Lung Expansion Therapy

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Chapter 39

Lung Expansion Therapy

Daniel F. Fisher

Chapter Objectives

After reading this chapter you will be able to:

Describe the various causes of atelectasis.

Identify which patients need lung expansion therapy.

Define the clinical findings seen in atelectasis.

Describe how lung expansion therapy works.

List the indications, hazards, and complications associated with the various modes of lung expansion therapy.

Describe the primary responsibilities of the respiratory therapist in planning, implementing, and evaluating lung expansion therapy.

Pulmonary complications are common serious problems seen in patients who have undergone thoracic or abdominal surgery.1,2 Such complications include atelectasis (alveolar collapse), pneumonia, and acute respiratory failure. These respiratory problems can be minimized or avoided if proper respiratory care is implemented during the perioperative period. The most common form of therapy used in high-risk patients is lung expansion therapy.

Lung expansion therapy encompasses a variety of respiratory care modalities designed to prevent or correct atelectasis. The most common modalities include deep breathing/directed cough, incentive spirometry (IS), continuous positive airway pressure (CPAP), positive expiratory pressure (PEP), and intermittent positive airway pressure breathing (IPPB). The common purpose that all of these techniques share is to guide the patient into improving pulmonary function by maximizing alveolar recruitment and optimizing airway clearance.

Various lung expansion therapies can be effective in preventing or correcting atelectasis in selected patients.¹ However, the precise method to apply in a given situation is not always clear because no advantage of any one method has been established. The most efficient use of resources is a primary concern with any plan to apply lung expansion therapy.

If all of the following therapies were to be compared, the common factor they share is that they all are designed to increase functional residual capacity (FRC). In other words, these all are supplemental techniques to simulate a deep breath or sigh. In an uncompromised patient, this mechanism is working effectively. In this context, the respiratory therapist (RT) plays a vital role. In consultation with the prescribing physician, the RT should assist in identifying patients most likely to benefit from lung expansion therapy, recommend and initiate the appropriate and most efficient therapeutic approach, monitor the patient’s response, and alter the treatment regimen as needed.

Causes and Types of Atelectasis

Although atelectasis can occur from a large variety of problems, this chapter focuses on the two primary types associated with postoperative or bedridden patients who are breathing spontaneously without mechanical assistance: (1) gas absorption atelectasis and (2) compression atelectasis. Gas absorption atelectasis can occur either when there is a complete interruption of ventilation to a section of the lung or when there is a significant shift in ventilation/perfusion (). Gas distal to the obstruction is absorbed by the passing blood in the pulmonary capillaries, which causes partial collapse of the nonventilated alveoli. When ventilation is compromised to a larger airway or bronchus, lobar atelectasis can develop.

Compression atelectasis results when the forces within the chest wall and lung—specifically, the pleural pressure—are exceeded by the transmural pressure, which is what distends and maintains the alveoli in an open state.2–4 Compression atelectasis is primarily caused by persistent use of small tidal volumes by the patient. This situation is common when general anesthesia is given, with the use of sedatives and bed rest, and when deep breathing is painful, as when broken ribs are present or surgery has been performed on the upper abdominal region. Weakening or impairment of the diaphragm can also contribute to compression atelectasis. Compression atelectasis results when the patient does not periodically take a deep breath and expand the lungs fully. It is a common cause of atelectasis in hospitalized patients. It may occur in combination with gas absorption atelectasis in a patient with excessive airway secretions who breathes with small tidal volumes for a prolonged period.

Factors Associated With Causing Atelectasis

Atelectasis can occur in any patient who cannot or does not take deep breaths periodically and in patients who are restricted to bed rest for any reason.⁵ Patients who have difficulty taking deep breaths without assistance include patients with significant obesity, patients with neuromuscular disorders or who are under heavy sedation, and patients who have undergone upper abdominal or thoracic surgery. Diaphragmatic position and function is the major contributor to the onset of atelectasis. In an anesthetized patient, there is a cephalad (toward the head) shift of the diaphragm. For patients who are supine, the lower, dependent portion of the diaphragm performs the most movement. The opposite occurs in patients who are paralyzed—the upper portion of the diaphragm is involved in movement.^3,4 Patients undergoing lower abdominal surgery are at less risk for atelectasis than patients undergoing upper abdominal or thoracic surgery, but they still may be at significant risk. Patients with spinal cord injury are prone to respiratory complications, the most common of which is atelectasis. Bedridden patients, such as patients recovering from major trauma, are particularly predisposed to developing atelectasis secondary to lack of mobility. Atelectasis is one of the most important determinants of hypoxemia after abdominal surgery and may account for 24% of deaths within 6 days of surgery.⁶ It is clinically prudent to consider atelectasis in every assessment of postoperative patients.

Impairment of the function of pulmonary surfactant can also have an impact on the development of atelectasis. Surfactants decrease the surface tension of the walls of the alveoli. When there is deterioration of the function of this vital protein, the relative increase in surface tension can cause the walls of the alveoli to collapse.⁴

Most postoperative patients also have problems coughing effectively because of their reduced ability to take deep breaths. An ineffective cough impairs normal clearance mechanisms and increases the likelihood of retained secretions, which could lead to the development of gas absorption atelectasis in a patient with excessive mucus production. Patients with a history of lung disease that causes increased mucus production (e.g., chronic bronchitis) are most prone to develop complications in the postoperative period. Similarly, a significant history of cigarette smoking should alert the RT to the high risk for respiratory complications with surgery. Such patients must be identified in the preoperative period and considered strong candidates for airway clearance and lung expansion therapy. Elective surgery for these patients may need to be postponed in some cases until such therapies can be included in the treatment plan. Lung expansion therapy and chest physical therapy in the postoperative period may help improve clearance of secretions by improving the effectiveness of coughing and secretion removal.

Rule of Thumb

The closer the incision is to the diaphragm, the greater the risk for postoperative atelectasis. Patients with a history of inadequate nutritional intake, as shown by an albumin level less than 3.2 mg/dl, have an increased risk for pulmonary complications in the postoperative period. This increased risk is most likely due to inadequate strength of the inspiratory muscles to maintain a normal FRC and VC.

Mini Clini

Risk Factors for Atelectasis

Problem

The RT is called to evaluate a 47-year-old obese man admitted to the hospital for upper abdominal surgery. He has a 60 pack-year smoking history and is scheduled for surgery tomorrow morning. Examination reveals bilateral inspiratory and expiratory coarse crackles and expiratory wheezes. He is alert and oriented with normal vital signs. His past medical history is positive for diabetes and kidney stones. What factors are present that predispose this patient for postoperative atelectasis, and what treatment plan should the RT recommend?

Discussion

Several important risk factors are present in this patient. The three most important are positive smoking history, obesity, and the site of surgery (upper abdomen). The findings of adventitious lung sounds and positive smoking history are very suggestive of a current pulmonary problem that would probably require bronchial hygiene, humidity therapy, and bronchodilators before surgery. Delaying the surgery may be necessary if significant secretion retention is present. Postoperatively, this high-risk patient would need careful monitoring and IS to minimize the risk of atelectasis.

Clinical Signs of Atelectasis

RTs must be able to recognize the clinical signs of atelectasis in patients so that appropriate therapy can be implemented in a timely fashion. The patient’s medical history often provides the first clue in identifying atelectasis. Recent upper abdominal or thoracic surgery in any patient should suggest possible atelectasis. A history of chronic lung disease or cigarette smoking or both provides additional evidence that the patient is prone to respiratory complications after major surgery or prolonged bed rest.

The physical signs of atelectasis may be absent or very subtle if the patient has minimal atelectasis. When the atelectasis involves a more significant portion of the lungs, the patient’s respiratory rate increases proportionally. Fine, late-inspiratory crackles may be heard over the affected lung region. These crackles are produced by the sudden opening of distal airways with deep breathing. Bronchial-type breath sounds may be present as the lung becomes more consolidated with atelectasis. Diminished breath sounds are common when excessive secretions block the airways and prevent transmission of breath sounds. Tachycardia may be present if atelectasis leads to significant hypoxemia. Patients with preexisting lung disease often present with significant abnormalities in respiratory and heart rates, even when atelectasis is not severe.

Rule of Thumb

There is a direct relationship between the spontaneous respiratory rate and the degree of atelectasis present. Typically, as atelectasis progresses, respiratory rate increases proportionally.

The chest radiograph is often used to confirm the presence of atelectasis. The atelectatic region of the lung has increased opacity. Evidence of volume loss is present in patients with significant atelectasis. Direct signs of volume loss on the chest film include displacement of the interlobar fissures, crowding of the pulmonary vessels, and air bronchograms. Indirect signs include elevation of the diaphragm; shift of the trachea, heart, or mediastinum; pulmonary opacification; narrowing of the space between the ribs; and compensatory hyperexpansion of the surrounding lung.

Lung Expansion Therapy

All modes of lung expansion therapy increase lung volume by increasing the transpulmonary pressure (Pl) gradient. As detailed elsewhere in this text, P_L gradient represents the difference between the alveolar pressure (Palv) and the pleural pressure (Ppl):

< ?xml:namespace prefix = "mml" />PL=Palv−Ppl

With all else being constant, the greater the Pl gradient, the more that the alveoli expand.

As depicted in Figure 39-1, the Pl gradient can be increased by either (1) decreasing the surrounding Ppl (see Figure 39-1, A) or (2) increasing the Palv (see Figure 39-1, B). A spontaneous deep inspiration increases the Pl gradient by decreasing the Ppl. The application of positive pressure to the lungs increases the Pl gradient by increasing the pressure inside the lung.

FIGURE 39-1 Transpulmonary pressure gradients with spontaneous inspiration **(A)** and positive pressure inspiration **(B).**

All lung expansion therapies use one of these two approaches. IS enhances lung expansion via a spontaneous and sustained decrease in Ppl. Positive airway pressure techniques increase Palv in an effort to expand the lung. Positive pressure lung expansion therapies may apply pressure during inspiration only (as in IPPB), during expiration only (as in PEP and expiratory positive airway pressure [EPAP]), or during both inspiration and expiration (CPAP). Although all of these approaches are used in lung expansion therapy, the methods that decrease Ppl (e.g., IS) have more of a physiologic effect than the methods that increase Palv and often are most effective. However, they require an alert, cooperative patient who is capable of taking a deep breath.

The goal of any lung expansion therapy should be to implement a plan that provides an effective strategy in the most efficient manner. Staff time and equipment are the two major issues related to efficiency. For a patient with minimal risk of postoperative atelectasis, deep breathing exercises, frequent repositioning, and early ambulation are usually effective and can be done with minimal coaching and time from clinicians and without equipment.⁴ For a patient at high risk for atelectasis (e.g., a patient undergoing upper abdominal surgery), IS is usually instituted. The additional staff time and equipment are justified in this high-risk group. Positive pressure therapy requires significantly more staff time and equipment and is reserved for high-risk patients who cannot perform IS techniques. The remainder of this chapter describes the use of IS and positive pressure therapy for the prevention or correction of atelectasis.

Incentive Spirometry

The purpose of IS is to guide the patient to take a sustained maximal inspiratory effort resulting in a decrease in Ppl and maintain the patency of airways at risk for closure. Because of its simplicity, IS has been the mainstay of lung expansion therapy for many years. IS devices are designed to mimic natural sighing by encouraging patients to take slow, deep breaths. IS can be performed using devices that provide visual cues to patients when the desired inspiratory flow or volume has been achieved. IS has been shown to be an efficient and effective prophylaxis against postoperative atelectasis in high-risk patients.⁵ The first documented use of incentive spirometry as a therapy was in 1972, and this led to the development of a visual feedback device in 1973.⁷

The desired volume and number of repetitions to be performed are initially set by the RT or other qualified caregiver. The inspired volume goal is set on the basis of predicted values or observation of initial performance. The true benefit from IS is best achieved by repeated use and proper technique.⁸ The American Association for Respiratory Care (AARC) has developed and published a clinical practice guideline on IS; excerpts from this guideline appear in Clinical Practice Guideline 39-1.

39-1 Incentive Spirometry

AARC Clinical Practice Guideline (Excerpts)*

Indications

• Presence of conditions predisposing to the development of pulmonary atelectasis (upper abdominal surgery, thoracic surgery, surgery in patients with COPD)

• Presence of pulmonary atelectasis

• Presence of restrictive lung defect associated with quadriplegia or dysfunctional diaphragm

Contraindications

• Patient cannot be instructed or supervised to ensure appropriate use of device

• Patient cooperation is absent, or patient is unable to understand or demonstrate proper use of device

• Patient is unable to deep breathe effectively (e.g., with VC < 10 ml/kg or IC < predicted)

• Presence of an open tracheal stoma is not a contraindication but requires adaptation of the spirometer

Hazards and Complications

• Ineffective unless closely supervised or performed as ordered

• Inappropriate as sole treatment for major lung collapse or consolidation

• Hyperventilation

• Barotrauma (emphysematous lungs)

• Discomfort secondary to inadequate pain control

• Hypoxia owing to break in mask O₂ therapy

• Exacerbation of bronchospasm

• Fatigue

Assessment of Need

• Surgical procedure involving upper abdomen or thorax

• Conditions predisposing to atelectasis, including immobility, poor pain control, and abdominal binders

• Presence of neuromuscular disease involving respiratory musculature

Assessment of Outcome

• Absence of or improvement in signs of atelectasis

• Decreased respiratory rate

• Resolution of fever

• Normal pulse rate

• Absence of crackles or presence of or improvement in previously absent or diminished breath sounds

• Normal chest radiograph

• Improved PaO₂ and decreased alveolar-arterial O₂ tension gradient

• Increased VC and peak expiratory flows

• Return of FRC or VC to preoperative values, in absence of lung resection

• Improved inspiratory muscle performance (e.g., attainment of preoperative flow and volume levels, increased FVC)

Monitoring

Direct supervision of every patient performance is unnecessary after the patient has demonstrated mastery of technique; however, preoperative instruction, volume goals, and feedback are essential to optimal performance.

• Observation of patient performance and use

• Frequency of sessions

• Number of breaths per session

• Inspiratory volume or flow goals achieved and 3- to 5-second breath hold maintained

• Effort and motivation

• Periodic observation of patient compliance with technique, with additional instruction as necessary

• Device within reach of patient and patient encouraged to perform independently

• New and increasing inspiratory volumes established each day

• Vital signs

^*For complete guidelines, see American Association for Respiratory Care: Clinical practice guidelines: incentive spirometry. Respir Care 36:1402, 1991.

Physiologic Basis

The basic maneuver of IS is a sustained maximal inspiration (SMI). An SMI is a slow, deep inhalation from the functional residual capacity (FRC) up to (ideally) the total lung capacity, followed by a 5- to 10-second breath hold. An SMI is functionally equivalent to performing an inspiratory capacity (IC) maneuver, followed by a breath hold. Figure 39-2 compares the alveolar and Ppl changes occurring during a normal spontaneous breath and an SMI during IS.

FIGURE 39-2 Alveolar *(solid lines)* and pleural *(dotted lines)* pressure changes during spontaneous breathing *(A)* and SMI *(B)*. Note the difference in Pl gradients *(double arrows)*.

During the inspiratory phase of spontaneous breathing, the decrease in Ppl caused by expansion of the thorax is transmitted to the alveoli. With Palv now negative, a pressure gradient is created between the airway opening and the alveoli. This transrespiratory pressure gradient causes gas to flow from the airway into the alveoli. Within certain limits, the greater the transrespiratory pressure gradient, the more that lung expansion occurs.

Indications

Indications for IS are listed in Box 39-1. The primary indication for IS is to treat existing atelectasis. IS may also be used as a preventive measure when conditions exist that make the development of atelectasis likely.⁶

Box 39-1 Indications for Incentive Spirometry

• Presence of pulmonary atelectasis

• Presence of conditions predisposing to atelectasis

• Upper abdominal surgery

• Thoracic surgery

• Surgery in patients with COPD

• Presence of a restrictive lung defect associated with quadriplegia or dysfunctional diaphragm

Contraindications

IS is a simple and safe modality. For this reason, contraindications are few (Box 39-2).

Box 39-2 Contraindications for Incentive Spirometry

• Patient cannot be instructed or supervised to ensure appropriate use of device

• Patient cooperation is absent, or patient is unable to understand or demonstrate proper use of device

• Patients unable to deep breathe effectively (VC < 10 ml/kg or IC < predicted)

Hazards and Complications

Given its normal physiologic basis, IS presents few major hazards and complications; those that can occur are listed in Box 39-3. Acute respiratory alkalosis is the most common problem and occurs when the patient performs IS too rapidly. Dizziness and numbness around the mouth are the most frequently reported symptoms associated with respiratory alkalosis. This problem is easily corrected with careful instruction and monitoring of the patient. Discomfort with deep inspiratory efforts secondary to pain is usually the result of inadequate pain control in a postoperative patient. This problem can be rectified by ensuring appropriate analgesia. In addition, pain medication should be coordinated with IS activity.

Box 39-3 Hazards and Complications of Incentive Spirometry

• Hyperventilation and respiratory alkalosis

• Discomfort secondary to inadequate pain control

• Pulmonary barotrauma

• Exacerbation of bronchospasm

• Fatigue