ACID BASE ANALYSIS

N. Lakshmi Sowmya.
Moderator: Dr. Anand Ram.
ABG TEST
 INTRODUCTION  
An arterial blood gas (ABG) is a test that measures:

 oxygen tension (PaO2)

 carbon dioxide tension (PaCO2)

 acidity (pH)

 oxyhemoglobin saturation (SaO2)

 bicarbonate (HCO3) concentration in arterial blood.

Some blood gas analyzers also measure:

methemoglobin, carboxyhemoglobin, and hemoglobin levels.
 ARTERIAL SAMPLING
Arterial blood is required for an ABG.
obtained by : percutaneous needle puncture or from an indwelling
arterial catheter.

 A) Needle puncture — 
• Percutaneous needle puncture refers to the withdrawal of arterial
blood via a needle stick.
• Needs to be repeated every time an ABG is performed, since an
indwelling catheter is not inserted.
Site selection 
The initial step :locating a palpable artery.

Common sites : radial, femoral, brachial, dorsalis pedis, or axillary

artery.

The radial artery is used most often.

Reason :
• Accessible
• easily positioned
• more comfortable for the patient than the alternative sites.
1.The radial artery is best palpated between the distal radius and the
tendon of the flexor carpi radialis when the wrist is extended.

The arm should be positioned on an arm-board with the palm facing

upward.

A large roll of gauze should be placed between the wrist and the arm-
board in a position that extends the wrist.

Taping the forearm and palm to the

arm-boardhelps maintain the position.
2.The brachial artery is best palpated medial to the biceps tendon
in the antecubital fossa, when the arm is extended and the palm is
facing up.

The needle should be inserted just above the elbow crease.

3.The femoral artery is best palpated just below the midpoint of the
inguinal ligament, when the lower extremity is extended.

The needle should be inserted at a 90 degree angle just below the

inguinal ligament.
4.The dorsalis pedis artery is best palpated lateral to the extensor
hallucis longus tendon.
It receives collateral flow from the lateral plantar artery through an
arch similar to that in the hand.
5.The axillary artery is best palpated in the axilla, when the arm is
abducted and externally rotated.
There is good collateral flow to the arm through the thyrocervical
trunk and subscapular artery; thus, the risk of ischemic complications
to the arm is low.
The needle should be inserted as high into the axilla as possible 
Collateral circulation :

• The Allen test or modified Allen test can be performed in patients

undergoing radial artery puncture.

• These are bedside tests that demonstrate collateral flow through

the superficial palmar arch.

To perform the modified Allen test:

• The patient's hand is initially held high with the fist clenched and
both the radial and ulnar arteries compressed.

• This allows the blood to drain from the hand.

.
• The hand is then lowered, the fist is opened, and pressure is
released from the ulnar artery.

• Color should return to the hand within six seconds, indicating that
the ulnar artery is patent and the superficial palmar arch is intact.

• The test is considered abnormal if ten seconds or more elapses

before color returns to the hand
• The Allen test (from which the modified Allen test evolved) is
performed identically, except these steps are executed twice:
once with release of pressure from the ulnar artery and once
with release of pressure from the radial artery.
For patients undergoing dorsalis pedis artery puncture, the
dorsalis pedis artery can be occluded, followed by compression
of the nailbed of the great toe and assessment of the rapidity
with which color returns to the nailbed after pressure is released
from the great toe
Technique
Once a palpable artery has been located, blood is withdrawn using
the following steps.

1.The planned puncture site should be sterilely prepped.

2.Local analgesia prior to arterial puncture should be considered,

since it appears to prevent pain without adversely impacting the
success of the procedure.
3.The seal of a heparinized syringe should be broken by pulling its plunger.
• The plunger can then be pushed back into the syringe, leaving a small
empty volume (eg, less than 1 mL) in the syringe.
• A small needle (eg, 22 to 25 gauge) should then be attached to the
syringe.
4.Using one hand to gently palpate the artery and the other to
manipulate the syringe and needle
• The artery should be punctured with the needle at a 30 to 45
degree angle relative to the skin.
• The syringe will fill on its own (ie, pulling the plunger is
unnecessary). Approximately 2 to 3 mL of blood should be
removed.
5.To prevent coagulation, the syringe should be rolled between the
hands for a few seconds to allow blood to mix with the heparin.

6.After withdrawing a sufficient volume of blood, the needle should

be removed and pressure applied to the puncture site for five to ten
minutes to achieve hemostasis.
Complications 
Complications due to percutaneous needle puncture are rare.

They include:
• Persistent bleeding

• Bruising
• Injury to the blood vessel
• Circulation distal to the puncture site may also be impaired
following percutaneous needle puncture, presumably due to
thrombosis at the puncture site.
Indwelling catheters:

Arterial blood can also be obtained via an indwelling arterial catheter.

Provide continuous access to arterial blood - helpful when frequent blood gases are
needed (eg, respiratory failure).

•Sample should be analyzed as soon as possible

If iced sample can be stored

• » Glass syringe – 1 hour

• » Plastic syringe – 15 minutes

 TECHNICAL ERRORS
• HEPARIN:

• Sodium Heparin 1% solution should be used

• Ammonium heparin will alter pH

• Dry lithium heparin is OK

• Excessive Heparin
 Syringe FLUSHED with 0.5ml 1:1000 Heparin &
emptied

HEPARI DILUTIONAL HCO3-

N EFFECT pCO2
Risk of alteration of results increases with:

 1) ↑ size of syringe/needle

 2) ↓volume of sample

 Syringes must have > 50% blood

 Use only 3ml or less syringe

 25% lower values if 1 ml sample taken in 10 ml syringe (0.25 ml

heparin in needle)
Air Bubbles:

 pO2 150 mm Hg & pCO2 0 mm Hg

 ↑ pO2 & ↓ pCO2

 Seal syringe immediately after sampling.

↑ Cell count - ↓ in PO2

WBC Count:

 0.01 ml O2 consumed/dL/min

 Marked increase in high TLC/plt counts : ↓ pO2

 Chilling / immediate analysis

Body Temperature:

 Affects values of pCO2 and HCO3 only

 ABG Analyser is controlled for Normal temperatures.

 Any change in body temp at the time of sampling

leads to alteration in values detected by the
electrodes.
ABG Syringe must be transported earliest via COLD CHAIN

Change/10 min Uniced 370C Iced 40C

pH 0.01 0.001
pCO2 1 mm Hg 0.1 mm Hg

pO2 0.1% 0.01%

 ABG EQUIPMENT
 3 electrode system that measures three fundamental
variables - pO2, pCO2 and pH

 All others parameters such as HCO3- computed by software

using standard formulae.

ABG ELECTRODES

A. pH (Sanz Electrode) :

• Measures H+ ion concentration of sample against a known pH

in a reference electrode, hence potential difference.

• Calibration with solutions of known pH (6.384 to 7.384)

B. P CO2 (Severinghaus Electrode):

• CO2 reacts with solution to produce H+

higher C02  more H+  higher P CO2 measured

C. P 02 (Clark Electrode) :

• 02 diffuses across membrane producing an electrical current

measured as P 02
 VENOUS BLOOD GASES AND OTHER ALTERNATIVES
TO ARTERIAL BLOOD GASES
• A venous blood gas (VBG) is an alternative method of estimating
systemic carbon dioxide and pH that does not require arterial blood
sampling.

• Performing a VBG rather than an ABG is particularly convenient in

the intensive care unit, since most patients have a central venous
catheter from which venous blood can be quickly and easily
obtained.
Sampling sites 
A VBG can be performed using a
• peripheral venous sample (obtained by venipuncture)
• central venous sample (obtained from a central venous catheter)
• mixed venous sample (obtained from the distal port of a
pulmonary artery catheter).

Central venous blood gases are preferred because their correlation

with arterial blood gases is the most well-established by research and
clinical experience.
Peripheral venous blood gases are an alternative for patients who do not
have central venous access.
• If a tourniquet is used to facilitate venipuncture, it should be released
about one minute before the sample is drawn to avoid changes induced
by local ischemia.
Mixed venous blood gases are a reasonable alternative for patients
whose venous access is a pulmonary artery catheter; however, a
pulmonary artery catheter should not be inserted for the sole
purpose of venous blood sampling

Measurements 
A VBG measures :

• The venous oxygen tension (pvo2)

• Carbon dioxide tension (pvco2)

• Acidity (ph)

• Oxyhemoglobin saturation (svo2)

• Serum bicarbonate (HCO3) concentration

• PvCO2, venous pH, and venous serum HCO3 concentration are used to
assess ventilation and/or acid-base status .

• SvO2 is used to guide resuscitation during severe sepsis or septic shock,

a process called early goal-directed therapy

• PvO2 has no practical value at this time. It is not useful in assessing

oxygenation because oxygen has already been extracted by the tissues
by the time the blood reaches the venous circulation.

• The inability of a VBG to measure oxygenation is the major drawback

compared with an ABG.

• To overcome this limitation, VBGs are often considered in combination

with pulse oximetry.
Correlation with arterial blood gases :

Central venous:

• The central venous pH is usually 0.03 to 0.05 pH units lower than

the arterial pH

• The PCO2 is usually 4 to 5 mmHg higher

• Little or no increase in serum HCO3.

Mixed venous blood gives results similar to central venous blood.
Peripheral venous :
• The pH is approximately 0.02 to 0.04 pH units lower than the
arterial pH

• The venous serum HCO3 concentration is approximately 1 to 2

meq/L higher

• the venous PCO2 is approximately 3 to 8 mmHg higher.

There are no venous to arterial conversions for the central venous,

mixed venous, or peripheral venous PvO2 or SvO2.
Comparison of Blood Gas Analysis at different sites
Misleading results 

• The correlation between arterial and venous blood gas

measurements varies with the hemodynamic stability of the
patient.

• This observation has two practical consequences:

• First, clinicians should be wary of VBG results and preferentially

obtain an ABG in hypotensive patients.

• Second, periodic correlation of the venous measurements with

arterial measurements should be performed whenever venous
measurements are used for serial monitoring.
 INTERPRETATION OF ABG

• OXYGENATION
• ACID BASE ANALYSIS
 OXYGENATION STATUS

 PaO2 vs SpO2

 Alveolar-arterial O2 gradient

 PaO2/FiO2 ratio

 PaCO2
 As Age the expected PaO2

As FiO2 the expected PaO2

 HYPOXEMIA:

 Normal PaO2 : 95 – 100 mm Hg

 Mild Hypoxemia : PaO2 60 – 80 mm Hg

 Moderate Hypoxemia : PaO2 40 – 60 mm Hg – tachycardia,

hypertension, cool extremities

 Severe Hypoxemia :PaO2 <40mmHg– severe arrhythmias,

brain injury, death
Alveolar-arterial O2 gradient:

o P(A-a)O2 is the alveolar-arterial difference in partial pressure of

oxygen
o PAO2 = 150 – PaCO2/RQ

o Normal range : 5 - 25 mm Hg (increases with age)

o Increase P(A-a)O2 : lung parenchymal disease
PaO2 / FiO2 ratio:
 Berlin criteria for ARDS severity

ARDS is characterized by an acute onset within 1 week, bilateral radiographic

pulmonary infiltrates, respiratory failure not fully explained by heart failure or
volume overload, and a PaO2/FiO2 ratio < 300 mm Hg
BERLIN’S CRITERIA FOR ARDS
Hypercapnia

o PaCO2 is directly proportional to CO2 production and inversely

proportional to alveolar ventilation
o Normal PaCO2 is 35 – 45 mm Hg
ACID BASE STATUS
 Basics

• Nano equivalent =1×10-9

pH = -log [H+] : Sorensen

formula
• [H+] = 40 nEq/L (16 to 160 nEq/L) at pH-7.4
 HENDERSON-HASSELBALCH
EQUATION

o Correlates metabolic & respiratory

regulations

HCO -
3
pH = pK + log ----------------
.03 x [PaCO2]
o Simplified
HCO -
3
pH ~ ---------
PaCO2
 Bicarbonate Buffer System

carbonic anhydrase
CO2 + H2O H2CO3 H+ + HCO3-

Acidosis : Acid = H+
H+ + HCO - H CO2 + H2O
CO
3
2
Alkalosis : Alkali
3 + Weak Acid = H2CO3
-
CO2 + H20 H2CO3 +
HCO3 + H
+
Alkali
• Phosphate buffer system:

• Major buffer in ICF and renal tubular fluid.

• Buffering low in ECF – only 8% concentration.

• Phosphates are concentrated in renal tubular fluid.

• HCl + NaH2PO4 NaH2PO4 + NaCl

• NaOH + Na2H2PO4  Na2HPO4 + H2O

Protein buffer system:

• Important ICF buffer

• All cell membranes except RBC membrane permit only a small
amount of diffusion of H+ ions and HCO3.
• Slow process.

• Rapid equilibrium in RBC.

• Hb + H+  HHb
 Respiratory Regulation

ALVEOLAR
H+ VENTILATIO PaCO2
N

ALVEOLAR

H+
VENTILATIO
N
PaCO2
 Renal Regulation
Kidneys control the acid-base balance by excreting either a basic or an
acidic urine

• Excretion of HCO3 -
• Regeneration of HCO -3
with excretion of H+
 Excretion of excess H+ & generation of new
HCO3 : The Ammonia Buffer System
-

GLUTAMINE

REABSORBED HCO3- NH3 NH3 + H+ NH4+

EXCRETE
D

• In chronic acidosis, the dominant mechanism

+
of acid eliminated excretion of NH4
 Response…

• Bicarbonate Buffer System

• Acts in few seconds

• Respiratory Regulation

• Starts within minutes good response by 2hrs, complete

by 12-24 hrs

• Renal Regulation

• Starts after few hrs, complete by 5-7 days

 Abnormal Values
pH < 7.35
• Acidosis (metabolic
and/or respiratory)
pH > 7.45
• Alkalosis (metabolic
and/or respiratory)
paCO2 > 45 mm Hg
• Respiratory acidosis (alveolar
hypoventilation)
paCO2 < 35 mm Hg
• Respiratory alkalosis (alveolar
hyperventilation)
HCO3- < 22 meq/L
• Metabolic acidosis
HCO3- > 26 meq/L
• Metabolic alkalosis
 Acid-Base Disorders
Simple acid base disorder – A single primary process
of acidosis or alkalosis with or without
compensation
 TYPES OF ACID-BASE DISORDERS

(A) Simple acid-base disorders: are common clinical

disturbances where compensation is incomplete and pH is
abnormal.
• Examples are –

• Metabolic acidosis
• Metabolic alkalosis
• Respiratory acidosis
• Respiratory alkalosis
 Compensation…

The body always tries to normalize the pH so…

 Primary respiratory disturbances (primary changes in PaCO2 ) invoke

compensatory metabolic response – secondary changes in HCO3 .

 Similarly primary metabolic disturbances cause compensatory

respiratory responses.

 pCO2 and HCO3 rise & fall together in simple disorders

 Compensation never overcorrects the pH

 Lack of compensation in an appropriate time defines a 2nd disorder

 Require normally functioning lungs and kidneys

 Characteristics of primary acid-base
disorders
DISORDER PRIMARY RESPONSE COMPENSATORY
RESPONSE
Metabolic  [H+ ]  PH  HCO3-  pCO2
acidosis

Metabolic  [H+ ]  PH  HCO3-  pCO2

alkalosis

Respiratory  [H+ ]  PH  pCO2  HCO3-

acidosis

Respiratory  [H+ ]  PH  pCO2  HCO3-

alkalosis
 DISORDER COMPENSATORY RESPONSE

Respiratory acidosis

Acute
↑ HCO3– 1 mEq/L per 10 mm Hg ↑ pCO2
Chronic
Respiratory alkalosis
Acute
↓ HCO3– 2 mEq/L per 10 mm Hg ↓ pCO2
chronic
↓ HCO3– 5 mEq/L per 10 mm Hg ↓ pCO2
Metabolic acidosis
↓ pCO2 1.3 mm Hg per 1 mEq/L ↓ HCO3–
(Limit of CO2 is 10 mm Hg)
Metabolic alkalosis
↑ pCO2 0.7 mm Hg per 1 mEq/L ↑ HCO3–
(Limit of CO2 is 55 mm Hg)
(B) Mixed acid-base disturbances : are not merely
compensatory disturbances but independently coexisting
disorders seen in critically ill patients with extreme changes

Clues to a mixed disorder:

o Normal pH with abnormal HCO3 or pCO2.

o pCO2 and HCO3 move in opposite directions.

o pH changes in an opposite direction for a known primary disorder.
 PHYSIOLOGIC EFFECTS OF ACIDOSIS AND
ALKALOSIS
 ON CVS:

• Acidemia can cause a decrease in cardiac contractility that is

directly proportional to the degree of fall in pH.
• Both metabolic and respiratory acidemia cause a similar
degree of myocardial depression, but the effect of the later
occurs more promptly, presumably because of the rapid entry
of CO2 into the cardiac cell.
• Although metabolic acidemia decreases the threshold for
ventricular fibrillation is established acidemia has no effect on
the success of defibrillation.

• Acidemia also causes stimulation of the sympathetic-adrenal

axis, and in severe acidemia this effect is countered by a
depressed responsiveness of adrenergic receptors to circulating
catecholamines.

• Alkalemia appears to increase myocardial contractility, at least

to a pH of 7.7.

• There is little effect on the threshold for ventricular fibrillation.

 ON CNS:

• Acute respiratory acidemia  marked increases in cerebral blood

flow.

• Acute elevations of PCO2 > 60 mmHg  confusion and headache

• > 70 mmHg  loss of consciousness and seizures can occur.

• Chronic elevations in CO2 are typically well tolerated, even when it

is as high as 150 mmHg.

• Acute hypercapnia depression of diaphragmatic contractility and

a ↓in endurance time.

• The effect of metabolic acidemia on the respiratory muscles is less

clear, but probably also consists of depression of contractility.

• Acute respiratory alkalemia  ↓ in cerebral blood flow, an effect

that last only about 6 hours.

• It produces confusion, myoclonus, asterixis, loss of consciousness

and seizures.
On Electrolytes:

• Acute infusions of HCI  ↑serum potassium.

• However, administration of organic acids, such as lactic acid and

ketoacids, does not raise potassium levels, and may even lower it.

• The hyperkalemia commonly observed in both lactic acidosis and

ketoacidosis is due to factors other than the pH change.

• Acute respiratory academia causes no change, or a slight

increment, in serum potassium.

• Both respiratory and metabolic academia  ↑extracellular

phosphate concentrations.
• Clinically, lactic acidosis and ketoacidosis are associated with
hyperphosphatemia.
• Acute hypocapnea causes a slight reduction in the serum levels of
sodium, potassium and phosphorus.
• Alkalemia  ↑ hemoglobin’s affinity for oxygen.
• Increase in the concentration of 2, 3 DPG in red blood cells and a
change in its morphology, oppose this effect.
• The clinical effect of alkalemia-induced changes in oxygen delivery
are minimal, and only in patients with tissue hypoxia are the small,
acute changes potentially relevant.
• Most common causes of acid-base disorders should be kept in
mind. Such as :
• i) Chronic renal failure expected to cause metabolic acidosis.
• ii) Intestinal obstruction and chronic vomiting likely to cause
metabolic alkalosis.
• iii) COPD patients or patients with overdose of sedatives usually
exhibit respiratory acidosis.
• iv) Patients with pneumonia, sepsis or cardiac failure frequently
have respiratory alkalosis.
• Metabolic acidosis :

• Causes :

• 1) Increased endogenous acid production (eg. Lactate and Ketoacids)

• 2) Loss of HCO3 (Diarrhoea)

• 3) Accumulation of endogenous acid (eg. Renal facture)

• Clinical metabolic acidosis are of 2 types –

• (1) High A.G. acidosis,

• (2) Normal AG or Hyperchloremic acidosis.

 ANION GAP

AG = [Na+ ] - [Cl- +HCO3-]

• Elevated anion gap represents metabolic acidosis

• Normal value: 12 ± 4 mEq/L
• Major unmeasured anions
– albumin
– phosphates
– sulfates
– organic anions
 Anion gap =Metabolic Acidosis

Unmeasured
cations Unmeasured
anions

Cl-
Na+

HCO3-
Cations = Anions
 Normal Anion Gap Increased Anion Gap

o Gastrointestinal loss of o Diabetic Ketoacidosis

bicarbonate(Diarrhea , Urinary
diversion) o Chronic Kidney Disease

o Small bowel, pancreatic, or bile o Lactic Acidosis

drainage (fistulas, surgical o Alcoholic Ketoacidosis
drains) o Aspirin Poisoning
o Renal loss of bicarbonate (or o Methanol Poisoning
bicarbonate equivalent) Renal
tubular acidosis, Recovery o Ethylene Glycol Poisoning
phase of Ketoacidosis , Renal o Starvation
Insufficiency.
o Paraldehyde poisoning
o Acidifying Substances HCl,
NH4Cl, Arginine HCl, Lysine HCl,
Sulfur.
• Lactic acidosis is the most common and most important
acidosis encountered in the ICU.
 Delta Gap
o The difference between patient’s AG & normal AG
o The coexistence of 2 metabolic acid-base
disorders may be apparent

Delta gap = Anion gap – 12

Delta Gap + HCO3 - = 22-26 mEq/l

 If >26, consider additional metabolic alkalosis

 If <22, consider additional non AG metabolic
acidosis
• Metabolic alkalosis:
• As the normal kidney can excrete HCO3 up to 10 meqkg-1day-1, for

metabolic alkalosis to persist there must be both a process that

elevates its serum levels and a stimulus for renal reabsoption.

• The former is usually acid loss from the stomach or from the

kidney, and the last due to hypovolemia with a Cl deficit (renal

tubules with a strong sodium avidity), hypokalemia or an increase

in mineralocorticoid activity.
• When Cl deficit is present, HCO3 is reabsorbed with sodium and

metabolic alkalosis will persist until the Cl deficit is replaced.

• Hypokalemia increases tubular HCO3 reabsorption and

mineralocorticoid excess increases HCO3 by increased secretion of

H+ ions in the cortical collecting tubule.

• major causes in the ICU are
 Vomiting
 Nasogastric suction
 Diuretics

 Corticosteroids,
 Overventilation of patients with chronically increased HCO3 levels

 Acetate used in total parenteral nutrition.

• Respiratory acidosis:
• Respiratory alkalosis:
STEP-BY-STEP ANALYSIS
OF
ACID-BASE STATUS
1. Look at the pO2 (<80 mmHg) and O2 saturation
(<90%) for hypoxemia.

2. Look at the pH
 < 7.35 : ACIDOSIS
 > 7.45 : ALKALOSIS
 7.35 – 7.45 : normal/mixed disorder.

3. Look at pCO2
 > 45 mm Hg : Increased (Acidic)
 < 35 mm Hg : Decreased (Alkalotic)
4. Look at the HCO3-

 > 26 mEq/L : Increased (Alkalotic)

 < 22 mEq/L : Decreased (Acidic)

5.Determine the acid-base disorder, match either the pCO2 or

the HCO – with pH.
 6. Compensation…are the CO2 or HCO3- of opposite type ?
Is the compensation adequate??

• METABOLIC DISORDER PCO2expecte

d

•PCO2measured ≠ PCO2expected MIXED DISORDER

•RESPIRATORY DISORDER pHexpecte

d

• pHm ≠ pHe range MIXED DISORDER

7. Calculate the anion gap if it is more there is Metabolic acidosis

8.Does the anion gap explain the change in HCO3-?

Calculate Delta gap

(rule out co-existence of 2 acid-base disorders)

9. Examine the patient to determine whether the clinical signs are

compatible with the acid-base analysis
THANK YOU!!!