ABG INTERPRETATION

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     1  12/30/02 ABG Interpretation 1 ABG INTERPRETATION Marc D. Berg, MD – DeVos Children’s Hospital Rita R. Ongjoco, DO – Sinai Hospital of Baltimore
     2  12/30/02 ABG Interpretation 2 ABG Interpretation First, does the patient have an acidosis or an alkalosis Second, what is the primary problem – metabolic or respiratory Third, is there any compensation by the patient – respiratory compensation is immediate while renal compensation takes time
     3  12/30/02 ABG Interpretation 3 ABG Interpretation It would be extremely unusual for either the respiratory or renal system to overcompensate The pH determines the primary problem After determining the primary and compensatory acid/base balance, evaluate the effectiveness of oxygenation
     4  12/30/02 ABG Interpretation 4 Normal Values pH 7.35 to 7.45 paCO2 36 to 44 mm Hg HCO3 22 to 26 meq/L
     5  12/30/02 ABG Interpretation 5 Abnormal Values pH < 7.35 Acidosis (metabolic and/or respiratory) pH > 7.45 Alkalosis (metabolic and/or respiratory) paCO2 > 44 mm Hg Respiratory acidosis (alveolar hypoventilation) paCO2 < 36 mm Hg Respiratory alkalosis (alveolar hyperventilation) HCO3 < 22 meq/L Metabolic acidosis HCO3 > 26 meq/L Metabolic alkalosis
     6  12/30/02 ABG Interpretation 6 Putting It Together - Respiratory So paCO2 > 44 with a pH < 7.35 represents a respiratory acidosis paCO2 < 36 with a pH > 7.45 represents a respiratory alkalosis For a primary respiratory problem, pH and paCO2 move in the opposite direction For each deviation in paCO2 of 10 mm Hg in either direction, 0. 08 pH units change in the opposite direction
     7  12/30/02 ABG Interpretation 7 Putting It Together - Metabolic And HCO3 < 22 with a pH < 7.35 represents a metabolic acidosis HCO3 > 26 with a pH > 7.45 represents a metabolic alkalosis For a primary metabolic problem, pH and HCO3 are in the same direction, and paCO2 is also in the same direction
     8  12/30/02 ABG Interpretation 8 Compensation The body’s attempt to return the acid/base status to normal (i.e. pH closer to 7.4) Primary Problem Compensation respiratory acidosis metabolic alkalosis respiratory alkalosis metabolic acidosis metabolic acidosis respiratory alkalosis metabolic alkalosis respiratory acidosis
     9  12/30/02 ABG Interpretation 9 Expected Compensation Respiratory acidosis Acute – the pH decreases 0.08 units for every 10 mm Hg increase in paCO2; HCO3 ?0.1-1 mEq/liter per ?10 mm Hg paCO2 Chronic – the pH decreases 0.03 units for every 10 mm Hg increase in paCO2; HCO3 ?1.1-3.5 mEq/liter per ?10 mm Hg paCO2
     10  12/30/02 ABG Interpretation 10 Expected Compensation Respiratory alkalosis Acute – the pH increases 0.08 units for every 10 mm Hg decrease in paCO2; HCO3 ??0-2 mEq/liter per ?10 mm Hg paCO2 Chronic - the pH increases 0.17 units for every 10 mm Hg decrease in paCO2; HCO3 ??2.1-5 mEq/liter per ?10 mm Hg paCO2
     11  12/30/02 ABG Interpretation 11 Expected Compensation Metabolic acidosis paCO2 = 1.5(HCO3) + 8 (?2) paCO2 ?1-1.5 per ?1 mEq/liter HCO3 Metabolic alkalosis paCO2 = 0.7(HCO3) + 20 (?1.5) paCO2 ?0.5-1.0 per ?1 mEq/liter HCO3
     12  12/30/02 ABG Interpretation 12 Classification of primary acid-base disturbances and compensation Acceptable ventilatory and metabolic acid-base status Respiratory acidosis (alveolar hypoventilation) - acute, chronic Respiratory alkalosis (alveolar hyperventilation) - acute, chronic Metabolic acidosis – uncompensated, compensated Metabolic alkalosis – uncompensated, partially compensated
     13  12/30/02 ABG Interpretation 13 Acute Respiratory Acidosis paCO2 is elevated and pH is acidotic The decrease in pH is accounted for entirely by the increase in paCO2 Bicarbonate and base excess will be in the normal range because the kidneys have not had adequate time to establish effective compensatory mechanisms
     14  12/30/02 ABG Interpretation 14 Acute Respiratory Acidosis Causes Respiratory pathophysiology - airway obstruction, severe pneumonia, chest trauma/pneumothorax Acute drug intoxication (narcotics, sedatives) Residual neuromuscular blockade CNS disease (head trauma)
     15  12/30/02 ABG Interpretation 15 Chronic Respiratory Acidosis paCO2 is elevated with a pH in the acceptable range Renal mechanisms increase the excretion of H+ within 24 hours and may correct the resulting acidosis caused by chronic retention of CO2 to a certain extent
     16  12/30/02 ABG Interpretation 16 Chronic Respiratory Acidosis Causes Chronic lung disease (BPD, COPD) Neuromuscular disease Extreme obesity Chest wall deformity
     17  12/30/02 ABG Interpretation 17 Acute Respiratory Alkalosis paCO2 is low and the pH is alkalotic The increase in pH is accounted for entirely by the decrease in paCO2 Bicarbonate and base excess will be in the normal range because the kidneys have not had sufficient time to establish effective compensatory mechanisms
     18  12/30/02 ABG Interpretation 18 Respiratory Alkalosis Causes Pain Anxiety Hypoxemia Restrictive lung disease Severe congestive heart failure Pulmonary emboli Drugs Sepsis Fever Thyrotoxicosis Pregnancy Overaggressive mechanical ventilation Hepatic failure
     19  12/30/02 ABG Interpretation 19 Uncompensated Metabolic Acidosis Normal paCO2, low HCO3, and a pH less than 7.30 Occurs as a result of increased production of acids and/or failure to eliminate these acids Respiratory system is not compensating by increasing alveolar ventilation (hyperventilation)
     20  12/30/02 ABG Interpretation 20 Compensated Metabolic Acidosis paCO2 less than 30, low HCO3, with a pH of 7.3-7.4 Patients with chronic metabolic acidosis are unable to hyperventilate sufficiently to lower paCO2 for complete compensation to 7.4
     21  12/30/02 ABG Interpretation 21 Metabolic Acidosis Elevated Anion Gap Causes Ketoacidosis - diabetic, alcoholic, starvation Lactic acidosis - hypoxia, shock, sepsis, seizures Toxic ingestion – salicylates, methanol, ethylene glycol, ethanol, isopropyl alcohol, paraldehyde, toluene Renal failure - uremia
     22  12/30/02 ABG Interpretation 22 Metabolic Acidosis Normal Anion Gap Causes Renal tubular acidosis Post respiratory alkalosis Hypoaldosteronism Potassium sparing diuretics Pancreatic loss of bicarbonate Diarrhea Carbonic anhydrase inhibitors Acid administration (HCl, NH4Cl, arginine HCl) Sulfamylon Cholestyramine Ureteral diversions
     23  12/30/02 ABG Interpretation 23 Effectiveness of Oxygenation Further evaluation of the arterial blood gas requires assessment of the effectiveness of oxygenation of the blood Hypoxemia – decreased oxygen content of blood - paO2 less than 60 mm Hg and the saturation is less than 90% Hypoxia – inadequate amount of oxygen available to or used by tissues for metabolic needs
     24  12/30/02 ABG Interpretation 24 Mechanisms of Hypoxemia Inadequate inspiratory partial pressure of oxygen Hypoventilation Right to left shunt Ventilation-perfusion mismatch Incomplete diffusion equilibrium
     25  12/30/02 ABG Interpretation 25 Assessment of Gas Exchange Alveolar-arterial O2 tension difference A-a gradient PAO2-PaO2 PAO2 = FIO2(PB - PH2O) - PaCO2/RQ* arterial-Alveolar O2 tension ratio PaO2/PAO2 arterial-inspired O2 ratio PaO2/FIO2 P/F ratio *RQ=respiratory quotient= 0.8
     26  12/30/02 ABG Interpretation 26 Assessment of Gas Exchange ABG A-a grad PaO2 PaCO2 RA 100% Low FIO2 ? ? N* N Alveolar hypoventilation ? ? N N Altered gas exchange Regional V/Q mismatch ? ?/N/? ? N/? Intrapulmonary R to L shunt ? N/? ? ? Impaired diffusion ? N/? ? N Anatomical R to L shunt (intrapulmonary or intracardiac) ? N/? ? ? * N=normal
     27  12/30/02 ABG Interpretation 27 Summary First, does the patient have an acidosis or an alkalosis Look at the pH Second, what is the primary problem – metabolic or respiratory Look at the pCO2 If the pCO2 change is in the opposite direction of the pH change, the primary problem is respiratory
     28  12/30/02 ABG Interpretation 28 Summary Third, is there any compensation by the patient - do the calculations For a primary respiratory problem, is the pH change completely accounted for by the change in pCO2 if yes, then there is no metabolic compensation if not, then there is either partial compensation or concomitant metabolic problem
     29  12/30/02 ABG Interpretation 29 Summary For a metabolic problem, calculate the expected pCO2 if equal to calculated, then there is appropriate respiratory compensation if higher than calculated, there is concomitant respiratory acidosis if lower than calculated, there is concomitant respiratory alkalosis
     30  12/30/02 ABG Interpretation 30 Summary Next, don’t forget to look at the effectiveness of oxygenation, (and look at the patient) your patient may have a significantly increased work of breathing in order to maintain a “normal” blood gas metabolic acidosis with a concomitant respiratory acidosis is concerning
     31  12/30/02 ABG Interpretation 31 Case 1 Little Billy got into some of dad’s barbiturates. He suffers a significant depression of mental status and respiration. You see him in the ER 3 hours after ingestion with a respiratory rate of 4. A blood gas is obtained (after doing the ABC’s, of course). It shows pH = 7.16, pCO2 = 70, HCO3 = 22
     32  12/30/02 ABG Interpretation 32 Case 1 What is the acid/base abnormality? Uncompensated metabolic acidosis Compensated respiratory acidosis Uncompensated respiratory acidosis Compensated metabolic alkalosis
     33  12/30/02 ABG Interpretation 33 Case 1 Uncompensated respiratory acidosis There has not been time for metabolic compensation to occur. As the barbiturate toxicity took hold, this child slowed his respirations significantly, pCO2 built up in the blood, and an acidosis ensued.
     34  12/30/02 ABG Interpretation 34 Case 2 Little Suzie has had vomiting and diarrhea for 3 days. In her mom’s words, “She can’t keep anything down and she’s runnin’ out.” She has had 1 wet diaper in the last 24 hours. She appears lethargic and cool to touch with a prolonged capillary refill time. After addressing her ABC’s, her blood gas reveals: pH=7.34, pCO2=26, HCO3=12
     35  12/30/02 ABG Interpretation 35 Case 2 What is the acid/base abnormality? Uncompensated metabolic acidosis Compensated respiratory alkalosis Uncompensated respiratory acidosis Compensated metabolic acidosis
     36  12/30/02 ABG Interpretation 36 Case 2 Compensated metabolic acidosis The prolong history of fluid loss through diarrhea has caused a metabolic acidosis. The mechanisms probably are twofold. First there is lactic acid production from the hypovolemia and tissue hypoperfusion. Second, there may be significant bicarbonate losses in the stool. The body has compensated by “blowing off” the CO2 with increased respirations.
     37  12/30/02 ABG Interpretation 37 Case 3 You are evaluating a 15 year old female in the ER who was brought in by EMS from school because of abdominal pain and vomiting. Review of system is negative except for a 10 lb. weight loss over the past 2 months and polyuria for the past 2 weeks. She has no other medical problems and denies any sexual activity or drug use. On exam, she is alert and oriented, afebrile, HR 115, RR 26 and regular, BP 114/75, pulse ox 95% on RA.
     38  12/30/02 ABG Interpretation 38 Case 3 Exam is unremarkable except for mild abdominal tenderness on palpation in the midepigastric region and capillary refill time of 3 seconds. The nurse has already seen the patient and has sent off “routine” blood work. She hands you the result of the blood gas. pH = 7.21 pCO2= 24 pO2 = 45 HCO3 = 10 BE = -10 saturation = 72%
     39  12/30/02 ABG Interpretation 39 Case 3 What is the blood gas interpretation? Uncompensated respiratory acidosis with severe hypoxia Uncompensated metabolic alkalosis Combined metabolic acidosis and respiratory acidosis with severe hypoxia Metabolic acidosis with respiratory compensation
     40  12/30/02 ABG Interpretation 40 Case 3 Metabolic acidosis with respiratory compensation This is a patient with new onset diabetes mellitus in ketoacidosis. Her pulse oximetry saturation and clinical examination do not reveal any respiratory problems except for tachypnea which is her compensatory mechanism for the metabolic acidosis. The nurse obtained the blood gas sample from the venous stick when she sent off the other labs.
     41  12/30/02 ABG Interpretation 41 References The ICU Book – Paul L. Marino, 1991, Algorithms for acid-base interpretations, p415-426 Textbook of Pediatric Intensive Care 3rd Edition – edited by Mark C. Rogers, 1996, Respiratory Monitoring: Interpretation of clinical blood gas values, p355-361 Pediatric Critical Care – Bradley Fuhrman and Jerry Zimmerman, 1992, Acid-Base Balance and Disorders, p689-696 Critical Care Physiology – Robert Bartlett, 1996, Acid-Base physiology p165-173.