arterial blood gas

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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

• Room air : PAO2 (60) – PaO2 (60) = 0 (N:< 25-30)

• Common cause:

– Flail chest injury

– Opiate/ BNZ toxicity

– Inhaled foreign body

– Neuromuscular disorders

– COPD*

• Acute

• Chronic

Type 1 Respiratory Impairment

• Low PaO2 with normal or low PaCO2

• Defective oxygenation despite adequate ventilation

• Room air= PAO2 (110) - PaO

2 (55)

=55

• Common cause:

– V/Q mismatch

– Right to left shunt

– Pneumonia

– Pulmonary oedema

– Acute asthma

– COPD*

• Assesing severity:

• PaO2 SaO2PaO2 SaO2

Mild 60-79 mmHg 90-94 %

Moderate 40-59 mmHg 75-89 %

Severe < 40 mmHg < 75%

Mixed respiratory failure

High PaCO2 and

• Room air = Increase PAO2- PaO

2 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• AcidosisRespiratory Effects

· Hyperventilation (·· Kussmaul respirations)

· Shift of oxyhaemoglobin dissociation curve to the right

Cardiovascular Effects

· Depression of myocardial contractility (this effect predominates at pH < 7.2 ) , Sympathetic over-activity, Resistance to the effects of catecholamines

· Peripheral arteriolar vasodilatation, Venoconstriction of peripheral veins , Vasoconstriction of pulmonary arteries ,Effects of hyperkalemia on heart

Central Nervous System Effects

· Cerebral vasodilation

· Very high pCo2 levels will cause central depression

Other Effects

· Increased bone resorption (chronic metabolic acidosis only)

· Shift of K+ out of cells causing hyperkalemia

· Increase in extracellular phosphate concentration

• Alkalosis• Respiratory Effects

· Shift of oxyhaemoglobin dissociation curve to the left (impaired unloading of oxygen

· Inhibition of respiratory drive via the central & peripheral chemoreceptors

Cardiovascular Effects

· Depression of myocardial contractility , ·Arrhythmias

Central Nervous System Effects

· Cerebral vasoconstriction leads to a decrease in cerebral blood flow (result in confusion, muoclonus, asterixis, loss of consciousness and seizures) Only seen in acute respiratory alkalosis. Effect last only about 6 hours.

· Increased neuromuscular excitability ( result in paraesthesias such as circumoral tingling & numbness; carpopedal spasm)

Other Effects

· Causes shift of hydrogen ions into cells, leading to hypokalemia.

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+ → NH

4+

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 base balance

• When an alkalosis or acidosis developed

• Compensated acid base balance

• Partially compensated

• (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 :

• The body produces too much acid,

• When the kidneys are not removing enough acid from the body,

• Through excessive loss of base (HCO

3)

• Etiology:

• K = Ketoacidosis (DKA,alcoholic ketoacidosis, starvation)

• U = Uremia (Renal Failure)

• L =Lactic acidosis

• T = Toxins (Ethylene glycol, methanol, paraldehyde, salicylate)

• To help making dd/:• Anion gap= ( [Na+] ) - ( [Cl-]+[HCO3-] )

– Normal AG: 12 ± 2 mmol/L

• In patient with severe hypoalbuminemia:

• Corrected AG=Actual AG – {2.5(4.5-album)}

• Elevated anion gap:

• Renal failure, Ketoacidosis, Lactic acidosis

• Normal anion gap:

• Gi tract loss, Renal HCO3- loss, volume Rescucitation of Normal Saline

• 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 1A 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 ), PO

2: 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