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` Blood Gas Analysis : review By: dr.Jeansen

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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)

Acute Chronic

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) =55

Common cause: V/Q mismatch Right to left shunt Pneumonia Pulmonary oedema Acute asthma COPD*

Assesing severity: Mild Moderate Severe PaO2 PaO2 60-79 mmHg 40-59 mmHg < 40 mmHg SaO2 SaO2 90-94 % 75-89 % < 75%

Mixed respiratory failureHigh 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 death

Alkalosis : CNS overexcitability

Acidosis

Physiologic Effect

AlkalosisRespiratory Effects Shift of oxyhaemoglobin dissociation curve to the left (impaired unloading of oxygen Inhibition of respiratory drive via the central & peripheral chemoreceptors

Respiratory 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

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)

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

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 fornoncarbonic 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 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 (HCO3) Etiology:K = Ketoacidosis (DKA,alcoholic ketoacidosis, starvation) U = Uremia (Renal Failure)

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(4.5album)}

Elevated anion gap:

Renal failure, Ketoacidosis, Lactic acidosisNormal anion gap:Gi tract loss, Renal HCO3- loss, volume Rescucitation of Normal Saline

L =Lactic acidosis T = Toxins (Ethylene glycol, methanol, paraldehyde, salicylate)

For Elevated anion gap (to determine if a mixed acid base disorder is present) : Delta ratio:AG-12 24- [HCO3-]

Measured anion gap Normal anion gap = Normal [HCO3-] Measured [HCO3-] Ratio table : < 0.4 0.4 to 0.8 1 1 to 2 >2

- Hyperchloraemic normal anion gap acidosis - Combined high AG and normal AG acidosis - Common in DKA due to urinary ketone loss - Typical pattern in high anion gap metabolic acidosis

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 AlkalosisAny process ,other than a fall in CO2 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 transfusion), Antacids, Bicarbonate. b. Impaired HCO3 excretion : Compensation : Hypoventilation GFR (blood

HCO3 and pH

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 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 AlkalosisHyperventilation 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 ), 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