VENTILATION Mechanical Ventilation for COPD AirTrap Control, Trigger Lockout and Expiratory Pressure Ramp
Foreword This brochure explains the underlying disorders in respiratory mechanics in cases of COPD (Chronic Obstructive Pulmonary Disease) with emphysemic components and the difficulties those disorders present for spontaneous breathing and mechanical ventilation. It also covers therapeutic options developed to optimize ventilation treatment for affected patients. In the first section the reader should acquire a basic understanding of the pathophysiology of the clinical pictures of COPD and pulmonary emphysema and the effects on respiratory mechanics. The second section describes special ventilator functions specifically developed to overcome these constraints under mechanical ventilation. 2 Mechanical Ventilation for COPD
Contents Abnormality in Respiratory Mechanics in COPD... 4 Closure of Small Airways... 5 Expiratory Flow Limitation and Dynamic Hyperinflation... 9 I:E Ratio... 11 Fluctuations in Expiratory Flow Curve...12 Overview of Disorders... 13 Therapeutic Functions for Ventilation in COPD Cases...15 AirTrap Control... 15 Trigger Lockout...18 Expiratory Pressure Ramp... 21 Overview of Mechanical Ventilation Functions...24 Summary...25 Bibliography...27 Mechanical Ventilation for COPD 3
Abnormality in Respiratory Mechanics in COPD Patients with Chronic Obstructive Pulmonary Disease (COPD) often suffer from dyspnea, or severe respiratory distress. Various disorders of respiratory mechanics result in insufficient ventilation, which can be life-threatening. The main characteristic of these disorders is a limitation of expiratory flow, which can give rise to the diverse consequences described on the following pages. expiratory flow inspiratory flow time Figure 1: Breath of a patient with COPD 4 Mechanical Ventilation for COPD
Closure of Small Airways Healthy Lung Tissue Lung Tissue with tendency to collapse elastic suspension in small airways + 5 hpa + 3 hpa loss of elastic structure + 2 hpa + 3 hpa reduced airway pressure and closure paw = 1 hpa paw = 2 hpa Edema and secretions elastic recoil + 3 hpa + 6 hpa + 4 hpa Healthy Alveoli Emphysema reduced elastic recoil + 1 hpa Thoracic cavity + 3 hpa Figure 2: Depiction of airway's tendency to close due to pulmonary emphysema and chronic obstructive bronchitis in comparison to healthy lung tissue. In this numerical example, the numbers are only representative of possible pressure ratios at the start of expiration. Mechanical Ventilation for COPD 5
The cause of flow limitations lies in the joint appearance of two phenomena. 1 1. Inflammatory changes to airways (chronic obstructive bronchitis) cause constriction of the bronchial muscles, the development of mucosal membrane edema and increased secretion production. These changes result in a narrowing of the airway lumen and an increased resistance to inspiratory and expiratory flow. 2. The development of pulmonary emphysema means the degradation of alveolar walls and decreased elastic recoil of lung tissue. The loss of structure in the lung parenchyma results in a reduction in the elastic recoil required for expiration and in the connective tissue of the small airways. The sometimes severe effects of these two phenomena are shown in a numerical example (Figure 2) and explained in the following paragraphs: Elastic recoil of the alveolar walls is responsible for the outward flow of air during expiration. For deep respiratory positions, additional inwardly directed forces come into effect due to the prestrained thorax. This pressure contributes to elastic recoil, but at the same time it presses against the airways, potentially causing them to collapse. The difference between the airway pressure and intrathoracic pressure is the physical factor which, together with the elastic suspension in the pulmonary structure, determines the caliber of the airway lumen and, in extreme cases, whether the airway remains open or closes. Elastic recoil of the alveolar walls is high in healthy lung tissue. In cases of emphysema, the expulsion force is reduced and the elastic suspension of the airways in the connective lung tissue is decreased. This condition combined with the obstruction-caused pressure loss along the airways results in unfavorable pressure distribution typical of COPD and can cause localized collapses. The narrowing of the airways leads to increased pressure loss during the outward flow. The intrabronchial pressure along the flow toward the upper airways decreases much faster than in a healthy lung. For lungs impaired by chronic obstructive bronchitis and emphysema, these unfavorable conditions cause the regional pressure to sink below the intrathoracic pressure at a certain point along the airway. 6 Mechanical Ventilation for COPD
At that point the affected bronchial branch collapses and the expiratory flow ceases for the moment. The decreased elastic suspension in the bronchial walls caused by emphysema exacerbates the tendency of the airway to collapse. After a breakdown in regional flow, an equalization of pressure occurs with the pulmonary area at the alveolar level and the affected airway can once again be opened if the remaining elastic recoil in the emphysematous area is greater than the intrathoracic pressure. The depicted events involving the closing and re-opening of the bronchial branches can recur in a cyclical fashion. These events often accompany after peak flow is exceeded the early phase of expiration and typically disappear later. Mechanical Ventilation for COPD 7
Explanation of tendency to collapse, based on numerical examples from figure 2 on page 5: The pressure figures in Figure 2 are examples only and could vary greatly from reality. In healthy lungs the contraction of the alveolar walls generates expulsion pressure of 6 hpa at the start of expiration, but the pressure is only 4 hpa in patients with emphysema. This pressure is generated by the joint effect of thoracic tension with the resulting positive pressure of 3 hpa and the respective elastic recoil in the alveolar or emphysematous wall. In this example recoil leads to a pressure of 1 hpa for emphysema, which is lower than the pressure of 3 hpa in the healthy alveoli. Along the constricted airway in the diseased lung (right), a severe pressure loss (ΔpAW) of 2 hpa occurs with the expiratory flow up to a certain point in the airway. While the intrabronchial pressure in the healthy lung is always greater than the ambient thoracic pressure in the schematically portrayed section of flow, the pressure at this point in the diseased lung has an absolute value of 2 hpa, which is already below thoracic pressure. The elastic suspension of the bronchial walls is lower than in the healthy lungs. Under these pressure conditions, the airway collapses. Healthy Lung Tissue Lung Tissue with tendency to collapse elastic suspension in small airways + 5 hpa + 3 hpa loss of elastic structure + 2 hpa + 3 hpa reduced airway pressure and closure Figure 2, thumbnail illustration paw = 1 hpa paw = 2 hpa Edema and secretions elastic recoil + 3 hpa + 6 hpa + 4 hpa Healthy Alveoli Emphysema reduced elastic recoil + 1 hpa Thoracic cavity + 3 hpa 8 Mechanical Ventilation for COPD
Expiratory Flow Limitation and Dynamic Hyperinflation Time Exspiratory flow Vte (EFL) Vte (normal) Collapse of small airways Expiratory Flow Limitation Figure 3: Expiratory Flow Limitation and reduction of expiratory volume physiological expiration curve, expiration curve with flow limitation and decreased expiratory tidal volume V T. At the large airway level the distally occurring collapses in total are recognized as Expiratory Flow Limitation (EFL). A corresponding flow curve is shown in Figure 3 together with a physiological flow curve. Because the area below the flow curve (integral) represents expiratory volume, it is immediately recognizable that the expiratory volume is lower than in the physiological flow curve. In contrast to expiratory flow, the inspiratory flow in COPD is not impaired by the airways' tendency to collapse and thus the inhaled volume is less limited than expiratory volume. Inspiration follows an incomplete expiration. When this imbalance persists, a shift in the respiratory position occurs with decreasing inspiratory reserve and increasing end-expiratory volume and in- Mechanical Ventilation for COPD 9
upper inflection point V p C = 50 ml/ mbar TLC lower inflection point V p p V C = 100 ml/ mbar C = 50 ml/ mbar FRC RV intrapulmonary pressure (mbar) Figure 4: Compliance curve of the lungs showing areas of normal compliance and lower elasticity close to the 'inflection points' trinsic positive end-expiratory pressure (PEEPi) rises. This process is called "dynamic hyperinflation" or "air trapping". The intrinsic PEEP thus generated requires increased respiratory effort in that the patient works harder to overcome this threshold loading with every spontaneous breath on top of the workload proportional to the depth of the breath. A further consequence of hyperinflation is a lowered diaphragm, a mechanically unfavorable position, which translates into a significant loss of strength. Thoracic movements take place in the upper range of the compliance curve (see Figure 4). At that point the lungs are restricted, a situation which, coupled with the reduced effectiveness of muscular contraction, further increases the work of breathing. These aspects of the mechanically unfavorable situation in COPD and pulmonary emphysema result in increased respiratory effort with decreased volume displacement. Spontaneous breathing is 10 Mechanical Ventilation for COPD
made significantly more difficult and ventilatory reserves are severely limited. This situation particularly during physical exercise can lead to the pulmonary system's inability to respond to instructions from the respiratory center. The patient suffers from dyspnea. Mechanical ventilation is also made more difficult by the functional restriction in the upper range of the compliance curve. In some circumstances, sufficient mechanical ventilation is possible only with high ventilation pressures. I:E Ratio Expiratory Flow Limitation inevitably leads to a breathing pattern adjustment on the part of the patient. The proportion of time for expiration increases, yielding the low I:E ratios typically observed in cases of COPD. bronchial muscles can also contribute to variance in the breathing pattern. The extent of an obstruction which changes during the course of a day, for example, may also require different settings to be made on the ventilator. The selection of correct ventilation settings is made more difficult by this situation. A suitable I:E ratio is dependent upon the extent of the current hyperinflation and can require extreme value settings, particularly for ventilation of exacerbations. A variable tone in the Mechanical Ventilation for COPD 11
Fluctuations in Expiratory Flow Curve The reopening of the airways, as described above, may follow a regional expiratory closure. The interaction of numerous flow fractions in the expiratory flow subject to this phenomenon, leads to behavior characteristic of emphysema. The cyclical closing and reopening provoke flow fluctuations at the level of large airways, where all flow fractions overlap. The fluctuations can be observed at a point in time after expiratory peak flow values are exceeded. Figure 5 shows a corresponding typical curve with signal fluctuations. For the ventilator these fluctuations pose a significant challenge. Spontaneous (S mode) or spontaneous timed (ST mode) BiLevel ventilation can be greatly impaired under these conditions. Fluctuation-caused short-term flow increases mislead the trigger algorithm and can be falsely interpreted as inspiratory effort by the ventilator. In this case asynchrony between patient and ventilator threat- Time Expiratory flow Normal expiratory flow Expiratory flow in pulmonary emphysema Fluctuation due to cyclical bronchial collapse and subsequent re-opening Figure 5: Expiratory flow curve with flow limitation and signal disruptions caused by cyclical closing and reopening of bronchial branches. The disruptions are exaggerated for emphasis. 12 Mechanical Ventilation for COPD
ens and patient "fighting" with the ventilator may occur. These problems prompt users to make device settings with less sensitive trigger thresholds in order to achieve synchronization between ventilator and patient. A high trigger threshold at the start of inspiration is unfavorable. The patient's work of breathing is increased and the extent to which the ventilator can unload the respiratory pump is minimized. Overview of Disorders The abnormalities of respiratory mechanics typically observed in COPD and pulmonary emphysema are summarized in Figure 6. The aspects listed give rise to notable difficulties under ventilation too. Results of non-invasive ventilation in particular are less positive for COPD patients than for patients with neuromuscular disorders or chest wall deformities. 2 The difficulties with regard to synchronization of patient and ventilator are pronounced in assisted ventilation, especially in cases of COPD. 3 Moreover, it is often difficult for patients to achieve adequate therapy compliance. The ventilation functions presented on the following pages can help to improve mechanical ventilation and increase patients' compliance. Mechanical Ventilation for COPD 13
Cyclical closing of small airways Expiratory Flow Limitation Fluctuations in flow curve Dynamic hyperinflation False triggering Increase in PEEPi Lowered diaphragm and reduction of effective diaphragmatic strength Functional Restriction Setting of less sensitive trigger levels Increase in work of breathing under S/ST BiLevel ventilation Increase in work of breathing High ventilation pressures Asynchronism with ventilator Difficult therapy / low patient compliance Effect of disorder on ventilation General effect on respiratory mechanics Figure 6: Airway closure in cases of COPD and pulmonary emphysema during expiration and the effects on respiratory mechanics for spontaneous breathing and mechanical ventilation 14 Mechanical Ventilation for COPD
Therapeutic Functions for Ventilation in COPD Cases AirTrap Control Ventilation pressure IPAP Switch to Inspiration Expiratory flow Pressure EPAP exp. flow 0 Time T E from frequency setting Figure 7: Incomplete expiration due to ventilator's premature switchover to inspiration. The disruptions are exaggerated to show the comparison to real conditions. Air Trapping or dynamic hyperinflation is the major complication of expiratory flow limitation with the previously described ramifications for respiratory mechanics. During ventilation the phenomenon of air trapping can be provoked or worsened (possibly only in phases) if the device settings are not precisely attuned to the current needs of the patient. Figure 7 shows a sample expiration flow curve that is prematurely interrupted by the ventilator. The patient flow at the switchover to inspiration is not equal to zero; therefore the expiration is incomplete and the threat of air trapping is present. AirTrap Control offers a way to monitor expiration with respect to potential hyperinflation under timed (T mode) or spontaneous/ timed (ST mode) BiLevel ventilation of COPD. The effect of AirTrap Control can be seen in the sample of the curve Mechanical Ventilation for COPD 15
in Figure 8. As part of expiration curve monitoring, a check is made of whether residual flow is present at the end of the pre-set expiratory time. If over the course of respiration air trapping and an increase in intrinsic PEEP are detected, the mandatory (T mode) or the maximum allowable expiration time (ST mode) is adjusted in order to permit fuller expiration and to counteract dynamic hyperinflation. When necessary, additional expiration time is allowed to prevent hyperinflation of the lungs and to sink the functional residual capacity in favor of increased inspiratory capacity. Expiratory flow Pressure Ventilation pressure EPAP Corrected timing of switch to inspiration made by AirTrap Control Time T E from frequency setting + extension Figure 8: Delay in the timing of switch to inspiratory pressure (compared to Figure 7) by means of AirTrap Control based on analyzed flow curve. A complete expiration takes place. 16 Mechanical Ventilation for COPD
Under AirTrap Control, therefore, a decrease in end-expiratory lung volume and a reduction of intrinsic PEEP (PEEPi) are favored. Lung compliance increases (as seen in the compliance curve in Figure 4) as the respiratory position lowers to yield a sufficient gap to total lung capacity. Ventilation is thus simplified and at the same ventilation pressure the tidal volume is increased. The present rate can be reduced by opportunistic extension of respiratory cycle times. At increasing tidal volumes, the reduced rate can nevertheless have a positive effect on respiratory minute volume. When alveolar ventilation (i.e., the extent of gas exchange in the alveoli) is regarded in place of externally measured minute ventilation, we see favorable effects from reducing the rate in phases while simultaneously increasing tidal volume as the proportion of anatomical dead space is less significant. Carbon dioxide elimination can also be improved by a temporarily decreased respiratory rate. Particularly in the long term, better ventilation is to be expected through a reduction of the resting respiratory level and an increase in inspiratory reserve. Alveolar Minute Ventilation V alv = (V tidal V Dead space) respiratory rate Limitation of expiratory extension Numerous critera ensure that under ventilation with AirTrap Control, the resulting minimal rate can sink to a limited extent only. Limitation of expiratory prolongation The pre-set time for expiration (T E) is prolonged by a maximum of 50 %. T E is prolonged for a maximum of 0.8 seconds. Maximum TE is 8 seconds at minimum rate. The smallest possible rate with AirTrap Control is f min = 6 /min. Mechanical Ventilation for COPD 17
Trigger Lockout Expiratory flow Pressure IPAP EPAP Switch to inspiratory pressure prompted by fluctuations in flow signal Time Brief T E on part of device through false triggering Ventilation pressure Figure 9: Assisted ventilation with false triggering caused by fluctuations in the flow curve with a sensitively set trigger without trigger lockout. The fluctuations are exaggerated in relation to realratios. In practice the expiratory flow is affected by the pressure increase, which is not shown for sake of simplicity. We saw in Section 1 that in some phases expiration is accompanied by fluctuations which can mislead the trigger algorithm in ventilators. Figure 9 shows a typical situation in a pressure curve during ventilation with a sensitive trigger setting without a preset lockout period. The steep rise in the expiration curve along the fluctuations can be interpreted by the ventilator as inspiratory effort. In spontaneous (S mode) or spontaneous/timed (ST mode) modes, the ventilator responds to such rises by prematurely switching to the inspiratory phase in accordance with the pre-set sensitive threshold. It is quite likely that asynchronism will develop between patient and ventilator in such situations and that patient fighting will ensue. The standard practice is to select a trigger level with low sensitivity in order to avoid the problem. However, the low sensitivity increases the work of breath- 18 Mechanical Ventilation for COPD
ing for the patient because the ventilator unloads the patient's respiratory pump at a later point during inspiration, making the unloading less effective. The function trigger block offers a solution. When the trigger lockout is activated, the switch to the inspiratory pressure level is temporarily blocked for a pre-set period measured from the start of expiration. When the pre-set period is over, the ventilator is then allowed to react to the trigger signal and switch to the inspiratory phase, during which a patient-initiated inspiration is expected. Because the fluctuations described decrease or disappear entirely when the expiration time is increased, the trigger sensitivity can be raised with an activated trigger block without running the risk of provoking false triggering. The work of breathing can be decreased further than with conventional assisted ventilation through the use of a sensitive trigger setting which is active during the crucial phase in the respiratory cycle only. Figure 10 shows the effect of the function when a properly chosen trigger lockout is Expiratory flow Pressure EPAP Trigger lockout period prevents a premature switch to inspiratory pressure when fluctuations occur in flow curve. Time Trigger lockout period Ventilation pressure Figure 10: Prevent the ventilator from making a premature switch to inspiratory phase (see Figure 9) with the setting of a suitable trigger lockout period. Mechanical Ventilation for COPD 19
used. At the start of expiration within the locked period, the ventilator ignores patient-generated signals which can misrepresent the start of an inspiration. First when the trigger lockout period has passed, the switch to inspiration is permitted. The setting of the trigger lockout is made (as shown in Figure 11) in relation to the maximum amount of time available for expiration, which is derived from the pre-set backup respiratory rate and the I:E ratio. Trigger Scaled display of lockout period (here 1.1 sec.) Expiration cycle Online display of position in expiration cycle Figure 11: Setting of trigger lockout period on ventilator. If the trigger for inspiration is blocked during activated trigger lockout time, a "B" is shown in the display. A spontaneously triggered respiratory phase change is indicated by an "S" in the display. 20 Mechanical Ventilation for COPD
Advantages of trigger lockout period Reduced risk of false triggering Setting of sensitive trigger level possible; a properly chosen level reduces the work of breathing Improved synchronism between patient and ventilator and thus stabilization of ventilation situation. The Expiratory Pressure Ramp An unrestrained expiration and a quick transition from high inspiratory ventilation pressure to expiratory pressure (PEEP) in a case of pulmonary emphysema can lead to or promote local collapse of airways and flow limitation, as described in Section 1. The airway altered by disease is left to its own devices and subject to the described adverse mechanical conditions. Figure 12 shows a corresponding flow curve in the presence of pulmonary emphysema, together with a ventilation pressure curve with a steep transition from inspiration pressure to expiration pressure. However, it is possible to protect the small airways from collapse with use of a quickly acting pneumatic splint at the start of expiration. For spontaneous breathing, for example, the Deutsche Atemwegsliga (German society of respiratory/pneumology experts) recommends the application of expiratory stenosis to effect an increase in intrabronchial pressure. 4 This pressure increase shifts the balance of forces on the bronchial wall in favor of increased airway width and can, in an ideal situation, keep the airways open in general or at least for a longer period of time. A comparable effect can be achieved through a prolongtion of Mechanical Ventilation for COPD 21
IPAP Steep pressure decrease Expiratory flow Pressure EPAP Expir. flow curve in case of pulmonary emphysema without "splinting" Time Ventilation pressure Figure 12: Expiratory flow curve under ventilation with steep pressure decrease and EPAP or PEEP 0 the expiratory pressure ramp (see flow curve in Figure 13). The application of a slowly decreasing expiratory pressure ramp is of course possible without the ventilator's use of an increased extrinsic PEEP or EPAP. A pressure ramp is particularly effective because the counterpressure helps in the phase in which the flow's contribution is great and the local thoracic pressure is particularly high due to hyperinflation. The risk of collapse in this early expiratory phase is especially high. An expiratory ramp similar to the effect of pursed lips breathing is an effective countermeasure. The alternative raising of end-expiratory pressure, on the other hand, can be disadvantageous because either the effective ventilation pressure (pressure difference between IPAP and PEEP) will be reduced or the inspiratory pressure will have to be increased further. 22 Mechanical Ventilation for COPD
IPAP Gradual pressure decrease Expiratory flow Pressure EPAP Raising of the expiratory flow curve through phased "splinting" of airways Time Ventilation pressure Figure 13: Effect of a flat pressure transition between inspiratory pressure and expiratory pressure in the flow curve in expiration (dotted line: curve with steep pressure decrease; solid line: curve with flat pressure decrease): The flow remains larger on average and the expiration volume can be increased by the temporary splint. The expiratory collapse can be counteracted by the intrabronchial pressure increase at the start of expiration and a carefully monitored reduction of the expiratory peak flow. The expiratory flow remains larger on average; the volume can be exhaled more easily and respiratory position can be lowered. Mechanical Ventilation for COPD 23
Overview of Mechanical Ventilation Functions Enhanced ventilation functionality through: AirTrap Control Expiratory pressure ramp Trigger lockout period Increase of tidal volume Splinting of small airways No premature switch to inspiration phase Decrease of PEEPi and reduction of functional restriction Increased synchrony between patient and ventilator Improved alveolar ventilation Greater unloading of respiratory pump Figure 14: Overview of mechanical ventilation functions and their effect on ventilation of COPD patients 24 Mechanical Ventilation for COPD
Summary COPD and pulmonary emphysema are characterized by limitations in respiratory mechanics as seen in the cyclical collapse of airways during expiration. The causes are airway obstructions and loss of structural integrity in the lung parenchyma. These pathophysiological features of respiratory mechanics greatly impair more than just the patient's spontaneous breathing. Achieving sufficient ventilation by means of a mechanical ventilator can also be more difficult in cases of COPD than in other diseases requiring similar treatment. Unloading of the respiratory pump can also be more challenging in the presence of these particular disorders. Nevertheless, mechanical ventilation is an essential element in the treatment of COPD with hyperinflation and an overloaded respiratory pump. Ventilation therapy can be expanded and optimized with the addition of various therapeutic options. With AirTrap Control, for instance, spontaneous/timed (ST mode) or timed (T mode) BiLevel ventilation can be more effectively adapted to dynamic hyperinflation and a concomitant functional stiffening caused by an upward shift in the resting expiratory level. Hyperinflation can be counteracted or deflation made possible when the expiratory flow curve is monitored. With the help of the trigger lockout, spontaneous (S mode) or spontaneous/ timed (ST mode) BiLevel ventilation can be better adjusted to the course of the expiratory flow curve with signal fluctuations. With the trigger temporarily disabled at the start of expiration, high trigger sensitivity is permitted in the phase which is crucial for the switchover to the next inspiration. Ventilation is stabilized and the synchrony between patient and ventilator is improved while the respiratory pump is more effectively unloaded by the ventilator. A temporary pneumatic splint in the particularly critical phase at the start of expiration is realized by means of a suitable expiratory pressure ramp. The effect is physically comparable to the respiratory method of pursed lips breathing used by spontaneously breathing patients. In this way the expiratory flow limitation and dynamic hyperinflation can be counteracted at its "roots". These therapeutic functions add to the "arsenal" available for use in mechanical ventilation. The single or combined application of these functions should be considered for Mechanical Ventilation for COPD 25
COPD. At the very latest, these functions should be tried if ventilation and unloading of the respiratory pump remain insufficient after conventional ventilation has been fully exploited. 26 Mechanical Ventilation for COPD
Bibliography 1 O'Donnell DE and Laveneziana P: Physiology and consequences of lung hyperinflation in COPD. Eur Respir. Rev 2006; 15: 100, 61-67. 2 Elliot MW: Non-Invasive Ventilation in Chronic Obstructive Pulmonary Disease. In: Simonds AK, editor. Non-Invasive Respiratory Support, 3rd ed. London: Hodder Arnold; 2007. p.216. 3 Nava S, Carlucci A and Ceriana P: Patient-ventilator interaction during noninvasive ventilation: practical assessment and theoretical basis. Breathe 2009; 5: 323-332 4 Vogelmeier C, Buhl R, Criée CP et al.: Guidelines for the Diagnosis and Therapy of COPD Issued by Deutsche Atemwegsliga and Deutsche Gesellschaft für Pneumologie und Beatmungsmedizin Pneumologie 2007: e1-e40. Pneumologie 2007: e1-e40. Mechanical Ventilation for COPD 27
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