q

What is the physiological response to metabolic acidosis?

A
  • Buffering
  • Compensation
108
Q

How does buffering try to reverse metabolic acidosis?

A
  • Acute ↑[H+] resisted by bicarbonate buffering, causing ↓HCO3-
  • Protein buffering important in chronic acidosis
109
Q

How does the respiratory centre compensate in metabolic acidosis?

A
  • Respiratory centre stimulated à hyperventilation (blows off CO2)
  • Self-limiting, as generates additional CO2
110
Q

How do the kidneys compensate in metabolic acidosis?

A
  • Urine H+ excretion maximised
  • Increased rate of regeneration of bicarbonate
111
Q

How can metabolic acidosis be treated?

A

Sodium bicarbonate (sometimes):

  • Careful administration of IV sodium bicarbonate
    • Usually only given if pH <7.00
  • Oral bicarbonate
    • CKD, RTA types 1 and 2
112
Q

Why must care be taken when treating metabolic acidosis with sodium bicarbonate?

A
  • Rapid correction impairs O2 delivery
  • Rebound alkalosis possible
113
Q

How is pH, [H+], pCO2, HCO3- and pO2 affected in metabolic alkalosis?

A
  • pH increased
  • [H+] decreased
  • pCO2 N/increased
  • HCO3- increased
  • pO2 decreased
114
Q

What are the typical signs and symptoms of metabolic alkalosis?

A
  • Usually related to underlying disorder
  • More severe alkalosis increases protein binding of Ca2+, leading to hypocalcaemia
    • Causes headache, lethargy and neuromuscular excitability, sometimes with delirium, tetany and seizures
  • Lowers threshold for arrhythmias
115
Q

What are the 3 main causes of metabolic alkalosis?

A
  1. Administration of bicarb
  2. Potassium depletion
  3. Loss of H+
116
Q

Why can hypokalaemia cause a metabolic alkalosis?

A
  • Kidneys
    • Excretion of H+ favoured in order to spare K+ at aldosterone-controlled renal transporter
  • Cells
    • ​K+ ions are transported out of RBCs to increase plasma concentration –> H+ ions move into cells to maintain electroneutrality. This leads to a decrease in plasma [H+]
117
Q

What can cause a loss of H+?

118
Q

How do buffers try to reverse metabolic alkalosis?

A

Release of H+ from buffers

119
Q

How can the respiratory centre try to compensate for metabolic alkalosis?

A
  • Reduced respiratory rate in order to retain CO2
  • Self-limiting, as an increase in pCO2 stimulates the respiratory centre
120
Q

How can the kidneys try to compensate for metabolic alkalosis?

A

This is difficult –> ↓GFR leads to inappropriately high bicarbonate reabsorption. Potassium deficiency contributes to persistence of alkalosis.

121
Q

What is the management for metabolic alkalosis?

A

Treat underlying cause

Treat factors that sustain alkalosis e.g. replace potassium

122
Q

How is pH, [H+], pCO2, HCO3- and pO2 affected in respiratory acidosis?

A
  • pH decreased
  • [H+] increased
  • pCO2 increased
  • HCO3- N/increased
  • pO2 decreased
123
Q

What are the signs and symptoms of respiratory acidosis?

A
  • Usually related to underlying disorder
  • Some patients may complain of dyspnoea
124
Q

What are the 2 main causes of respiratory acidosis?

A
  1. Defective control of respiration
  2. Defective respiratory function
125
Q

What can cause a defective control of respiration?

A
  • CNS depression
    • Anaesthetics, sedatives etc
    • Narcotics, opiates etc
  • CNS disease
    • Trauma
    • Haemorrhage
    • Infarction
    • Tumour
    • Infection
  • Neurological disease
    • Spinal cord lesions
    • MND
    • Guillain-Barre
126
Q

What can cause a defective respiratory function?

A
  • Mechanical
    • Myopathies
    • Pneumothorax
    • Pleural effusion
    • Inadequate mechanical ventilation
  • Pulmonary disease
    • E.g. COPD, severe asthma etc
    • Impaired perfusion (e.g. massive pulmonary embolism)
127
Q

How does buffering try to reverse respiratory acidosis?

A

Limited buffering by Hb

128
Q

How does the respiratory centre try and compensate for respiratory acidosis?

A

↑pCO2 stimulates respiratory centre, but disease prevents adequate response

129
Q

How do the kidneys try and compensate for respiratory acidosis?

A
  • Maximal bicarbonate reabsorption (takes a while to reach maximal effect)
  • Almost all phosphate excreted as H2PO4- (rather than HPO42-)
  • Marked increase in urinary NH4+
130
Q

What is the management for respiratory acidosis?

A
  • Treat underlying cause
  • Maintain adequate arterial pO2, but avoid loss of hypoxic stimulus to respiration
  • Avoid rapid correction of pCO2 (risk of alkalosis due to persistence of compensation)
131
Q

How is pH, [H+], pCO2, HCO3- and pO2 affected in respiratory alkalosis?

A
  • pH increased
  • [H+] decreased
  • pCO2 decreased
  • HCO3- N/decreased
  • pO2 increased
132
Q

What are the signs and symptoms in respiratory alkalosis?

A
  • Usually related to underlying disorder
  • More severe alkalosis increases protein binding of Ca2+, leading to hypocalcaemia
    • Causes headache, lethargy and neuromuscular excitability, sometimes with delirium, tetany and seizures
133
Q

What are the 3 main causes of respiratory alkalosis?

A
  1. Central
  2. Pulmonary
  3. Iatrogenic
134
Q

What are the central causes of respiratory alkalosis?

A
  • Head injury
  • Stroke
  • Hyperventilation
  • Drugs (e.g. salicylates)
  • Sepsis (cytokines)
  • Chronic liver disease (toxins)
135
Q

What are the pulmonary causes of respiratory alkalosis?

A

Pulmonary embolism

Pneumonia

Asthma

Pulmonary oedema

136
Q

What are the iatrogenic causes of respiratory alkalosis?

A

Excessive mechanical ventilation

137
Q

How does buffering respond to respiratory alkalosis?

A

Release of H+ from non-bicarbonate buffers

138
Q

How does the respiratory centre try and compensate for respiratory alkalosis?

A

Inhibitory effect of ↓pCO2 overwhelmed by primary cause

139
Q

How does the kidneys try and compensate for respiratory alkalosis?

A

Decreased renal regeneration of bicarbonate (CO2 is substrate, therefore CO2 is preserved)

140
Q

What is the management for respiratory alkalosis?

A

Treat underlying cause

Rapid symptomatic relief by re-breathing

Sedation or prevention of hyperventilation by mechanical ventilation

141
Q

What are mixed acid-base disorders?

A
  • Mixed disorders: two or more primary acid-base disorders presenting in the same patient
  • Can be either additive or counterbalancing
142
Q

What type of mixed disorder can respiratory failure cause? Explain

A

Additive:

  • Respiratory acidosis (↑pCO2) and metabolic acidosis (↑lactic acid)
143
Q

What type of mixed disorder can vomiting and CCF cause? Explain

A

Additive:

  • Metabolic alkalosis (loss of H+) and respiratory alkalosis (↑ resp. rate)
144
Q

What type of mixed disorder can salicylate poisoning cause? Explain

A

Counterbalancing: Metabolic acidosis and respiratory alkalosis (↑ resp. rate)

145
Q

What type of mixed disorder can vomiting and renal failure cause? Explain

A

Counterbalancing: Metabolic alkalosis (loss of H+) and metabolic acidosis (↓renal H+ excretion)

146
Q

What is CCF?

A

congestive cardiac failure

147
Q

Case 1

A
  • What is the pH? –> 7.59 (alkalotic)
  • What is the pCO2? –> Essentially normal (the alkalosis is not respiratory - ↑HCO3 concurs)
  • What is the primary acid-base disorder? –> Metabolic alkalosis
  • Is there any compensation? –> Not really. pCO2 is essentially normal
  • How is this acid-base disorder classified? –> Non-compensated metabolic alkalosis
  • What is the cause? –> Vomiting (loss of HCl)
  • What is the likely cause of the hypokalaemia? –> Vomiting (indirectly)
148
Q

Why can vomiting cause hypokalaemia?

A

Gastric fluid is not especially rich in potassium, but it is very rich in H+ ions. Loss of H+ ions from vomiting causes potassium depletion by the following mechanisms:

  • Kidneys: Excretion of K+ favoured in order to spare H+ ions at aldosterone-controlled renal transporter
  • Cells: H+ ions are transported out of RBCs to increase plasma concentration –> K+ ions move into cells to maintain electroneutrality. This leads to a decrease in plasma [K+]

N.B. a metabolic alkalosis can cause hypokalaemia and hypokalaemia can cause a metabolic alkalosis

149
Q

Case 2:

A
  • What is [H+]? –> 83 nmol/L (acidotic)
  • What is the pCO2? –> pCO2 is high (therefore the acidosis is respiratory)
  • What is the primary acid-base disorder? –> Respiratory acidosis
  • Is there any compensation? –> No. Bicarbonate is not elevated
  • How is this acid-base disorder classified? –> Uncompensated respiratory acidosis
  • What is the cause? –> ↓CO2 excretion
150
Q

Case 3:

A
  • What is the pH? –> 7.60 (alkalotic)
  • What is the pCO2? –> pCO2 is low (therefore the alkalosis is respiratory in origin)
  • What is the primary acid-base disorder? –> Respiratory alkalosis
  • Is there any compensation? –> Mild. HCO3- is slightly low (metabolic compensation)
  • Is the compensation full or partial? –> pH has not returned to normal, therefore partial
  • How is this acid-base disorder classified? –> Partially-compensated respiratory alkalosis
  • What is the cause? –> Hyperventilation (blowing off CO2), hypocalcaemia caused by alkalosis (note paraesthesia)
151
Q

What is paraesthesia?

A

an abnormal sensation, typically tingling or pricking (‘pins and needles’), caused chiefly by pressure on or damage to peripheral nerves.

152
Q

How can acidosis lead to hypercalcaemia?

A

As H+ binds to albumin to reduce plasma [H+], Ca2+ must be released –> hypercalcaemia

153
Q

How can alkalosis lead to hypocalcaemia?

A

As H+ is released from albumin to increase plasma [H+], Ca2+ must bind to albumin –> hypocalcaemia

154
Q

Case 4:

A
  • What is the pH? –> 7.05 (acidotic)
  • What is the pCO2? –> pCO2 is low (therefore the acidosis is not respiratory - ↓HCO3 concurs)
  • What is the primary acid-base disorder? –> Metabolic acidosis
  • Is there any compensation? –> Yes. pCO2 is low (respiratory compensation)
  • Is the compensation full or partial? –> pH has not returned to normal, therefore partial
  • How is this acid-base disorder classified? –> Partially-compensated metabolic acidosis
  • What is the cause? –> Diabetic ketoacidosis (DKA)
155
Q

Summary:

A
  • Acid-base homeostasis is maintained by a combination of processes in the lungs, kidneys, liver and GI tract
  • When homeostasis is disturbed, buffering and compensatory mechanisms begin in an attempt to return the pH to neutral
  • Respiratory disorders can be compensated by metabolic processes
  • Metabolic disorders can be compensated by respiratory processes
  • Over-compensation does not occur
156
Q

What is HCO3- replaced by in the RBC when Hb is acting as a buffer?

157
Q

What is RTA type 1?

A

Type 1 (distal) RTA Type 1 is impairment in hydrogen ion secretion in the distal tubule, resulting in a persistently high urine pH (>5.5) and systemic acidosis.

158
Q

What is RTA type 2?

A

Type 2 is impairment in bicarbonate resorption in the proximal tubules

159
Q

Which acid-base disorder will RTA type 1 cause?

A

Decreased H+ excretion –> metabolic acidosis

160
Q

Which acid-base disorder will RTA type 2 cause?

A

Decreased bicarb reabsorption –> metabolic acidosis

Yr 2 - EMS (60 decks)

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