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Blood gases. Worked examples
1. Blood gases
What is most likely to be wrong with the patient and how will
you manage them?
2. The Rules
All units in mmo/L and mmHg
Anion Gap = Na - (Cl + HCO3)? N < 15, > 30 = DKA or lactic
acidosis
Rule of thumb Cl normal = HAGMA
A-a gradient N = age/4+4
A = FIO2 x 713 (at sea level) - pCO2 x 1.25
= 150 - pCO2 x 1.25 at sea level on room air
Predicted pCO2 for metabolic acidosis = 1.5 x HCO3 + 8 +/-
2
3. Metabolic alkalosis: Expected PCO2 = 0.9 [HCO3] + 9
Compensation for respiratory acidosis
* Acute:? HCO3 incr 1 for each 10mmHg rise pCO2 above 40
* Chronic: HCO3 incr 4 for each 10mmHg rise pCO2 above 40
* To a maximum HCO3 of 45
Respiratory alkalosis predicted HCO3 drop
* acute 2 for each 10mmHg pCO2 below 40
* chronic 5 for each 10mmHg pCO2 below 40 minimum HCO3 12-
15 after 2-3 days.
Estimated osmolality = 2 Na + urea + glucose
Corrected sodium = glucose/3.5 + measured Na
5. NAGMA
GI or renal loss / decr production of HCO3
HARDUP
Hyperchloraemia
Acetazolamide, Addison’s disease
Renal tubular acidosis
Diarrhoea, vomiting, ileostomies, fistulae
Ureteroenterostomies
Pancreatoenterostomies
8. Case 1: 75F
Arterial
FIO2 0.5
pH 7.289 7.35-7.43
pO2 147 69-116
pCO2 26.4 32-45
BXS 13.1 -2 - +2
HCO3 12.3 22-26
Na 155 136-146
K 4.4 3.5-5.0
Cl 120 99-106
Glucose 46 3.9-5.8
Lactate 4.3 0.5-1.6
Hb 163 130-180
Before we do any calculations look at the numbers, give me a
couple of diagnoses and tell me your management
9. Case 1: 75F
Arterial
FIO2 0.5
pH 7.289 7.35-7.43
pO2 147 69-116
pCO2 26.4 32-45
BXS 13.1 -2 - +2
HCO3 12.3 22-26
Na 155 136-146
K 4.4 3.5-5.0
Cl 120 99-106
Glucose 46 3.9-5.8
Lactate 4.3 0.5-1.6
Hb 163 130-180
DKA or HHS + relative
hypoxia + hypoperfusion ?
septic
Rehydrate slowly
Add insulin and K+
replacement once K+
known
Seek and treat source
CXR
15. Respiratory compensation for metabolic acidosis
Predicted pCO2 = 1.5 x HCO3 + 8 (+/- 2) at 24 - 48 hours
= 26.45
Which is what is measured.
This would suggest there is no respiratory component to this
patients presentation, which, given the A-a gradient, is not
correct
So ? partially compensated metabolic acidosis which would
cause a CO2 greater than 26.45 + a respiratory alkalosis
driving the CO2 down to the measured 26.4
17. Corrected Sodium
Corrected Na = glucose/3.5 + measured Na
= 46/3.5 + 155
= 171
Na > 160 has 75% mortality high incidence of neurological
deficits in survivors.
21. Raised anion gap metabolic acidaemia, extreme
hyperglycaemia, hyperosmolality + lactic acidosis.
At this age most likely to be HHS rather than DKA. With lactic
acidosis the acidosis, though likely to be a component of
renal failure
K normal but patient likely to be whole body K deficient and
likely to become hypoK with treatment.
Marked A-a gradient suggesting a respiratory component to
the presentation, with hypoxia prehospital causing the
lactic acidosis
Source of deterioration needs to be sought and corrected eg
pneumonia, CCF, MI.
22. The patient needs volume replacement initially with isotonic
crystalloid until perfusion is normalised then with hypotonic saline
to correct hyperosmolality (patient is relatively more deficient in
free water than sodium). There is a risk of cerebral and
pulmonary oedema if osmolality and dehydration is corrected
too quickly. If there is pulmonary oedema before resuscitation the
patient will need ventilatory support as volume is replaced.
1L NS/1H till intravascularly euvolamic then 1/2NS at 250ml/hr
(maximum of 50ml/kg over first 4 hours). Add K 20mmol/hour
when passing urine. Change to 1/2NS + 5% dextrose + 40mmol KCL
when BSL < 16.5
Use of insulin is controversial as may cause too rapid correction of
hyperosmolality. I would use low dose insulin at 0.1U/kg and
monitor BSL and osmolality Q2H. BSL should not be reduced
below 14mmol/L until mental state and hyperosmolarity
25. Case 2 85F
Arterial
FIO2 1.0
pH 7.186 7.35-7.43
pO2 87.5 69-116
pCO2 37.8 32-45
BXS -12.9 -2 - +2
HCO3 13.7 22-26
Na 139 136-146
K 9.4 3.5-5.0
Cl 117 99-106
Glucose 8.6 3.9-5.8
Lactate 0.6 0.5-1.6
Hb 124 130-180
Before we do any calculations look at the numbers,
give me a couple of diagnoses and tell me your
management
26. Case 2 85F
Arterial
FIO2 1.0
pH 7.186 7.35-7.43
pO2 87.5 69-116
pCO2 37.8 32-45
BXS -12.9 -2 - +2
HCO3 13.7 22-26
Na 139 136-146
K 9.4 3.5-5.0
Cl 117 99-106
Glucose 8.6 3.9-5.8
Lactate 0.6 0.5-1.6
Hb 124 130-180
Life threatening
hyperkalaemia
Hypoxia
Severe acidosis with poor
respiratory compensation ?
Decr LOC
Salbutamol
Calcium gluconate
ECG
Repeat K+ sample
27. Most important thing
Life threatening hyperK: 9.4
Needs to be confirmed and simultaneously treated
â—Źsafe to start a salbutamol neb while ECG and repeat gas is
being done
Other treatment options? What would you do?
31. Predicted Respiratory Compensation
pCO2 = 1.5 x HCO3 + 8
= 28.5
Measured CO2 is 37.8 so some respiratory acidosis (eg
pneumonia, decr LOC) (driving the CO2 up) and/or
metabolic alkalosis (eg vomiting) (driving the HCO3 down)
32. A-a Gradient
A = 713 x FIO2 - pCO2 x 1.25
= 713 - 47.25
= 665.75
A-a = 665.75 - 87.5
= 578 (N = age/4 +4
= 25)
= bad!
Despite a SaO2 of 96%
34. Conclusion
Life threatening hyperkalaemia
Marked NAGMA / hyperchloraemic metabolic acidosis
Acidosis and hyperK likely to be on the basis of renal failure
The hyperK needs urgent treatment and confirmation
Find cause of renal failure: Hx, examination and further
examination
If appears volume depleted she needs replacement with K
free crystaloid till euvolaemic
Likely to need urgent dialysis if she is a candidate
36. Case 3: 3 year old with tachypnoea
Venous
FIO2 0.21
pH 7.22 7.35-7.43
pO2 48 69-116
pCO2 24 32-45
BXS -2 - +2
HCO3 10 22-26
Na 139 136-146
K 1.9 3.5-5.0
Cl 118 99-106
Glucose 4.1 3.9-5.8
Lactate 2.5 0.5-1.6
Hb 107 130-180
37. Case 3: 3 year old with tachypnoea
Venous
FIO2 0.21
pH 7.22 7.35-7.43
pO2 48 69-116
pCO2 24 32-45
BXS -2 - +2
HCO3 10 22-26
Na 139 136-146
K 1.9 3.5-5.0
Cl 118 99-106
Glucose 4.1 3.9-5.8
Lactate 2.5 0.5-1.6
Hb 107 130-180
NB venous
Hypokalaemia ? Secondary to B2 agonist
Or diarrhoeal illness
Needs oxygen
38. Most important finding
Life threatening hypoK
Needs to be immediately confirmed and treated
IV KCL max 0.4mg/kg/hour with ECG monitoring
Estimated weight 14kg (2(age+4))
KCL 5.6mmol/hour
Will get onto how to do that.
42. What's going on and what are you going to do?
Probable gastroenteritis with life threatening hypokalaemia.
Mx (lots of ways to do it)
If really shocked IV boluses eg Hartmann's (K = 5mmol/L) 20mmol/kg boluses
till clinically intravascularly euvolaemic.
Then
Eg 20mmolKCL in 1/2NS + 5% dextrose run at double maintenance
(Maintenance = 4ml/kg for 1st 10kg + 2ml/kg for next 10kg + 1ml/kg
thereafter, (but in Alice they use 5ml/kg if under ) 40 + 8 ml/hour. Double
maintenance = 96ml/hour
43. Alternatively (RCH): 250ml/hour NS + KCL 20mmol/L for first 6 hours
if severely dehydrated (=5mmolKCL/hour), or 150ml/kg thereafter
Alternatively (CC) 280ml boluses of Hartmann's if shocked. Then or
otherwise: 250 0r 150ml/hour (depending on severity) NS + 5%
Dextrose + KCL 20mmol/L. Offer ORS. Stop IV fluid when taking >
10ml/kg/hour ORS.
ORS (liquid or icy pole) contains KCL 20mmol/kg.
Ondansetron 2mg SL wafer or IV
See http://sites.google.com/a/emergency-medicine-
tutorials.org/www/Home/medical-
3/gastroenterology/gastroenteritis
Also note anaemia - probably nutrition related, needs further
assessment and mx.
45. Is there an acid base disorder present? If so what?
No acidaemia or alkalaemia but probably respiratory acidosis (low HCO3, high CO2 and
hypoxia (or could be metabolic alkalosis with full compensation - but hypoxia
suggests respiratory process and don't usually get full compensation for metabolic
acidosis).
Compensation for respiratory acidosis:
â—Źacute: HCO3 1mmol/10mmHg pCO2 above 40
â—Źchronic: HCO3 4mmol/10mmHg pCO2 above 40
pO2 50.8 so max HCO3 should be 24 +4 = 28
Measured (actually, calculated) HCO3 = 32.4
So some other process driving HCO3 higher or pCO2 lower
â—Źmetabolic alkalosis eg vomiting, diuretics
â—Źacute respiratory alkalosis eg acute respiratory compensation on back ground of
chronic respiratory disease
46. Other disorder?
K = 2.7
Most common causes diuretics and GIT loss
â—Ź Decreased intake
o rare
â—Ź Redistribution
o Alkalaemia (think of cells pumping out H in exchange for K to correct alkalaemia)
o Insulin
o Beta agonists - eg salbutamol - quite likely in this patient
o Thyrotoxic periodic paralysis
o Familial hypokalaemic periodic paralysis
o Aldosterone excess
â—Ź Loss
o GIT
 especially vomiting to give alkalosis
o Renal
 Diuretics
 Hyperaldosteronism
 Primary
 Secondary
 Renal hypoperfusion
 CCF
 Renal artery stenosis
 CRF
 Liver disease (splanchnic shunting through varices)
 Post ATN
 Renal tubular acidosis
 Bartters
 hypoMag
 Leukaemias
48. A-a gradient
Patient on room air oops!
A = 150 - 50.8 x 1.25
= 86.5
A-a = 86.5 - 41.9
= 44.6 N = age/4 +4
= 23
49. Conclusion
Severely unwell patient who requires oxygen.
She has hypoxic and hypercapnic respiratory failure.
She is not acidaemic or alkalaemic probably on the basis of a compensated
chronic respiratory acidosis + another process eg
â—Źmetabolic alkalosis from vomiting or diuretics (also causing hypo K)
â—Źacute respiratory acidosis
She is hypokalaemic from eg
â—Źvomiting
â—Źdiuretics
â—Źalkalosis
â—Źsalbutamol
She needs urgent correction of her hypoxia as first line therapy. She is likely
to require ventilatory support. Her K needs to be corrected.
51. A-a gradient
A = 150 - 43 x 1.25
= 96.25
A - a = 96.25 - 28.8
= 67.45 (N = age/4 + 4 = 21.75)
Severe A-a gradient
52. Acid base disorder
Metabolic alkalosis
Causes
Most common GIT loss (vomiting) or diuretics
Chloride responsive
â—Ź GI loss
â—ŹDiuretics
â—ŹChloride wasting disease
o cystic fibrosis
Non-chloride responsive
â—Źhyperaldosteronism
oExpect hyperNa and hypoK
oeg renal artery stenosis, CCF, liver failure, nephrotic syndrome
53. Compensation for metabolic alkalosis
Expected PCO2 = 0.9 [HCO3] + 9
= 0.9 x 49.1 + 9
= 53
Measured 43
So probable respiratory alkalosis also, especially as severely
hypoxic.
54. Severe hypoK: 1.9
Likely to be as a result of vomiting
â—ŹKidneys retain H at expense of K
Needs urgent correction and cardiac monitoring
55. Hyponatraemia: 129
Likely to be due to vomiting
Usually classified as
â—ŹSpurious
â—ŹHypertonic
oHyperglycaemia, Mannitol
â—ŹHypotonic
oHypovolaemic
Decr intake or loss eg GI loss, 3rd spacing, burns
oEuvolaemic
SIADH, Drugs, Glucocorticoid deficiency, Excess water
intake (psych, potomania, novice athletes)
oHypervolaemic
renal failure, cirrhosis, nephrotic syndrome, CCF
56. Hyponatraemia does NOT need urgent correction
Criteria for urgent correction
â—ŹNa ~< 115 and
oSeizure or
oComa or
ofocal neurological deficit
58. Conclusion
Severe hypoxaemia requiring oxygen and probably ventilatory
support.
Hypoxaemia likley to be as a result of aspiration from
vomiting and exacerbated by respiratory compensation for
metabolic alkalosis
Given Hx of persistent vomiting, vomiting is probable cause of
metabolic alkalosis.
Needs volume, Na, Cl and K replacement eg NS + 40mmolKCL/
1 hour with cardiac monitoring
60. Respiratory alkalosis
Predicted HCO3 drop
â—Źacute 2 for each 10mmHg pCO2 below 40
â—Źchronic 5 for each 10mmHg pCO2 below 40 minimum HCO3
12-15 after 2-3 days.
Predicted HCO3 drop 1.5 - 6.5 -> 22.5-17.5
Measured = 20.1 So probably full compensation and single
process depending on chronicity