ABG INTERPRETATION Debbie Sander PAS-II Objectives What’s an ABG? Understanding Acid/Base Relationship General approach to ABG Interpretation Clinical causes Abnormal ABG’s Case studies Take home What is an ABG Arterial Blood Gas Drawn from artery- radial, brachial, femoral It is an invasive procedure. Caution must be taken with patient on anticoagulants. Helps differentiate oxygen deficiencies from primary ventilatory deficiencies from primary metabolic acid-base abnormalities What Is An ABG? pH [H+] PCO2 Partial pressure CO2 PO2 Partial pressure O2 HCO3 Bicarbonate BE Base excess SaO2 Oxygen Saturation Acid/Base Relationship This relationship is critical for homeostasis Significant deviations from normal pH ranges are poorly tolerated and may be life threatening Achieved by Respiratory and Renal systems Case Study No. 1 60 y/o male comes ER c/o SOB. Tachypneic, tachycardic, diaphoretic and Cyanotic. Dx acute resp. failure and ABG’s Show PaCO2 well below nl, pH above nl, PaO2 is very low. The blood gas document Resp. failure due to primary O2 problem. Case Study No. 2 60 y/o male comes ER c/o SOB. Tachypneic, tachycardic, diaphoretic and Cyanotic. Dx acute resp. failure and ABG’s Show PaCO2 very high, low pH and PaO2 is moderately low. The blood gas document Resp. failure due to primarily ventilatory insufficiency. Buffers There are two buffers that work in pairs H2CO3 Carbonic acid NaHCO3 base bicarbonate These buffers are linked to the respiratory and renal compensatory system Respiratory Component function of the lungs Carbonic acid H2CO3 Approximately 98% normal metabolites are in the form of CO2 CO2 + H2O H2CO3 excess CO2 exhaled by the lungs Metabolic Component Function of the kidneys base bicarbonate Na HCO3 Process of kidneys excreting H+ into the urine and reabsorbing HCO3- into the blood from the renal tubules 1) active exchange Na+ for H+ between the tubular cells and glomerular filtrate 2) carbonic anhydrase is an enzyme that accelerates hydration/dehydration CO2 in renal epithelial cells Acid/Base Relationship H2O + CO2 H2CO3 HCO3 + H+ Normal ABG values pH 7.35 – 7.45 PCO2 35 – 45 mmHg PO2 80 – 100 mmHg HCO3 22 – 26 mmol/L BE -2 - +2 SaO2 >95% Acidosis pH < 7.35 Alkalosis pH > 7.45 PCO2 > 45 PCO2 < 35 HCO3 < 22 HCO3 > 26 Respiratory Acidosis Think of CO2 as an acid failure of the lungs to exhale adequate CO2 pH < 7.35 PCO2 > 45 CO2 + H2CO3 pH Causes of Respiratory Acidosis emphysema drug overdose narcosis respiratory arrest airway obstruction Metabolic Acidosis failure of kidney function blood HCO3 which results in availability of renal tubular HCO3 for H+ excretion pH < 7.35 HCO3 < 22 Causes of Metabolic Acidosis renal failure diabetic ketoacidosis lactic acidosis excessive diarrhea cardiac arrest Respiratory Alkalosis too much CO2 exhaled (hyperventilation) PCO2, H2CO3 insufficiency = pH pH > 7.45 PCO2 < 35 Causes of Respiratory Alkalosis hyperventilation panic d/o pain pregnancy acute anemia salicylate overdose Metabolic Alkalosis plasma bicarbonate pH > 7.45 HCO3 > 26 Causes of Metabolic Alkalosis loss acid from stomach or kidney hypokalemia excessive alkali intake How to Analyze an ABG = 80 – 100 mmHg 1. PO2 NL 2. pH NL = 7.35 – 7.45 Acidotic <7.35 Alkalotic >7.45 3. PCO2 NL = 35 – 45 mmHg Acidotic >45 Alkalotic <35 4. HCO3 NL = 22 – 26 mmol/L Acidotic < 22 Alkalotic > 26 Four-step ABG Interpretation Step 1: Examine PaO2 & SaO2 Determine oxygen status Low PaO2 (<80 mmHg) & SaO2 means hypoxia NL/elevated oxygen means adequate oxygenation Four-step ABG Interpretation Step 2: pH acidosis alkalosis <7.35 >7.45 Four-step ABG Interpretation Step 3: study PaCO2 & HCO 3 respiratory irregularity if PaCO2 abnl & HCO3 NL metabolic irregularity if HCO3 abnl & PaCO2 NL Four-step ABG Interpretation Step 4: Determine if there is a compensatory mechanism working to try to correct the pH. ie: if have primary respiratory acidosis will have increased PaCO2 and decreased pH. Compensation occurs when the kidneys retain HCO3. ~ PaCO – pH Relationship 2 80 7.20 60 7.30 40 7.40 30 7.50 20 7.60 ABG Interpretation Acidosis CO2 Change c/w Abnormality CO2 More Abnormal CO2 Expected CO2 Less Abnormal Compensated Respiratory Acidosis Respiratory Acidosis Mixed Respiratory Metabolic Acidosis CO2 Normal CO2 Change opposes Abnormality Metabolic Compensated Metabolic Acidosis Metabolic Acidosis ABG Interpretation Alkalosis CO2 Change c/w Abnormality CO2 More Abnormal CO2 Expected CO2 Less Abnormal Compensated Respiratory Alkalosis Respiratory Alkalosis Mixed Respiratory Metabolic Alkalosis CO2 Normal CO2 Change opposes Abnormality Metabolic Alkalosis Compensated Metabolic Alkalosis Respiratory Acidosis pH 7.30 PaCO2 60 HCO3 26 Respiratory Alkalosis pH 7.50 PaCO2 30 HCO3 22 Metabolic Acidosis pH 7.30 PaCO2 40 HCO3 15 Metabolic Alkalosis pH 7.50 PCO2 40 HCO3 30 What are the compensations? Respiratory acidosis metabolic alkalosis Respiratory alkalosis metabolic acidosis In respiratory conditions, therefore, the kidneys will attempt to compensate and visa versa. In chronic respiratory acidosis (COPD) the kidneys increase the elimination of H+ and absorb more HCO3. The ABG will Show NL pH, CO2 and HCO3. Buffers kick in within minutes. Respiratory compensation is rapid and starts within minutes and complete within 24 hours. Kidney compensation takes hours and up to 5 days. Mixed Acid-Base Abnormalities Case Study No. 3: 56 yo neurologic dz required ventilator support for several weeks. She seemed most comfortable when hyperventilated to PaCO2 28-30 mmHg. She required daily doses of lasix to assure adequate urine output and received 40 mmol/L IV K+ each day. On 10th day of ICU her ABG on 24% oxygen & VS: ABG Results pH PCO2 PO2 HCO3 BE K+ 7.62 30 mmHg 85 mmHg 30 mmol/L 10 mmol/L 2.5 mmol/L BP Pulse RR VT MV 115/80 mmHg 88/min 10/min 1000ml 10L Interpretation: Acute alveolar hyperventilation (resp. alkalosis) and metabolic alkalosis with corrected hypoxemia. Case study No. 4 27 yo retarded with insulin-dependent DM arrived at ER from the institution where he lived. On room air ABG & VS: pH PCO2 PO2 HCO3 BE 7.15 22 mmHg 92 mmHg 9 mmol/L -30 mmol/L Interpretation: BP Pulse RR VT MV 180/110 mmHg 130/min 40/min 800ml 32L Partly compensated metabolic acidosis. Case study No. 5 74 yo with hx chronic renal failure and chronic diuretic therapy was admitted to ICU comatose and severely dehydrated. On 40% oxygen her ABG & VS: pH PCO2 PO2 HCO3 BE 7.52 55 mmHg 92 mmHg 42 mmol/L 17 mmol/L BP Pulse RR VT MV 130/90 mmHg 120/min 25/min 150ml 3.75L Interpretation: Partly compensated metabolic alkalosis with corrected hypoxemia. Case study No. 6 43 yo arrives in ER 20 minutes after a MVA in which he injured his face on the dashboard. He is agitated, has mottled, cold and clammy skin and has obvious partial airway obstruction. An oxygen mask at 10 L is placed on his face. ABG & VS: pH 7.10 BP 150/110 mmHg PCO2 60 mmHg Pulse 150/min PO2 125 mmHg RR 45/min HCO3 18 mmol/L VT ? ml BE -15 mmol/L MV ? L . Interpretation: Acute ventilatory failure (resp. acidosis) and acute metabolic acidosis with corrected hypoxemia Case study No. 7 17 yo, 48 kg with known insulin-dependent DM came to ER with Kussmaul breathing and irregular pulse. Room air ABG & VS: pH PCO2 PO2 HCO3 BE 7.05 12 mmHg 108 mmHg 5 mmol/L -30 mmol/L BP Pulse RR VT MV 140/90 mmHg 118/min 40/min 1200ml 48L Interpretation: Severe partly compensated metabolic acidosis without hypoxemia. Case No. 7 cont’d This patient is in diabetic ketoacidosis. IV glucose and insulin were immediately administered. A judgement was made that severe acidemia was adversely affecting CV function and bicarb was elected to restore pH to 7.20. Bicarb administration calculation: Base deficit X weight (kg) 4 30 X 48 = 360 mmol/L 4 Admin 1/2 over 15 min & repeat ABG Case No. 7 cont’d ABG result after bicarb: pH PCO2 PO2 HCO3 BE 7.27 25 mmHg 92 mmHg 11 mmol/L -14 mmol/L BP Pulse RR VT MV 130/80 mmHg 100/min 22/min 600ml 13.2L Case study No. 8 47 yo was in PACU for 3 hours s/p cholecystectomy. She had been on 40% oxygen and ABG & VS: pH PCO2 PO2 HCO3 BE SaO2 Hb 7.44 32 mmHg 121 mmHg 22 mmol/L -2 mmol/L 98% 13 g/dL BP Pulse RR VT MV 130/90 mmHg 95/min, regular 20/min 350ml 7L Case No. 8 cont’d Oxygen was changed to 2L N/C. 1/2 hour pt. ready to be D/C to floor and ABG & VS: pH PCO2 PO2 HCO3 BE SaO2 Hb 7.41 10 mmHg 148 mmHg 6 mmol/L -17 mmol/L 99% 7 g/dL BP Pulse RR VT MV 130/90 mmHg 95/min, regular 20/min 350ml 7L Case No. 8 cont’d What is going on? Case No. 8 cont’d If the picture doesn’t fit, repeat ABG!! pH PCO2 PO2 HCO3 BE SaO2 Hb 7. 45 31 mmHg 87 mmHg 22 mmol/L -2 mmol/L 96% 13 g/dL BP Pulse RR VT MV Technical error was presumed. 130/90 mmHg 95/min 20/min 350ml 7L Case study No. 9 67 yo who had closed reduction of leg fx without incident. Four days later she experienced a sudden onset of severe chest pain and SOB. Room air ABG & VS: pH PCO2 PO2 HCO3 BE SaO2 7.36 33 mmHg 55 mmHg 18 mmol/L -5 mmol/L 88% BP 130/90 mmHg Pulse 100/min RR 25/min MV 18L Interpretation: Compensated metabolic acidosis with moderate hypoxemia. Dx: PE Case study No. 10 76 yo with documented chronic hypercapnia secondary to severe COPD has been in ICU for 3 days while being tx for pneumonia. She had been stable for past 24 hours and was transferred to general floor. Pt was on 2L oxygen & ABG &VS: pH 7.44 BP 135/95 mmHg PCO2 63 mmHg Pulse 110/min PO2 52 mmHg RR 22/min HCO3 42 mmol/L BE +16 mmol/L MV 10L SaO2 86% .Interpretation: Chronic ventilatory failure (resp. acidosis) with uncorrected hypoxemia Case No. 10 cont’d She was placed on 3L and monitored for next hour. She remained alert, oriented and comfortable. ABG was repeated: pH 7.36 BP 140/100 mmHg PCO2 75 mmHg Pulse 105/min PO2 65 mmHg RR 24/min HCO3 42 mmol/L BE +16 mmol/L MV 4.8L SaO2 92% . Pt’s ventilatory pattern has changed to more rapid and shallow breathing. Although still acceptable the pH and CO2 are trending in the wrong direction. High-flow oxygen may be better for this pt to prevent intubation Take Home Message: Valuable information can be gained from an ABG as to the patients physiologic condition Remember that ABG analysis if only part of the patient assessment. Be systematic with your analysis, start with ABC’s as always and look for hypoxia (which you can usually treat quickly), then follow the four steps. A quick assessment of patient oxygenation can be achieved with a pulse oximeter which measures SaO2. It’s not magic understanding ABG’s, it just takes a little practice! Any Questions? References 1. Shapiro, Barry A., et al; Clinical Application of Blood Gases; 1994 2. American Journal of Nursing1999;Aug99(8):34-6 3. Journal Post Anesthesia Nursing1990;Aug;5(4)264-72 4. Irvine, David;ABG Interpretation, A Rough and Dirty Production Practice ABG’s 1. PaO2 2. PaO2 3. PaO2 4. PaO2 5. PaO2 6. PaO2 7. PaO2 8. PaO2 9. PaO2 10. PaO2 90 60 95 87 94 62 93 95 65 110 SaO2 95 SaO2 90 SaO2 100 SaO2 94 SaO2 99 SaO2 91 SaO2 97 SaO2 99 SaO2 89 SaO2 100 pH 7.48 pH 7.32 pH 7.30 pH 7.38 pH 7.49 pH 7.35 pH 7.45 pH 7.31 pH 7.30 pH 7.48 PaCO2 32 PaCO2 48 PaCO2 40 PaCO2 48 PaCO2 40 PaCO2 48 PaCO2 47 PaCO2 38 PaCO2 50 PaCO2 40 HCO3 HCO3 HCO3 HCO3 HCO3 HCO3 HCO3 HCO3 HCO3 HCO3 24 25 18 28 30 27 29 15 24 30 Answers to Practice ABG’s 1. Respiratory alkalosis 2. Respiratory acidosis 3. Metabolic acidosis 4. Compensated Respiratory acidosis 5. Metabolic alkalosis 6. Compensated Respiratory acidosis 7. Compensated Metabolic alkalosis 8. Metabolic acidosis 9. Respiratory acidosis 10. Metabolic alkalosis
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