08. Blood Gases and Acid Base Disorders | Clinicians Pocket Reference, 11th Edition

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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

Measurement	Arterial Blood	Mixed Venous Blood^a	Venous Blood
pH (range)	7.40 (7.37 7.44)	7.36 (7.31 7.41)	7.36 (7.31 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

^aObtained from the right atrium, usually through a pulmonary artery catheter.

Venous Blood Gases

There is little difference between arterial and venous pH and [HCO₃] (except in severe CHF and shock). Venous blood gas levels may occasionally be used to assess acid base status, but venous O₂ levels are significantly less than arterial values (see Table 8 1).

Capillary Blood Gases

A CBG is obtained from a highly vascularized capillary bed. CBG is often used for pediatric patients because obtaining the sample is easier (through the heel) and less traumatic (no risk of arterial thrombosis, hemorrhage) than obtaining an ABG sample. (See Chapter 13, Heelstick Technique.)

When interpreting a CBG, apply the following rules:

pH: Same as arterial or slightly lower (Normal = 7.35 7.40)
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. Saturation is probably more useful than PO₂ itself in interpretation of a CBG.

General Principles of Blood Gas Determinations

Interpretation of O₂ values is discussed in Hypoxia

1. The blood gas analyzers in most labs measure pH and PCO₂ as well as PO₂. [HCO₃] and base difference are calculated with the Henderson Hasselbalch equation:

or the Henderson equation:

2. For a rough estimate of [H⁺], [H⁺] = (7.80 pH) x 100, or add 1 mEq/L to 40 mEq for every 0.01 below 7.40 and subtract 1 mEq/L from 40 mEq for every 0.01 above 7.40 (accurate for pH 7.25 7.48); 40 mEq/L = [H⁺] at the normal pH of 7.40. pH is a log scale; for every change of 0.3 in pH from 7.40 the [H⁺] doubles or halves. For pH 7.10, [H⁺] = 2 x 40, or 80 nmol/L, and for pH 7.70, [H⁺] = 1/2 40, or 20 nmol/L.

3. The calculated [HCO₃] should be within 2 mEq/L of the [HCO₃] of a venous measurement drawn at the same time. If not, an error has been made in collection or in determination of the values, and both samples should be recollected.

4. Two additional relationships derived from the Henderson Hasselbalch equation should be committed to memory. These two rules are helpful in interpreting blood gas results, 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 0.08 units. As PCO₂ decreases, pH increases; as the PCO₂ increases, pH decreases.

Rule II:

A pH change of 0.15 is equivalent to a base change of 10 mEq/L. A decrease in base (ie, [HCO₃]) is termed a base deficit, and an increase in base is termed a base excess.

Acid Base Disorders: Definition

1. Acid base disorders are common clinical problems. Acidemia is a pH < 7.37, and alkalemia is a pH > 7.44. Acidosis and alkalosis are used to describe the process by which pH changes. The primary causes of acid base disturbances are abnormalities in the respiratory, metabolic, and renal systems. As the Henderson Hasselbalch equation shows, a respiratory disturbance leading to an abnormal PCO₂ alters the pH, and similarly a metabolic disturbance altering [HCO₃] changes the pH.

2. Any primary disturbance in acid base homeostasis invokes a normal compensatory response. A primary metabolic disorder leads to respiratory compensation, 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.

3. The degree of compensation can be expressed in terms of the degree of primary acid base disturbance. Table 8 2 lists the major categories of primary acid base disorders, the primary abnormality, the secondary compensatory response, and the expected compensation based on the primary abnormality. These changes are defined graphically in Figure 8 1.

Table 8 2 Simple Acid Base Disturbances

Acid Base Disorder	Primary Abnormality	Expected Compensation	Expected Degree of Compensation
Metabolic acidosis	[HCO₃]	PCO₂	PCO₂ = (1.5 x [HCO₃])+8
Metabolic alkalosis	[HCO₃]	PCO₂	in PCO₂ = [HCO₃] x 0.6
Acute respiratory acidosis	PCO₂	[HCO₃]	in [HCO₃] = PCO₂/10
Chronic respiratory acidosis	PCO₂	[HCO₃]	in [HCO₃] = 4 x PCO₂/10
Acute respiratory alkalosis	PCO₂	[HCO₃]	in [HCO₃] = 2 x PCO₂/10
Chronic respiratory alkalosis	PCO₂	[HCO₃]	in [HCO₃] = 5 x PCO₂/10

Mixed Acid Base Disorders

1. Most acid base disorders result from a single primary disturbance of the normal physiologic compensatory response (called simple acid base disorders). In some cases (eg, serious illness), two or more primary disorders may occur simultaneously, resulting in a mixed acid base disorder. The net effect of mixed disorders can be additive (eg, metabolic acidosis and respiratory acidosis) and result in extreme alteration of pH. Or, the effects can be opposite (eg, metabolic acidosis and respiratory alkalosis) and nullify somewhat the effect of the other on pH.

2. To determine the presence of a mixed acid base disorder with a blood gas value, follow the six steps in the Interpretation of Blood Gases. Alterations in either [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.

Interpretation of Blood Gases

Use a consistent, stepwise approach to interpretation of blood gases. (See Figure 8 1.)

Figure 8 1.

Step 1:

Determine whether the numbers fit.

The right side of the equation should be within about 10% of the left side. If the numbers do not fit, obtain another ABG and chemistry panel for [HCO₃].

Example. pH 7.25, PCO₂ 48 mm Hg, [HCO₃] 29 mEq/L.

This blood gas cannot be interpreted, and samples for ABG and [HCO₃] must be recollected. The most common reason for the numbers not fitting is that the ABG and the chemistry panel [HCO₃] were obtained at different times.

Step 2:

Next, determine whether acidemia (pH < 7.37) or alkalemia (pH > 7.44) is present.

Step 3:

Identify the primary disturbance as metabolic or respiratory. For example, if acidemia is present, is the PCO₂ > 44 mm Hg (respiratory acidosis), or is the [HCO₃] < 22 mEq/L (metabolic acidosis)? In other words, identify which component, respiratory or metabolic, is altered in the same direction as the pH abnormality. If both components act in the same direction eg, 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). The primary disturbance is the one that varies the most from normal. That is, with a [HCO₃] of 6 mEq/L and PCO₂ of 50 mm Hg, the primary disturbance would be metabolic acidosis; the [HCO₃] is only 25% of normal, whereas the increase in PCO₂ is only 25% above normal.

Step 4:

After identifying the primary disturbance, use the equations in Table 8 2 to calculate the expected compensatory response. If the difference between the actual value and the calculated value is great, a mixed acid base disturbance is present.

Step 5:

Calculate the anion gap:

A normal anion gap is 8 12 mEq/L. If the anion gap is increased, proceed to Step 6.

Step 6:

If the anion gap is elevated, compare the changes from normal between the anion gap and [HCO₃]. If the change in anion gap is similar to the change in [HCO₃] from normal, gap acidosis is present and there is no metabolic alkalosis or nongap metabolic acidosis. If the change in anion gap is greater than the change in [HCO₃] from normal, metabolic alkalosis is present in addition to gap metabolic acidosis. If the change in the anion gap is less than the change in [HCO₃] from normal, nongap metabolic acidosis is present in addition to gap metabolic acidosis. (See Examples 5, 6, and 7.)

Finally, be sure the interpretation of the blood gas is consistent with the clinical setting.

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

The diagnosis of metabolic acidosis (Figure 8 2) can be classified as anion gap or non anion gap acidosis. The anion gap (Normal range, 8 12 mEq/L) is calculated as:

Figure 8 2.

Differential diagnosis of metabolic acidosis.

Anion Gap Acidosis:

Anion gap > 12 mEq/L; caused by a decrease in [HCO₃] balanced by an increase in an unmeasured acid ion from either endogenous production or exogenous ingestion (normochloremic acidosis).

Non Anion Gap Acidosis:

Anion gap = 8 12 mEq/L; caused by a decrease in [HCO₃] balanced by an increase in chloride (hyperchloremic acidosis). Renal tubular acidosis is a type of nongap acidosis that can be associated with a variety of pathologic conditions (Table 8 3). The anion gap is helpful in identifying metabolic gap acidosis, nongap acidosis, and mixed metabolic gap and nongap acidosis. If an elevated anion gap is present, a closer look at the anion gap and [HCO₃] helps differentiate (a) pure metabolic gap acidosis, (b) metabolic nongap acidosis, (c) mixed metabolic gap and nongap acidosis, and (d) metabolic gap acidosis and metabolic alkalosis.

Table 8 3 Renal Tubular Acidosis: Diagnosis and Management

Clinical Condition	Renal Defect	GFR	Serum [HCO₃] (mmol/L)	Serum [K+] (mmol/L)	Minimal Urine pH	Associated Disease States	Treatment
Normal	None	N	24 28	3.5 5	4.8 5.2	None	N/A
Proximal RTA (type II RTA)	Proximal H⁺ secretion	N	15 18		<5.5	Drugs, Fanconi syndrome, various genetic disorders, dysproteinemic states, secondary hyperparathyroidism, toxins (heavy metals), tubulointerstitial diseases, nephrotic syndrome, paroxysmal nocturnal hemoglobinuria	NaHCO₃ or KHCO₃ (10 15 mmol/kg/d), thiazide diuretics
Classic distal RTA (type I RTA)	Distal H⁺ secretion	N	20 30		>5.5	Various genetic disorders, autoimmune diseases, nephrocalcinosis, drugs, toxins, tubulointerstitial diseases, hepatic cirrhosis, empty sella syndrome	NaHCO₃ (1 3 mmol/kg/d)
Buffer deficiency (type III RTA)	Distal NH₃ delivery		15 18	N	<5.5	Chronic renal insufficiency, renal osteodystrophy, severe hypophosphatemia	NaHCO₃ (1 3 mmol/kg/d)
Generalized distal RTA (type IV RTA)	Distal Na⁺ reabsorption, K⁺ secretion, and H⁺ secretion		24 28		<5.5	Primary mineralocorticoid deficiency (eg, Addison disease), hyporeninemic hypoaldosteronism, diabetes mellitus, tubulointerstitial diseases, nephrosclerosis, drugs), salt-wasting mineralocorticoid-resistant hyperkalemia	Fludrocortisone (0.1 0.5 mg/d) dietary K+ restriction, NaHCO₃ (1 3 mmol/kg/d) furosemide (40 160 mg/d)

Treatment of Metabolic Acidosis

1. Correct the underlying disorder (eg, control diarrhea).

2. Bicarbonate therapy is reserved for severe metabolic gap acidosis. If the pH < 7.20, correct to above 7.20 with sodium bicarbonate. The total replacement dose of HCO₃ can be calculated as follows:

3. Replace with one-half the total amount of bicarbonate over 8 12 h and reevaluate. Be aware of sodium and volume overload during replacement. A normal or isotonic bicarbonate drip is made with 3 amp NaHCO₃ (50 mEq NaHCO₃/amp) in 1 L D₅W.

Metabolic Alkalosis: Diagnosis and Treatment

Metabolic alkalosis represents an increase in [HCO₃] with a compensatory rise in PCO₂.

Differential Diagnosis

In two basic categories of diseases the kidneys retain HCO₃ (Figure 8 3). 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," or "random" urine for chloride (U_Cl).

Figure 8 3.

Differential diagnosis of metabolic alkalosis.

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). This chloride depletion results in renal sodium conservation leading to a corresponding reabsorption of HCO₃ by the kidney. In this category of metabolic alkalosis, the urinary [Cl ] is < 10 mEq/L, and the disorders respond to treatment with intravenous NaCl.

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. The urinary [Cl ] > 10 mEq/L, and these disorders do not respond to NaCl administration.

Treatment of Metabolic Alkalosis

Correct the underlying disorder.

1. Chloride-responsive

a. Replace volume with NaCl if depleted.

b. Correct hypokalemia if present.

c. NH₄Cl and HCl should be reserved for extreme cases.

2.Chloride-resistant

a. Correct the underlying problem, such as stopping exogenous steroids.

Respiratory Acidosis: Diagnosis and Treatment

Respiratory acidosis is a primary rise in PCO₂ with a compensatory rise in plasma [HCO₃]. Increased PCO₂ occurs in clinical situations in which decreased alveolar ventilation occurs.

Differential Diagnosis

Neuromuscular Abnormalities with Ventilatory Failure:

Muscular dystrophy, myasthenia gravis, Guillain Barr syndrome, hypophosphatemia

Central Nervous System:

Drugs (sedatives, analgesics, tranquilizers, ethanol), CVA, central sleep apnea, spinal cord injury (cervical)

Airway Obstruction:

Chronic (COPD), acute (asthma), upper airway obstruction, obstructive sleep apnea

Thoracic Pulmonary Disorders:

Bony thoracic cage (flail chest, kyphoscoliosis), parenchymal lesions (pneumothorax, severe pulmonary edema, severe pneumonia), large pleural effusions, scleroderma, marked obesity (pickwickian syndrome)

Treatment of Respiratory Acidosis

Improve Ventilation:

Intubate patient and initiate mechanical ventilation, increase ventilator rate, reverse narcotic sedation with naloxone (Narcan), etc.

Respiratory Alkalosis: Diagnosis and Treatment

Respiratory alkalosis is a primary fall in PCO₂ with a compensatory decrease in plasma [HCO₃]. Respiratory alkalosis occurs with increased alveolar ventilation.

Differential Diagnosis

Central Stimulation:

Anxiety, hyperventilation syndrome, pain, head trauma or CVA with central neurogenic hyperventilation, tumors, salicylate overdose (often mixed metabolic gap acidosis and respiratory alkalosis), fever, early sepsis

Peripheral Stimulation:

PE, CHF (mild), interstitial lung disease, pneumonia, altitude, hypoxemia of any cause (see Hypoxia)

Miscellaneous:

Hepatic insufficiency, PRG, progesterone, hyperthyroidism, iatrogenic mechanical overventilation

Treatment of Respiratory Alkalosis

Correct the underlying disorder.

Hyperventilation Syndrome:

Best controlled by having the patient rebreathe into a paper bag to increase PCO₂, decrease ventilator rate, increase amount of dead space with ventilator, or manage underlying cause.

Hypoxia

The second type of information gained from a blood gas level, in addition to acid base results, is oxygenation. Results usually are given as PO₂ and O₂ saturation (see Table 8 1 for normal values). These two parameters are related to each other.

Oxygen saturation at any given PO₂ is influenced by temperature, pH, and the level of 2,3-diphosphoglycerate (2,3-DPG) as shown in Figure 8 4.

Figure 8 4.

Oxyhemoglobin dissociation curve.

Oxygenation can also be determined noninvasively with pulse oximetry. Pulse oximetry is used to measure pulse rate and SaO₂ and can reduce the need for ABG measurements. The transcutaneous technique (detector placed on the finger, toe, top of the ear, earlobe of adults and the foot, palm, great toe, or thumb of children) is sensitive in the detection of arterial desaturation only. The technology is based on the different red and infrared light absorption characteristics of oxygenated and deoxygenated hemoglobin. The technique may be less accurate in cases of poor perfusion, motion, sensor exposure to ambient light, skin pigmentation (usually at saturations < 80% only), use of IV contrast agents, and the presence of abnormal hemoglobins (carboxy hemoglobin, methemoglobin). Normal pulse oximetry readings should be 95 99% in a healthy person on room air and can vary slightly according to age, state of fitness, and altitude. Anemia, elevated bilirubin, and sickle cell disease do not affect readings.

Hypoxia Differential Diagnosis

/ Abnormalities:

COPD (emphysema, chronic bronchitis, asthma), atelectasis, pneumonia, PE, ARDS, pneumothorax, pneumoconiosis, CF, obstructed airway

Alveolar Hypoventilation:

Skeletal abnormalities, neuromuscular disorders, pickwickian syndrome, sleep apnea

Decreased Pulmonary Diffusing Capacity:

Pneumoconiosis, pulmonary edema, drug-induced pulmonary fibrosis (bleomycin), collagen vascular diseases

Right-to-Left Shunt:

Congenital heart disease (eg, tetralogy of Fallot, transposition of the great arteries)

Sample Acid Base Problems

In each of these examples, 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, PCO₂ 55 mm Hg, and [HCO₃] 29 mEq/L.

Step 1:

The numbers fit because the difference between the calculated and observed values is < 10%.

Step 2:

pH < 7.37, acidemia.

Step 3:

PCO₂ > 44 mm Hg, and [HCO₃] is not < 22 mEq/L, respiratory acidosis.

Step 4:

Normal compensation for chronic (COPD) respiratory acidosis (from Table 8 2).

Expected [HCO₃] is 24 mEq/L + 6 = 30, which is close to the measured [HCO₃] of 29 mEq/L, simple respiratory acidosis. This patient has chronic respiratory acidosis due to hypoventilation (simple acid base disorder).

Example 2

Immediately after cardiac arrest a patient has pH 7.25, PCO₂ 28 mm Hg, and [HCO₃] 12 mEq/L.

Step 1:

The numbers fit.

Step 2:

pH < 7.37, acidemia.

Step 3:

[HCO₃] is < 22 mEq/L and PCO₂ is not > 44 mm Hg, metabolic acidosis.

Step 4:

(See Table 8 2)

The expected PCO₂ of 26 mm Hg is very similar to the measured value of 28 mm Hg, so this condition is simple metabolic acidosis. The patient has lactic acidosis following cardiopulmonary arrest (simple acid base disorder).

Example 3

A young man with a fever of 103.2 F and a fruity odor on his breath has a blood gas of pH 7.36, PCO₂ 9 mm Hg, and [HCO₃] 5 mEq/L.

Step 1:

The numbers fit.

Step 2:

pH < 7.37 indicates acidemia.

Step 3:

[HCO₃] < 22 mEq/L and PCO₂ is not > 44 mm Hg, thus metabolic acidosis is present.

Step 4:

The expected compensation in PCO₂ can be calculated as follows (see Table 8 2):

The expected PCO₂ is 17.5 mm Hg, but the reading is 9 mm Hg, indicating a second process, respiratory alkalosis. This patient has metabolic acidosis due to DKA and concomitant respiratory alkalosis possibly due to early sepsis and fever (mixed acid base disorder).

Example 4

A 30-year-old woman who is 30 wk PRG presents with nausea and vomiting. Blood gas analysis reveals pH 7.55, PCO₂ 25 mm Hg, and [HCO₃] 22 mEq/L.

Step 1:

The numbers fit.

Step 2:

pH < 7.44 indicates alkalemia.

Step 3:

PCO₂ < 36 mm Hg, and [HCO₃] is not > 26 mEq/L, thus respiratory alkalosis is present.

Step 4:

The expected compensation for chronic respiratory alkalosis (ie, pregnancy) is calculated from Table 8 2:

The calculated [HCO₃] is 24 7.5, or 16 17 mEq, but the actual [HCO₃] is 22 mEq/L, indicating relative secondary metabolic alkalosis ([HCO₃] is higher than expected). This patient has respiratory alkalosis due to pregnancy and relative secondary metabolic alkalosis due to vomiting.

Example 5

A 19-year-old patient with diabetes has an anion gap of 29 mEq/L and a [HCO₃] of 6 mEq/L.

Step 1:

Step 2:

Actual [HCO₃] is 6 mEq/L, close to the expected [HCO₃] of 5 mEq/L. Thus pure metabolic gap acidosis is present, most likely from DKA.

Example 6

A 21-year-old patient with diabetes presents with nausea, vomiting, and abdominal pain. The anion gap is 23 mEq/L, and the [HCO₃] is 18 mEq/L.

Step 1:

Step 2:

The [HCO₃] is 18 mEq/L and not the 11 mEq/L expected from pure metabolic gap acidosis. Because the actual [HCO₃] is higher than expected, this condition is mixed metabolic gap acidosis and metabolic alkalosis. The patient has metabolic gap acidosis from DKA and metabolic alkalosis from vomiting.

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, and the [HCO₃] is 10 mEq/L.

Step 1:

Step 2:

Actual [HCO₃] is 10 mEq/L and not the expected 17 mEq/L of pure metabolic gap acidosis. Because the actual [HCO₃] is lower than expected, mixed metabolic gap acidosis and metabolic nongap acidosis must be present. The patient has metabolic nongap acidosis from diarrhea and metabolic gap acidosis from alcoholic ketoacidosis.