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Blood gases
What is most likely to be wrong with the patient and how will
you manage them?
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
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
HAGMA
Lactate or DKA
The restL CAT MUDPILES
CO, CN
Alcoholic ketoacidosis
Toluene
Methanol
Uraemia
DKA
Phenformin, Paracetamol, Pyroglutamic metabolic acidosis, Paraldehyde
Iron, isoniazid
Lactate
Ethylene glycol, ethanol
Salicylates
NAGMA
GI or renal loss / decr production of HCO3
HARDUP
Hyperchloraemia
Acetazolamide, Addison’s disease
Renal tubular acidosis
Diarrhoea, vomiting, ileostomies, fistulae
Ureteroenterostomies
Pancreatoenterostomies
Raised Osmolar Gap
MIME ELK
Methanol/mannitol
Isopropyl alcohol
Methylene glycol
Ethylene glycol
Ethanol
Lactate
Ketones
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
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
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
Anion Gap
Anion Gap
Anion Gap = Na - (HCO3 + Cl)
= 155 - (12.3 + 120)
= 22.7 (N < 15)
Causes of a raised anion gap metabolic acidosis
â—ŹDKA
â—ŹRenal failure
â—ŹLactic acidosis
olocalised ischaemia
oshock
ohypoxia
â—ŹToxins
A-a Gradient
A-a Gradient
A = FIO2 x Dry atmospheric pressure - pCO2/0.8
= FI02 x 713 (at sea level) - pCO2 x 1.25
= 0.5 x 713 - 26.4 x 1.25
= 356 - 33
= 323
A-a = 323 - 147
= 176 (N = age/4 +4
= 23)
So he’s got something going on in his lungs
Respiratory compensation for metabolic acidosis
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
Corrected Sodium
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.
Estimated Osmolality
Estimated Osmolality
Osmolality = 2Na + glucose + urea
= 310 + 46 + urea - which is likely to be high
= 356 + urea (278-305)
Conclusion
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.
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
Reference for HHS: UpToDate
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
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
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
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?
Anion Gap
Anion Gap
Anion Gap = Na - (HCO3 + Cl)
= 139 - (13.7 + 117)
= 8.3 (N < 15)
NAGMA
Hyperchloraemic metabolic acidosis
â—ŹDiuretics
â—ŹRenal disease
oclassically Renal Tubular Acidosis
orenal failure
â—ŹGI losses
Predicted Respiratory Compensation
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)
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%
Conclusion
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
Significant pulmonary pathology needs to be addressed based
on further assessment.
Prognosis: poor.
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
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
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.
Anion gap
Anion gap
AG = Na - (HCO3 + Cl)
= 139 - (10 + 118)
= 11
= N
NAGMA / Hyperchloraemic metabolic acidois
â—ŹDiuretics
â—ŹGIT loss
â—ŹRenal disease
What's going on and what are you going to do?
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
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.
Case 4 78F SOB
Arterial
FIO2 0.21
pH 7.421 7.35-7.43
pO2 41.9 69-116
pCO2 50.8 32-45
BXS 7.8 -2 - +2
HCO3 32.4 22-26
Na 140 136-146
K 2.7 3.5-5.0
Cl 99 99-106
Glucose 6.0 3.9-5.8
Lactate 0.9 0.5-1.6
Hb 104 130-180
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
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
HypoK
Most likley secondary to any or all of:
â—ŹAlkalosis
â—ŹSalbutamol
â—ŹDiuretics
â—ŹVomiting
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
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.
Case 5. 71F with persistent vomiting
Arterial
FIO2 0.21
pH 7.671 7.35-7.43
pO2 28.2 69-116
pCO2 43 32-45
BXS 25.7 -2 - +2
HCO3 49.1 22-26
Na 129 136-146
K 1.9 3.5-5.0
Cl 71 99-106
Glucose 6.0 3.9-5.8
Lactate 1.8 0.5-1.6
Hb 136 130-180
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
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
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.
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
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
Hyponatraemia does NOT need urgent correction
Criteria for urgent correction
â—ŹNa ~< 115 and
oSeizure or
oComa or
ofocal neurological deficit
Estimated Osmolality
2Na + glucose + urea = 158 + 6.0 + urea
= 164 + urea
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
Case 6 74M SOB
Arterial
FIO2 0.21
pH 7.49 7.35-7.43
pO2 38.4 69-116
pCO2 26.7 32-45
BXS -2.8 -2 - +2
HCO3 20.1 22-26
Na 139 136-146
K 4.2 3.5-5.0
Cl 108 99-106
Glucose 6.2 3.9-5.8
Lactate 1.4 0.5-1.6
Hb 121 130-180
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
A-a gradient
A = 150 - 26.7 x 1.25
= 116.6
A-a = 116.6 - 38.4
= 78 (N = age/4 +4 = 22.5)
Anion Gap
139 - (20.1 + 108) = 10.9
= N
Conclusion
Severe hypoxic respiratory failure.
Patient requires oxygen and treatment of underlying process

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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
  • 4. HAGMA Lactate or DKA The restL CAT MUDPILES CO, CN Alcoholic ketoacidosis Toluene Methanol Uraemia DKA Phenformin, Paracetamol, Pyroglutamic metabolic acidosis, Paraldehyde Iron, isoniazid Lactate Ethylene glycol, ethanol Salicylates
  • 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
  • 6. Raised Osmolar Gap MIME ELK Methanol/mannitol Isopropyl alcohol Methylene glycol Ethylene glycol Ethanol Lactate Ketones
  • 7. 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
  • 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
  • 11. Anion Gap Anion Gap = Na - (HCO3 + Cl) = 155 - (12.3 + 120) = 22.7 (N < 15) Causes of a raised anion gap metabolic acidosis â—ŹDKA â—ŹRenal failure â—ŹLactic acidosis olocalised ischaemia oshock ohypoxia â—ŹToxins
  • 13. A-a Gradient A = FIO2 x Dry atmospheric pressure - pCO2/0.8 = FI02 x 713 (at sea level) - pCO2 x 1.25 = 0.5 x 713 - 26.4 x 1.25 = 356 - 33 = 323 A-a = 323 - 147 = 176 (N = age/4 +4 = 23) So he’s got something going on in his lungs
  • 14. Respiratory compensation for metabolic acidosis
  • 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.
  • 19. Estimated Osmolality Osmolality = 2Na + glucose + urea = 310 + 46 + urea - which is likely to be high = 356 + urea (278-305)
  • 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
  • 23. Reference for HHS: UpToDate
  • 24. 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
  • 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?
  • 29. Anion Gap Anion Gap = Na - (HCO3 + Cl) = 139 - (13.7 + 117) = 8.3 (N < 15) NAGMA Hyperchloraemic metabolic acidosis â—ŹDiuretics â—ŹRenal disease oclassically Renal Tubular Acidosis orenal failure â—ŹGI losses
  • 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
  • 35. Significant pulmonary pathology needs to be addressed based on further assessment. Prognosis: poor.
  • 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.
  • 40. Anion gap AG = Na - (HCO3 + Cl) = 139 - (10 + 118) = 11 = N NAGMA / Hyperchloraemic metabolic acidois â—ŹDiuretics â—ŹGIT loss â—ŹRenal disease
  • 41. What's going on and what are you going to do?
  • 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.
  • 44. Case 4 78F SOB Arterial FIO2 0.21 pH 7.421 7.35-7.43 pO2 41.9 69-116 pCO2 50.8 32-45 BXS 7.8 -2 - +2 HCO3 32.4 22-26 Na 140 136-146 K 2.7 3.5-5.0 Cl 99 99-106 Glucose 6.0 3.9-5.8 Lactate 0.9 0.5-1.6 Hb 104 130-180
  • 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
  • 47. HypoK Most likley secondary to any or all of: â—ŹAlkalosis â—ŹSalbutamol â—ŹDiuretics â—ŹVomiting
  • 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.
  • 50. Case 5. 71F with persistent vomiting Arterial FIO2 0.21 pH 7.671 7.35-7.43 pO2 28.2 69-116 pCO2 43 32-45 BXS 25.7 -2 - +2 HCO3 49.1 22-26 Na 129 136-146 K 1.9 3.5-5.0 Cl 71 99-106 Glucose 6.0 3.9-5.8 Lactate 1.8 0.5-1.6 Hb 136 130-180
  • 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
  • 57. Estimated Osmolality 2Na + glucose + urea = 158 + 6.0 + urea = 164 + urea
  • 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
  • 59. Case 6 74M SOB Arterial FIO2 0.21 pH 7.49 7.35-7.43 pO2 38.4 69-116 pCO2 26.7 32-45 BXS -2.8 -2 - +2 HCO3 20.1 22-26 Na 139 136-146 K 4.2 3.5-5.0 Cl 108 99-106 Glucose 6.2 3.9-5.8 Lactate 1.4 0.5-1.6 Hb 121 130-180
  • 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
  • 61. A-a gradient A = 150 - 26.7 x 1.25 = 116.6 A-a = 116.6 - 38.4 = 78 (N = age/4 +4 = 22.5)
  • 62. Anion Gap 139 - (20.1 + 108) = 10.9 = N
  • 63. Conclusion Severe hypoxic respiratory failure. Patient requires oxygen and treatment of underlying process