THIS IS A SEMINA BASED ON ACID BASE ANALYSIS AND DISORDERS BOTH .

1. ACID BASE DISORDERS
PRESENTER : DR. RAJESH MUNIGIAL
MODERATOR : DR SAGAR S M
HOD : DR ARUNKUMAR AJJAPPA
SSIMS & RC , DAVANGERE , KARNATAKA

2. • History
• Definitions
• Buffers
• Acidosis
• Alkalosis
• Analysis of ABG
• Case scenarios

3. HISTORY
• In early 1831 o’Shaugnessy identified loss of
carbonate of soda from blood in patients dying of
cholera.
• This led directly to crystalloid replacement
therapy for hypovolemic shock
• In 1909 J.Henderson coined the term acid base
balance.
• Henderson’s work was later refined by
hesselbasch in 1916.

4. DEFINITIONS
• Acid : substance that donates proton .
• Base : substance that accepts proton.
• Strong acid : readily and almost irreversibly
gives proton.
• Strong base : avidly binds H+

5. • PH : signifies free hydrogen ion concentration,
inversely related to H+ ion concentration.
• BUFFER : A buffer is a solution that contains a
weak acid and its conjugate base or a weak
base and its conjugate acid ( conjugate pairs ).
Buffers minimize any change in [H + ] by readily
accepting or giving up hydrogen ions

7. Henderson-Hasselbalch Equation:
pH = pK + log 10 [(HCO3)/(H2CO3 + CO2)]
(at normal) = 6.1 + log 10 (24/pCO2 x .03)
= 6.1 + log (24/1.2) = 6.1 + log 20 = 6.1 + 1.3
= 7.4
• If the ratio of bicarbonate to pCO2 is doubled or
reduced by half, the pH changes by 0.3

8. BASE EXCESS ! BASE DEFICIT !
• Base excess is the amount of acid or base
(expressed in mEq/L) that must be added for
blood pH to return to 7.40 and Pa co 2 to return
to 40 mm Hg at full O 2 saturation and 37°C.
Base excess – alkalosis
Base deficit – acidosis

9. STRONG ION DIFFERENCE
• It is the difference between the sum of strong
cations and srong anions .

10. BODY BUFFERS

11. • Physiological responses to changes in [H + ] are
characterized by three phases:
• (1) immediate chemical buffering,
• (2) respiratory compensation (whenever possible),
and
• (3) a slower but more effective renal compensatory
response that may nearly normalize arterial pH
even if the pathological process remains present.
• Disorders in any of these systems leads to
alterations in blood pH

12. BICARBONATE BUFFER
• The bicarbonate system is, however, important for two
reasons:
• (1) bicarbonate (HCO 3 − ) is present in relatively high
concentrations in extracellular fluid, and
• (2) more importantly—Pa co 2 and plasma [HCO 3 − ] are
closely regulated by the lungs and the kidneys, respectively

13. RESPIRATORY COMPENSATION
• Changes in alveolar ventilation responsible for
the respiratory compensation of Paco2 are
mediated by chemoreceptors within the
brainstem .
• These receptors respond to changes in
cerebrospinal spinal fluid pH.
• Minute ventilation increases 1–4 L/min for
every (acute) 1 mm Hg increase in Paco2 .

14. • During metabolic acidosis: Decreases in
arterial blood pH stimulate medullary
respiratory centers. The resulting increase in
alveolar ventilation lowers Paco2 and tends to
restore arterial pH toward normal
• During metabolic alkalosis :Increases in arterial
blood pH depress respiratory centers. The
resulting alveolar hypoventilation tends to
elevate Paco2 and restore arterial pH toward
normal.

15. RENAL COMPENSATION
• DURING ACIDOSIS
The renal response to acidemia is 3-fold:
• (1) increased reabsorption of the filtered HCO 3 − ,
• (2) increased excretion of titratable acids, and
• (3) increased production of ammonia.

16. INCREASE REABSORPTION OF BICARBONATE

17. INCREASE EXCRETION OF TITRABLE ACIDS

18. INCREASE FORMATION OF AMMONIA

19. Regulation of acid base balance

20. ABG INTEPRETATION
• Mainly 4 approaches
1. Boston approach- Henderson-Hasselbalch
equation
2. Copenhegan approach (Base excess)-siggard
Anderson formula
3. Anion gap based approach- widely used at
bedside
4. Stewart Fencl strong ion difference approach

21. STEPWISE ABG ANALYSIS
1. pH: Is acidemia or alkalemia present?
2. Examine Paco2 : Is the change in Pa co 2 consistent with a
respiratory component?
3. If the change in Pa co2 does not explain the change in arterial pH,
does the change in [HCO 3 − ] indicate a metabolic component?
4. Make a tentative diagnosis
5. If the compensatory response is more or less than expected, by defi
nition, a mixed acid–base disorder exist
6. Calculate the plasma anion gap in the case of metabolic acidosis.
7. . Measure urinary chloride concentration in the case of metabolic
alkalosis.

22. Normal values
Measured : Ph , Pao2, Pco2
Calculated : Hco3 , So2

23. ACID BASE DISORDERS
• Simple/Primary acid–base disorders : when
compensation is appropriate
• A respiratory change is called “acute” or
“chronic” depending on whether a secondary
change in the bicarbonate concentration has
occurred .
• Mixed acid–base disorders – When compensation
is inappropriate i.e. the secondary response differs
from that which would be expected

24. PRIMARY ACID BASE DISORDERS

25. ACIDOSIS
PHYSIOLOGICAL CHANGES (PH <7.2)
• Sympathodrenal activation
• Myocardial depression – contractility reduced
• Smooth muscle depression : reduced PVR
• Tissue hypoxia
• Decreased responsiveness to endogenous and exogenous
catecholamines
• Reduced threshold for arrhythmias
• CNS depression with respiratory acidosis (co2 narcosis)

26. RESPIRATORY ACIDOSIS
• CNS DEPRESSION
• NEUROMUSCULAR
• DISORDERS
• CHEST WALL
ABNOMALITES
• PLEURAL
ABNORMALITIES
• AIRWAY OBSTRUCTION
• PARENCHYMAL LUG
DISEASES
• THYROID STORM
• LARGE CALORIC FOODS
• INTENSIVE SHIVEIRNG
• MALIGNANT
HYERTHERMIA

28. TREATMENT
• Reverse the imbalance between CO2 production and
alveolar ventilation
• By increasing alveolar ventilation
• bronchodilation, reversal of narcosis, or improving lung
compliance (diuresis)
• Severe acidosis (pH <7.20), CO2 narcosis and respiratory
muscle fatigue are indications for mechanical ventilation.
• Intravenous NaHCO 3 is rarely necessary, unless Hco3 is
<6

29. • Case scenario: Following sleeping pill ingestion, patient
presented in drowsy state with sluggish respiration
with rate of 4/min
– pH 7.1
– HCO3 28 mEq/l
– PaCO2 80 mmHg
– PaO2 42 mmHg
• Which acid-base disorder is present?
• ACUTE RESPIRATORY ACIDOSIS

30. METABOLIC ACIDOSIS
• primary decrease in [HCO 3 − ]
• (1) consumption of HCO 3 − by a strong
nonvolatile acid,
• (2) renal or gastrointestinal wasting of
bicarbonate, or
• (3) rapid dilution of the extracellular fluid
compartment with a bicarbonate-free fluid.

31. HIGH ANION GAP METABOLIC
ACIDOSIS (HAGMA)
• Failure to Excrete
Endogenous Nonvolatile
Acids
• . Increased Endogenous
Nonvolatile Acid
Production
• Ingestion of Exogenous
Nonvolatile Acids

33. • DKA : FLUID THERAPY
• LACTIC ACIDOSIS : OXYGENATION AND
PERFUSION

34. NAGMA
• Increased
Gastrointestinal Loss of
HCO3
• Increased Renal Loss of
HCO3
• Other Causes of
Hyperchloremic Acidosis
: A dilutional
hyperchloremic acidosis

36. Test Case # 2
23 year old AIDS patient c/o weakness and pr
olonged severe diarrhea. He appears mark
edly dehydrated.
pH 7.25 pCO2 25 pO2 110 HCO3 11
151 129 60
2.0 12 2.0

37. Test Case # 2
• Anion Gap= 151-(129 + 11)= 11 (normal)
• The patient is Acidemic (pH 7.25)
• Respiratory compensation normal?
1.5 (HCO3) + 8 plus or minus 2
1.5 (11) + 8= 24.5 (compare with 25)
Dx: Uncomplicated Non-AG Metabolic Aci
dosis

38. Treatment : when to give bicarb?
• Ph < 7.2
HCO3 level < 6
– Drawback
Bicarbonate moeity of NAHCO3 provides buffer
for hydrogen ions , generating co2 ….increasing
alveolar ventilatioon.
– If pCO2 > 1.5 (HCO3) + 8
• then ventilate better

39. • The amount of NaHCO 3 given is derived from the
base excess
• ABG IS MUST TO CHECK OVERSHOT ALKALOSIS
AND SODIUM OVERLOAD
• Raising arterial pH to >7.25 is usually sufficient to
overcome the adverse physiological effects of the
acidemia.
• Profound or refractory acidemia may require acute
hemodialysis with a bicarbonate dialysate.

40. Is the compensation adequate
• Acute metabolic acidosis:
– pCO2 = 1.5 x HCO3 + 8 (+/- 2)
–hyperventilation
• Acute metabolic alkalosis:
– pCO2 = 0.9 x HCO3 + 15
–hypoventilation

41. Metabolic acidosis - Example
18 y.o. presents in DKA
ABG: pH 7.00 pCO2 25 Bicarbonate 6
If Pure metabolic acidosis, then pCO2=(1.5)(6) + 8=
17
metabolic acidosis with respiratory acidosis:
--chronic lung disease
-fatigue from compensation or hypokalemia or hy
pophosphatemia
-This patient is at risk for tiring out and becoming
extremely acidotic.

42. ANESTHETIC CONSIDERATIONS IN
PATIENTS WITH ACIDOSIS
• Acidemia can potentiate the depressant effects of most sedatives and
anesthetic agents on the central nervous and circulatory systems.
• Increased sedation and depression of airway reflexes may predispose
to pulmonary aspiration.
• The circulatory depressant effects of both volatile and intravenous
anesthetics can also be exaggerated.
• Halothane is more arrhythmogenic in the presence of acidosis.
• Succinylcholine should generally be avoided in acidotic patients with
hyperkalemia

43. ALKALOSIS
PHYSIOLOGICAL EFFECTS OF ALKALOSIS :
• ODC shift to left
• Hypokalemia
• Hypocalcemia
• Coronary vasospasm
• Bronchoconstriction

44. RESPIATORY ALKALOSIS
• Respiratory alkalosis is defined as a primary
decrease in Paco2 .
• The mechanism is usually an inappropriate
increase in alveolar ventilation relative to CO2
production

45. CAUSES
• Central stimulation
• Pain
• Anxiety
• Ischemia Stroke
• Tumour
• Infection
• Fever
• Drug-induced Salicylates
Progesterone (pregnancy)
• Peripheral stimulation
• Hypoxemia
• High altitude
• Pulmonary disease
• Congestive heart failure
• Non cardiogenic pulmonary
edema
• Asthma
• Pulmonary embolism
• Severe anemia
• Ventilator induced
• sepsis

47. TREATMENT
• Correction of the underlying process
• For severe alkalosis (ph>7.6), intravenous
hydrochloric acid , arginine chloride,
ammonium chloride

48. Respiratory alkalosis - example
18 y.o. with several days of SOB due to
pneumonia:
pH 7.43 pCO2 25 Bicarbonate 16
• Chronic hypocapnia

49. METABOLIC ALKALOSIS
Metabolic alkalosis is defined as a primary
increase in plasma [HCO3−].
(1) Those associated with NaCl deficiency and
extracellular fluid depletion, often described as
chloride sensitive, and
(2) Those associated with enhanced
mineralocorticoid activity, commonly referred to
as chloride-resistant

50. Chloride-Sensitive Metabolic Alkalosis
Depletion of extracellular fluid causes the renal
tubules to avidly reabsorb Na + .
Because not enough Cl − is available to
accompany all of the Na + ions reabsorbed,
increased H + secretion must take place to
maintain electroneutrality.
In effect, HCO3- ions that might otherwise have
been excreted are reabsorbed, resulting in
metabolic alkalosis

51. Causes
• Chloride-sensitive
Gastrointestinal
• Vomiting
• Gastric drainage
Renal
• Diuretics
Sweat
• Cystic fibrosis
• Chloride-resistant
• Increased
mineralocorticoid activity
• Primary
hyperaldosteronism
• Edematous disorders
(secondary
hyperaldosteronism)
• Cushing’s syndrome
• Severe hypokalemia

52. Miscellaneous
• Massive blood transfusion
• Acetate-containing colloid solutions
• Alkaline administration with renal insufficiency
Alkali therapy
Combined antacid and cation-exchange resin therapy
Hypercalcemia
Milk-alkali syndrome
Bone metastases
Sodium penicillins
Glucose feeding after starvation

53. • ABG of a patient with CHF on furosemide
– pH 7.48
– HCO3 34 mEq/l
– PaCO2 48 mmHg
• Which acid-base disorder is present?
PRIMARY METABOLIC ALKALOSIS

55. Treatment
• IV NACL
• IV KCL
• H2 BLOCKER THERAPY when excessive gastric
fluid loss
• Acetazolamide in edematous patients.

56. ANESTHETIC IMPICATIONS IN ALKALOSIS
• Prolong duration of opioid induced respiratory
depression
• Decreased cerebral blood flow: cerebral
ischaemia , particularly during hypotension.
• Arythmmias
• Potentiation of NMB

58. ABG Examples of Alkalosis
Metabolic, Resp., and Mixed
Normal Simple
Metabolic
Resp. Mixed
Severe
Mixed
Mild
Na 140 139 139 139 139
K 4 3 3.5 2.8 3.0
Cl 105 89 107 92 92
HCO3 24 35 20 32 32
AG 11 15 12 17 8
pCO2 40 47 25 30 39
pH 7.40 7.49 7.54 7.65 7.53

59. Mixed Respiratory acidosis and metabolic alkalosis
Acute resp
acidosis
Simple
acute resp
acidosis
Simple
Chronic
resp
acidosis
Simple
metabolic
alkalosis
Mixed resp
acid and
met
alkalosis
Na 140 140 140 140 140
K 4.0 4.5 4.5 3.0 3.5
Cl 105 105 94 92 86
HCO3 25 27 36 36 42
AG 10 8 10 12 12
pCO2 40 70 70 48 70
pH 7.40 7.13 7.33 7.49 7.40

60. MIXED ACID BASE DISORDERS
• If the Arterial pH is relatively normal and the
PCO2 and/or HCO3 are abnormal, one can
assume that a mixed abnormality is present.

61. Mixed Acid-Base Disorders:
• Is the degree of respiratory compensation for
a metabolic acidosis too much or too little?
pCO2 lower than calculated
Superimposed Resp. Alk.
pCO2 higher than calculated
Superimposed Resp. Acidosis
Salicylate poisoning
Sepsis
Increase ICP + Shock
Sedative OD + Shock
Ventilatory Impairment
Remember: 1.5 x Bicarb + 8

62. WHAT IS DELTA GAP

63. Delta ratio
Delta ratio = AG – 12 / 25 – HCO3
< 0.4 due to a pure NAGMA
0.4 – 0.8 due to a mixed NAGMA + HAGMA
0.8 – 2.0 due to a pure HAGMA
>2.0 due to a mixed HAGMA + metabolic
alkalosis

65. Mixed Acid-Base: Example 1
27 y.o man with polyuria and polydipsia for one
week, and intractable vomiting for 4 days. Tod
ay he is critically ill with a temp. of 104 F.
pH 7.50 pCO2 26 pO2 100
150 100 50
3.8 20 1.8
650
AG= 30
Bicarb=24-20= 4
AG=30-12= 18
Na/Cl > 1.4

66. • Is the magnitude of the increase in AG equal
to the magnitude of the decrease in serum
bicarb?
Vomiting + DKA + AKA
AG Change >> Bicarb Change (chloride is r
elatively low)
Superimposed Met. Alkalosis

67. • Repiratory alkalosis
• Anion Gap Metabolic Acidosis
• Concurrent Metabolic Alkalosis

68. Mixed Acid-Base: Example 2
25 y.o. woman admitted 6 hours ago with severe
DKA. Her initial pH was 6.9 with a pCO2 of 10,
and serum bicarb of 2.4. After insulin and NS
hydration, her lab values returned as follows…
140 110
10
AG= 20
Bicarb= 24-10= 14
AG= 20-12= 8
pH 7.25 pCO2 23

69. • Anion Gap Metabolic Acidosis
• Hyperchloremic Metabolic Acidosis.
• Respiratory alkalosis

70. CASE 1
An 80 year old man has been confused and c/o
SOB for one week. He also has a hearing problem
and has seen 3 ENT docs in the past month.
Family denies medications.
pH 7.53 pCO2 15 pO2 80 HCO3 12
140 108
3.0 13
120 Diagnosis?
AG = 140 - 121 = 19

71. CASE 1
Anion Gap= 140-(108+13)= 19, Δ AG = 7
Δ Bicarb= 24-13= 11
pCO2= 1.5 (12) + 8= 26 (compared/w 15)
Patient is Alkalemic (pH= 7.53) indicating a Su
perimposed Respiratory Alkalosis
Dx: Metabolic Acidosis and Respiratory Alkalosis

72. Case 3
45 y.o. alcoholic man has been vomiting for 3 da
ys. Vitals: BP 100/70, P 110. Intern administe
red Valium 30 mg for tremulousness.
pH 7.30 pCO2 40
145 96
3.0 19
Serum Ketones +
Diagnosis?

73. Case 3
• Anion Gap= 145- (96 + 19)= 30
• Δ Bicarb= 24-19= 5
• Δ AG= 30-12= 18
• Change in AG >> Change in Bicarb
• Superimposed Metabolic Alkalosis
• Respiratory compensation?
1.5 x (19) + 8= 36 (compared with pCO2=40)

74. Case 3
• Anion Gap Metabolic Acidosis (AKA)
• Metabolic Alkalosis (Persistent Vomiting)
• Mild Respiratory Acidosis (Oversedation)

75. Case 5
33 y.o. woman c/o leg pain and SOB which sta
rted suddenly yesterday.
pH 7.45 pCO2 20 pO2 80
140 116
4.0 14 Diagnosis?

76. Case 5
• Anion gap= 140- (116 + 14)= 10
Dx: Respiratory Alkalosis (PE) with
Metabolic acidosis

77. Summary of Expected Compensation and
Other Equations
• pH = pKa + log HCO3/H2CO3
• [H+] = 24 x pCO2/HCO3
• for each doubling of [H+], pH drops by 3
• In acute respiratory alkalosis, if mild, the pH changes by 0.
08 for every 10 mmHg change in pCO2

78. Expected Compensation (cont.)
• pure stable met. acidosis: pCO2 = 1.5 x HCO3 + 8 =-- 2
• pure stable met. alkalosis: pCO2 = .9 (HCO3) + 15
more commonly pCO2 = .9(HCO3) + 9

79. Summary of important points
• Doubling or halving the pCO2:HCO3 ratio changes pH by 0.3
• Bicarbonate therapy based on bicarb ≤ 6,
• Low pH with bicarb > 6 needs Rx with ventilation
• Know the anion gap and MUDPILES
• Anion Gap > 18 is metabolic acidosis
– no matter what the pH, pCO2, or bicarb.
• Winter’s formula: pCO2 should be = 1.5 x HCO3 + 8

80. THANK YOU !!