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WORKING WITH BLOOD GASES

WORKING WITH BLOOD GASES. Martha Richter MSN, CRNA. OBJECTIVES. This lecture should help you Analyze blood gas results Discuss implications on anesthesia management when states of alkalosis/acidosis exist List the variations in acidosis/alkalosis states. ACID BASE & ABGS.

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WORKING WITH BLOOD GASES

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  1. WORKING WITH BLOOD GASES Martha Richter MSN, CRNA

  2. OBJECTIVES • This lecture should help you • Analyze blood gas results • Discuss implications on anesthesia management when states of alkalosis/acidosis exist • List the variations in acidosis/alkalosis states

  3. ACID BASE & ABGS • Henderson-Hasselbach’s equation describes the equilibrium between acids & bases • Disturbances • Metabolic – HCO3 • Respiratory- PaCO2 • Ph=(-)log of H ion concentration; describes acidity or alkalinity

  4. ACID BASE & ABG • What are the normal values: • pH- 7.35-7.45 • PaO2 – 90-100 • PaCO2 35-45 • Bic 21-27 mEq/l

  5. ABGS • What are the different states? • Metabolis alkalosis • Metabolis acidosis • Respiratory alkalosis • Respiratory acidosis • Compensated states of the above

  6. METABOLIC ALKALOSIS • pH >7.45 Bic >27 mEq/l • Assoc with increased mortality in the critically ill • Caused by: N/G suction, diuretics, renal hypoperfusion, hypokalemia, hypochloremia

  7. METABOLIC ALKALOSIS • Physiological effects • Hypokalemia + alkalosis = ventricular arrhythmias; potentiates dig. • May generate compensatory hypoventilation, generating hypercarbia = PaO2 dec • Inc bronchial tone + dec vent effort = atelectesis contributor • Oxyhemoglobin dissoc curve shifts to L = dec availability of O2 to tissues • Dec CO

  8. METABOLIC ALKALOSIS • Remember: • the majority of CO2 is carried as bicarb. • The greatest amount of CO2 is eliminated thru the lungs. • Do not compound metabolic alkalosis with respiratory alkalosis! • CV depression • arrhythmias

  9. METABOLIC ALKALOSIS • What are the treatment options? • Volume expansion to inc renal perfusion • K to correct • Consider 0.9NS instead of LR • Administer H • Ammonium cl, arginine HCl, 0.1 N-hydrocholic acid • Acetazolamide (carbonic anhydrase inhibitor-influences renal bicarb wasting) • Acid dialysis

  10. METABOLIC ACIDOSIS • pH <7.35 Bicarb <21 mEq/l • Anion gap calculation • Na-[Cl]+[HCO3]=<13 mEq/l normal • External losses as cause = normal anion gap • Anion gap >13 when:lactic/ketoacidosis, uremic retention of waste products, toxin ingest (ASA, ethylene glycol, methanol)

  11. METABOLIC ACIDOSIS • EFFECTS OF LOW PH • Dec myocardial contractility • Inc pulmonary vasc resist • Increase SVR • Impaired response to catechols by CV system • Normally, the body compensates with hyperventilation. Patients who are unable to compensate in this way may require mechanical ventilation

  12. METABOLIC ACIDOSIS • ASSESS THE PATIENT • RX aimed at correcting the underlying influences • Hypovolemia • Hypoperfusion • How is the renal function • Does any pulmonary pathology interfere with gas exchange

  13. METABOLIC ACIDOSIS • INTRAOP CARE • Art line to facilitate ABG “tracking” • PA catheter • Remember the exaggerated response to drugs & PPV

  14. WHAT ABOUT BICARB RX? • Severe acidosis may require IV NaBicarb • One calc: Wt kgX0.3X(24mEq/l-actual HCO3)/2 This is a half-correction used for the initial dose. Req. ABG recheck at freq intervals. The use of Bicarb remains controversial.

  15. RESPIRATORY ALKALOSIS • pH >7.45 PaCO2 <35 • Response to inc minute volume • Pain • Anxiety • Hypoxemia • CNS disease • Sepsis

  16. RESPIRATORY ALKALOSIS • May produce • Hypokalemia • Hypocalcemia • Dysrhthmias • Bronchoconstriction • Hypotension • Potentiation Dig toxicity

  17. RESPIRATORY ALKALOSIS • Remember the effect on CBF • Acute profound hypocapnia = <20mmHg • Cerebral ischemia! • Rx the underlying cause!

  18. RESPIRATORY ACIDOSIS • pH <7.35 PaCO2 >45 (always) • Causes • Minute vol insuff to eliminate CO2 • CNS depression (drugs/injury) • Increased work of breathing=tired • Airway obstruction • Neuromuscular dysfunction • Inc Vd dut to pulmonary embolism,COPD,acute respiratory failure • Acute/chronic • Increase in CO2 prod

  19. RESPIRATORY ACIDOSIS • When d/t intrinsic pulmonary dis • Remember to “handle with care” • Postop pain management issues • Art line to allow ABG sampling • Aim for a normal pH in CO2 retainers • Acute resp acid requires mechanical vent if the underlying cause can’t be treated quickly

  20. INTERPRETING THE ABG • Need to know the hx, ABG, lytes • Identify what needs immed intervention • Resp acid pH<7.1=vent, ETT • Metabol acid pH<7.1=alkalinizing RX What’s the disturbance? Acidosis/alkalosis resp/metabol/mixed Is it simple resp acute? Low pCO2 should have elev pH with low HCO3.

  21. INTERPRETING THE ABG • A calculation for determining acute condition • pH decreases 0.1 for every 10mm inc PaCO2 • HCO3 dec 2mEq/l for every 10mmHg dec PaCO2 • If your numbers don’t follow this rule, consider a chronic condition • When you can’t describe acute/chronic resp changes, consider metabolic process

  22. COMPENSATION RULES • Respiratory comp occurs more quickly then metabolic • Overcompensation is rare • Inadequate/excess compen suggests additional primary process • Metabolic acidosis assoc with inc anion gap is never compensatory • Rules of thumb approximate pH-H relationship • The presence of an anion gap sorts out the presence of metabolic acidosis

  23. COMPENSATION • Respiratory compensation for metabolic processes happens immediately • Metabolic compensation for respiratory processes happens slowly (1-2 days)

  24. WHY IS THE TEMPERATURE IMPORTANT? • CO2 is more soluble in cold blood. • Request ABGs at true body temp • The difference is important when comparing ABGs with ETCO2 or gas results from pump-oxygenator

  25. REMEMBER THE BASE EXCESS • Base excess • (-) = metabolic component in the face of acidosis • (+)= compensated in the face of acidosis • As BE goes down, reflects cellular hypoperfusion/hypoxia-correct the underlying problem

  26. EXAMPLES • Pure (Uncompensated) Respiratory • Acute • Acidosis: PCO2=52, pH=7.3 • Hypoventilation • Requires 1-2 days for compensation • Alkalosis:PCO2=28, pH=7.5 • Acute hyperventilation • Requires 1-2 days for compensation

  27. EXAMPLES • Compensated Respiratory • Chronic acidosis: pH7.3, PaCO2=64 • COPD • Chronic alkalosis: pH 7.45, PaCO2 – 28 • High altitude response to hypoxia

  28. EXAMPLES • COMPENSATED METABOLIC Acidosis pH 7.3, PaCO2 28 compensation after lactic acidosis Alkalosis pH 7.5, PaCO2 52 comp after vomiting/aspiration

  29. EXAMPLES • MIXED • Acidosis • pH 7.1 PaCO2 64 • Following trauma with tissue ischem &resp depression • Alkalosis • pH 7.6 PaCO2 28 • Gastric aspiration with mechan hyperventilation

  30. RULES OF THUMB Barash • Dec PaCO2 • pH inc 0.1 for every 10 mmHg dec PaCO2 • Bicarb dec 2 mEq/l for every 10 mmHg dec in PaCO2 • pH will nearly normalize hypocarbia is sustainable • Bicarb will dec 5-6 mEq/l for each chronic 10 mmHg dec PaCO2

  31. RULES OF THUMB Barash • Increased PaCO2 • pH will dec 0.05 for every acute PaCO2 inc 10 mmHg • Bicarb will inc 1.0 mEq/l for every PaCO2 inc of 10 mmHg • pH will return toward normal if hypercarbia is sustained • Bicarb will increase 4 mEq/l for ea chronic 10 mmHg inc PaCO2

  32. ACID BASE & ABGS • Be logical in your analysis • Keep it simple

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