This patient appears to be in hemorrhagic shock from his injuries sustained in the motor vehicle crash. His thready pulse and low blood pressure indicate he has lost a significant amount of blood and is hypovolemic. Immediate treatment should focus on resuscitation with intravenous fluids and blood products to restore circulating volume and improve end organ perfusion. His condition requires prompt intervention to prevent further hemodynamic instability and potential organ dysfunction or failure.

1. Acid Base Balance
Presenter : DR B Sharath Chandra
Kumar
Post Graduate
Anaesthesiology
Moderator : DR B Syama Sundara
Rao,
Prof, MD;DA

2. History
 The concept of acids and bases is relatively new
 In the early part of the 20th century, it was known that in
critical illness the CO2 content of the blood decreased.
 In 1831, O'Shaughnessy identified loss of “carbonate of
soda” from the blood as a fundamental disturbance in
patients dying of cholera.
 We now know that the loss of bicarbonate was related to
hyperventilation and buffering of free hydrogen ions in
dysmetabolic states

3.  1903, the revolutionary theory of Arrhenius
 Arrhenius acid is any substance that delivers a hydrogen ion
into the solution. A base is any substance that delivers a
hydroxyl ion into the solution
 In 1909, Henderson coined the term acid-base balance
 that later was refined by Hasselbalch in 1916
 In 1923, Brønsted and Lowry proposed an expanded theory
of acids and bases. They defined acids as proton donors and
bases as proton acceptors. All Arrhenius acids and bases
were also Brønsted-Lowry acids and bases
Acid: H+ donor
Base: H+ acceptor

4. Introduction
 H+ has variations in local production & clearance
 Deviations from normal range can cause marked alterations
in protein structure & function, enzyme activity, & cellular
functions
 H+ produced in large amounts from oxidation of
carbohydrates
 H+ concentration regulated to maintain a
pH of 7.35 to 7.45
 pH = - log[H+] nmol/L
pH=-log [H+]

5. Henderson-Hasselbalch equation

 pKa = the ionisation exponent of the
acid
pH = pKa + log [salt/base] / [acid]

6. Why [H+], why not Na+
 Because H+ conc. are low relative to other cations
 At normal pH, H+ conc = 40 nmol/L, where as
Na + conc= 140000000 nmol/L
 Osmotic effect of H+ is negligeble when compared to
Na+
 a decrease of pH by 0.3= doubling of H+
 a increase of pH by 1.0= 10 fold ↓ of H+

7. What is p in pH
 p means –ve logarithm
 E.g. , pH= -log H+, pKa= -log Ka

8. Hydrogen ions ( nmol/L ) pH
100 7.0
80 7.1
63 7.2
50 7.3
42 7.38
40 7.4
38 7.42
32 7.5
25 7.6
20 7.7

9. Production of acids in human body
1. Volatile :
 As a metabolic byproduct during carbohydrate
metabolism in the form of carbon dioxide.
 200ml/min or 288L/day.
 Acid production 12960 meq/d.
 the gas is eliminated via lung, there fore called as volatile
2. Nonvolatile :
 usually during protein degradation
e.g. sulfuric acid,HCl, phosphoric acid
 Accounts for 70mmol/d
 Lactic acid is often neglected to calculate as it is further
degraded to CO2 in liver.

10. Acid base homeostasis
 Requires both elimination/production of acid or
recovery of base
 The H+ conc compatible with life can vary 10 fold i.e.
from 16-160 nmol/L (pH 6.8-7.8 )

11. Regulation of hydrogen ions
1.Buffer system
a. bicarbonate buffer
b. hemoglobin buffer
c. protein buffer
d. phosphate buffer
2.Ventilatory response
3.Renal response

12. 1. Buffer system
 Definition :A buffer is defined as a solution or
reagent that resists a change in pH with the addition of
either an acid or a base
 It is a mixture of a weak acid or weak base and its salts
that resists changes in pH when a strong acid or base is
added to the solution.
 Effectiveness of a buffer depends on
◦ the pK of the buffering system and
◦ the pH of the environment in which it is placed

13. 1a. Carbonic acid- Bicarbonate buffer
 Major buffer of metabolic acid/base in the plasma
 Does not function to buffer respiratory acid. pKa- 6.1
 A strong acid like HCl if increases
 A strong base like NaOH if increases
 If Co2 is added to this system H+ & HCO3- are equally
produced
HCl+NaHCO3 -------> NaCl+H2CO3-----NaCl+H2O+CO2
NaOH+H2CO3--- NaHCO3+H2O
CO2+H2O+NaHCO3---- H+ + HCO3- + NaHCO3

14. The effectiveness of the buffer system is
based on -
1) Its present in high concentration (> 20 mmol/L)
2) The lungs can dispose of readily or retain CO2 (as
changes in CO2 modify the ventilation rate)
3) The bicarconate (HCO3
-) can be readily disposed
of or reclaimed by the kidneys.

15. 1b. Hemoglobin buffer
 Predominant non carbonic buffer in ECF. pKa-6.8
 Buffers both resp & metabolic acids
 Buffers CO2 by 2 methods
- allows CO2 to combine directly with A.A to form
carbamino compound. Accounts for 15-25% of total
CO2 transport
- CO2 is catalyzed in RBC to H+ & HCO3- by carbonic
anhydrase enzyme. H+ buffered by Hb to HHb. The free
HCO3 diffuses into plasma in exchange to Cl-, known as
chloride shift

17. 1c. Protein buffers
 Play as buffer due to large total concentration & some
have free acid/basic radicals
 AA having free acid radicals in the form of COOH can
buffer alkali by liberating H+
 AA having free base radicals in the form of NH3OH can
buffer acid
COOH+OH- ----- COO- + H2O
NH3OH + H+ ----- NH3+ + H2O

18. 1d.Phosphate buffer
 Largest inorganic buffer
 Predominantly intracellular
 pKa 6.8
 For strong acid
 For strong base
HCl + Na2HPO4 --- NaH2PO4 =NaCl
NaOH + NaH2PO4 --- Na2HPO4 = H2O

19. 2. Ventilatory response
 Limited to CO2 excretion by lung
 Regulated by medullary centres sensitive primarily to H+
 Also serves to compensate metabolic acid-base
disturbances
 A decrease in HCO3- decreases pH, increases ventilation
and vice-versa

20. 3. Renal Response
 Mainly to recover HCO3- and eliminate H+
 Bicarbonate filtered by kidney is 4320 mmol/day
 HCO3- is absorbed into the interstitium with the help of
carbonic anhydrase
 Apart from re-absorption HCO3- is generated newly in
the proximal tubules by glutamate metabolism

21. Methods of assesment of acid-base balance
In vitro tests:
1) Hendersen Hasselbach equation
2) Alkali reserve
3) Standard HCO3-
4) Astrup method
5) Buffer base and buffer excess system

22. In vivo tests:
 In vivo titration curves are derived from collation of
normal human values of pH PaCO2 and HCO3- in acute
and chronic disorders
 Clinical sample values are then compared with these
values and the deviation from them may be
characterized and quantified for both acute and chronic
disorders

23. Stewart Approach
2. Weak Acid “Buffer” Solutions
A TOT = weak ions , mainly albumin & phosphate
3. CO2 content

24. Carbon Dioxide–Bicarbonate (Boston)
Approach
 acid-base chemistry using acid-base maps and the
mathematical relationship between CO2 tension and
serum bicarbonate (or total CO2),

26. Base Deficit/Excess (Copenhagen) Approach
 The standardized base excess (SBE) =
0.9287 [ HCO3- - 24.4 + (pH-7.4) ]

27. Assessment of A-B balance
Arterial blood Mixed venous blood
range range
pH 7.40 7.35-7.45 pH 7.33-7.43
pCO2 40 mmHg 35 – 45 pCO2 41 – 51
pO2 95 mmHg 80 – 95 pO2 35 – 49
Saturation 95 % 80 – 95 Saturation 70 – 75
BE 2 BE
HCO3
- 24 mEq/l 22 - 26 HCO3
- 24 - 28

28. Acid Base disturbances
Acidosis: pH<7.35
 Metabolic and respiratory
Alkalosis: pH>7.45
 Metabolic and respiratory

30. Respiratory Acidosis
 Any event (drug or disease) that decreases
alveolar ventilation results in an increased
concentration of dissolved carbon dioxide in the
plasma (increased PaCO2).
 By convention, carbonic acid resulting from
dissolved carbon dioxide is considered a
respiratory acid, and respiratory acidosis is present
when the pH is <7.35.
 Dissolved CO2 produces equal amounts of H+ and
HCO3- but still pH falls because the relative
increase in H+ is greater than the relative increase
in HCO3-

31. Respiratory alkalosis
 Due to increased ventilation, removing excess CO2
 May be due to hypoxia or iatrogenic or psychological
 Increases pH> 7.45
 Hypocalcemia accompanies it, may precipitate tetany

32. Metabolic Acidosis
 Any acid other than due to CO2 retention is considered
metabolic
 Bicarbonate deficit - blood concentrations of bicarb
drop below 22mEq/L
 Causes:
◦ Loss of bicarbonate through diarrhea or renal
dysfunction
◦ Accumulation of acids (lactic acid or ketones) which
may occur in DM,starvation,high fever.
◦ Failure of kidneys to excrete H+

33. Anion gap
 sum of anion and cations is always equal
 sodium and potassium accounts for 95% of cations
 chloride and bicarbonate accounts for 68% of anions
 there is difference between measured anion and cation
 the unmeasured anions constitute the ANION GAP.
 they are protein anions ,sulphates ,phosphates and
organic acid
 AG can be calculated as (Na+ + K+)—(HCO3
- + Cl-)
 high anion gap acidosis:renal failure,DM
 normal anion gap acidosis:diarrhea
 hyperchloremic acidosis

35. Metabolic alkalosis
 Due to excessive vomitings, nasogastric suction, chronic
thiazide use, excessive aldosterone

36. Clinical effects of acid base disorders
CVS:
 Heart rate: increases as pH decreases from 7.4 to 7.1
due to release of catecholamines from adrenal medulla.
In a sympathetically blocked patient the effect of
acidemia is bradycardia due to vagal stimulus
 Cardiac rhythm: Both atrial and ventricular arrhythmias
are more common in acidosis. It may be due to rise in
ECF potassium in acidosis
 Myocardial contractility: On isolated heart direct
depression. In sympathetically active heart contraction
increases due to catecholamine increase upto a certain
level

37.  Cardiac Output: Mild acidosis increases Cardiac Output
but as acidosis increases cardiac output falls
Systemic vascular Effects:
 With acidosis, Vasodilatation on systemic arteries
except on splanchnic vessels
 On venous system acidosis causes constriction

38. Respiratory Effects:
 With acidosis, minute ventilation increases due to
medullary centre stimulation
 Airway resistance: Acidosis causes variable response,
whereas alkalosis causes broncho-constriction

39. Renal effects:
 Renal vascular resistance increases as the pH falls
Utero-placental effects:
 Effects fetus directly through placenta and indirectly by
changing placental blood flow
 CO2 has more effect than H+ or HCO3-
 Acidosis has same effects on fetal organ function as in
adults
 Acidosis causes increased uterine blood flow
 Alkalosis causes a left shift of ODC, causing decreased
O2 delivery to fetus

40. Neuro-endocrine effects:
 CBF increases with increase in pCO2 and vice-versa
 With increase in cerebral CO2 mental changes occur and
lead to coma
 Hypothermia occurs in respiratory acidosis
 Acidosis causes increase in catecholamine levels
Electrolyte balance:
 Acidosis causes increased serum ionized calcium and
vice-versa
 pH and serum K+ are inversely proportional: 0.1 units of
pH change causes 0.6 mmol/L change in K+

41. Effect of temperature on pH
 As the temperature falls, CO2 becomes more soluble
causing PCO2 to fall , H+ to be more buffered by Hb and
an increase in pH
 1 fall in temp -- 0.015 units rise in pH

42. pH stat management
 Return of pH & pCO2 of hypothermic blood to normal
by adding CO2
 Advantage : better cerebral circulation
 Disadvantage : cerebral micro embolus
 Uses : surgery for congenital heart disease, during
cooling stage, before profound hypothermic circulatory
arrest

43.  The degree of ionisation (alpha) of the imidazole groups
of intracellular proteins remains constant despite
change in temperature.
 The pH will be corrected and reported by machine for
37 C
 Even though the actual pH is alkaline in
hypothermia, the enzyme function will be retained
because of alpha of the imidazole groups
Alpha stat

44. Simple acid-base disturbances can be
evaluated using the following strategy:
Step 1. Look at the pH (three possibilities):
 <7.35—acidosis
 7.35-7.45—normal or compensated acidosis
 >7.45—alkalosis
Step 2. Look for respiratory component (volatile acid = CO2):
 PCO2 <35 mm Hg—respiratory alkalosis or compensation for
metabolic acidosis (if so, BD * > -5)
 PCO2 35-45 mm Hg—normal range
 PCO2 >45 mm Hg—respiratory acidosis (acute if pH <7.35,
chronic if pH in normal range and BE[†]> +5)

45. Step 3. Look for a metabolic component (i.e., buffer base
utilization):
 BD >-5—metabolic acidosis
 BE -5 to +5—normal range
 BE >5—alkalosis

46.  Put this information together.
 Options:
1. Acidosis, CO2 <35 mm Hg, BD >-5—acute metabolic
acidosis
2. Normal range pH CO2 <35, BD >-5—acute metabolic
acidosis plus compensation
3. Acidosis, PCO2 >45 mm Hg, normal range BE—acute
respiratory acidosis
4. Normal range pH, PCO2 >45 mm Hg, BE >+5—prolonged
respiratory acidosis
5. Alkalosis, PCO2 >45 mm Hg, BE >+5—metabolic alkalosis
6. Alkalosis, PCO2 <35 mm Hg, BDE normal range—acute
respiratory alkalosis
7. If the acid-base picture does not conform to any of
these, a mixed picture is present.

47.  A 45-year-old man is admitted after a motor
vehicle crash. He is bleeding, and his pulse is
thready. Blood pressure is 90/50 mm Hg, heart
rate is 120 beats/min, respiratory rate is
36/min, and temperature is 35°C.
 A serum chemistry and blood gas are taken.
Does he have any acid-base disturbances?
 Na+ 144, K+ 4, Cl- 110, total CO2 8, urea 10,
creatinine 2, albumin 4, lactate 16, pH 7.28,
PCO2 24, HCO3
- 8, BE -16
 Anion gap = 26
 Corrected anion gap = 27.25

48. .4