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Respiratory (Revision) > 9 - Acid Base Balance > Flashcards

9 - Acid Base Balance Flashcards

1
Q

What is the normal pH of blood?

A
  1. 35 - 7.45
  2. 5 - 35.5 nmol per litre H+
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2
Q

What is more dangerous, alkalemia or acidaemia?

A

Alkalaemia

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3
Q

What pH range causes high mortality in alkalosis and why?

A

Reduces solubility of Ca salts so more free Ca leaves the ECF to bind to bones and proteins. Hypocalcaemia leads to excitable nerves, paraesthesia and tetany

  • Paraesthesia and tetany above 7.45
  • 45% mortality at 7.5
  • 80% mortality at 7.65
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4
Q

What pH range causes high mortality in acidosis and why?

A

High H+ affects enzyme function and leads to K+ movement out of cells so hyperkalaemia leading to arrythmias.

  • Effects seen at 7.1
  • Life threatening below 7
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5
Q

What is the main buffer system for pH in the ECF?

A

- Carbon Dioxide/Hydrogen carbonate system

    • pCO2 determined by ventilation* so disturbed by respiratory disease
    • HCO3- determined by kidneys* so disturbed by metabolic or kidney disease
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6
Q

How do the kidneys maintain plasma pH in general terms?

A
  • Variable recovery of HCO3- produced by RBC
  • Secretion of H+
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7
Q

What parameters change to get the following outcomes in the blood:

  • Respiratory acidosis
  • Respiratory alkalosis
  • Metabolic acidosis
  • Metabolic alkalosis
A

- Resp acid: increased pCO2

- Resp alk: decrease pCO2

  • Met acid: decreased HCO3- due to reaction with metabolic acids, e.g lactate and ketoacids

- Met alk: increased HCO3-

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8
Q

How does the body compensate for the following:

  • Respiratory acidosis
  • Respiratory alkalosis
  • Metabolic acidosis
  • Metabolic alkalosis
A

- Respiratory acidosis: kidneys retain more HCO3-

- Respiratory alkalosis: kidneys lose more HCO3-

- Metabolic acidosis: hyperventilation

- Metabolic alkalosis: limited by the hypoxia that comes with hypoventilation

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9
Q

How do we stop HCO3- depleting in the body when the body produces metabolic acids like lactate that react with HCO3- ?

A
  • Kidneys recover all filtered HCO3- (80% PCT and 15% DCT in intercalated cells)
  • PCT makes HCO3- from AA putting NH4+ onto urine
  • DCT makes HCO3- from CO2 and H2O and the H+ is buffered by ammonia and phosphate
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10
Q

How is HCO3- in the kidney produced?

A
  • H+ ions actively secreted in the DCT
  • H+ buffered by phosphate (titratable) and ammonia
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11
Q

What is the major adaptive response of the kidney to an increased acid load?

A
  • Production of NH3 from glutamate that moves throughout interstitiums
  • H+ actively pumped into lumen of DCT and CT
  • H+ reacts with NH3 to make NH4+ which is excreted in urine
  • Allows HCO3- to be reabsorbed to buffer and loses H+
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12
Q

What is the minimum pH of urine?

A

- 4.5

  • All HCO3- has been recovered
  • Some H+ in the urine buffered by ammonia to ammonium and phosphate to stop urinary tract being damaged
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13
Q

What can happen to potassium levels in alkalosis and acidosis?

A

Hyperkalaemia can cause metabolic acidosis or the acidosis can cause hyperkalaemia etc.

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14
Q

Why does hyper/hypokalaemia lead to acidosis/alkalosis?

A
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15
Q

What will the following blood parameters look like:

  • Compensated respiratory acidosis
  • Compensated respiratory alkalosis
  • Compensated metabolic acidosis
A

- Comp Resp Acidosis: high pCO2, high HCO3-, normal pH

- Comp Resp Alkalosis: low pCO2, low HCO3-, normal pH

- Comp Met Acidosis: low HCO3-, low pCO2, normal pH

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16
Q

What is the anion gap and what can it tell us?

A
  • Difference between measure cations and ions
  • Normal 10-18 mmol/L
  • Gap increased if HCO3- is replaced by ions other than Cl-, e.g metabolic acids
  • If metabolic acidosis but no change in ion gap then this is a renal cause as not making enough HCO3- but replaced by Cl-
17
Q

If the pH drops due to a metabolic acidosis what processes occur to correct this?

A
  • Peripheral chemoreceptors detect
  • Increase ventilation
  • Decreased pCO2
18
Q

What conditions can lead to metabolic and respiratory acidosis?

A

Respiratory:

  • Type 2 resp failure with low pO2 and high pCO2
  • Severe COPD
  • Severe asthma
  • Drug OD
  • Neuromuscular diseases

(chronic are compensated to near normal pH by HCO3-)

Metabolic:

Increased anion gap:

  • Ketoacidosis in diabetes
  • Lactic acidosis, poor tissue perfusion
  • Uraemic acidosis in advanced renal failure so reduced acid seccretion

Normal anion gap:

  • Renal tubular acidosis
  • Persistant diarrhoea (replaced by Cl-)
19
Q

What conditions can lead to metabolic and respiratory alkalosis?

A

Respiratory:

  • Hyperventilation in panic attack/anziey
  • Type 1 Resp failure leading to chronic hyperventilation but compensated

Metabolic:

  • Severe vomiting or mechanical drainage of stomach as HCO3- produced in response to H+ in stomach but no H+
  • Potassium depletion/excess mineralcorticoid excess
  • Certain diuretics, e.g loops
20
Q

What is renal tubular acidosis?

A
  • Type 1 (distal) = inability to pump out H+
  • Type 2 (proximal) = issues with HCO3- reabsorption

RARE

21
Q

What can be an issue with correcting metabolic alkalosis e.g in persistent vomiting?

A
  • Increased HCO3- so just excrete more

- HOWEVER: if patient is volume depleted then their capacity to lose HCO3- is reduced due to high rate of Na+ recovery to raise volume. In PCT

22
Q

What does metabolic alkalosis do to potassium levels in the blood?

A
23
Q

If pCO2 is high, HCO3- is high and pH relatively normal, what is this called?

A

Compensated respiratory acidosis as can’t have compensated metabolic alkalosis

24
Q

If pCO2 is low, HCO3- is low and pH relatively normal, what is this called?

A
  • Compensated resp alkalosis or compensated metabolic acidosis
  • If no respiratory disease or altitude exposure unlikely to be respiratory
  • Check anion gap as this will be increased in metabolic acidosis
25
Q

For each set of ABG results, state the acid base status:

A
26
Q

How should you treat someone with hypoxia and chronic hypercapnia?

A
  • Hypercapnia would occur as the central chemoreceptors set to a new high pCO2 (by choroid plexus)
  • If given oxygen their peripheral chemoreceptors detect increase in pO2 and lower respiratory rate but this raises the pCO2

Respiratory (Revision) (23 decks)

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