Clinical acid base Flashcards

1
Q

What is the state of the blood in terms of respiratory alkalosis? (think pH and CO2)

A
  • alkalaemia (high pH ~7.6)

- low pCO2

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2
Q

What are the potential causes of respiratory alkalosis?

A
  • hyperventilation
  • any cause of impaired oxygenation
  • central cerebral stimulation: fever, pain, drugs, sepsis
  • panic/anxiety
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3
Q

What is the state of the blood in terms of respiratory acidosis? (think pH and CO2)

A
  • acidaemia (low pH ~7.2)

- high pCO2

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4
Q

What are the potential causes of respiratory acidosis?

A
  • Reduced ventilation:
    1. airway disease
    2. neuromuscular or chest wall disease
    3. reduced respiratory drive: opiates or reduced consciousness
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5
Q

How might a person with respiratory acidosis present?

A
  • Breathless - high resp rate
  • Drowsy
  • Wheeze throughout chest
  • Low O2 sats
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6
Q

A patient with COPD presents to A&E after a fall, they are hypercapnic, normal (borderline) pO2, low O2 sats but are NOT acidotic. How should this respiratory status be managed?

A

They have type 2 respiratory failure and compensated respiratory acidosis
No need to rush treating this patient - continue to monitor ABGs but as they have no clinical symptoms they should be fine
–> norma for someone with COPD

*high HCO3- will show that it is being compensated for

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7
Q
Patient presents with extreme breathlessness. Their respiratory status is as follows:
pH = 7.11		(7.35-7.45)
pCO2 = 2.8    (4.5-6 kPa)
pO2	 = 15	(10-13 kPa)
HCO3- = 12	(22-28mmol/L)

Why is this patient breathless?

A
  • patient has metabolic acidosis
  • trying to compensate b y lowering CO2
  • breathing more to breathe out more CO2 = breathless

*typical in diabetic patients –> at this point you would need to test blood glucose levels

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8
Q

What substances in the body can cause high anion gap metabolic acidosis?

A
  1. Kentones:
    - DKA
    - Starvation or alcoholic ketoacidosis
  2. Lactate:
    - tissue hypoxia/poor perfusion
    - altered cellular respiration
    - D-lactate (rare)
  3. Titrable acid:
    - renal failure
  4. Ingested acid:
    - ethylene glycol, methanol, salicylate
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9
Q

State whether pH, HCO3- and CO2 are high or low in lactic acidosis/ketoacidosis?

A

all are usually low

same for renal failure acidosis and ingested acidosis

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10
Q

What is normal anion gap metabolic acidosis also called? How does it usually arise?

A
  • = hyperchloraemic metabolic acidosis
  • usually due to bicarbonate loss
  • -> kidney: renal tubular acidosis
  • -> gut: diarrhoea
  • compensatory rise in chloride to maintain electrical neutrality
  • also seen in iatrogenic chloride administration
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11
Q

What are the potential causes of renal tubular acidosis?

A
  • diarrhoea
  • external drainage of pancreas/biliary tree
  • urinary diversion
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12
Q

What are the acute/severe and chronic complications of acidosis?

A

Acute/severe:

  • negative inotropic effects
  • confusion
  • Kussmaul’s breathing
  • hyperkalaemia

Chronic:

  • bone reabsorption, calciuria stones
  • insulin resistance
  • progressive renal impairment
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13
Q

Why does HCO3- rise with chloride and potassium depletion?

A

Chloride depletion:

  1. As H+ is lost:
    - diarrhoea
    - diuretics
    - mineralocorticoid excess
    - vomiting/NG drainage

Postassium depletion:

  1. A H+ is lost:
    - vomiting/NG drainage
    - rare hypokalaemia disorders
  2. As H+ moves into cells:
    - hypokalaemia
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