Gunn: Acid/Base Physiology 3 Flashcards

1
Q

What is metabolic alkalosis?

A
  • If plasma bicarbonate > 24mmols/L, HCO3 is excreted by the kidneys
    • Rapid correction of circulationg alkali
  • Thus a metabolic alkalosis requires both:
    • An initiator
    • Impaired renal correction
  • Steady state reflects
    • reabsorption of all filtered HCO3
    • Excretion of filtered fixed acid/regeneration of plasma HCO3
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2
Q

Initator of matabolic alkalosis?

A
  • Gain of alkali in the ECF
    • exogenous (eg. IV NaHCO3 infusion, citrate in transfused blood)
    • endogenous (eg. matabolism of ketoanions to produce bicarbonate)
  • Loss of H+ from ECG
    • Kidneys (eg. use of diuretics)
    • Gut (vomiting gastric fluid, NG suction) - (eg. pyloric stenosis in babies)
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3
Q

Chloride’s role in Metabolic alkalosis?

A

Lack of Cl- leads to increased HCO3- reabsorption

  • Cl- nad HCO3- are the only anions present in appreciable quantities in ECF
  • When Na+ and K+ are reabsorbed we need a balancing anion
  • Thus a deficiency of one leads to the increased reabsorption of the other

(eg. Diuretics such as frusemide resuly in a loss of NaCl and there is a risk if the patient is already volume depleted leaving them with elevated alosterone, and they have a low dietary chlorine intake)

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4
Q

Potassium depletion results from? leads too?

A

Hyperaldosteronism: Primary: Conn’s; secondary: Bartters

  • Increased distal tubular Na+ reabsorption and Increased K+, H+ loss
  • Increased HCO3- reabsorption matches the incresed H+ loss
  • *Indirect**: Increased Na+ reabsorption leads to an increased nagative cell voltage promoting H+ secretion
  • *Direct**: Stuimulates H+ ATPase

Upregulaters anion exchanger, facilitating HCO3/Cl exchange

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5
Q

What is the anion gap?

A

The anion gap is the difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum.

Anion Gap = (Na+ + K+) - (Cl- + HCO3-)

  • If K+ is not used in the measurement the normal range is 8 - 16 mmol.L-1
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6
Q

What is the purpose of the anion gap calculation?

A

It is a useful way of identifying the cause of metabolic acidosis.

  • If the anion of the non-volatile acid is Cl- (metabolic acidosis due to diarrhoea or renal dysfunction) the anion gap will be normal.
  • If the anion of the non-volatile acid is not Cl- (e.g lactate or beta-hydroxybutyrate) the anion gap will increase.
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7
Q

The alveolar gas equation and estimating the Alveolar O2?

A

We know that the PaCO2 = PACO2 and so:

PAO2 = PIO2 - PACO2/R + F (R = resp exchange ratio)

PAO2 = 150 - 40/0.8 + 2

Alveolar O2 = 102 mmHg

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8
Q

What value difference between PAO2 and PaO2 indicates impaired oxygen diffusion in the lungs? Some common examples of this?

A

Young Adults = >12mmHg at sea level

Elderly = >25mmHg at sea level

  • A widened gap would make a major contribution to a patients severe hypoxaemia. COPD is commonly associated with diffusion defects which give rise to such gradients.
  • These is also common in HF as the lungs become oedematous and CO2 diffuses normally but O2 struggles with the increased diffusion distance
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9
Q

What are the steps involved in the analysis and interpretation of arterial blood gases?

A
  1. pH - Normal, acidaemic, alkalaemic?
  2. PCO2, HCO3- and BE - Acidosis, Alkalosis, Respiratory or Metabolic?
  3. PCO2, HCO3- and BE - Compensated or Uncompensated? Simple/mixed?
  4. Anion Gap - Normal or Increased?
  5. PO2 - Normal, Low or High? (relative to the FIO2 and therfore alveolar PO2)
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10
Q

Symptoms felt from Alkalosis and acidosis?

A

Alkalosis: Nerve effects are common such as tingling of the fingers

Acidosis: Non-specific, general unwell/decreased consciousness with nausea especially in cases of acute ketone acidosis

DKA: pretty much everyone presents with 2-3 weeks of polyuria, polydypsia and waking in the night multiple times to urinate (not caused by much else)

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