a summarized presentation about acid base balance & its practical application in the ICU. To download send me an email to sherif_badrawy@yahoo.com

1. ACID BASE BALANCE
INTERPRETATION
Dr.Sherif Badrawy

2. ‫اﻟﺮﺣﯿﻢ‬ ‫اﻟﺮﺣﻤﻦ‬ ‫ﷲ‬ ‫ﺑﺴﻢ‬
♻ This is a summarized presentation about
acid base balance & its practical application
in the ICU.
♻ I hope this will help in simplifying this
important ICU topic.
♻ All comments are welcome & highly
appreciated.
1a

3. 1b
Dr. Sherif
Badrawy
Digitally signed by Dr.
Sherif Badrawy
DN: cn=Dr. Sherif Badrawy,
o=KKUH, ou=Critical Care,
email=sherif_badrawy@ya
hoo.com, c=SA
Date: 2015.08.25 18:40:56
+03'00'

4. Osmolar Gap
2a

5. Screening test for detecting abnormal
low MW solutes (e.g. ethanol, methanol
& ethylene glycol [Normal is < 10]
↑Osmolar Gap ➜ >10 ➜ indirect
evidence for the presence of an abnormal
solute in significant amounts
2b

6. Osmolar gap =
3a

7. Osmolality - Osmolarity
Osmolality (measured),
Osmolarity (calculated)
3b

8. Osmolality (measured) ➜
Units:
4a

9. mOsm/kg
Measured in laboratory and
returned as the plasma
osmolality
4b

10. Osmolarity (calculated) ➜
Units:
5a

11. mOsm/l
Osmolarity = (1.86 x [Na+]) +
[glucose] + [urea] + 9 (using
values measured in mmol/l)
5b

12. Compensation rules for
Metabolic Acidosis
6a

13. Expected PCO2 = 1.5 x HCO3
+ 8 ± 2
6b

14. Compensation rules for
Metabolic Alkalosis
7a

15. Expected PCO2 = 0.7 x HCO3
+ 21 ± 2
7b

16. Compensation rules for
Respiratory Acidosis
8a

17. 8b

18. Compensation rules for
Respiratory Alkalosis
9a

19. 9b

20. How to calculate metabolic
compensation in respiratory
acidosis and alkalosis (aka the
1-2-3-4-5 rule)
10a

21. 10b

22. Adverse effects of metabolic
acidosis
11a

23. ◒ ↓myocardial contractility,
arrhythmias, VC
◒ Pulmonary VC, hyperventilation
◒ ↓Splanchnic and renal blood flow
◒ ↑metabolic rate, catabolism, ↓ATP
synthesis, ↓2,3DPG synthesis
11b

24. Working out a Metabolic
Acidosis
◒ Calculate AG or AGc, if:
◒ High:
12a

25. ◒ Unmeasured anions likely ➜ measure osmolality.
➜ If there is no obvious cause for an elevated AGc, ➜
specific assays (glucose, renal function,
rhabdomyolysis, L-lactate, D-lactate, β-
hydroxybutyrate, salicylate)
◒ Calculate osmolar gap. If high AG and high OG
then ketones, lactate, ethanol, ethylene glycol,
methanol, mannitol.
12b

26. Working out a Metabolic
Acidosis
◒ Calculate AG or AGc, if:
◒ Normal:
13a

27. Do Urinary AG
13b

28. Working out a Metabolic
Acidosis
◒ Calculate AG or AGc, if:
◒ Low:
14a

29. - Lab error: ↑Cl, ↓Na
- ↓anions (eg Alb)
- ↑cations: Ca, Mg, IgG, Li
14b

30. Causes of Normal Anion gap
metabolic acidosis ?
15a

31. 【U S E D C A R PAR T S】
✺ U ⇨ Ureterosigmoidostomy
✺ S ⇨ saline administration (in the face of renal dysfunction)
✺ E ⇨ Endocrine〘Addisons〙
✺ D ⇨ Diarrhea
✺ C ⇨ Carbonic anhydrase inhibitors
✺ A ⇨ Ammonium chloride
✺ R ⇨ Renal tubular acidosis
✺ PAR ⇨PARathyroid Adenoma
✺ T ⇨ Triamterene, amiloride
✺ S ⇨ Spironolactone
15b

32. Causes of High Anion gap
metabolic acidosis ?
16a

33. 【MUDPILES】
★ M-Methanol
★ U-Uremia (chronic renal failure)
★ D-Diabetic ketoacidosis
★ P-Propylene glycol,Paraldehyde
★ I-Infection, Iron, Isoniazid, Inborn errors of metabolism
★ L-Lactic acidosis
★ E-Ethylene glyco,Ethanol
★ S-Salicylates
16b

34. Low anion gap
17a

35. ✪ Increase in unmeasured cations
(Increased Li, K, Ca, Mg, and IgG)
✪ Decreased unmeasured anions
(Decreased PO4, albumin)
✪ Chloride over-estimation
(anion) (Hypercholesterolemia)
17b

36. [H+] =
18a

37. 24 X PC02/[HC03]
[H+] = 24 x (40/24) = 40
nEq/L
18b

38. Calculating Anion Gap
19a

39. Na - (CL + HC03) = 12 ±4
mEq/L (range = 8 to 16
mEq/L)
19b

40. Influence of Albumin on the
Anion Gap
20a

41. albumin is the major unmeasured anion
in plasma. This means that a decrease in
serum albumin will decrease the
AG,(e.g., a high AG metabolic acidosis
can present with a normal AG in the
presence of hypoalbuminemia).
20b

42. Albumin corrected anion gap
(AGc)
21a

43. AGc = AG + 0.25 × (40 -
albumin)
21b

44. What is the Gap-Gap ?
22a

45. In the presence of a high AG metabolic
acidosis, it is possible to detect another
metabolic acid-base disorder (a
normal AG metabolic acidosis or a
metabolic alkalosis)
by comparing the AG excess to the HC03
deficit
22b

46. Calculation of Gap-Gap ?
23a

47. AG Excess /HC03 Deficit =
(AG - 12)/(24 - HC03)
23b

48. explanation of Gap-Gap 1
24a

49. ☼ Mixed Metabolic Acidoses
↑AG metabolic acidosis the ↓in serum HC03 = the ↑in
AG, and the AG excess/HC03 deficit ratio is unity
(=1) when a hyperchloremic acidosis appears, the↓in
HCO3 is > ↑in the AG, and the ratio (AG
excess/HCO3 deficit) falls below unity (<1),( as 24-
HCO3 ➜ will be a bigger number dt ↓in HCO3).
∴Gap-Gap <1 indicates the coexistence of a ↑AG
metabolic acidosis + normal AG metabolic acidosis
24b

50. explanation of Gap-Gap 2
25a

51. ☼ Metabolic Acidosis and Alkalosis
When alkali is added in the presence of a ↑AG
metabolic acidosis, the ↓in HCO3 is < the ↑in
AG, and the gap-gap (AG excess /HCO3
deficit) is greater than unity (>1).
∴Gap-Gap > 1 indicates the coexistence of a
↑AG metabolic acidosis + normal AG
metabolic Alkalosis
25b

52. Precise explanation of Gap-
Gap
26a

53. 26b

54. Hyperlactaemia:
27a

55. a level from 2 mmols/l to 5
mmol/l.
27b

56. Severe Lactic Acidosis:
28a

57. - when levels are greater than 5 mmols/l
- As levels rise above 5mmols/l, the associated mortality
rate can become very high.
- The brief and often very high lactate levels that occur
with severe exercise or generalised convulsions (eg up to
30 mmol/l) are associated with an extremely low
mortality rate so the absolute lactate level (alone) is not a
good predictor of outcome unless the cause of the high
level is also considered.
28b

58. physiology of lactate
29a

59. Each day the body produce >
1500 mmols of lactate (about
20 mmols/kg/day) ➜ blood
stream a ➜ metabolised
mostly in the liver
29b

60. Relationship of lactate to
pyruvate
30a

61. - Lactate is produced from pyruvate in a
reaction catalysed by lactate
dehydrogenase
This reaction considered to be always in
an
equilibrium situation. Normally the ratio
of lactate to pyruvate in the cell is 10 to 1.
30b

62. Type A Lactic Acidosis :
31a

63. 【Inadequate Tissue Oxygen Delivery】
(i)Anaerobic muscular activity (eg sprinting,
generalised convulsions)
(ii)Tissue hypoperfusion (eg shock -septic,
cardiogenic or hypovolaemic; hypotension; cardiac
arrest; acute heart failure; regional hypoperfusion
esp mesenteric ischaemia)
(iii) Reduced tissue oxygen delivery or utilisation (eg
hypoxaemia, CO poisoning, severe anaemia)
31b

64. levels at which Type A Lactic
Acidosis occurs
32a

65. - If hypoxaemia is the only factor present, it
needs to be severe (eg paO2 < 35mmHg) to
ppt lactic acidosis dt protection afforded by
the body's compensatory
mechanisms which ↑tissue blood flow.
Similarly anaemia needs to be severe (eg
[Hb] <5g/dl) if present alone because tissue
blood flow is increased in compensation.
32b

66. Type B Lactic Acidosis
33a

67. no clinical evidence of
reduction in tissue oxygen
delivery.
33b

68. i) type B1 :
34a

69. Associated with underlying diseases
- LUKE leukaemia, lymphoma
- TIPS thiamine deficiency, infection,
pancreatitis, short bowel syndrome
- FAILURES hepatic, renal , diabetic
failures
34b

70. (ii) type B2:
35a

71. Assoc with drugs & toxins (eg metformin,
cyanide, beta-agonists, methanol,
adrenaline, salicylates, nitroprusside,
ethanol intoxication in chronic
alcoholics, anti-retroviral drugs,
paracetamol, fructose, sorbitol,
isoniazid)
35b

72. (iii) type B3:
36a

73. Assoc with inborn errors of
metabolism (eg congenital forms of
lactic acidosis with various enzyme
defects eg pyruvate dehydrogenase
deficiency)
36b

74. D-Lactic Acidosis
37a

75. D-lactate generated by bacterial fermentation in the
bowel can enter the systemic circulation and produce
a metabolic acidosis, often combined with a
metabolic encephalopathy, 【after extensive small
bowel resection or after jejunoileal bypass】 for
morbid obesity, can ↑anion gap, but the standard lab
assay for lactate measures only l-lactate. If d-lactic
acidosis is suspected, you must request a specific d-
lactate assay.
37b

76. The principles of management
of patients with lactic acidosis
are:
38a

77. (i) Diagnose and correct the underlying
condition (if possible)
(ii) Restore adequate tissue oxygen
delivery (esp restore adequate perfusion)
(iii) Ensure appropriate compensatory
hyperventilation where possible
38b

78. patients with severe acidosis (pH
<7.1), HD unstable, a trial infusion
of HCO3 can be attempted by
administering 1/2 of the estimated
bicarbonate deficit
39a

79. HCO3 deficit (mEq)=0.6 x wt
(kg) x (15-plasma HCO3)
39b

80. Use of bicarbonate in Lactic
Acidosis
40a

81. two RCT of bicarbonate in
lactic acidosis and shock
found no beneficial effects on
cardiac function or any other
effects of pH correction
40b

82. potential SEs of bicarbonate in
Lactic Acidosis
41a

83. (i) acute hypercapnia
(ii) ionised hypocalcaemia
(iii) intracellular acidosis due to CO2 crossing cell
membranes rapidly
(iv) acute intravascular overload
(v) bicarbonate ↑lactate production by ↑activity of
the rate limiting enzyme phosphofructokinase, ➜
shifts Hb-O2 dissociation curve, ↑O2 affinity of Hb
➜ ↓DO2 to tissue
41b

84. potential indications: of
bicarbonate in Lactic Acidosis
42a

85. ❂ PHTN in whom pulmonary VC may
↑by acidosis
❂ significant IHD in whom severe
acidosis ↓threshold for arrhythmia
❂ TCA or Aspirin overdose
❂ Consider slow bicarbonate infusion to
keep pH > 7.15
42b

86. Management of Lactic
Acidosis
43a

87. ☼ Lactate is a question not any
answer: exclude occult sepsis,
inadequate resuscitation, localised
ischaemia or CVS failure
☼ Stop NRTIs in HIV
43b

88. Volume deficits average in
DKA
44a

89. 50 to 100 mL/kg
44b

90. Uses of Ethylene glycol
45a

91. antifreeze and deicing
solutions
45b

92. Etiology of Hypokalemia with
alkalosis ?
46a

93. ❂ Vomiting
❂ Diuretics
❂ Cushing's syndrome
❂ Conn's syndrome (primary
hyperaldosteronism)
46b

94. Etiology of Hypokalemia with
acidosis ?
47a

95. ❂ Diarrhea
❂ RTA
❂ Acetazolamide
❂ Partially treated DKA
47b

96. Causes of Metabolic Alkalosis
?
48a

97. loss of hydrogen ions or a gain of bicarbonate 【CLEVER PD】
✵ Contraction (volume)
✵ Liquorice☯
✵ Endo: (Conn's/Cushing's/Bartter's)☯
✵ Vomiting/ aspiration (e.g.Peptic ulcer➜ pyloric stenosis, NG
suction)
✵ Excess Alkali☯
✵ Refeeding Alkalosis☯
✵ Post-hypercapnia
✵ Diuretics
☯ = Associated with High Urine Cl levels
48b

98. Mechanism of metabolic
alkalosis ?
49a

99. ✪ Activation of (RAAS) is a key factor
✪ Aldosterone ➜ reabsorption of Na+ in exchange
for H+ in the DCT
✪ ECF depletion (vomiting, diuretics) ➜ Na+ and
Cl- loss activation of RAAS➜ ↑ aldosterone levels
✪ In Hypokalemia, K+ shift from cells ➜ ECF.
Alkalosis is caused by shift of H+ into cells to
maintain neutrality
49b

100. Rx of metabolic alkalosis ?
50a

101. ❂ Stop precipitants
❂ Hydrate with NaCl (concept of saline responsive vs non-
responsive, urinary Cl <20 if responsive).
❂ +/- correct albumin
❂ Correct KCl (Cl most helpful, K disappears into depleted
intracellular space)
❂ More difficult where CCF, CRF, liver disease ➜ ↑aldosteronism
in presence of ↑ECF. Prefer K
❂ Acetazolamide: increase urinary SID. Carbonic Anhydrase
inhibitor. 250 - 500 mg bd
❂ Dialysis
50b