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ARTERIAL BLOOD GASES

1. How did ABGs come about? 2. What are they for? 3. What can we determine when we look at an ABG? 4. How do we interpret ABGs? 5. How will the ABG help us in managing the patient?

Henderson Hasselbach equation- direct association between the acid and the base in order to maintain an optimal internal environment which is essential to life [H+] = 24 x pco2 HCO3

Patterns of Acid- Base interpretation 1. Observe pH 2. Identify the primary acid-base disturbance 3. Acute or chronic 4. Degree of compensation 5. Identify second acid-base disturbances (mixed)

Compensation for Acid-bases Disturbances via the lungs and the kidneys Primary abnormality Respiratory acidosis hypoventilation Compensatory responses Decrease HCO3 excretion Respiratory hyperventilation Increase HCO3 alkalosis excretion Metabolic acidosis Loss of HCO3 Hyperventilation Metabolic alkalosis Increase in HCO3 Hypoventilation - Compensation does not necessarily mean pH goes back to NORMAL - Renal compensation is not immediate (several hours)

Indications of ABG 1. Ventilator, acid-base status 2. oxygenation status

4 Main ACID-BASE disturbances a. Respiratory acidosis b. Respiratory alkalosis c. Metabolic acidosis d. Metabolic alkalosis

Normal values: pH= 7.35 7.45 pCO2= 35-45 pO2= 80-100 HCO3= 22-27

Interpretation of ABGs A. Respiratory acidosis- when the level of alveolar ventilation decreases below that necessary to excrete CO2 produced [H+]= 24 x pCO2 HCO3

Acute change in pH = ^pCO2 x 0.007 Chronic change in pH = ^pCO2 x 0.003 ^[H+] = Actual [H+] Normal [H+] ^pCO2 = Actual pCO2 Normal pCO2

<0.3 --- chronic 0.3 0.7 --- chronic in acute exacerbation >0.7 --- acute

A. Acute Respiratory Acidosis: Increase pCO2 10 mmHg with corresponding increase 1 mEq HCO3 (limit: 30 mEq/L) B. Chronic Respiratory Acidosis: Increase pCO2 10 mmHg with corresponding increase 4 mEq HCO3 (limit: 45 mEq/L) Ex : 7.38 / 53.8 / 122 / 31.4 / 98.3% [H+] = 53.8 x 24 = 41.1 31.4 53.8 40 = 13.8 (^pCO2) 13.8 divided by 10 = 1.3 1.3 x 4 = 5.2 Acute ^pH = 13.8 x 0.007 = 0.096 7.4 0.096 = 7.3 41.1 40 = 0.08 (chronic) 53.8 40 = 5.2 + 22 = 27.2 + 26 = 31.2

Chronic ^pH = 13.8 x 0.003 = 0.04 7.4 0.04 = 7.36 Expected pH = 7.30 7.36 If actual pH is less than expected, there is a concomitant metabolic acidosis If actual pH is more than expected, there is a concomitant metabolic alkalosis

Causes of Hypercapnea (Increase pCO2) A. Decrease VE (minute ventilation) 1. Decrease ventilator drive 2. Drug overdose 3. Destructive brain lesion 4. Pickwickian syndrome B. Increase VE 1. Pulmo parenchymal dse 2. Inc. airway resistance (asthma) 3. Increase compliance (emphysema)

C. Neuromuscular diseases 1. Cord transaction 2. GBS, MG 3. Muscular dystrophy

B. Respiratory alkalosis- results when level of alveolar ventilation is increased above that necessary to excrete CO2 produced Acute decrease pCO2 10 mmHg, corresponding decrease 2 mEq HCO3 (limit: 18 mEq/L) Chronic decrease pCO2 10 mmHg, corresponding decrease 5 mEq HCo3 (limit : 12 -15 mEq/L) Causes: CNS Excitation 1. acute anxiety 2. drugs 3. CNS infection Peripheral Chemoreceptor Activation 1. Arterial hypoxemia (<50 mmHg) 2. Metabolic acidosis

Idiopathic 1. Exercise 2. restrictive lung disease

Ex : 20 y/o Navy, presents with 3 day history of non productive cough, fever of 38.5C and diffuse alveolar filling on CXR ABG: 7.45 / 28 / 40 / 20 40 28 = 12 12 divided by 10 = 1.2 1.2 x 5 = 6 24 6 = 18 2 16 20 mEq Simple Respiratory Alkalosis

C. Metabolic Acidosis- results if there is either loss of extracellular buffer (HCO3) or the addition of a fixed acid PaCO2 = 1.5 x observed HCO3 + 8 2 Limit of compensation: 10 mmHg Anion gap= serum Na+ - (Cl + HCO3) Normal = 10-12 mEq/L

Ex: 7.18 / 17.4 / 126.3 / 6.9 / 97.6% (1.5 x 6.9) + 8 2 pCO2 = 18.3 2 16 20 If actual pCO2 is more than expected, there is a concomitant respiratory acidosis If actual pCO2 is less than expected, there is a concomitant respiratory alkalosis

Causes: a. Increase anion gap 1. Renal failure 2. Ketoacidosis (diabetic, alcoholic, lactic) 3. Toxins (salicylates, methanol, and ethylene glycol) b. Decrease anion gap 1. Diarrhea 2. Small bowel, biliary, pancreatic drainage 3. RTA 4. Urinary, GI anastomosis 5. Addition of HCl or congeners

4. Metabolic Alkalosis- results when there is either loss of fixed acids or gain in body buffers (HCO3) Expected pCO2 = ( actual normal HCO3) x 0.75 + 40 Limit : 55 mmHg Ex: 7.45 / 40.4 / 96.8 / 29 / 97.5% Expected pCO2 = (29 24) x 0.75 + 40 = 43.75 41 - 45 If actual pCO2 is more than expected, there is a concomitant respiratory acidosis If actual pCO2 is less than expected, there is a concomitant respiratory alkalosis

Causes: a. Loss of acids 1. extrarenal = vomiting 2. renal = diuretic 3. potassium depletion 4. primary aldosteronism b. Gain of Acid 1. HCO3 administration

OXYGENATION Normal values 1. seated: 104.2 0.27 (age in years) 2. Supine: 103.5 0.42 (age in years)

Room Air (FiO2= 0.21) = # of LPM x 4 +2o Patient <60 years old: pO2 = 100 20 Patient >60 years old: subtract 1 from 80 for every year above 60 years of age

On supplemental oxygen (FiO2 > 0.21) - compute for the P/F ratio

Causes of Hypoxemia 1. Central hypoventilation 2. Low FiO2 3. Decreased diffusing capacity 4. V/Q mismatched 5. Shunt 6. Low mixed venous oxygen

Indices of Oxygenation: AaDO2, aAO2, P/F a. aAO2 = >0.75 b. P/F = 400 500 c. AaO2 = <25 29 or (age) +4 4 the wider the gradient the more hypoxemic

1. aAO2 PAO2 = (Pbarometric PH2O) (FiO2)- pCO2 0.8 Pbarometric = 760 PH2O = 47 Ex = 7.38/ 38 / 90 / 22.4 / 96.6% at 48% FiO2 PAO2 = (760 47) x 0.48 - 38 0.8 = 713 x 0.48 - 38 0.8 = 295 aAO2 = actual pO2 in the ABG pAO2 = 90 295 aAO2 = 0.30

2. AaDO2 = difference in O2 in the alveolus and arterial blood Determines diffusing capacity/ efficiency of diffusion across the alveolar-capillary barrier pAO2 paO2 (found in blood gas) AaDO2 = 295 90 = 205 Interpret: corrected hypoxemia at FiO2 48% 3. P/F Ratio = pO2 FiO2 Normal for patient <60 = 400-500 Normal for patient >60 = multiply every year above 60 by 5 then subtract the total from 400 If the actual P/F ratio is less than expected, the patient is hypoxemic If the actual P/F ratio is equal to the expected value, the patient is non-hypoxemia

HYPOXEMIA - Relative deficiency of Oxygen tension in arterial blood - Causes: 1. Hypoventilation- decrease volume of air moving in and out of the mouth/min (decrease minute ventilation) Ex: a. Drug induced CNS suppression (barbiturate overdose) b. Increase ICP due to brainstem compression c. Idiopathic (pickwickian syndrome)

Clinical detection: decrease Vt and decrease RR 2. Decreased Inspired O2 tension ascent to altitude leading to decrease in barometric pressure leading to decrease PAO2 and decrease PaO2 - Concern for respiratory patients in high altitudes

3. Diffusion abnormalities- rarely cause hypoxemia at rest - Significant only in patient with pre existing abnormalities in lung function who undergo exercise

4. V/Q Mismatch- low ventilation in normal perfused lung unit due to a. increase Raw (asthma, bronchitis) b. decrease Compliance (stiff lung: restrictive lung dse) c. increase compliance (emphysema) V/Q < 1

5. Shunt no ventilation with persistent perfusion in lung unit due to: a. airway closure (atelectasis) b. alveolar filling (aspiration, pneumonia, drowning) V/Q = 0

Differentiating Causes of Arterial Hypoxemia

Mechanism

AaO2

PaO2

Central N hypoventilation Shunt >60 Dec V/Q due to: Inc airway 30-50 resistance Inc compliance 30-50 Dec compliance >60

increase decrease

Response CXR to 100% O2 N N Abn White lung

N, inc N, inc decrease

N N N

Black lung Black lung

Evaluation of Hypoxemia Room air, patient < 60 year old 1. Mild hypoxemia, PaO2 < 80 mmHg 2. Moderate hypoxemia, PaO2 <60 mmHg 3. Severe hypoxemia, PaO2 <40 mmHg

Oxygen therapy: 1. Uncorrected hypoxemia: PaO2 < RA acceptable limit 2. Corrected hypoxemia: PaO2 > RA minimal acceptable limit; < 100 mmHg 3. Excessively corrected hypoxemia: PaO2 = 100mmHg < minimal predicted