presentation i did in my 2 nd year of post graduation

1. ACID BASE DISORDERS
By Dr Arighna Mukherjee
Moderator Dr D. Mukherjee
Professor NRSMCH
Dept of Anaesthesiology

2. INTRODUCTION
• Acid base disorders is one of the most common disorders affecting 90
percent patients admitted to ICU.Therefore a structured approach to the
identification of acid base disorders is required for quick identification and
management of these disorders
• The blood gas machines in most labs measure the pH, pco2 and the pO2.
• The [HCO3-] and base difference is calculated using the Henderson-
HasselbacH equation

3. DEFINITIONS
• An acid is a molecule that releases hydrogen ions in solution
• A base is a molecule that accepts hydrogen ion in solution
• A buffer is a substance that reversibly binds hydrogen ion in solution

4. NORMAL BLOOD GAS VALUES
• Normal range of pH, pCO2 and HCO3 are as follows
• pH=7.35-7.45
• pCO2=36-44 mm Hg
• HCO3=22-26 mEq/lMeasurement Arterial Mixed venous Venous
pH 7.35-7.45 7.31-7.41 7.31-7.41
pO2{mm Hg} 80-100 35-40 30-50
pCO2{mm Hg} 36-44 41-51 40-52
O2 saturation >95 60-80 60-85
HCO3 meq/l 22-26 22-26 22-28
Base deficit -2 to +2 -2 to +2 -2 to +2

5. HYDROGEN ION CONCENTRATION
AND P H
• pH means the power of hydrogen and is a logarithmic function of [H+]
• pH =- log[H+]
• The physiological range of pH and corresponding [H+] is shown below

6. • Features of pH
• It is a dimensionless number with no chemical or physiological relevance
• Varies in opposite direction to [H+]
• Changes in pH are not linearly related to changes in [H +] as seen from previous
table
• Hydrogen ion as trace element
• [H+] is expressed as neq/l whereas principal extracellular elements sodium and
chloride is expressed in meq/l which is a million times less, therefore changes in[H+]
are just one of several physicochemical changes taking place and thus explains why
same degree of acidosis is more life threatening in lactic acidosis than in
ketoacidosis

7. CLASSIFICATION OF ACID BASE DISORDERS
• The relationship between partial pressure of CO2 and [HCO3-]in the body is as
follows:[H+]=24*[PCO2/HCO3-]
• The PCO2/HCO3 ratio identifies the primary acid base disorder as shown below
• Secondary responses should not be called compensatory responses because they do not completely correct
the change in[H+] produced by the primary disorder
The picture can't be displayed.

8. RESPONSES TO METABOLIC DISORDERS
• Metabolic acidosis: Increased minute ventilation and
subsequent decrease in pCO2
• Appears in 30-120 minutes and takes 12-24 hours to
complete
Metabolic alkalosis :Decreased mv and subsequent
increased pCO2
Not as vigorous as metabolic acidosis because the peripheral
chemoreceptors are easier to stimulate than inhibit as they
are not very active normally

9. RESPONSES TO RESPIRATORY DISORDERS
• Changes occur in kidney via HCO3 reabsorption in proximal tubules to
produce appropriate change
• Slow response takes 2-3 days to complete hence divided into acute or chronic
disorders

10. • Predictive equations for evaluating secondary responses to primary acid base disorders
The picture can't be displayed.

11. STEPWISE APPROACH TO ACID BASE ANALYSIS
The picture can't be displayed.

12. The picture can't be displayed.
The picture can't be displayed.

13. The picture can't be displayed.

14. • Example - PaCO2=23,pH =7.54,HCO3-=31
The PaCO2 and pH are in opposite directions indicating a primary respiratory
disorder
and pH is alkaline indicating a primary respiratory alkalosis.
HCO3 is abnormal indicating a chronic respiratory disorder, using relevant
equations Change in PaCO2= 17 mmHg expected HCO3-=24+(.4*17) =31 mm
Hg rounded off
Therefore HCO3- is as expected
If HCO3- <31 it would indicate chronic respiratory alkalosis with incomplete
renal response
If > 31 would indicate a secondary metabolic acidosis

15. ANION GAP
• It is the difference between unmeasured anions and unmeasured cations in blood
• Generally measured ions are Na+,Cl-and HCO3-
• Therefore AG=UA-UC=Na-(Cl+HCO3)
• Normal range 8-16 meq/l
The picture can't be displayed.

16. INFLUENCE OF ALBUMIN
• Albumin is the principal unmeasured anion and the principal determinant of
anion gap
• It is a weak acid that contributes about 3 meq/l to the AG for each 1g/dl of
albumin in plasma at normal pH
• A low albumin could in plasma will lower the AG and could mask the presence
of an unmeasured anion eg lactate that is contributing to metabolic acidosis
hence corrected anion gap is proposed as follows
• AGc =AG + 2.5*(4.5-[albumin in g/dl])

17. CLASSIFICATION OF METABOLIC ACIDOSIS ACCORDING
TO ANION GAP
The picture can't be displayed.

18. GAP-GAP RATIO
• It is the ratio between AG excess (difference between measured and normal
AG) to the HCO3 deficit (difference between measured and normal HCO3 in
plasma)
• AG excess / HCO3 deficit =(AG-12)/(24-HCO3) considering AG =12 meq/l
and HCO3 24 meq/l normally in plasma
• In the presence of high anion gap metabolic acidosis a ratio <1 indicates the
coexistence of normal anion gap metabolic acidosis
• A ratio >1 indicates the coexistence of a metabolic alkalosis similarly

19. The picture can't be displayed.

20. BASE DEFICIT EXCESS APPROACH
• It is the amount of strong acid or base required to return the pH to 7.4
assuming pCO2 is constant at at 40 mm Hg and temperature is 37 degree
celsius
• It employs the buffer base concept which is equal to [Na+]+[K+]-[Cl-]and
mainly includes bicarbonate, albumin, phosphate and haemoglobin
• BDE=(HCO3-24.4+[2.3*Hb+7.7]*[pH -7.4])*(1-.023*Hb)
• In vivo it is converter into following equation considering Hb as 5g/dl known
as standard base excess SBE=.93*(HCO3-24.4+14.83)*[pH -7.4]
• Considering all these following conclusion’s can be drawn

21. The picture can't be displayed.

22. The picture can't be displayed.

23. STRONG ION DIFFERENCE
• It is the difference in the summed concentration of strong readily dissociated
cations and anions in extracellular fluid expressed as follows
• SID=(Na+K+Mg+Ca)-(Cl –Lactate) in physiological pH
• To maintain electrical neutrality SID +[H+]+[OH-]=0.
• Since [OH-] has negligible influence at physiological pH
• SID =[H+].
• If pH is used we see that SID and pH Change in the same direction
• Increase in lactate will decrease the SID and this will decrease plasma pH

24. RESPIRATORY ACIDOSIS
• Occurs in the presence of an acute increase in PaCO2 associated with
respiratory failure
• Clinically signs are cyanosis, vasodilation and narcosis due to CO2 retention
• Recent studies suggest‘permissive hypercapnia’for acute respiratory failure is
well tolerated and may indeed be beneficial
• According to patients breathing pattern it may be as follows

26. RESPIRATORY ALKALOSIS
• Occurs when an acute decrease in PaCO2 results from hyperventilation in
response to anxiety or pain, central respiratory stimulation (as occurs in
early salicylate poisoning) or excessive artificial ventilation
• Presents with signs and symptoms of vasoconstriction :light headedness, visual
disturbances, dizziness and perhaps hypocalcaemia from increased binding of
calcium to albumin
• Hypocalcaemia is caused by increased available negative charge on albumin
in alkaline states
• It frequently coexists with metabolic acidosis. Example a multitrauma
patient in whom massive blood loss leads to lactic acidosis and a flail chest
causes respiratory acidosis

27. LACTIC ACIDOSIS
• Occurs when production of lactate is greater than livers capacity to clear it
• Formed physiologically as a product of glucose metabolism from pyruvate via
lactate dehydrogenase
• Normal lactate :pyruvate ratio is <20:1
• Increases in vigorous exercise or following exogenous infusion ( epinephrine
or norepinephrine)
• It is of 2 types :Type A due to global inadequate oxygen delivery eg-
hypovolaemic or hemorrhagic shock
• Type B:normal oxygen delivery and tissue perfusion but excess circulating
catecholamines eg-trauma, sepsis, cyanide poisoning

28. APPROACH TO LACTIC ACIDOSIS

29. DIABETIC KETOACIDOSIS
• Usually seen in insulin dependent diabetic patients
• Definition according to American Diabetes Association is
• Glucose> 250mg /dl, plasma HCO3 <18 mEq/ L, plasma pH < or = 7.30 an
elevated anion gap and evidence of ketones in blood or urine however
exceptions can be seen

30. MANAGEMENT

31. ALCOHOLIC KETOACIDOSIS
• Appears 1-3 days after a period of heavy binge drinking.
• Mechanisms involved are reduced nutrient intake increasing ketone
production, hepatic oxidation of ethanol (which enhances β hydroxybutyrate
production) and dehydration (which impairs ketone excretion).
• Clinical features :nausea vomiting and abdominal pain, electrolyte
abnormalities.
• Mixed acid base abnormalities are common like lactic acidosis or metabolic
alkalosis as seen in protracted vomiting.

32. • Diagnosis :Suggested by the clinical setting i. e. after a period of binge drinking, elevated anion gap, presence of
ketones in blood and urine.
• Nitroprusside reaction maybe negative as oxidation of ethanol generates NADH which converts acetoacetate
to β hydroxybutyrate and results in low concentration of acetoacetate in blood and urine.
• MANAGEMENT :Thiamine supplementation followed by infusion of dextrose containing saline solutions.

33. METABOLIC ALKALOSES
• Most common acid base disorder in hospitalised patients
• Defined as an increase in bicarbonate in ECF>26 meq/l
• Once developed can sustain itself by increase in HCO3 reabsorption and
decrease in HCO3 secretion
• PATHOGENESIS: 5 main processes 1)bicarbonate reabsorption
• 2)bicarbonate secretion
• 3)chloride depletion
. 4) hypokalaemia .
5) aldosteronism.

35. CLINICAL MANIFESTATIONS
• Neurologic :depressed consciousness, generalized seizures, paraesthesias and
carpopedal spasms. However it is more seen in respiratory alkalosis and
metabolic alkaloses due to baking soda ingestion
• Hypoventilation :Given by the equation ΔPaCO2=.7*ΔHCO3
• Oxygen-Hb dissociation curve:shifts to the left and there is decreased
tendency of Hb to release O2 in tissues… Mainly theoretical.

36. TYPES

37. MANAGEMENT
• Saline responsive :The picture can't be displayed.

38. • Saline resistant or in edematous states:
• 1)KCL-As hypokalaemia is a contributing factor.
• Diuretic induced hypokalaemia can be resistant to potassium replacement if there is concurrent
magnesium depletion therefore plasma magnesium should also be checked before K + replacement is initiated.
• 2)Acetazolamide
• 3)HCL infusion :Reserved for extreme cases, very risky, major side effect is severe tissue necrosis

39. THANKYOU