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Blood Gas Analysis : review

By: dr.Jeansen
 Clinical Case
 A 25 year old man, with no significant past medical history,
presents to the emergency department with a 2 day history of
fever , productive cough and worsening breathlessness.
 He is hot and flushed with a temperature of 39.3 oC. He doesn't
appeared distress but is using accessory muscles of respiration.
 There is diminished chest expansion on the left with dullness to
percussion, bronchial breathing and coarse crackles in the left
lower zone posteriorly.

P: 104 x/min, RR : 28 x /min, BP: 118/70 mmHg, SpO2: 89%
Question :Describe the probability of his gas
exchange!
Disorders of Gas
Exchange
Type 2 Respiratory Impairment

• High PaCO2 and is due to inadequate alveolar

ventilation

• PaO2 usually low too

• Room air = PAO2 (60) - PaO2(60)= 0

• High PaCO2 • Acute
• Room air : PAO2 (60) – PaO2
• Chronic
(60) = 0 (N:< 25-30)
• Common cause:
– Flail chest injury
– Opiate/ BNZ toxicity
– Inhaled foreign body
– Neuromuscular
disorders
– COPD*
Type 1 Respiratory Impairment

• Low PaO2 with normal or low

PaCO2
• Defective oxygenation despite
adequate ventilation
• Room air= PAO2 (110) - PaO2 (55)
• Common cause: • Assesing severity:
PaO2 SaO2
– V/Q mismatch • PaO2 SaO2
Mild 60-79 mmHg 90-94 %
– Right to left shunt Moderate 40-59 mmHg 75-89 %

Severe < 40 mmHg < 75%

– Pneumonia
– Pulmonary oedema
– Acute asthma
– COPD*
 Mixed respiratory failure
High PaCO2 and
• Room air = Increase PAO2- PaO2 gradient
– Example :
• Acute exacerbation of COPD
• Decompensated CHF ( type1 ) combined with pulmonary
disease (type 2)
 Clinical Case
 A 25 year old man, with no significant past medical history,
presents to the emergency department with a 2 day history of
fever , productive cough and worsening breathlessness.

He is hot and flushed with a temperature of 39.3 oC. He doesn't
appeared distress but is using accessory muscles of respiration.
 There is diminished chest expansion on the left with dullness to
percussion, bronchial breathing and coarse crackles in the left
lower zone posteriorly.
 P: 104 x/min, RR : 28 x /min, BP: 118/70 mmHg, SpO2: 89%

 Probability: Type 1 respiratory failure

• BGA : (on room air)
• pH : 7.5 ( N: 7.35 – 7.45)
• PCO2 : 28 mmHg ( N : 35 – 45 )
• PHCO3 : 24 mmol/L ( N: 22- 28 )
• PO2: 57.8 mmHg ( N: > 80)

• Describe his Acid Base status!

ACID BASE BALANCE
• Why acid base balance is so important?
– For celular processes ( include enzymes) to occur
efficiently
– Acidosis : CNS depression → death
– Alkalosis : CNS overexcitability → death
 Physiologic Effect
• Acidosis • Alkalosis
Respiratory Effects
• Respiratory Effects
· Hyperventilation (·· Kussmaul respirations)
· Shift of oxyhaemoglobin dissociation curve to the
left (impaired unloading of oxygen
· Shift of oxyhaemoglobin dissociation curve to the
right
· Inhibition of respiratory drive via the central &
peripheral chemoreceptors
Cardiovascular Effects
Cardiovascular Effects
· Depression of myocardial contractility (this effect
predominates at pH < 7.2 ) ,Sympathetic over-
· Depression of myocardial contractility , ·
activity, Resistance to the effects of catecholamines
Arrhythmias
· Peripheral arteriolar vasodilatation,
Central Nervous System Effects
Venoconstriction of peripheral veins ,
Vasoconstriction of pulmonary arteries ,Effects of
hyperkalemia on heart · Cerebral vasoconstriction leads to a decrease in
cerebral blood flow (result in confusion, muoclonus,
asterixis, loss of consciousness and seizures) Only
Central Nervous System Effects
seen in acute respiratory alkalosis. Effect last only
about 6 hours.
· Cerebral vasodilation
· Increased neuromuscular excitability ( result in
· Very high pCo2 levels will cause central depression paraesthesias such as circumoral tingling &
numbness; carpopedal spasm)
Other Effects
Other Effects
· Increased bone resorption (chronic metabolic
acidosis only) · Causes shift of hydrogen ions into cells, leading to
hypokalemia.
· Shift of K+ out of cells causing hyperkalemia

· Increase in extracellular phosphate concentration

Sources of H+ ions in our bodies:
1. Breakdown of fat and sugars for energy
2. Metabolism of protein → metabolic acids

Normal extracellular pH: 7.35 - 7.45

 Body Acid Base Regulation
• A. Chemical buffer system :
• 1. H2CO3 : HCO3 buffer pair = Primary ECF buffer for
noncarbonic acid
– CO2 + H2O↔ H2CO3 ↔ H+ + HCO3
• 2. Protein buffer system:
– Mostly by albumin
• 3. Phosphate buffer system
• 4. Hemoglobin buffer system = H+ buffer system generated
from CO2
• H++ Hb ↔ HHb
• B. Respiratory System = removal of CO2
– Limitation : can return pH only 50-75% toward
normal
• C. Renal :
– Conserve or excrete HCO3
– Energy dependent H+ carriers in the tubular cells
• Phosphate ( derived from excess ingested Phosphate )
• Amonia : from glutamine released by the renal tubular
cells when pH ↓
• NH3 + H+ → NH4+
Terms
 Mixed acid base disturbance
• When a primary respiratory disturbance and
primary metabolic occur simultaneously
• Ex : 1. Salycilate poisoning
– Primary Hyperventilation ( resp.alkalosis )
– salicylate acid ( metab.acidosis )

– 2. Severe ventilatory failure

– Rising PaCO2
– Lower PO2 → lactic acidosis
• Uncompensated acid • Compensated acid
base balance base balance
• When an alkalosis or • Partially compensated
acidosis developed • (pH still abnormal)
• Fully compensated
• (pH has returned back
to normal)
• Tips: the overcompensation doesn't
occur
Acid Base Balance Disorder
 Disorders of Acid Base Balance
• Henderson Haselbach
equation:
 Metabolic Acidosis
• Occurs when : • To help making dd/:
• The body produces too much • Anion gap= ( [Na+] ) - ( [Cl-]+[HCO3-] )
acid,
– Normal AG: 12 ± 2 mmol/L
• When the kidneys are not
• In patient with severe
removing enough acid from the hypoalbuminemia:
body,
• Corrected AG=Actual AG – {2.5(4.5-
• Through excessive loss of base album)}
(HCO3)
• Etiology: • Elevated anion gap:

• K = Ketoacidosis (DKA,alcoholic ketoacidosis, • Renal failure, Ketoacidosis, Lactic acidosis

starvation)
• Normal anion gap:
• U = Uremia (Renal Failure)
• Gi tract loss, Renal HCO3- loss, volume
• L =Lactic acidosis Rescucitation of Normal Saline
• T = Toxins (Ethylene glycol, methanol,
paraldehyde, salicylate)
• For Elevated anion gap (to determine if a mixed acid base disorder is present) :

• Delta ratio:
Measured anion gap – Normal anion gap = AG-12

Normal [HCO3-] – Measured [HCO3-] 24- [HCO3-]

Ratio table :

< 0.4 - Hyperchloraemic normal anion gap acidosis

0.4 to 0.8 - Combined high AG and normal AG acidosis

1 - Common in DKA due to urinary ketone loss

1 to 2 - Typical pattern in high anion gap metabolic acidosis

>2 Check for either a co-existing Metabolic Alkalosis (which would elevate [HCO3]) or a co-existing
Chronic Respiratory Acidosis (which results in compensatory elevation of [HCO3])

Cara lain : ∆gap: { AG - 12 } – {24 - HCO3-} Normal ∆ gap : 0 ± 6

Positive ∆ gap : High AG acidosis and a concurrent metabolic alkalosis

Negative ∆ gap : High AG & normal AG acidosis

Expected PaCO2 = 1.5 x [HCO3] + 8 (range: +/- 2)

 Metabolic Alkalosis
Any process ,other than a fall in CO2 → HCO3 and pH ↑
Etiology:
a. ↑ HCO3 generation:
Chloride depleted ( Urine Cl < 20mmol/L): Profound potassium depletion
Chloride expanded (Urine Cl > 20mmol/L) : Diuretics, Emesis, NGT,
Excess admin. Alkali : Acetate in parentral infusion, Citrate (blood
transfusion), Antacids, Bicarbonate.
b. Impaired HCO3 excretion : ↓ GFR
Compensation : Hypoventilation

Expected PaCO2 = 0.7 [HCO3] + 20 (range: +/- 5)*

 Respiratory Acidosis
• Hypoventilation causes ↑ blood CO2 and ↓ pH
• Etiology : Narcotics, CNS injury, pulmonary disease,
abdominal compartment syndrome
• Acute vs Chronic
• Acute respiratory acidosis :
• The PaCO2 is elevated with an accompanying acidemia (pH
<7.35)
• Decrease in pH = (PaCO2-40) x 0.08
• 10
• The [HCO3] will increase by 1 mmol/l for every 10 mmHg
elevation in pCO2 above 40 mmHg.
• Expected [HCO3] = 24 + { (Actual PaCO2 - 40) / 10 }
• Chronic respiratory acidosis :
• The PaCO2 is ↑ above the upper limit of the reference range,
with a normal blood pH (7.35 to 7.45) or near-normal pH
secondary to renal compensation and an elevated serum
bicarbonate (HCO3− >30 mm Hg).
– Decrease in pH = 0,03 x PaCO2 – 40
» 10
• The [HCO3] will increase by 4 mmol/l for every 10 mmHg
elevation in pCO2 above 40mmHg.
• Expected [HCO3] = 24 + 4 { (Actual PaCO2 - 40) / 10}
 Respiratory Alkalosis
Hyperventilation causes ↓ blood CO2 and ↑ pH
Etiology : pain, anxiety, fever,drugs (salycilate), thyrotoxicosis
Acute vs Chronic
Acute respiratory alkalosis :
The PaCO2 is decreased with an accompanying alkalosis ( pH >
7.45)
Increase in pH = (40 - PCO2) x 0.08
10
• The [HCO3] will decrease by 2 mmol/l for every 10
mmHg decrease in pCO2 below 40 mmHg.
• Expected [HCO3] = 24 - 2 { ( 40 - Actual pCO2) / 10 }
Chronic respiratory alkalosis :
• The PaCO2 is ↓ below the lower limit of the reference range,
with a normal blood pH (7.35 to 7.45) or near-normal pH
secondary to renal compensation and a decreased serum
bicarbonate.
– Increase in pH = 0,03 x 40 - PaCO2
10

The [HCO3] will decrease by 5 mmol/l for every 10 mmHg

decrease in pCO2 below 40 mmHg.
• Expected [HCO3] = 24 - 5 { ( 40 - Actual pCO2 ) / 10 } +/- 2)
 Clinical Case 1
A 25 year old man, with no significant past medical history, presents to the
emergency department with a 2 day history of fever , productive cough and
worsening breathlessness.
He is hot and flushed with a temperature of 39.3 oC. He doesn't appeared
distress but is using accessory muscles of respiration.
There is diminished chest expansion on the left with dullness to percussion,
bronchial breathing and coarse crackles in the left lower zone posteriorly.
P: 104 x/min, RR : 28 x /min, BP: 118/70 mmHg, SpO2: 89%
BGA : (on room air) , pH : 7.5 ( N: 7.35 – 7.45), PCO2 : 28 mmHg ( N : 35 – 45 ),
PHCO3 : 24 mmol/L ( N: 22- 28 ), PO2: 57.8 mmHg ( N: > 80)

Describe his gas exchange!

Acid base status?
Therapy?
 Clinical Case 2
• An 18 years old is admitted to the toxicology unit having taken
a large overdose of an unknown substance 5 hours earlier .
She complains of nausea.
• On examination : she is mildly confused,Her respirations are
increased in both rate and depth. P: 100x/mnt. RR: 26x/mnt,
BP: 132/100 mmHg, T: 37,6 0 C, O2 : 99%
• ABG: pH : 7.41 , PCO2 : 22.6 mmHg, PO2 : 97 mmHg,
HCO3: 17,6 mmol/L, K: 3,6 mmol/L, Na: 140mmol/L, Cl :
99mmol/L, Lactate : 1,4 (N: 0.4-1.5)
• Describe her gas exchange !
• Describe her acid base status !
– The anion gap?
• Is there any mixed acid base disorder?
• Thank You