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Metabolism 2 > Clinical Acid and Base > Flashcards

Clinical Acid and Base Flashcards

1
Q

name the key components of blood gas analysis

A
  • pH: compensated or decompensated (=sick!)
  • pCO2: respiratory component
  • HCO3- (and ‘base excess’): metabolic component
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2
Q

what other useful information is on an ABG

A
  • pO2/sO2: Oxygenation
  • Electrolytes: To calculate anion gap
  • Other values – glucose, lactate, Hb etc
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3
Q

describe an ABG

A
  • Use a special type of medium such as heparin in it so the blood doesn’t clot
  • Go into the radial artery most common part
  • Syringe will self fill if you hit the artery
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4
Q

what artery do you measure an ABG from

A

radial

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5
Q 
Case 1 
20 year old
Very anxious
Breathless – respiratory rate 28/min
Chest examination unremarkable
Clear lung field on CXR

pH 7.58 (7.35-7.45)
pCO2 2.9 (4.5-6 kPa)
pO2 8.1 (10-13 kPa)
HCO3- 24 (22-28mmol/L)

Na		137		(135-145 mmol/L)
K		4.0		(3.5-5 mmol/L
Cl		104		(97-107 mmol/L)
A

respiratory alkalosis

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6
Q

what are the causes of respiratory alkalosis

A
  • hyperventilation
  • any cause of impaired oxygenation

central cerebral stimulation

  • panic anxiety
  • fever
  • pain
  • drugs
  • sepsis
  • hypoxia
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7
Q 
Case 2 
80 year old
Lifelong smoker
Brought in by ambulance
Breathless – respiratory rate 22/min
Drowsy
Wheeze throughout chest
Sats 95% on 60% oxygen

pH 7.09 (7.35-7.45)
pCO2 9.7 (4.5-6 kPa)
pO2 17 (10-13 kPa)
HCO3- 24 (22-28mmol/L)

Na		137		(135-145 mmol/L)
K		4.0		(3.5-5 mmol/L
Cl		104		(97-107 mmol/L)
A

respiratory acidosis

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8
Q

what are the causes of respiratory acidosis

A

Reduced ventilation:
Airways disease
Neuromuscular or chest wall disease
Reduced respiratory drive: opiates or reduced consciousness

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9
Q 
case 3 
80 year old
Lifelong smoker, COPD
Admitted to hospital after a fall
‘Routine’ blood gas done in emergency department
pH		7.38		(7.35-7.45)
pCO2	8.9		(4.5-6 kPa)
pO2		8.1		(10-13 kPa)
HCO3-	35		(22-28mmol/L)
sO2		88%
Na		137		(135-145 mmol/L)
K		4.0		(3.5-5 mmol/L
Cl		104		(97-107 mmol/L)
A

compensated respiratory acidosis

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10
Q

describe what you would see in compensated respiratory acidosis

A

normal pH
high pCO2
compensatory high bicarbonate

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11
Q

what can cause compensatory respiratory acidosis

A
  • metabolic compensation may take a few days

- intercalated cells in distal nephrons actively excrete hydrogen ions and reclaim bicarbaotne

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12
Q 
case 4 
24 year old
Very breathless and anxious
Chest examination and CXR normal
Appears unwell

pH 7.11 (7.35-7.45)
pCO2 2.8 (4.5-6 kPa)
pO2 15 (10-13 kPa)
HCO3- 12 (22-28mmol/L)

Na		137		(135-145 mmol/L)
K		4.0		(3.5-5 mmol/L
Cl		98		(97-107 mmol/L)
A

metabolic acidosis

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13
Q

what can cause high anion gap metabolic acidosis

A

Acid ‘added’ to the blood:
Ketones:
DKA
Starvation or alcoholic ketoacidosis

Lactate:
Tissue hypoxia/poor perfusion
Altered cellular respiration
Rarely: D-lactate

‘Titrable acid’
Renal failure

Ingested acid
Ethylene glycol, methanol, salicylate

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14
Q

describe what lactic acidosis/ketoacidosis looks like e

A

Low pH, low HCO3-, often low CO2

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15
Q

what causes lactic acidosis/ketoacidosis

A
  • impaired oxygenation or glucose enters
  • decrease in bicarbonate
  • leads to lactate and ketones forming
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16
Q

what happens in renal failure acidosis

A
  • decrease in tithable or dietary acid
  • decrease in bicarbonate
  • failure to clear titrable acid using phosphate/ammonium
17
Q

Case 5
18 year old man
Attends A+E with renal colic

pH 7.25 (7.35-7.45)
pCO2 4.2 (4.5-6 kPa)
pO2 12 (10-13 kPa)
HCO3- 13 (22-28mmol/L)

Na		137		(135-145 mmol/L)
K		3.2		(3.5-5 mmol/L
Cl		116		(97-107 mmol/L)
A

normal anion gap metabolic acidosis = Hyperchloraemic metabolic acidosis

18
Q

what is normal anion gap metabolic acidosis due to

A

Usually due to bicarbonate loss
Kidneys: Renal tubular acidosis
Gut: diarrhoea

Compensatory rise in chloride to maintain electrical neutrality

19
Q

what are the types of renal tubular acidosis

A 
Bicarbonate lost in urine:
 Type 1 ‘distal’
 Type 2 ‘proximal’
Type 3 very rare
Type 4 hyperkalaemic

1,2,3 rare and genetic
4 is more common

20
Q

what is renal tubular acidosis

A
  • Not able to get acid into the urine

- If you have a patient and you think if the patient has renal tubular acidosis – test the urine pH

21
Q

what are the acute consequences of acidosis

A

Negative inotropic effects
Confusion
Kussmaul’s breathing
Hyperkalaemia

22
Q

what are the chronic consequences of acidosis

A

Bone reabsorption, calciuria, stones
Insulin resistance
Progressive renal impairment

23
Q 
case 6 
74 year old man
Multiple chronic health problems
Admitted two days ago with bowel obstruction
Clinical deterioration
pH		7.2		(7.35-7.45)
pCO2	6.8		(4.5-6 kPa)
pO2		9.5		(10-13 kPa)
HCO3-	16		(22-28mmol/L)
Na		137		(135-145 mmol/L)
K		6		(3.5-5 mmol/L
Cl		98		(97-107 mmol/L)
Lactate 	5.6		(<2mmol/L)
A

mixed acidosis

24
Q

describe what mixed acidosis is caused by

A 
Likely two (or more) underlying processes
Sick!
25
Q 
case 7 
80 year old woman
Heart failure
Long term steroid use
Admitted with vomiting and dizziness
pH		7.6		(7.35-7.45)
pCO2	6		(4.5-6 kPa)
pO2		9.5		(10-13 kPa)
HCO3-	35		(22-28mmol/L)
Na		137		(135-145 mmol/L)
K		3.2		(3.5-5 mmol/L
Cl		95		(97-107 mmol/L)
A

metabolic alkalosis

26
Q

why does bicarbonate rise

A 
As H+ is lost:
Vomiting/NG drainage
Diarrhoea
Diuretics
Mineralocorticoid excess
Rare hypokalaemic disorders

As H+ moves into cells:
- Hypokalaemia
If alkali is administered

frist list is with chloride deletion
last 2 and 2nd part is with potassium depletion

27
Q

what is the treatment of metabolic alkalosis

A

Replacement of H+:

  • Normal saline (NaCl) if chloride deplete
  • Potassium supplementation
  • Treat underlying cause

Metabolism 2 (40 decks)

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