Acid Base, Arterial Blood Gas
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This document provides an overview of arterial blood gas (ABG) analysis, including how to interpret an ABG test result. It discusses how an ABG measures oxygen, carbon dioxide, acidity levels and other values in arterial blood. The document outlines the technique for arterial blood sampling, including common sites and proper technique. It also discusses specimen care and transport. Finally, it provides guidance on how to interpret ABG results, including how to assess oxygenation/hypoxemia, acid-base disorders, and the compensatory responses of the body. Key areas like normal values, mechanisms of acid-base imbalances, and the steps to analyze an ABG result are summarized.
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Acid Base, Arterial Blood Gas
- 1. Basic ABG Interpretation Jose Socrates ‘DEE’ Evardone Year Level I Department of Internal Medicine Cebu Doctors University Hospital
- 2. arterial blood gas (ABG) • test that measures the: –1) oxygen tension (PaO2), –2) carbon dioxide tension (PaCO2), –3) acidity (pH), –4) oxyhemoglobin saturation (SaO2), and –5) bicarbonate (HCO3) concentration in arterial blood. • Some blood gas analyzers also measure the methemoglobin, carboxyhemoglobin levels
- 3. ARTERIAL BLOOD GASES • ARTERIAL SAMPLING • Needle puncture – - Site selection – - Collateral circulation – - Technique – - Complications • Indwelling catheters • SPECIMEN CARE • TRANSPORT • ANALYSIS • INTERPRETATION – Normal values
- 4. ARTERIAL BLOOD GASES • ARTERIAL SAMPLING: • Common sites include: – 1) radial, – 2) femoral, – 3) brachial, – 4) dorsalis pedis, or – 5) axillary artery • the radial artery is used most often because it is – accessible, – easily positioned, and – more comfortable for the patient than the alternative sites
- 5. ARTERIAL BLOOD GASES Technique ●Local analgesia ●The seal of a heparinized syringe should be broken by pulling its plunger. ●the artery should be punctured with the needle at a 30 to 45 degree angle relative to the skin ●rolled between the hands ●pressure applied to the puncture site for five to ten minutes to achieve hemostasis. 30-45-degree angle (for radial artery), 45-60-degree angle (for brachial artery), 45-90-degree angle (for femoral artery) with the bevel of the needle turned up
- 17. ARTERIAL BLOOD GASES SPECIMEN CARE Gas diffusion through the plastic syringe is a potential source of error. - Using a glass syringe - placed on ice and analyzed within 15 minutes
- 18. ARTERIAL BLOOD GASES SPECIMEN CARE The HEPARIN decrease in the pH dilute the PaCO2 heparin solution should be minimized and at least 2 mL of blood should be obtained
- 19. ARTERIAL BLOOD GASES SPECIMEN CARE Air bubbles that exceed 1 to 2 percent of the blood volume falsely high PaO2 falsely low PaCO2 gently removing the bubbles without agitation and analyzing the sample as soon as possible
- 20. ARTERIAL BLOOD GASES INTERPRETATION "Oxygenation and mechanisms of hypoxemia“ and "Simple and mixed acid-base disorders"
- 21. ARTERIAL BLOOD GASES "Oxygenation and mechanisms of hypoxemia“ MEASURES OF OXYGENATION: 1) Arterial oxygen saturation (SaO2) 2) Arterial oxygen tension (PaO2) 3) A-a oxygen gradient 4) PaO2/FiO2 ratio 5) a-A oxygen ratio 6) Oxygenation index
- 22. ARTERIAL BLOOD GASES Arterial oxygen saturation (SaO2)
- 23. ARTERIAL BLOOD GASES Arterial oxygen tension (PaO2)
- 24. ARTERIAL BLOOD GASES A-a oxygen gradient A-a oxygen gradient = PAO2 - PaO2 A-a gradient = 2.5 + 0.21 x age in years
- 25. ARTERIAL BLOOD GASES PaO2/FiO2 ratio A normal PaO2/FiO2 ratio is 300 to 500 mmHg less than 300 mmHg indicating abnormal gas exchange less than 200 mmHg indicates severe hypoxemia
- 26. ARTERIAL BLOOD GASES a-A oxygen ratio a-A oxygen ratio = PaO2 ÷ PAO2 lower limit of normal is 0.77-0.82 most reliable when the FiO2 is less than 0.55
- 27. ARTERIAL BLOOD GASES Oxygenation index OI = [mean airway pressure x FiO2 ÷ PaO2] x 100
- 28. ARTERIAL BLOOD GASES MECHANISMS OF HYPOXEMIA Hypoventilation V/Q mismatch Right-to-left shunt Diffusion limitation Reduced inspired oxygen tension
- 29. ARTERIAL BLOOD GASES "Simple and mixed acid-base disorders"
- 30. ARTERIAL BLOOD GASES Normal Values (Harrisons)
- 31. Normal Values • pH = 7.35 – 7.45 • pCO2 = 35 – 45 mmHg lungs (Reference Value = 40) • HCO3 = 22 – 26 mmol/L kidneys (Reference value = 24)
- 32. Definition Of Terms • Acidemia- Arterial pH < 7.56 • Alkalemia- Arterial pH > 7.45 • Acidosis- A process that tends to lower the extracellular pH (Hydrogen ion concentration increases) • Alkalosis- A process that tends to raise the extracellular pH (hydrogen ion concentration decreases)
- 33. Definition Of Terms • Metabolic acidosis- A disorder that reduces the serum Hc03 and pH • Metabolic Alkalosis- A disorder that elevates serum Hc03 and pH • Respiratory Acidosis- A disorder that elevates the arterial pC02 and reduces the pH • Respiratory Alkalosis- A disorder that reduces the arterial pC02 and elevates the pH
- 34. Definition Of Terms • Simple Acid Base Disorder- Appropriate Respiratory or Renal Compensation for the Disorder • Mixed Acid Base Disorder- Presence of More than one acid base Disorder
- 38. ARTERIAL BLOOD GAS ANALYSIS • 1) Look at the pH – Acidemia or alkalemia – The cause is in the same direction • 2) Look at pCO2 – Decreased in alkalosis – Increased in acidosis • 3) Look at HCO3 – Decreased in acidosis – Increased in alkalosis • 4) Remember, the body does NOT overcompensate • 5) Compensation can be COMPLETE or INCOMPLETE Example # 1 PH – 7.34 pCO2 – 52 HCO3 - 19
- 39. ARTERIAL BLOOD GAS ANALYSIS • 1) Look at the pH – Acidemia or alkalemia – The cause is in the same direction • 2) Look at pCO2 – Decreased in alkalosis – Increased in acidosis • 3) Look at HCO3 – Decreased in acidosis – Increased in alkalosis • 4) Remember, the body does NOT overcompensate • 5) Compensation can be COMPLETE or INCOMPLETE Example # 2 PH – 7.34 pCO2 – 50 HCO3 - 31
- 40. ARTERIAL BLOOD GAS ANALYSIS • 1) Look at the pH – Acidemia or alkalemia – The cause is in the same direction • 2) Look at pCO2 – Decreased in alkalosis – Increased in acidosis • 3) Look at HCO3 – Decreased in acidosis – Increased in alkalosis • 4) Remember, the body does NOT overcompensate • 5) Compensation can be COMPLETE or INCOMPLETE Example # 3 PH – 7.38 pCO2 – 24 HCO3 - 19
- 41. ARTERIAL BLOOD GAS ANALYSIS • 1) Look at the pH – Acidemia or alkalemia – The cause is in the same direction • 2) Look at pCO2 – Decreased in alkalosis – Increased in acidosis • 3) Look at HCO3 – Decreased in acidosis – Increased in alkalosis • 4) Remember, the body does NOT overcompensate • 5) Compensation can be COMPLETE or INCOMPLETE Example # 4 PH – 7.46 pCO2 – 42 HCO3 - 31
- 42. ARTERIAL BLOOD GAS ANALYSIS • 1) Look at the pH – Acidemia or alkalemia – The cause is in the same direction • 2) Look at pCO2 – Decreased in alkalosis – Increased in acidosis • 3) Look at HCO3 – Decreased in acidosis – Increased in alkalosis • 4) Remember, the body does NOT overcompensate • 5) Compensation can be COMPLETE or INCOMPLETE Example # 5 PH – 7.39 pCO2 – 41 HCO3 - 25
- 43. ARTERIAL BLOOD GAS ANALYSIS • 1) Look at the pH – Acidemia or alkalemia – The cause is in the same direction • 2) Look at pCO2 – Decreased in alkalosis – Increased in acidosis • 3) Look at HCO3 – Decreased in acidosis – Increased in alkalosis • 4) Remember, the body does NOT overcompensate • 5) Compensation can be COMPLETE or INCOMPLETE Example # 6 PH – 7.41 pCO2 – 51 HCO3 - 33
- 44. Calculations for the Medicine Floors
- 46. A 45 y.o. doctor ran a 6:12 mile, then fell down on all 4’s
- 47. A 45 y.o. doctor ran a 6:12 mile, then fell down on all 4’s ACIDOSIS ALKALOSIS Metabolic Respiratory CHRONIC RESP
- 53. DETERMINE PRIMARY DISORDER • Check the trend of the pH, HCO3, pCO2 • The change that produces the pH is the primary disorder pH = 7.25 HCO3 = 12 pCO2 = 30 ACIDOSIS ACIDOSIS ALKALOSIS METABOLIC ACIDOSIS
- 54. DETERMINE PRIMARY DISORDER • Check the trend of the pH, HCO3, pCO2 • The change that produces the pH is the primary disorder pH = 7.25 HCO3 = 28 pCO2 = 60 ACIDOSIS ALKALOSIS ACIDOSIS RESPIRATORY ACIDOSIS
- 55. DETERMINE PRIMARY DISORDER • Check the trend of the pH, HCO3, pCO2 • The change that produces the pH is the primary disorder pH = 7.55 HCO3 = 19 pCO2 = 20 ALKALOSIS ACIDOSIS ALKALOSIS RESPIRATORY ALKALOSIS
- 56. DETERMINE PRIMARY DISORDER • If the trend is the same, check the percent difference • The bigger %difference is the 10 disorder pH = 7.25 HCO3 = 16 pCO2 = 60 ACIDOSIS ACIDOSIS ACIDOSIS RESPIRATORY ACIDOSIS (24- 16)/24 = 0.33 (60-40)/40 = 0.5
- 57. DETERMINE PRIMARY DISORDER • If the trend is the same, check the percent difference • The bigger %difference is the 10 disorder pH = 7.55 HCO3 = 38 pCO2 = 30 ALKALOSIS ALKALOSIS ALKALOSIS METABOLIC ALKALOSIS (38-24)/24 = 0.58 (40-30)/40 = 0.25
- 59. • PREDICTION OF COMPENSATORY RESPONSES ON SIMPLE ACID BASE DISORDERS • Metabolic Acidosis PaCO2 = (1.5 X HCO3) + 8 • Metabolic Alkalosis PaCO2 will increase 0.75 mmHg per meq/L increase in HCO3 • Respiratory Acidosis Acute HCO3 will increase 1 meql/L per 10 mmHg increase in PaCO2 Chronic HCO3 will increase 4 meq/L per 10 mmHg increase in PaCO2 • Respiratory Alkalosis Acute HCO3 will decrease 2 meq/L per 10 mmHg decrease in PaCO2 Chronic HCO3 will decrease 4 meq/L per 10 mmHg decrease in PaCO2
- 60. COMPENSATORY RESPONSE METABOLIC ACIDOSIS PaCO2 = (1.5 X HCO3) + 8 HCO3 =12 pCO2 =1.5 X 12 + 8 = 26 pCO2 = 1.5 X 7 + 8 = 18.5HCO3 =7
- 61. COMPENSATORY RESPONSE HCO3 =35 pCO2 =11 X 0.75 = 8.25 = 8.25 + 40 = 48 pCO2 = 52HCO3 =40 METABOLIC ALKALOSIS PaCO2 will increase 0.75 mmHg per meq/L increase in HCO3
- 62. COMPENSATORY RESPONSE pCO2 =55 HCO3 = 25.5 HCO3 = 28pCO2 =80 ACUTE RESPIRATORY ACIDOSIS HCO3 will increase 1 meq/L per 10 mmHg increase in PaCO2
- 63. COMPENSATORY RESPONSE RESPIRATORY ALKALOSIS Acute: HCO3 will decrease 2 meq/L per 10 mmHg decrease in PaCO2
- 64. Check for Secondary Acid Base Disorders Primary Acid Base Disorder Compensation Secondary Base Disorder Metabolic Acidosis Actual reduction of pC02 from baseline is HIGHER than that of calculated compensation Secondary RESPIRATORY ALKALOSIS is present Actual reduction of pC02 from baseline is LESS than that of calculated compensation Secondary RESPIRATORY ACIDOSIS is present
- 65. Check for Secondary Acid Base Disorders Primary Acid Base Disorder Compensation Secondary Base Disorder Metabolic Alkalosis Actual increase of Pc02 from baseline is HIGHER than that of calculated compensation Secondary RESPIRATORY ACIDOSIS is present Actual reduction of pC02 from baseline is LESS than that of calculated compensation Secondary RESPIRATORY ACIDOSIS is present
- 66. Check for Secondary Acid Base Disorders Primary Acid Base Disorder Compensation Secondary Base Disorder Respiratory Acidosis Actual increase of Hc03 from baseline is HIGHER than that of calculated compensation Secondary Metabolic Alkalosis is present Actual increase of Hc03 from baseline is LESS than that of calculated compensation Secondary METABOLIC ACIDOSIS is present
- 67. Check for Secondary Acid Base Disorders Primary Acid Base Disorder Compensation Secondary Base Disorder Respiratory Alkalosis Actual decrease of Hc03 from baseline is HIGHER than that of calculated compensation Secondary Metabolic Acidosis is present Actual decrease of Hc03 from baseline is LESS than that of calculated compensation Secondary METABOLIC Alkalosis is present
- 68. ANION GAP Na – (HCO3 + Cl) = 10-12 mmol/L Na = 135 HCO3 = 15 Cl = 97 RBS = 100 mg% AG = 135 – 112 = 23
- 69. ANION GAP Na – (HCO3 + Cl) = 10-12 Na = 135 HCO3 = 15 Cl = 97 RBS = 500 mg% Corrected AG = Na + RBS mg% -100 x 1.4 100 AG = 135 + 5.6 – 112 = 28.6
- 70. DETERMINE CLUES FROM THE CLINICAL SETTING
- 71. CLUES FROM CLINICAL SETTING HIGH ANION GAP METABOLIC ACIDOSIS (HAGMA) M Methanol U Uremia D Diabetic Ketoacidosis P Paraldehyde I Isoniazid, Iron L Lactic Acidosis E Ethylene Glycol, Ethanol S Salicylates
- 72. CLUES FROM CLINICAL SETTING NORMAL ANION GAP METABOLIC ACIDOSIS (NAGMA) H Hyperalimentation A Acetazolamide R Renal Tubular Acidosis D Diarrhea U Ureteropelvic shunt P Post Hypocapnia
- 73. CLUES FROM CLINICAL SETTING METABOLIC ALKALOSIS Vomiting Remote diuretic use Post hypercapnea Chronic diarrhea Cystic fibrosis Acute alkali administration
- 74. CLUES FROM CLINICAL SETTING METABOLIC ALKALOSIS Bartter’s syndrome Severe potassium depletion Current diuretic use Hypercalcemia Hyperaldosteronism Cushing’s syndrome Gastric aspiration
- 75. CLUES FROM CLINICAL SETTING RESPIRATORY ACIDOSIS CHRONIC: COPD, intracranial tumors ACUTE: pneumonia, head trauma, general anesthetics, sedatives RESPIRATORY ALKALOSIS Hyperventilation, Pregnancy, Liver failure, Methylxanthines
- 76. CASE 1 56F with vomiting and diarrhea 3 days ago despite intake of loperamide. Her last urine output was 12 hours ago. PE showed BP = 80/60, HR = 110, RR = 28. There is poor skin turgor.
- 77. CASE 1 serum Na = 130 pH = 7.30 K = 2.5 pCO2 = 30 Cl = 105 HCO3 = 15 BUN = 42 pO2 = 90 crea = 2.0 RBS = 100 BCR = BUN / crea = 21 PRE-RENAL
- 78. CASE 1 serum Na = 130 pH = 7.30 K = 2.5 pCO2 = 30 Cl = 105 HCO3 = 15 BUN = 42 pO2 = 90 crea = 2.0 RBS = 100 pH = acidosis, pCO2 =alk, HCO3 = acidosis Metabolic Acidosis
- 79. CASE 1 serum Na = 130 pH = 7.30 K = 2.5 pCO2 = 30 Cl = 105 HCO3 = 15 BUN = 42 pO2 = 90 crea = 2.0 RBS = 100 pCO2 = 15 x 1.5 + 8 = 30.5 Compensated Metabolic Acidosis
- 80. CASE 1 serum Na = 130 pH = 7.30 K = 2.5 pCO2 = 30 Cl = 105 HCO3 = 15 BUN = 42 pO2 = 90 crea = 2.0 RBS = 100 AG= 130 – (105+15) = 10 NAGMA
- 81. CASE 2 19F, fashion model, is surprised to find her K=2.7 mmol/L because she was normokalemic 6 months ago. She admits to being on a diet of fruit and vegetables but denies vomiting and the use of diuretics or laxatives. She is asymptomatic. BP = 90/55 with subtle signs of volume contraction.
- 82. CASE 2 serum Na 138 63 K 2.7 34 Cl 96 0 HCO3 30 0 pH 7.45 5.6 pCO2 45 Metabolic Alkalosis Plasma Urine pH = alk, pCO2 =acidosis HCO3 = alkalosis
- 83. COMPENSATORY RESPONSE HCO3 =35 pCO2 =11 X 0.75 = 8.25 = 8.25 + 40 = 48 pCO2 = 52HCO3 =40 METABOLIC ALKALOSIS PaCO2 will increase 0.75 mmHg per mmol/L increase in HCO3
- 85. CASE 3 AG= 138 – (96+30) = 12 NAG Plasma Urine serum Na 138 63 K 2.7 34 Cl 96 0 HCO3 30 0 pH 7.45 5.6 pCO2 45
- 86. CASE 3 Plasma Urine serum Na 138 63 K 2.7 34 Cl 96 0 HCO3 30 0 pH 7.45 5.6 pCO2 45 What is the cause of the acid base disorder?
- 87. CASE 4 73M with long standing COPD (pCO2 stable at 52-58 mmHg), cor pulmonale, and peripheral edema had been taking furosemide for 6 months. Five days ago, he had anorexia, malaise, and productive cough. He continued his medications until he developed nausea. Later he was found disoriented and somnolent
- 88. CASE 4 PE: BP 110/70, HR 110, RR 24, T=40 respiratory distress prolonged expiratory phase postural drop in BP drowsy, disoriented scattered rhonchi and rales BLFs distant heart sounds trace pitting edema
- 89. CASE 4 admission after 48 hrs pH = acidosis pCO2 =acidosis, HCO3 = alk Respiratory Acidosis serum Na 136 139 K 3.2 3.9 Cl 78 86 HCO3 40 38 pH 7.33 7.42 pCO2 78 61 pO2 43 56
- 90. COMPENSATORY RESPONSE pCO2 =55 HCO3 = 25.5 HCO3 = 28pCO2 =80 ACUTE RESPIRATORY ACIDOSIS HCO3 will increase 1 mmol/L per 10 mmHg increase in PaCO2
- 91. serum Na 136 139 K 3.2 3.9 Cl 78 86 HCO3 40 38 pH 7.33 7.42 pCO2 78 61 pO2 43 56 CASE 4 admission after 48 hrs HCO3 = 25.5 Respiratory Acidosis & M. Alkalosis
- 92. Check for Secondary Acid Base Disorders Primary Acid Base Disorder Compensation Secondary Base Disorder Respiratory Acidosis Actual increase of Hc03 from baseline is HIGHER than that of calculated compensation Secondary Metabolic Alkalosis is present Actual increase of Hc03 from baseline is LESS than that of calculated compensation Secondary METABOLIC ACIDOSIS is present
- 93. CASE 5 42M, alcoholic, brought to the ER intoxicated. He was found at Rizal park in a pool of vomitus. PE showed unkempt and incoherent patient with a markedly contracted ECF volume. T=390 C with crackles on the RULF.
- 94. serum Na = 130 pH = 7.53 K = 2.9 pCO2 = 25 Cl = 80 HCO3 = 20 BUN = 34 pO2 = 60 crea = 1.4 alb = 38 RBS = 15 mmol/L CASE 5 PRE-RENALBCR = 24
- 95. serum Na = 130 pH = 7.53 K = 2.9 pCO2 = 25 Cl = 80 HCO3 = 20 BUN = 12 pO2 = 60 crea = 120 alb = 38 RBS = 15 mmol/L CASE 5 Respiratory Alkalosis %pCO2 =38, %HCO3 = 18
- 96. COMPENSATORY RESPONSE RESPIRATORY ALKALOSIS Acute: HCO3 will decrease 2 mmol/L per 10 mmHg decrease in PaCO2
- 97. serum Na = 130 pH = 7.53 K = 2.9 pCO2 = 25 Cl = 80 HCO3 = 20 BUN = 12 pO2 = 60 crea = 120 alb = 38 RBS = 15 mmol/L CASE 5 Compensated Respiratory Alkalosis HCO3 = 21
- 98. serum Na = 130 pH = 7.53 K = 2.9 pCO2 = 25 Cl = 80 HCO3 = 20 BUN = 12 pO2 = 60 crea = 120 alb = 38 RBS = 15 mmol/L CASE 5 HAGMA + RAlkAG = 130 – (80 + 20) = 30
- 99. QUESTIONS?
Editor's Notes
- ARTERIAL SAMPLING — Arterial blood is required for an ABG. It can be obtained by percutaneous needle puncture or from an indwelling arterial catheter. There is no evidence that any site is superior to the others.
- Technique — Once a palpable artery has been located, blood is withdrawn using the following steps. ●The planned puncture site should be sterilely prepped. ●Local analgesia ●The seal of a heparinized syringe should be broken by pulling its plunger. The plunger can then be pushed back into the syringe, leaving a small empty volume (eg, less than 1 mL) in the syringe. A small needle (eg, 22 to 25 gauge) should then be attached to the syringe. Arterial blood gas kits are available, which contain a heparinized plastic syringe with the plunger already pulled back to allow for the collection of 2 mL of blood without the need to break the seal. ●Using one hand to gently palpate the artery and the other to manipulate the syringe and needle, the artery should be punctured with the needle at a 30 to 45 degree angle relative to the skin. The syringe will fill on its own (ie, pulling the plunger is unnecessary). Approximately 2 to 3 mL of blood should be removed. ●To prevent coagulation, the syringe should be rolled between the hands for a few seconds to allow blood to mix with the heparin. ●After withdrawing a sufficient volume of blood, the needle should be removed and pressure applied to the puncture site for five to ten minutes to achieve hemostasis.
- The radial artery is best palpated between the distal radius and the tendon of the flexor carpi radialis when the wrist is extended To get the wrist into this position, the arm should be positioned on an armboard with the palm facing upward and a large roll of gauze should be placed between the wrist and the armboard in a position that extends the wrist. Taping the forearm and palm to the armboard helps maintain the position.
- Schematic representation of the relationship of the brachial artery to the antecubital crease and the median nerve. The artery should be entered just above the antecubital crease.
- Technique of brachial artery puncture. The brachial artery is palpable in the antecubital fossa just medial to the biceps tendon. The needle should enter the brachial artery just above the antecubital crease.
- Schematic representation of the relationship of the common femoral artery to the femoral vein and femoral nerve.
- Technique of femoral artery puncture. The femoral artery can be palpated just below the midpoint of the inguinal ligament. The needle should be inserted at a 90 degree angle toward the pulsation for a single sampling of arterial blood. For catheter placement, the needle should be inserted at a 45º angle in a cephalad direction (as shown).
- The dorsalis pedis artery is located lateral to the extensor hallucis longus tendon.
- Technique of cannulation of the dorsalis pedis artery. Before placement of a catheter in this artery, adequacy of collateral flow should be demonstrated. The artery should be occluded by pressure, and the great toe should be blanched by compression of the toenail for several seconds. While the dorsalis pedis artery is still being compressed, color should return rapidly to the toe after pressure on the nail is released.
- The axillary artery is palpated within the axilla when the arm is abducted and externally rotated.
- Technique of axillary artery puncture. The arm should be hyperabducted and externally rotated. The needle should be inserted into the artery as high as possible within the axilla.
- The patient's hand is initially held high while the fist is clenched and both radial and ulnar arteries are compressed (A); this allows the blood to drain from the hand. The hand is then lowered (B) and the fist is opened (C). After pressure is released over the ulnar artery (D), color should return to the hand within six seconds, indicating a patent ulnar artery and an intact superficial palmar arch.
- Gas diffusion through the plastic syringe is a potential source of error. However, it appears that the clinical significance of the error is minimal if the sample is placed on ice and analyzed within 15 minutes [6-9]. Using a glass syringe will also prevent this error.
- The heparin that is added to the syringe as an anticoagulant can decrease in the pH if acidic heparin is used. It can also dilute the PaCO2, resulting in a falsely low value Thus, the amount of heparin solution should be minimized and at least 2 mL of blood should be obtained. ●Air bubbles that exceed 1 to 2 percent of the blood volume can cause a falsely high PaO2 and a falsely low PaCO2 [11]. The magnitude of this error depends upon the difference in gas tensions between blood and air, the exposure surface area (which is increased by agitation), and the time from specimen collection to analysis. The clinical significance of this error can be decreased by gently removing the bubbles without agitation and analyzing the sample as soon as possible [7,12].
- Air bubbles that exceed 1 to 2 percent of the blood volume can cause a falsely high PaO2 and a falsely low PaCO2 The clinical significance of this error can be decreased by gently removing the bubbles without agitation and analyzing the sample as soon as possible [7,12].
- Arterial oxygen saturation (SaO2) — Most of the oxygen that diffuses from the alveolus to the pulmonary capillary binds to hemoglobin in red blood cells. The arterial oxygen saturation (SaO2) is the proportion of red blood cells whose hemoglobin is bound to oxygen. It is most commonly measured noninvasively by pulse oximetry, but can also be measured by arterial blood gas Hypoxia is defined as a condition where the oxygen supply is inadequate either to the body as a whole (general hypoxia) or to a specific region (tissue hypoxia). Abnormal SaO2 has not been defined because a threshold below which tissue hypoxia occurs has not been identified. This reflects with multifactorial nature of tissue hypoxia. It seems reasonable to consider a resting SaO2 ≤95 percent or exercise desaturation ≥5 percent abnormal, although these values should not be considered in isolation [1]. As an example, a resting SaO2 of 95 percent could be abnormal if a patient previously had a resting SaO2 of 99 percent.
- Arterial oxygen tension (PaO2) — A small amount of the oxygen that diffuses from the alveolus to the pulmonary capillary dissolves into the plasma. The arterial oxygen tension (PaO2) is the amount of oxygen dissolved in the plasma, which is measured by arterial blood gas. Similar to oxygen saturation, an abnormal PaO2 has not been defined because a threshold below which tissue hypoxia occurs has not been identified. However, it seems reasonable to consider a PaO2 <80 mmHg abnormal, although the value should not be considered in isolation
- The alveolar to arterial (A-a) oxygen gradient is a common measure of oxygenation (“A” denotes alveolar and “a” denotes arterial oxygenation). It is the difference between the amount of the oxygen in the alveoli (ie, the alveolar oxygen tension [PAO2]) and the amount of oxygen dissolved in the plasma (PaO2) (calculator 1): A-a oxygen gradient = PAO2 - PaO2. PaO2 is measured by arterial blood gas, while PAO2 is calculated using the alveolar gas equation: PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 ÷ R) where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level), PH2O is the partial pressure of water (47 mmHg at 37 degrees C), PaCO2 is the arterial carbon dioxide tension, and R is the respiratory quotient. The respiratory quotient is approximately 0.8 at steady state, but varies according to the relative utilization of carbohydrate, protein, and fat. The A-a gradient calculated using this alveolar gas equation may deviate from the true gradient by up to 10 mmHg. This reflects the equation's simplification from the more rigorous full calculation and the imprecision of several independent variables (eg, FiO2 and R). The normal A-a gradient varies with age and can be estimated from the following equation, assuming the patient is breathing room air (calculator 1) [3]: A-a gradient = 2.5 + 0.21 x age in years The A-a gradient increases with higher FiO2. When a patient receives a high FiO2, both PAO2 and PaO2 increase. However, the PAO2 increases disproportionately, causing the A-a gradient to increase. In one series, the A-a gradient in men breathing air and 100 percent oxygen varied from 8 to 82 mmHg in patients younger than 40 years of age and from 3 to 120 mmHg in patients older than 40 years of age
- PaO2/FiO2 ratio — The PaO2/FiO2 ratio is another common measure of oxygenation. A normal PaO2/FiO2 ratio is 300 to 500 mmHg, with values less than 300 mmHg indicating abnormal gas exchange and values less than 200 mmHg indicates severe hypoxemia As an example, a patient whose PaO2 is 60 mmHg while receiving an FiO2 of 0.50 (ie, 50 percent) has a PaO2/FiO2 ratio of 120 mmHg
- a-A oxygen ratio = PaO2 ÷ PAO2 The a-A oxygen ratio is commonly used to predict the change in PaO2 that will result when the FiO2 is changed. Its lower limit of normal is 0.77-0.82 and it is most reliable when the FiO2 is less than 0.55 (ie, 55 percent)
- Oxygenation index — The oxygenation index (OI) is most commonly used in neonates with persistent pulmonary hypertension of the newborn to determine the severity of hypoxemia and to guide the timing of interventions, such as inhaled nitric oxide [8,9]. OI = [mean airway pressure x FiO2 ÷ PaO2] x 100 A high OI (eg, ≥25) indicates severe hypoxemic respiratory failure.
- MECHANISMS OF HYPOXEMIA Hypoventilation V/Q mismatch Right-to-left shunt Diffusion limitation Reduced inspired oxygen tension Hypoventilation — Both arterial (PaCO2) and alveolar (PACO2) carbon dioxide tension increase during hypoventilation, which causes the alveolar oxygen tension (PAO2) to decrease. As a result, diffusion of oxygen from the alveolus to the pulmonary capillary declines. The net effect is hypoxemia. Hypoxemia due to pure hypoventilation can be identified by two characteristics. First, it readily corrects with a small increase in the fraction of inspired oxygen (FiO2). Second, the A-a gradient is usually normal. An exception exists when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient [11]. Abnormalities that cause pure hypoventilation include: CNS depression, such as drug overdose, structural CNS lesions, or ischemic CNS lesions that impact the respiratory center Obesity hypoventilation (Pickwickian) syndrome Impaired neural conduction, such as amyotrophic lateral sclerosis, Guillain-Barré syndrome, high cervical spine injury, phrenic nerve paralysis, or aminoglycoside blockade Muscular weakness, such as myasthenia gravis, idiopathic diaphragmatic paralysis, polymyositis, muscular dystrophy, or severe hypothyroidism Poor chest wall elasticity, such as a flail chest or kyphoscoliosis V/Q mismatch — Ventilation-perfusion (V/Q) mismatch refers to an imbalance of blood flow and ventilation. It causes the composition of alveolar gas to vary among lung regions: Lung regions with low ventilation compared to perfusion will have a low alveolar oxygen content and high CO2 content Lung regions with high ventilation compared to perfusion will have a low CO2 content and high oxygen content In the normal lung, there is V/Q mismatch because perfusion and ventilation are heterogeneous. Both ventilation and perfusion are greater in the bases than in the apices. However, the difference between apical and basilar ventilation is smaller than the difference between apical and basilar perfusion. As a result, the V/Q ratio is higher in the apices than in the bases. V/Q mismatch is responsible for the normal A-a gradient. In the diseased lung, V/Q mismatch increases because heterogeneity of both ventilation and perfusion worsen. The net effect is hypoxemia. Hypoxemia due to V/Q mismatch can be corrected with low to moderate flow supplemental oxygen and is characterized by an increased A-a gradient. Common causes of hypoxemia due to V/Q mismatch include obstructive lung diseases, pulmonary vascular diseases, and interstitial diseases. Right-to-left shunt — A right-to-left shunt exists when blood passes from the right to the left side of the heart without being oxygenated. There are two types of right-to-left shunts: Anatomic shunts exist when the alveoli are bypassed. Examples include intracardiac shunts, pulmonary arteriovenous malformations (AVMs), and hepatopulmonary syndrome. Physiologic shunts exist when non-ventilated alveoli are perfused. Examples include atelectasis and diseases with alveolar filling (eg, pneumonia, acute respiratory distress syndrome). Right-to-left shunts cause extreme V/Q mismatch, with a V/Q ratio of zero in some lung regions. The net effect is hypoxemia, which is difficult to correct with supplemental oxygen. The degree of shunt can be quantified from the shunt equation (calculator 3): Qs/Qt = (CcO2 - CaO2) ÷ (CcO2 - CvO2) where Qs/Qt is the shunt fraction, CcO2 is the end-capillary oxygen content, CaO2 is the arterial oxygen content, and CvO2 is the mixed venous oxygen content. CaO2 and CvO2 are calculated from arterial and mixed venous blood gas measurements, respectively. CcO2 is estimated from the PAO2. (See "Oxygen delivery and consumption", section on 'Definitions'.) Diffusion limitation — Diffusion limitation exists when the movement of oxygen from the alveolus to the pulmonary capillary is impaired. It is usually a consequence of alveolar and/or interstitial inflammation and fibrosis, such as that due to interstitial lung disease. In such diseases, diffusion limitation usually coexists with V/Q mismatch, which makes the relative contribution of each to the patient's hypoxemia uncertain. Diffusion limitation is characterized by exercise-induced or -exacerbated hypoxemia. This is illustrated by the following: During rest, blood traverses the lung relatively slowly. Thus, there is usually sufficient time for oxygenation to occur even if diffusion limitation exists. During exercise, cardiac output increases and blood traverses the lung more quickly. As a result, there is less time for oxygenation. In the healthy individuals, several compensatory mechanisms occur. Pulmonary capillaries dilate, which increases the surface area available for gas exchange by perfusing additional regions of lung. PAO2 also increases, which promotes oxygen diffusion by increasing the oxygen gradient from the alveolus to the artery. The net effect is that full oxygenation is sustained. In patients with diffusion limitation (such as with pulmonary fibrosis), there is insufficient time for oxygenation to occur. In addition, most such patients have parenchymal destruction, which renders it impossible to recruit additional surface area for gas exchange. The net effect is measurable hypoxemia. Reduced inspired oxygen tension — The inspired oxygen tension (PiO2) is a component of the alveolar gas equation that was described above. It can be determined by the equation: PiO2 = FiO2 x (Patm - PH2O) where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level), and PH2O is the partial pressure of water (47 mmHg at 37 degrees C). Reduction of the PiO2 will decrease the PAO2. This impairs oxygen diffusion by decreasing the oxygen gradient from the alveolus to the artery. The net effect is hypoxemia. A reduced PiO2 is most commonly associated with high altitude