ARTERIAL BLOOD

GAS ANALYSIS
Aa sh i sh Ne g i
 Introduction
◦ Cardiorespiratory care requires precise
knowledge of patient’s oxygenation,
ventilatory, and acid-base status
◦ This information is obtained by arterial blood
samples.
◦ Interpretation of arterial blood gas parameters
best reflect the lung’s ability to exchange O2
and CO2 with the blood, the blood’s O2
carrying capacity, and its acid-base status
 Indications for ABG
◦ Symptoms
◦ Medical history
◦ Physical examination
◦ Laboratory investigations
1. Anyone of it if suggest respiratory or acid-base abnormality
2. Helps in evaluating effects of treatment
 Sampling and Measurement
◦ Invasive approaches require sampling of blood by needle puncture or
indwelling catheter
◦ Analysis of an arterial blood sample is the gold standard to accurately evaluate
oxygenation, ventilation and acid base status.
◦ Measurement of arterial pH, PaCO2, and PaO2 typically is provided by a blood
gas analyzer, which also uses programmed equations to compute the HCO3
and SaO2 values.
◦ Arterial puncture and indwelling catheter (A line) is used to draw arterial blood
sample
 Assessment of oxygenation
◦ Parameters indicating oxygenation status includes;
1. Partial pressure of oxygen in arterial blood (PaO2),

2. Oxyhemoglobin saturation (SpO2, SaO2) and

3. Arterial O2 content (CaO2)

 Partial Pressure of Oxygen (Pao2)
REFERENCE RANGE : 80 to100 mm Hg breathing room air
◦ Pressure exerted by dissolved oxygen in the arterial blood.
◦ Reflects the lung’s ability to transfer O2 from the inspired gas into the circulating blood
◦ Depends on both environmental factors (O2 concentration and barometric pressure) and lung function
◦ Assuming normal lung function and environmental factors, Alveolar oxygen is determined by equation:
PAO2 = FIO2 (PB −PH2O) − (PaCO2 × 1.25)
(PAo2 = partial pressure of oxygen in the alveoli; FIo2 = fraction of inhaled oxygen; PB = barometric pressure; PH2O= water vapor pressure in alveoli,
47 mm Hg at BTPS; PaCO2 = arterial partial pressure of CO2 (assumed to approximate the alveolar Pco2); and 1.25 = factor based on the ratio of CO2
production to O2 consumption (respiratory quotient).
◦ With normal lungs breathing at sea level, there exists on average a 10 mm Hg
gradient between the PAO2 and PaO2, yielding a normal PaO2 in the 90 to 100
mm Hg range.
◦ This difference—called the alveolar-arterial oxygen tension gradient and
abbreviated as P(A-a)O2—increases with increasing age, owing to a
progressive decline in lung function.
◦ It is estimated by multiplying patients age by 0.3. For example, we would
estimate the P(A-a)o2 of an otherwise healthy 70-year-old patient as being 0.3
× 70, or about 20 mm Hg
 Hypoxemia and severity causes
◦ When PaO2 is less than 80mmHg it is known as Hypoxemia
◦ Causes of hypoxemia includes hypoventilation (decreased rate of CO2 removal), ventilation-
perfusion (V/Q) mismatch, pulmonary shunting, diffusion defect, breathing at low partial
pressure of Oxygen e.g. high altitiude
◦ Patient complains of shortness of breath, especially with exertion additional common clinical
manifestations of hypoxemia include mental confusion, tachycardia, tachypnea, hypertension,
and cyanosis.
 Oxyhemoglobin
◦ Normally, more than 98% of the O2 in arterial blood is chemically bound to hemoglobin.
◦ This bonding depends on:
a. Total Hb concentration
b. Proportion of oxygen bound to it
◦ Each gram of normal hemoglobin has the capacity to bind with 1.34 mL O2
◦ Average Hb content of 15 g/dL, this means that each 100 mL of blood has the potential for carrying
about 20 mL O2 (1.34 mL/g × 15 g/dL = 20.1 mL/dL).
◦ Complete assessment of patient oxygenation must include knowledge of Hb content, as determined by
either CO-oximetry or a complete blood cell count (CBC).
Oxygen dissociation curve
 Arterial O2 Content (Cao2)

REFERENCE RANGE : 16 to 20 mL/dL

◦ represents the total oxygen content in the arterial blood, measured in
mL/dL.
◦ Dissolved O2 = 0.003 mL/dL/mm Hg × 100 mm Hg = 0.3 mL/dL
◦ Average Hb content of 15 g/dL, this means that each 100 mL of
blood has the potential for carrying about 20 mL O2 (1.34 mL/g ×
15 g/dL x 0.97 = 19.5 mL/dL).
◦ CaO2 = 0.3 mL/dL + 19.5 mL/dL = 19.8 mL/dL
Comparison of the forms of hypoxia
Parameter Hypoxaemic Anemic Circulatory Histotoxic

PaO2 Decreased Normal Normal Normal

CaO2 Decreased Decreased Normal Normal

DO2 Decreased Decreased Decreased Decreased

 pH
◦ measurement of the hydrogen ion concentration in the plasma, abbreviated as H+
◦ REFERENCE RANGE : 7.35 to 7.45
◦ majority of body functions occur optimally at or near a pH of 7.40
◦ pH values below 7.35 indicate an abnormally high blood H+ or acidemia
◦ Effects of Acidosis: depress CNS function (lethargy and confusion), may worsen to coma, reduced
myocardial contractility and decreased blood flow throughout the body
◦ pH values above 7.45 indicate an abnormally low blood H+ or alkalemia
◦ Effects of alkalosis: overexcitability of the CNS and peripheral nerves (tetany, muscle spasms,
respiratory failure of muscle of respiration involved)
 Partial Pressure of Carbon Dioxide
(Paco2)
◦ measures the adequacy of ventilation relative to the metabolic production of
CO2 by the tissues
◦ REFERENCE RANGE : 35 to 45 mm Hg
◦ Presence of a PaCO2 above 45 mm Hg is termed hypercapnia, resulting from
hypoventilation (decreased removal of Carbon dioxide)
◦ The presence of a PaCO2 below 35 mm Hg is termed hypocapnia resulting
from hyperventilation (increased removal of carbon dioxide)
◦ It is the best measure for evaluating the effectiveness of ventilation and should
be interpreted in light of the patient’s minute ventilation (VE).
 Plasma Bicarbonate (HCO3-)

◦ Reference range: 22-26 mmol/l

◦ Plasma HCO3- primarily reflects the metabolic component of acid-base balance and is regulated by the
renal system
◦ functions chemically as base therefore changes in its concentration will cause opposite direction changes
in pH (H+)
◦ primary increase in HCO3- causes alkalemia (pH > 7.45) is termed metabolic alkalosis
◦ A primary decrease in HCO3- causes acidemia (pH < 7.35) is termed metabolic acidosis
◦ Values may also change as a compensatory or secondary response to primary changes in Paco2 levels;
usually requires at least 12 to 24 hours to occur,and takes around 3 days for full compensation
Simple acid base imbalance
 Respiratory Acidosis
◦ abnormal condition in which there is a primary reduction in alveolar ventilation relative to the rate of CO2
production, that is, inadequate ventilation resulting in elevated PaCO 2 levels and decreased pH.
◦ occurs in a variety of respiratory and non-respiratory abnormalities
◦ Respiratory
a) Acute upper airway obstruction
b) Severe diffuse airway obstruction (acute or chronic)
c) Massive pulmonary edema
◦ Non-respiratory
a) Drug overdose
b) SCI and TBI
c) Neuromuscular disease
d) Thoracic trauma
e) obesity
 Clinical manifestations
◦ Acutely dyspnea and tachypnea
◦ CNS depression (semiconscious, confused)
◦ At PaCO2 levels more than 70mmHg- Comatose
◦ Systemic vasodilation (warm flushed skin and a bounding
pulse)
◦ Cerebral vasodilation (elevated intracranial pressures,retinal
venous distention, papilledema, and headache)
 Respiratory Alkalosis
◦ abnormal condition in which there is a primary increase in alveolar
ventilation relative to the rate of CO2 production (i.e.,
hyperventilation.)
◦ Hyperventilation usually is the result of an increased stimulus or drive
to breathe e.g. pain, anxiety, and hypoxemia (PaO2 <60 mm Hg) and
as a compensatory response to metabolic acidosis
◦ Clinical signs and symptoms: tachypnea, dizziness, sweating, tingling
in the fingers and toes (paresthesia), and muscle weakness or spasm
 Metabolic Acidosis
◦ abnormal condition resulting from a net gain in fixed blood acids or reduction in buffer base.
◦ causes of two types of metabolic acidosis include the following:
◦ Increase in fixed acids:
a) Ketoacidosis (e.g., diabetes/starvation)
b) Renal failure (distal tubules/retention of H+)
c) Lactic acidosis (shock/anaerobic metabolism)
◦ Loss of base (HCO3-)
a) Diarrhea
b) Renal failure (proximal tubules/loss of HCO 3-)
Sign and symptoms: dyspnea, headache, nausea, and vomiting acutely. Confusion, stupor and dysrhythmias may
follow
 Metabolic Alkalosis
◦ Simple metabolic alkalosis is an abnormal condition resulting from a net gain in buffer base or loss in
fixed acids.
◦ Common causes of metabolic alkalosis include:
a) Hypokalemia or hypochloremia
b) Nasogastric suction (loss of stomach acid)
c) Persistent vomiting (loss of stomach acid)
d) Diuretic therapy
e) Steroid therapy
f) Excessive administration of sodium bicarbonate
Hypoventilation, CNS depression is present
THANKS FOR
PATIENCE