ABG

APPROACH TO INTERPRETATION OF ABG Know the primary disorder Compute for the range of compensation For metabolic acidosis  get anion gap For high anion gap  get change in anion gap and compare with change in bicarbonate

COMPENSATORY RESPONSE DisorderpHPrimary Disturbance Compensatory Response Metabolic Acidosis Dec HCO3 (loss of HCO3 or gain in H+) Dec pCO2 (hyperventilation) Respiratory Acidosis Inc pCO2 (hypoventilation) Inc HCO3 (HCO3 generation) Metabolic Alkalosis Inc HCO3 (gain in HCO3 or loss of H+) Inc pCO2 (hypoventilation) Respiratory Alkalosis Dec pCO2 (hyperventilation) Dec HCO3 (HCO3 consumption)

COMPENSATORY RESPONSES DISORDERPRIMARYCOMPENSATORY RESPONSE Metabolic Acidosis ↓HCO mmHg decrease in PCO 2 for every 1meq/L fall in HCO 3 Metabolic Alkalosis ↑HCO mmHg elevation in PCO 2 for every 1meq/L rise in HCO 3 Respiratory Acidosis ↑PCO 2 1meq/L increase in HCO 3 for every 10mmHg rise in PCO 2 Respiratory Alkalosis ↓PCO 2 2meq/L reduction in HCO 3 for every 10mmHg fall in PCO 2

Case 1 A 55 year-old female, a known diabetic for 10 years, came in at the ER for a 3 day history of fever and productive cough with anasarca, abdominal pain and vomiting Labs: –RBS – 22 (396) –BUN – 3.6 –Crea- 323 mmol/L –Ca – 1.88 –Alb – 22 –Urine ketone +++ –Na –K – 3.8 –Cl – 98 –Phos – 3.2 –USG – ABG: pH – pCO2 – 20.2 pO2 – 89 HCO3 – 12.4 BE – -9.0 O2 sats – 98%

Case 1 Interpret ABG – Look at the pH Acidotic – What caused the pH Metabolic acidosis – Compute for compensation Decrease in pCO2 = 1.2 x change in bicarbonate – Expected pCO2: Expected pCO2 = 26 Expected pCO2 is higher than actual pCO2 (20.2), therefore there is concomitant respiratory alkalosis ABG: pH – pCO2 – 20.2 pO2 – 89 HCO3 – 12.4 BE – -9.0 O2 sats – 98% Room air

Case 1: Interpret ABG – If metabolic, compute the anion gap Get the corrected Na: – Corrected Na = (RBS – 100) x Na – Corrected Na = 134 Compute the anion gap: – Anion gap = Na – HCO3 – Cl – Anion gap = 23.6 – HAGMA

Case 1: Interpret ABG – Get delta-delta: Change in anion gap – Change = AG - 12 – Change = 11.6 Change in bicarbonate – Change = 24 – bicarbonate – Change = 11.6 Change in AG = change in bicarbonate – Therefore: pure HAGMA Otherwise: – Change in AG > change in bicarbonate: HAGMA + metab alkalosis – Change in AG < change in bicarbonate: HAGMA + NAGMA

Case 1: Interpret ABG – Check for pO2 Correlate with FiO2 – LPM to FiO2 at nasal cannula: 4 x LPM + 20 Hypoxemia (pO2 at FiO2 21%) – Mild: – Moderate: – Severe: < 60 ABG: pH – pCO2 – 20.2 pO2 – 89 HCO3 – 12.4 BE – -9.0 O2 sats – 98% Room air

Case 1: Final ABG interpretation: – High anion gap metabolic acidosis with concomitant respiratory alkalosis, mild hypoxemia

Case 1: Conditions that lead to metabolic acidosis: – HAGMA DKA Alcoholic ketoacidosis Lactic acidosis Renal insufficiency Starvation Salicylate intoxication Methanol intoxication Ethylene glycol intoxication – NAGMA Diarrhea Pancreatic fluid loss Ileostomy Carbonic anhydrase inhibitors RTA Arginine and lysine in parenteral nutrition

Case 2: Case 2: A 55 year-old female, a known diabetic for 10 years came in at the ER for a 3-day history of fever and productive cough with anasarca, abdominal pain and vomiting RBS – 22 BUN – 13.2 Crea – 323 Ca – 1.62 Alb – 22 Urine ketone + Na – 117 K – 2.8 Cl – 98 Phos – 6.2 USG – ABG: pH – pCO2 – pO2 – HCO3 – BE – 6.0 O2 sats – 98%

Case 2: Interpret ABG – Look at the pH Alkalotic – What caused the pH Metabolic alkalosis – Compute for compensation increase in pCO2 = 0.7 x change in bicarbonate – Expected pCO2: Expected pCO2 = Expected PCO2 is near actual pCO2. Therefore, patient has compensated metabolic alkalosis ABG: pH – pCO2 – pO2 – HCO3 – BE – 6.0 O2 sats – 98% 10 lpm

Case 2: Interpret ABG – Check for pO2 Correlate with FiO2 – LPM to FiO2 at nasal cannula: 4 x LPM + 20 Hypoxemia (pO2 at FiO2 21%) – At FiO2 21%, pO2 should be at least 90 – Target pO2 = 90 / 0.21 x FiO2 – Target pO – hypoxemia ABG: pH – pCO2 – pO2 – HCO3 – BE – 6.0 O2 sats – 98% 10 lpm

Case 2 Final ABG interpretation: – Compensated metabolic alkalosis, with hypoxemia

Case 2: Conditions associated with metabolic alkalosis: – Diuretic therapy – Posthypercapnia – Vomiting – Nasogastric suction – NaHCO3 – Refeeding alkalosis – Primary aldosteronism – Hyperreninism – Liddle’s syndrome – Licorice (exogenous mineralocorticoids)

Case 3: A 50 year old male, with a 50 pack year smoking history presents at the ER for chronic cough, weight loss, with a 3 day history of high-grade fever and dyspnea for which he took cotrimoxazole 800/160 mg TID. Early this morning, he was found unresponsive and was then brought to the ER. On PE, there was note of tachypnea, poor air entry and ocassional wheezing all over RBS – 6.3 BUN – 8.3 Crea- 96 Ca – 1.92 Alb – 22 USG – Na – 163 K – 7.8 Cl – 98 Phos – L ECG – ST, NA, NSSTWCs ABG: pH – pCO2 – 70.2 pO2 – HCO3 – BE – -2.0 O2 sats – 78%

Case 3: Interpret ABG – Look at the pH acidotic – What caused the pH Respiratory acidosis – Compute for compensation increase in HCO3 = 1/10 x change in pCO2 (acute) Increase in HCO3 = 3/10 x change in pCO2 (chronic) – Expected HCO3: (acute) Expected HCO3 = 27 Expected HCO3 is higher than actual HCO3 (24.20). Therefore, patient has uncompensated respiratory acidosis ABG: pH – pCO2 – 70.2 pO2 – HCO3 – BE – -2.0 O2 sats – 78% 5 LPM

Case 3: Interpret ABG – Check for pO2 Correlate with FiO2 – LPM to FiO2 at nasal cannula: 4 x LPM + 20 Hypoxemia (pO2 at FiO2 21%) – Expected pO2 = 90/0.21 x FiO2 – Expected pO2 = 171 – hypoxemia ABG: pH – pCO2 – 70.2 pO2 – HCO3 – BE – -2.0 O2 sats – 78% 5 LPM

Case 3 Final ABG interpretation: – Uncompensated respiratory acidosis with hypoxemia

Case 3 Conditions associated respiratory acidosis: – Airway obstruction – Respiratory center depression – Neuromuscular defects – Restrictive defect

Case 4: A 50 year old male, with a 50 pack-year smoking history presents at the ER for chronic cough, weight loss, with 3 day history of low grade fever and dyspnea for which he took cotrimoxazole 800/160 mg TID. Early this morning, he was found unresponsive and was then brought to the ER. On PE, there was note of tachypnea, poor air entry and occasional wheezing all over RBS – 6.3 BUN – 14.3 Crea – 96 Ca Alb – 22 USG – Na – 113 K – 7.8 Cl – 98 Phos – L ECG – ST, NA, shortened Qt, peaked T waves ABG: pH – 7.48 pCO2 – 30.2 pO2 – HCO3 – BE – -1.8 O2 sats – 78%

Case 4: Interpret ABG – Look at the pH alkalosis – What caused the pH Respiratory alkalosis – Compute for compensation decrease in HCO3 = 2/10 x change in pCO2 (acute) decrease in HCO3 = 5/10 x change in pCO2 (chronic) – Expected HCO3: (acute) Expected HCO3 = Expected HCO3 is lower than actual HCO3 (25.50). Therefore, patient has concomitant metabolic alkalosis ABG: pH – 7.48 pCO2 – 30.2 pO2 – HCO3 – BE – -1.8 O2 sats – 78% 6 LPM

Case 4: Interpret ABG – Check for pO2 Correlate with FiO2 – LPM to FiO2 at nasal cannula: 4 x LPM + 20 Hypoxemia (pO2 at FiO2 21%) – Target pO2 = 90/0.21 x FiO2 – Target pO2 = 189 – hypoxemia ABG: pH – 7.48 pCO2 – 30.2 pO2 – HCO3 – BE – -1.8 O2 sats – 78% 6 LPM

Case 4: Final ABG interpretation: – Respiratory alkalosis with concomitant metabolic alkalosis

Case 4: Conditions associated with respiratory alkalosis: – High altitude – V/Q mismatch – Severe anemia – Infection – trauma – Hepatic failure – Gram negative septicemia – Interstitial lung disease – Pneumonia – Pulmonary embolism – Pulmonary edema