Acid base balance & Arterial blood gas analysis

1. ACID –BASE BALANCE &
INTERPRETATION OF ABG
Dr. Anuradha

2. Terminology
• pH : negative logarithm of H+
• Acid : a H+ ion donor
• Acidosis: abnormal process which lowers arterial
pH
• Acidemia: blood pH lower than acceptable range
• Base: H+ ion acceptor
• Alkalosis: abnormal process that lowers arterial pH
• Alkalemia: blood pH higher than acceptable range

3. How is it done ?
• ABG analysis is performed in whole blood
• PaO2, PaCO2 and pH are directly measured
with standard electrodes and digital analysers
• Oxygen saturation is derived from the oxygen
dissociation curve
• HCO3- concentration is calculated from
Hendersson- Hasselbach equation

4. • pH = pKa + Log { HCO3- / H2CO3 }
• pKa is the negative logarithm of dissociation
constant of carbonic acid.
•
• Base excess is also calculated.
• Also measures electrolytes, hemoglobin,
lactate and glucose

5. Indications for ABG
• To assess adequacy of oxygenation and
ventilation
• Assess changes in acid base haemostasis and
guide treatment for acid base abnormalities
• Establish diagnosis and severity of respiratory
failure and refractory COPD exacerbations
• To guide oxygen therapy, mechanical
ventilation and weaning

6. • Manage pts in ICU with heart/ renal/ hepatic /
multi organ failure, polytrauma, sepsis, DKA,
burns, various poisoning
• During cardiopulmonary surgery
• To determine prognosis in critically ill patients

7. Limitations
• ABG value represents only one point of time
• Must look at trends rather than a single value
• Avoid excessive blood sampling

8. 8 Steps in Evaluation of Acid- Base
Disorder
• STEP 1
• Check for accuracy of ABG
• If temperature, Hb, FiO2, Barometric pressure
are correctly entered in ABG machine.
• Result maybe incorrect if these values are not
proper

9. • STEP 2
• Look for adequacy of oxygenation
• Look at PaO2, SaO2, FiO2
• PaO2 changes with age.
• Correlate PaO2 with FiO2
• PaO2 maybe predicted as
• FiO2 X 5 in healthy lungs &
• FiO2 X 3 In COPD
PaO2 in mm Hg % of SaO2
Normal in air > 80 > 95
Mild hypoxia 60- 79 90 – 94
Moderate hypoxia 40 - 59 75 – 89
Severe hypoxia < 40 < 75

10. NormalValues
• pH 7.35 – 7.45 7.4 to remember
• pCO2 35 – 45 mmHg. 40 to remember
• HCO3- 22- 26 mmol/L 24 „ „
• Anion Gap 12 +/- 2 mmol/L. 12 „ „

11. • STEP 3
• Look at pH
• If it is normal, acidemic or alkalemic
• pH 7.35- 7.45 is normal
• pH < 7.35 is acidemia , uncompensated
• pH > 7.45 is alkalemia, uncompensated

12. STEP 4 : Analyse the primary disorder
– if respiratory or metabolic
What disorder is present? pH pCO2 or HCO3
RespiratoryAcidosis pH low pCO2 high
Metabolic Acidosis pH low HCO3 low
RespiratoryAlkalosis pH high pCO2 low
Metabolic Alkalosis pH high HCO3 high

13. • STEP 5
• Evaluate compensation and correlate with pH,
pCO2 and HCo3-
• If primary issue is respiratory, there will be
change in HCO3- to compensate for the change
in PaCO2
• In metabolic issues, there will be compensation
by change in PaCO2

14. • STEP 6
• Calculate compensation seen in ABG and
match it with expected
Disorder Event Compensation
A/C Respiratory Acidosis 10 mmHg rise in PaCO2 1 meq/L rise in HCO3-
C/C Respiratory acidosis 10 mmHg rise in PaCO2 4 meq/L rise in HCO3-
A/C Respiratory alkalosis 10 mmHg fall in PaCO2 2 meq/L fall in HCO3-
C/C Respiratory alkalosis 10 mmHg fall in PaCO2 14 meq/L fall in HCO3-
Metabolic acidosis 1 meq/L fall in HCO3- 1.25 mmHg fall in PaCO2
Metabolic alkalosis 1 meq/L rise inHCO3- 0.75 mmHg rise in PaCO2

15. • STEP 7
• Analyse if the disorder is mixed- 2 methods
• A] Check relative movement of pH in relation
to PaCO2 and HCO3-. If both pairs are moving
and in correct direction, it’s a Mixed disorder
• B] Analyse compensation assuming the
primary disorder as respiratory or metabolic.
If analysis shows no compensation, it is a
Mixed disorder.

16. Mixed Disorder- examples
• 1)Metabolic Acidosis+ Metabolic Alkalosis
• Renal failure and vomiting
• Vomiting & hypotension (lactic acidosis)
• 2) Metabolic Acidosis + Respiratory Acidosis
• Cardiac arrest
• Severe pulmonary oedema
• Drug ingestion with CNS depression
• 3)Metabolic Acidosis + Respiratory Alkalosis
• Septic shock
• Salicylate overdose

17. • 4) Metabolic Alkalosis + Respiratory Acidosis
• Chronic diuretic use in chronic lung disease
• 5) Metabolic Alkalosis + Respiratory Alkalosis
• Rare... In patients on ventilator being
hyperventilated and on diuretics/ Naso gastric
tube aspiration
• 6) Mixed Acute & Chronic Respiratory Acidosis
• Chronic respiratory failure with an acute
decompensation

18. • STEP 8
• Unmask hidden disorders – by using serum
electrolytes
• 3 calculations- AnionGap, Bicarbonate Gap, Delta
ratio
• a) Anion Gap
• Normal AG= (Na + K)– (cl + HCO3)
= 16+/-4 mEq/L
• Normal AG without K+ is 12 +/- 4 mEq/L
• ΔAG (Change in AG) = Measured AG- 12

19. PHYSIOLOGY

21. Buffers
• extracellular
– carbonic acid / bicarbonate
(H2CO3 / HCO3
-)
– haemoglobin
• intracellular
– proteins
– phosphoric acid / hydrogen
phosphate (H3PO4 / H2PO4
- +
HPO4
2-)
Henderson-Hasselbalch equation:
pH = 6.1 + log([HCO3
-] / 0.03 pCO2)

22. Organs involved in the regulation of
A-B-balance
– Equilibrium with plasma
– High buffer capacity
• Haemoglobin – main buffer for CO2
– Excretion of CO2 by alveolar ventilation:
– minimally 12,000 mmol/day
– Reabsorption of filtered bicarbonate: 4,000 to 5,000
mmol/day
– Excretion of the fixed acids (acid anion and associated
H+): about 100 mmol/day

23. Organs involved in the regulation of
A-B-balance
– CO2 production from complete oxidation of substrates
• 20% of the body’s daily production
– metabolism of organic acid anions
• such as lactate, ketones and amino acids
– metabolism of ammonium
• conversion of NH4
+ to urea in the liver results in an
equivalent production of H+
– Production of plasma proteins
• esp. albumin contributing to the anion gap
– Bone inorganic matrix consists of hydroxyapatite
crystals (Ca10(PO4)6(OH)2]
• bone can take up H+ in exchange for Ca2+, Na+ and K+
(ionic exchange) or release of HCO3
-, CO3
- or HPO4
2-

25. Respiratory system - CO2
• differences in the stimulation of respiration by
pCO2, H+ and pO2
• alveolar ventilation
• Disturbances – acidosis or alkalosis

26. Renal system – fixed H+ & HCO3
-
• Proximal tubular
mechanisms:
– reabsorption of HCO3
-
filtered at the glomerulus
– production of NH4
+
• Distal tubular mechanisms:
– net excretion of H+
• normally 70mmol/day
• max. 700mmol/day
– together with proximal
tubule excretion of H+
could increase up to
1000x!!! (pH of urine 4.5)
– Formation of titratable
acidity (TA)
– Addition of NH4
+ to luminal
fluid
– Reabsorption of remaining
HCO3
-

27. Respiratory acidosis (RA)
• primary disorder is a pH due to PaCO2 (>40
mmHg), i.e. hypercapnia
• time course:
– acute (pH)
– chronic (pH or normalisation of pH)
• Renal compensation – retention of HCO3
-, 3-4 days
• causes:
– decreased alveolar ventilation
– presence of excess CO2 in the inspired gas
– increased production of CO2 by the body
paCO2 =VCO2 /VA

28. Resp. Acidosis - compensation
• Acute RA - buffering only!
– 99% of buffering
intracellularly
• proteins (Hb and
phosphates) most
important buffers for
CO2
• Issue: concentration
is low relative to
amount of CO2
– the bicarbonate system
– no role in acute resp.
acidosis
• Chronic RA - renal bicarbonate retention
•
– takes 3 or 4 days to reach its
maximum
– paCO2  pCO2 in proximal tubular
cells  H+ secretion into the
lumen:
•  HCO3 production crosses
basolateral membrane and enters
the circulation (so plasma [HCO3]
increases)
•  Na+ reabsorption in exchange
for H+
•  NH3 production to 'buffer' the
H+ in the tubular lumen (so
urinary excretion of NH4Cl
increases)

29. RA - correction (i.e. treatment)
• the pCO2 rapidly returns to normal with
restoration of adequate alveolar ventilation
– treatment needs to be directed to correction of the primary
cause if this is possible
• Rapid fall in pCO2 (especially if the RA has
been present for some time) can result in:
– severe hypotension
– ‘post hypercapnic alkalosis’

30. Metabolic acidosis (MA)
• primary disorder is a pH due to HCO3
-:
Unmeasured anions in metabolic acidosis are
– Lactate
– Ketones (DM, starvation)
– Renal acids (sulphates, phosphates)
AG = [Na+] - [Cl-] - [HCO3
-]

31. MA - causes
• ketoacidosis
– diabetic, alcoholic,
starvation
• lactic acidosis
• acute renal failure
• toxins
• renal tubular acidosis
• GIT loss of HCO3
– diarrhoea
– drainage of
pancreatic or bile
juice
Na+
Cl-
AG
HCO3
-
normal
anion gap
Na+
Cl-
AG
HCO3
-
physiologic
situation
Na+
Cl-
AG
HCO3
-
high
anion gap

32. Compensatory Response in
Metabolic Acidosis
one half of acid load is buffered by nonbicarbonate buffers =
Bone, protein, red cells..
• PCO2  (Kussmaul)
• compensatory response after 15-30 minutes
• 5 days up to maximal
• Kidney:
• Metabolic acidosis
•  processing of glutamine into NH4
+ (ammonia to
ammonium for better H-excretion) and
• Bicarbonate generation (and reclaiming)

33. Metabolic alkalosis
 Calculate the urinary cl- to differentiate saline responsive vs saline resistant.
Must be off diuretics in order to interpret urine chloride
i. Urine chloride < 10 implies responsivenss to saline : ECF volume depletion
ii. Urine chloride >10 implies resistance to saline : severe K+ depletion ,
mineralcorticoid excees syndrome Etc
Saline responsive UCL<10 Saline-resistant UCL >10
Vomiting If hypertensive: Cushings, Conn’s, RAS, renal failure with alkali
administartion
NG suction If not hypertensive: severe hypokalemia, hypomagnesemia,
Bartter’s, Gittelman’s, licorice ingestion
Over-diuresis Exogenous corticosteroid administration
Post-hypercapnia

34. Lactic acidosis
• Overproduction or inadequate clearance.
• Is degradation product of glucose metabolism
• Increases in Anaerobic conditions- vigorous
exercise
• & Aerobic conditions: β-adrenergic stimulation in
skeletal muscle by stress or exogenous infusion
(Adr, NA)
• Lactate is converted to CO2 and H2O by the liver
• Lactate in Ringer lactate solution is functionally
HCO −3 .

35. • 2 types of lactic acidosis --.Type A & B
• Type A ,global inadequate oxygen delivery, in
hypovolemic or hemorrhagic shock. SvO2 low
• Type B occurs despite normal global oxygen delivery
and tissue perfusion.
• In regional hypoperfusion. Eg. Bowel ischemia .
• Excess circulating catecholamines (endogenous or
exogenous). Eg. Exercise, trauma or sepsis.
• Cyanide poisoning (in sodium nitroprusside),
biguanides (metformin)
• hypercatabolic diseases, such as lymphoma, leukemia,
AIDS, DKA.

36. • Lactic acidosis is a sensitive marker of disease
severity & adverse outcome if uncorrected
• Normal systemic indices of perfusion does not
exclude significant regional hypoperfusion or
mitochondrial failure.
• Dynamic measurements of lactate over time
are better predictors of outcome than are
static measures.
• Lactate clearance proposed as an end point
of resuscitation in sepsis.

37. APPROACHESTO ACID BASE
BALANCE

38. 3 Approaches to acid base balance
• Descriptive approach uses Pco2 and HCO3
- Boston approach based on Henderson
Hasselbach equation.
- Also anion gap
• Semiquantitative: Copenhagen approach.
Bufferbase concept, the standardized base
deficit-excess (BDE) and base-deficit gap.
• Quantitative approach: Stewart Fencl approach.
Uses SID and ATOT, is quantified using the strong
ion gap (SIG).

39. Henderson- Hasselbach equation
• Henderson- Hasselbach (in 1909/1916) described
‘acid base balance’ in terms of carbonic acid
• CO2 + H2O → H2CO3 → H+ + HCO3-
• pH = pKa + Log { HCO3- / H2CO3 }
• pKa is the negative logarithm of dissociation
constant of carbonic acid = 6.1
• Total CO2= HCO3- +dissolved CO2 +carbamino
CO2 +H2CO3
• ,, = PCO2 x 0.03 mmol CO2 / L / mmHg
• pH = 6.1 + log [ HCO3- ] / PCO2 x 0.03

40. Boston Approach
• Schwartz and colleagues atTufts University in Boston
• Descriptive approach.
• 2 independent variables: Paco2 and [HCO3 −].
• derived from the Henderson-Hasselbalch equation
• Uses acid-base maps and the mathematic relationship
between CO2 tension and serum HCO − 3 (or total
CO2)
• In simple disturbances, this is a reasonable approach

41. Descriptive Approach- Normogram
• Respiratory Disorders
• Acute RespiratoryAcidosis
• Expected [HCO3 − ] = 24 + [(Measured
PaCO2 − 40) /10]
• Chronic Respiratory Acidosis
• Expected [HCO3 − ] = 24 + 4 [(Measured
PaCO2 − 40) /10]
• Acute RespiratoryAlkalosis
• Expected [HCO3 − ] = 24 − 2 [(40 −
Measured PaCO2) /10]
• Chronic Respiratory Alkalosis
• Expected [HCO3 − ] = 24 − 5 [(40 −
Measured PaCO2) /10] (range: ± 2)
• Metabolic Disorders
• Metabolic Acidosis
• Expected PaCO2 = 1.5 × [HCO3 − ] + 8
(range: ± 2)
• Metabolic Alkalosis
• Expected PaCO2 = 0.7 × [HCO3 − ] + 20
(range: ± 5)

42. • Pitfalls :
• Confusing maps ,to learn formulas and perform
mental arithmetic.
• Not useful in complex acid base abnormalities
( hypoalbuminemia, hyperchloremic acidosis, or
dilutional acidosis or patients with lactic acidosis
in the setting of chronic respiratory acidosis).

43. Anion Gap approach
• By Emmet & Narins in 1975. Law of electrical neutrality.
• Looked at weak acids (phosphate and albumin) and UMAs .
• UnmeasuredAnion Gap, UMA “gap” of −10 to −12 mEq/L normal.
• AG, Simple = Na+ – [cl- + HCO3-] = 12-14 mEq/L
• AG, conventional= [Na+ + K+]- [cl- + HCO3-]= 14 to 18 ,,
• AG, modern = = [Na+ + K+]- [cl- + HCO3- + Lactate-]= 14 to 18
• Gap “widens” in acidosis caused by UMAs: renal acids or ketones.
• If the gap does not widen, then the anions are being measured,
and the acidosis has been caused by hyperchloremia (HCO −3
cannot independently influence acid-base status) or lactate (if
used).

44. Metabolic acidosis: Increased Anion
gap acidosis

45. Nongap metabolic acidosis
Causes of nongap metabolic acidosis - DURHAM
Diarrhea, ileostomy, colostomy, enteric fistulas
Ureteral diversions or pancreatic fistulas
RTA type I or IV, early renal failure
Hyperailmentation, hydrochloric acid administration
Acetazolamide, Addison’s
Miscellaneous – post-hypocapnia, toulene, sevelamer, cholestyramine ingestion
For non-gap metabolic acidosis, calculate the urine anion gap
UAG = UNA + UK – UCL
If UAG >0 : renal problem
If UAG <0 : non renal problem (most commonlyGI)
Most common is diarhoea and IV fluids

46. • B) Bicarbonate Gap, BG
• Calculate this if AG is elevated
• BG = ΔAG - ΔCO2
• BG outside +/- 6 strongly suggests another coexisting
acid base disorder
• BG > +6 = metabolic alkalosis with bicarbonate
retention as compensation for respiratory acidosis
• BG < +6 = Hyperchloremic metabolic acidosis with
bicarbonate excretion as compensation

47. Delta Anion gap
• Another version of the anion gap . Useful in critical illness
• Delta ratio = Δ Anion gap/ Δ [HCO3 − ] or ↑ Anion gap/ ↓ [HCO3 − ]
• =Measured anion gap − Normal anion gap
Normal [HCO3 − ] − Measured [HCO3 − ]
• = (Anion gap − 12)/ (24 − [HCO3 − ])
• Delta ratio & Clinical assessment
• <0.4 Hyperchloremic normal AG acidosis
• <1 High AG and normal AG acidosis
• 1 -2 Pure anion gap acidosis
Lactic acidosis: average value 1.6
DKA ratio closer to 1 (because of urine ketone loss)
• >2 High AG acidosis and concurrent metabolic alkalosis or
preexisting compensated respiratory acidosis

48. Albumin & Acid- Base Balance
• Most critically ill patients are hypoalbuminemic, and
maybe hypophosphatemic
• Why doesAlbumin deficits occur in critical illness?
1) reprioritization of hepatic protein production – more
acute phase reactants & less albumin synthesis
(2) capillary leak with loss of albumin into the
interstitium
(3) breakdown of preexisting albumin (constituent
amino acids can be used for protein synthesis)
(4) replacement of plasma with protein free fluids.

49. Impact of hypoalbuminemia on acid-
base balance
• . Albumin is the core negative charge
• Hypoalbuminemia may mask the detection of
acidosis caused by UMAs when using
conventional methods (pH, HCO3 − ,base
deficit,AG)
• Hypoalbuminemia- associated with alkalosis
• Hyperalbuminemia is very rare- in cholera,with
hemoconcentration, it is linked with acidosis.

50. Corrected anion gap
• By Fencl and Figge
• More accurate, corrects for albumin
• Anion gap corrected (for albumin) =
Calculated anion gap + 2.5 × (Normal
albumin g/dL − Observed albumin g/dL)

51. SEMIQUANTITATIVE APPROACH: BASE
DEFICIT OR EXCESS (COPENHAGEN)
• Uses algorithms. Based on Na+, cl-, albumin
• Calculates standardized base excess (BE for ECF) from Van
Slyke equation
• SBE = 0.9287 [HCO3- - 24.4 + (PH – 7.4)
• [It is independent of Henderson-Hasselbalch equation]
• Principle: In metabolic acidosis, anions increases and HCO3-
falls. Change in the HCO3- from baseline(delta HCO3-)
reflects net anions gained.
• The buffer base= HCO −3 + non volatile buffer ions
(serum albumin, phosphate,Hb)
• Drawback- values affected by Hb .

52. • Copenhagen approach
normogram • based on Pco2 and base
deficit/excess, referred to as
standard base excess (SBE).
• Calculation of Base Deficit/
Excess of Sodium, Chloride, and
FreeWater and Albumin
• BDENaCl=[Na+]−[Cl−] − 38
• BDEAlb =0.25 (42 – Alb. g/L)
• BDENaCl −BDEAlb = BDEcalc
• BDE − BDEcalc = BDE gap =
The effect of unmeasured
anions or cations

53. • Relatively accurate in most
• Limitation:
• does not distinguish between
- acidosis caused by lactate or Cl−
- alkalosis resulting from dehydration or
hypoalbuminemia.

54. Stewart Fencl Approach
• More accurate
• Basic concept- electrical neutrality
• In plasma, Stewart identified 3 independent
determinants that dictate acid–base status.
• (i) CO2
• (ii) electrolytes (strong ions)
• (iii) weak acids.
• Strong ions dissociate completely in solution,
weak ions partially

55. • In plasma, strong cations (mainly Na+) outnumber
strong anions (mainly Cl-); the difference between
the two is the strong ion difference (SID):
• SID = [Na+ + K+ + Ca2+ + Mg2+] -- [Cl- + lactate-]
• Normal plasma SID is 40–44 mmol / litre
• (Note that bicarbonate is not a strong ion).
• SID affects water dissociation,ie. H+ concentration.

56. • The remaining negative charges that balance SID (to
maintain electrical neutrality) come from CO2 and weak
acids; hence:
• SID = CO2 + A-
• Effective SIDe = [HCO3− ] +[Charge on albumin] +
[Charge on Pi] in mmol/L
• Weak acids are mainly albumin and phosphate.
• Stewart used the term ATOT to represent the total
concentration of weak ions, that is, AH + A-
• Hypoalbuminaemia has a slightly alkalinizing effect and
the body adapts by decreasing SID.

57. • Metabolic acidosis is produced by
• a decrease in SID.
• Or increase in CO2, Phosphates or albumin
• As SID decreases (i.e. becomes less positive),
more water dissociates to maintain electrical
neutrality. Hence, free H+ concentration
increases and pH decreases.
• In contrast, metabolic alkalosis occurs as a result
of an inappropriately large SID

58. Physiological mechanisms controlling
strong ion difference
• Kidney - main organ controlling strong ions
• Most imp.is chloride balance, filtering , reabsorbing.
• (Note that H+ excretion is irrelevant because water provides
an infinite source of H+).
• NH4+ is important in acid–base balance because of its co-
excretion with Cl-.
• Hepatic generation of NH4+ is important in AA balance
• Hepatic glutamine synthesis is stimulated by acidosis.
Glutamine is used by the kidney to generate NH4+ and thus
excrete chloride.
• The gastrointestinal tract also has important effects on SID

59. • Stewart approach - six independent simultaneous
equations.
• They are applications, require a computer to solve.
• [H+] x [OH-] = K’w
• [H+] x [A-] = Ka x HA
• [HA] + [A-] = ATOT
• [H+] x [HCO3-] = Kc x PCO2
• [H+] x [CO3 2-] = Ka x [HCO3-]
• SID + [H+] - [HCO3-] - [CO3 2-] - [A-] - [OH-] = O

60. Fencl– Stewart approach.
• Modified to five equations in the Fencl– Stewart
approach.
• Basis: sodium and chloride are the main strong ions
and albumin the main weak ion in ECF
• Simpler equation by Story and colleagues ; approach
to clinical diagnosis of abnormal SBE:
• (i) SBE from a blood gas machine
• (ii) sodium–chloride effect on BE = [Na+] - [Cl-] - 38
• (iii) albumin effect = 0.25 (42 - [albumin])
• (iv) unmeasured ion effect = SBE - (Na+ - Cl- effect) -
(albumin effect)

61. Eg.Thinking differently about fluids
through Stewart angle.....
• I.V. fluids equilibrate with ECF, altering
extracellular SID and ATOT.
• The CO2TOT of the infused fluid does not
affect extracellular SID andATOT.
• In other words, it is not the presence of
HCO3- in sodium bicarbonate preparations
that reverses a metabolic acidosis
• Rather it is the high SID (100 mmol /litre for
8.4% NaHCO3-) and the absence of ATOT.

62. Common Periop Acid- Base
Disturbances
• Respiratory Acidosis :
• Hypoventilation
• Narcosis
• Incomplete reversal of neuromuscular blockade
• Respiratory Alkalosis:
• Hyperventilation
• Anxiety
• Pain

63. • MetabolicAcidosis
• From measured anions ( hyperchloremic
acidosis)
• Hyperchloremia - from NS and saline
containing fluids
• RTA
• Bladder reconstruction

64. • MetabolicAcidosis
• From UMA - wideAG acidosis
• Hypoperfusion- lactic acidosis
• DKA

65. • Metabolic Acidosis
• Due to free water excess
• ( Hyponatremia, dilutional acidosis)
• Hypotonic fluid
• Sodium loss
• Diarrhoea
• Administering hyperosmolar fluids- mannitol,
alchohol
• Hyperproteinemia

66. • MetabolicAlkalosis:
•
• Hyper ventilation of COPD

67. Thank you

68. A CASE
• 75 year old lady, h/o diabetes 11 years
• h/o fall 6 days ago , #femur
• No other illness
• Reduced food intake
• 17/ 7/17 : Posted for sx
• In OT , BK = 6.5 , GRBS previous day 350 – 490
mg/dl.
• sx cancelled, to ICU.

69. • In ICU BK <1 . Started onVRIII.
• 19/7/17
• ABG taken
• 20/7/17
• BK > 5, ABG not bad, DKA protocol started

70. Variable 17/7
VBG
19/7 20/7
10am
20/7 5pm 20/7 6 pm 20/7 7pm
FiO2 % 21 21 21 21 29
pH 7.32 7.44 7.42 7.411 7.39
pCO2 mmHg 22 29 25 31 36
pO2 mmHg 53 84 79 72 41
K+ mmol/L 4.1 3 2.8 3.1 2.8
Na+ ,, 129 135 131 133 134
Ca2+ ,, 1.1 3 3.33 4.7 4.6
Cl- ,, 106 101 100 102 106
Lac ,, 1.3 1.5 0.8 0.7 0.8
sO2 % 83 95 94 91 67
HCO3-
mmol/L
14.2 21.5 19 21 22
SBE c ,, 13.6 -- 3.9 -- 6.8 -- 4.4 -- 2.3
Anion gap c ,, 12 14.9 14.7 11 6.5
Blood ketone 6 .... 0.8 1.5 5 1.8
Rx VRIII VRIII DKA DKA proto

71. • Arrhenius concept in 1903:
• Acid delivers H+ ion into solution & base delivers
OH- ion
• Water is a highly ionising and substances with
polar bonds will dissociate into component parts
in water
• Bronsted & Lowry concept:
• Acid is proton/ H+ donor & base is proton/ H+
acceptor