Physical Therapy for a Patient in Acute Respiratory Failure.

This case report highlights the potential role and contributions of 24-hour access to physical therapy by patients who have acute respiratory failure.

Physical therapy may be indicated for patients in the intensive care setting when they have retained secretions and radiological evidence of atelectasis or infiltrate, or as prophylaxis in conditions such as acute head injury and smoke inhalation.[1] Physical therapy interventions include postural drainage, breathing exercises, percussion, vibration, manual hyperinflation, coughing, huffing, and suction. Body positioning, which primarily aims to optimize ventilation-perfusion ratios, and mobilization and exercise are physical therapy interventions not traditionally considered as part of the treatment for these patients. Dean,[2] based on extensive reviews of physiologic evidence, concluded that body positioning and mobilization and exercise should be the first-line interventions for patients with cardiopulmonary system dysfunctions.

Few studies have examined the effectiveness of physical therapy interventions for patients who are critically ill and in intensive care units (ICUs). Mackenzie and colleagues[3-5] applied physical therapy, consisting of postural drainage, percussion, vibration, and suction, to patients with atelectasis, lung contusions, pneumonia, and acute respiratory distress syndrome. Each session of physical therapy lasted about an hour. They concluded that treatment resulted in a decrease in intrapulmonary shunt,[4] an increase in total lung/thorax compliance(*) for up to 2 hours,[4,5] resolution of radiographically visible infiltrates,[3] and no adverse cardiopulmonary complications.[3,4] None of their studies, however, included a control group. Stiller and colleagues[6,7] investigated the most effective combination of physical therapy interventions for treating patients with acute lobar atelectasis. They demonstrated that physical therapy consisting of modified postural drainage (without head-down tilt), manual hyperinflation, and suction (or, for patients who were not intubated, modified postural drainage, deep breathing, coughing, and huffing, interspersed with relaxed breathing) led to greater radiographically visible resolution of lobar atelectasis compared with physical therapy that did not include modified postural drainage or physical therapy that also included chest wall vibration.[6,7] Furthermore, physical therapy administered hourly for 6 hours was shown to be more effective than physical therapy given once in 6 hours.[6]

Several researchers also have documented the adverse effects of physical therapy on oxygenation[8] and hemodynamic stability[9-13] in patients with respiratory or hemodynamic compromise needing airway clearance. In these studies, physical therapy consisted of percussion and suction in both side-lying positions. This combination of interventions, which is different from the physical therapy administered in the other studies cited, is questionable because alternate side-lying positioning is not specific to the underlying lung pathology and percussion alone has been shown to cause atelectasis,[14] cardiac arrhythmias,[15] and fewer benefits compared with other physical therapy interventions such as manual hyperinflation.[16] Instead, percussion (and vibration), if indicated (especially for facilitating movement of secretions), should be applied during deep breathing and interspersed with relaxed breathing (also known as "breathing control"). These techniques are used in conjunction with coughing and huffing, in a series of maneuvers called "active cycle of breathing techniques."[17] The cycle begins and ends with breathing control. Deep breathing exercises with or without percussion and vibration are included in the cycle. The cycle continues until coughing or huffing is dry and nonproductive. The active cycle of breathing techniques has been shown to be effective in secretion clearance in patients with cystic fibrosis.[17,18] These techniques may be useful for other patients who are not intubated and ventilated.

In recent years, physical therapy services for patients with respiratory failure have come under scrutiny as a result of limited financial resources.[19] In 1991, the Task Force on Guidelines of the Society of Critical Care Medicine recommended "24 hr/day availability of measures aimed at pulmonary secretion control, specifically chest physiotherapy and postural drainage"[20(p276)] for patients with acute respiratory failure on mechanical ventilatory support. In reality, physical therapy is not always available 24 hours a day. In Australia, for instance, 24-hour access to physical therapy was available in 19 (45%) out of 42 hospitals surveyed.[21] Five other hospitals (12%) provided physical therapy after normal working hours, but these hours were limited to 5:00 to 9:00 PM or 5:00 PM to midnight.[21] In hospitals that previously had 24-hour access, physical therapy was reduced to cover from 4:00 PM to 11:00 PM.[22] The purpose of this case report is to document the contributions of 24-hour availability of physical therapy to the care of a patient with acute respiratory failure in an intensive care setting.

Case Description

Subject and History

The patient was a 66-year-old Chinese man. He was originally admitted via the emergency department for increasing dyspnea that was associated with productive coughs of a large amount of mucopurulent sputum. He was diagnosed, based on the chest radiograph on admission, as having a moderate pneumothorax (20%) on the right side. He had a history of chronic obstructive pulmonary disease (COPD), and spontaneous pneumothorax is not uncommon. Re-expansion of the lung was immediate following chest tube insertion.

A day after re-expansion of the lung, he complained of pain arising from chest tube insertion, inability to urinate, and severe dyspnea. A urinary catheter was inserted, resulting in passage of urine (200 cc from 7:30 AM to 2:30 PM on that day), and subsequently dyspnea was relieved. Analgesics were prescribed to relieve his pain. Two days later, the urinary catheter was removed. That night, he experienced severe abdominal pain, with elevated serum creatine phosphokinase (CPK) (279 U [multiplied by] [L.sup.-1]; normal range=40-210 U [multiplied by] [L.sup.-1]), but normal levels of aspartate aminotransferase (25 U [multiplied by] [L.sup.-1]; normal range=15-33 U [multiplied by] [L.sup.-1]) and lactate dehydrogenase (295 U [multiplied by] [L.sup.-1]; normal range=180-380 U [multiplied by] [L.sup.-1]). His prothrombin time (14.7 seconds; normal range=11-14 seconds) and partial thromboplastin time (PTT) (34.5 seconds; normal range=21-32 seconds) were elevated. His white blood cell count (14.66 x [10.sup.9] [multiplied by] [L.sup.-1]; normal range =4-10 x [10.sup.9] [multiplied by] [L.sup.-1]) and differential counts, which included neutrophils (75%; normal range=40%-75%), monocytes (10.1%; normal range=2%-10%), and basophils (1.1%; normal range=0%-1%), also were elevated. An inverted T wave in the [V.sub.2] lead was observed on the electrocardiograph (ECG), possibly indicating myocardial ischemia.

The primary physician, with the assistance of the medical team, considered diagnoses of acute intestinal obstruction, perforated abdomen, or acute myocardial infarction. The team ruled out a cardiac event because (1) the patient did not have symptoms of angina, (2) his CPK level was only slightly elevated, and (3) no abnormal ST segments were recorded on the ECG. Furthermore, palpation of the patient's abdomen showed it was tender with muscle guarding. The decision was then made to undertake an exploratory laparotomy. Intraoperatively, he was observed to have a "wheezy and tight" chest and an unstable systemic blood pressure, with systolic blood pressure plummeting from 160 mm Hg to 90 mm Hg and diastolic blood pressure dropping from 90 mm Hg to 40 mm Hg. Nebulized Ventolin([dagger]) (1 mL in 1 mL of normal saline given every 4 hours) and intravenously administered aminophylline (250 mg in 12 hours) were given to relieve acute bronchospasm. Dopamine, a catecholamine that improves blood pressure, was administered intravenously at 10 [micro]g [multiplied by] [kg.sup.-1] [multiplied by] [min.sup.-1]. The laparotomy yielded nothing abnormal. He was subsequently transferred to the surgical ICU for observation. Postoperatively, he developed an episode of supraventricular tachycardia (170 beats per minute), which was treated with intravenous administration of verapamil (3 mg), a calcium channel blocker that slows the ventricular response. When the patient was awake, in addition to his abdominal pain, he complained of pain from the operative site. His hemodynamic status was stabilized sufficiently to return to the high-dependency unit (HDU) a day later.

The evening following surgery, while the patient was still in the HDU, he became severely dyspneic, with a respiratory rate of over 35 breaths per minute and a pulse oxygen saturation (Sp[O.sub.2]) of 60% on fraction of inspired oxygen ([FIO.sub.2]) of 1.0 administered via a nonrebreathing face mask. His arterial blood gases were pH 7.37, his arterial carbon dioxide tension (Pa[CO.sub.2] was 26.4 mm Hg, his arterial oxygen tension (Pa[O.sub.2] was 39.7 mm Hg, and his arterial oxygen saturation (Sa[O.sub.2] 74.8%. The patient was in type I respiratory failure (hypoxemia without hypercapnia). He was also hyperventilating, thus resulting in a lowered Pa[CO.sub.2]. When he became tachycardiac and hypotensive, he was transferred to the ICU with the intention of providing mechanical ventilation and hemodynamic stabilization. There were widespread tactile fremitus and coarse crackles on auscultation. Aspiration was unlikely to be the reason for his respiratory distress, as he was still under an order to receive nothing by mouth. He was severely distressed and had difficulty expectorating. The medical diagnosis was acute respiratory failure, possibly from a chest infection. On consultation with the physical therapist in the ICU, the medical staff decided to delay intubation and try antibiotic therapy and intensive physical therapy.

Physical Therapy Examination

During the interview and conversations with the patient, he became dyspneic while trying to respond verbally to the therapist's questions. Dyspnea was further exacerbated by abdominal pain and coughing. The patient was a cooperative gentleman who followed instructions except when they might cause him to become more dyspneic, such as moving in bed, turning, and coughing. He appeared to be poorly nourished, as indicated by his emaciated appearance, his report that he ate poorly because of his dyspnea, and his "nothing by mouth" order following surgery. He required some assistance to move in bed. His temperature was 37.6 [degrees] C (99.7 [degrees] F). Sinus tachycardia with a rate of 143 beats per minute was recorded. Systemic blood pressure was 121/53 mm Hg. Respiratory rate was 28 to 30 breaths per minute, and Sp[O.sub.2] ranged from 88% to 100% on 8 L [multiplied by] [min.sup.-1] of oxygen ([FIO.sub.2] = 1.0) via the nonrebreathing face mask. His cough was labored and moist, but unproductive. Upper chest breathing was evident, with no basal expansion on palpation. On auscultation, breath sounds were absent on the right lateral and posterior basal segments and decreased on the left posterior basal segments, with occasional low-pitched wheezes.

His chest radiograph (Fig. 1) showed loss of right-sided hemidiaphragm, silhouette signs on the right heart border, and blunting of costophrenic angles. His arterial blood gases at entry into the ICU, but before physical therapy, showed compensated respiratory acidosis (pH=7.346, Pa[CO.sub.2]=57.8 mm Hg, Pa[O.sub.2]=106.7 mm Hg, Sa[O.sub.2]=98.5%, base excess=8.2). Alveolar-arterial oxygen difference (Aa[DO.sub.2], based on an unabridged version of the alveolar gas equation,[23] was estimated to be 196.1 mm Hg. The Aa[DO.sub.2] describes the efficiency of gas exchange[23] and thus enables clinicians to distinguish between hypoxemia due to hypoventilation and hypoxemia due to impaired gas exchange. His white blood cell count was elevated at 19.38 x [10.sup.9] [multiplied by] [L.sup.-1], although hemoglobin (12.5 g [multiplied by] d[L.sup.-1]), red blood cell count (4.42 x [10.sup.12] [multiplied by] [L.sup.-1]), and platelet count (315 x [10.sup.9] [multiplied by] [L.sup.-1]) were within acceptable limits. His bleeding times, prothrombin time and PTT (17.4 seconds and 34.8 seconds, respectively), remained elevated.

[Figure 1 ILLUSTRATION OMITTED]

The patient's main problems were assessed to be impaired gas exchange arising from atelectasis, chest infection, and difficulty of expectoration, which resulted in secretion retention. Difficulty of expectoration could be due to pain from the laparotomy incision, leading to poor alveolar hypoventilation and atelectasis. His ineffective cough could also be due to abdominal muscle weakness as a result of poor nutrition (from surgery and COPD) and fear of dyspnea. Patients with COPD often eat poorly because of dyspnea, and he had been on a "nothing by mouth" order following his abdominal surgery; it was then 7 days postadmission. He had general muscle weakness, possibly from prolonged bed rest for his medical and surgical conditions.

The short-term physical therapy goal was to reduce the gas exchange impairment by optimizing the ventilation-perfusion ratio, decreasing his work of breathing, instructing him on effective coughing or huffing, removing or facilitating removal of secretions, and educating him on self-administered bronchial hygiene within exercise tolerance. The long-term goals, when he became less dyspneic, were to assess and improve exercise tolerance and to facilitate independent management of dyspnea and bronchial hygiene.

Intervention

Physical therapy intervention was based on Dean's physiologic treatment hierarchy for patients with impaired oxygen transport (Tab. 1).[2] The upright position was considered the position of choice for intervention because the patient's arousal was at its greatest, his ventilation-perfusion ratio was optimal, and his diaphragm muscle excursion was maximal in an upright position. His work of breathing was also reduced in that position. The active cycle of breathing techniques was incorporated with periods of breathing control, deep breathing, mobilization/exercise, and cough (Fig. 2).

[Figure 2 ILLUSTRATION OMITTED]

Table 1.

Dean's Hierarchy for Treatment of Patients With Impaired Oxygen Transport(a)

Premise: Position of optimal physiological function is
being upright and moving

I.      Mobilization and Exercise

Goal:   To elicit an exercise stimulus that addresses one of the
        three effects on the various steps in the oxygen
        transport pathway, or some combination

        A. Acute effects
        B. Long-term effects
        C. Preventative effects

II.     Body Positioning

Goal:   To elicit a gravitational stimulus that simulates being
        upright and moving as much as possible (ie, active,
        active assisted, or passive)

        A. Hemodynamic effects related to fluid shifts
        B. Cardiopulmonary effects on ventilation and its
           distribution, perfusion, ventilation, and perfusion
           matching and gas exchange

III.    Breathing Control Maneuvers

Goal:   To augment alveolar ventilation, faciliate mucociliary
        transport, and stimulate coughing

        A. Coordinated breathing with activity and exercise
        B. Spontaneous eucapnic hyperventilation
        C. Maximal tidal breaths and movement in three
           dimensions
        D. Sustained maximal inspiration
        E. Pursed lip breathing to end-tidal expiration
        F. Incentive spirometry

IV.     Coughing Maneuvers

Goal:   To facilitate mucociliary clearance with the least effect
        on dynamic airway compression and adverse
        cardiovascular effects

        A. Active and spontaneous cough with closed glottis
        B. Active assist (self-supported or by other)
        C. Modified coughing interventions with open glottis
           (eg, forced expiratory technique, huff)

V.      Relaxation and Energy Conservation
        Interventions

Goal:   To minimize the work of breathing, of the heart, and
        oxygen demand overall

        A. Relaxation procedures at rest and during activity
        B. Energy conservation (ie, balance of activity to rest,
           performing activities in an energy-efficient
           manner, improved movement economy during
           activity)
        C. Pain control interventions

VI.     ROM Exercises (Cardiopulmonary Indications)

Goal:   To stimulate alveolar ventilation and alter its
        distribution

        A. Active
        B. Assisted active
        C. Passive

VII.    Postural Drainage Positioning

Goal:   To facilitate airway clearance using gravitational effects

        A. Bronchopulmonary segmental drainage positions

VIII.   Manual Techniques

Goal:   To facilitate airway clearance in conjunction with specific
        body positioning

        A. Autogenic drainage
        B. Manual percussion
        C. Shaking and vibration
        D. Deep breathing and coughing

IX.     Suctioning

Goal:   To facilitate the removal of airway secretions collected
        centrally

        A. Open suction system
        B. Closed suction system
        C. Tracheal tickle
        D. Instillation with saline
        E. Use of manual inflation bag (bagging)

(a) Reprinted with permission from Dean.[2(pp258-259)]

ROM = range of motion.

During the breathing control period, the patient was instructed to perform normal tidal breathing using the lower chest wall and to relax his upper chest and shoulders. Verbal input and tactile input (ie, the therapist's hand was placed over the patient's abdomen) were given until the patient was able to achieve breathing control. During deep breathing, the patient was instructed to inhale deeply (ie, slowly over 3-5 seconds) to inspiratory reserve volume (when he began using his accessory muscles) and exhale passively. The emphasis was on lower chest wall expansion. Three to four repetitions of deep breathing were followed by a period of breathing control.

Percussion and expiratory vibration techniques were initially incorporated to assist secretion mobilization, but he was unable to tolerate these techniques and responded with increased dyspnea. Percussion and vibration were omitted from the active cycle of breathing. Mobilization and exercise in the form of arm elevation and thoracic mobility (rotation) exercises (10-20 times or as tolerated) were prescribed to optimize the various steps of the oxygen transport system, particularly to stimulate maximal inspiration and facilitate mucociliary transport rate. Active mobilization and exercise were also safer than continuing with percussion because of the patient's elevated prothrombin time and PTT and, therefore, risk of bleeding. Physical therapy sessions were kept short, about 20 minutes in duration. Repetitions of exercises were progressively increased as the patient's dyspnea improved and he was more able to tolerate the physical therapy program. The patient's heart rate, blood pressure, respiratory rate, and Sp[O.sub.2] were monitored for responses to mobilization and exercise. Instead of hourly intervention, as advocated in the literature,[6,7] intervention occurred every 2 hours because the patient was too dyspneic to tolerate more frequent sessions and to allow the nebulized Ventolin to achieve maximal bronchodilator effects between sessions. Analgesia was provided by bolus intravenous administration of morphine as required (ie, by patient's complaint) before, during, or after physical therapy. Morphine was administered by the nursing staff.

Outcomes and Progress

On the patient's first day in the ICU, a total of 6 treatment sessions were provided. The clinical tools used for establishing the outcomes of intervention were auscultation and chest radiographs, both of which have established reliability and validity.[24,25] Following the initial interventions, breath sounds increased in all segments on auscultation, chest radiographs showed resolution of infiltrates (Figs. 3 and 4), and oxygenation improved (Fig. 5). He was ready to be transferred out of the ICU after 2 days. His Aa[DO.sub.2] fell to 140.2 mm Hg by the time he was transferred out of the ICU and then to 22.2 mm Hg in the general ward, indicating that gas exchange was normalized. Coughing and huffing were initially assisted by anterior chest wall or lateral costal compressions. During the patient's 48-hour stay in the ICU, he could cough and huff independently when he became less dyspneic. He was producing a large amount of sputum ([is greater than] 30 mL per day). Early inspiratory to mid-inspiratory coarse crackles, primarily over the posterior basal regions on both sides, were still present, suggesting that pulmonary secretions were in the large airways. Wheezes were also heard after physical exertion. The patient was given physical therapy 5 times on the second day in the ICU and then 2 times when he was transferred out of the ICU into the general ward. Clinical improvements continued in the general ward (Fig. 5).

[Figures 3-5 ILLUSTRATION OMITTED]

When the patient became less dyspneic, further interviews and examination were attempted to ascertain his home situation for discharge planning. He was a retiree from a shipping company after serving as senior supervisor for over 30 years, He was unmarried and lived with his brother's family. He had no caregivers; his medical expenses were borne by his previous company. Although he claimed to have stopped smoking for 6 years after 40 pack-years of smoking (ie, 1 pack of cigarettes a day for 40 years), he was still smoking 1 to 2 cigarettes a day. He lived in a private residential apartment with an elevator taking him to the floor of his unit. He was not an active person; it appeared he spent most of his time conserving his energy. He was on long-term oxygen therapy (2-3 L [multiplied by] [min.sup.-1]) via nasal cannula for his COPD, and he independently managed his activities of daily living. At the time of his stay in the hospital, he was reluctant to do a 6-minute walk test, fearing his dyspnea might worsen. He would do upper-extremity and thoracic rotation exercises, but not exercises with thoracic flexion, extension, or lateral flexion because they made him breathless.

The patient stayed in the ICU for 48 hours, avoiding intubation and mechanical ventilation. His prothrombin time and PTT (15.7 seconds and 30.6 seconds, respectively) were improved with fresh frozen plasma. His resting heart rate was about 70 to 80 beats per minute with sinus rhythm. His dyspnea improved, but the abdominal pain, although it had subsided, was still present. By the time he returned to the general ward, his sputum had cultured positive for methicillin-resistant Staphylococcus aureus, and he was therefore isolated. Although the sputum specimen was obtained while he was still in the ICU, this finding suggested that he still had pulmonary secretion production. Therefore, it was important to reinforce effective coughing in this patient.

Physical therapy continued daily over the next 4 days with the aims of (1) improving expectoration using active cycle of breathing techniques, (2) facilitating independent bronchial hygiene (ability to independently clear airways through effective coughing and huffing efforts), and (3) reinforcing dyspnea management using body positioning (forward lean positions in sitting and standing) and energy conservation strategies (eg, more breaks, bursts of activities, breaking up complex tasks into simpler and smaller tasks, exhaling with activities) (Tab. 2). He was able to cough out his sputum on his own, the amount of which had become less ([is less than] 20 mL per day). His cough was strong, dry, and unproductive. He was encouraged to sit in a chair, instead of sitting in bed, and to walk short distances 3 to 4 times a day. He became fatigued easily and, therefore, stopped walking frequently; otherwise, he safely and independently walked about 10 m, often using pursed lip breathing to control his dyspnea. By the fifth day after he left the ICU, he was visited by the physical therapist twice to ensure independence in bronchial hygiene and dyspnea management. He was discharged on the same day. Overall, he received 21 sessions of physical therapy (ie, 11 sessions during his 48-hour stay in the ICU, 2 sessions daily for 4 days in the general ward, and 2 sessions on the day of discharge).

Table 2.

Chronology of Events During Patient's Hospitalization

  Day   Event

    1   Right-sided pneumothorax; chest tube inserted with
        immediate re-expansion of the chest

    2   Patient complained about inability to urinate; urinary
        catheter inserted

    4   Patient complained about severe abdominal pain

    5   Exploratory laparotomy was done; patient admitted to
        surgical intensive care unit (ICU) due to intraoperative
        and postoperative events

    7   Return to high-dependency unit; patient became
        dyspneic overnight; readmitted to surgical ICU

  8-9   Intensive physical therapy in ICU

10-13   Return to general ward

   14   Patient discharged

Discussion

During their initial discussions, the ICU physicians and the physical therapist acknowledged the patient's known chronic respiratory failure due to COPD, requiring long-term oxygen therapy. The physical therapist, with input from the ICU physicians, considered oxygenation, rather than ventilation, to be the patient's main problem. As a result, intubation and mechanical ventilation were postponed, and intensive physical therapy evaluation and treatment were requested. The decision, as it turned out, was prudent (Fig. 5) because weaning the patient with respiratory failure secondary to COPD from mechanical ventilation could be difficult.[26]

Physical therapy intervention in this case report was chiefly based on the work of Dean,[2] with adaptation of the active cycles of breathing techniques[17,18] to accommodate the patient's breathlessness. Dean's approach, although based on physiologic principles, has not been shown to be clinically beneficial. This case report has shown application of the technique and avoidance of invasive medical procedures.

The outcome of physical therapy (with 24-hour availability) in this case was consistent with the findings of a recent study that examined the effects of longer availability of physical therapy per day.[27] In that study, the effects of physical therapy administered twice during daytime working hours (8:30 AM to 5:00 PM) (n = 15) were compared with the effects of physical therapy administered twice during daytime working hours (8:30 AM to 5:00 PM) and at least once in the evening (5:00 PM to 9:00 PM) (n = 16).[27] The study demonstrated that elderly patients who had undergone abdominal surgery and who received additional physical therapy (consisting of body positioning; mobilization [getting patient out of bed]; and percussion, vibration, and coughing or airway suctioning) in the evening had lower intrapulmonary shunt, and therefore enhanced gas exchange, than those who received only daytime physical therapy. Patients receiving only daytime physical therapy also remained intubated longer ([bar]X=18.1 hours, SD=12.9 hours) than those receiving daytime and evening physical therapy ([bar]X=9.4 hours, SD=17.9 hours).[27] The study appeared to suggest that longer availability of physical therapy allowed for more frequent, and thus more effective, interventions.[27]

The patient in this report was admitted to the ICU for 2 days for an episode of acute respiratory failure. The cost of physical therapy during that time was $330 in Singapore currency ($198 in US currency) for 11 sessions. Had the patient been intubated and mechanically ventilated, the cost of the intubation procedure, monitoring of the mechanically ventilated patient, and physical therapy would have been $505 in Singapore currency ($303 in US currency) for the 2 days. Given the difficulty of weaning intubated patients with COPD from mechanical ventilation, it would be very likely for him to remain intubated and ventilated for longer than 48 hours, thus further escalating the cost.

In conclusion, the case report has highlighted the potential role and contributions of 24-hour access to physical therapy by patients who have acute respiratory failure. Invasive medical procedures were avoided with favorable clinical outcomes following interventions based on Dean's approach.

(*) Static total lung/thorax compliance ([C.sub.T]) was calculated as [C.sub.T]=(inspired volume - compressible volume) / (end-inspiratory "plateau" pressure - positive end-expiratory pressure).[5] Measurements were made before administration of physical therapy, immediately after physical therapy, and every half hour for up to 2 hours thereafter.[5]

([dagger]) Glaxo Wellcome Inc, Five Moore Dr, Research Triangle Park, NC 27709.

References

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[3] Mackenzie CF, Shin B, McAslan TC. Chest physiotherapy: the effect on arterial oxygenation. Anesth Analg. 1978;57:28-30.

[4] Mackenzie CF, Shin B. Cardiorespiratory function before and after chest physiotherapy in mechanically ventilated patients with post-traumatic respiratory failure. Crit Care Med. 1985;13:483-486.

[5] Mackenzie CF, Shin B, Hadi F, Imle PC. Changes in total lung/ thorax compliance following chest physiotherapy. Anesth Analg. 1980; 59:207-210.

[6] Stiller K, Geake T, Taylor J, et al. Acute lobar atelectasis: a comparison of two chest physiotherapy regimens. Chest. 1990;98:1336-1340.

[7] Stiller K, Jenkins S, Grant R, et al. Acute lobar atelectasis: a comparison of five physiotherapy regimens. Physiotherapy Theory and Practice. 1996;12:197-209.

[8] Connors AF Jr, Hammon WE, Martin RJ, Rogers RM. Chest physical therapy: the immediate effect on oxygenation in acutely ill patients. Chest. 1980;78:559-564.

[9] Weissman C, Kemper M, Damask MC, et al. Effect of routine intensive care interactions on metabolic rate. Chest. 1984;96:815-818.

[10] Swinamer DL, Phang PT, Jones RL, et al. Twenty-four hour energy expenditure in critically ill patients. Crit Care Med. 1987;15:637-643.

[11] Weissman C, Kemper M. The oxygen uptake-oxygen delivery relationship during ICU interventions. Chest. 1991;99:430-435.

[12] Weissman C, Kemper M, Harding J. Response of critically ill patients to increased oxygen demands: hemodynamic subsets. Crit Care Med. 1994;22:1809-1816.

[13] Horiuchi K, Jordan D, Cohen D, et al. Insights into the increased oxygen demand during chest physiotherapy. Crit Care Med. 1997;25: 1347-1351.

[14] Zidulka A, Chrome JF, Wight DW, et al. Clapping or percussion causes atelectasis in dogs and influences gas exchange. J Appl Physiol. 1989;66:2833-2838.

[15] Hammon WE, Connors AF Jr, McCaffree DR. Cardiac arrhythmias during postural drainage and chest percussion of critically ill patients. Chest. 1992;102:1836-1841.

[16] Jones AYM, Hutchinson RC, Oh TE. Effects of bagging and percussion on total static compliance of the respiratory system. Physiotherapy. 1992;78:661-666.

[17] Pryor JA, Webber BA, Hodson ME, Batten JC. Evaluation of the forced expiration technique as an adjunct to postural drainage in the treatment of cystic fibrosis. BMJ. 1979;2:417-418.

[18] Webber BA, Hofmeyr JL, Morgan MDL, Hodson ME. Effects of postural drainage, incorporating the forced expiration technique, on pulmonary function in cystic fibrosis. Br J Dis Chest. 1986;80:353-359.

[19] Alexander E, Weingarten S, Mohsenifar Z. Clinical strategies to reduce utilization of chest physiotherapy without compromising patient care. Chest. 1996;10:430-432.

[20] Task Force on Guidelines, Society of Critical Care Medicine. Guidelines for standards of care for patients with acute respiratory failure on mechanical ventilatory support. Crit Care Med. 1991;19: 275-278.

[21] Ntoumenopoulos G, Greenwood KM. Variation in the provision of cardiothoracic physiotherapy in Australian hospitals. Australian Journal of Physiotherapy. 1991;37:29-36.

[22] Prendergast M, O'Callaghan CM. An experience with an in-hospital evening physiotherapy service for patients with specific respiratory compromise [abstract]. Physiotherapy Canada. 1996;48(2):insert.

[23] Martin L. Abbreviating the alveolar gas equation: an argument for simplicity. Respir Care. 1985;30:964-968.

[24] Albaum MN, Hill LC, Murphy M, et al. Interobserver reliability of the chest radiograph in community-acquired pneumonia. Chest. 1996; 110:343-350.

[25] Brooks D, Thomas J. Interrater reliability of auscultation of breath sounds among physical therapists. Phys Ther. 1995;75:1082-1088.

[26] Hilbert G, Gruson D, Portel L, et al. Noninvasive pressure support ventilation in COPD patients with postextubation hypercapnic respiratory insufficiency. Eur Respir J. 1998; 11:1349-1353.

[27] Ntoumenopoulos G, Greenwood KM. Effects of cardiothoracic physiotherapy on intrapulmonary shunt in abdominal surgical patients. Australian Journal of Physiotherapy. 1996;42:291-303.

WP Wong, PT, BPhty(Hons), is Principal Physiotherapist, Physiotherapy Department, Singapore General Hospital, Outram Road, Singapore 169608, Singapore ([e-mail]).

Mr Wong provided concept/research design, writing, and data collection and analysis. He thanks the patient for the learning experience, the staff of the Surgical Intensive Care Unit of the Singapore General Hospital, Singapore, and the physical therapists working at night.

This article was submitted July 19, 1999, and was accepted March 3, 2000.