Attenuation of the Hemodynamic Responses to Chest Physical Therapy

Patti Klein, Marcia Kemper, Charles Weissman, Stanley H. Rosenbaum, Jeffrey Askanazi and Allen I. Hyman Chest 1988;93;38-42 DOI 10.1378/chest.93.1.38

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Attenuation of the Hemodynamic Responses to Chest Physical Therapy*

Patti Klein, M.D.;t Marcia Kemiper, B.A.;t Charles Weissman, Al.D., Stanley H. Rosenbaum, M.D.;I! Jeffrey Askanazi, M.D., EC.C.P; and Allen I. Hymtan, M.D.;
*

Chest physiotherapy (CPT) is a commonly used technique in mechanically ventilated critically ill patients. This study examines the hemodynamic and metabolic changes associated with CPT and measures the attenuation by two doses of intravenous fentanyl (1.5 pLg/kg and 3.0 1Lg/kg) on these changes. Heart rate, systolic and mean blood pressures, cardiac output, oxygen consumption (Vo2), and carbon dioxide production (VcoO) all increased during CPT. De-

creases in arterial pH and VE and increases in PaCO, were also observed. The higher, but not lower dose, of fentanyl significantly attenuated increases in blood pressure and heart rate during CPT and no substantial hemodynamic changes occurred once CPT had stopped. The increases in Vo2 and Vco, were not attenuated. Short acting narcotics attenuate the hemodynamic responses to stressful stimuli such as CPT.

C lhest physiotherapy (CPT) is commonly used in mechanically ventilated critically ill patients to mnobilize pulmonary secretions and facilitate their removal.'2 The CPT consists of varying amounts of percussion, chest wall vibration, postural drainage, and suctioning.') The efficacy of CPT in various diseases is controversial.3 5 Tlhough a stressful procedure that may have significant metabolic and hemodyinamic effects,6 surprisingly few studies have examinied thlis. Hemodyinamic disturbances are of special conicern sirnce critically ill patients may lack the cardiac reserve necessary to tolerate stress. The purpose of this study was twofold as follows: (1) to measure the hiemodynamic and metabolic changes that occur with CPT, and (2) to examnine wlhether narcotic analgesics carn attenuate these responses.
METHODS
Twenty-three postoperative mechanically ventilated patients in the Surgery-Anesthesiology Intensive Care Unit of the Columbia Presbyteriani Medical Center were studied on 26 occasions. The patients had undergone major abdominal or thoracic surgery within the previous week. All were hemodynamically stable, sorne were receiving low doses of inotropic medication (dopamine 2-4 FLg/kg/ min) and continuous intravenous analgesia with fentanyl (0. 5-1. 0 >Lg/ kg/h). The CPT consisted of percussion, vibration, and suctioning. Each patient ieceived two ten-ininiute CPT sessions, separated by at
*From the Departments of Anesthesiology and Medicine, College of Physicians and Surgeons, Columbia University, New York. tFellow, Department of Anesthesiology. Currently at Departrnent of Anesthesiology, New York University School of Medicine, New York. tStaff Associate, Department of Anesthesiology. Assistant Professor of Anesthesiology and Medicine. lAssociate Professor of Clinical Anesthesiology and Medicine. Assistant Professor of Anesthesiology. * *Professor of Anesthesiology and Pediatrics. Manuscript received March 12; revision accepted May 12. Reprint requests: Dr Weissman, 630 West 168th Street, New York City 10032 38

least a 30-minute interval. Group 1 (n=10) received 1.5 ,ug/kg of fentanyl or placebo intravenously in randorn order, three minutes before each CPT session. Group 2 (n= 10) similarly received two sessions of CPT, preceded by 3 [mg/kg of fentanyl or placebo intravenously. Group 3 (n =6) received only placebo before each CPT session. This group served as a control group to account for the consistency in performance of CPT as well as the diurnal changes in hemodynamic and metabolic parameters. The drug or placebo was administered after baseline values had been obtained by one of two coauthors (P.K. or C.W), and it was unknown to the therapist performing CPT (M.K.) whether fentanyl or placebo had been given. Each CPT sessioii was preceded by a 15-minute resting period (resting has been previously definied as "a state where the patient was not aroused by surrounding events").5 Each session consisted of turning the patient onto his or her side (ie, lateral decubitus position), then perforniing percussion and vibration for three rniinutes, repeating the procedure on the opposite side, then placing the patient supine to suction the trachea. Suctioining was limited to one minrute. The CPT session was then followed by a 20-minute rest period. Metabolic and hemodyniamic measurements were made duririg the procedure and rest period. Oxygen consumption (Vo2), carbon dioxide production (Vco2), minute ventilation (VE), and respiratory quotient (RQ) were measured and recorded continuously throughout the CPT session and continued unitil the patient returned to a resting state. Measurements were made of heart rate (HR), and blood pressure (systolic, diastolic, and mean). These data were collected at the following timnes, 15, ten, and five minutes before CPT session (patient supine), one minute after the patient was turned into the lateral decubitus position in preparation for CPT (side 1), three rninutes after CPT was begun on side 1, three minutes after CPT was begun on side 2, immediately after suctioning the patient, and ten, 15, and 20 minutes following the completion of the CPT sessioni. Arterial blood gas values were obtained as follow: 15 minutes before CPT, three minutes after CPT was begun on side 2, and 15 minutes after cornpletion of side 2 CPT. In some patients, cardiac output was measured by thermodilution at 15 minutes and one miiiute before CPT (side 1), immediately after completion of CPT on side 2 (patient supine), and 15 minutes after completion of CPT (patienit in "resting state"). Heart rate and direct blood pressure were monitored continuously using indwelling 20 g radial artery catheters conrlected to HewlettPackard pressure amplifier modules with Benitley Trantec pressure
Hemodynamic Responses to Chest Physical Therapy (Klein et al)

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Table 1-Values of Systolic and Mean Blood Pressure (mean + SD)

Baseline*
Group 1 (n= 10) S DIug
M

Turn

CPT1

CPT2

SXN

Rest

134+27
85+12 129 26 83- 11

Placebo

S
M

14124 94.- 14 149 22

96-- 10

142 29 9318 155 231: 99-9:

14631
95 18

154 171+ 100 I4-I

13930 9017 149 23 94 20

12227
8911

131+ 31
85+ 15

Group 2 (n = 10) S Dirug NI S Placebo M Group 3 (N =6) S Placebo M S Placebo M

140 t 33 89 22 149 32 93+17

115 12

155 104 167 106

137 93 138 95

39 26T: 36 25
39T: 20t 15T

156 29t 104 191 1 186 35

118234
134 26t

157 t 29t 101 19 188 314 119+19T

138 28T:

140 38 89 t 23 178 39T

11125t:
132 +22t

121 16 8011 149 32 9416

114 15

13T *Baseline is mean of values, 15, ten, and five minutes prior to CPT; CPT 1, first CPT session. CPT 2, second CPT sessioni; SXN, suctioning; rest, mean of values ten, 15, and 20 minutes after CPT; S, systolic blood pressure (mm Hg); and NI, inean blood pressure (mm Hg). tSignificantly different than baseline values (p<0.05). 1:Significantly different than baseline values (p<0.01). Difference between baseline value significantly different when drug and placebo compared (p 0.01).

74+9 116 16 76 11

90 21t 143 17T 95 111

93-21t
145 25t 97 141:

83 15 135 24T 93 +20t

69 13 117 19 78 15

transducers. In patients with pulmonary artery catheters, thermodilution cardiac outputs were measured with an Edwards cardiac output computer. The rate pressure product (RPP) was calculated from the systolic blood pressure and heart rate. Metabolic date (Vo2, Vco2, RQ) and minute ventilation (VE) were measured with a Horizoii metabolic measurement cart. A Puritan-Bennett AO-I blender was placed between the gas sources and the Bear I ventilator and was used to ensure consistency ofthe FIo2.7 The Flo2 sampling line was placed above the outlet port of the cascade humidifier. The mixed expired gas flowed from the expiratory port of the Bear I to the mixing chamber of the Horizon metabolic measurement cart via six feet of 22 mm tubing. Sampled gas was thoroughly dried before reaching the analyzers. The volume, temperature, CO2 and 02 analyzers were fully calibrated before each study. This study was approved by the Institutional Review Board, Columbia Univerisity Health Sciences Center. WAritten informed consent was obtained fromn the patient or a close faimiily member. Statistical analysis was performed using paired and unpaired Student's t-test with Bonferroni correction and three-way analysis of
variance.

RESULTS

Table 2-Heart Rate

Baselirne Turn
CPT1*

CPT2

SXN

Rest

Chest physical therapy resulted in significant metabolic and hemodynamic changes with placebo. Heart rate, systolic and mean blood pressures, and cardiac output were all increased during the chest physical therapy sessions (Tables 1 through 3). Sirnilar increases were seen in Vo2 and Vco2 (Table 4). In some groups, arterial pH dropped significantly and PaCO2 increased while VE decreased or did niot change during CPT (Table 4). Some patients had decreases in PaO2. In Group 3, there was no significant differences in the hemodynainic, respiratory, and rnetabolic respoinses between the two CPT sessionis. The administration of 1.5 ,utg/kg fentanyl immediately prior to CPT resulted in no differences when compared to placebo. However, wlhen 3.0 1.g/kg was administered, there was significant attenuation of the increase in systolic and mean blood pressure, as well as suppression of the heart rate increase. No decrease in the attenuation was found in patients receiving background sedation (continuous intravenous infusion of
Table 3-Cardiac Output
Baseline
Group 1 (n 6) Drug Placebo Group 2 (n 6) Drug Placebo 5 Group 3 (n =2) Placebo
5.2+0.8 5.1+0.6 5.3 0.9 .4 0.8
6.5 0.03

Group 1 (N = 10) + Drug 86 13 94 12 95t12T 95 t 16t 95 15t 84 11 Placebo 84 13 92101: 95511T100111: 94 14: 85+ 11 Group 2 (N =10) Drug 101 9 108 11 107 14 112 14 106 13 95 6 Placebo 98 +9 109 12: 112 11+ 116 16: 117 161 101 12 Group 3 (N 6) Placebo 99 6 104+10 112'11t110 t15t 112121: 97 11 Placebo 93 7 102 + 17 106 t 14t 109 t 10t 108 131+ 98 12 *CPT 1 is initial chest physical therapy session; CPT 2. second chest physical therapy session; anld, SXN, suctioniiig. tSigriificantly different than baseline values (p<005).

CPT
6.0+ I.lt

Rest 5.2+0.6 5.1+0.5

4.8 1.0 5.7 1.3

6.8+1.3t
6.2 +1. Ot

75 +2.3t

*Significantly different than baseline values (p<0.01). Difference between baseline value significantly different when drug and placebo compared (p<.Ol).

9.2 0 lt

6.1+ 0.03

*Nlean -1-SD; CPT, chest physical therapy. tSignificantly different than baseline values (p<0.01).
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Table 4-Metabolic and Respiratory Data

Vo2,
mi/min
VCo2, ml/min VE, L/min

PaO2,

RQ

pH

mm

Hg

mm

PCO2, Hg

Group 1 (n = 10)
Drug

Baseline
CPT Rest

20446 260+68*

200+53t
201 50 272+51* 207 43t

17833 20352* 17836t 180 32 21331* 17624t

8.92.1 9.02.3 9.02.4 9.9+ 1.9 9.4 1.7* 9.2+2.0

0.890.1 0.780.1 0.920.2

0.92 0.2 0.810.1 0.900.1

7.45+05 7.40+0.1* 7.42+0.1

7.45 0.0 7.41+0.1* 7.459.1

12924 11127 11815

12717 12125 12827

373

433*
41+4 38 + 3

Placebo Baseline
CPT Rest

435*
39+5

Group 2 (n 10)
Drug

Baseline
CPT Rest

239 71 331105*

205 57 24787*

11.2 2.6 11.33.5

0.86 0.1 0.75+0.1

23149t
24249 33090* 241 58t

20351t
20551 24768* 21560t

10.82.7
11.62.6 12.22.9 10.92.8

0.88+0.1
0.840.1 0.770.1 0.890.1

7.48 0.1 7.410.1* 7.450.1t

113 26 10325

37 + 3

435*
38+4

117+22
115+35 97+25 10620

Placebo Baseline
CPT Rest

7.470.01 7.430.1*

383 415
39+4

7.450.It

Group 3 (n 6)
Placebo Baseline
CPT Rest

265 59 310 167 26277

224 48 25451 22253 218 41 244 45 21943

11.1 2.9 12.33.1 11.13.0 10.8 + 2.1 12.4 3.0 10.42.2

0.85 0.1 0.830.1 0.860.1

0.92 0.1 0.86 0.1 0.890.1

7.48 0.02 7.460.02 7.470.02 7.47 0.02 7.46 0.02 7.480.01

117 28 12628 116+20

120 9 119 25 11322

36 2

373 37+2
37 1.0 39 2.2

Placebo Baseline CPT

Rest

241_ 57 295 75 24653

372.4

*Significantly different than baseline values (p<0.05). tSignificantly different than CPT values (p<O.O5).

fentanyl) or inotropic support. Fentanyl did not alter the metabolic response during CPT even at the higher dose (Table 4). No cross-over effect was noted in groups 1 and 2, ie, there was no difference of giving fentanyl for
the initial CPT session
session.
DISCUSSION
vs

giving

it for the second

heart rate, and rate pressure product than did any other routine daily intensive care procedure. Laws and McIntyre8 found 50 percent increases in cardiac output with CPT and lung hyperinflations; Mackenzie and Shin9 examined the cardiac and respiratory effects of CPT in young adult patients with posttraumatic respiratory failure and found no changes in their cardiac index after CPT but did not make measurements

Previous studies have shown that CPT is a stressful procedure. Weissman et a16 observed that CPT caused greater increases above resting levels of Vo2, Vco2,

fore, it would be beneficial to suppress the hemodynamic response so that CPT could be performed in this group of patients. The major criteria in choosing a drug to suppress these responses were rapid onset and short duration, to suppress the responses during CPT without causing hypotension during and after the procedure was completed. Fentanyl, a narcotic analgesic, has a rapid onset and a short duration of action." Doses of fentanyl have been shown to attenuate the

hemodynamic stresses associated with such procedures as laryngoscopy and intubation during standard"'3 and rapid sequence'4 anesthetic induction.
Our results confirm the previous observation that CPT can cause major alterations in both hemodynamic and metabolic parameters.68 Mean increases of approximately 50 percent in cardiac output, 25 percent in mean and systolic blood pressure, and 15 percent in heart rate were observed. The rate pressure product (RPP), an indicator of myocardial oxygen deinand, was elevated. During the study, RPP frequently exceeded 15,000, a level at which ischemia can occur in patients with coronary artery disease.'3 Similarly, Aitkenhead et al'6 noted that RPP increased from 14,331+1,145 pre-CPT to 18,776+ 1,732 during CPT They also observed that plasma epinephrine and norepinephrine
Hemodynamic Responses to Chest Physical Therapy (Klein et al)

during therapy. Although its efficacy45 is controversial, CPT is practiced in many intensive care units. Because of its associated hemodynamic and metabolic stresses, it is frequently denied to patients with cardiovascular dysfunction. These patients are often those that can least afford to suffer pulmonary deterioration. There40

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increased 150 percent and 50 percent, respectively, above baseline values during CPT and began returning to baseline values during the 15 minutes after CPT We found that during CPT in some of the groups, there was a small but significant increase in PaCO2 (and decrease in pH). This was associated with a rise in .Jco2 without a parallel increase in VE. The lack of increase in VE is not unexpected due to the nature of these patients' underlying pulmonary pathology and of the respiratory depressant effects of narcotics. Small decreases in PaO2 were observed in some patients while others had substantial drops in PaO2. Other investigators have also observed decreases in PaO2 during CPT Huseby et al'7 studied 18 acutely ill, mechanically ventilated patients with pneumonia and found a mean decrease of 19 mm Hg in PaO2 during CPT. Connors et al"' observed a mean decrease of 17 mm Hg in a similar group of patients. Both authors attributed this fall in PaO2 to an increase in ventilation/perfusion disturbances caused by changes in cardiac output and regional ventilation in intubated patients with unilateral lung disease.'9 Gormenzano and Branthwaite2" reported decreases in arterial oxygen tension following CPT in 13 postoperative patients with cardiac compromise. Mechanisms involved to explain their findings included decreases in venous return secondary to increases in intrathoracic pressure resulting in decreases in cardiac output, increases in intrapulmonary shunt or increases in oxygen consumption, the latter of which was seen in the present study. Tyler and colleagues2' performed a regression analysis of the relationships between baseline PaO2 and the lowest PaO2 obtained during therapy. These observations reinforce the prudence of increasing the F1o0 to 1.0 during CPT. The attempt at attenuating the response to CPT with fentanyl demonstrated dose dependency. At the lower dose of fentanyl (1.5 pLg/kg), no significant attenuation was observed. However, at the higher dose (3. 0 pLg/kg), there was significant reduction in the increases in blood pressure and heart rate. Systolic blood pressure increased an average of 30 percent without fentanyl and only 12 percent when the higher dose of drug was administered. Similar degrees of attenuation were seen with mean blood pressure and heart rate. Comparison of pre-CPT baseline data with post-CPT resting values demonstrated that when the higher dose of fentanyl was administered, there was a small but significant decrease in heart rate, something not unexpected given the vagotonic action of fentanyl. It is interesting to note that although there was suppression of the hemodynamic response, there was no change in the metabolic response. This dissociation between metabolic and hemodynamic response is not unexpected, since only at rather large doses of narcotics (eg, 4 mg/kg of morphine or 75 to 100 pLg/kg of fentanyl) is there suppression of the metabolic and hormonal

responses to stress.22 This is consistent with the findings in the current study, that at the lower doses of fentanyl used in this study, there was suppression of the hemodynamic changes with little alteration in the metabolic changes. In summary, this study demonstrates that CPT produces major hemodynamic and metabolic stress and that the hemodynamic response to CPT can be attenuated but not abolished by prior administration of a moderate intravenous dose of fentanyl. It also demonstrates that this dose of fentanyl does not cause clinically significant falls in blood pressure or heart rate once the procedure has finished. This does of fentanyl did not, however, alter the metabolic response. Our study examined whether narcotics can attenuate the response to stressful stimuli in the critically ill, mechanically ventilated patients. The ability of shortacting narcotic agents to attenuate, but not abolish, the hemodynamic response to a stressful situation such as CPT shows that there is a need to examine whether higher doses of fentanyl or other drugs can further suppress and possibly abolish this response without causing major hemodynamic disruption once the procedure has been completed.
ACKNOWLEDGMENTS: The authors would like to thank the nursing staff of the Surgery-Anesthesiology Intensive Care Unit for their assistance, Mrs. Claire French for her secretarial assistance, and Dr. Paul Mendelowitz for his technical assistance.

REFERENCES
1 Kigin CM. Advances in chest physical therapy. In: O'Donohue WJ. Current advances in respiratory care. Park Ridge, IL: American College of Chest Physicians, 1984:37-71 2 Mackenzie RF, Ciesla N, Imle PC, Klemic N. Chest physiotherapy in the intensive care unit. Baltimore: Williams and Wilkins, 1981 3 Pierce AK. Conference on the scientific basis of in-hospital respiratory. Am Rev Respir Dis 1980; 122:1-2 4 Kiri Hoff LH, Owens GR, Rogers RM, Mazzocco MC. Does chest physical therapy work? Chest 1985; 88:3 5 Morrarca L, Finlay IG, Matheson M, McKay AJ, Wilson N, McArdle CS. Randomized controlled trial of physiotherapy for postoperative pulmonary complications. Br J Anesth 1983; 55:1113-17 6 Weissman C, Kemper M, Damask MC, Askanazi J, Hyman AL, Kinney JM. The effect of routine intensive care interactions on metabolic rate. Chest 1984; 86:815- 18 7 Browning JA, Linberg SE, Turney SZ, Chodoff P The effects of fluctuation Flo2 on metabolic measurements in mechanically ventilated patients. Crit Care Med 1982; 10:82-85 8 Laws AK, McIntyre RW. Chest phsyiotherapy: a physiological assessment during intermittent positive pressure ventilation in respiratory failure. Can Anesth Soc J 1969; 12:481 9 Mackenzie CF, Shin B. Cardiorespiratory function before and after chest/physiotherapy in mechanically ventilated patients with post-traumatic respiratory failure. Crit Care Med 1985; 13:483-86 10 Schleimer R, Benjamini E, Eisele H, Henderson G. Pharmacokinetics of fentanyl as determined by radioimmuno assay. Clin Pharmacol Ther 1978; 23:188 11 Dahlgren N, Messoter K. Treatment of stress response to laryngoscopy and intubation with fentanyl. Anesthesia 1981; 36:1022-26
CHEST / 93 / 1 / JANUARY, 1988
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12 Martin DE, Rosenberg H, Aukberg SJ, Bartkowski RR, Edwards MW, Greenhow DE. Low dose fentanyl blunts circulatory responses to tracheal intubation. Anesth Analg 1982; 61:680-4 13 Parker EO, Ross AL. Low dose fentanyl effects on thiopental requirements and hemodynamic response during induction and intubation. Anesthesiology 1982; 57:322 14 Cork RC, Weiss JL, Hamersoft SK, Bently J. Fentanyl preloading for rapid sequence induction of anesthesia. Anesth Analg 1984, 63:60-64 15 Gobel FL, Nordenstrom LA, Nelson RR, Jorgensen CR, Wang Y The rate pressure product as an index of myocardial oxygen consumption during exercise in patients with angina pectoris circulation. Circulation 1978; 57:549-56 16 Aitkenhead AR, Taylor S, Hunt CW, Acholak C, Smith G. Effect of respiratory therapy on plasma catecholamines. Anesthesiology 1984; 61:44 17 Huseby J, Hudson L, Stark K, Tyler M. Oxygenation during

chest physiotherapy (abstract). Chest 1976; 70:430 18 Conners AF, Hammar WE, Martin AH, Rogers RM. Chest physical therapy: the immediate effect of oxygenation in acutely ill patients. Chest 1980; 78:559-64 19 Buscaglia AJ, St. Marie MS. Oxygen saturation during chest physiotherapy for acute exacerbation of severe obstructive pulmonary disease. Respir Care 1983; 28:1009-13 20 Gorrnezano J, Branthwaite MA. Effects of physiotherapy during intermittent positive pressure v'entilation. Anesthesia 1972, 27:258-63 21 Tyler ML, Hudson LD, Grose BL, NMoseby JS. Prediction of oxygenation during chest physiotherapy in critically ill patients. Am Rev Respir Dis 1980; 12:218 22 George JM, Reier CE, Lanese RR, Rowen JM, Morphine anesthesia blocks the cortisol arid growth hormone response to surgical stress in humans. J Clin Endocrinol Metabol 1974; 38:736-40

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Hemodynamic Responses to Chest Physical Therapy (Klein et al)

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Attenuation of the Hemodynamic Responses to Chest Physical Therapy Patti Klein, Marcia Kemper, Charles Weissman, Stanley H. Rosenbaum, Jeffrey Askanazi and Allen I. Hyman Chest 1988;93; 38-42 DOI 10.1378/chest.93.1.38 This information is current as of May 14, 2009
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