VIEWS: 9 PAGES: 30 POSTED ON: 12/14/2011
ARTERIAL BLOOD GASES Dr.Balamugesh ABG - Introduction Blood gas and pH analysis has more immediacy and potential impact on patient care than any other laboratory determination.(National committee for Laboratory Standards). Cornerstone in the diagnosis & management of clinical oxygenation and acid-base disturbances. Of all the concepts employed in the diagnosis and treatment of respiratory disorders, few are more important or less well understood than those of blood gas interpretation. Information from ABGs OXYGENATION VENTILATION & ACID BASE 1. OXYGENATION:- FiO2 (0.21 – 1.0) P/F ratio A-a gradient PaO2 2. VENTILATION & ACID BASE CO2 +H2O H2CO3 H+ + HCO3- Tissues Expired CO2 H+ Normal Ranges PaO2 >80mm Hg – In supine posture PaO2=109-(0.43 Х age) – PaO2=100mmHg in 10 year old child, PaO2 falls approximately 5mmHG for every 10 years upto 90 years. – 5 mmHg higher in the sitting position that supine position Normals pH 7.35-7.45 pCO2 35-45 HCO3 24+2 Blood samples must be drawn only when the patient is in steady state. 20 to 30 min waiting period is recommended before taking ABG after a change in oxygen therapy or ventilation in those with pulmonary disease. Sampling errors -Air contamination Most important change: PaO2 tends to increase towards 158mm Hg, Less significant change: PaCO2 falls, pH rises All air bubbles should be expelled immediately All samples with visually apparent froth should be discarded. Venous sampling/admixture Mixed venous blood – pH 7.38, pCO2 48mmHg, PaO2 40mmHg, SaO2 75% Flash of blood on entering artery, pulsations during syringe filling, auto-filling of syringe, correlate with pulse oximetry. Addition of one-tenth of venous blood to an arterial sample could produce 25% drop in measure PaO2. Blood Volume (ml) PaO2 Arterial 4.5 86 Venous 0.5 31 Mixed 5.0 56 Anticoagulant effects 0.05ml of heparin(1,000units/ml) is required to anticoagulate 1 ml of blood. Dead space of a standard 5ml syringe with 22G needle is 0.2ml; i.e. filling the syringe dead space with heparin provides sufficient volume to anticoagulate a 4ml blood sample. Heparin – weak acid equilibrated with room air Initially PaCO2 falls, In extreme dilution pH and bicarbonate falls PaO2 usually unchanged. Time delay - metabolism Samples should be analyzed within 20 min to avoid error. Measurement Direction Magnitude/Hour pH ↓ 0.05 PCO2 ↑ 5 PaO2 ↓ 20 150 (initial >250mmHg) Placing the sample in iced water slows metabolism to 10%. Leukocyte Larceny – Rapid fall in PaO2 in blood samples with high leukocyte counts – due to metabolism by leukocytes. Approach to Hypoxia Six basic mechanisms of hypoxia 1. Decrease in inspired PO2 2. Hypoventilation 3. Shunting 4. V/Q mismatching 5. Diffusion barrier – least common cause 6. Increased tissue consumption – not significant if lungs are normal Alveolar-arterial oxygen gradient(A-a gradient) Driving force for oxygen to enter blood Indicator of the extent of parenchymal dysfunction in the lung PAO2=[FiO2 Х (PB-PH20)] – PaCO2/R PAO2=150-[1.25 Х PaCO2] Normal= <15mmHg in <30yr old Increases by ~3mmHg per decade PaCO2=60; PaO2=35; pH=7.36. Mechanism of Hypoxia? AO2=150 – 1.25 Х 60 = 75 A-a gradient=75-35=40. Ans: hypoventilation with another mechanism. P/F ratio (PaO2/FiO2) Easy to calculate index of pulmonary parenchymal dysfunction Does not consider PaCO2. Normal 400-500 Moderate pulmonary dysfunction 200-400 Substantial pulmo. Dysfunction <200. Helps to decide the safe limits of reduction of FiO2 during weaning from oxygen. E.g: PaO2-160 on FiO2 of 0.8. If we want PaO2 of 80 reduce FiO2 to 0.4. Steps in Acid-base classification 1. pH classification 2. PaCO2 classification 3. Metabolic classification 4. Compensation evaluation 5. Complete acid-base classification Verification of internal consistency Henderson-Hasselbalch equation pH=6.1 + HCO3 / ( 0.031 Х PCO2) pH classification 7.35-7.45 – Normal <7.35 – acidosis >7.45 - alkalosis PaCO2 assessment Normal 35-45 Respiratory acidosis >45 Respiratory alkalosis<35 Metabolic assessment BE HCO3 Normal 0 ±2 24 ±2 Met.acidosis <-2 <22 Met.alkalosis >+2 >26 Anion gap: Plasma anions not measured by routine laboratory. AG= (Na+K) – (Cl+HCO3). Normal = 12 + 4 mEq/L Respiratory Acidosis In Respiratory Failure CO2 retention Causes – from cerebral cortex to the peripheral nerve innervating respiratory muscle; from large airway to pleura.. Treatment – mechanical ventilation, cause. Respiratory Alkalosis As in Hyperventilation Results in Hypocarbia Causes- Anxiety, cerebral stimulation, sepsis, drugs, hypoxia. Treatment - Cause, rebreathing Metabolic Acidosis- Check too much Heparin ?? Increased Anion gap – Sepsis, renal Failure, Ketoacidosis, Drugs and Poisons Normal Anion Gap – GI-loss, Renal tubular acidosis, Endocrine (steroid def, renin def) Drugs ( Spironolactone, Amiloride, Triamterene ) Treatment – Cause, Bicarb to replace buffer. Metabolic Alkalosis Causes – - Vomiting as in Gastric outlet obstruction; loss of HCl acid, - Renal with increased steroids, - K+ depletion as with loop diuretics, - Iatrogenic as with bicarbonate therapy. Treatment – correct perpetuating cause(s): volume depletion, potassium correction Compensation assessment Return of an abnormal pH towards normal by the component that was not primarily affected. Body does not over compensate for a primary acid-base disturbance. In other words, when the pH reaches the normal range, compensatory mechanisms are no longer triggered. Expected compensation Disorder Initial change Compensation Met. Acidosis ↓ in HCO3 1.2 mmHg ↓in PCO2 for every 1 ↓ in HCO3 Met. Alkalosis ↑ in HCO3 0.6 ↑ in PCO2 for every 1 ↑ in HCO3 Resp.acidosis – Acute ↑ in PCO2 1 ↑ in HCO3 for every 10 ↑ in PCO2 Resp.acidosis – 3.3 ↑ in HCO3 for Chronic every 10 ↑in PCO2 Resp.alkalosis – Acute ↓ in PCO2 2.2 ↓ in HCO3 for every 10 ↓ PCO2 Resp.alkalosis – 4.4 ↓ in HCO3 for Chronic every 10 ↓ in PCO2. pH PaCO2 HCO3 Diagnosis 7.6 30 31 MAlk+RAlk 7.1 70 14 MAci+RAci 7.5 25 21 RespAlk 7.4 20 12 MAc+Ralk 7.5 47 36 MAlk THANK YOU
"ARTERIAL BLOOD GAS"