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Renal > Acid Base Balance and ABGs > Flashcards

Acid Base Balance and ABGs Flashcards

1
Q

What is the normal range for blood pH?

A

7.37-7.43

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2
Q

What is the normal range for bicarbonate in the blood?

A

22-26 mmol/L

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3
Q

What is the equation used to express the state of equilibrium maintained between bicarbonate, hydrogen ions, carbonic acid and CO2 and water?

A
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4
Q

Which direction does the bicarbonate buffering equation shift when additional hydrogen ions are added?

A

The addition of hydrogen ions drives the reaction to the right, decreasing the plasma bicarbonate concentration [HCO3−] and increasing the arterial carbon dioxide pressure (PaCO2). THis means that bicarbonate must be produced/reabsorbed to buffer this acid challenge

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5
Q

Why does acidaemia stimulate increased respiration?

A

Due to increased CO2 production due to acid load -> bicarbonate buffer system shifts right -> resp system detects rise in PaCO2 -> increased resp effort

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6
Q

What are the main mechanisms for increasing bicarbonate availibility?

A
  • Bicarbonate regeneration
  • Bicarbonate reabsorption
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7
Q

Where does bicarbonate rabsorption take place?

A

Kidneys

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8
Q

Where is the majority of bicarbonate reabsorbed in the kidney?

A

Proximal convoluted tubule - 85-90%

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9
Q

Why is the majority of bicarbonate reabsorbed in the proximal convoluted tubule?

A

Greater quantity of luminal (brush border) carbonic anhydrase in the proximal tubule than in the distal nephron

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10
Q

Draw the process by which bicarbonate is reabsorbed in the proximal convoluted tubule of the kidney

A
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11
Q

How is bicarbonate reabsorbed into lumenal cells of the proximal convoluted tubule?

A

Carbonic acid is converted by Carbonic anhydrase to CO2 and H2O - freely moves into luminal cells, where it is converted back to HCO3-

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12
Q

How is bicarbonate converted to carbonic acid in the lumen of the proximal convoluted tubule?

A

H+ is excreted from luminal cells in exchange for Na+

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13
Q

How does H2CO3 become bicarbonate in the luminal cells to allow it’s bicarbonate portion to enter the blood?

A

Dissociates with H+

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14
Q

What is proximal tubular bicarbonate reabsorption driven by?

A

Na+/K+ ATPase pump located in the basolateral luminal cell membrane - By exchanging peritubular potassium ions for intracellular sodium ions, the pump keeps the intracellular sodium concentration low, allowing sodium ions to enter the cell by moving down the sodium concentration gradient from the tubule lumen to the cell interior

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15
Q

What buffer systems are involved in acid secretion?

A
  • Titratable acids such as phosphate
  • Ammonia system
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16
Q

How is H+ excreted in the distal convoluted tubule?

A

Titratable acid system - primarily phosphate excretion

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17
Q

How does the titratable acid buffer system work?

A

Hydrogen ions bind to the conjugate anions of the titratable acids and are excreted in the urine. For each hydrogen ion excreted in this form, a bicarbonate ion is regenerated within the cell and returned to the blood

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18
Q

What buffer system is the most important under heavy acid load?

A

Ammonium buffer system - creates the most bicarbonate

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19
Q

Why is the titratable acid system limited in terms of how much it can buffer acid in the blood?

A

Titratable acids cannot increase significantly because the availability of titratable acid is fixed by the plasma concentration of the buffer and by the GFR.

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20
Q

Draw the ammonium buffer system in the proximal convoluted tubule

A
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21
Q

Draw the ammonium buffer system in the distal convoluted tubule

A
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22
Q

In the ammonium buffer system, what is ammonia formed from in the cell?

A

Glutamine -> Glutamate

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23
Q

What is the name of the enzyme which deaminates glutamine to glutamate in luminal cells to produce NH3?

A

Renal glutanimase

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24
Q

Write out the henderson-Hasselback equation

A
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25
Q

Give the following for uncompensated respiratory acidosis:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - Decreased
  • PaCO2 - Increased
  • HCO3<strong>-</strong> - normal
26
Q

What are the main tests done on ABG?

A
  • pH: 7.35 – 7.45
  • PaCO2: 4.7-6.0 kPa
  • PaO2: 11-13 kPa
  • HCO3-: 22-26 mEg/L
  • Base excess: -2 to +2 mmol/L
  • Can also have lactate, and electrolytes
27
Q

Give the following for uncompensated respiratory alkalosis:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - increased
  • PaCO2 - decreased
  • HCO3<strong>-</strong> - normal
28
Q

Give the following for compensated respiratory acidosis:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - normal/increased
  • PaCO2 - increased
  • HCO3<strong>-</strong> - increased
29
Q

Give the following for compensated respiratory alkalosis:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - normal/increased
  • PaCO2 - decreased
  • HCO3<strong>-</strong> - Decreased
30
Q

Give the following for metabolic acidosis:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - decreased
  • PaCO2 - normal
  • HCO3<strong>-</strong> - Decreased
31
Q

Give the following for metabolic alkalosis with respiratory compensation:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - increased
  • PaCO2 - increased
  • HCO3<strong>-</strong> - increased
32
Q

Give the following for metabolic alkalosis:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - increased
  • PaCO2 - normal
  • HCO3<strong>-</strong> - increased
33
Q

Give the following for metabolic acidosis with respiratory compensation:

  • pH
  • PaCO2
  • HCO3-
A
  • pH - decreased
  • PaCO2 - decreased
  • HCO3<strong>-</strong> - decreased
34
Q

Why would metabolic acidosis with respiratory compensation have decreased PaCO2?

A

Due to increased respiratory drive blowing off CO2

35
Q

How long does it take for compensation mechanisms in the kidney to reach maximum effect?

A

3-5 days

36
Q

What is important to note when taking an ABG?

A

Assess clinical status and FiO2:

  • A normal PaO2 in a patient on high flow oxygen – you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy
  • A normal PaCO2 in a hypoxic asthmatic patient – a sign they are tiring and need ITU intervention
  • A very low PaO2 in a patient who looks completely well, is not short of breath and has normal O2 saturations – likely a venous sample
37
Q

What is type 1 respiratory failure?

A

Hypoxia (PaO2 <8 kPa) with normocapnia (PaCO2 <6.0 kPa).

38
Q

What is type 2 respiratory failure?

A

Hypoxia (PaO2 <8 kPa) with hypercapnia (PaCO2 >6.0 kPa).

39
Q

What causes type 1 respiratory failure?

A

Ventilation/perfusion (V/Q) mismatch - volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue. Examples include:

  • Reduced ventilation and normal perfusion – e.g. pulmonary oedema, bronchoconstriction
  • Reduced perfusion with normal ventilation – e.g. pulmonary embolism
40
Q

Why is PaCO2 normal in type 1 respiratory failure?

A

As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves.

41
Q

What causes type II respiratory failure?

A

Alveolar hypoventilation - prevents patient from being able to adequately oxygenate and eliminate enough CO2 from their blood. Examples include:

  • Increased airway resistance due to obstruction (e.g. COPD)
  • Reduced compliance of the lung tissue/chest wall – (e.g. pneumonia/rib fractures/obesity)
  • Reduced strength of the respiratory muscles (e.g. Guillain–Barré / motor neurone disease)
  • Drugs acting on the respiratory centre reducing overall ventilation (e.g. opiates)
42
Q

What is base excess?

A

Another surrogate marker of metabolic acidosis or alkalosis.

43
Q

What does a high (> +2mmol/L) base excess indicate?

A

There is a higher than normal amount of HCO3- in the blood, which may be due to a primary metabolic alkalosis or a compensated respiratory acidosis.

44
Q

What does a low (< -2mmol/L) base excess indicate?

A

There is a lower than normal amount of HCO3- in the blood, suggesting either a primary metabolic acidosis or a compensated respiratory alkalosis.

45
Q

How can respiratory alkalosis/acidosis be compensated for?

A

Can be metabolically compensated by increasing or decreasing the levels of HCO3–

46
Q

How can metabolic acidosis/alkalosis be compensated for?

A

Can be compensated by the respiratory system retaining or blowing off CO2 in an attempt to move the pH closer to the normal range

47
Q

What can you assume if you see a metabolic compensation for a respiratory acidosis/alkalosis?

A

Can assume that the respiratory derangement has been ongoing for at least a few days, if not more.

48
Q

What is the anion gap?

A

A derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions. To work out if the metabolic acidosis is due to:

  • Increased acid production or ingestion
  • Decreased acid excretion or loss of HCO3–
49
Q

What does an increased anion gap incdicate?

A

Increased acid production or ingestion

50
Q

What does a decreased anion gap indicate?

A

Decreased acid excretion or loss of HCO3–

51
Q

How would you calculate the anion gap?

A

ANION GAP = {[Na+] + [K+]} − {[HCO3−] + [Cl−]}

52
Q

What are the main anions used to calculate the anion gap?

A
  • Na+
  • K+
53
Q

What are the main cations used to calculate the anion gap?

A
  • Cl-
  • HCO3-
54
Q

What are causes of respiratory acidosis?

A

Type II respiratory failure

  • COPD
  • Exhaustion in asthma, pulmonary oedema, pneumonia
  • Respiratory depression (e.g. opiates)
  • Guillain-Barre – paralysis leads to an inability to adequately ventilate
55
Q

What type of respiratory failure can lead to respiratory acidosis?

A

Type II

56
Q

What are causes of respiratorry alkalosis?

A

Often type I respiratory failure

  • Anxiety – often referred to as a panic attack
  • Pain – causing increased respiratory rate
  • Hypoxia – resulting in increased alveolar ventilation in an attempt to compensate e.g. asthma
  • Pulmonary embolism
  • Altitude
  • Pneumothorax
  • Stroke
  • Subarachnoid bleed
  • Meningitis
57
Q

What are causes of metabolic acidosis with an increased anion gap?

A

Increased acid production/ingestion

  • Lactic acidaemia - shock, infection, tissue ischaemia
  • Urate - renal failure
  • Ketones - DKA, alcohol
  • Drugs/Toxins
58
Q

What are causes of metabolic acidosis with normal anion gap?

A

Decreased acid excretion or loss of HCO3–

  • Renal tubular acidosis
  • Diarrhoea/Ileostomy
  • Drugs - acetazolamide
  • Addison’s Disease
  • Pancreatic fistula
  • Ammonium cholride ingestion
59
Q

What are causes of metabolic alkalosis?

A
  • Vomiting
  • Diuretics - K+ depletion
  • Burns
  • Ingestion of a base
60
Q

What mnemonic can you use to remember the causes of metabolic acidosis with a high anion gap?

A

CAT MUDPILES

  • Cyanide, carbon monoxide
  • Alcoholic ketoacidosis
  • Toluene
  • Methanol, metformin
  • Uraemia
  • Diabetic ketoacidosis
  • Phenformin, pyroglutamic acid, paraldehyde, propylene glycol, paracetamol
  • Iron, isoniazid
  • Lactate (numerous causes)
  • Ethanol, ethylene glycol
  • Salicylates

Renal (19 decks)

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