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Manual hyperinflation causes norepinephrine release
ISSUES IN PULMONARY NURSING
Manual hyperinflation causes norepinephrine release Jennifer Paratz, MPhty, FACP, PhDa,b,c and Jeffrey Lipman, MBBCh (Wits), FFA (Crit Care), FFICANZCAa
OBJECTIVE: To measure hemodynamics and plasma catecholamines during manual hyperinflation (MHI) in ventilated patients. METHODS: MHI was performed with a Mapleson “C” circuit, 2l-reservoir bag; peak inspiratory pressure was standardized to 35 mL water; and positive expiratory-end pressure of 5 mL water was administered to seven mechanically ventilated patients with septic (6) and cardiogenic (1) shock (67.2 ⫾ 5.2 years, Acute Physiology Assessment and Chronic Health Evaluation II score 22.1 ⫾ 3.1). Diastolic (DAP) and mean arterial pressure (MAP), continuous cardiac index, pulmonary artery occlusion pressure, dynamic compliance, plasma norepinephrine and epinephrine, and arterial blood gases were recorded, and systemic vascular resistance index (SVRI) and oxygenation ratio were calculated. RESULTS: There were no significant changes in pulmonary artery occlusion pressure, mean arterial pressure, or PaO2/FiO2. There were significant increases in SVRI (P ⬍ .001), DAP (P ⬍ .001), dynamic compliance (P ⬍ .01), and plasma norepinephrine (P ⬍ .001) and a decrease in cardiac index (P ⬍ .05) after MHI. CONCLUSIONS: The increases in DAP, SVRI, and plasma norepinephrine suggest a sympathetic vasoconstrictive response during the application of MHI. (Heart Lung® 2006;35:262–268.)
M
anual hyperinflation (MHI), the technique of using a bag valve resuscitator with a reservoir bag to deliver larger-than-baseline tidal volume (VT) to ventilated patients, was originally in common use to reverse the iatrogenic effects of endotracheal suction.1 With the advent of closed suction systems, this function has became superfluous2; however, it is still in wide use in the United Kingdom, Asia, South Africa, and Australia3-5 as a physiotherapy technique to reverse the effects of mechanical ventilation, ie, loss of compliance and secretion retention. The slow inspiration and inspiratory plateau aims to recruit areas of ateleca
From Department of Anaesthesiology and Critical Care, University of Queensland, Royal Brisbane Hospital, Brisbane, Australia; Department of Physiotherapy, University of Queensland, Brisbane, Australia; and cAlfred Hospital/La Trobe University Cardiopulmonary Research Centre, Melbourne, Australia. Reprint requests: Jennifer Paratz MPhty, FACP, PhD, Department of Intensive Care, Royal Brisbane Hospital, Herston, Brisbane, Queensland, Australia 4029. 0147-9563/$ – see front matter Copyright © 2006 by Mosby, Inc. doi:10.1016/j.hrtlng.2005.12.002
b
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tatic lung,6 whereas the fast expiration acts as an “artificial cough” to increase expiratory flow rate7 and assist in mobilization of secretions.7 It has been demonstrated to be effective in improving total lung and thorax compliance,8-11 resolving atelectasis,12 decreasing inspiratory resistance,8 and increasing the amount of secretions obtained on suction.11 Despite the beneficial effect of MHI on respiratory parameters, the increased VT and reversed inspiratory-to-expiratory (I:E) ratio does have the potential to alter hemodynamics and thus overall oxygen delivery.13 This makes it difficult to establish the risk-to-benefit of using this technique in critically ill patients. There have been a range of effects in previous studies on hemodynamics10,14-18; however, a variety of personnel, peak inspiratory pressures (PIPs), positive end-expiratory pressures (PEEPs), and VTs were employed. Patient selection and treatment parameters in some studies14 did not conform to accepted guidelines for MHI.4 More recent studies10,17,18 that have controlled PIP and inclusion criteria have demonstrated minimal hemodynamic effects. We recently completed a study10 JULY/AUGUST 2006
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standardizing PIP, PEEP, and I:E ratio during MHI with minimal changes in hemodynamics. Despite no alteration in cardiac output (CO), systemic vascular resistance index (SVRI) and diastolic arterial pressure (DAP) increased after MHI, suggesting that compensatory vasoconstriction may have occurred in response to a decrease in venous return.19 Because CO was recorded by the thermodilution method, there was a delay in the final measurement, and it is possible that CO may have decreased during the procedure. We thought it important to repeat this study using a continuous method of CO to determine immediate changes in CO. Because vasoconstriction occurred after MHI in the previous study,10 we wished to investigate whether this was a compensatory response by the sympathetic system. An increase in plasma norepinephrine, with all other factors constant, indicates vasoconstriction in response to a sympathetic response20; therefore, plasma catecholamines were also measured in this study. The main dependent variables were continuous CO indexed to body surface area, SVRI, DAP, and plasma epinephrine and norepinephrine. Pulmonary artery occlusion pressure (PAOP), mean arterial blood pressure (MAP), VT, dynamic compliance (Cdyn), intrinsic PEEP (PEEPi), and PaO2/FiO2 were also recorded.
METHODS This study was a prospective within-subjects design and was completed in a tertiary intensive care facility. Approval for the study was obtained from the Royal Brisbane Hospital Ethics Committee, and written informed consent obtained from each patient’s next of kin. Subjects suitable for inclusion in this study were those who were intubated and ventilated; who had an arterial line and Vigilance™ (Baxter Edwards Critical Care, Irwin, CA) pulmonary artery catheter21 in situ; and who had PAOP⬎8 and ⬍17 mmHg, SaO2 ⬎92, and no cardiac arrhythmias present. In this unit, pulmonary artery monitoring is only used in cases of shock resistant to initial therapy. Patients were not enrolled for the study unless they had been deemed hemodynamically stable and adequately fluid loaded in the case of septic shock22 by the treating intensive care physician. Exclusion criteria included patients with fulminant pulmonary edema, severe head injury, PEEP ⬎7.5 mL water, FiO2 ⬎.7, MAP less than target MAP associated with adequate tissue perfusion, PIP ⬎40 mL water, nitric oxide, and undrained pneumothorax. Subjects were HEART & LUNG
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sedated so they could be ventilated adequately and were taking a minimal amount of spontaneous breaths. To standardize procedures, all patients were turned to a supine position for 20 minutes before the baseline measurements were recorded. All medications and ventilator parameters were kept constant during the time of measurement. Pressure monitoring was zeroed at the midaxillary level before measurement. MHI was performed for 3 minutes using a Mapleson “C” with expiratory valve (model no. CIG DF 655; Medishield) and a 2-L reservoir bag (model no. BS 3352; Warne Surgical Products, UK) connected to 100% wall oxygen at 15 L/min. The waveform consisted of inspiration for 2 seconds, sustained inspiration for 2 seconds, and a fast release of the valve to ensure a short expiration as described by McCarren et al.23 The I:E ratio was 2:1. A PIP of 30 mL water has been demonstrated to reverse atelectasis24 without causing barotrauma25; therefore, this figure was used in this study. A PEEP of 5 mL water was maintained in the MHI circuit during the procedure. One experienced operator (J.P.) performed all MHI. There was continuous feedback from the visual display downloaded to the personal computer from the Ventrak respiratory mechanics monitor (model no. 1550; Novametrix Medical Systems, Wallingford, CT) so that the correct PIP, PEEP, and I:E ratio were used. Vt, PIP, I:E ratio, MAP, Cdyn, PEEP, and PEEPi were recorded continuously throughout MHI from the respiratory mechanics monitor by way of a pneumotach placed in the MHI circuit. This was downloaded to a computer and analyzed using Analysis Plus™. Diastolic and MAP were recorded (Merlin pressure module M1006reA; Hewlett Packard) 1 minute before, during disconnection from the ventilator, at 1, 2, and 3 minutes during MHI, and at 1 and 5 minutes after MHI. The information was downloaded to a computerized information system. PAOP was taken immediately before and after MHI at end expiration.26 CO was measured by the Vigilance Cardiac Output System (Baxter Edwards Critical Care, Irwin, CA). This system21,27 employs a heated filament wrapped around a balloon flotation pulmonary artery catheter, which is positioned in the right atrium and ventricle. The heating results in a temperature change that is detected downstream in the pulmonary artery. This temperature change is cross-correlated with the input sequence and a thermodilution washout curve generated by the system’s computer (Vigilance). The CO and CI are then calculated by the computer using a modified Stewart-Hamilton equation.21 Determinations were www.heartandlung.org
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Table 1 Student t test means (SDs) of hemodynamic and respiratory variables before and after MHI Variable
Before MHI
After MHI
Mean difference (SD)
Confidence intervals
PAOP (mm Hg) SVRI (dyn s/cm5/m2) Plasma norepinephrine Plasma epinephrine PEEPi mL H2O Cdyn mL/mL H2O PaO2/FiO2
12.6(2.2) 1576.1(57.8) 2.3(1.2) 0.3(0.1) 2.50(0.51) 41.8(14.1) 243.9(69.8)
12.7(1.6) 1621.6(57.8)*** 5.2(2.2)*** 0.3(0.1) 2.53(0.47) 45.5(15.5)** 285.7(73.5)
⫺0.3(0.8) ⫺45.4(1.5) ⫺2.8(1.3) 0.0014(0.0003) ⫺.034(0.15) ⫺3.7(2.17) ⫺41.8(73.7)
⫺0.78, 0.73 ⫺46.8, ⫺44.0 ⫺4.1, ⫺1.6 ⫺0.002, 0.004 ⫺0.116, 0.047 ⫺5.73, ⫺1.7 ⫺110.0, 26.36
*P ⬍ .05; **P ⬍ .01, ***P ⬍ .00.
made automatically every 30 seconds (continuous CO indexed to body surface area). The accuracy and reliability of the Vigilance system has been extensively assessed compared with thermodilution.21,27,28 The previously mentioned measurements were used to derive SVRI. Blood samples for plasma epinephrine and norepinephrine were taken from the indwelling arterial catheter immediately before and after MHI. Arterial blood was collected into a precooled lithium heparin tube, to which an antioxidant, 0.1 mL sodium metabisulphite, had previously been added. This was centrifuged, separated, and analyzed for plasma norepinephrine and epinephrine by high-performance liquid chromatography with electrochemical detection.20 The lower limit for detection was 0.1 nmol/L, and linearity ranged from the lower limit of detection to 6.7 nmol/L. The coefficients of variation were 0.52 and 0.46 for norepinephrine and epinephrine, respectively. Arterial blood was also analyzed by an ABL620 Radiometer Copenhagen immediately before and after MHI. The results were used to derive PaO2/FiO2. From our previous study,10 15 subjects were needed for a 2-sided significance level of 5% and a power of 80%.29 We recruited 7 subjects, and power for continuous cardiac index was calculated as 76% at this stage.
DATA ANALYSIS Results were calculated using SPSS (version 11.0; SPSS, Chicago, IL). The distribution and range of scores for subjects were examined to ensure that parametric statistics could be used. Mean changes scores, SDs, and 95% confidence intervals (CIs) were calculated between times for all dependent variables. Paired Student t test was used to compare pre 264
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and post measurements of PAOP, SVRI, and plasma norepinephrine and epinephrine. A repeated-measures analysis of variance (ANOVA) compared baseline values of CCI, MAP, and DAP with values at disconnection, at 1, 2, and 3 minutes during MHI, and at 1 and 5 minutes after MHI. These are summarized as means and SDs (Tables 1 and 2). Planned comparisons were completed for any significant main effects; therefore, Bonferroni correction was not required. A probability of P ⬍ .05 was considered statistically significant.
RESULTS Seven subjects were enrolled, and all completed the study. Admitting etiology, age, ventilation parameters, Acute Physiology Assessment and Chronic Health Evaluation II scores30 (day of intensive care unit [ICU] admission), Murray lung injury scores,31 radiographic changes, sedation, and inotrope requirements are listed in Table 3. All subjects were on the Bennetts 7200 Ventilator (Nellcor-Puritan-Bennett, CA), had at least a rate of 12 on synchronized intermittent mandatory ventilation, were receiving a Vt of 8 to 10 mL/kg (with inspiratory pause pressures ⱕ30 mL water, and were defined as having mild to moderate lung injury31. As listed in Table 3, 6 subjects had septic shock,32 and 1 subject had cardiogenic shock secondary to the listed causes. As a set PIP was delivered, the resultant Vt delivered during MHI varied directly with dynamic lung compliance. The mean (SD) Vt delivered during MHI was 121.5% (⫾11.3) of the patient’s ventilator volume. Respiratory rate was 12.1 (⫾1.2) bpm. There was no change in PEEPi from baseline levels during MHI (Table 2). The mean PaO2/FiO2 ratio did not alter significantly overall (Table 2). Cdyn increased JULY/AUGUST 2006
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Table 2 Means (SDs) for hemodynamic variables before, during, and after MHI Before MHI Variable 2
CCI (L/min/m ) MAP (mm Hg) DAP (mm Hg)
During MHI
Baseline
Disconnection
1 min
2 min
3 min
1 min
5 min
3.59 (0.42) 83.6 (2.3) 61.7 (4.3)
3.61 (0.42) 83.7 (1.8) 62.8 (5.0)
3.56 (0.41) 83.9 (1.7) 63.8 (5.5)
3.54 (0.40) 84.5 (2.7) 67.0 (4.3)**
3.53 (0.40)* 85.0 (2.3) 67.5 (4.4)**
3.6 (0.41) 84.8 (2.6) 66.7 (4.2)**
3.61 (0.41) 84.5 (1.6) 65.0 (4.4)**
significantly after MHI (t(6) ⫽ ⫺4.52, P ⬍ .01, ␦ ⫽ .3). Hemodynamic parameters are detailed in Tables 1 and 2. CCI decreased during the third minute of MHI (F(1,6) ⫽ 2.42, P ⬍ .05, ␦ ⫽ .3). SVRI increased after MHI (t(6) ⫽ ⫺7.95, P ⬍.001, ␦ ⫽ .8), and DAP increased significantly (F(1,6) ⫽ 35.19, P ⬍ .001, ␦ ⫽ .8) during the procedure. All other hemodynamic parameters, ie, PAOP and MAP, did not alter during or after MHI. Plasma norepinephrine increased significantly (t(6) ⫽ ⫺5.63, P ⬍ .001, ␦ ⫽ .5) after MHI, whereas plasma epinephrine did not alter.
DISCUSSION There is no doubt that increased positive pressure has the capacity to alter hemodynamics.33 However, the effects will vary according to respiratory and cardiovascular pathophysiology and the method of delivery of positive pressure. Because beneficial respiratory effects from MHI have been documented,8-12 it is important to investigate which patients can tolerate this increase in positive pressure without deterioration in hemodynamics and, subsequently, oxygen delivery. Our previous study10 documented no change in CO after MHI with increases in SVRI and DAP. This suggested that vasoconstriction had occurred and that CO had actually decreased during MHI, which could not be detected with the intermittent method of thermodilution. The present study has provided further information and explanation regarding the effect of MHI on hemodynamics. In this group of patients with septic shock, there were small but statistically significant decreases in CCI during MHI. Because the decrease was a mean of only .08l/min/m2, this was not clinically significant. Increases occurring in SVRI, DAP, and plasma norepinephrine after MHI strongly suggest that sympathetic compensation caused vasoconstriction in response to the changes in CCI. Decreases in venous return and CO caused by positive pressure are usually offset by a compensaHEART & LUNG
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tory mechanism (vasoconstriction) modulated by the sympathetic system.19 When mechanical ventilation is applied, consideration is given to the hemodynamic effect of positive pressure, and a ventilatory pattern of short inspiration, long expiration, no inspiratory plateau, and decreased airway pressure is recommended. However, when MHI is applied, the pattern used is (1) a long inspiration with an inspiratory plateau to assist collateral ventilation6,34 and stabilization of alveoli and (2) a short expiration to maximize mean expiratory flow and mobilize secretions, ie, a reverse I:E ratio.7 Concerns regarding this pattern of ventilation on the hemodynamic system have been previously raised.13 It has not been known previously whether the hemodynamic system, having provided compensation on the initial application of mechanical ventilation, is able to compensate again on further application of positive pressure, ie, MHI. The fact that CCI decreased minimally and that this was followed by increased DAP and SVRI indicates that these patients did have adequate sympathetic compensation. Because plasma norepinephrine increased, this gives further evidence to the sympathetic nervous system being responsible for the compensation.20 Hjemjadl20 in an extensive review, stated that an increase in plasma norepinephrine, with all other factors constant, indicates vasoconstriction in response to a sympathetic response. The fact that plasma epinephrine did not increase demonstrated that this was not a stress response. No patients in this study failed to compensate for the increase in intrathoracic pressure. Lack of compensation would have been indicated by a clinically significant decrease in CO and no increase in DAP and SVRI.19 Conditions that result in a lack of compensation during positive pressure include hypovolaemia, hypocarbia, head up-tilt, administration of beta-blockers, and spinal injury. Chernow et al35 found that plasma norepinephrine levels correlated inversely with decreases in CO www.heartandlung.org
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Table 3 Demographic and baseline data of subjects Variable
Mean
Age (y) Gender (M/F) Admission APACHE II LIS Day of admission to ICU Admitting etiology Multitrauma/sepsis Cardiogenic shock Primary sepsis syndrome Community acquired pneumonia/sepsis Elective abdominal surgery/sepsis Radiographic features (unilateral/bilateral) Ventilation parameters PEEP (mLH2O) FiO2 Vt (mL) PIP PS RR (bpm) (ventilator/patient) Vasoactive support Norepinephrine (g/min) Epinephrine (g/min) Sedation Morphine/midazolam (mg/h) Glasgow Coma Scale
67.2 5/2 22 1.62 3
SD
Range
⫾ 5.2
55–76
⫾ 3.1 ⫾ 0.1 ⫾ 0.25
18–26 1.25–1.75 3–4
⫾ 1.0 ⫾ 0.1 ⫾ 122.4 ⫾ 4.1 ⫾ 2.0 0.5/0.5
5–7.5 0.30–0.55 600–900 22–35 10–15 12–14/0–3
1 1 1 2 2 4/3 5.4 0.45 770 27.1 10.9 12.6/1.1 11.2 8.9 5/5 4.1
⫾ 4.8 ⫾ 5.7 ⫾ 2.1/2.3 ⫾ 1.1
3–5
LIS, Lung Injury Score; PS, pressure support; RR, respiratory rate.
produced by PEEP in ventilated dogs. Because plasma epinephrine levels did not increase with increasing PEEP, they also considered that the response was caused by sympathetic activity. Our study confirmed this result using an intermittent method of increasing intrathoracic pressure in a clinical population. The values of plasma norepinephrine and epinephrine found in this study agreed with previous values quoted in studies.20,36,37 Kong et al37 found higher values of catecholamines in critically ill patients; however, their patients had not been well sedated before measurement. The patients in the current study were well sedated with morphine/midazolam and had a mean Glasgow coma scale of 4.1 (Table 3). Hjemdahl20 also stated that lack of specificity and reproducibility are problems encountered in measuring plasma levels catecholamines. However, because the samples in this study before and after MHI were measured by the same method and laboratory with no other intervention but MHI, the results are highly likely to be valid. 266
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In a survey on MHI, King and Morrell4 found that most physiotherapists considered medium to high inotrope requirements a contraindication to MHI. It appears that in this population, MHI has minimal effects. However, these measurements were taken at a very specific time in septic shock, ie, when fluid loading had been completed and peripheral vascular tone had returned to normal. Previous studies that have investigated increased positive pressure during septic shock10,16 have found that if patients were in a hyperdynamic state, as shown by high CO and low SVRI, there was a large decrease in CO in response to positive pressure because of the relative hypovolemia caused by peripheral vasodilatation. It may therefore be important to give consideration to hemodynamic values in these patients before selecting them for this technique, because if SVRI is low, CO may decrease significantly after positive pressure. The present study also measured only the technique of MHI. Selective positioning, MHI, and endotracheal suction are usually performed in sequence clinically to remove any secreJULY/AUGUST 2006
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tions mobilized by MHI. Significant hemodynamic effects on disconnection from the ventilator, ie, increase in preload attributed to loss of positive pressure and PEEP have previously been found.38,39 Further studies investigating both MHI and suction should be done. Strict inclusion criteria as to level of PEEP and FiO2 before disconnection as well as PAOP were followed-up in this study, which may be another reason for the differing results found in other studies.14 The effects of positive pressure can vary according to ventricular loading conditions. Pinsky et al40 found that in normal cardiac function, left ventricular stroke volume decreases after increased positive pressure. We have also demonstrated clinically significant decreases in CO in an animal model with normal cardiac function during MHI.41 An FiO2 of 1.0 was used during MHI because it was believed that if alveoli were recruited by the hyperinflation procedure, desaturation caused by pulmonary hypoxemic vasoconstriction may have occurred.42 This, however, could have had an effect on hemodynamics because an FiO2 of 1.0 can decrease CO and peripheral resistance.43 Further work is planned to compare the hemodynamic and respiratory effects of various FiO2 levels. Previous studies17 have applied MHI with an FiO2 ⬍ 1.0 with no detrimental effect on gas exchange. In recent studies, set parameters of PIP ⬍ 35 mL water have been used during MHI, resulting in smaller VTs but still resulting in improvements in static/dynamic compliance, oxygenation, and amount of secretions obtained.10,11 This is compared with previous studies where large, uncontrolled PIP and VTs were noted.14,44 This study also found an improvement in Cdyn after MHI. If beneficial respiratory and minimal hemodynamic effects can be obtained, it is obviously better to use these set limits, especially in view of protective lung strategy currently used in the ICU.45 An inverse I:E ratio such as that used in MHI has also been blamed for decreasing coronary blood flow46 and causing PEEPi.47 One patient in this study developed ischemic changes on the electrocardiogram at the end of MHI, indicating that ischemic heart disease may be a precaution for MHI. There was, however, no increase in PEEPi after MHI. This study has clinical relevance to staff working in ICUs. There was a strong indication that although cardiac index initially decreased on application of MHI in this group of patients, it did so by a clinically insignificant figure, and the patients were able to compensate by vasoconstriction. This study gives further knowledge as to patient selection for MHI. Patients on medium to high doses of inotropes are sometimes considered too unstable for physiotherHEART & LUNG
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apy intervention,4 but this study has shown that as long as the patient is adequately fluid loaded, MHI appears to be safe.
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Manual hyperinflation causes norepinephrine release Jennifer Paratz, MPhty, FACP, PhDa,b,c and Jeffrey Lipman, MBBCh (Wits), FFA (Crit Care), FFICANZCAa
OBJECTIVE: To measure hemodynamics and plasma catecholamines during manual hyperinflation (MHI) in ventilated patients. METHODS: MHI was performed with a Mapleson “C” circuit, 2l-reservoir bag; peak inspiratory pressure was standardized to 35 mL water; and positive expiratory-end pressure of 5 mL water was administered to seven mechanically ventilated patients with septic (6) and cardiogenic (1) shock (67.2 ⫾ 5.2 years, Acute Physiology Assessment and Chronic Health Evaluation II score 22.1 ⫾ 3.1). Diastolic (DAP) and mean arterial pressure (MAP), continuous cardiac index, pulmonary artery occlusion pressure, dynamic compliance, plasma norepinephrine and epinephrine, and arterial blood gases were recorded, and systemic vascular resistance index (SVRI) and oxygenation ratio were calculated. RESULTS: There were no significant changes in pulmonary artery occlusion pressure, mean arterial pressure, or PaO2/FiO2. There were significant increases in SVRI (P ⬍ .001), DAP (P ⬍ .001), dynamic compliance (P ⬍ .01), and plasma norepinephrine (P ⬍ .001) and a decrease in cardiac index (P ⬍ .05) after MHI. CONCLUSIONS: The increases in DAP, SVRI, and plasma norepinephrine suggest a sympathetic vasoconstrictive response during the application of MHI. (Heart Lung® 2006;35:262–268.)
M
anual hyperinflation (MHI), the technique of using a bag valve resuscitator with a reservoir bag to deliver larger-than-baseline tidal volume (VT) to ventilated patients, was originally in common use to reverse the iatrogenic effects of endotracheal suction.1 With the advent of closed suction systems, this function has became superfluous2; however, it is still in wide use in the United Kingdom, Asia, South Africa, and Australia3-5 as a physiotherapy technique to reverse the effects of mechanical ventilation, ie, loss of compliance and secretion retention. The slow inspiration and inspiratory plateau aims to recruit areas of ateleca
From Department of Anaesthesiology and Critical Care, University of Queensland, Royal Brisbane Hospital, Brisbane, Australia; Department of Physiotherapy, University of Queensland, Brisbane, Australia; and cAlfred Hospital/La Trobe University Cardiopulmonary Research Centre, Melbourne, Australia. Reprint requests: Jennifer Paratz MPhty, FACP, PhD, Department of Intensive Care, Royal Brisbane Hospital, Herston, Brisbane, Queensland, Australia 4029. 0147-9563/$ – see front matter Copyright © 2006 by Mosby, Inc. doi:10.1016/j.hrtlng.2005.12.002
b
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tatic lung,6 whereas the fast expiration acts as an “artificial cough” to increase expiratory flow rate7 and assist in mobilization of secretions.7 It has been demonstrated to be effective in improving total lung and thorax compliance,8-11 resolving atelectasis,12 decreasing inspiratory resistance,8 and increasing the amount of secretions obtained on suction.11 Despite the beneficial effect of MHI on respiratory parameters, the increased VT and reversed inspiratory-to-expiratory (I:E) ratio does have the potential to alter hemodynamics and thus overall oxygen delivery.13 This makes it difficult to establish the risk-to-benefit of using this technique in critically ill patients. There have been a range of effects in previous studies on hemodynamics10,14-18; however, a variety of personnel, peak inspiratory pressures (PIPs), positive end-expiratory pressures (PEEPs), and VTs were employed. Patient selection and treatment parameters in some studies14 did not conform to accepted guidelines for MHI.4 More recent studies10,17,18 that have controlled PIP and inclusion criteria have demonstrated minimal hemodynamic effects. We recently completed a study10 JULY/AUGUST 2006
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standardizing PIP, PEEP, and I:E ratio during MHI with minimal changes in hemodynamics. Despite no alteration in cardiac output (CO), systemic vascular resistance index (SVRI) and diastolic arterial pressure (DAP) increased after MHI, suggesting that compensatory vasoconstriction may have occurred in response to a decrease in venous return.19 Because CO was recorded by the thermodilution method, there was a delay in the final measurement, and it is possible that CO may have decreased during the procedure. We thought it important to repeat this study using a continuous method of CO to determine immediate changes in CO. Because vasoconstriction occurred after MHI in the previous study,10 we wished to investigate whether this was a compensatory response by the sympathetic system. An increase in plasma norepinephrine, with all other factors constant, indicates vasoconstriction in response to a sympathetic response20; therefore, plasma catecholamines were also measured in this study. The main dependent variables were continuous CO indexed to body surface area, SVRI, DAP, and plasma epinephrine and norepinephrine. Pulmonary artery occlusion pressure (PAOP), mean arterial blood pressure (MAP), VT, dynamic compliance (Cdyn), intrinsic PEEP (PEEPi), and PaO2/FiO2 were also recorded.
METHODS This study was a prospective within-subjects design and was completed in a tertiary intensive care facility. Approval for the study was obtained from the Royal Brisbane Hospital Ethics Committee, and written informed consent obtained from each patient’s next of kin. Subjects suitable for inclusion in this study were those who were intubated and ventilated; who had an arterial line and Vigilance™ (Baxter Edwards Critical Care, Irwin, CA) pulmonary artery catheter21 in situ; and who had PAOP⬎8 and ⬍17 mmHg, SaO2 ⬎92, and no cardiac arrhythmias present. In this unit, pulmonary artery monitoring is only used in cases of shock resistant to initial therapy. Patients were not enrolled for the study unless they had been deemed hemodynamically stable and adequately fluid loaded in the case of septic shock22 by the treating intensive care physician. Exclusion criteria included patients with fulminant pulmonary edema, severe head injury, PEEP ⬎7.5 mL water, FiO2 ⬎.7, MAP less than target MAP associated with adequate tissue perfusion, PIP ⬎40 mL water, nitric oxide, and undrained pneumothorax. Subjects were HEART & LUNG
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sedated so they could be ventilated adequately and were taking a minimal amount of spontaneous breaths. To standardize procedures, all patients were turned to a supine position for 20 minutes before the baseline measurements were recorded. All medications and ventilator parameters were kept constant during the time of measurement. Pressure monitoring was zeroed at the midaxillary level before measurement. MHI was performed for 3 minutes using a Mapleson “C” with expiratory valve (model no. CIG DF 655; Medishield) and a 2-L reservoir bag (model no. BS 3352; Warne Surgical Products, UK) connected to 100% wall oxygen at 15 L/min. The waveform consisted of inspiration for 2 seconds, sustained inspiration for 2 seconds, and a fast release of the valve to ensure a short expiration as described by McCarren et al.23 The I:E ratio was 2:1. A PIP of 30 mL water has been demonstrated to reverse atelectasis24 without causing barotrauma25; therefore, this figure was used in this study. A PEEP of 5 mL water was maintained in the MHI circuit during the procedure. One experienced operator (J.P.) performed all MHI. There was continuous feedback from the visual display downloaded to the personal computer from the Ventrak respiratory mechanics monitor (model no. 1550; Novametrix Medical Systems, Wallingford, CT) so that the correct PIP, PEEP, and I:E ratio were used. Vt, PIP, I:E ratio, MAP, Cdyn, PEEP, and PEEPi were recorded continuously throughout MHI from the respiratory mechanics monitor by way of a pneumotach placed in the MHI circuit. This was downloaded to a computer and analyzed using Analysis Plus™. Diastolic and MAP were recorded (Merlin pressure module M1006reA; Hewlett Packard) 1 minute before, during disconnection from the ventilator, at 1, 2, and 3 minutes during MHI, and at 1 and 5 minutes after MHI. The information was downloaded to a computerized information system. PAOP was taken immediately before and after MHI at end expiration.26 CO was measured by the Vigilance Cardiac Output System (Baxter Edwards Critical Care, Irwin, CA). This system21,27 employs a heated filament wrapped around a balloon flotation pulmonary artery catheter, which is positioned in the right atrium and ventricle. The heating results in a temperature change that is detected downstream in the pulmonary artery. This temperature change is cross-correlated with the input sequence and a thermodilution washout curve generated by the system’s computer (Vigilance). The CO and CI are then calculated by the computer using a modified Stewart-Hamilton equation.21 Determinations were www.heartandlung.org
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Table 1 Student t test means (SDs) of hemodynamic and respiratory variables before and after MHI Variable
Before MHI
After MHI
Mean difference (SD)
Confidence intervals
PAOP (mm Hg) SVRI (dyn s/cm5/m2) Plasma norepinephrine Plasma epinephrine PEEPi mL H2O Cdyn mL/mL H2O PaO2/FiO2
12.6(2.2) 1576.1(57.8) 2.3(1.2) 0.3(0.1) 2.50(0.51) 41.8(14.1) 243.9(69.8)
12.7(1.6) 1621.6(57.8)*** 5.2(2.2)*** 0.3(0.1) 2.53(0.47) 45.5(15.5)** 285.7(73.5)
⫺0.3(0.8) ⫺45.4(1.5) ⫺2.8(1.3) 0.0014(0.0003) ⫺.034(0.15) ⫺3.7(2.17) ⫺41.8(73.7)
⫺0.78, 0.73 ⫺46.8, ⫺44.0 ⫺4.1, ⫺1.6 ⫺0.002, 0.004 ⫺0.116, 0.047 ⫺5.73, ⫺1.7 ⫺110.0, 26.36
*P ⬍ .05; **P ⬍ .01, ***P ⬍ .00.
made automatically every 30 seconds (continuous CO indexed to body surface area). The accuracy and reliability of the Vigilance system has been extensively assessed compared with thermodilution.21,27,28 The previously mentioned measurements were used to derive SVRI. Blood samples for plasma epinephrine and norepinephrine were taken from the indwelling arterial catheter immediately before and after MHI. Arterial blood was collected into a precooled lithium heparin tube, to which an antioxidant, 0.1 mL sodium metabisulphite, had previously been added. This was centrifuged, separated, and analyzed for plasma norepinephrine and epinephrine by high-performance liquid chromatography with electrochemical detection.20 The lower limit for detection was 0.1 nmol/L, and linearity ranged from the lower limit of detection to 6.7 nmol/L. The coefficients of variation were 0.52 and 0.46 for norepinephrine and epinephrine, respectively. Arterial blood was also analyzed by an ABL620 Radiometer Copenhagen immediately before and after MHI. The results were used to derive PaO2/FiO2. From our previous study,10 15 subjects were needed for a 2-sided significance level of 5% and a power of 80%.29 We recruited 7 subjects, and power for continuous cardiac index was calculated as 76% at this stage.
DATA ANALYSIS Results were calculated using SPSS (version 11.0; SPSS, Chicago, IL). The distribution and range of scores for subjects were examined to ensure that parametric statistics could be used. Mean changes scores, SDs, and 95% confidence intervals (CIs) were calculated between times for all dependent variables. Paired Student t test was used to compare pre 264
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and post measurements of PAOP, SVRI, and plasma norepinephrine and epinephrine. A repeated-measures analysis of variance (ANOVA) compared baseline values of CCI, MAP, and DAP with values at disconnection, at 1, 2, and 3 minutes during MHI, and at 1 and 5 minutes after MHI. These are summarized as means and SDs (Tables 1 and 2). Planned comparisons were completed for any significant main effects; therefore, Bonferroni correction was not required. A probability of P ⬍ .05 was considered statistically significant.
RESULTS Seven subjects were enrolled, and all completed the study. Admitting etiology, age, ventilation parameters, Acute Physiology Assessment and Chronic Health Evaluation II scores30 (day of intensive care unit [ICU] admission), Murray lung injury scores,31 radiographic changes, sedation, and inotrope requirements are listed in Table 3. All subjects were on the Bennetts 7200 Ventilator (Nellcor-Puritan-Bennett, CA), had at least a rate of 12 on synchronized intermittent mandatory ventilation, were receiving a Vt of 8 to 10 mL/kg (with inspiratory pause pressures ⱕ30 mL water, and were defined as having mild to moderate lung injury31. As listed in Table 3, 6 subjects had septic shock,32 and 1 subject had cardiogenic shock secondary to the listed causes. As a set PIP was delivered, the resultant Vt delivered during MHI varied directly with dynamic lung compliance. The mean (SD) Vt delivered during MHI was 121.5% (⫾11.3) of the patient’s ventilator volume. Respiratory rate was 12.1 (⫾1.2) bpm. There was no change in PEEPi from baseline levels during MHI (Table 2). The mean PaO2/FiO2 ratio did not alter significantly overall (Table 2). Cdyn increased JULY/AUGUST 2006
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Table 2 Means (SDs) for hemodynamic variables before, during, and after MHI Before MHI Variable 2
CCI (L/min/m ) MAP (mm Hg) DAP (mm Hg)
During MHI
Baseline
Disconnection
1 min
2 min
3 min
1 min
5 min
3.59 (0.42) 83.6 (2.3) 61.7 (4.3)
3.61 (0.42) 83.7 (1.8) 62.8 (5.0)
3.56 (0.41) 83.9 (1.7) 63.8 (5.5)
3.54 (0.40) 84.5 (2.7) 67.0 (4.3)**
3.53 (0.40)* 85.0 (2.3) 67.5 (4.4)**
3.6 (0.41) 84.8 (2.6) 66.7 (4.2)**
3.61 (0.41) 84.5 (1.6) 65.0 (4.4)**
significantly after MHI (t(6) ⫽ ⫺4.52, P ⬍ .01, ␦ ⫽ .3). Hemodynamic parameters are detailed in Tables 1 and 2. CCI decreased during the third minute of MHI (F(1,6) ⫽ 2.42, P ⬍ .05, ␦ ⫽ .3). SVRI increased after MHI (t(6) ⫽ ⫺7.95, P ⬍.001, ␦ ⫽ .8), and DAP increased significantly (F(1,6) ⫽ 35.19, P ⬍ .001, ␦ ⫽ .8) during the procedure. All other hemodynamic parameters, ie, PAOP and MAP, did not alter during or after MHI. Plasma norepinephrine increased significantly (t(6) ⫽ ⫺5.63, P ⬍ .001, ␦ ⫽ .5) after MHI, whereas plasma epinephrine did not alter.
DISCUSSION There is no doubt that increased positive pressure has the capacity to alter hemodynamics.33 However, the effects will vary according to respiratory and cardiovascular pathophysiology and the method of delivery of positive pressure. Because beneficial respiratory effects from MHI have been documented,8-12 it is important to investigate which patients can tolerate this increase in positive pressure without deterioration in hemodynamics and, subsequently, oxygen delivery. Our previous study10 documented no change in CO after MHI with increases in SVRI and DAP. This suggested that vasoconstriction had occurred and that CO had actually decreased during MHI, which could not be detected with the intermittent method of thermodilution. The present study has provided further information and explanation regarding the effect of MHI on hemodynamics. In this group of patients with septic shock, there were small but statistically significant decreases in CCI during MHI. Because the decrease was a mean of only .08l/min/m2, this was not clinically significant. Increases occurring in SVRI, DAP, and plasma norepinephrine after MHI strongly suggest that sympathetic compensation caused vasoconstriction in response to the changes in CCI. Decreases in venous return and CO caused by positive pressure are usually offset by a compensaHEART & LUNG
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tory mechanism (vasoconstriction) modulated by the sympathetic system.19 When mechanical ventilation is applied, consideration is given to the hemodynamic effect of positive pressure, and a ventilatory pattern of short inspiration, long expiration, no inspiratory plateau, and decreased airway pressure is recommended. However, when MHI is applied, the pattern used is (1) a long inspiration with an inspiratory plateau to assist collateral ventilation6,34 and stabilization of alveoli and (2) a short expiration to maximize mean expiratory flow and mobilize secretions, ie, a reverse I:E ratio.7 Concerns regarding this pattern of ventilation on the hemodynamic system have been previously raised.13 It has not been known previously whether the hemodynamic system, having provided compensation on the initial application of mechanical ventilation, is able to compensate again on further application of positive pressure, ie, MHI. The fact that CCI decreased minimally and that this was followed by increased DAP and SVRI indicates that these patients did have adequate sympathetic compensation. Because plasma norepinephrine increased, this gives further evidence to the sympathetic nervous system being responsible for the compensation.20 Hjemjadl20 in an extensive review, stated that an increase in plasma norepinephrine, with all other factors constant, indicates vasoconstriction in response to a sympathetic response. The fact that plasma epinephrine did not increase demonstrated that this was not a stress response. No patients in this study failed to compensate for the increase in intrathoracic pressure. Lack of compensation would have been indicated by a clinically significant decrease in CO and no increase in DAP and SVRI.19 Conditions that result in a lack of compensation during positive pressure include hypovolaemia, hypocarbia, head up-tilt, administration of beta-blockers, and spinal injury. Chernow et al35 found that plasma norepinephrine levels correlated inversely with decreases in CO www.heartandlung.org
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Table 3 Demographic and baseline data of subjects Variable
Mean
Age (y) Gender (M/F) Admission APACHE II LIS Day of admission to ICU Admitting etiology Multitrauma/sepsis Cardiogenic shock Primary sepsis syndrome Community acquired pneumonia/sepsis Elective abdominal surgery/sepsis Radiographic features (unilateral/bilateral) Ventilation parameters PEEP (mLH2O) FiO2 Vt (mL) PIP PS RR (bpm) (ventilator/patient) Vasoactive support Norepinephrine (g/min) Epinephrine (g/min) Sedation Morphine/midazolam (mg/h) Glasgow Coma Scale
67.2 5/2 22 1.62 3
SD
Range
⫾ 5.2
55–76
⫾ 3.1 ⫾ 0.1 ⫾ 0.25
18–26 1.25–1.75 3–4
⫾ 1.0 ⫾ 0.1 ⫾ 122.4 ⫾ 4.1 ⫾ 2.0 0.5/0.5
5–7.5 0.30–0.55 600–900 22–35 10–15 12–14/0–3
1 1 1 2 2 4/3 5.4 0.45 770 27.1 10.9 12.6/1.1 11.2 8.9 5/5 4.1
⫾ 4.8 ⫾ 5.7 ⫾ 2.1/2.3 ⫾ 1.1
3–5
LIS, Lung Injury Score; PS, pressure support; RR, respiratory rate.
produced by PEEP in ventilated dogs. Because plasma epinephrine levels did not increase with increasing PEEP, they also considered that the response was caused by sympathetic activity. Our study confirmed this result using an intermittent method of increasing intrathoracic pressure in a clinical population. The values of plasma norepinephrine and epinephrine found in this study agreed with previous values quoted in studies.20,36,37 Kong et al37 found higher values of catecholamines in critically ill patients; however, their patients had not been well sedated before measurement. The patients in the current study were well sedated with morphine/midazolam and had a mean Glasgow coma scale of 4.1 (Table 3). Hjemdahl20 also stated that lack of specificity and reproducibility are problems encountered in measuring plasma levels catecholamines. However, because the samples in this study before and after MHI were measured by the same method and laboratory with no other intervention but MHI, the results are highly likely to be valid. 266
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In a survey on MHI, King and Morrell4 found that most physiotherapists considered medium to high inotrope requirements a contraindication to MHI. It appears that in this population, MHI has minimal effects. However, these measurements were taken at a very specific time in septic shock, ie, when fluid loading had been completed and peripheral vascular tone had returned to normal. Previous studies that have investigated increased positive pressure during septic shock10,16 have found that if patients were in a hyperdynamic state, as shown by high CO and low SVRI, there was a large decrease in CO in response to positive pressure because of the relative hypovolemia caused by peripheral vasodilatation. It may therefore be important to give consideration to hemodynamic values in these patients before selecting them for this technique, because if SVRI is low, CO may decrease significantly after positive pressure. The present study also measured only the technique of MHI. Selective positioning, MHI, and endotracheal suction are usually performed in sequence clinically to remove any secreJULY/AUGUST 2006
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tions mobilized by MHI. Significant hemodynamic effects on disconnection from the ventilator, ie, increase in preload attributed to loss of positive pressure and PEEP have previously been found.38,39 Further studies investigating both MHI and suction should be done. Strict inclusion criteria as to level of PEEP and FiO2 before disconnection as well as PAOP were followed-up in this study, which may be another reason for the differing results found in other studies.14 The effects of positive pressure can vary according to ventricular loading conditions. Pinsky et al40 found that in normal cardiac function, left ventricular stroke volume decreases after increased positive pressure. We have also demonstrated clinically significant decreases in CO in an animal model with normal cardiac function during MHI.41 An FiO2 of 1.0 was used during MHI because it was believed that if alveoli were recruited by the hyperinflation procedure, desaturation caused by pulmonary hypoxemic vasoconstriction may have occurred.42 This, however, could have had an effect on hemodynamics because an FiO2 of 1.0 can decrease CO and peripheral resistance.43 Further work is planned to compare the hemodynamic and respiratory effects of various FiO2 levels. Previous studies17 have applied MHI with an FiO2 ⬍ 1.0 with no detrimental effect on gas exchange. In recent studies, set parameters of PIP ⬍ 35 mL water have been used during MHI, resulting in smaller VTs but still resulting in improvements in static/dynamic compliance, oxygenation, and amount of secretions obtained.10,11 This is compared with previous studies where large, uncontrolled PIP and VTs were noted.14,44 This study also found an improvement in Cdyn after MHI. If beneficial respiratory and minimal hemodynamic effects can be obtained, it is obviously better to use these set limits, especially in view of protective lung strategy currently used in the ICU.45 An inverse I:E ratio such as that used in MHI has also been blamed for decreasing coronary blood flow46 and causing PEEPi.47 One patient in this study developed ischemic changes on the electrocardiogram at the end of MHI, indicating that ischemic heart disease may be a precaution for MHI. There was, however, no increase in PEEPi after MHI. This study has clinical relevance to staff working in ICUs. There was a strong indication that although cardiac index initially decreased on application of MHI in this group of patients, it did so by a clinically insignificant figure, and the patients were able to compensate by vasoconstriction. This study gives further knowledge as to patient selection for MHI. Patients on medium to high doses of inotropes are sometimes considered too unstable for physiotherHEART & LUNG
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apy intervention,4 but this study has shown that as long as the patient is adequately fluid loaded, MHI appears to be safe.
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