Chest physical therapy.

The immediate effect on

oxygenation in acutely ill patients.
A F Connors, Jr, W E Hammon, R J Martin and R M Rogers

Chest 1980;78;559-564
DOI 10.1378/chest.78.4.559
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© 1980 American College of Chest Physicians
 *
Chest Physical Therapy
The Immediate Effect on Oxygenation in Acutely Ill
Patients
Alfred F. Connors, Jr., M.D.;t Willy E. Hammon, R.P.T.;
Richard J. Martin, M.D., F.C.C.P.; and Robert M. Rogers, M.D., F.C.C.P.

There is no documentation in the literature of the risk of postural drainage alone, and had fallen another 5.3 mm
hypoxemia after chest percussion in acutely ill adults Hg (P < 0.01)30 minutes after return to the pretreatment
with nonsurgical pulmonary disorders. We studied the position. There was no significant change in Pa02 in 12
immediate effect of postural drainage and chest percus- patients who produced moderate to large amounts of mu-
sion (PDP) on oxygenation in 22 hospitalized patients copurulent secretions. The fall in Pa02 was probably due
with a variety of acute, nonsurgical pulmonary disor- to increased ventilation-perfusion mismatch since this fall
ders. Heart rate, respiratory rate, blood pressure, and was avoided in two patients restudied while receiving 100
arterial blood gas levels were measured at four points percent oxygen. We conclude that all acutely ill patients
before, during, and after PDP. There was a significant receiving PDP should he carefully monitored and, if
fall in Pa02 after chest percussion in ten patients who necessary, should receive increased levels of inspired
produced no sputum or small amounts of mucoid sputum. oxygen to avoid hypoxemia. Our data suggest that the
The mean Pa02 fell 16.8 mm Hg (P < 0.05) immediately use of PDP in patients without sputum production is not
after PDP, when compared to the value obtained after indicated and is potentially dangerous.

C hest physical therapy in the form of postural tion following PDP. Holloway et a17 reported a
drainage and percussion (PDP) has long been decrease in Pa02 in neonates after PDP. Gormezano
used as adjunct therapy in the care of patients with and Branthwaite8 demonstrated a significant reduc-
acute and chronic pulmonary disease. In 1953, Pal- tion in PaOz in 13 postoperative patients who had
mer and Sellick1 showed PDP to be of value in the cardiovascular complications, but no change in 11
prevention of atelectasis after abdominal surgery. patients treated for respiratory failure. One study,9
Since that time, PDP has been used increasingly reported in abstract form, found a significant drop in
in the care of patients with chronic lung disease, Pa02 in 17 patients, but the patients and their dis-
both in the stable phase of their illness and during eases were not described. Thus, there are only two
acute exacerbations, and in patients with acute pul- reports in adult patients of a fall in Pa02 result-
monary disease such as pneumonia, acute bronchitis, ing from PDP, and the only complete published
aspiration, and atelectasis. Despite the widespread study concerns postoperative patients with cardio-
employment of this form of therapy, Jones,2 in his vascular complications. The risk of hypoxemia with
review of the subject, found little objective data to PDP in acutely ill, adult, nonsurgical patients, prob-
support its use in chronic and acute lung disease. ably the largest group receiving this therapy in the
Studies of the immediate effects of PDP on oxy- hospital setting, has not been documented.
genation have produced equivocal results. Finer and This fact, along with reports of significant ar-
Boyd3 reported a significant increase in arterial oxy- rhythmias9 and even cardiac arrest1#{176}during chest
gen tension (Pa02) after PDP in a controlled study physical therapy, prompted us to assess this treat-
of 20 neonates with respiratory distress. A number of ment modality in a population of acutely ill, adult,
studies in patients with stable chronic bronchi- nonsurgical patients with a variety of lung disorders.
tis, stable chronic obstructive pulmonary disease Our study was designed to document the risk, if any,
(COPD), or trauma found no change in oxygena- of hypoxemia after PDP and to characterize the
population at risk.
From the Departments of Medicine and Rehabilitative Serv-
ices, University of Oklahoma Health Sciences Center, Okla-
homa City. METHODS
Supported by the Oklahoma Lung Association and the Na-
tional Institute of Health grants HLO 7155 and HLO 7210. A total of 22 patients (13 men and 9 women), ranging in
fParker B. Francis Fellow in Pulmonary Research. age from 23 to 95 years, were included in this study. They
Manuscript received September 14; revision accepted De- were drawn from inpatients at the University of Oklahoma
cember 4.
Health Sciences Center who were referred by their primary
Repnn* requests: Dr. Rogers, University of Oklahoma Health
Sciences Center, P0 Box 26901, Oklahoma City 73190 physicians to the physical therapy department for postural

CHEST, 78: 4, OCTOBER, 1980 CHEST PHYSICAL THERAPY 559

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© 1980 American College of Chest Physicians
drainage and chest percussion. All patients were hospitalized either from the radial artery with a 22-gauge needle or
with an acute illness and were studied during an acute phase through an indwelling radial artery line (Jelco 20-gauge, 13i
of that illness. Twelve patients were studied while in the inch, Teflon catheter). Blood gases were immediately placed
intensive care unit; the remaining ten were on the hospital on ice and analyzed within 15 minutes of the time they were
floors. Two patients were studied twice, the repeat study drawn. Analysis was done on a pH/blood gas analyzer
following a change in their respiratory status. The pulmonary (Instrumentation Laboratory 813) which was calibrated be-
disorders present in the study population were as follows: fore each determination. The numerical data obtained were
acute pneumonia, 10; bronchiectasis, 3; quadriplegia of re- analyzed using repeated measures analysis of variance and
cent onset (all with left lower lobe atelectasis), 3; acute Duncan’s multiple range test. Since data analysis was not
bronchitis, 3; cardiac arrest with aspiration, 2; pulmonary done until after the study was completed, the correlations
edema, 1; chronic bronchitis, 13 (history unobtainable in reported below were not known at the time the PDP was
three patients); and chronic airways obstruction (FEy1 given, thus avoiding bias on the part of the therapist adminis-
<1.5), 12. tering the chest percussion.
Each patient gave informed consent to a protocol ap-
proved by the Human Experimentation Committee. In the RESULTS
case of those patients who were unconscious or otherwise
unable to give consent, consent was obtained from a mem-
After analysis of the data, the patients were clear-
ber of the immediate family. A detailed respiratory history ly separated into two groups. One group (group 1)
was obtained using a standard questionnaire. consisted of 12 patients who produced moderate to
The study protocol duplicated the routine manner of giving large amounts
of mucopurulent sputum as a result of
PDP by the physical therapy department in our hospital. We
postural drainage and percussion. The other group
were particularly interested in the Trendelenburg position, as
this was the position most commonly associated with the
(group 2) consisted of ten patients (12 studies) who
episodes of cyanosis, dyspnea, and cardiac arrhythmias noted produced no sputum in nine studies and small to
by our nurses and physical therapists. Therefore, we inten- large amounts of thin, mucoid sputum in three stud-
tionally limited our patients to those with lower lobe disease. ies. The groups are characterized in Table 1.
Observations were made of the heart rate, arterial blood Group 2 had a significant fall in mean Pa02 at
pressure, respiratory rate, and arterial blood gas levels at four
point three, following chest percussion. This fall
different points before, during, and after therapy: (1)
after the patient had been reclining in bed with the head
persisted 30 minutes later. (The data are sum-
elevated 30 for at least ten minutes; (2) after the patient marized in Table 2.) Group 1 had no change in PaOa
had been lying in the lateral decubitus position with the at point three and a slight but not significant rise in
diseased lung up and with the foot of the bed elevated 12 Pa02 at point four. Group 2 had a higher baseline
inches (approximately 10 of Trendelenburg) for at least
mean PaOa (86.0 mm Hg) than group 1 (69.6 mm
five minutes (postural drainage alone); (3) immediately
after ten minutes of chest percussion to the affected lobe
Hg). This is probably due to the fact that 5 of the 12
(PDP); and (4) after the patient had returned to the studies in group 2 involved patients receiving
baseline position and remained there for 30 minutes. Sputum
Table 1-Comparison of Group 1 and Group 2
was collected throughout the study period, the total volume
was measured, and the sputum was classified as mucoid or Group 1Group 2
mucopurulent.1’

The percussion consisted of striking the chest with a

No. of patients 12 10 (12 studies)
cupped hand at a rate of 80 to 90 beats per minute for ten Age, mean (range) 49.7 (34-71) 54.3 (23-95)
minutes, followed by one to two minutes of vibration and
Sex (male:female) 6:6 ‘7:3
chest compression. The same therapist (W. H.) administered
the chest percussion to all patients. After measurements had Sputum obtained during
been made at point three, the patients were encouraged to study period
cough, and suctioning was done in those patients with Volume-large > 5 ml 9/12 2/12
tracheostomy or endotracheal tubes. The oxygen therapy that moderate 2 to 5 ml 3/12 0/12
the patient had been receiving prior to the study was con- small <2 ml o 1/12
tinued during the entire study. In 12 studies, supplemental none 0 9/12
oxygen was supplied by nasal cannula or Venturi mask. These Quality-mucoid o 3/12
were checked at each point to be sure that they were mucopurulent 12/12 0
positioned correctly and functioning properly. Seven studies
Supplemental oxygen therapy 10/12 11/12
were done on six patients who were being supported by
mechanical ventilators (Bennett MA-i); three were on the Mechanical ventilation 2/12 5/12
assist-control mode, thus setting their own respiratory rate;
and four were receiving intermittent mandatory ventilation
Acute infiltrate on chest
(IMY). The patients receiving IMV were not receiving sighs x-ray film 8/12 8/10

at the time of the study. Those on the assist-control mode had Smoking history 8/12 7/7*
their sighs turned off from the time they were placed in the > 30 pack years 5/8 7/7*
Trendelenburg position until the measurements were taken at Number of cigarettes/day 28 32
point 3, a period of approximately 15 minutes. All other
Chronic bronchitis 8/12 5/7*
respirator settings were left unchanged. All four blood pres-
sure measurements were taken on the same arm using a > 5 years 7/8 4/5
standard blood pressure cuff. All blood gases were drawn tHistory unobtainable in three patients.

560 CONNORS ET AL CHEST, 78: 4, OCTOBER, 1980

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© 1980 American College of Chest Physicians
 Table 2-Arterial Blood Gas, Heart Rate, and three had the study repeated while receiving 100
Blood Pressure Data
percent oxygen (both patients were being mechan-
Points ically ventilated). The previously demonstrated re-
duction at point 3 was not seen during 100 percent
1 2 3 4
oxygen (Fig 2a and b).
Group I It is noteworthy that, while the change in mean
Pa02, mm Hg 69.6±2.2* 70.8±1.8 70.8±2.3 72.4±2.3 Pa02 in group 1 was not significant, three patients
PaCO2,mmHg 53.7±6.0 53.9±6.3 53.9±6.4 51.7±6.5
had an increase in Pa02 of greater than 15 percent
pH 7.42±.01 7.43±.02 7.42±02 7.44±.01
HR, above baseline (15 to 31 percent). Two of the three
beats/mm 101.2±5.5 97.8±5.1 100.3±4.9 98.0±5.7 patients had severe bronchiectasis. The third had
BP (systolic), acute pneumonia with copious purulent sputum.
mm Hg 117.6 ±4.6 112.9 ±7.8 113.9 ±4.7 116.2 ±4.6
Respiratory
120
rate 0,

, .
(breaths/mm) 24.1 ±2.4 25.0 ±2.4 24.6 ±2.4 22.3 ± 1.9
/ /
100
Group 2
so
Pa02, mm Hg 86.0 ±9.4 90.0 ± 12.4 73.2 ± 6.Ot 67.9 ±4.6t /
a 0
PaCO2,mmllg 41.6 ± 3.5 41.8 ± 3.5 41.3 ± 3.5 41.0 ± 3.4 80 /
C
pH 7.44±.02 7.44±02 7.45±.02 7.45±.01 a /5

HR,beats/min 90.9 ±5.3 91.5 ±6.8 95.2 ±5.7 91.4 ±4.7 a /

BP (systolic), .0 80- /
E /
mmHg 117.0±7.0 115.3±6.2 115.8±7.4 116.3±7.3 /
0
Respiratory 40- /
0
rate
C
(breaths/mm) 20.8±2.4 20.9±2.1 20.8±1.9 20.3±2.0
a
20
*All numbers are mean (3
± SEM.
fP <0.05 between points 1 and 4, and points 2 and 3. C
0
P <0.01 between points 2 and 4.

mechanical ventilation, and consequently, higher

-20
concentrations of inspired oxygen (FIos). Neither : .6. 10cm PEEP
group had a fall in PaOa after five minutes in the o_ -o F,02 = 1.0, 10cm PEEP
-40.
Trendelenburg position. A graph of the percentage
of change in Pa02 for both groups is shown in Fig-
ure 1. There was no significant change in Pcos, pH,
1 2 3 4
systolic blood pressure, heart rate, or respiratory
FIGURE 2A. Percent change of PaO. from baseline is plotted
rate in either group. at four study points for two patients with reduced Pa02 after
Two patients who had a reduced Pa02 at point chest percussion who were restudied on 100 percent oxygen.
10 This patient had an initial rise in Pa02 at an F1o2 of .8 and
a 1.0, but subsequent fall at points 3 and 4 on 60 percent oxy-
C gen was not present on 100 percent oxygen.
5. -o
a 0
.35
.0 -. .___________S
: 5
0 o__0FIQ2:1.O
0 a
a
- - Os
0 .0
5.
E
-5 0
0.0
0 o
- -10- Oc
C 00
0
0 o 10
15. .-. Group I 0__
C
0
0- -o Group II
-15
-20- a
0 0.

-20
I I I

Ficums
groups
1. Percent
is plotted at point
1
change
in Pa02
1, baseline;
from baseline
2
for both
point 2, after 5 minutes
3 4
- 1
I

2
I

3
I

4
I

of postural drainage alone; point 3, after 10 minutes of chest FIGURE 2B. This patient had fall in Pa02 seen both after
percussion; and point 4, 30 minutes after return to baseline postural drainage alone and after PDP. This fall was not
position. (Actual values for Pa02 are recorded on Table 2.) present on 100 percent oxygen.

CHEST, 78: 4, OCTOBER, 1980 CHEST PHYSICAL THERAPY 561

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© 1980 American College of Chest Physicians
 DISCUSSION percussion. Several patients in this group had a
marked improvement in their PaOs, while only two
Our results show that there is a significant risk of
hypoxemia after postural drainage and chest percus-
patients had a fall in Pa02 of greater than 10 percent
sion in certain acutely-ill, nonsurgical, adult patients.
(11 percent and 17 percent). When the studies of
These findings concur with Gormezano and Branth-
the short-term effects of PDP reported in the litera-
waite’s8 report of a similar fall in PaOm after PDP in
ture are re-examined, we find, as did Murray’8 in a
recent editorial, that those studies done on subjects
13 postoperative patients with cardiovascular com-
producing large volumes of sputum are, on the
plications and with an abstract by Huseby et a19
whole, the same studies which show a significant
showing a fall in Pa02 of 19 mm Hg following PDP
in 17 patients whose diseases were not specified. benefit from PDP. Cochrane et al’3 studied 23 pa-
Thus, PDP appears to carry with it a risk of by-
tients with bronchiectasis, cystic fibrosis, and chronic
poxemia, but what are the benefits from this therapy bronchitis, all producing greater than 30 ml of spu-
tum per day, and found significant improvement in
to offset this risk?
Postural drainage and percussion are presumed to specific airways conductance and FEy1. Feldman et

augment the clearance of sputum from the airways al,14 in a study of 19 patients with cystic fibrosis or
by bringing the force of gravity and vibration to the chronic bronchitis who expectorated an average of
aid of the normal airway clearance mechanisms. If 15 ml of sputum during a one-hour study period,
PDP succeeds in doing this, then, acutely, measur- found a significant increase in expiratory flow rates
able improvement should be seen in several related at low lung volumes. Recently, Bateman et al’#{176}
factors. These factors would include increased spu- reported increased clearance of deposited radio-
tum production, more even distribution of ventila- aerosol and increased sputum volume in ten patients

tion, increased expiratory flow rates, reduced airway with stable chronic airways obstruction and an aver-
resistance, increased vital capacity, and improved age daily sputum volume of 100 ml. Thus, PDP does
oxygenation. The expected long-term results of this seem to have desirable acute effects in patients with

therapy would be more rapid improvement in the large volumes of secretions. Conversely, there is
clinical signs of disease, x-ray abnormalities, pulmo- little documentation of acute benefit from PDP in
nary function, and gas exchange. Indeed, there is a
patients with small amounts of secretions. Thus, the
significant increase in sputum volume acutely after same group which we have shown to be at risk for
postural drainage and percussion.4 Measurements of hypoxemia after PDP also appears to be the least
likely to benefit from this treatment.
acute changes in lung volume and flow rates give
conflicting and inconclusive results,4’5’2”3 al- The cause of hypoxemia noted after PDP is un-
though recently, Feldman et al’4 found significant known; however, there are a number of possible
improvement in flows at low lung volumes despite mechanisms which might explain it. An increase in
no change in FEy,. Those studies which measure ventilation-perfusion (V/ Q) mismatch can cause an
airway resistance and specific conductance also give acute reduction in PaOi. There are several events
conflicting results.5”3 Three controlled long-term which might lead to uneven V/Q matching during
studies of PDP in hospitalized patients with acute and after chest percussion: (1) shifting of mucus
exacerbations of chronic bronchitis’5”6 or acute from peripheral airways to converge in a large, cen-
pneumonia’7 show no increase in sputum volume, tral airway could reduce ventilation to a larger area
no change in the rate of defervescence, no change in of perfused lung; (2), bronchospasm could cause an
the resolution of x-ray abnormalities, and no im- acute increase in V/Q mismatch (Campbell et aP2
provement of pulmonary function or gas exchange. demonstrated a decrease in FEy, after PDP in
Thus, the effectiveness of PDP as a treatment seven patients with an exacerbation of their chronic
modality in acute and chronic pulmonary disease is bronchitis which was reversible with bronchodila-
subject to question. tors); and (3) lung compression due to chest per-
The volume and character of the sputum appear cussion may cause narrowing of airways or even
to be important factors in separating the patients premature airway closure at the resulting smaller
that develop hypoxemia from those who do not. We lung volumes, reducing ventilation to these areas.
found a significant reduction in PaOm after chest Ventilation-perfusion mismatch is the likely cause of
percussion only in those patients who produced no the hypoxemia noted in our patients since adrninis-
sputum or small amounts of mucoid secretions as a tration of 100 percent oxygen in two of our patients
result of the therapy. The patients in group 1, who blocked the reduction in PaOi at point three.
produced moderate to large amounts of muco- We assume that the fall in PaOs corresponds with
purulent sputum, had a slight, but not significant, an increase in alveolar-arterial oxygen difference
improvement in oxygenation as a result of chest (P{A-a]Os). The P(A-a)Om was not determined in

562 CONNORS ET AL CHEST, 78: 4, OCTOBER, 1980

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© 1980 American College of Chest Physicians
this study because 12 of the 22 patients were receiv- rise in Pco2 was noted in either group and there was
ing supplemental oxygen by means which preclude no significant change in Pa02 after five minutes in
accurate measurement of the F1o2, ie, nasal cannula the Trendelenburg position. An increase in shunt
or Venturi mask. In patients receiving oxygen by fraction would also cause a decrease in Pa0. There
either of these means, an increase in inspiratory flow are two mechanisms by which PDP might cause an
rate associated with hyperventilation could result in increased shunt fraction: first, airway closure may
increased dilution of the administered oxygen with occur due to lung compression from chest percussion
air, reducing the F1o2 and consequently, the alveo- resulting in unventilated areas of the lung; and,
lar Po2 (PAO2). In that case, there could be a fall in second, shifting of mucus from peripheral airways to
PaOs without a change in P (A-a) 02. However, the a larger, central airway might totally block the air-
PaCO2 and respiratory rate in our subjects were way and acutely increase the percentage of unventi-
stable at all four points in both groups (see Table lated lung. However, the two patients studied
2). There was no change in ventilatoiy pattern suffi- receiving 100 percent oxygen did not have an in-
cient to produce a reduction in F1o2. We conclude creased shunt fraction after chest percussion.
that the change in Pa02 was associated with an In conclusion, this study of acutely ill, nonsurgical
increase in P (A-a) 02, rather than a change in Fbi, adults reveals a significant risk of a fall in Pa02 after
PaCO2, or respiratory quotient. chest percussion in severely ill patients with absent
A fall in cardiac output is another mechanism or mucoid secretions. This fall appears to be due to
which may explain the hypoxemia that developed. If an increase in V/Q mismatch. There was no fall in
oxygen consumption, alveolar Po2, and shunt frac- Pa02 noted after postural drainage alone.
tion are constant, a fall in cardiac output will result We feel the following recommendations are justi-
in a fall in the oxygen content of mixed venous fied. First, avoid chest percussion in acutely ill pa-
blood, due to increased oxygen extraction by the tients with little or no secretions since there is little
tissues, which when mixed with the oxygenated end- objective evidence of benefit to this group, and, in
capillary blood will result in a lower arterial oxygen our study, this is the group most likely to experience
content and Pa02. Barrell and Abbas2#{176}recently a fall in PaO2. Second, assure adequate oxygenation
observed a significant fall in mixed venous oxygen during chest percussion in the acutely ill patient; 100
(14 patients) and cardiac output (5 patients) dur- percent oxygen appears to prevent the fall in Pa02
ing chest percussion in patients studied several days noted immediately after chest percussion.
after open heart surgery for mitral valve replace-
ACKNOWLEDGMENTS: We are grateful to Dr. Mimi Lam
ment. Laws and Mclntyr&#{176} noted a fall in cardiac and Dr. Barry A. Cray for their help reviewing this paper
output in three of eight patients on ventilators dur- and preparing it for publication.

ing hyperinflations, chest compression, and vibra- REFERENCES

tion. The three patients who had a fall in cardiac
1 Palmer KNV, Sellick BA: The prevention of postoperative
output were described as “unconscious or too ill to pulmonary atelectasis. Lancet 1953; 1:184-168
resist the physiotherapist’s efforts.” The fall was felt 2 Jones NL: Physical therapy: present state of the art. Am
to be due to the increased intrathoracic pressure Rev Respir Dis 1974; 110:132-136
obtained during hyperinilation and impairment of 3 Finer NN, Boyd J: Chest physiotherapy in the neonate: a
controlled study. Pediatrics 1978; 61:282-285
the normal compensatory mechanisms to a rise in
4 May DB, Munt PW: Physiologic effects of chest percus-
intrathoracic pressure. sion and postural drainage in patients with stable chronic
We did not measure cardiac output and have no bronchitis. Chest 1979; 75:29-32
clear evidence that a fall in cardiac output was a 5 Newton DAG, Stephenson A: The effect of physiotherapy
on pulmonary function: a laboratory study. Lancet 1978;
factor in the decrease in Pa02 we demonstrated in
2:228-230
Group 2. The study which demonstrated a fall in
6 Mackenzie CF, Shin B, McAslan TC: Chest physio-
cardiac output after PDP2#{176}
was done on a small therapy: the effect on arterial oxygenation. Anesth Analg
number of patients and did not delineate the cause 1978; 57:28-30
of the fall in cardiac output. Hence, there is a need 7 Holloway R, Adams EB, Desai SD, Thambiran AK:
Effect of chest physiotherapy on blood gases of neonates
for further study of the effect of PDP on cardiac
treated by intermittent positive pressure respiration.
output and the possible mechanisms which mfght
Thorax 1969; 24:421-426
mediate a fall in this parameter after PDP. 8 Gormezano J, Branthwaite MA: Effects of physiotherapy
Other factors should also be considered as possi- during intermittent positive pressure breathing: changes
ble causes of the fall in Pa02 noted after chest in arterial blood gas tensions. Anaesthesia 1972; 27:258-
264
percussion. Hypoventilation due to the fall in vital
9 Huseby J, Hudson L, Stark K, Tyler M: Oxygenation
capacity seen in patients placed in the Trendelen- during chest physiotherapy abstracted. Chest 1976;
burg position might have played a role. However, no 70:430

CHEST, 78: 4, OCTOBER, 1980 CHEST PHYSICAL THERAPY 563

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© 1980 American College of Chest Physicians
10 Laws AK, McIntyre RW: Chest physiotherapy: a physio- tions in chronic bronchitis. Acta Med Scand 1964; 175:
logical assessment during intemuttent positive pressure 715-719
ventilation in respiratory failure. Can Anaesth Soc J 1969; 16 Petersen Esmann
ES, Y, Honcke P, Munkner C: A
16:487-493 controlled study of the effect of treatment on chronic
11 A Report to the Medical Research Council by their bronchitis: an evaluation using pulmonary function tests.
Committee on the Aetiology of Chronic Bronchitis: defini- Acta Med Scand 1967; 182:293-304
tion and classification of chronic bronchitis for clinical and 17 Graham WGB, Bradley DA: Efficacy of chest physio-
epidemiological purposes. Lancet 1965; 1:775-779 therapy and intermittent positive-pressure breathing in
12 Campbell AH, O’Connell JM, Wilson F: The effect of the resolution of pneumonia. N Engl J Med 1978; 299:
chest physiotherapy upon the FEY1 in chronic bronchitis. 624-627
Med J Aust 1975; 1:33-35 18 Murray JF: The ketchup bottle method. N Engi J Med
13 Cochrane GM, Webber BA, Clarke SW: Effects of spu- 1979; 300:1155-1157
tum on pulmonary function. Br Med J 1977; 2:1181- 19 Bateman JRM, Newman SP, Daunt KM, Pavia D, Clarke
1183 SW: Regional lung clearance of excessive bronchial secre-
14 Feldman J, Traver GA, Taussig LM: Maximal expiratory tions during chest physiotherapy in patients with stable
flows after postural drainage. Am Rev Respir Dis 1979; chronic airways obstruction. Lancet 1979; 1:294-297
119:239-245 20 Barrell SE, Abbas HM: Monitoring during physiotherapy
15 Anthonisen P, Bus P, Sogard-Andersen T: The value of after open heart surgery. Physiotherapy 1978; 64:272-
lung physiotherapy in the treatment of acute exacerba- 273

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© 1980 American College of Chest Physicians
 Chest physical therapy. The immediate effect on oxygenation in acutely ill
patients.
A F Connors, Jr, W E Hammon, R J Martin and R M Rogers
Chest 1980;78; 559-564
DOI 10.1378/chest.78.4.559
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