Normal Values

2SD Normal Clinically acceptable

pH 7.35 - 7.45 7.30 - 7.50

pCO2 35 - 45 30- 50

PO2 (21%O2) 97 >80

(On ventilator) 60 - 90

HCO3 24 - 28
 Definition of terms

pH - Negative logarithm of the H+ ion activity

ACID - A H+ ion donor

BASE - A H+ ion acceptor

ACIDOSIS - An abnormal process which tends

to lower the arterial pH
ALKALOSIS - An abnormal process which tends to
increase arterial pH
ACIDEMIA - Blood pH lower than acceptable range

ALKALEMIA - Blood pH higher than acceptable range

 ACID BASE BALANCE

 50 to 100 mmols of H+ released into extra

cellular
fluid each day

 Extra cellular fluid H+ concentration

maintained
between 35 to 40 nmols

 pH of ECF = 7.38
 H+ Balance maintained

Mainly by

 Excretion of H+ in urine

 CO2 indirectly plays a role

Principal source of H+ ions
 Metabolism of amino acids

 Incomplete metabolism of carbon skeletons

of organic compounds.
 Buffering of H+

Replacement of strong acid with a weaker

one with a consequent reduction of number
of free H+
Henderson’s – Hasselbach equation

pH = pK + Log (base / acid)

For Bicarbonate buffer system

pH = 6.1 + Log (HCO3 / PCO2 x s)

If PCo2 is expressed in

 KPa s = 0.23

 mmHg s = 0.03
 Hydrogen Homeostasis
H+ concentration in body maintained tightly by
following mechanisms

 H+ can be incorporated into water (by

combination with HCO3)

 Removed temporarily by the buffering

mechanism of body

 H+ lost permanently from the body through

kidneys & intestine
Buffering systems in Body

 Bicarbonate buffering system

 Phosphate buffering system

 Plasma proteins

 Ammonia buffering system

0

Most important is Bicarbonate Buffering

system

H+ + HCO3 H2CO3 CO2H2O

Because
 It accounts for over 60% of the body
buffering capacity

 Necessary for efficient buffering by

hemoglobin

 H+ secretion of the kidney depends on it.

Control systems for Bicarbonate buffering
 Control of CO2 by the Respiratory centre and
the lungs

 Control of bicarbonate by the kidney and

erythrocytes

 Carbonic anhydrase system

 Bicarbonate generation by erythrocytes

 Bicarbonate formation in the gastro intestinal

tract
Kidneys play central role in maintenance of Acid
Base balance
(Carbonic anhydrase plays key role)

 Bicarbonate reclamation No net loss

of H+  maintain steady state

 Bicarbonate generation  net loss of H+ 

important mechanism for correcting acidosis
Phosphate and ammonia Buffering system
play important roles as urinary buffers
Disturbances of Hydrogen Ion
homeostasis

Acidosis  fall in ratio of HCO3 : PCO2

 Metabolic

 Respiratory

Alkalosis  rise in ratio of HCO3 : PCO2

 Metabolic

 Respiratory
 Metabolic Acidosis

 Primary abnormalities in bicarbonate buffer

systems is a reduction in HCO3
 Fall in HCO3 may be due to
• Its use in buffering H+ more rapidly than
it is generated .
• Loss in urine and GIT
• Impaired production
 Metabolic acidosis

 Increased anion gap acidosis

 Normal anion gap acidosis

 Anion gap = K+ + Na+ - Cl- – HCO3-

 Increased anion gap acidosis

 Increased production of lactic acid -

exercise, shock, hypoxia, liver failure,
Biguanides, trauma etc.,

 Acid from metabolism – as in

ketoacidosis
(diabetes, alcohol, starvation)
 Increased anion gap Metabolic acidosis

 Partial or complete compensatory

respiratory alkalosis occurs

 Chloride level remain normal

before &
after compensation
 Normal anion gap acidosis
Occurs in

Renal tubular acidosis

 Addison’s disease

 Diarrhea

 Carbonic anhydrase inhibitor therapy

 Uretero sigmoidostomy
 Hyperkalemic acidosis
Common finding in metabolic acidosis
 Hypokalemic acidosis seen in
Renal tubular acidosis
Carbonic anhydrase inhibitor therapy
 Hyperchloremic acidosis
Uretero sigmoidostomy
 Biochemical finding in metabolic acidosis

 HCO3 always low

 pCO2 usually low (Compensated change)

 pH low (uncompensated or partially

compensated)
or normal (fully compensated

 Treatment  aimed at correcting the cause

 Respiratory acidosis
 Primary abnormality  rise in pCO2 due to CO2
retention

 Compensatory rise in HCO3 in plasma due to

accelerated carbonic anhydrase mechanism
in erythrocyte & renal tubules

 Urine becomes more acidic.

 Arterial Blood Findings

 pCO2 always raises

In acute respiratory failure
 pH low
 HCO3 high normal or slightly raised
In chronic respiratory failure
 pH normal or low, depending on chronicity
 HCO3 raised
 Alkalosis
Metabolic Alkalosis
Primary abnormality is rise in HCO3
Occur in three situation.
 K+ depletion with generation of bicarbonate
in the kidney (commonest)
 Bicarbonate Generation by gastric mucosa
when
H+ & cl- are lost because of pyloric stenosis
or
gastric aspiration (Hypochloremic alkalosis)
 Bicarbonate administration
 Compensatory Changes in metabolic
alkalosis are ineffective

Treatment:

 Volume correction

 K+ correction

 Treatment of cause
 Respiratory Alkalosis

Primary abnormality is a fall in PCO2 due to

abnormally deep or rapid respiration when

CO2 transport capacity of pulmonary alveoli is

normal
 Causes
 Hysterical over breathing
 Raised intracranial pressure
 Hypoxia
 Excessive artificial ventilation
 Hyperthyroidism
 Pregnancy
 Fever
Compensatory change is a fall in plasma
HCO3

Arterial blood finding:

 PCO2 always reduced

 HCO3 low or normal

 pH raised (uncompensated or partially

compensated) or normal (fully compensated)
 Clinical manifestation due to underlying
causes of acid base disorders

Signs & Symptoms Suspected acid

base disorder
1. CNS
Coma Respiratory acidosis or
alkalosis
Seizure Metabolic acidosis
2. Cardiovascular
CCF Respiratory alkalosis
Shock Metabolic acidosis
3. Respiratory
Tachypnoea Respiratory alkalosis
Hyperpnoea
Bradypnoea
Hypopnoea Respiratory acidosis
 Clinical manifestation due to underlying
causes of acid base disorders
Signs & Symptoms Suspected acid
base disorder
4. GIT
Vomiting Metabolic alkalosis
Diarrhoea Metabolic acidosis
Abdominal pausi Respiratory alkalosis
5. Renal
Oliguria Metabolic acidosis
Polyuria Metabolic acidosis
(Ketoacidosis) or
Alkalosis (Diuretics)
6. Endocrine
Mgxoedema Respiratory acidosis
Hypertension Metabolic acidosis
(Ketoacidosis) or
Alkalosis (Diuretics)
Clinical manifestation due to altered pH & HCO3

Acisosis
Depressed senosrium
Depressed myocardial squeeze
Hypercapnia
Headaches
Papilloedema
Asterixis
Alkalemia
Seizures
Ventricular arrhythmias
Muscle weakness
Tetany
Hypocapnia
ST elevation
Coronary spasm
 Laboratory markers of acid base disorders

Lab Variable Disorder

Serum HCO3
 Metabolic alkalosis or respiratory acidosis
 Metabolic acidosis or respiratory alkalosis

Serum Potassium
 Hyperkalemia distal RTA
 Metabolic alkalosis, RTA

Serum Anion Gap

 markedly Organic acidosis
Metabolic alkalosis
 Simple acid base disorders

pH pCO2 HCO3 Disorder

   Metabolic acidosis

   Respiratory acidosis

   Metabolic alkalosis

   Respiratory alkalosis
APPROACH TO EVALUATION OF ACID BASE PROBLEM

Detect the problem

Explain the process

Acidosis / alkalosis are not final diagnosis

Need to explain underlying condition

Correct the disorder

 ‘2 SECOND’ SOLVERS

1) A 52 year old man has been on a ventilator for

2 days

pH 7.5

paCO2 25

HCO3 20

ABG Status ?
APPROACH TO EVALUATION OF ACID BASE PROBLEM

Detect the problem

Explain the process

Acidosis / alkalosis are not final diagnosis

Need to explain underlying condition

Correct the disorder

2) A 40 years old chronic smoker admitted with dyspnoea

pH 7.3

paCO2 80

HCO3 40

ABG status ?
3) 30yrs Old lady admittedto ICU with post op fever

pH 7.10

paCO2 30

HCO3 9

Diagnosis?
4) Chronic CCF on diuretics worsening dyspnoea

pH 7.5

paCO2 45

HCO3 36

Diagnosis ?
5) 20 yrs old man profuse diarrhoea

pH 7.15

paCO2 12

HCO3 12

ABG ?
40yrs old vomiting following ingestion of unknown poison

pH 7.4

paCO2 20

HCO3 12

Diagnosis ?
 CASE-1
 36\F Underwent laprotomy
 3rd pod pt develops breathlessness, oliguria
 WBC count and  blood urea nitrogen
 Chest x ray – clear
 Urine analysis – plenty of pus cells
 Wound clear.
 Diagnosis …… ??
 Treatment ….. ??
6) 40yrs old vomiting following ingestion of unknown
poison

pH 7.4

paCO2 20

HCO3 12

Diagnosis ?
 CASE-4

 56/ m diabetic with rapid breathing&sweatin

 Altered sensorium

 Glucose ….. 436 mgs/dl

 Urine – ketones +

 Treatment …… ??
 CASE-5
 50/f hypertensive with pedal edema
 Facial puffiness, oliguria, breathlessness
 Altered sensorium
 Blood urea nitrogen - raised
 K+ ……..??
 Hco3 ….. ??
 Treatment …… ??
B1) Mr. A 53yrs old presented to casualty with the
following ABG

pH - 7.51, paCO2 - 50, HCO3 - 40, paCO2 40 (on 21%

O2) found to be in CCF

Treatment:
Supplemental O2 and diuretics
3 days later, ABG
b) pH 7.35, paCO2 60, HCO3 41, paCO2 70 (on 24% O2)
B2) Mr. B 65yrs old

pH - 7.45, paCO2 - 55, HCO3 - 38

Na 155, K- 5.5, Cl 90, Glucose 90 Urea 180

Diagnosis ?
B3) Ms. C 18yrs old

Acute severe asthmatic attack unresponsive to

therapy in casualty
ABG (initial) in room air
a) pH - 7.4, paCO2 - 33, HCO3 - 20, paCO2 55
2hrs later, ABG on 40% O2 was
b) pH - 7.20, paCO2 - 50, HCO3 - 20, paCO2 65

Diagnosis ?
B4) Mr. D 72yrs odl COPD / CCF
Sys BP 70mmHg
initial ABG (on 40% O2)
a) pH - 7.1, paCO2 - 70, HCO3 - 21, paCO2 35
intubated & ventilated
subsequent ABG’s (on 40% O2)

b) pH - 7.28, paCO2 - 40, HCO3 - 17, paCO2 88

Na 150, K- 3.5, Cl 110

initial & subsequent ABG status ?

B5) Mr. G 45yrs old alcoholic
Several admissions for abdominal pain due to
pancreatitis
Vomiting for several days
alert dehydrated
Sys BP 80mmHg
HR 120/min
initial ABG on room air
a) pH - 7.47, paCO2 - 48, HCO3 - 34, paCO2 78
Na 130, K- 2.9, Cl - 77, Urea 120, Creatinine 2.5
Treated with IV saline and K replacement 6hrs later
pH - 7.51, paCO2 - 43, HCO3 - 30, paCO2 69
Na 135, K- 3.2, Cl - 94
improved over the next days
Investigations pH - 7.30, paCO2 - 32, HCO3 - 17, paCO2 79
Na 137, K- 4.2, Cl - 98, Urea 5
Changes in AB & Elect comp in patients with Resp acidosi
Overshoot alkalosis