1. DIAGNOSIS AND TREATMENT OF
ACID BASE DISORDERS

2. Why pH is important ?
• Precise regulation of the pH in a narrow range of 7.35-
7.45 is essential.
• pH is vital for normal cellular enzymatic reactions and
for normal ionic concentration.
• Extreme ranges of pH (<7.2 or >7.5) are potentially life
threatening (for eg cardiac arrhythmias )as can cause
disruption of many vital cellular enzymatic reactions
and physiological processes.
Buffering: the concentration of free hydrogen is controlled by buffers which acts as
hydrogen sponge.
When H conc is low (high pH) , hydrogen sponges release hydrogen and increase the
free H conc.
When H conc is high (low pH), hydrogen sponges engulf the free hydrogen and
decrease the free H conc.
The major Hydrogen buffers are Bicarbonate, phosphate ,hemoglobin and bone.

3. Acid base terminology 1/3
Clinical terminology Criteria
Normal pH 7.4 (7.35-7.45)
Acidemia pH < 7.35
Alkalemia pH > 7.45
Normal PaCO2 40 (35- 45 ) mm of Hg
Respiratory acidosis (failure) PaCO2 > 45 mm Hg and
low pH
Respiratory alkalosis
(hyperventilation)
PaCO2 < 35 mm Hg and
high pH
Normal HCO3 24 (22- 26 ) mEq/L
Metabolic Acidosis HCO3 < 22 mEq/L and
low pH
Metabolic Alkalosis HCO3 > 26 mEq/L and
high pH

4. Acid base terminology 2/3
pH: pH signifies free hydrogen ion concentration. pH is
inversely related to H ion concentration.
• Increase in pH means H ion is decreasing.
• Decrease in pH means H ion is Increasing.
Acid: A substance that can “donate” H ion or when added
to solution raises H ion (ie. Lowers pH)
Base: A substance that can accept H ion or when added to
solution lowers H ion (ie. Raises pH)
Anion: An ion with negative charge is anion (ie. Cl, HCO3)
Cation: An ion with positive charge is cation (ie. Na, K, Mg)
If cation and anion is confusing
Anion “n” –negative charge.
Cation “t” – Positive (+) charge.

5. Acid base terminology 3/3
• Acidemia and alkalemia : The “-aemia” is the same suffix
found in anemia . It means “blood”.
• Acidemia : means “acid blood” refers to a blood pH below
normal (pH < 7.35) and increased H ion concentration.
• Alkalemia : means “alkaline blood” refers to a blood pH
above normal (pH > 7.35) and decrease H ion
concentration.
• Acidosis : Abnormal process or disease which reduce pH
due to increase in acid or decrease in alkali is called
acidosis.
• Alkalosis : Abnormal process or disease which increases pH
due to decrease in acid or increase in alkali is called
alkalosis.

6. Basic Concepts : Hydrogen Ion Concentration
and pH
• The hydrogen ion concentration [H1] in extracellular
fluid is determined by the balance between the
partial pressure of carbon dioxide (PCO2) and the
concentration of bicarbonate (HCO3) in the fluid. This
relationship is expressed as follows(The Henderson
Equation)
• Using a normal arterial PCO2 of 40 mm Hg and a
normal serum HCO3 concentration of 24 mEq/L, the
normal [H+] in arterial blood is 24 × (40/24) = 40
nEq/L.
  


3
2
24
HCO
PaCO
H

8. Respiratory regulation
• By excreting volatile acids, lung regulates
PaCO2.
• Normally CO2 production and excretion are
balanced which maintain CO2 at 40 mm hg.
• When rate of CO2 production increases it will
stimulate PaCO2 sensitive chemoreceptors at
central medulla with resultant rise in rate and
depth of breathing. This hyperventilation will
maintain PaCO2 at normal range.

9. When the respiratory regulation falls
what will be the consequences ?
1. If the underlying disorder (respiratory or CNS)
causes hypoventilation, CO2 excretion is
reduced. Retained PaCO2 (hypercapnia) causes
fall in pH leading to respiratory acidosis.
2. If the underlying disorder causes
inappropriately high hyperventilation, CO2 is
washed out. Low PaCO2 (hypocapnia) causes
rise in pH leading to respiratory alkalosis.
Hypoventilation= Hypercapnia= Respiratory Acidosis
Hyperventilation= Hypocapnia= Respiratory Alkalosis

10. Renal regulation
• The role of kidney is to maintain plasma HCO3
concentration and there by pH regulation.
• 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.

11. How kidney responds to metabolic
ABD and regulate HCO3 ?
1. In response to acid load, normal kidneys are
able to increase net acid excretion greatly.
Increased excretion of H ions along with
regeneration of HCO3 will correct plasma
HCO3 to normal range.
2. When there is primary increase in plasma
HCO3 ,there will be increase renal excretion
of HCO3 in urine.

12. When does metabolic regulation falls ?
• Metabolic acidosis occurs when excess HCO3
is lost (diarrhea), acids are added (DKA/lactic
acidosis)/Salicyclate overdose or bicarbonate
is not generated (renal failure ).
• Metabolic alkalosis occurs when excess H ion
is lost (vomiting), or renal bicarbonate
excretion fails (hypovolemia).

13. one feature of metabolic disorders with respiratory is that
the pH, bicarbonate and PCO2 all changes in the same
direction.

14. In respiratory acid-base disorders, the pH changes in
the opposite direction as the change in bicarbonate
and PCO2.

15. • THOUGH SECONDARY RESPONSES SHOULD
NOT BE CALLED “COMPENSATORY
RESPONSES” BECAUSE THEY DO NOT
COMPLETELY CORRECT THE CHANGE
PRODUCED BY PRIMARY ACID BASE
DISORDER.

16. Compensation
Disorder Expected compensation
Metabolic Acidosis Expected PaCO2= HCO3 X 1.5 +
8
Metabolic Alkalosis Rise in PaCO2 = Rise in HCO3 X
0.75
Respiratory
Acidosis
Rise in HCO3 = Rise in Paco2 X
0.1
Respiratory
Alkalosis
Fall in HCO3 = Fall in PaCo2 X
0.2

17. Characteristics of Primary acid-base
disorders
Basic disorder pH Primary
change
2nd change
Metabolic
Acidosis
Low HCO3
Low
PaCO2
decreased
Metabolic
Alkalosis
Hig
h
HCO3
High
PaCO2
Increased
Respi Acidosis Low PaCO2
High
HCO3
Increased
Respi Alkalosis Hig
h
PaCO2
Low
HCO3
decreased

19. High

20. Clinical conditions
Clues to possible ABD Type
CNS
Coma (hypo/hyperventilation Respiratory Acidosis/alkalosis
CVS
Congestive heart failure
Shock (decrease perfusion/lactic acid
production)
Respiratory Alkalosis
Metabolic Acidosis/ Respiratory Alkalosis
Respiratory
Tachypnea (Co2 washout)
Bradypnea (CO2 retention)
Respiratory Alkalosis
Respiratory Acidosis
GI
Vomiting (loss of H)
Diarrhea (Loss of HCO3)
Abdominal pain
Metabolic alkalosis
Metabolic Acidosis
Respiratory Alkalosis

21. Clinical conditions
Clues to possible ABD Type
Renal
Oliguria/ anuria
Polyuria
Metabolic Acidosis
Metabolic Alkalosis
Endocrine
Myxedema (bradypnea)
Hypertension (Na gain
and H loss)
Respiratory acidosis
Metabolic alkalosis

22. Common mixed Acid base disorder
Disorders Common causes
Metabo
lic
Acidosi
s
Respi
Acidosis
↓ pH, ↓ HCO3,
↑PCO2
Cardiac arrest
(hypoventilation +
lactic acidosis)
Respi
Alkalosis
↔pH, ↓HCO3, ↓
PCO2
Salicyclate
intoxication
Liver failure with
hyperventilation
Metabo
lic
Alkalosi
s
Respi
Acidosis
↔ pH, ↑ HCO3, ↑
PCO2
COPD with diuretics
Respi
Alkalosis
↑pH, ↑ HCO3,
↓PCO2
Pneumonia with
vomiting

23. 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.
2/3/2016

24. • 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
2/3/2016

25. 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
2/3/2016

27. • If pH and PaCO2 changes in same direction,
the primary disorder is metabolic and if they
change in opposite direction ,the primary
disorder is respiratory.
Step II: determine the primary
disorder
Chemical
change
Primary
disorder
Compensation pH
Low HCO3- Metabolic
acidosis
Respiratory
alkalosis
low pH
High HCO3- Metabolic
alkalosis
Respiratory
acidosis
High pH
High PaCO2 Respiratory
acidosis
Metabolic
alkalosis
Low pH
Low PaCO2 Respiratory
alkalosis
Metabolic
acidosis
High pH

29. • Normal pH is 7.4
• Calculate the change in pH (from 7.4)
A. in acute respiratory disorder (acidosis / alkalosis)
change in pH = 0.008 X [PaCO2 -40]
expected pH = 7.4 +/-change in pH
B. in chronic respiratory disorder (acidosis/alkalosis)
change in pH = 0.003 X [PaCO2 -40 ]
expected pH = 7.4 +/- change in pH
Compare the pH on ABG
if pH on ABG is close to A, it is acute disorder
if pH on ABG is close to B, it is chronic disorder
Step III: if primary disorder is respiratory, determine
acute / chronic disorder

34. Unmeasured Anions Unmeasured Cation
Albumin: 15 mEq/L Calcium: 5 mEq/L
Organic Acids: 5 mEq/L Potassium: 4.5 mEq/L
Phosphate: 2 mEq/L Magnesium: 1.5 mEq/L
Sulfate: 1 mEq/L
Total UA: 23 mEq/L Total UC: 11 mEq/L
Anion AG = UA – UC = 12 mEq/L
Determination of anion gap
Adjusted AG = calculated AG + 2.5 X [4 – S.albumin gm%]

35. Pneumonic Causes
M Methanol
U Uremia
D Diabetic ketoacidosis
P Paraldehyde
I Isoniazid / iron
L Lactate
E Ethanol, ethylene glycol
R Rhabdomyolysis / renal failure
S Salicylate / sepsis
Causes of a raised AG metabolic
acidosis

36. Pneumonic Causes
H Hyper alimentation
A Acetazolamide
R Renal tubular acidosis
D Diarrhea
U Uremia (acute)
P Post ventilation hypocapnia
Causes of a non – AG metabolic
acidosis

37. • Check urinary AG in non-AG metabolic acidosis
• U Na + U K – U Cl
• Normal : negative
• Non-renal loss of bicarbonate [diarrhea] :
negative
• Renal loss of bicarbonate[ RTA / H+ excretion]
: positive
Urinary AG

38. • In less obvious cases, the coexistence of two metabolic
acid-base disorders may be apparent by calculating the
difference between the change in AG [delta AG] and
the change in serum HCO3- [delta HCO3-].
• e.g. Diabetic ketoacidosis
• This is called the Delta gap or gap –gap.
Step VII: for an increased anion gap metabolic
acidosis; are there other disorders

39. • Delta gap = delta AG – delta HCO3-
• Where delta AG = patient’s AG – 12 mEq/L
• Delta HCO3- = 24 mEq/L – patient’s HCO3-
• Normally the delta gap is zero :
– AG acidosis
• A positive delta gap of more than 6 mEq/L :
– metabolic alkalosis and/or HCO3- retention.
• The delta gap of less than 6 mEq/L :
– Hypercholremic acidosis and/or HCO3- excretion.
Delta Gap

40. GENERATION OF M.AKL
FACTORS EX
I. LOSS OF ACID FROM ECS
A. LOSS OF GASTRIC ACID VOMITING
B. LOSS OF ACID IN URINE PRIMARY ALDOSTERONISM+DIURETIC
C. SHIFT OF ACID INTO THE CELL POTASSIUM DEFICIENCY
D. LOSS OF ACID INTO THE STOOL CONGENITAL CHLORIDE LOSING
DIARRHEA
II. EXCESSIVE BICARBONATE LOAD
A. ABSOLUTE
ORAL /PARENTRAL HCO3 MILK ALKALI SYNDROME
CONVERSION OF SALTS OF ORGANIC
ACIDS INTO HCO3
LACTATE/CITRATE/ACETATE
ADMINSTRATION
B. RELATIVE NaCO3 DIALYSIS
III.POST HYPERCAPNEIC STATES Correction (e.g., by mechanical ventilatory
support) of chronic hypercapnia

41. • Metabolic alkalosis is associated with
1. hypokalemia,
2. ionized hypocalcemia,
3. secondary ventricular arrhythmias,
4. increased digoxin toxicity,
5. and compensatory hypoventilation
(hypercarbia), although compensation rarely
results in Paco2 >55 mm Hg
6. Alkalemia may reduce tissue oxygen availability
by shifting the oxyhemoglobin dissociation curve
to the left and by decreasing cardiac output.

42. • In patients in whom arterial blood gases have
not yet been obtained, serum electrolytes and a
history of major risk factors, such as vomiting,
nasogastric suction, or chronic diuretic use, can
suggest metabolic alkalosis.
• Total CO2 -should be about 1.0 mEq/L greater
than [HCO3
-] on simultaneously obtained
arterial blood gases. If either calculated [HCO3
-]
on the arterial blood gases or “CO2” on the
serum electrolytes exceeds normal (24 and 25
mEq/L, respectively) by >4.0 mEq/L, either the
patient has a primary metabolic alkalosis or has
conserved bicarbonate in response to chronic
hypercarbia.

43. Classification of metabolic alkalosis

44. 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 -
 acetazol-amide (a carbonic anhydrase inhibitor that causes renal
bicarbonate wasting), (5-10mg/kg iv/po)
 infusion of [H+] in the form of ammonium chloride, arginine
hydrochloride, or 0.1 N hydrochloric acid (100 mmol/L),
 or dialysis against a high-chloride/low bicarbonate dialysate.
 0.1 N hydrochloric acid most rapidly corrects life-threatening
metabolic alkalosis but must be infused into a central vein;
peripheral infusion will cause severe tissue damage.

46. Infusion rate 0.2mEq/l/hr

47. METABOLIC ACIDOSIS
• hypobicarbonatemia (<21 mEq/L)
• an acidemic pH (<7.35)
• Metabolic acidosis occurs as a consequence of-
1. endogenous or exogenous acid loads
2. abnormal external loss of bicarbonate.
• Approximately 70 mmol of acid metabolites are produced,
buffered, and excreted daily; -
1. 25 mmol of sulfuric acid from amino acid metabolism,
2. 40 mmol of organic acids, and phosphoric and other acids.
• Extracellular volume in a 70-kg adult contains 336 mmol
of bicarbonate buffer (24 mEq/L × 14 L of extracellular
volume). Glomerular filtration of plasma volume
necessitates reabsorption of 4,500 mmol of bicarbonate
daily, of which 85% is reabsorbed in the proximal tubule,
10% in the thick ascending limb, and the remainder is
titrated by proton secretion in the collecting duct

48. • Calculation of the anion gap
• [(Na+ - ([Cl-] + [HCO3
-])] distinguishes between two
types of metabolic acidosis
• The anion gap - normal (<13 mEq/L.)
• In metabolic acidosis associated with a high anion gap,
bicarbonate ions are consumed in buffering hydrogen
ions, while the associated anion replaces bicarbonate
in serum.
• Because three quarters of the normal anion gap
consists of albumin, the calculated anion gap should be
corrected for hypoalbuminemia
• Corrected AG = AG+2.5x(4.5-albumin in g/dl)

49. DIFFERENTIAL DIAGNOSIS OF M.AC
ELEVATED A.G NORMAL A.G
THREE DISEASES RENAL TUBULAR ACIDOSIS
UREMIA DIARRHEA
KETOACISOSIS CARBONIC ANHYDRASE INHIBITOR
LACTIC ACIDOSIS URETERAL DIVERSION
TOXINS EARLY RENAL FAILURE
METHANOL HYDRONEPHROSIS
ETHYLENE GLYCOL HCL ADMINISTRATION
SALISYLATES CHLORIDE ADMINISTRATION
PARALDEHYDE

50. METABOLIC ACIDOSIS CAUSES
• Decrease myocardial contractility,
• increase pulmonary vascular resistance,
• and decrease systemic vascular resistance.

51. ANESTHETIC IMPLICATION
• A patient with hyperchloremic metabolic acidosis may be
relatively healthy, those with lactic acidosis, ketoacidosis,
uremia, or toxic ingestions will be chronically or acutely ill.
 Preoperative assessment should emphasize volume status
and renal function.
• If shock has caused metabolic acidosis,-
1. direct arterial pressure monitoring
2. preload may require assessment via echocardiography or
pulmonary arterial catheterization.
 Intraoperatively, one should be concerned about the
possibility of exaggerated hypotensive responses to drugs
and positive pressure ventilation.
 In planning intravenous fluid therapy, consider that
balanced salt solutions tend to increase [HCO3
-] (e.g., by
metabolism of lactate to bicarbonate) and pH and 0.9%
saline tends to decrease [HCO3
-] and pH

52. 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 NaHCO3
-.
• Hyperventilation, although an important
compensatory response to metabolic acidosis,
is not definitive therapy for metabolic
acidosis.

53. • 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 [HCO3
-] 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.

54. DILUTIONAL ACIDOSIS
• It occurs when the plasma bicarbonate
concentration is decreased due to
extracellular volume expansion with
solutions(NS, albumin) that contain neither
acid nor alkali.
• A hyperchloremic metabolic acidosis may
accompany large volume infusion of isotonic
saline I/O complicated with blood loss and
extensive tissue dissection.

55. RESPIRATORY ALKALOSIS
• hypocarbia (Paco2 ≤35 mm Hg)
• alkalemic pH (>7.45),
• results from an increase in minute ventilation that is greater than that
required to excrete metabolic CO2 production.
• respiratory alkalosis may be a sign of pain, anxiety, hypoxemia, central
nervous system disease, or systemic sepsis, the development of
spontaneous respiratory alkalosis in a previously normocarbic patient
requires prompt evaluation.
• Respiratory alkalosis, like metabolic alkalosis, may produce
1. hypokalemia,
2. hypocalcemia,
3. cardiac dysrhythmias,
4. bronchoconstriction,
5. and hypotension,
6. and may potentiate the toxicity of digoxin.
7. In addition, both brain pH and cerebral blood flow are tightly regulated
and respond rapidly to changes in systemic pH.Doubling minute
ventilation reduces Paco2 to 20 mm Hg and halves cerebral blood flow;
conversely, halving minute ventilation doubles Paco2 and doubles
cerebral blood

56. 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.
• Preoperative recognition of chronic
hyperventilation necessitates intraoperative
maintenance of a similar Paco2.

57. RESPIRATORY ACIDOSIS
• hypercarbia (Paco2 ≤45 mm Hg)
• low pH (<7.35),
• occurs because of a decrease in minute alveolar ventilation
(VA), an increase in production of carbon dioxide (VCO2) or
both, from the equation:
• PaCO2=k x VCO2 / VA where
• K = constant
• Respiratory acidosis -
 acute, without compensation by renal [HCO3
-] retention
 chronic, with [HCO3
-] retention offsetting the decrease in
Ph.

58. CAUSES
• A reduction in VA may be due to an overall decrease in
minute ventilation (VE) or to an increase in the amount
of wasted ventilation (VD), according to the equation;
• VA= VE-VD
• Decreases in VE –
1. central ventilatory depression by drugs or
2. central nervous system injury.
3. airway obstruction
4. neuromuscular dysfunction.
• Increases in VD –
1. with chronic obstructive pulmonary disease,
2. pulmonary embolism, and most acute forms of
respiratory failure.
3. VCO2 may be increased by sepsis, high-glucose
parenteral feeding, or fever

59. ANESTHETIC IMPLICATION
• Patients with chronic hypercarbia due to intrinsic
pulmonary disease require careful preoperative
evaluation.
• The ventilatory restriction imposed by upper
abdominal or thoracic surgery may aggravate
ventilatory insufficiency after surgery.
• Administration of narcotics and sedatives, even in small
doses, may cause hazardous ventilatory depression.
• Preoperative evaluation should consider direct arterial
pressure monitoring and frequent intraoperative blood
gas determinations, as well as strategies to manage
postoperative pain with minimal doses of systemic
opioids.

60. • Intraoperatively, a patient with chronically
compensated hypercapnia should be ventilated
to maintain a normal pH.
• Inadvertent restoration of normal VA may result
in profound alkalemia.
• Postoperatively, prophylactic ventilatory support
may be required for selected patients with
chronic hypercarbia
• Epidural narcotic administration may provide
adequate postoperative analgesia while limiting
depression of ventilatory drive.

61. 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 is indicated unless
severe metabolic acidosis is also present or unless
mechanical ventilation is ineffective in reducing acute
hypercarbia.
• chronic respiratory acidosis is rarely managed with
ventilation but rather with efforts to improve
pulmonary function.

62. Changes of [HCO3
-] and pH in Response to Acute
and Chronic Changes in Paco2
• Decreased PaCO2
pH increases 0.10 per 10 mm Hg decrease in PaCO2
• [HCO3
-] decreases 2 mEq/L per 10 mm Hg decrease in PaCO2
• pH will nearly normalize if hypocarbia is sustained
• [HCO3
-] will decrease 5 to 6 mEq/L per 10 mm Hg chronic ↓ in
PaCO2
a
• Increased PaCO2
pH will decrease 0.05 per acute 10 mm Hg increase PaCO2
• [HCO3
-] will increase 1.0 mEq/L per 10 mm Hg increase PaCO2
• pH will return toward normal if hypercarbia is sustained
• [HCO3
-] will increase 4–5 mEq/L per chronic 10 mm Hg increase in
PaCO2

63. Consequences of acidosis

64. Consequences of alkalosis