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ABG Interpretation

ABG Interpretation. Normal Arterial Blood Gas Values. PH 7.35-7.45 PaCo2 35-45 mm Hg PaO2 70-100 mm Hg (depends on age) SaO2 93-98% HCo3- 22-26 mEq/L %MetHg <2% %COHb <2% Base Excess -2.0-2.0 mEq/L CaO2 16-22 ml O2/dl. The Keys to Understanding Arterial Blood Gases.

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ABG Interpretation

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  1. ABG Interpretation

  2. Normal Arterial Blood Gas Values • PH 7.35-7.45 • PaCo2 35-45 mm Hg • PaO2 70-100 mm Hg (depends on age) • SaO2 93-98% • HCo3- 22-26 mEq/L • %MetHg <2% • %COHb <2% • Base Excess -2.0-2.0 mEq/L • CaO2 16-22 ml O2/dl

  3. The Keys to Understanding Arterial Blood Gases • The determinants of PaCo2 (PaCo2 equation) • The determinants of the PAo2 and Pao2 (Alveolar gas equation) • Acid Base Balance (Henderson Hasselbalch equation)

  4. Determinants of Hypercapnia • PaCo2 is based on the production of Co2 (VCo2) and on alveolar Ventilation (VA) • Alveolar Ventilation (VA) is defined as minute ventilation (VE) minus dead space ventilation (VD) • PaCo2 = VCo2 x 0.86 or VCo2 x 0.86 VA VE - VD

  5. Determinants of Hypercapnia • PaCo2 increases with increased production of Co2 • Hypermetabolism, malignant hypothermia, high carbohydrate diet • The decrease in (VA) may be due to a decrease in minute ventilation (VE) or an increase in dead space ventilation (VD) since VA = VE-VD

  6. Determinants of Hypercapnia • Clinical examples of an inadequate minute ventilation VE leading to hypercapnia include • Sedative Drug Overdose • Respiratory muscle paralysis • Central hypoventilation • Examples of increased dead space ventilation (VD) leading to hypercapnia include • COPD • Severe restrictive lung disease with rapid shallow breathing

  7. Dangers of Hypercapnia • An elevated PaCo2 will lower the PaO2 • An elevated PaCo2 will lower the PH and cause acidemia • The Higher the baseline PaCo2 the greater it will rise for a given decrease in Alveolar Ventilation (VA)

  8. Alveolar Gas Equation (Oxygenation) • The partial pressure of oxygen in the alveolus PAo2 is based on: • Inspired Fio2 • Pb ( barometric pressure ) (760 mm hg at sea level) • The water vapor pressure (47mm hg at normal body temperature) • PACo2 ( equal to the PaCo2/RQ or PaCo2/0.8) • Thus the PAo2 = Fio2 * (Pb-47mmHg)-PaCo2 / 0.8 • In a pt breathing RA • PAo2 = 150 – PaCo2/ 0.8

  9. Alveolar Gas Equation (Oxygenation) PAo2 = Fio2 * (Pb – 47) – PaCo2 / 0.8 • The PAo2 decreases with: • Decreased inspired Fi02 • Decreased Barometric Pressure (altitude) • Increased PACo2 or PaCo2

  10. P(A-a) O2 • The partial pressure difference between Alveolar and arterial O2 is commonly referred to as the A-a gradient • A normal A-a gradient is between 5-25 mm Hg and it increases with age. Part of this is due to normal shunting via the thesbian circulation • (Age/4) + 4 estimates the normal A-a gradient for a given age • An elevated A-a gradient indicates that oxygen is not adequately transferred from the alveoli to the pulmonary capillaries • This usually signifies a lung problem or a cardiac shunt

  11. Causes of a Low PaO2 • Non Respiratory Causes • Cardiac R to L Shunt ( increased A-a gradient, does not respond to increased Fio2) • Decreased inspired Fio2 or decreased barometric pressure (normal A-a gradient) • Low mixed venous O2 saturation ( due to increased extraction of O2, not usually significant unless there is also a VQ mismatch or diffusion barrier) • Respiratory Causes • Pulmonary R to L Shunt (Increased A-a gradient) • VQ mismatch (Increased A-a gradient) • Diffusion barrier (Increased A-a gradient) • Hypoventilation (Increased PaCo2 with a normal A-a gradient)

  12. Acid Base Balance • Henderson-Hasselbalch Equation PH = pK + Log [HCo3-] .03 [PaCo2] The 2 determinants of PH are the [HCo3-] and the [PaCo2]

  13. Acid Base Balance • The first step in proper ABG interpretation involves obtaining an accurate history and physical exam. This will often provide clues to the prevailing acid-base disorder and can aid in narrowing the differential diagnosis • A given set of acid base parameters is never in and of itself diagnostic • This is especially true for pts with drug ingestion, vomiting, diarrhea, and diabetes mellitus.

  14. Verifying the Accuracy of the Data • The components of the Hco3-Co2 system should always be in equilibrium in the blood • The PH, PaCo2 and serum HCo3 must be consistent with the Henderson-Hasselbalch equation. The HCo3 from the ABG is a calculated HCo3 • ABG and chemistries should be drawn at the same time • If the measurements do not fit reasonably well into these equations an error in one or more of the values has likely occurred and a repeat ABG and serum Hco3 should be obtained

  15. Henderson Equation • The first step in ABG interpretation is determining internal consistency • [H+] = 24 * PaCo2 [HCo3-] A [H+] of 40 is equal to a PH of 7.40 For every 1 mmol/L change in the [H+] the PH inversely changes by .01

  16. Values for PH and corresponding [H+] PH[H+] (mEq/L) 7.55 28 7.50 32 7.45 35 7.40 40 7.35 45 7.30 50 7.25 56

  17. Determining the Serum Anion Gap • The anion gap is the difference between the unmeasured anions (negatively charged molecules) and the unmeasured cations (positively charged molecules) in the serum • The Concentration of all anions and cations in the serum must balance • Therefore: Na + UC = [Cl + HCo3] + UA • Rearranged UA – UC = Na – [Cl + HCo3] • Normal in most labs is 10 + or - 2 • Hypoalbuminemia, hyponatremia, and increased [k], [mg],[ca] and [NH4] may all lower the anion gap. • A decrease of the serum albumin by 50% can decrease the anion gap by 5 meq/l.

  18. Determinants of the Anion Gap Unmeasured AnionsUnmeasure Cations Proteins (15 meq/L) Calcium (5 meq/L) Organic Acids (5 meq/L) Potassium (4.5 meq/L) Phosphates (2 meq/L) Mg (1.5 meq/L) Sulfates (1meq/L) ____________________ __________________ UA = 23 meq/L UC = 11 meq/L Anion gap = UA – UC = 12 meq/L

  19. Determining the Delta Gap • If a serum anion gap is present a Delta gap should be calculated to evaluate for an additional metabolic derangement • The Delta gap can be calculated by the following equation • (calculated AG – normal AG) – (Normal HCo3 – Measured HCo3) Or (Calculated AG – 12) – (24 – measured HCo3)

  20. Interpreting the Delta Gap • A normal Delta gap is 0 indicating that the anion gap metabolic acidosis is the only metabolic derangement. • A postive delta gap may indicate the presence of an additional metabolic alkalosis or a respiratory acidosis with metabolic compensation • Conversely a negative delta gap may indicate an additional metabolic acidosis or a respiratory alkalosis with metabolic compensation

  21. Determining the Osmolar Gap • The Osmolal gap is used to detect the presence of ingested toxins such as ethylene glycol, methanol or isopropyl alcohol • These Toxins often cause an increased AG acidosis. The Osmolal gap is the difference between the measured osmolality and the calculated osmolality • The calculated osmolality is determined by 2*[Na] + Serum Glucose/18 + BUN/2.8 +Ethanol/4.5 • An Osmolal gap >10mOsm suggests the presence of an ingested toxin as a contributor to the anion gap acidosis

  22. Simple Acid Base Abnormalities • The term simple acid-base disorder denotes the presence of a single abnormality associated with an expected compensatory response • The Four simple acid base disorders are metabolic acidosis, metabolic alkalosis, respiratory acidosis (both acute and chronic) and respiratory alkalosis (acute and chronic)

  23. Simple Acid Base Disorders • Metabolic Acidosis – primary disturbance is a decrease in HCo3 with compensatory hyperventilation and a decreased PaCo2. • The Predicted PaCo2 is determined using the Winter’s equation • PaCo2 = (1.5 x HCo3) + 8 + or – 2 • Any significant deviation from the predicted PaCo2 signifies an additional respiratory disorder • A PaCo2 higher than predicted signifies an additional Respiratory Acidosis • A PaCo2 lower than predicted signifies an additional Respiratory Alkalosis

  24. Simple Acid Base Disorders • Metabolic Alkalosis – Primary disturbance is an increase in HCo3 with compensatory hypoventilation and an increased PaCo2 • Predicted PaCo2 = (0.7 x HCo3) + 21 + or – 1.5 • Any significant deviation from the predicted PaCo2 signifies an additional Respiratory disorder

  25. Simple Acid Base Disorders • Respiratory Acidosis – primary derangement is an increased PaCo2 with a compensatory increase in HCo3. • In acute resp acidosis for every increase of 10 mm Hg of PaCo2 the PH should drop by .08. • Increase in [HCo3] = change PaCo2/10 + or - 3 • In Chronic resp acidosis for every 10 mm Hg rise of the PaCo2 the PH should drop by .03 as compensation but not correction • Increase in [HCo3] = 3.5 x change Paco2/10 • Changes greater than those predicted signify an additional metabolic disorder

  26. Simple Acid Base Disorders • Respiratory Alkalosis – primary derangement is a decreased PaCo2 with a compensatory decrease in the HCo3 • For every 10 mm Hg decrease in the PaCo2 the PH should increase by .08 in an acute disorder • Decrease in [HCo3] = 2x change in PaCo2/10 • For every 10 mm Hg decrease in the PaCo2 the PH should increase by .03 in a chronic disorder • Decrese in [HCo3] = 5 x change in the PaCo2/10 • Changes greater than those predicted signify an additional metabolic disorder

  27. Complex Acid Base DisordersFramework for Metabolic Acidosis • First as always take a thorough Hx and perform a physical examination • Next determine the internal consistency of the ABG • Look at the PH. If it is less than 7.35 there is a primary acidosis. If the HCo3 and PaCo2 are both low it is a primary metabolic acidosis • Calculate the predicted PaCo2 using the Winters equation [PaCo2= (1.5 x Hco3) +8 + or – 2]. If the PaCo2 is lower than predicted there is an additional respiratory alkalosis. If the PaCo2 is higher than predicted there is an additional respiratory acidosis • Calculate the AG. If there is an AG present calculate the Delta gap. If the Delta gap is 0 there is no additional metabolic derangement. If there is a + delta gap there may be an additional metabolic alkalosis. If it is negative there may be an additional non ag metabolic acidosis • Lastly if there is an AG present with no obvious etiology calculate the osmolal gap looking for toxic ingestion.

  28. Classification of Metabolic Acidosis • Increased Anion gap • Lactic Acidosis • Ketoacidosis (Diabetes, Alcohol, Starvation) • Renal Failure • Toxic Ingestion • Salicylates, Methanol, Ethylene Glycol, Paraldehyde, INH • Normal anion gap (Hyperchloremic metabolic Acidosis) • GI loss of HCo3 • Renal Loss of HCo3 • Renal Tubular Disease • Pharmacological ( Ammonium Chloride, Dilutional, Hyperalimentation) • Urine Anion gap may be used to differentiate GI vs Renal causes of a non ag metabolic Acidosis • Urine AG = UA – UC = Na – [K + Cl] • A negative value usually indicates a GI loss of HCo3. A value of zero or a positive value signifies a renal cause

  29. Metabolic AcidosisClinical Signs and Symptoms • Kussmaul’s Respirations – deep and rapid breathing • Arrhythmias • Suppressed myocardial contractility • R shift of the oxyhemoglobin dissociation curve • Hyperkalemia • Increased protein catabolism • Insulin resistence

  30. Metabolic Alkalosis • The primary disturbance in metabolic alkalosis is an increase in HCo3 or the loss of acid. • The compensatory respiratory response is a rise in PaCo2. • Calculate the predicted PaCo2 using the following equation: PaCo2= (0.7 x HCo3) +21 + or – 1.5. • If the PaCo2 is less than predicted there is an additional respiratory alkalosis. If the PaCo2 is higher than predicted there is an additional respiratory acidosis. • Metabolic Alkalosis may be Hypovolemic Cl- depleted or hypervolemic Cl- expanded

  31. Metabolic Alkalosis • The etiology of the hypovolemic Cl - depleted form includes: • GI loss of H+ • Vomiting, Gastric suctioning, Cl- rich diarrhea • Renal loss of H+ • Diuretics • Post hypercapnia • High dose carbenicillin • The etiology of the hypervolemic Cl-expanded form includes: • Primary hyperaldosteronism, hypercortisolism • ACTH excess, Hydrocortisone and mineralicorticoid excess • Renin secreting tumor • Hypokalemia, milk-alkali syndrome, Massive blood transfusion • History and Urine Chloride can be helpful in differentiating the two • Urine Chloride is usually less than 20 in the chloride depleted form and greater than 20 in the chloride expanded form

  32. Metabolic AlkalosisClinical Signs and Symptoms • Tachycardia • Arrhythmias • Obtunted mental Status • Increased risk of seizures • Decreased cerebral blood flow • Hypocalcemia • hypokalemia

  33. Respiratory Acidosis • The major disturbance in respiratory acidosis is ineffective ventilation and or increased production of Co2. • In acute disorders for every increase of 10 mm Hg in the PaCo2 the PH decreases by .08. • If there is a further decrease in the PH there is an additional metabolic acidosis. Likewise if the PH is higher than predicted there is likely a metabolic alkalosis. • In chronic respiratory acidosis for every 10 mm Hg increase of the PaCo2 the PH decreases by .03. Further changes signify additional metabolic derangements • The Maximum Renal compensation for chronic respiratory acidosis is a HCo3 of 45. If the serum HCo3 is greater than 45 there must be an additional metabolic alkalosis

  34. Respiratory AcidosisCauses, Clinical Signs and Symptoms • Causes • Airway obstruction, depression of the respiratory center ( brain injury drugs ) • Increased Co2 production ( hyperthermia, hypermetabolism, high carbohydrate diet ) • Neuromuscular diseases • Pulmonary disorders ( obstructive, restrictive, ARDS/ALI, OHS, Flail chest • Clinical Signs and Symptoms • Confusion, HA • Asterixis • Hypertension • Arrhythmias and peripheral vasodilitation

  35. Respiratory Alkalosis • The primary derangement in respiratory alkalosis is hyperventilation • The compensatory responses are the same numerically as they are in respiratory acidosis although in the opposite directions for both acute and chronic disorders • Common causes of respiratory alkalosis are: • Hypoxia, acute or chronic pulmonary disease • Overstimulation of the respiratory center (sepsis, pregnancy, liver disease, progesterone, salicylates, pain, and organic brain disease)

  36. Respiratory AlkalosisClinical Signs and Symptoms • Confusion • Seizures • Parasthesias • Arrhythmias • Muscle cramps • Hypokalemia • Hypophosphatemia • hypocalcemia

  37. Examples # 1 • A 28 y/o male presents with 1 day hx of acute SOB and Diarrhea • ABG 7.32/24/104/12/99% • Serum HCo3 23 • What is the Acid base disorder?

  38. Example # 1 • First step in ABG interpretation is checking the internal consistency using the henderson equation • [H] = 24 x [PaCo2] / [HCo3] • [H] = 24 x (24/23) = 25 • The expected PH for a [H] of 25 = 7.55 • The ABG and serum HCo3 are not internally consistent. An ABG and serum HCo3 need to be repeated simultaneously

  39. Example #2 • A 72 y/o m with a Pmhx of COPD presents with sob and AMS. He is intubated in the ED on arrival and placed on mechanical ventilation. ABG 1 hr after intubation reveals PH 7.5 PCo2 50. • What must The serum HCo3 be in order for the PH to be internally consistent? • What is the predominant acid base disorder

  40. Example #2 • PH 7.5 is equal to a [H] of 30 • 30 = 24 x 50/x • X = 40, so the serum HCo3 must be 40 • The predominant acid base disorder is a post hypercapnic metabolic alkalosis due to overventilation in a pt with chronic Co2 retention

  41. Example #3 • A physically fit 23 y/o f goes jogging. After 20 minutes of running her RR has doubled. If an ABG was performed at that time what would you expect it to show • A) normal PCo2 and PH • B)Low PCo2 and high PH • C)High PCo2 and low PH • D)Low PCo2 and low PH

  42. Example # 3 • Answer. Normal PCo2 and normal PH. During exercise Co2 production increases. In a physically fit person alveolar ventilation increases accordingly keeping PaCo2 and PH in the normal range • Remember PaCo2 = VCO2/ VE - VD

  43. Example # 4 • A 26 y/o homeless male is admitted to the ICU with AMS and persitent vomiting • ABG 7.4 / 38 / 90 / 99% • Na 149 K 3.8 Cl 100 HCo3 24 BuN 110 • Cr 8.7 • What is ( are ) the acid base disorder(s)

  44. Example #4 • Upon cursory review there appears to be no acid base disorder • However there is an AG of 25 upon closer inspection. 149 – [100 + 24] = 25 • The Delta gap [25 – 12] – [24-24] is also + with a value of 13. • Therefore there is an ag metabolic acidosis and a metabolic alkalosis • This is likely secondary to uremia + vomiting • Given Ams and renal failure an osmolal gap should also be calculated

  45. Example #5 • A mountain climber ascends from sea level to 18 K feet over a 2 day period. Supplemental O2 is not used. Which of the following will not change • A) Fio2 • B) barometric pressure • C) PaO2 • D) PaCo2 • E) PH

  46. Example # 6 • Since the early 1980’s mountain climbers have climbed Mt Everest without supplemental O2. How is this possible? • Barometric Pressure at the summit is 253 mm Hg. Assume a PaCo2 of 40 • PAo2 = Fi02 * ( 253 – 47 ) – 40/0.8 • PA02 = .21 (206) – 50 = -6.7 ?? • If we take into account a nml A-a gradient of 5 the PaO2 is –11.7??

  47. Example # 6 • In Fact these climbers profoundly hyperventilate and have PaCo2 usually < 10 mm Hg. If we plug this into the Alveolar gas equation we get a PAo2 of about 35 mm Hg. • Although this is profoudly low a physically fit person can survive this, although they develop dizziness, confusion and SOB

  48. The END

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