5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

c.2 and 4 only

d.1 and 3 only

1In 1956, DuBois et al. described the forced oscillation technique (FOT) as a tool to measure lung function using sinusoidal sound waves of single frequencies generated by a loud speaker and passed into the lungs during tidal breathing. Dubois, A. B., Brody, A. W., Lewis, D. H., et al. (1956). Oscillation mechanics of lungs and chest in man. Journal of Applied Physiology 8, 587-594.

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Metabolic Acidosis With Complete Respiratory Compensation

Metabolic Acidosis With Partial Respiratory Compensation

Metabolic Alkalosis

Metabolic Alkalosis With Complete Respiratory Compensation

Metabolic Alkalosis With Partial Respiratory Compensation

Acid-Base Abnormalities

As the pathologic processes of a respiratory disorder intensify, the patient's arterial blood gas (ABG) values are usually altered to some degree. Table 5.1 lists the normal ABG values. Box 5.1 provides an overview of the common respiratory and metabolic acid-base disturbances. In the profession of respiratory care, knowledge and understanding of the acid-base disturbances are absolute and unconditional prerequisites to the assessment and treatment of the patient with a respiratory disorder. Because of the fundamental importance of this subject, this chapter provides the following review:

TABLE 5.1

Normal Blood Gas Values

*Technically, only the oxygen (PaO2) and carbon dioxide (PaCO2) pressure readings are true blood gas values. The pH indicates the balance between the bases and acids in the blood. The bicarbonate (HCO3–) reading is an indirect measurement that is calculated from the pH and PaCO2 levels.

Box 5.1

Acid-Base Disturbance Classifications

Respiratory Acid-Base Disturbances

•Acute alveolar hyperventilation (acute respiratory alkalosis)

•Acute alveolar hyperventilation with partial renal compensation (partially compensated respiratory alkalosis)

•Chronic alveolar hyperventilation with complete renal compensation (compensated respiratory alkalosis)

•Acute ventilatory failure (acute respiratory acidosis)

•Acute ventilatory failure with partial renal compensation (partially compensated respiratory acidosis)

•Chronic ventilatory failure with complete renal compensation (compensated respiratory acidosis)

•Acute alveolar hyperventilation superimposed on chronic ventilatory failure

•Acute ventilatory failure superimposed on chronic ventilatory failure

Metabolic Acid-Base Disturbances

•Metabolic acidosis

•Metabolic acidosis with partial respiratory compensation

•Metabolic acidosis with complete respiratory compensation

•Metabolic alkalosis

•Metabolic alkalosis with partial respiratory compensation

•Metabolic alkalosis with complete respiratory compensation

Combined Acid-Base Disturbances

•Combined metabolic and respiratory acidosis

•Combined metabolic and respiratory alkalosis

Highlighted terms are included in the Key Terms list and glossary.

•The PCO2/HCO3–/pH relationship—an essential cornerstone of ABG interpretations

•The most common acid-base abnormalities seen in the clinical setting

•The metabolic acid-base abnormalities

•Errors associated with ABG measurements

The PCO2/HCO3–/pH Relationship

To fully understand the clinical significance of the acid-base disturbances listed in Box 5.1, a fundamental knowledge of the PCO2/HCO3–/pH relationship is essential. The PCO2/HCO3–/pH relationship is graphically illustrated in the PCO2/HCO3–/pH

nomogram shown in Fig. 5.1. The PCO2/HCO3–/pH nomogram is an excellent clinical tool to identify acid-base disturbances. See Appendix XII on the Evolve site for a pocket-size PCO2/HCO3–/pH nomogram card that can be cut out, laminated, and used as a handy ABG reference tool in the clinical setting.

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encountered PCO2/HCO3–/pH relationships is important: (1) an acute PCO2 increase and its effects on the pH and HCO3– values, and (2) an acute PCO2 decrease and its effects on the pH and HCO3– values.1

How Acute PCO2 Decreases Affect pH and HCO3– Values

The red normal PCO2 blood buffer bar shown on the PCO2/HCO3–/pH nomogram is also used to identify the pH and HCO3– values that will result immediately in response to a sudden decrease in PCO2—for example, as a result of alveolar hyperventilation. For example, if the patient's PaCO2 were suddenly to decrease to, say, 25 mm Hg, the pH would immediately increase to about 7.55 and the HCO3– level would decrease to about 21 mEq/L. In addition, the PCO2/HCO3–/pH nomogram shows that these ABG values represent acute alveolar hyperventilation (acute respiratory alkalosis). This is shown by the fact that (1) all of the ABG values (i.e., PCO2, HCO3–, and pH) intersect within the red normal PCO2 blood buffer bar, and (2) the pH and HCO3– readings are precisely what are expected for an acute increase in the PCO2 of 25 mm Hg (Fig. 5.2).

FIGURE 5.2 Acute alveolar hyperventilation is confirmed when the reported PCO2, pH, and HCO3– values all intersect within the red-colored “Respiratory Alkalosis” bar. For example, when the reported PCO2 is 25 mm Hg at a time when the pH is 7.55 and

the HCO3– is 21 mEq/L, acute alveolar hyperventilation is confirmed (see black arrows). (From Terry Des Jardins, with permission.)

How Acute PCO2 Increases Affect the pH and HCO3– Values

As mentioned previously, the red normal PCO2 blood buffer bar shown on the PCO2/HCO3–/pH nomogram is used to identify the pH and HCO3– values that will result immediately in response to a sudden increase in PCO2, such as a result of net alveolar hypoventilation. For example, if the patient's PaCO2 were to suddenly increase to 60 mm Hg, the pH would immediately fall to about 7.28 and the HCO3– level would increase to about 26 mEq/L. Furthermore, the PCO2/HCO3–/pH nomogram shows that these ABG values represent acute ventilatory failure (acute respiratory acidosis). This is shown by

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Acute Decreases in PaCO2 (e.g., Acute Hyperventilation).

Using the normal ABG values as a baseline (e.g., pH 7.40, PaCO2 40 mm Hg, and HCO3– 24 mEq/L), for every 5 mm Hg the PaCO2 decreases, the pH will increase about 0.06 units (from 7.40), and the HCO3– will decrease about 1 mEq/L. Or, by way of another example, for every 10 mm Hg the PaCO2 decreases, the pH will increase about 0.12 units (from 7.40), and the HCO3– will decrease about 2 mEq/L. Thus if the patient's PaCO2 suddenly decreases to, say, 30 mm Hg, the expected pH change would be around 7.52 and the HCO3– would be about 22 mEq/L.

Again, it should be noted that if the patient's PaO2 is also very low, lactic acid may be present. In such cases, the patient's pH and HCO3– values would both be lower than expected for a particular PaCO2 level.

Table 5.2 provides a summary of the effects of acute PaCO2 changes on pH and HCO3– levels (see previous discussion). Note that the pH and HCO3– changes with hypoventilation (increased PaCO2) and hyperventilation (decreased PaCO2) are not equal. Based on the PCO2/ HCO3–/pH relationship presented in Table 5.2, Table 5.3 provides a general rule of thumb— an excellent and handy clinical tool—to determine the expected pH and HCO3– changes that occur in response to an acute increase or decrease in the PCO2 level.

TABLE 5.2

Summary of Acute PaCO2 Changes on pH and HCO3– Levels

TABLE 5.3

General Rule of Thumb for the PCO2/HCO3–/pH Relationship in the Clinical Setting

Common Acid-Base Abnormalities Seen in the Clinical Setting

The most common acid-base abnormalities associated with the respiratory disorders presented in this textbook are (1) acute alveolar hyperventilation (acute respiratory alkalosis), (2) acute ventilatory failure (acute respiratory acidosis), (3) chronic ventilatory failure (compensated respiratory acidosis), (4) acute alveolar hyperventilation superimposed on chronic ventilatory failure (acute respiratory alkalosis on compensated respiratory acidosis), (5) acute ventilatory failure superimposed on chronic ventilatory failure (acute respiratory acidosis on compensated respiratory acidosis), (6) metabolic alkalosis, and (7) metabolic acidosis (especially lactic acidosis). A brief overview of these common acid-base abnormalities follows.

Acute Alveolar Hyperventilation (Acute Respiratory Alkalosis)

Acute alveolar hyperventilation is defined as a pH above 7.45 and a PaCO2 level below 35 mm Hg and an HCO3– level

down slightly. Table 5.4 provides an example of acute alveolar hyperventilation. The most common cause of acute alveolar hyperventilation is hypoxemia. The decreased PaO2 seen during acute alveolar hyperventilation usually develops from a

decreased ventilation-perfusion ratio (V/Q ratio), capillary shunting (or a relative shunt or shunt-like e ect), and venous admixture associated with the pulmonary disorder. The PaO2 continues to drop as the pathologic effects of the disease

intensify. Eventually the PaO2 may decline to a point low enough (a PaO2 of about 60 mm Hg) to significantly stimulate the

peripheral chemoreceptors, which in turn causes the ventilatory rate to increase (Fig. 5.4). The increased ventilatory response in turn causes the PaCO2 to decrease and the pH to increase (Fig. 5.5). Box 5.2 lists additional pathophysiologic

mechanisms in respiratory disorders that can contribute to an increased ventilatory rate and a reduction in PaCO2.

TABLE 5.4

Acute Alveolar Hyperventilation (Acute Respiratory Alkalosis)

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FIGURE 5.4 Relationship of venous admixture to the stimulation of peripheral chemoreceptors in response to alveolar consolidation.

FIGURE 5.5 PaO2 and PaCO2 trends during acute alveolar hyperventilation.

Box 5.2

Pathophysiologic Mechanisms That Lead to a Reduction in PaCO2

•Decreased lung compliance

•Stimulation of the central chemoreceptors

•Activation of the deflation reflex

•Activation of the irritant reflex

•Stimulation of the J receptors

•Pain and anxiety

Acute Ventilatory Failure (Acute Respiratory Acidosis)

Acute ventilatory failure is defined as a pH below 7.35, a PaCO2 level above 45 mm Hg, and an HCO3– level slightly

increased. Table 5.5 provides an example of acute ventilatory failure. Acute ventilatory failure is a condition in which the lungs are unable to meet the metabolic demands of the body in terms of CO2 homeostasis and typically tissue oxygenation.

In other words, the patient is unable to provide the muscular, mechanical work necessary to move gas into and out of the lungs to meet the normal CO2 production of the body. This condition leads to an increased PACO2 and subsequently an

increased PaCO2. The increased PACO2 causes a decrease in the PAO2, which in turn leads to a decreased PaO2 in the arterial blood.

TABLE 5.5

Acute Ventilatory Failure (Acute Respiratory Acidosis)

Acute ventilatory failure is not associated with a typical ventilatory pattern. For example, the patient may demonstrate apnea, severe hyperpnea, or tachypnea. The bottom line is that acute ventilatory failure can develop in response to any ventilatory pattern that does not provide adequate alveolar ventilation. When an increased PaCO2 is accompanied by

acidemia (decreased pH), acute ventilatory failure, or respiratory acidosis, is said to exist. Clinically, this is a medical emergency that may require mechanical ventilation.

Chronic Ventilatory Failure (Compensated Respiratory Acidosis)

Chronic ventilatory failure (compensated respiratory acidosis) is defined as a greater than normal PaCO2 level with a normal pH status and, typically, a decreased PaO2 on room air. Table 5.6 provides an example of chronic ventilatory failure.

Although chronic ventilatory failure is most commonly seen in patients with severe chronic obstructive pulmonary disease, it is also seen in several chronic restrictive lung disorders (e.g., severe tuberculosis, kyphoscoliosis). Box 5.3 lists common respiratory diseases associated with chronic ventilatory failure during the advanced stages of the disorder.

TABLE 5.6

Chronic Ventilatory Failure (Compensated Respiratory Acidosis)

Box 5.3

Respiratory Diseases Associated With Chronic Ventilatory Failure

During Advanced Stages

Chronic Obstructive Pulmonary Disorders (Most Common)

•Chronic bronchitis

•Emphysema

•Bronchiectasis

•Cystic fibrosis

Restrictive Respiratory Disorders

•Tuberculosis

•Fungal diseases

•Kyphoscoliosis

•Chronic interstitial lung diseases

•Bronchopulmonary dysplasia

The basic pathophysiologic mechanisms that produce ABGs associated with chronic ventilatory failure are as a respiratory disorder gradually worsens, the work of breathing progressively increases to a point at which more oxygen is consumed than is gained. Although the exact mechanism is unclear, the patient slowly develops a breathing pattern that uses the least amount of oxygen for the energy expended. In essence, the patient selects a breathing pattern based on work efficiency rather than ventilatory efficiency. (See the discussion of airway resistance and its effect on the ventilatory pattern in Chapter 3, The Pathophysiologic Basis for Common Clinical Manifestations.) As a result, the patient's alveolar ventilation slowly decreases, which in turn causes the PaO2 to decrease and the PaCO2 to increase further (Fig. 5.6). As the

PaCO2 increases, the pH falls.

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