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1. Acid Base Balance

2. 1. Introduction
2. Regulation of acid base balance
3. Blood buffers
4. Respiratory mechanism
5. Renal mechanism
6. Acid base disorders
7. ABG Analysis
Learning Objectives

3.  Normal blood PH : 7.35-7.45
 Maintenance of blood pH - important
homeostatic mechanism of the body.
 PH less than 7.35 leads to acidosis and
pH more than 7.45 leads to alkalosis.
Introduction

4. Acid Base Balance
• pH : Signifies free hydrogen ion concentration. pH is
inversely related to H+ ion concentration.
• Acid: Substance that can donate H+ ion, i.e. lowers pH.
• Base: Substance that can accept H+ ion, i.e. raises pH.
• Anion: Ion with negative charge.
• Cation: Ion with positive charge.
• Acidemia: Blood pH< 7.35 with increased H+ concentration.
• Alkalemia: Blood pH>7.45 with decreased H+
concentration.
• Acidosis: Abnormal process or disease which reduces pH due
to increase in acid or decrease in alkali.
• Alkalosis: Abnormal process or disease which increases pH due
to decrease in acid or increase in alkali.

5. Acid Base Balance
 The body produces acids daily
• 15,000 mmol CO2
• 50-100 mEq Nonvolatile acids
 The primary source is from metabolism of sulfur containing
amino acids (cystine, methionine) and resultant formation
of sulfuric acid.
 Other sources are non metabolized organic acids,
•Phosphoric acid, lactic acid, citric acid.
The lungs and kidneys attempt to maintain balance

6. Respiratory Regulation
 10-12 mol/day CO2 is accumulated and is
transported to the lungs as Hb-generated
HCO3 and Hb-bound carbamino compounds
where it is freely excreted.
H2 O + CO2 ↔H2 CO3 ↔H+ + HCO3-
 Accumulation/loss of Co2 changes pH within
minutes

7. Respiratory Regulation
 Normally CO2 production and excretion are balanced which
maintain CO2 at 40 mm hg.
 When rate of CO2 production increases it will stimulate
PaCO2 chemoreceptors at central medulla with resultant rise
in rate and depth of breathing.
 This hyperventilation will maintain PaCO2 at normal range.
 Response to alkalosis is biphasic. Initial hyperventilation to
remove excess pCO2 followed by suppression to increase
pCO2 to return pH to normal

8. Renal Regulation
 Kidneys are the ultimate defense against the addition of
non-volatile acid/alkali
 Kidneys play a role in the maintenance of this HCO3¯ by:
The kidneys regulate HCO3 by:
1. Excretion of H ions by tubular secretion.
2. Reabsorption of filtered bicarbonate ions.
3. Production of new HCO3 ions.
 Kidneys balance nonvolatile acid generation during
metabolism by excreting acid.

9. Renal Regulation
 Renal Excretion of acid –
combining hydrogen ions
with either urinary buffers to
form titrable acid. eg:
Phosphate, urate, ammonia

10. Acid Base Disorders
Acidosis/Alkalosis
 Any process that tends to increase/decrease pH
 Metabolic: Primarily affects Bicarbonate
 Respiratory: Primarily affects PaCO2
Acidemia/Alkalemia
 Net effect of all primary and compensatory changes
on arterial blood pH.

11. Response to ACID BASE challenge
1. Blood buffers : First line of defence
2. Respiratory regulation : Second line of defence
3. Renal regulation : Third line of defence

12. 1. Blood Buffer System
 Can not remove H+ ions from the body.
 Temporarily acts as a shock absorbant to reduce the free H+
ion.
 3 buffer system :
 Bicarbonate buffer
 Phosphate buffer
 Protein buffer

13. Blood buffer systems act instantaneously
Regulate pH by binding or releasing H⁺
 Limitations of Buffer Systems
 Provide only temporary solution to acid– base
imbalance
 Do not eliminate H+ ions
 Supply of buffer molecules is limited

14. 2. Respiratory Acid-Base Control Mechanisms
 When chemical buffers alone cannot prevent changes in
blood pH, the respiratory system is the second line of defence
against changes.
 Eliminate or Retain CO₂
 Change in pH are RAPID
 Occuring within minutes
 PCO₂ ∞ VCO₂/VA

15. 3. Renal Acid-Base Control Mechanisms
 The kidneys are the third line of defence against wide
changes in body fluid pH.
Movement of bicarbonate
Retention/Excretion of acids
Generating additional buffers
 Long term regulator of ACID – BASE balance
 May take hours to days for correction

16. Renal regulation of acid base balance
 Role of kidneys is preservation of body’s bicarbonate stores.
 Accomplished by:
Reabsorption of 99.9% of filtered bicarbonate
Regeneration of titrated bicarbonate by excretion of:
Titratable acidity (mainly phosphate)
Ammonium salts

17. Evaluation and investigations
History and examination :
•Careful history and examination can provide clue for underlying
clinical disorders.
Diarrhea or Ketoacidosis  Metabolic acidosis
Presence of Kussmaul’s breathing Metabolic acidosis

18.  Basic investigations are essential as they may provide
clue for underlying disorders.
 Most useful investigations are serum sodium,
potassium, chloride, Hco3 and anion gap.
 Other relevant investigations are CBC, urine
examination, urine electrolytes, blood sugar, renal
function test etc.
Primary investigations

19. Indications for ABG
1. Critical and unstable patients where significant acid base
disorder is suspected.
2. If history, examination and serum electrolytes suggest severe
progressive acid base disorders.
3. Sick patient with significant respiratory distress, secondary to
acute respiratory diseases or exacerbation of chronic
respiratory diseases

21. Acid Base Disorders
ACIDOSIS: PH <7.35
a ) METABOLIC ACIDOSIS
b ) RESPIRATORY ACIDOSIS
ALKALOSIS : PH >7.45
a ) METABOLIC ALKALOSIS
b ) RESPIRATORY ALKALOSIS

23. DEFINITIONS AND TERMINOLOGY
Component Terminology
I. Acidosis/Alkalosis
II. Respiratory/Metabolic
 Compensated/Uncompensated

24. Acid Base Disorders
The primary disorders:
1. Respiratory Acidosis
a) Acute
b) Chronic
2. Respiratory Alkalosis
a) Acute
b) Chronic
3. Metabolic Acidosis
4. Metabolic Alkalosis

25. Metabolic Acidosis
 Primary Acid Base disorder
 ↓HCO₃⁻ → ↓ pH
 Gain of strong acid
 Loss of base(HCO₃⁻)

26.  The sum of cations and anions in ECF is always equal, so as
to maintain the electrical neutrality.
 Commonly measured electrolytes in plasma are Na+, K+,Cl,
HCO3- .
 Unmeasured anion in the plasma constitutes the anion gap.
Anion Gap

27.  This is due to presence of protein anions, sulphate, phosphate
and organic acids.
 Anion gap = (Na + k) - ( HCO3+ Cl- ) .
 Normally anion gap is about 15 mEq/l
 Normal range = 8-18 mEq/l.

28. High anion gap acidosis
I. Renal failure
II. Diabetic ketoacidosis
III. Lactic acidosis
IV. Starvation
 Normal anion gap acidosis
I. Diarrhoea
II. Hyperchloremic acidosis
III. External pancreatic or small-bowel drainage
IV. Ureterosigmoidostomy, jejunal loop, ileal loop
Low anion gap
I. Multiple myeloma

29. Compensation for Metabolic acidosis
 H+ buffered by ECF HCO - & Hb in RBC; Plasma
 Hyperventilation – to reduce PCO₂
 ↓pH sensed by central and peripheral chemoreceptors
 ↑ in ventilation starts within minutes,well advanced at 2 hours
 Maximal compensation takes 12 – 24 hours

30. Acid–Base Balance Disturbances
.Responses to Metabolic Acidosis

31. Metabolic acidosis
Symptoms are specific and a result of the underlying pathology
I. Respiratory effects:
 Hyperventilation
II. CVS:
 ↓ myocardial contractility
 Sympathetic over activity
 Resistant to catecholamines
III. CNS:
 Lethargy,disorientation,stupor,muscle twitching,COMA, CN
palsies
 Others : hyperkalemia

32. TREATMENT
• The treatment of metabolic acidosis consists of the
treatment of the primary pathophysiologic process, that is,
hypo- perfusion, hypoxia, and if pH is severely decreased,
administration of NaHCO -3
.
• Hyperventilation, although an important compensatory
response to metabolic acidosis, is not definitive therapy for
metabolic acidosis.

33.  The initial dose of NaHCO3 can be calculated as:
NaHCO3 (mEq/L)=WT(kgs)x 0.3(24mEq/L-
actual HCO3) / 2
 0.3 = the assumed distribution space for bicarbonate and 24
mEq/L is the normal value for [HCO 3-] on arterial blood gas
determination.
 The calculation markedly underestimates dosage in severe
metabolic acidosis. In infants and children, a customary initial
dose is 1.0 to 2.0 mEq/kg of body weight.

34. Metabolic Alkalosis
↑ pH due to ↑HCO₃⁻ or ↓acid
Initiation process
 ↑in serum HCO₃⁻
 Excessive secretion of net daily production of fixed acids
Maintenance
 ↓HCO₃⁻ excretion or ↑ HCO₃⁻ reclamation
 Chloride depletion
 Pottasium depletion
 ECF volume depletion
 Magnesium depletion

35. CAUSES OF METABOLIC ALKALOSIS
I. Exogenous HCO3 − loads
A.Acute alkali administration
B.Milk-alkali syndrome
II. Gastrointestinal origin
A. Vomiting
B. Gastric aspiration
C. Congenital chloridorrhea
D. Villous adenoma
III. Renal origin
1.Diuretics
2.Posthypercapnic state
3.Hypercalcemia/hypoparathyroidis
m
4.Recovery from lactic acidosis or
ketoacidosis
5.Nonreabsorbable anions including
penicillin, carbenicillin
6.Mg2+ deficiency
7.K+ depletion

36. Chloride responsive alkalosis
Low urinary chloride concentration(<15 meq/L)
 Gastric acid loss
 Diuretic therapy
 Volume depletion
 Renal compensation for hypercapnea
Chloride resistant alkalosis
Elevated urinary chloride (>25 meq/L)
 Primary mineralocorticoid excess
 Severe pottasium depletion
 Associated with volume expansion

37. Compensation for Metabolic Alkalosis
 Respiratory compensation: HYPOVENTILATION
 Maximal compensation: PCO₂ 55 – 60 mmHg
 Hypoventilation not always found due to
 Hyperventilation causes may be
 Pain
 Pulmonary congestion
 Hypoxemia(PO₂ < 50mmHg)

38. TREATMENT
Etiologic therapy-
 Expansion of intravascular volume or the administration of
potassium.
 Infusion of 0.9% saline will dose-dependently increase
serum [Cl-] and decrease serum [HCO3-].
Nonetiologic therapy -
 Acetazolamide (a carbonic anhydrase inhibitor that causes
renal bicarbonate wasting)
 Infusion of [H+] in the form of ammonium chloride,
arginine hydrochloride, or 0.1 N hydrochloric acid
 or dialysis against a high-chloride/low bicarbonate dialysate.

39. Acid–Base Balance Disturbances
.
Metabolic Alkalosis

40. Metabolic Alkalosis
 Decreased myocardial contractility
 Arrythmias
 ↓ cerebral blood flow
 Confusion
 Mental obtundation
 Neuromuscular excitability
• Hypoventilation
 pulmonary micro atelectasis
 V/Q mismatch(alkalosis inhibits HPV)

41. Respiratory Acidosis
 ↑ PCO₂ → ↓pH
 Acute(< 24 hours)
 Chronic(>24 hours)

42. RESPIRATORY ACIDOSIS - CAUSES
 CNS Depression
1) Drugs: Opiates,sedatives,anaesthetics
2) Obesity hypoventilation syndrome
3) Stroke
 Neuromuscular Disorders
1) Neurologic: MS, Polio, GBS, Tetanus, Botulism, High Cord
lesions
2) MUSCLE:↓K⁺,↓PO₄, Muscular Dystrophy
 Airway Obstruction
 COPD, Acute aspiration, Laryngospasm

43.  Chest wall restriction
 Pleural: Effusions, Pneumothorax
 Chest Wall: Scleroderma, Ankylosing spondylitis, Obesity
 Severe pulmonary restrictive disorders
 Pulmonary fibrosis
 Parenchymal Infiltration: Pneumonia, edema
 Abnormal blood CO₂ transport
 Decreased Perfusion: HF, Cardiac Arrest
 Severe anemia

44. Compensation in Respiratory Acidosis
Acute respiratory acidosis:
 Mainly due to intracellular buffering(Hb, PO₄)
 HCO₃⁻ ↑ = 1mmol for every 10 mmHg ↑ PCO₂
 Minimal increase in HCO₃⁻
 pH change = 0.008 x (40 - PaCO₂)
Chronic respiratory acidosis:
 Renal compensation (acidification of urine & bicarbonate
retention) comes into action
 HCO₃⁻ ↑= 3.5 mmol for every 10 mm Hg ↑PCO₂
 pH change = 0.003 x (40 - PaCO₂)
 Maximal response : 3 - 4 days

45. Acid–Base Balance Disturbances
Respiratory Acid–Base Regulation.

46. • Respiratory System
 Stimulation of ventilation ( tachypnea)
• CNS:
 ↑Cerebral blood flow→ ↑ICT
 CO₂ NARCOSIS (Disorientation,confusion,headache,lethargy)
 COMA(arterial hypoxemia,↑ICT, Anaesthetic effect of ↑ PCO₂
> 100mmHg)
• CVS:
 Tachycardia
• Others:
 peripheral vasodilatation(warm,flushed,sweaty)

47. TREATMENT
The treatment of respiratory acidosis depends on whether the
process is acute or chronic.
Acute respiratory acidosis –
 Require mechanical ventilation unless a simple etiologic factor
(i.e., narcotic overdosage or residual muscular blockade) can be
treated quickly.
 Bicarbonate administration rarely indicated unless severe
metabolic acidosis or mechanical ventilation is ineffective in
reducing acute hypercarbia.
Chronic respiratory acidosis is rarely managed with
ventilation but rather with efforts to improve pulmonary
function.

48. Respiratory Alkalosis
 Most common Acid base abnormality in critically ill
 ↓PCO₂ → ↑pH
 Primary process: Hyperventilation
 Acute: PaCO₂ ↓,pH-alkalemic
 Chronic: PaCO₂↓,pH normal / near normal

49. CAUSES OF RESPIRATORY ALKALOSIS
A. Central nervous system
stimulation
1. Pain
2. Anxiety, psychosis
3. Fever
4. Cerebrovascular accident
5. Meningitis, encephalitis
6. Tumor
7. Trauma
B. Hypoxemia or
tissue hypoxia
1. High altitude
2. Septicemia
3. Hypotension
4. Severe anemia

50. C. Drugs or hormones
1. Pregnancy, progesterone
2. Salicylates
3. Cardiac failure
D. Stimulation of chest
receptors
1. Hemothorax
2. Flail chest
3. Cardiac failure
4. Pulmonary embolism
E. Miscellaneous
1. Septicemia
2. Hepatic failure
3. Mechanical ventilation
4. Heat exposure
5. Recovery from metabolic
 acidosis

51. Compensation for respiratory Alkalosis
Acute respiratory alkalosis:
 Intracellular buffering response-slight decrease in HCO₃⁻
 Start within 10 mins ,maximal response 6 hrs
Chronic respiratory alkalosis:
 Renal compensation (acid retention,HCO₃⁻ loss)
 Starts after 6 hours, maximal response 2- 3 days

52. Acid–Base Balance Disturbances
Respiratory Acid–Base Regulation.

53. Respiratory alkalosis
CNS:
 ↑ neuromuscular irritability
(tingling, circumoral
numbness)
 Tetany
 ↓ ICT
 ↓Cerebral blood flow
 Light headedness, confusion
CVS:
 CO& Systolic BP ↑
 Arrythmias
 ↓ myocardial contractility
Others:
 Hypokalemia,
hypophosphatemia
 ↓Free serum calcium
 Hyponatremia,
hypochloremia

54. TREATMENT
 Treatment of respiratory alkalosis per se is often not
required.
 The most important steps are recognition and treatment
of the underlying cause.
 For instance, correction of hypoxemia or hypoperfusion-
induced lactic acidosis should result in resolution of the
associated increases in respiratory drive.

55. MIXED ACID BASE DISORDER
Diagnosed by combination of clinical assessment, application of
expected compensatory responses , assessment of the anion gap, and
application of principles of physiology.
Respiratory acidosis and alkalosis never coexist
Metabolic disorders can coexist Eg: lactic acidosis/ DKA
with vomiting
Metabolic and respiratory Acid base disorders can coexist Eg:
salicylate poisoning (Metabolic acidosis + Respiratory alkalosis)

57. Components of the Arterial Blood Gas
The arterial blood gas provides the following values:
1. pH (Normal range is 7.35 to 7.45)
2. PaO2 (Normal range is 80 to 100 mm Hg.)
3. SaO2 (Normal range is 95% to 100%.)
4. PaCO2 (Normal range is 35 to 45 mm Hg)
5. HCO3 (Normal range is 22 to 26 mEq/liter)
6. Base Excess (Normal range is –2 to +2 mEq/liter)
 The base excess indicates the amount of excess or insufficient level of
bicarbonate in the system.
 (A negative base excess indicates a base deficit in the blood.)

58. Steps to an Arterial Blood Gas Interpretation
Acid-base evaluation requires a focus on three of the
reported components:
1. pH,
2. PaCO2 and
3. HCO3

59. This process involves three steps.
Step 1
Assess the pH to determine if the blood is within normal
range, alkalotic or acidotic.
a) If it is above 7.45, the blood is alkalotic.
b) If it is below 7.35, the blood is acidotic.

60. Step 2
If the blood is alkalotic or acidotic, determine if it is caused
primarily by a
a) Respiratory or
b) Metabolic problem.
To do this, assess the PaCO2 level.
Remember that with a respiratory problem, as the pH decreases
below 7.35, the PaCO2 should rise.
If the pH rises above 7.45, the PaCO2 should fall. Compare the
pH and the PaCO2 values. If pH and PaCO2 are indeed moving
in opposite directions, then the problem is primarily respiratory
in nature.

61. Step 3
Finally, assess the HCO3 value.
With a metabolic problem, normally as the pH increases, the
HCO3 should also increase. Likewise, as the pH decreases, so
should the HCO3.
Compare the two values. If they are moving in the same
direction, then the problem is primarily metabolic in nature.

62. The following chart summarizes the relationships
between pH, PaCO2 and HCO3.

63. Thank you