5 курс / Пульмонология и фтизиатрия / Clinical_Manifestations_and_Assessment_of_Respiratory

3.Pursed-lip breathing

4.Dull percussion note

a.1 and 4 only

b.1 and 3 only

c.2, 3, and 4 only

d.1, 2, 3, and 4

6.According to the American Association for Respiratory Care (AARC), the purpose(s) of respiratory TDPs is/are to:

1.Deliver individualized diagnostic and therapeutic respiratory care to patients

2.Assist the physician with evaluating patients’ respiratory care needs and optimize the allocation of respiratory care services

3.Determine the indications for respiratory therapy and the appropriate modalities for providing high-quality, cost-effective care that improves patient outcomes and decreases length of stay

4.Empower respiratory therapists to allocate care using signand symptom-based algorithms for respiratory treatment

a.1 only

b.3 only

c.1, 2, and 3 only

d.1, 2, 3, and 4

7.A patient experiencing a severe asthmatic episode would probably demonstrate a variety of objective clinical indicators to justify the assessments that call for the administration of which of the following protocols:

1.Oxygen Therapy Protocol

2.Airway Clearance Therapy Protocol

3.Aerosolized Medication Therapy Protocol

4.Lung Expansion Therapy Protocol

a.1 and 3 only

b.3 and 4 only

c.1, 2, and 4 only

d.1, 2, and 3 only

8.On the previous page, the Aerosolized Medication Protocol appears with one or more steps left out. Which steps have been omitted?

1.Discharge training/documentation has been left out

2.Effect of treatment with MDI/spacer has not been evaluated

3.Failure to be able to breath hold has not been related to muscle weakness, following the finding of a reduced inspiratory capacity

4.Use of additional protocols has not been considered in view of the patient's failure to improve on aerosol therapy via small-volume nebulizer treatment or intermittent positive-pressure breathing

a.1 and 3 only

b.2 and 4 only

c.2, 3, and 4 only

d.1, 2, 3, and 4

9.A patient with recent thoracic surgery, who has developed both left and right lower lung lobe atelectasis, would most likely benefit from which of the following protocols?

a.Oxygen Therapy Protocol

b.Airway Clearance Therapy Protocol

c.Aerosolized Medication Therapy Protocol

d.Lung Expansion Therapy Protocol

10.An obese 37-year-old man enters the emergency department in respiratory distress. He stated that he had been bedridden for the past 8 days with the flu. He thought he was getting better but had been short of breath for the past 2 days. His vital signs are blood pressure 175/125, respiratory rate 25 breaths/min, and heart rate 110 bpm. He has bilateral bronchial breath sounds over the lower lobes and dull percussion notes over the bases. His arterial blood gases show that he has acute alveolar hyperventilation with moderate hypoxemia. His chest x-ray image revealed bilateral atelectasis throughout his right and left lower lobes. Which of the following protocols would initially be the most beneficial?

a.Oxygen Therapy Protocol

b.Airway Clearance Therapy Protocol

c.Aerosolized Medication Therapy Protocol

d.Lung Expansion Therapy Protocol

1Available online at http://www.aarc.org.

2The AARC Protocol Implementation Committee has developed a PowerPoint presentation of the complete survey, which is intended to assist in understanding the barriers and developing successful strategies to implement protocol utilization (http://www.aarc.org; search for AARC Protocol Implementation Committee).

3The “teach” edition reflects the recognition that has been given to patient education as an important part of the hospital stay.

4Sample protocols for mechanical ventilation are provided in Chapter 11, Respiratory Insufficiency, Respiratory Failure and Ventilatory Management Protocols, page 169.

5Protocols for mechanical ventilation are provided in Chapter 11, Respiratory Insufficiency, Respiratory Failure and Ventilatory Management Protocols.

6The authors would like to thank the Respiratory Care Department at the Kettering Health Network, in Dayton, Ohio, for

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providing the use of their Oxygen Therapy Protocol, Airway Clearance Therapy Protocol, Lung Expansion Protocol, and Aerosolized Medication Therapy Protocol. The Kettering Health Network (KHN) protocols shown here serve only as examples. The modalities and medications reflect only those that KHN is currently using in their patient care. This is particularly true in the case of ventilators discussed in Chapter 11, Respiratory Insufficiency, Respiratory Failure, and Ventilatory Management Protocols, where clearly not every ventilator or ventilator modality is being used by the KHN.

7The memorization of the protocols, algorithms, or specific medications presented in this chapter is not recommended. This is because protocols frequently change as updated CPGs become available, and local institutional practice mandates vary. However, it is important to commit to memory the kinds of protocols available in your institution (e.g., Oxygen Therapy Protocol) and the types of therapy used in them (e.g., ultra-high-flow oxygen therapy, hyperbaric oxygen therapy, etc.). The protocols in this textbook reflect the availability of modalities from the Respiratory Care Department at Kettering Health Network, and Dayton Children's Hospital, in Dayton, Ohio, which have recently been modified to reflect the most recent AARC CPGs.

8The Case Study Discussion Section at the end of each respiratory disease chapter often refers the reader back to these clinical scenarios, correlating various clinical manifestations to specific pathophysiologic mechanisms and alterations of the lungs.

9The mechanical ventilation protocols are presented in Chapter 11, Respiratory Insufficiency, Respiratory Failure, and Ventilatory Management Protocols.

C H A P T E R 1 1

Respiratory Insufficiency, Respiratory

Failure, and Ventilatory Management

Protocols

CHAPTER OUTLINE

Classifications of Respiratory Failure

Hypoxemic Respiratory Failure—Type I (Oxygenation Failure)

Hypercapnic Respiratory Failure—Type II (Ventilatory Failure) Types of Ventilatory Failure

Mechanical Ventilation

Standard Criteria for Instituting Mechanical Ventilation Prophylactic Ventilatory Support

Key Clinical Indicators for Ventilatory Support in Hypercapnic and Hypoxemic Respiratory Failure Ventilatory Support Strategy

Mechanical Ventilation Protocols

Mechanical Ventilation Discontinuation (Weaning) Ventilator Graphics

Ventilator Hazards

Barotrauma and Volutrauma

Lung Protective Strategies Ventilator Malfunctions

Charting the Progress of Ventilated Patients

Self-Assessment Questions

CHAPTER OBJECTIVES

After reading this chapter, you will be able to:

•Define respiratory failure.

•Identify the six major anatomic alterations of the lungs and subsequent clinical scenarios that can lead to respiratory failure.

•Differentiate between the two major classifications of respiratory failure.

•Describe hypoxemic respiratory failure (type I) (oxygenation failure).

•List respiratory disorders associated with hypoxemic respiratory failure.

•Discuss the pathophysiologic mechanisms of hypoxemic respiratory failure.

•Describe the benefit of the alveolar-arterial oxygen radiant [P(A-aO)2] in the treatment of respiratory failure.

•Describe hypercapnic respiratory failure (type II) (ventilatory failure).

•Describe the pathophysiologic mechanisms of hypercapnic respiratory failure.

•List respiratory disorders associated with hypercapnic respiratory failure.

•Differentiate the types of ventilatory failure.

•Describe the major components of a mechanical ventilation protocol.

•Identify good “starting points” for selection of ventilator modes and settings.

•Describe the benefits of ventilator graphics in modern ventilator management.

•Describe the etiology, pathogenesis, and presentation of ventilator-induced/ventilator-associated lung injury (VILI/VALI)

•Discuss the concept and application of lung-protective strategies in mechanical ventilation.

•Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

KEY TERMS

Absolute Shunt

Acute Alveolar Hyperventilation Superimposed on Chronic Ventilatory Failure

Acute Ventilatory Failure

Acute Ventilatory Failure Superimposed on Chronic Ventilatory Failure

Adaptive Support Ventilation (ASV)

Alveolar-Arterial Oxygen Tension Difference [P(A-a)O2]

Alveolar Flooding

Alveolar Hypoventilation

Anatomic Shunt

Apnea

ARDSNet Protocol

Arterial Oxygen Tension (PaO2)

Arterial Oxygen Tension to Fractional Inspired Oxygen Ratio (PaO2/FIO2)

Arterial to Alveolar Oxygen Tension Ratio (PaO2/PAO2 ratio)

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Barotrauma Bohr Equation Capillary Shunt

Chronic Ventilatory Failure

Continuous Positive Airway Pressure (CPAP) Ventilation Dead Space/Tidal Volume Ratio (VD/VT) Ratio

Diffusion Defect

Hypercapnic Respiratory Failure (Type II) Hypoxemic (Type I) Respiratory Failure Impending Ventilatory Failure Intermittent Mandatory Ventilation (IMV) Invasive Mechanical Ventilation Maximum Inspiratory Pressure (MIP) Mechanical Dead Space

Neurally Adjusted Ventilatory Assist (NAVA) Noninvasive Ventilation (NIV) Patient-Ventilator Interaction

Permissive Hypercapnia Pressure Time Index (PTI) Prone Positioning

Prophylactic Ventilatory Support Protective Lung Strategies Pulmonary Shunting

Rapid Shallow Breathing Index (RSBI) Relative Shunt

Respiratory Failure

Richmond Agitation Sedation Scale Shunt-Like Effect

Spontaneous Breathing Trial (SBT) Static Lung Compliance (CL)

Type III Respiratory Failure Venous Admixture

Ventilator-Associated Lung Injury (VALI) Ventilator-Induced Lung Injury (VILI) Ventilation-Perfusion Mismatch Ventilatory Failure

Volutrauma

Respiratory failure (also called ventilatory failure) is a general term used to describe the inability of the respiratory system to establish and maintain adequate oxygen uptake and carbon dioxide removal from the body. The arterial blood gas (ABG) criteria for respiratory failure in the normal individual are an arterial partial pressure of oxygen (PaO2) less than 60 mm Hg, an arterial partial pressure of carbon dioxide (PaCO2)

greater than 50 mm Hg, or a mixture of both. These ABG values constitute the definition for respiratory failure. Additional objective findings include cardiac arrhythmias, both hypertension and preterminally hypotension, coma, and death. Subjective findings (symptoms) of respiratory failure include dyspnea, anxiety, restlessness, and rapid and shallow breathing. Respiratory failure is a life-threatening clinical condition that the respiratory therapist must be 100% proficient in consistently recognizing, assessing, and managing.

Virtually every respiratory disorder presented in this textbook can result in respiratory failure. Each respiratory disorder can cause one or more of the anatomic alterations of the lung, which in turn activate specific and very predictable pathophysiologic mechanisms and clinical manifestations that can progressively worsen if not identified and treated. The interrelationship between the anatomic alterations of the lungs, the pathophysiologic mechanisms, and the clinical manifestations are collectively referred to as clinical scenarios (see Chapter 10, The Therapist-Driven Protocol Program).

As discussed in detail in Chapter 10, there are six basic anatomic alterations of the lungs, which in turn cause six different clinical scenarios that can result in respiratory failure. These scenarios are (1) atelectasis (see Fig. 10.7), (2) alveolar consolidation (see Fig. 10.8), (3) increased alveolar-capillary membrane thickness (see Fig. 10.9), (4) bronchospasm (see Fig. 10.10), (5) excessive bronchial secretions (see Fig. 10.11), and (6) distal airway and alveolar weakening (see Fig. 10.12).

Classifications of Respiratory Failure

On the basis of the ABG values, respiratory failure is commonly classified as (1) hypoxemic respiratory failure (also called type I respiratory failure), (2) hypercapnic respiratory failure (also called type II respiratory failure), or (3) a combination of both. The term hypoxemic respiratory failure is used when the primary problem is inadequate oxygenation exchange between the alveoli and the pulmonary capillary system, which results in a decreased PaO2. The term hypercapnic respiratory failure is used when the primary problem is alveolar hypoventilation, which

results in an increased PaCO2 and, without supplemental oxygen, a decreased PaO2.

In the clinical setting, hypercapnic respiratory failure is commonly called ventilatory failure. Based on the PaCO2 and pH values, ventilatory failure is further classified as being either acute ventilatory failure (high PaCO2 and low pH) or chronic ventilatory failure (high PaCO2 and

normal pH). Because acute ventilatory changes (i.e., hyperventilation or hypoventilation) are often seen in patients with chronic ventilatory failure, the patient also may present with either (1) acute alveolar hyperventilation superimposed on chronic ventilatory failure or (2) acute ventilatory failure superimposed on chronic ventilatory failure.

The different types of respiratory failures are described in the following section.

Hypoxemic Respiratory Failure—Type I (Oxygenation Failure)

Hypoxemic respiratory failure (type I) is used to describe a patient whose primary problem is inadequate oxygenation. Patients with hypoxemic respiratory failure typically demonstrate hypoxemia—a low PaO2—and a normal or low PaCO2 value.1 The low PaCO2 is usually

attributable to the alveolar hyperventilation associated with hypoxemia (see Figs. 3.5 and 3.6). Box 11.1 provides a listing of common respiratory disorders that can cause hypoxemic respiratory failure. The major pathophysiologic causes of hypoxemic respiratory failure are (1) alveolar hypoventilation, (2) pulmonary shunting, and (3) ventilation-perfusion (V/Q) mismatch. Although less common, a decrease in inspired oxygen pressure (PIO2) (e.g., exposure at high altitudes) also can cause hypoxemic respiratory failure.

Box 11.1

Respiratory Disorders Associated With Hypoxemic Respiratory Failure (Oxygenation

Failure)

Restrictive Pulmonary Disorders*

•Pneumonia

•Pulmonary edema

•Interstitial lung diseases

•Acute respiratory distress syndrome

•Alveolar atelectasis

Chronic Obstructive Pulmonary Disorders†

•Emphysema

•Chronic bronchitis

•Asthma

•Cystic fibrosis

Neoplastic Disease*

• Cancer of the lung

Newborn and Early Childhood Respiratory Disorders*

•Meconium aspiration syndrome

•Transient tachypnea of the newborn

•Respiratory distress syndrome

•Pulmonary air leak syndromes

•Respiratory syncytial virus infection

•Congenital diaphragmatic hernia

•Bronchopulmonary dysplasia‡

•Croup syndrome†

*Primary pulmonary shunting disorders.

†Primarily a decreased V/Q ratio and alveolar hypoventilation disorders.

‡Pulmonary shunting, decreased.

The primary pathophysiologic mechanisms of hypoxemic respiratory failure are discussed in more detail in the following sections.

Pathophysiologic Mechanisms of Hypoxemic Respiratory Failure

Alveolar hypoventilation develops when the minute volume of alveolar ventilation (VA) is not adequate for the body's metabolic needs. It is characterized by an increased PaCO2 level and, without supplemental oxygen, a decreased PaO2. Common causes of alveolar hypoventilation

include central nervous system depressants, head trauma, chronic obstructive pulmonary disease (COPD), obesity, sleep apnea, and neuromuscular disorders (e.g., amyotrophic lateral sclerosis [ALS], myasthenia gravis, or Guillain-Barré syndrome). The current epidemic of opioid and sedative substance abuse has increased the number of cases of alveolar hypoventilation to a frightening extent. Box 11.2 lists the substances currently monitored by authorities with urinary or blood screening.

Box 11.2

Urinary and Drug Screens Commonly Monitored for Substance Use and Abuse*

• Benzodiazepines	• Methadone
• Barbiturates	• Opioids
• Codeine	• Methamphetamine
• THC (marijuana)	• Fentanyl
• Amphetamines

*Modified from Hammond, S., et al. (2017). Drug screens used to monitor opioid use in monitoring chronic pain. The Journal of the American Medical Association, 318, 11, 1061-1062.

The results of alveolar hypoventilation are hypoxia, hypercapnia, respiratory acidosis, and, in severe cases, pulmonary hypertension with cor pulmonale. It should be emphasized, however, that even though alveolar hypoventilation causes hypoxemia, the alveoli are still able to efficiently transfer oxygen into the pulmonary capillary blood—assuming the inspired oxygen can be delivered to the alveoli. Thus treatment of alveolar hypoventilation primarily consists of ventilatory support.

Pulmonary Shunting.

Pulmonary shunting is defined as that portion of the cardiac output that moves from the right side to the left side of the heart without being exposed to alveolar oxygen (PAO2). Pulmonary shunting is divided into the following two categories: (1) absolute shunt and (2) relative shunt. As

discussed in more detail in the following section, all forms of pulmonary shunting lead to venous admixture and a decreased PaO2 level.

Absolute Shunt.

Absolute shunts (also called true shunts) are classified as either an anatomic shunt or a capillary shunt. Both types, anatomic and capillary shunts, are classified under the general heading of absolute shunts.

Anatomic shunts occur when blood flows from the right side of the heart to the left side without coming in contact with an alveolus for gas exchange (Fig. 11.1B). In the healthy lung, there is a normal anatomic shunt of about 3% of the cardiac output. This normal shunting is caused by nonoxygenated blood completely bypassing the alveoli and entering (1) the pulmonary vascular system by means of the bronchial venous drainage and (2) the left atrium by way of the thebesian veins. These natural anatomic shunts explain the small normal difference between the partial pressure of oxygen in the alveoli (PAO2) and the arterial blood (PaO2)—that is, the normal P(A-a)O2 difference of 7 to 15 mm Hg.

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FIGURE 11.1 Pulmonary shunting. (A) Normal alveolar-capillary unit. (B) Anatomic shunt. (C) Types of capillary shunt. (D) Types of relative or shunt-like effect.

Common abnormal causes of anatomic shunt include the following:

•Congenital heart disease

•Intrapulmonary fistula

•Vascular lung tumors

Capillary shunts are caused by (1) alveolar collapse or atelectasis, (2) alveolar fluid accumulation, or (3) alveolar consolidation or pneumonia (see Fig. 11.1C).

The sum of both the anatomic shunt and capillary shunt makes up the absolute (also called the true shunt). The patient with absolute shunting responds poorly to oxygen therapy because of the two pathologic mechanisms:

1.In an anatomic shunt the alveolar oxygen does not come in direct contact with the shunted blood—that is, the nonoxygenated blood completely bypasses the ventilated alveoli and mixes downstream with the oxygenated blood.

2.When a capillary shunt is present, the nonoxygenated blood passes alveoli that are not ventilated and, as a result, moves downstream as venous blood and mixes with the oxygenated blood (see section on Venous Admixture).

The patient with absolute shunting is refractory to oxygen therapy. In other words, the reduced arterial oxygen level caused by this type of pulmonary shunting cannot be easily treated by increasing the concentration of oxygen for these two major reasons: (1) because of the pathology associated with an absolute shunt, the alveoli are unable to accommodate any form of ventilation, and (2) the blood that bypasses the normal, functional alveoli is unable to carry more oxygen once it has become fully saturated, except for a very small amount of oxygen that dissolves in the plasma (PO2 × 0.003 = Dissolved O2).

Relative Shunt.

When pulmonary capillary perfusion is in excess of alveolar ventilation, a relative shunt (also referred to as a shunt-like effect) is said to be present (see Fig. 11.1D). A relative shunt can be caused by an airway obstruction, an alveolar-capillary diffusion defect, or a combination of both.

Airway obstruction leads to poor ventilation of the distal airways. As a result, the pulmonary capillary blood flow is greater than the alveolar ventilation—in short, a decreased V/Q ratio exists. This condition results in a relative shunt, or shunt-like e ect, which in turn causes the PaO2

to fall (see Fig. 11.1D). Common respiratory disorders that cause airway obstruction include emphysema, chronic bronchitis, asthma, and cystic fibrosis.

Alveolar-capillary diffusion defects occur when an abnormality in the structure of the alveolar-capillary membranes slows the movement of oxygen between the alveoli and the pulmonary capillary blood. Under these conditions, the pulmonary capillary blood passing by the alveolus does not have enough time to equilibrate with the alveolar oxygen tension. This condition results in a relative shunt, or shunt-like effect, which in turn causes the PaO2 to fall (see Fig. 11.1D).

Common causes of diffusion defects include interstitial pulmonary edema and interstitial lung disorders (e.g., asbestosis, scleroderma, or idiopathic pulmonary fibrosis). Relative shunting also may occur after the administration of drugs that cause an increase in cardiac output or dilation of the pulmonary vessels. Unlike an absolute shunt, which is refractory to oxygen therapy, conditions that cause a shunt-like effect are more easily corrected (at least partially) by oxygen therapy and alveolar expansion techniques such as continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP).

Table 11.1 illustrates the type of pulmonary shunting associated with common respiratory disorders.

TABLE 11.1

Type of Pulmonary Shunting Associated With Common Respiratory Diseases

Respiratory Diseases	Capillary Shunt	Relative or Shunt-Like Effect
Chronic bronchitis		X
Emphysema		X
Asthma		X
Croup/epiglottitis		X
Sleep apnea		X
Bronchiectasis*	X	X
Cystic fibrosis*	X	X
Interstitial lung disease*	X	X
Cancer of the lungs	X	X
Guillain-Barré syndrome	X	X
Myasthenia gravis	X	X
Pneumonia	X
Tuberculosis	X
Pulmonary edema	X
Flail chest	X
Pneumothorax	X
Kyphoscoliosis	X
Interstitial lung disease	X
Acute respiratory distress syndrome	X
Pleural diseases	X
Respiratory distress syndrome	X
Near drowning	X
Smoke inhalation	X
Atelectasis	X

*Relative or shunt-like effect is most common.

Venous Admixture.

Venous admixture is defined as the mixing of shunted, nonoxygenated blood with reoxygenated blood distal to the alveoli—that is, downstream in the pulmonary venous system in route to the left side of the heart (Fig. 11.2). When venous admixture occurs, the shunted—nonoxygenated— blood gains oxygen molecules while at the same time the reoxygenated blood loses oxygen molecules. This process continues until (1) the PO2

throughout all the plasma of the newly mixed blood is in equilibrium and (2) all the hemoglobin molecules carry the same number of oxygen molecules.

FIGURE 11.2 Venous admixture occurs when reoxygenated blood mixes with nonreoxygenated blood distal to the alveoli. Technically, the PO2 in the pulmonary capillary system will not equilibrate completely because of the normal P(A-a)O2. The PO2 in the pulmonary capillary system is normally a few millimeters of mercury less than the PO2 in the alveoli.

The final result of venous admixture is (1) a “downstream” blood mixture that has a higher PO2 and CaO2 than the original shunted, nonoxygenated blood and (2) a lower PO2 and CaO2 than the original reoxygenated blood—in other words, a blood mixture with PaO2 and CaO2

values somewhere between those of original values of the reoxygenated and nonoxygenated blood. The overall final outcome of venous admixture is a reduced PaO2 and CaO2 level returning to the left side of the heart via the systemic venous system. Clinically, it is this oxygen

mixture that is evaluated downstream (e.g., from the radial artery) to assess the patient's ABGs.

To calculate the amount of a patient's pulmonary shunting, see the discussion of pulmonary shunt fraction in Chapter 6, Assessment of Oxygenation, page 86.

Ventilation-Perfusion (V̇/Q̇) Ratio Mismatch

Under normal conditions, the overall alveolar ventilation is about 4 L/min and pulmonary capillary blood flow is about 5 L/min, making the average overall ratio of alveolar ventilation to blood flow about 4 : 5 or 0.8. This relationship is expressed as the ventilation-perfusion (V/Q) ratio (Fig. 11.3).

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FIGURE 11.3 The normal overall pulmonary ventilation-perfusion ratio (V̇/Q̇) is approximately 0.8.

In some disorders, such as pulmonary embolism (see Chapter 21, Pulmonary Vascular Disease: Pulmonary Embolism and Pulmonary Hypertension), the lungs receive less blood flow in relation to ventilation. When this condition develops, the V/Q ratio increases. A larger portion of the alveolar ventilation therefore will not be physiologically effective and the patient will be said to demonstrate “wasted” or dead-space ventilation (Fig. 11.4).

FIGURE 11.4 Dead-space ventilation (V̇).

2

In other lung disorders (e.g., asthma, emphysema, pulmonary edema, or pneumonia), the lungs receive relatively less ventilation in relation to blood flow. When this condition develops, the V/Q ratio decreases. A decreased ratio leads to a relative shunt, or shunt-like e ect, which in turn leads to venous admixture and a decreased PaO2 (see Fig. 11.1D).

Ratio of Dead Space to Tidal Volume

In the clinical setting, the patient's alveolar dead space is often expressed as the dead space/tidal volume (VD/VT) ratio. The VD/VT ratio provides a good reference of the patient's wasted ventilation (i.e., both the anatomic and alveolar dead space) per each breath. The calculation

of the VD/VT ratio requires both a sample of the patient's arterial CO2 (PaCO2) and the mixed expired CO2 (). The PaCO2 is obtained from

a routine ABG sample, and the is collected in a sampling bag or balloon or estimated via capnography. The calculation of the VD/VT ratio uses a modified form of the Bohr equation, which assumes that there is no CO2 in the inspired gas. The VD/VT ratio is written as follows:

where PaCO2 is the arterial CO2 tension, and is the expired CO2 tension. Thus if a patient has a PaCO2 of 40 mm Hg and a of 30 mm Hg, the VD/VT ratio would be calculated as follows:

The VD/VT ratio in the normal adult breathing spontaneously ranges between 20% and 40%. For patients receiving mechanical ventilation, the normal VD/VT ratio ranges between 40% and 60%, because of the mechanical dead space added by the endotracheal tube, etc. The VD/VT ratio increases with diseases that cause significant dead space, such as pulmonary embolism.

Decreased Partial Pressure of Inspired Oxygen (Decreased PIO2)

Hypoxemia also can develop from decreases in inspired concentrations of oxygen. For example, hypoxemia can develop at high altitudes. This is because the partial pressure of inspired oxygen progressively decreases in response to the falling barometric pressure that occurs at high altitudes. The higher the altitude above sea level, the lower is the barometric pressure. The lower the barometric pressure, the lower is the partial pressure of inspired oxygen. For example, at an altitude of 18,000 to 19,000 feet, the barometric pressure is about half the sea-level value of 760 mm Hg (380 mm Hg).

The barometric pressure on the summit of Mount Everest (altitude 29,028 feet) is about 250 mm Hg (the atmospheric PO2 is about 43 mm Hg).

To compensate for this, it is not uncommon for a mountain climber to use an oxygen mask. At an altitude of about 65,000 feet, the barometric pressure falls below the pressure of water vapor, and tissue fluids begin to “boil” or “vaporize.” Airlines correct for the decreased barometric pressure by pressurizing their cabins.2 However, the individual with chronic hypoxemia may still require supplemental oxygen during the flight. The effects of chronic hypoxia and hyperoxia are being increasingly more appreciated, and steps to remedy the problems range from high-flow oxygen therapy, pressurized hospital rooms, hyperbaric oxygen therapy, and—recently reported—even the use of oxygen generators in some carriages in a train3 running from China to Lhasa, Tibet. This train frequently passes through altitudes near 5000 meters, and supplemental oxygen is bled into the carriage to relieve the symptoms of altitude sickness of passengers.

Identifying the Pathophysiologic Mechanisms of Acute Hypoxemic Respiratory Failure

To more effectively treat the patient, the alveolar-arterial oxygen tension difference [P(A-a)O2] is used clinically to identify the primary

cause of the hypoxemic respiratory failure—alveolar hypoventilation, pulmonary shunting, or V/Q mismatch. The clinical determination of the P(A-a)O2 is made by subtracting the PaO2 (obtained from an ABG value) from the PAO2, which is obtained from the ideal alveolar gas equation:

where PB is the barometric pressure, PAO2 is the partial pressure of oxygen within the alveoli, PH2O is the partial pressure of water vapor in the alveoli (which is 47 mm Hg), FIO2 is the fractional concentration of inspired oxygen, PaCO2 is the partial pressure of arterial carbon dioxide, and RQ is the respiratory quotient. The RQ is the ratio of carbon dioxide production (VCO2) divided by oxygen consumption (VO2).

Under normal circumstances, about 250 mL of oxygen per minute is consumed by the tissue cells and about 200 mL of carbon dioxide is excreted into the lung. Thus the RQ is normally about 0.8, but can range from 0.7 to 1.0. Clinically, 0.8 is generally used for the RQ. For example, consider the following case example:

Case Example

If a patient is receiving an FIO2 of 0.30 on a day when the barometric pressure is 750 mm Hg, and if the patient's PaCO2 is 70 mm Hg and PaO2 is 60 mm Hg, the P(A-a)O2 can be calculated as follows:

Using the PaO2 obtained from the ABG, the P(A-a)O2 now can be easily calculated as follows:

The normal P(A-a)O2 on room air at sea level ranges from 7 to 15 mm Hg and should not exceed 30 mm Hg. Although the P(A-a)O2 may be useful in patients breathing a low FIO2, it loses some of its sensitivity in patients breathing a high FIO2. The P(A-a)O2 increases at high oxygen concentrations. Because of this, the P(A-a)O2 has less value in the critically ill patient who is breathing a high oxygen concentration. The normal P(A-a)O2 for an FIO2 of 1.0 is between 25 and 65 mm Hg. The critical value of the P(A-a)O2 on the 100% oxygen is greater than 350 mm Hg.

When conditions such as obesity or drug overdose lead to alveolar hypoventilation and subsequent hypoxemic respiratory failure, the (P[A- a]O2) is normal, thus indicating that the lungs are normal but alveolar ventilation is not. In these cases, the treatment management is directed

at a ventilatory support strategy. These patients readily respond to ventilator therapy and not to oxygen therapy alone.

When V/Q mismatch, pulmonary shunting, or di usion blockade is the primary cause of the hypoxemic respiratory failure, the (P[A-a]O2) is

elevated. In these cases, the administration of oxygen is used to identify the specific pathologic basis of the hypoxemic respiratory failure—that is, a V/Q mismatch or pulmonary shunting. The patient with a V/Q mismatch shows significant improvement with oxygen therapy, indicating that the patient's V/Q status may not have been permanently altered. For example, the use of bronchodilators may improve the patient's bronchoconstriction and thus improve his alveolar hypoventilation and his altered V/Q status. By contrast, the patient with an absolute shunt shows little to no improvement with oxygen therapy, even at an FIO2 of 1.0. In these cases, the treatment needs to focus on the cause of the

intrapulmonary shunting. For example, therapeutic efforts are directed at opening collapsed alveoli (in cases of atelectasis or alveolar flooding), reducing pulmonary edema, or mobilizing excessive secretions that lead to atelectasis. The (PA-Pa) is a helpful tool in the early diagnosis of the patient's disease process (and in following its progress), especially when the FIO2 varies during the course of therapy.

Summary of Causes of Hypoxemic Respiratory Failure.

Table 11.2 summarizes the major causes of hypoxemic respiratory failure, the pathophysiologic mechanisms involved, the typical P(A-a)O2 findings, the expected patient response to oxygen therapy, and types of patients who demonstrate the mechanism.

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TABLE 11.2

Causes of Hypoxemic Respiratory Failure

	Cause of Hypoxemic	Pathophysiologic Mechanism	P(A-a)O2	General Response to	Examples
	Respiratory Failure		Findings	Oxygen Therapy
	Alveolar hypoventilation	Decreased minute ventilation: Increased PaCO2,	Normal	Fair/good, with ventilatory	Drug overdose
		decreased PaO2		support or increased	Oversedation
				alveolar ventilation	Obesity
					Head trauma
					Myasthenia
					gravis
					Guillain-Barré
					syndrome
	Pulmonary shunting	Venous admixture (venous blood mixing with	Increased	Poor	Atelectasis
		arterial blood)			Pneumonia
					Alveolar fibrosis
					ARDS
					Pulmonary
					edema
	Ventilation-perfusion	Venous admixture (nonoxygenated blood mixing	Increased	Good	Emphysema
	mismatch	with arterial blood)			Chronic
					bronchitis
					Asthma
					Pulmonary
					embolus
	Decrease in inspired	Decreased oxygen concentration or decreased	Normal	Good	High altitude
	oxygen (decreased	inspired oxygen pressure (e.g., decreased			Low oxygen
	FIO2 or PIO2)	barometric pressure)			content of gas
					mixture
					Enclosed
					breathing
					spaces
					(suffocation)
	ARDS, Acute respiratory distress syndrome.

Hypercapnic Respiratory Failure—Type II (Ventilatory Failure)

Hypercapnic respiratory failure (type II) is the phrase used when the primary problem is alveolar hypoventilation. Patients with hypercapnic respiratory failure demonstrate an increased PaCO2 and, without supplemental oxygen, a decreased PaO2.4 The major pathophysiologic

mechanisms that result in hypercapnic respiratory failure are (1) alveolar hypoventilation, (2) increased dead-space disease, and (3) severe V/Q ratio mismatch. Box 11.3 provides common respiratory disorders associated with hypercapnic respiratory failure.

Box 11.3

Respiratory Disorders Associated With Hypercapnic Respiratory Failure* (Ventilatory

Failure)

Pulmonary Disorders

•Emphysema

•Chronic bronchitis

•Asthma

•Cystic fibrosis

Respiratory Center Depression

•Drug overdose

•Cerebral trauma or infarction

•Bulbar poliomyelitis

•Encephalitis

Neuromuscular Disorders

•Myasthenia gravis

•Guillain-Barré syndrome

•Spinal cord trauma

•Muscular dystrophy

Pleural and Chest Wall Disorders

•Flail chest

•Pneumothorax

•Pleural effusion

•Kyphoscoliosis

•Obesity

Sleep Apnea

*It should be noted that any of the pulmonary disorders associated with hypoxemic respiratory failure can—when severe enough—lead to hypercapnic respiratory failure.

Types of Ventilatory Failure

In the clinical setting, hypercapnic respiratory failure is commonly referred to as ventilatory failure. Based on the arterial blood PaCO2 and pH values, ventilatory failure can be further classified as either (1) acute ventilatory failure (high PaCO2 and low pH) or (2) chronic ventilatory failure (high PaCO2 and normal pH).

In addition, chronic ventilatory failure is often complicated by conditions that cause the patient to either hyperventilate or hypoventilate—that is, on top of (in addition to) their chronic ventilatory failure. In these cases, the patient is said to have either (1) acute alveolar hyperventilation superimposed on chronic ventilatory failure or (2) acute ventilatory failure (hypoventilation) superimposed on chronic ventilatory failure. The different classifications of ventilatory failure are discussed in more detail in the following paragraphs.