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Blood Gas Basics
Blood gases provide information concerning the oxygenation, ventilatory, and acid-base
status of the patient. Blood gas results are usually given as pH, PO2, PCO2, [HCO3–], base
excess or deficit (base difference), and O2 saturation. This test gives information on acid–
base homeostasis (pH, PCO2, [HCO3–], and base difference) and on blood oxygenation
(PO2, O2 saturation). Arterial blood gases (ABG) are most commonly measured; venous,
mixed venous, and capillary blood gases are measured less frequently. Indications for
blood gas determinations are as follows (Respir Care 2001;46:498–505):

To determine a patient's ventilatory (PaCO2), acid–base (pH and PaCO2), and
oxygenation and O2-carrying capacity (PaO2 and O2Hb)

To quantitate the response to therapeutic intervention (eg, supplemental O2
administration, mechanical ventilation) or diagnostic evaluation (eg, exercise
desaturation)

Monitoring the severity and progression of documented disease processes (eg,
COPD)

Normal Blood Gas Values
Normal values for blood gas analysis are given in Table 8–1, and capillary blood gases are
discussed in a following section. Mixed venous blood gases are reviewed in Chapter 20.
The bicarbonate concentration ([HCO3–]) from the blood gas is a calculated value
and should not be used in interpretation of blood gases; the [HCO3–] from a
concurrent chemistry panel should be used. Note: The HCO3– values on the chemistry
panel and those calculated from the blood gases should be about the same. A major
discrepancy (> 10% difference) means one or more of the three values is in error (pH,
PCO2, or [HCO3–]). The most common cause of discrepancies is drawing the blood gas and
chemistry panel samples at different times. ABGs and chemistry panels [HCO3–] should be
obtained at the same time for the most accurate interpretation.

Table 8–1 Normal Blood Gas Values

Saturation is probably more useful than PO2 itself in interpretation of a CBG. Venous blood gas levels may occasionally be used to assess acid–base status.36 (7. Heelstick Technique. (See Chapter 13.) When interpreting a CBG. apply the following rules:  pH: Same as arterial or slightly lower (Normal = 7. hemorrhage) than obtaining an ABG sample. . but venous O2 levels are significantly less than arterial values (see Table 8–1). Venous Blood Gases There is little difference between arterial and venous pH and [HCO3–] (except in severe CHF and shock).Measurement Arterial Blood Mixed Venous Blooda Venous Blood pH (range) 7.41) PO2 (mm Hg) (decreases with age) 80–100 35–40 30–50 PCO2 (mm Hg) 36–44 41–51 40–52 O2 saturation (%) [decreases with age] >95 60–80 60–85 HCO3– (mEq/L) 22–26 22–26 22–28 Base difference (deficit/excess) –2 to +2 –2 to +2 –2 to +2 a Obtained from the right atrium. Capillary Blood Gases A CBG is obtained from a highly vascularized capillary bed.40)  PCO2: Same as arterial or slightly higher (Normal = 40–45 mm Hg)  PO2: Lower than arterial (Normal = 45–60 mm Hg)  O2 saturation: > 70% is acceptable.35–7.44) 7.37– 7.31– 7. usually through a pulmonary artery catheter.41) 7.36 (7.31–7.40 (7. CBG is often used for pediatric patients because obtaining the sample is easier (through the heel) and less traumatic (no risk of arterial thrombosis.

01 below 7. Rule II: A pH change of 0. and similarly a metabolic disturbance altering [HCO3–] changes . 40 mEq/L = [H+] at the normal pH of 7. a respiratory disturbance leading to an abnormal PCO2 alters the pH. [HCO3–]) is termed a base deficit. These two rules are helpful in interpreting blood gas results. or add 1 mEq/L to 40 mEq for every 0. If not. For a rough estimate of [H+]. or 80 nmol/L. particularly in defining a simple versus a mixed blood gas disorder: Rule I: A change in PCO2 up or down 10 mm Hg is associated with an increase or decrease in pH of 0.15 is equivalent to a base change of 10 mEq/L.48). 4. [HCO3–] and base difference are calculated with the Henderson–Hasselbalch equation: or the Henderson equation: 2. metabolic. pH is a log scale. [H+] = (7. as the PCO2 increases. As the Henderson– Hasselbalch equation shows. A decrease in base (ie.80 – pH) x 100. or 20 nmol/L.08 units. [H+] = 1/2 40.10.General Principles of Blood Gas Determinations Interpretation of O2 values is discussed in Hypoxia 1.40. an error has been made in collection or in determination of the values. and an increase in base is termed a base excess. The calculated [HCO3–] should be within 2 mEq/L of the [HCO3–] of a venous measurement drawn at the same time.3 in pH from 7.40 (accurate for pH 7. and both samples should be recollected.70. Two additional relationships derived from the Henderson–Hasselbalch equation should be committed to memory. and renal systems.37.25–7.40 and subtract 1 mEq/L from 40 mEq for every 0. The primary causes of acid–base disturbances are abnormalities in the respiratory. Acidemia is a pH < 7. pH increases.01 above 7. Acidosis and alkalosis are used to describe the process by which pH changes. The blood gas analyzers in most labs measure pH and PCO2 as well as PO2. Acid–Base Disorders: Definition 1. As PCO2 decreases. and for pH 7. 3. pH decreases.44. for every change of 0. For pH 7.40 the [H+] doubles or halves. [H+] = 2 x 40. Acid–base disorders are common clinical problems. and alkalemia is a pH > 7.

A primary metabolic disorder leads to respiratory compensation. Alterations in either . Table 8–2 lists the major categories of primary acid–base disorders. The net effect of mixed disorders can be additive (eg.the pH. follow the six steps in the Interpretation of Blood Gases. The degree of compensation can be expressed in terms of the degree of primary acid–base disturbance.6 in [HCO3–] = PCO2/10 in [HCO3–] = 4 x PCO2/10 in [HCO3–] = 2 x PCO2/10 in [HCO3–] = 5 x PCO2/10 Mixed Acid–Base Disorders 1.5 x [HCO3–])+8 in PCO2 = [HCO3–] x 0. two or more primary disorders may occur simultaneously. serious illness). 2. the effects can be opposite (eg. the secondary compensatory response. Table 8–2 Simple Acid–Base Disturbances Acid–Base Disorder Primary Abnormality Expected Compensation Metabolic acidosis [HCO3–] PCO2 Metabolic alkalosis [HCO3–] PCO2 Acute respiratory acidosis PCO2 Chronic respiratory acidosis PCO2 Acute respiratory alkalosis PCO2 Chronic respiratory alkalosis PCO2 [HCO3–] [HCO3–] [HCO3–] [HCO3–] Expected Degree of Compensation PCO2 = (1. Most acid–base disorders result from a single primary disturbance of the normal physiologic compensatory response (called simple acid–base disorders). Or. Any primary disturbance in acid–base homeostasis invokes a normal compensatory response. and the expected compensation based on the primary abnormality. metabolic acidosis and respiratory alkalosis) and nullify somewhat the effect of the other on pH. In some cases (eg. To determine the presence of a mixed acid–base disorder with a blood gas value. metabolic acidosis and respiratory acidosis) and result in extreme alteration of pH. These changes are defined graphically in Figure 8–1. 3. the primary abnormality. 2. and a primary respiratory disorder leads to an acute metabolic response due to the buffering capacity of body fluids and chronic compensation (1–2 d) due to alterations in renal function. resulting in a mixed acid–base disorder.

Originally published by Appleton & Lange.[HCO3–] or PCO2 that differ from expected compensation levels indicate a second process. . Two of the examples given in the following section illustrate the strategies used in identifying a mixed acid–base disorder.) Step 1: Determine whether the numbers fit. Nomogram for acid-base disorders. Inc. Interpretation of Blood Gases Use a consistent.) Figure 8–1. with permission. (Reprinted. stepwise approach to interpretation of blood gases. (See Figure 8–1. Copyright © 1991 by the McGraw-Hill Companies. from: Cogan MG: Fluid and Electrolytes.

If the anion gap is increased. Step 2: Next. respiratory or metabolic. is altered in the same direction as the pH abnormality. the [HCO3–] is only 25% of normal.37) or alkalemia (pH > 7.The right side of the equation should be within about 10% of the left side. and samples for ABG and [HCO3–] must be recollected.25. pH 7. The most common reason for the numbers not fitting is that the ABG and the chemistry panel [HCO3–] were obtained at different times. the primary disturbance would be metabolic acidosis. Step 3: Identify the primary disturbance as metabolic or respiratory. if acidemia is present. The primary disturbance is the one that varies the most from normal.44) is present. Step 4: After identifying the primary disturbance. Step 5: Calculate the anion gap: A normal anion gap is 8–12 mEq/L. whereas the increase in PCO2 is only 25% above normal. For example. both respiratory (PCO2 > 44 mm Hg) and metabolic [HCO3–] < 22 mEq/L) acidosis are present—then this is a mixed acid–base problem (see Step 4). If both components act in the same direction—eg. That is. or is the [HCO3–] < 22 mEq/L (metabolic acidosis)? In other words. determine whether acidemia (pH < 7. Step 6: . PCO2 48 mm Hg. proceed to Step 6. with a [HCO3–] of 6 mEq/L and PCO2 of 50 mm Hg. obtain another ABG and chemistry panel for [HCO3–]. Example. use the equations in Table 8–2 to calculate the expected compensatory response. identify which component. a mixed acid–base disturbance is present. If the numbers do not fit. If the difference between the actual value and the calculated value is great. [HCO3–] 29 mEq/L. This blood gas cannot be interpreted. is the PCO2 > 44 mm Hg (respiratory acidosis).

(See Examples 5.) Finally. caused by a decrease in [HCO3–] balanced by an increase in an . Differential Diagnosis The diagnosis of metabolic acidosis (Figure 8–2) can be classified as anion gap or non– anion gap acidosis. compare the changes from normal between the anion gap and [HCO3–]. Anion Gap Acidosis: Anion gap > 12 mEq/L. 8–12 mEq/L) is calculated as: Figure 8–2. be sure the interpretation of the blood gas is consistent with the clinical setting. gap acidosis is present and there is no metabolic alkalosis or nongap metabolic acidosis. The anion gap (Normal range. If the change in anion gap is greater than the change in [HCO3–] from normal. nongap metabolic acidosis is present in addition to gap metabolic acidosis. and 7. If the change in the anion gap is less than the change in [HCO3–] from normal. If the change in anion gap is similar to the change in [HCO3–] from normal. Metabolic Acidosis: Diagnosis and Treatment Metabolic acidosis represents an increase in acid in body fluids reflected by a decrease in [HCO3–] and a compensatory decrease in PCO2. Differential diagnosis of metabolic acidosis.If the anion gap is elevated. metabolic alkalosis is present in addition to gap metabolic acidosis. 6.

Table 8–3 Renal Tubular Acidosis: Diagnosis and Management Clinical Renal Conditio Defect n GF Serum R [HCO3– ] (mmol/ L) Serum [K+] (mmol/ L) Minim Associated al Disease States Urine pH Treatment Normal N 24–28 3.2 None N/A Proximal Proximal RTA (type H+ II RTA) secretion N 15–18 <5. (b) metabolic nongap acidosis. None . 3 autoimmune mmol/kg/d) diseases. nongap acidosis. nephrocalcinosis. (c) mixed metabolic gap and nongap acidosis. and (d) metabolic gap acidosis and metabolic alkalosis. dysproteinemic states. The anion gap is helpful in identifying metabolic gap acidosis. toxins (heavy metals).8–5. Renal tubular acidosis is a type of nongap acidosis that can be associated with a variety of pathologic conditions (Table 8–3). paroxysmal nocturnal hemoglobinuria NaHCO3 or KHCO3 (10– 15 mmol/kg/d). caused by a decrease in [HCO3–] balanced by an increase in chloride (hyperchloremic acidosis). tubulointerstitial diseases. Non–Anion Gap Acidosis: Anion gap = 8–12 mEq/L. a closer look at the anion gap and [HCO3–] helps differentiate (a) pure metabolic gap acidosis. various genetic disorders.5 Drugs. secondary hyperparathyroidi sm. and mixed metabolic gap and nongap acidosis.5 Various genetic NaHCO3 (1– disorders.5–5 4.unmeasured acid ion from either endogenous production or exogenous ingestion (normochloremic acidosis). thiazide diuretics Classic Distal H+ distal secretion RTA (type I RTA) N 20–30 >5. If an elevated anion gap is present. Fanconi syndrome. nephrotic syndrome.

toxins.20 with sodium bicarbonate. The total replacement dose of HCO3– can be calculated as follows: 3. drugs). hepatic cirrhosis. empty sella syndrome Buffer Distal NH3 deficiency delivery (type III RTA) 15–18 Distal Na+ reabsorpti on. and H+ secretion 24–28 Generaliz ed distal RTA (type IV RTA) N <5. 3 renal mmol/kg/d) osteodystrophy. severe hypophosphatemi a <5. hyporeninemic hypoaldosteronis m. nephrosclerosis. Be aware of sodium and volume overload during replacement. control diarrhea). NaHCO3 (1– 3 mmol/kg/d) furosemide (40–160 mg/d) Treatment of Metabolic Acidosis 1. 2.1–0. saltwasting mineralocorticoid -resistant hyperkalemia Fludrocortiso ne (0.5 Primary mineralocorticoid deficiency (eg.5 mg/d) dietary K+ restriction. tubulointerstitial diseases. A . Addison disease). diabetes mellitus. Correct the underlying disorder (eg. Replace with one-half the total amount of bicarbonate over 8–12 h and reevaluate. Bicarbonate therapy is reserved for severe metabolic gap acidosis.20. tubulointerstitial diseases. K+ secretion. correct to above 7.5 Chronic renal NaHCO3 (1– insufficiency. If the pH < 7.Clinical Renal Conditio Defect n GF Serum R [HCO3– ] (mmol/ L) Serum [K+] (mmol/ L) Minim Associated al Disease States Urine pH Treatment drugs.

Figure 8–3. Differential diagnosis of metabolic alkalosis. Chloride-Insensitive (Resistant) Metabolic Alkalosis: The pathogenesis in this category is direct stimulation of the kidneys to retain HCO3– irrespective of electrolyte intake and losses. Differential Diagnosis In two basic categories of diseases the kidneys retain HCO3– (Figure 8–3). The urinary [Cl–] > 10 mEq/L.normal or isotonic bicarbonate drip is made with 3 amp NaHCO3 (50 mEq NaHCO3/amp) in 1 L D5W. They can be differentiated in terms of response to treatment with sodium chloride and also by the urinary [Cl–] as determined by ordering a "spot. This chloride depletion results in renal sodium conservation leading to a corresponding reabsorption of HCO3– by the kidney." or "random" urine for chloride (UCl). Metabolic Alkalosis: Diagnosis and Treatment Metabolic alkalosis represents an increase in [HCO3–] with a compensatory rise in PCO2. and these . the urinary [Cl–] is < 10 mEq/L. Chloride-Sensitive (Responsive) Metabolic Alkalosis: The initial problem is a sustained loss of chloride out of proportion to the loss of sodium (either by renal or GI losses). In this category of metabolic alkalosis. and the disorders respond to treatment with intravenous NaCl.

acute (asthma). obstructive sleep apnea Thoracic–Pulmonary Disorders: Bony thoracic cage (flail chest.disorders do not respond to NaCl administration. large pleural effusions. Increased PCO2 occurs in clinical situations in which decreased alveolar ventilation occurs. 2. 1. hypophosphatemia Central Nervous System: Drugs (sedatives. CVA. Guillain–Barré syndrome. such as stopping exogenous steroids. Correct the underlying problem. c. scleroderma. upper airway obstruction. spinal cord injury (cervical) Airway Obstruction: Chronic (COPD). ethanol).Chloride-resistant a. parenchymal lesions (pneumothorax. tranquilizers. central sleep apnea. b. severe pulmonary edema. NH4Cl and HCl should be reserved for extreme cases. myasthenia gravis. Treatment of Metabolic Alkalosis Correct the underlying disorder. kyphoscoliosis). severe pneumonia). . Differential Diagnosis Neuromuscular Abnormalities with Ventilatory Failure: Muscular dystrophy. Correct hypokalemia if present. analgesics. Chloride-responsive a. Respiratory Acidosis: Diagnosis and Treatment Respiratory acidosis is a primary rise in PCO2 with a compensatory rise in plasma [HCO3–]. Replace volume with NaCl if depleted.

increase amount of dead space with ventilator. fever. hyperventilation syndrome. hypoxemia of any cause (see Hypoxia) Miscellaneous: Hepatic insufficiency. increase ventilator rate. decrease ventilator rate. Hyperventilation Syndrome: Best controlled by having the patient rebreathe into a paper bag to increase PCO2. early sepsis Peripheral Stimulation: PE. altitude. tumors. interstitial lung disease. head trauma or CVA with central neurogenic hyperventilation. progesterone. in addition to acid–base results.marked obesity (pickwickian syndrome) Treatment of Respiratory Acidosis Improve Ventilation: Intubate patient and initiate mechanical ventilation. or manage underlying cause. is oxygenation. Differential Diagnosis Central Stimulation: Anxiety. iatrogenic mechanical overventilation Treatment of Respiratory Alkalosis Correct the underlying disorder. reverse narcotic sedation with naloxone (Narcan). Respiratory Alkalosis: Diagnosis and Treatment Respiratory alkalosis is a primary fall in PCO2 with a compensatory decrease in plasma [HCO3–]. pneumonia. pain. Results usually are given as PO2 and O2 saturation (see Table 8–1 . salicylate overdose (often mixed metabolic gap acidosis and respiratory alkalosis). Hypoxia The second type of information gained from a blood gas level. hyperthyroidism. CHF (mild). Respiratory alkalosis occurs with increased alveolar ventilation. etc. PRG.

for normal values). earlobe of adults and the foot. toe. and sickle cell disease do not affect readings. The technology is based on the different red and infrared light absorption characteristics of oxygenated and deoxygenated hemoglobin. top of the ear. or thumb of children) is sensitive in the detection of arterial desaturation only. motion. The technique may be less accurate in cases of poor perfusion.3-DPG) as shown in Figure 8–4. Hypoxia Differential Diagnosis / Abnormalities: . The transcutaneous technique (detector placed on the finger. state of fitness. Oxygen saturation at any given PO2 is influenced by temperature. Figure 8–4. and altitude. and the presence of abnormal hemoglobins (carboxy hemoglobin. use of IV contrast agents. Normal pulse oximetry readings should be 95–99% in a healthy person on room air and can vary slightly according to age.3diphosphoglycerate (2. great toe. skin pigmentation (usually at saturations < 80% only). elevated bilirubin. These two parameters are related to each other. palm. pH. Oxyhemoglobin dissociation curve. Anemia. methemoglobin). sensor exposure to ambient light. Oxygenation can also be determined noninvasively with pulse oximetry. and the level of 2. Pulse oximetry is used to measure pulse rate and SaO2 and can reduce the need for ABG measurements.

pickwickian syndrome. sleep apnea Decreased Pulmonary Diffusing Capacity: Pneumoconiosis. obstructed airway Alveolar Hypoventilation: Skeletal abnormalities. use the technique in Step 1 of Interpretation of Blood Gases to identify the acid–base disorder. Example 1 A patient with COPD has a blood gas of pH 7.34. chronic bronchitis. neuromuscular disorders. CF. Step 2: pH < 7. Step 4: Normal compensation for chronic (COPD) respiratory acidosis (from Table 8–2). PE. Step 1: The numbers fit because the difference between the calculated and observed values is < 10%. transposition of the great arteries) Sample Acid–Base Problems In each of these examples. and [HCO3–] is not < 22 mEq/L. pneumoconiosis. pneumothorax. and [HCO3–] 29 mEq/L. drug-induced pulmonary fibrosis (bleomycin). pulmonary edema. . asthma).COPD (emphysema. collagen–vascular diseases Right-to-Left Shunt: Congenital heart disease (eg. tetralogy of Fallot. PCO2 55 mm Hg. respiratory acidosis. Step 3: PCO2 > 44 mm Hg. pneumonia.37. atelectasis. acidemia. ARDS.

and [HCO3–] 12 mEq/L. Step 4: (See Table 8–2) The expected PCO2 of 26 mm Hg is very similar to the measured value of 28 mm Hg. and [HCO3–] 5 mEq/L. Step 1: . Example 2 Immediately after cardiac arrest a patient has pH 7. Step 2: pH < 7. Example 3 A young man with a fever of 103. The patient has lactic acidosis following cardiopulmonary arrest (simple acid–base disorder).36.37. Step 3: [HCO3–] is < 22 mEq/L and PCO2 is not > 44 mm Hg. Step 1: The numbers fit. acidemia. simple respiratory acidosis.Expected [HCO3–] is 24 mEq/L + 6 = 30.25. PCO2 9 mm Hg. which is close to the measured [HCO3–] of 29 mEq/L.2°F and a fruity odor on his breath has a blood gas of pH 7. PCO2 28 mm Hg. metabolic acidosis. This patient has chronic respiratory acidosis due to hypoventilation (simple acid–base disorder). so this condition is simple metabolic acidosis.

but the reading is 9 mm Hg.44 indicates alkalemia.55. Step 3: PCO2 < 36 mm Hg. thus respiratory alkalosis is present.5 mm Hg. Step 4: The expected compensation in PCO2 can be calculated as follows (see Table 8–2): The expected PCO2 is 17. Example 4 A 30-year-old woman who is 30 wk PRG presents with nausea and vomiting. Blood gas analysis reveals pH 7. and [HCO3–] is not > 26 mEq/L. Step 3: [HCO3–] < 22 mEq/L and PCO2 is not > 44 mm Hg. thus metabolic acidosis is present. indicating a second process. Step 2: pH < 7. pregnancy) is calculated from Table 8–2: . This patient has metabolic acidosis due to DKA and concomitant respiratory alkalosis possibly due to early sepsis and fever (mixed acid–base disorder).The numbers fit. respiratory alkalosis. Step 4: The expected compensation for chronic respiratory alkalosis (ie.37 indicates acidemia. Step 1: The numbers fit. and [HCO3–] 22 mEq/L. PCO2 25 mm Hg. Step 2: pH < 7.

and abdominal pain. close to the expected [HCO3–] of 5 mEq/L. Example 6 A 21-year-old patient with diabetes presents with nausea. This patient has respiratory alkalosis due to pregnancy and relative secondary metabolic alkalosis due to vomiting. but the actual [HCO3–] is 22 mEq/L. Step 1: Step 2: Actual [HCO3–] is 6 mEq/L. The anion gap is 23 mEq/L. vomiting.5. or 16–17 mEq.The calculated [HCO3–] is 24 – 7. Thus pure metabolic gap acidosis is present. Example 5 A 19-year-old patient with diabetes has an anion gap of 29 mEq/L and a [HCO3–] of 6 mEq/L. indicating relative secondary metabolic alkalosis ([HCO3–] is higher than expected). Step 1: Step 2: . and the [HCO3–] is 18 mEq/L. most likely from DKA.

The patient has metabolic gap acidosis from DKA and metabolic alkalosis from vomiting. mixed metabolic gap acidosis and metabolic nongap acidosis must be present. Step 1: Step 2: Actual [HCO3–] is 10 mEq/L and not the expected 17 mEq/L of pure metabolic gap acidosis. .The [HCO3–] is 18 mEq/L and not the 11 mEq/L expected from pure metabolic gap acidosis. Example 7 A 55-year-old patient who drinks a fifth of whiskey per day has a 2-wk history of diarrhea. The anion gap is 17 mEq/L. The patient has metabolic nongap acidosis from diarrhea and metabolic gap acidosis from alcoholic ketoacidosis. Because the actual [HCO3–] is higher than expected. this condition is mixed metabolic gap acidosis and metabolic alkalosis. and the [HCO3–] is 10 mEq/L. Because the actual [HCO3–] is lower than expected.