Acid Base Balance Flashcards

1
Q

What is normal H+ conc in ECF?

A

35-45 nmol/l

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2
Q

What is normal pH and how do you calculate it?

A

pH 7.35 -7.46
pH = log 1/ [H+]

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3
Q

How is H+ made and excreted?

A

Metabolism of proteins, carbohydrates and fats produce carbon dioxide, water and hydrogen ions

Production of H+ (50-100 mmol/day)

Excretion by the kidney

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4
Q

Where do H+ ions travel?

A

Hydrogen ion produced in the tissues is transported via the circulation to the kidneys where it is excreted

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5
Q

What is buffering of H+ in the body?

A

One can add 14 mmol of hydrogen ion per litre of body water with an increase in hydrogen ion concentration of only 36 nmol/L.

ECF buffering of hydrogen is at the expense of bicarbonate
Bicarbonate buffering of H+ is only effective in the short term.
To maintain normal homeostasis the kidney needs to excrete hydrogen ions and regenerate bicarbonate.

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6
Q

How is bicarbonate handled in the nephron?

A

Bicarbonate reabsorption in the proximal tubule

H+ excretion & bicarbonate regeneration

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7
Q

How is CO2 handled in the body?

A

Production of CO2 (20,000-25,000 mmol/day)
Excreted by lungs

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8
Q

How does respiration control CO2?

A

Respiration is controlled by chemoreceptors in the hypothalamic respiratory centre

In health any increase in CO2 stimulates respiration thus tending to maintain a stable concentration of CO2

20-25,000 mmol/day of CO2 is excreted through the lungs in expired air.

In health CO2 produced in the tissues is transported via the circulation to the lungs where it is excreted

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9
Q

How does CO2 make H+?

A

By reacting with water to make bicarbonate and hydrogen ions (HHb)

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10
Q

How do the kidneys and lungs control acid base balance?

A

Kidneys- control bicarbonate
Lungs- control CO2

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11
Q

How do you calculate H+ using CO2 and bicarb?

A

k x (CO2 conc/ HCO3 conc)

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12
Q

What are the causes of metabolic acidosis?

A
  1. Increased H+ production e.g. diabetic ketoacidosis
  2. Decreased H+ excretion e.g. Renal tubular acidosis
  3. Bicarbonate loss e.g. intestinal fistula
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13
Q

What is respiratory compensation in metabolic acidosis?

A

This stimulates the respiratory centre
Identified by a fall in pCO2
H+ returns towards normal

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14
Q

What are the causes of acute respiratory acidosis?

A

Primary abnormality is increased CO2 producing increased H+ (decreased pH) and a slight increase in bicarbonate (2-4 mmol/L).

May be due to:
Decreased Ventilation
Poor Lung Perfusion
Impaired Gas Exchange

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15
Q

What happens in chronic respiratory acidosis?

A

Over the course of a few days this leads to increased renal excretion of H+ combined with generation of bicarbonate.
H+ may return to near normal but pCO2 and bicarbonate remain elevated

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16
Q

What are the causes of metabolic alkalosis?

A

H+ loss (e.g. pyloric stenosis)
Hypokalaemia
Ingestion of Bicarbonate

17
Q

What is the compensation of metabolic alkalosis?

A

This tends to inhibit the respiratory centre
Identified by a rise in pCO2
H+ returns towards normal

18
Q

What are the causes of respiratory alkalosis?

A

Due to Hyperventilation
Voluntary
Artificial ventilation
Stimulation of respiratory centre

19
Q

What happens in chronic respiratory alkalosis?

A

If prolonged this leads to decreased renal excretion of H+ and less bicarbonate generation
H+ may return to near normal but pCO2 and bicarbonate remain low

20
Q

How do you assess an ABG?

A

H+/pH tells us whether there is an overt acidosis or alkalosis
pCO2 tells us whether there is a respiratory disturbance (primary or secondary)
pO2 does not directly affect acid-base status but gives an indication of respiratory function and tissue oxygenation
Note: Bicarbonate predominantly reflects metabolic disturbances but is also affected by respiratory disturbances

21
Q

Abnormality?

A

Metabolic Acidosis with partial compensation

22
Q

64 year old female

3 week history of intermittent vomiting

abdominal pain

weight loss

O/E

Dehydrated

Jaundiced

Hypotensive

Oliguric

Urea 28.1 mmol/l (2.5-8.0)

Creatinine 387 mmol/l (60-125)

Sodium 129 mmol/l (135-145)

Potassium 1.6 mmol/l (3.5-5.5)

Bicarbonate 56 mmol/l (22-30)

Total protein 89 g/l (64-83)

Gas abnormality? Diagnosis?

A

Metabolic alkalosis with partial respiratory compensation

Hyperchloraemic hypokalaemia

Diagnosis: pyloric stenosis

23
Q

How does vomiting cause a metabolic alkalosis?

A

Loss of HCl in vomit produces a metabolic alkalosis

(Low H+, high bicarbonate)

Loss of fluid produces dehydration

(Raised urea, creatinine and total protein)

Dehydration stimulates renin/angiotensin/aldosterone mechanism

Low potassium as it is lost in vomit and urine

24
Q

pH 7. 55 (7.35-7.45)

H+ 28 nmol/l (35-46)

pCO2 3.0 kPa (4.7-6.0)

pO2 14.4 kPa (10.0-13.3)

Bicarbonate 20 mmol/l (22-30)

Abnormality?

A

Respiratory alkalosis (with little compensation)

25
Q

pH 7. 41 (7.35-7.45)

H+ 39 nmol/l (35-46)

pCO2 10.4 kPa (4.7-6.0)

pO2 7.8 kPa (10.0-13.3)

Bicarbonate 47 mmol/l (22-30)

Abnormality?

A

Compensated Resp acidosis/ met alkalosis

Resp acidosis - e.g. COPD

Met Alkalosis- e.g. hypokalaemia, loss of H+, too many rennies ;)

26
Q

A young woman was admitted to hospital 8 hours after she had taken an overdose of aspirin.

Arterial blood:

pH 7. 46 (7.35-7.45)

H+ 35 nmol/l (35-46)

pCO2 2.0 kPa (4.7-6.0)

pO2 17.8 kPa (10.0-13.3)

Bicarbonate 10 mmol/l (22-30)

Abnormality?

A

Respiratory alkalosis with partial compensation

27
Q

Arterial blood:

pH 6. 93 (7.35-7.45)

H+ 116 nmol/l (35-46)

pCO2 9.7 kPa (4.7-6.0)

pO2 65.8 kPa (10.0-13.3)

Bicarbonate 15 mmol/l (22-30)

Abnormality?

A

Mixed respiratory and metabolic acidosis