Blood Gas Analysis

• Arterial Blood Gases measures:

1. Partial pressures of O2, PaO2

2. Partial pressures of CO2, PaCO2
3. PH
4. HCO3¯¯
•   Arterial Blood Gas reveals information on:
Oxygen and Carbon Dioxide Exchange
Acid-base status

• A true arterial blood gas gives you three data points:

 PaO2- Partial pressure oxygen: 60-90 mm Hg

PaCO2- Partial pressure carbon dioxide: 36-44mmHg
pH -normal 7.35-7.45

• These values are derived from the measured values

above:

     HCO3- 22-26 meq/L: Calculated from the Henderson-Hasselbach

equation
Base deficit
 How is a arterial blood gas
obtained?

• Sample is obtained from an artery using

a "blood gas" syringe coated with heparin
• All air bubbles are removed and a cap
placed on syringe
• Best if run within 15 minutes
• Place on ice if it will be longer than 15
minutes
• Partial pressure of Arterial Oxygen PaO2
• Partial pressure of Alveolar Oxygen PAO2

Alveolar-arterial O2 gradient or A-
a gradient= PAO2-PaO2
Respiratory Membrane
A-a gradient
 A-a gradient
• The alveolar arterial oxygen difference can be
calculated by subtracting measured PaO2 from
calculated PAO2

• PaO2 < PAO2 by 5 mm Hg and PaCO2 >

PACO2 by 0.5 mm Hg (A-a gradient)

• In a healthy person the value is less than

15 mmHg
 A-a gradient
• A-a gradient is attributed shunt flow by
passing the gas exchange zone

• Anatomical shunts: post-pulmonary shunts,

bronchial circulation, ventricular septal defects

• Physiological shunts: ventilation/perfusion

inequalities
 SIGNIFICANCE
Arterial blood gas analysis is indicated
whenever the following clinically important
conditions occur:
• Hypoxemia
• Hypercapnia
• Acid-base Disturbances
 Hypoxemia
• Hypoxemia: PaO2 <60 mm Hg
• Mechanism of Hypoxemia

1. Decrease in inspired O2
2. Hypoventilation
3. Shunting
4. Ventilation/Perfusion V/Q mismatch
 Mechanisms

Decrease in Inspired O2 → ↓PAO2 →

↓PaO2→ ↔ A-a gradient

• Hypoventilation → ↓PAO2 → ↓PaO2
→ ↔ A-a gradient + ↑ PaCO2

• Problem:
– nervous system defects (CNS, NM junction)
– toxic drug effects (barbiturates, morphine)
• Solution:
O2 supplementation
– mechanical ventilation
– respiratory stimulants
• Diffusion Impairment
• ↓DLO2 ↓PaO2 ↑A-a gradient
• Problem:
– interstitial fibrosis (thickness of alveolar capillary
membrane)
– interstitial pneumonia ( thickness of alveolar cap
membrane)
– pulmonary edema with alveolar flooding (↓area gas
exchange)
• Solution:
↑ PAO2, but beware of oxygen toxicity
– acute 100% O2 (< 2 days) induces pulmonary
capillary permeability and alveolar edema
– chronic 100% O2 (> 2 days) induces interstitial
fibrosis
• Shunting → ↑A-a gradient + ↑ PaCO2
Problem:
• normal shunts: venous drainage from bronchial circ
• abnormal shunts: atrial or septal defects, patent ductus
arteriosus
Solution:
• surgical repair of arterial-venous anastomosis
• oxygen administration will not help (diagnostic test for
shunt)
• PaCO2 may not be raised above normal (40mm Hg)
• V/Q Mismatching → ↑A-a gradient + ↔↑ PaCO2

Problem:
– chronic obstructive pulmonary disease (COPD)
(emphysema, bronchitis)
– pulmonary embolism
Solution: ↑PAO2
– PaO2 is still improved with oxygen supplementation

• Supplemental oxygen distinguishes V/Q mismatching from true

shunt
 Hypercapnia
• Elevated partial pressure of CO2 in
blood.
           PaCo2>45mmHg
• Mechanism: Alveolar ventilation is
inadequate for the amount of CO2
produced
 Causes
1. Increased CO2 production
2. Decreased ventilatory drive
3. Malfunction of respiratory pump
4. Increased airway resistance
5. Inefficiency of gas exchange ( V/Q
mismatch)
 Acid Base balance
• Regulation of normal PH ( 7.35-7.45) depends
upon the Kidney and Lungs

• PH is a function of the ratio of HCO3¯

(regulated by the kidney) to PCO2 (regulated
by the lungs)
Acidosis: ↓PH
Alkalosis: ↑ PH
Many physiological mechanisms act to prevent
wide swings in the PH
Carbonic acid/Bicarbonate buffer system:
CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3-
 Metabolic Alkalosis

• Characteized by an increase in the plasma

bicarbonate concentration and plasma PH

• Compensatory rise is in PCO2 due to

hypoventilation
 Causes:
• H+ Ion loss
GI loss ( vomiting)
Exogenous steroids
Renal loss( Conn’s syndrome, Cushing’s)
Decreased Chloride intake
Diuretics
• HCO3 Retention
Bicarbonate administration
Contraction alkalosis
Milk-alkali syndrome
• H+ movement into cells
Hypokalemia
 Management
• If hypovolaemic metabolic alkalosis occurs due to
vomiting or diuretic use management is with
adequate intravenous fluid NaCl, which allows
kidney to remove excess alkali into the urine

• If metabolic alkalosis is assocoated with normal or

hypervolaemia , e.g. Conn’s syndrome, cushing’s
syndrom or steroid therapy than management
depends on correcting underlying cause
 Respiratory Alkalosis
• Respiratory alkalosis develops when there is a
period of sustained hyperventilation resulting in
the reduction of PCO2 and increase in plasma PH

• Compensatory response is Renal compensation by

reduction of tubular acid secreation and fall in
plasma bicarbonate
 Causes of Respiratory Alkalosis
• Hyperventilation of any cause
Anemia
Pulmonary embolus
Anxiety
Pain
Over vigorous assisted ventilation
Salicylates
 Management
• Clinical features are associated with the cause, e.g.
agitation, perioral and digital tingling

• Tetany or seizures may occur due to hypocalcemia

caused by increased binding of calcium to albumin
in alkalotic ECF

• Management is correction of causes, reduction of

anxiety and rebreathing in a closed paper bag to
allow CO2 levels to rise
 Metabolic Acidosis
• Develops when an acid other than carbonic acid
(due to CO2 retention) accumulates in the body
resulting in a fall in the plasma bicarbonate

• The fall in PH is blunted by hyperventilation,

resulting in a reduced PCO2

• If kidneys are normal, renal excretion of acid will

gradually increase over time raising plasma
bicarbonate and hence the PH towards normal
 Anion Gap

It is the difference between the main

measured cations ( Na+ + K+) and the
anions ( Cl¯+ HCO3¯)
Anion Gap=
     (Na+ + K+) - (HCO3- + Cl- )

Increased Gap = >11 meq/L

Normal Gap = 3-11 meq/ L
Normal Anion Gap Metabolic Acidosis
Addition of mineral acid (HCl) or loss of
bicarbonate buffer with no addition to the
plasma of a new acidic anion → Anion gap
is unchanged since plasma Cl¯ increases to
replace depleted HCO3
Increased Anion Gap Metabolic Acidosis
Addition of acid is accompanied by its
corresponding anion, which adds to the
unmeasured anion gap, while the chloride
concentration remains normal
 Causes of Metabolic Acidosis
Non-anion gap Metabolic Acidosis

• Diarrhea:
Loss of HCO3 in diarrhea
• Renal Tubular acidosis:
Urinary loss of HCO3 in proximal RTA; impaired
tubular secretion in distal RTA
 Anion gap Metabolic Acidosis

• Lactic acidosis:
Tissue hypoxia (e.g. shock) or liver disease
• Aspirin poisoning:
Accumulation of salicylates
• Methanol poisoning:
Accumulation of formate
• Renal failure:
Accumulation of organic acids
• Diabetic ketoacidosis:
Accumulation of ketones with hyperglycemia
• Isopropyl alcohol, ehylene glycol poisoning:
Accumulation of glycolate, oxalate
 Management
• Identifying and correcting the cause

• Intravenous fluid resuscitation replacing Na

and water

• HCO3 infusion required only if underlying

disorder is not readily corrected and acidosis is
severe (PH<7.15)
 Respiratory Acidosis

• Occurs when there is acculmulation of CO2

due to reduced effective alveolar ventilation

• Results in the rise in PCO2 with a

compensatory increase in plasma bicarbonate
concentrtion
 Causes and Management
• Hypoventilation of any cause
COPD
Pickwickian
Obesity
Suffocation
Opiates
Sleep apnea

Management depends on correction of cause but

ultimately external ventilatory support may be
necessary
 Primary Disturbances and their
Compensatory Responses
Disorder PH H+ Primary Compensation Mechanism of
Compensation

Metabolic ↓ ↓ PCO2 Increases

↓ ↑ respiratory rate
Acidosis HCO3

Metabolic ↑ ↑ PCO2 Decreases

↑ ↓ respiratory rate
Alkalosis HCO3

Respiratory ↑ ↑ HCO3 Renal absorption of

↓ ↑ Bicarbonate. Need
Acidosis PCO2
24-36 hours for
maximal effect
Respiratory ↑ ↓ ↓ ↓ HCO3 Renal loss of
Alkalosis PCO2 Bicarbonate