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Protocol for Artificial Airways.

Aerosolized Medication Therapy Protocol (Protocol 10.4, page 144)

The vast majority of the daily work performed by the respiratory therapist involves assessments and treatments associated with the cornerstone protocols mentioned previously.4 Done well, they are the essential foundations of a good TDP program. For example, a patient experiencing a severe asthmatic episode would probably demonstrate a variety of objective and subjective clinical indicators to justify the assessments that call for the administration of oxygen therapy (e.g., to treat hypoxemia), an aerosolized bronchodilator (e.g., to treat bronchospasm), air clearance therapy (e.g., to mobilize the thick white secretions associated with asthma), and mechanical ventilation (e.g., to treat acute ventilatory failure).

As shown in the algorithms in Protocols 10.1 through 10.4,5 a step-by-step, branching logic process directs the practitioner to (1) gather clinical data (clinical indicators), (2) make assessment decisions based on the clinical data, and

(3) either start, up-regulate, down-regulate, or discontinue a treatment modality. In fact, the primary reasons a good TDP program works is because a specific treatment modality cannot be started, stopped, or modified unless there are specific and measurable clinical indicators identified to justify the assessment and treatment decision.6

The treatment selections outlined in each of the previously mentioned protocols are based on current AARC Clinical Practice Guidelines (CPGs), which provide the most recent scientific evidence that justifies the administration of a specific treatment modality. Using the evidence-based methods mandated by the scientific community, evidence-based clinical practice guidelines provide the indications, contraindications, hazards and complications, assessment of need, assessment of outcome, and appropriate monitoring techniques used for specific therapy modalities. In other words, the CPGs are the gold standards used by the respiratory therapy profession to start, adjust, or discontinue a specific treatment modality. In Box 10.1 (see page 147), excerpts from the AARC's CPG on oxygen therapy for adults in the acute care facility provide a representative example of a CPG and, more importantly, describe current thinking on the scientific basis for the Oxygen Therapy (see Protocol 10.1, page 138).

Box 10.1

American Association for Respiratory Care Clinical Practice Guideline for Oxygen Therapy in the Acute Care Facility (Excerpts)*

Indications

Documented hypoxemia. Defined as a decreased PaO2 in the blood below normal range.

PaO2 <60 mm Hg or SaO2 <90% in persons breathing room air.

Acute care situations in which hypoxemia is suspected.

Severe trauma.

Acute myocardial infarction.

Short-term therapy or surgical intervention (e.g., postanesthesia recovery, hip surgery).

Contraindications

• No specific contraindications to oxygen therapy exist when indications are present.

Precautions and/or Possible Complications

PaO2 >60 mm Hg may depress ventilation in some patients with elevated PaCO2.

FIO2 >0.50, may cause absorption atelectasis, oxygen toxicity, and/or ciliary or leukocyte depression.

Supplemental oxygen should be administered with caution to patients with paraquat poisoning or to those receiving bleomycin.

During laser bronchoscopy, minimal FIO2 should be used to avoid intratracheal ignition.

Fire hazard is increased in the presence of increased oxygen concentration.

Bacterial contamination associated with nebulizers or humidifiers is a possible hazard.

Assessment of Need

Need is determined by measurement of inadequate oxygen tension and/or saturation, by invasive or noninvasive methods, and/or by the presence of clinical indicators.

Assessment of Outcome

Outcome is determined by clinical and physiologic assessment to establish adequacy of patient response to therapy.

Monitoring

Patient

Clinical assessment, including cardiac, pulmonary, and neurologic status.

Assessment of physiologic parameters (PaO2, SaO2, SpO2) in conjunction with the initiation of therapy or:

Within 12 hours of initiation with FIO2 <0.40

Within 8 hours with FIO2 ≥0.40 (including postanesthesia recovery)

Within 72 hours in acute myocardial infarction

Within 2 hours for any patient with principal diagnosis of chronic obstructive pulmonary disease

Equipment

All oxygen delivery systems should be checked at least once per day.

More frequent checks are needed in systems:

Susceptible to variation in oxygen concentration (e.g., hood, high-flow blending systems)

Applied to patients with artificial airways

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Delivering a heated gas mixture

Applied to patients who are clinically unstable or who require FIO2 >0.50

Care should be taken to avoid interruption of oxygen therapy in situations including ambulation or transport for procedure.

*See http://www.aarc.org/ (Clinical Practice Guidelines) for the most recent and complete list of clinical practice guidelines.

From Kalstrom, T. J.; American Association for Respiratory Care (AARC). (2002). AARC clinical practice guideline: Oxygen therapy for adults in the acute care facility—2002 revision and update. Respiratory Care 47, 6, 717-720. See this article for the complete guidelines.

On occasion, several different treatment selections may be listed under each of the protocols. In essence, the various treatment selections serve as a “therapy selection menu.” When the patient demonstrates the clinical indications associated with any of these protocols, the respiratory therapist is expected to select and administer the most efficient and most cost-effective treatment listed in that protocol. As already discussed, the treatment selection decision and the frequency with which the therapy is to be administered are based on (1) the identification of the appropriate clinical indicators, (2) the severity of the abnormality suggested by the clinical information, (3) the patient's ability to perform or tolerate the therapy, (4) the patient's response to the therapy, and (5) the local cost-effective conditions where appropriate.

In another example, the implementation of the Lung Expansion Therapy Protocol, Protocol 10.3 (see pages 142), would probably be indicated after thoracic surgery to prevent, or correct atelectasis. While a patient is on a mechanical ventilator, positive end-expiratory pressure (PEEP) is a time-honored way of treating this condition. If the patient was still breathing but was unconscious or unable to follow directions, a continuous positive airway pressure (CPAP) mask would be a more appropriate treatment selection (under the same protocol) than, say, incentive spirometry, even though both are designed to treat or prevent atelectasis. In this example, although treatment with CPAP mask therapy would be more expensive, it would be more appropriate than the less expensive incentive spirometry, which would require that the patient be alert.

Remember, the treatment portion of a protocol is based on the therapy that will best work to correct or offset the anatomic alterations and pathophysiologic mechanisms caused by the respiratory disorder in a timely and cost-efficient manner. Finally, even when a patient is transferred to the intensive care unit, intubated, and placed on a mechanical ventilator, the respiratory therapist usually must still administer one or more of the first four respiratory therapy treatment protocols listed in this section. For example, the patient would probably need CPAP, PEEP, or other lung expansion or airway clearance therapies to offset any alveolar atelectasis caused by airway mucous plugs via the Lung Expansion Therapy Protocol. The patient might require a bronchodilator agent to offset bronchospasm via the Aerosolized Medication Therapy Protocol.

Summary of a Good Therapist-Driven Protocol Program

As illustrated in Fig. 10.5, the essential components of a good TDP program are as follows. Every respiratory care plan must be directly linked to (1) a physician's order, (2) specific clinical indicators (obtained from the patient's chart, physical examination, and laboratory and x-ray results—all identified and documented), (3) a bedside respiratory assessment and severity assessment must be performed (diagnosis), (4) a treatment selection that is both therapeutic and cost-effective, and finally, (5) the evaluation of the patient's response to the treatment must be routinely performed.

FIGURE 10.5 Overview of the essential components of a good therapist-driven protocol program.

This step-by-step process mandates that the respiratory therapist (1) has a strong knowledge base of the major respiratory disorders, and (2) is competent in the actual assessment process. Fig. 10.6 provides an assessment form with common examples for each category (i.e., clinical indicators, respiratory assessments, and treatment plans). The data documented in Fig. 10.6 can be easily transferred to the subjective-objective evaluation, assessment, and treatment (SOAP) format. The SOAP format used in the assessment of respiratory diseases is discussed in more detail in Chapter 12, Recording Skills and Intraprofessional Communication.7

FIGURE 10.6 Therapist-driven protocol program assessment form.

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Common Anatomic Alterations of the Lungs

Although the respiratory therapist may at some time treat one or two cases of every respiratory disorder presented in this textbook, most of the therapist's professional career will be caring for patients with only a few of them. For example, the diagnosis-related group (DRG) system, which uses the most current edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) identification listings, shows the following short list of respiratory disorders: chronic bronchitis, emphysema, asthma, pneumonia, atelectasis, acute respiratory distress syndrome (ARDS), interstitial fibrosis, pulmonary edema/congestive heart failure, and acute and chronic respiratory failure with and without ventilatory support.

From this relatively short list of respiratory disorders identified through the DRG system, an even shorter list of the most common anatomic alterations of the lungs treated by the respiratory therapist can be derived. This list includes (1) atelectasis (e.g., which can occur from mucous plugging, upper abdominal surgery, pleural effusion, or pneumothorax), (2) alveolar consolidation (e.g., pneumonia), (3) increased alveolar-capillary membrane thickness (e.g., ARDS, pneumoconiosis, or pulmonary edema), (4) bronchospasm (e.g., asthma or bronchitis), (5) excessive bronchial secretions (e.g., chronic bronchitis, asthma, pulmonary edema, and bronchiectasis), and (6) distal airway and alveolar weakening (e.g., emphysema). Each of these anatomic alterations of the lung leads to a chain of events that can be summarized in the following clinical scenarios based on their most prominent pathophysiology.

Clinical Scenarios Activated by Common Anatomic Alterations of the Lungs

For the purposes of this text, we have chosen to refer to the interrelationships among the major anatomic alterations of the lung, the predominant pathophysiologic mechanisms, and the clinical manifestations that result as clinical scenarios. The specific anatomic alterations of the lung lead to the activation of specific and predictable pathophysiologic mechanisms and to their effects. The more common pathophysiologic mechanisms are listed in Box 10.2. The pathophysiologic mechanisms in turn activate specific—and predictable—clinical manifestations (see Fig. 10.3). To further enhance the reader's knowledge and understanding of the commonly encountered respiratory disorders, the clinical scenarios—caused by the anatomic alterations associated with these disorders—are provided in the following section.8

Box 10.2

Pathophysiologic Mechanisms Commonly Activated in Respiratory

Disorders

Decreased ventilation-perfusion (V/Q) ratio

Alveolar diffusion block

Decreased lung compliance

Stimulation of oxygen receptors

Deflation reflex

Irritant reflex

Pulmonary reflex

Increased airway resistance

Air trapping and alveolar hyperinflation

Atelectasis

Fig. 10.7 shows the pathophysiologic mechanisms caused by atelectasis (e.g., from a pneumothorax), the clinical manifestations that result, and the treatment protocols used to offset them. The hypoxemia that results from atelectasis is caused by partial or total capillary shunting. The type of hypoxemia produced by shunting is often refractory to oxygen therapy (see Fig. 11.1C). Therefore the implementation of modalities selected in the Lung Expansion Therapy Protocol may be more beneficial in the treatment of atelectasis-related hypoxemia than would be the Oxygen Therapy Protocol in such a patient.

FIGURE 10.7 Atelectasis clinical scenario.

Alveolar Consolidation

Fig. 10.8 illustrates the pathophysiologic mechanisms caused by alveolar consolidation (as classically seen in lobar pneumonia), the clinical manifestations that may result, and the treatment protocols used to offset them. The hypoxemia that develops as a result of consolidation is caused by capillary shunting. This type hypoxemia is often refractory to oxygen therapy.

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FIGURE 10.8 Alveolar consolidation clinical scenario.

Depending on the severity of the alveolar consolidation, the Lung Expansion Therapy Protocol or the Oxygen Therapy Protocol may be beneficial. In general, however, there is no effective, specific respiratory care treatment modality for alveolar consolidation. With pneumonia, the great temptation for the respiratory therapist is to do too much, such as instituting lung expansion therapy, bronchodilator therapy, and airway clearance therapy. Such treatment protocols generally are not indicated, especially during the early consolidation stages of the disease process. Appropriate antibiotics (prescribed by the physician), bed rest, fluids, and supplementary oxygen are all that are usually needed. When pneumonia is in its resolution stage, however, the patient may experience excessive secretions and atelectasis, accompanied by bronchoconstriction. At this time, other treatment modalities may be indicated.

Increased Alveolar-Capillary Membrane Thickness

Fig. 10.9 illustrates the major pathophysiologic mechanisms caused by increased alveolar-capillary membrane thickness (as seen in postoperative ARDS, pulmonary edema, asbestosis, and chronic interstitial lung disease), the clinical manifestations that develop, and the treatment protocols used to offset them. The hypoxemia that develops as a result of an increased alveolar-capillary membrane thickness is caused by an alveolar-capillary diffusion block. This type of hypoxemia often responds favorably to the Oxygen Therapy Protocol and the Lung Expansion Protocol.

FIGURE 10.9 Increased alveolar-capillary membrane thickness clinical scenario.

Bronchospasm

Fig. 10.10 shows the major pathophysiologic mechanisms activated by bronchospasm (as seen in asthma), the clinical manifestations that result, and the appropriate treatment protocols used to offset them. The Aerosolized Medication Therapy Protocol (bronchodilator therapy) is the primary treatment modality used to offset the anatomic alterations of bronchospasm (the original cause of the pathophysiologic chain of events). The Oxygen Therapy Protocol and Mechanical Ventilation Protocol9 are secondary treatment modalities used to offset the mild, moderate, or severe clinical manifestations associated with bronchospasm.

FIGURE 10.10 Bronchospasm clinical scenario.

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Excessive Bronchial Secretions

Fig. 10.11 illustrates the major pathophysiologic mechanisms caused by excessive bronchial secretions (e.g., as seen in chronic bronchitis, cystic fibrosis, and asthma), the clinical manifestations that result, and the appropriate treatment protocols used to correct them. The Airway Clearance Therapy Protocol is the primary treatment modality used to offset the anatomic alterations associated with excessive bronchial secretions.

FIGURE 10.11 Excessive bronchial secretions clinical scenario.

Distal Airway and Alveolar Weakening

Fig. 10.12 illustrates the major pathophysiologic mechanisms caused by distal airway and alveolar weakening (e.g., pulmonary emphysema), the clinical manifestations that result, and the appropriate treatment protocols used to offset them. Pulmonary rehabilitation and oxygen therapy may be all the practitioner can provide to treat the symptoms associated with distal airway and alveolar weakening.

FIGURE 10.12 Distal airway and alveolar weakening clinical scenario.

Overview of Common Anatomic Alterations Associated With Respiratory Disorders

When the safe and ready respiratory therapist knows and understands the chain of events (clinical scenarios) that develop in response to common anatomic alterations of the lungs, an accurate assessment and appropriate treatment protocol

design can be easily determined. Table 10.3 provides an overview of the most common anatomic alterations associated with the respiratory disorders presented in this textbook.

TABLE 10.3

Common Anatomic Alterations of the Lungs Associated With Respiratory Disorders

Respiratory

 

Alveolar

Increased Alveolar-

 

Excessive

Distal

Atelectasis

Capillary Membrane

Bronchospasm Bronchial

Airway

Disorder

Consolidation

 

 

 

Thickness

 

Secretions

Weakening

Chronic bronchitis

 

 

 

X*

X

 

Emphysema

 

 

 

X

X*

X

Asthma

 

 

 

X

X

 

Cystic fibrosis

X*

 

 

X*

X

 

Bronchiectasis

X

X

 

X

X

 

Atelectasis

X

 

 

 

 

 

Pneumonia

 

X

X

 

X*

 

Tuberculosis

 

X

X

 

 

 

Pulmonary edema

X

 

X

 

X

 

Pulmonary embolism

X

 

 

X

 

 

Flail chest

X

X

 

 

 

 

Pneumothorax

X

 

 

 

 

 

Pleural diseases

X

 

 

 

 

 

Kyphoscoliosis

X

 

 

 

X*

 

Cancer of the lung

X

X

 

 

X

 

Interstitial lung

 

 

X

X*

 

 

diseases

 

 

 

 

 

 

Acute respiratory

X*

X

X

 

 

 

distress syndrome

 

 

 

 

 

 

Guillain-Barré

X*

X*

 

 

X*

 

syndrome

 

 

 

 

 

 

Myasthenia gravis

X*

X*

 

 

X*

 

Meconium aspiration

X

X

 

 

X

 

syndrome

 

 

 

 

 

 

Transient tachypnea

 

 

X

 

X

 

of newborn

 

 

 

 

 

 

Respiratory distress

X

X

 

 

X

 

syndrome

 

 

 

 

 

 

Pulmonary air leak

X

 

 

 

 

 

syndromes

 

 

 

 

 

 

Respiratory syncytial

X

X

 

 

X

 

virus

 

 

 

 

 

 

Bronchopulmonary

X

 

X

 

X

 

dysplasia

 

 

 

 

 

 

Congenital

X

 

 

 

 

 

diaphragmatic

 

 

 

 

 

 

hernia

 

 

 

 

 

 

Near drowning

X

X

X

X

 

 

Smoke inhalation and

X

X

X

X

 

 

thermal injuries

 

 

 

 

 

 

*Common secondary anatomic alterations of the lungs associated with this disorder.

Fig. 10.13 provides a three-component overview model of a prototype airway to further enhance the reader's visualization of anatomic alterations of the lungs commonly associated with obstructive respiratory disorders (e.g., asthma, bronchitis, or emphysema) and the treatment plans commonly used to offset them.

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FIGURE 10.13 A three-component model of a prototype airway. Therapy may be directed at any or all components. (A) Airway lumen. (B) Airway wall. (C) Supporting structures. Therapy for A includes deep breathing and coughing, smoking cessation, suctioning, mucolytics, bland aerosols, systemic and parenteral hydration, and therapeutic bronchoscopy. Therapy for B includes bronchodilators, aerosolized antiinflammatory agents, aerosolized antibiotics, and aerosolized decongestants. Therapy for C includes pursed-lip breathing exercises (e.g., when the elastic recoil of the lungs is absent in emphysema—as represented by the broken spring in the upper left corner) and removal of external factors compressing the airway (e.g., bullae, pleural effusion, pneumothorax, tumor masses).

Self-Assessment Questions

1.Which of the following pathophysiologic mechanisms is/are associated with the “atelectasis” clinical scenario?

1.Air trapping

2.Decreased ventilation-perfusion ratio

3.Deflation reflex

4.Irritant reflex

a.1 and 4 only

b.2 and 3 only

c.1 and 4 only

d.2, 3, and 4 only

2.Which of the following clinical manifestations is/are associated with the “excessive bronchial secretions” clinical scenario?

1.Translucent radiographs

2.Increased forced vital capacity

3.Pursed-lip breathing

4.Air bronchograms

a.1 and 4 only

b.1 and 3 only

c.2, 3, and 4 only

d.1, 2, 3, and 4

3.Which of the following clinical manifestations is/are associated with the “atelectasis” clinical scenario? 1. Increased opacity in chest x-ray

2.Decreased forced vital capacity

3.Bronchial breath sounds

4.Diminished heart sounds

a.1 and 4 only

b.2 and 3 only

c.1, 2, and 3 only

d.2, 3, and 4 only

4.Which of the following pathophysiologic mechanisms is/are associated with the “bronchospasm” clinical scenario?

1.Air trapping

2.Decreased ventilation-perfusion ratio

3.Increased airway resistance

4.Irritant reflex

a.1 and 4 only

b.2 and 3 only

c.2, 3, and 4 only

d.1, 2, 3, and 4

5.Which of the following clinical manifestations is/are associated with the “distal airway and alveolar weakening” clinical scenario?

1.Diminished breath sounds

2.Decreased residual volume