A Negative Pressure Respirator Is

Crit Care. 2012; 16(2): R37.

Negative- versus positive-pressure ventilation in intubated patients with acute respiratory distress syndrome

Konstantinos Raymondos

¹Anaesthesiology and Intensive Intendance Medicine, Medical School Hanover, Carl-Neuberg-Strasse 1, D-30625 Hanover, Federal republic of germany

Ulrich Molitoris

¹Anaesthesiology and Intensive Care Medicine, Medical Schoolhouse Hanover, Carl-Neuberg-Strasse ane, D-30625 Hanover, Federal republic of germany

Marcus Capewell

^oneAnaesthesiology and Intensive Intendance Medicine, Medical School Hanover, Carl-Neuberg-Strasse 1, D-30625 Hanover, Germany

Björn Sander

^oneAnaesthesiology and Intensive Care Medicine, Medical School Hanover, Carl-Neuberg-Strasse 1, D-30625 Hanover, Germany

Thorben Dieck

¹Anaesthesiology and Intensive Care Medicine, Medical School Hanover, Carl-Neuberg-Strasse ane, D-30625 Hanover, Frg

Jörg Ahrens

^aneAnaesthesiology and Intensive Care Medicine, Medical School Hanover, Carl-Neuberg-Strasse 1, D-30625 Hanover, Germany

Christian Weilbach

²Anaesthesiology, St-Josefs-Hospital, Krankenhausstraße xiii, D-49661 Cloppenburg, Germany

Wolfgang Knitsch

³General, Visceral and Transplantation Surgery, Medical School Hanover, Hanover, Carl-Neuberg-Strasse 1, D-30625 Hanover, Federal republic of germany

Antonio Corrado

⁴Unita' di Terapia Intensiva Pneumologica e, Fisiopatologia Toracica, DAI, Specialità doctor-Chirurgiche, Azienda Ospedaliero-Universitaria Careggi, Padiglione San Luca, Via di San Luca ane, I-50136 Florence, Italy

Received 2011 Aug 23; Revised 2011 December 27; Accepted 2012 Mar 2.

Abstract

Introduction

Recent experimental data suggest that continuous external negative-pressure level ventilation (CENPV) results in amend oxygenation and less lung injury than continuous positive-pressure ventilation (CPPV). The effects of CENPV on patients with acute respiratory distress syndrome (ARDS) remain unknown.

Methods

We compared 2 h CENPV in a tankrespirator ("iron lung") with ii h CPPV. The 6 intubated patients developed ARDS after pulmonary thrombectomy (n = 1), aspiration (n = 3), sepsis (n = 1) or both (n = 1). Nosotros used a tidal volume of six ml/kg predicted body weight and matched lung volumes at terminate expiration. Haemodynamics were assessed using the pulse profile cardiac output (PiCCO) system, and pressure measurements were referenced to atmospheric pressure.

Results

CENPV resulted in amend oxygenation compared to CPPV (median ratio of arterial oxygen pressure to fraction of inspired oxygen of 345 mmHg (minimum-maximum 183 to 438 mmHg) vs 256 mmHg (minimum-maximum 123 to 419 mmHg) (P < 0.05). Tank pressures were -32.five cmH₂O (minimum-maximum -xxx to -43) at finish inspiration and -xv cmH₂O (minimum-maximum -15 to -19 cmH₂O) at end expiration. NO Inspiratory transpulmonary pressures decreased (P = 0.04) and airway pressures were considerably lower at inspiration (-one.v cmH₂O (minimum-maximum -3 to 0 cmH_twoO) vs 34.v cmH_iiO (minimum-maximum xxx to 47 cmH₂O), P = 0.03) and expiration (four.5 cmH₂O (minimum-maximum 2 to v) vs xvi cmH₂O (minimum-maximum 16 to 23), P =0.03). During CENPV, intraabdominal pressures decreased from xx.v mmHg (12 to 30 mmHg) to 1 mmHg (minimum-maximum -7 to five mmHg) (P = 0.03). Arterial pressures decreased by approximately x mmHg and fundamental venous pressures by xviii mmHg. Intrathoracic blood volume indices and cardiac indices increased at the initiation of CENPV by 15% and 20% (P < 0.05), respectively. Center rate and extravascular lung water indices remained unchanged.

Conclusions

CENPV with a tank respirator improved gas exchange in patients with ARDS at lower transpulmonary, airway and intraabdominal pressures and, at least initially improving haemodynamics. Our observations encourage the consideration of further studies on the physiological effects and the clinical effectiveness of CENPV in patients with ARDS.

Keywords: iron lung, tank respirator, external negative-force per unit area ventilation, acute lung injury

Introduction

Acute respiratory distress syndrome (ARDS) is usually treated with invasive continuous positive-pressure ventilation (CPPV) [1], which can aggravate both lung injury and multisystem organ failure [two]. Studies of mechanical ventilation in patients with ARDS take focused on low tidal book and high positive end-expiratory pressure (PEEP) [2-5]. Less injurious low tidal volume tin can lead to impaired oxygenation [4], and even very high PEEP can be insufficient to maintain lung volume in patients with severe ARDS [3]. Other approaches using mechanical ventilation have not been shown to farther better outcome, and mortality in patients with ARDS still reaches l% [1].

External negative-pressure ventilation with tank respirators is very successful in treating patients with chronic obstructive pulmonary disease [6], but in that location are no information regarding patients with hypoxaemic astute respiratory failure. Contempo experimental data suggest that continuous external negative-pressure ventilation (CENPV) may distend lungs in a fundamentally different manner from CPPV and may result in better oxygenation and less lung injury at lower transpulmonary pressures [vii]. Extrapolation to patients is difficult, and to appointment only continuous external negative-pressure (CENP) has been applied in three ARDS patients who breathed spontaneously in Emerson tank respirators [8-x]. Furthermore, cuirass [11] or poncho wrap systems [12,13] take been used for CENP during intermittent positive-pressure ventilation (IPPV), which resulted in improved cardiac output [11-thirteen]. However, both cuirass and poncho wrap systems decrease breast wall compliance when they are affixed to the torso [11-13], and effective ventilation in patients with ARDS has non been reported with either these systems or with tank respirators.

We speculated that, similarly to contempo experimental data, CENPV with a tank respirator would also consequence in better oxygenation in intubated patients with ARDS, even when low tidal volumes were used. Therefore, we performed a physiologic study to compare CENPV with CPPV using matched lung volumes at end expiration and matched low tidal volumes. Favourable physiologic effects may help to promote CENPV equally an applicable and even noninvasive ventilatory style for patients with ARDS.

Materials and methods

The written report was canonical past the upstanding committee of our institution, and informed consent was obtained from the patients' next-of-kin. We studied half-dozen intubated patients between January 2001 and January 2002. Technical personnel and approaches did non change during the study menstruum. Within 12 hours before study entry, all patients met ARDS criteria [14]. Their clinical characteristics, Simplified Acute Physiology Score II scores [15] and respiratory settings at that fourth dimension are listed in Table ane. The patients were placed nether sedation analgesia and did not breathe spontaneously. We performed a recruitment manoeuvre as described below to standardise the history of lung volume [16], and, to achieve more comparable conditions, we adjusted PEEP to sixteen cmH₂O in patients 1 through 5 (and to 23 cmH_twoO in patient 6). The patients were ventilated with a lung-protective strategy using a tidal book of 6 ml/kg predicted body weight (as calculated in [4]).

Table 1

Clinical characteristics and respiratory variables of the patients inside 12 hours earlier study entry^a

	Cause of lung injury		Demographics		Respiratory variables

Patient	Disorders predisposing to ARDS	Underlying disease	SAPS II	Body mass index	PaO₂/FiO_iiratio	Plateau pressure (cmH₂O)	PEEP (cmH₂O)	FiO₂	PaCO_two(mmHg)	pH	Days on ventilator	Outcomes
1	Aspiration	Encephalon injury	34	29.3	152	26	9	0.4	41	7.39	sixteen	Deceased
2	Severe pulmonary thromboembolism and thrombectomy	Parkinson's illness	33	25.seven	190	32	ten	0.4	46	7.40	iii	Survived
3	Sepsis, liver failure after valproate administration	Endometritis, epilepsy	35	31.1	153	30	14	0.5	45	7.43	5	Survived
4	Aspiration	Subarachnoid haemorrhage	33	27.6	190	28	9	0.five	44	7.48	3	Deceased
v	Aspiration	Gastric ulcer perforation	34	29.nine	153	36	13	0.half-dozen	49	7.32	2	Survived
half dozen	Sepsis, aspiration	Colon diverticulitis	42	thirty.four	118	46	22	0.8	65	seven.30	47	Deceased
Mean ± SD			35 ± three	29 ± 2	159 ± 27	33 ± 7	13 ± five	0.5 ± 02	48 ± nine	7.39 ± 0.07	18 ± 11

^aPatient 2 developed ARDS subsequently embolectomy and three days of mechanical ventilation at pulmonary artery wedge pressures below 18 mmHg. Patient half dozen adult ARDS already at admission due to a combination of sepsis after bowel suture insufficiency and aspiration and was treated with lung-protective ventilation already for 47 days at study entry. ARDS, acute respiratory distress syndrome; FiO₂, fraction of inspired oxygen pressure level; PaCO₂, arterial carbon dioxide pressure; PaO₂/FiO_ii, arterial oxygen-to-fraction of inspired oxygen pressure ratio; PEEP, positive end-expiratory force per unit area; SAPS 2, Simplified Acute Physiology Score 2 [fifteen].

We compared 2-hour CENPV using a tank respirator with ii-hour CPPV using biphasic positive airway pressure level/airway pressure release ventilation with an Evita ane ventilator (Dräger, Lübeck, Germany). We randomised the sequence of the ventilatory mode to residual the effects of the previous ventilation catamenia. The six patients were randomized to receive 2 hours of CENPV first and and then 2 hours of CPPV (n = three patients) or 2 hours of CPPV first and then 2 hours of CENPV (due north = 3 patients) in an unchanged supine position. Betwixt both ventilatory modes, we returned the ventilation, ventilation is the correct give-and-take to baseline, and the whole experiment lasted six to vii hours.

Nosotros matched tidal volume, respiratory frequency and the lung volume at end expiration that represented the divergence between functional residual chapters (FRC) with and without finish-expiratory pressure. The ratio of inspiration to expiration was 1:1. Subsequently a recruitment manoeuvre of six deep breaths with an inspiratory pressure of 60 cmH₂O, the lung volume at end expiration was measured by a sudden release of the relevant positive or negative pressure at end expiration with a spirometer (Volumeter 3000; Dräger). This step was repeated two more than times, and the average value of the three measurements was calculated. Side by side, lung volumes at cease expiration of the second ventilation mode were matched to those measured with the first one. To find out the corresponding pressure at end expiration, we beginning measured the lung volume at a similar positive or negative pressure. We and so increased or decreased pressure according to the achieved volumes and repeated the measurement manoeuvre until the divergence between lung volumes at cease expiration was smaller than 50 ml. Nosotros so performed three measurements again as described above.

To achieve comparable conditions, nosotros recruited the lungs again immediately before CPPV or CENPV with 25 deep breaths applied during 1 minute using inspiratory superlative pressures of 60 cmH_iiO. We performed this manoeuvre to standardise the history of lung book [16] to improve the comparability between both ventilatory modes. We used a fourth dimension interval of i minute to allow the states to take haemodynamic measurements during the recruitment manoeuvre using the PiCCO system (Pulsion Medical Systems, Munich, Germany).

Thanks to an initiative of Prof Ina Pichlmayr the tank respirator and the pump amass to generate negative pressures had been manufactured at our institution during the early 1980s [17]. The transparent plastic tank has been used in various clinical settings in patients without endotracheal tubes [xviii] with the caput placed outside the tank as commonly practiced [6-10]. Every bit we were studying intubated patients, it was not necessary to place the caput exterior the tank (Figure 1). Covering the whole body including the head avoided several problems such as air leakage at the cervix and improved the practicability of using the tank respirator. Nursing intendance was very limited, and therefore the whole tank was removed when complex nursing care was necessary. Like to archetype tank respirators [6-8], apertures at both sides allowed access to the patients, which enabled the use of nursing procedures such as endotracheal tube suctioning. In example of an emergency such as cardiac abort, the plastic tank can be removed inside a few seconds.

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The transparent plastic tank respirator during ventilation of the 2d patient (Table 1). The tank covered the whole patient, including the head. This setting improves the practicability of continuous external negative-force per unit area ventilation in an intubated patient in whom flow is delivered from the conventional mechanical ventilator through the endotracheal tube. Apertures in the lesser, beneath the wooden frame, were used to lead out all connections to the patient, and trimmed-to-fit sponge rubbers were used to seal these apertures. (The shoes were put on this patient to forbid contractions.).

During CENPV, the inspiratory changes of airway flow caused by the tank respirator triggered the conventional mechanical ventilator that delivered menstruation at a acme inspiratory pressure of 5 cmH₂O in the pressure support mode of the Evita 1 ventilator. The conventional ventilator was prepare to 0 cmH₂O at terminate expiration. The ventilatory circuits, arterial and central venous lines, gastric tube, urine catheter, electrocardiographic leads, pulse oximeters and other connections to the patient were led out of the tank via apertures from its bottom.

Airway pressures were measured via the side hole of a modified Swan-Ganz catheter that was introduced via the endotracheal tube and placed into the trachea 1 cm distal to the tip of the tube. Oesophageal pressures were measured with a conventional balloon catheter arrangement (CP-100 Pulmonary Monitor; BiCore Monitoring Systems, Irvine, CA, U.s.). The oesophageal airship catheter was passed to a depth of 60 cm, and placement of the balloon in the stomach was confirmed by a transient increment in pressure during gentle compression of the abdomen. We then withdrew the catheter until oesophageal placement was confirmed past the presence of cardiac artefacts and pressure changes during tidal ventilation [16]. Intraabdominal pressure level was obtained by measuring the force per unit area in the bladder via the urine catheter afterwards filling the empty bladder with 50 ml of saline using the midaxillary level as the reference line [19]. All pressure measurements were referenced to atmospheric force per unit area outside the tank [20].

Cardiac alphabetize, intrathoracic blood volume index, extravascular lung water alphabetize and stroke volume variation were assessed past thermal dilution using the PiCCO system with an arterial catheter inserted into a femoral avenue. The Wilcoxon signed-rank test was used to compare values between CENPV and CPPV, and P-values less than 0.05 were considered significant.

Results

Gas exchange

At the get-go of CENPV and CPPV, gas exchange was similar (Figure ii). During CENPV, oxygenation improved impressively compared to the respective values during CPPV. The mean arterial-to-inspired oxygen pressure ratio (PaO₂/FiO₂ratio) increased by 92 mmHg (40%) afterward 1 hour and by 76 mmHg (xxx%) after 2 hours. However, the individual responses varied considerably between patients during both CPPV and CENPV (Effigy 2). Furthermore, arterial carbon dioxide pressure (PaCO_ii) decreased and pH increased during CENPV, but statistical significance was reached but at one 60 minutes (Effigy ii).

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The grade of arterial oxygen-to-fraction of inspired oxygen pressure ratio (PaO_ii/FiO_two), arterial carbon dioxide partial force per unit area (PaCO_ii) and pH immediately before lung recruitment and during continuous positive-pressure ventilation (CPPV) and continuous external negative-force per unit area ventilation (CENPV). Measurements were taken at time 0 (5 minutes after the recruitment manoeuvre) immediately after starting the 2-hour ventilatory period of CPPV or CENPV. *P < 0.05 compared to respective values at 1 or 2 hours during CPPV.

Respiratory mechanics

Individual data of each patient regarding lung volumes and pressures are shown in Tables 2 and three. Lung volumes were well-matched and did not differ between CPPV and CENPV (Table 2). During CENPV, intraabdominal pressures decreased by xv to 26 mmHg (Table 2 Figure 3). Endotracheal airway pressures decreased by at to the lowest degree 30 cmH_iiO at inspiration and by at least 11 cmH₂O at expiration (Figure 3), and inspiratory transpulmonary pressures (airway pressure minus oesophageal pressure level) were also significantly lower during CENPV (Table iii). In contrast, transrespiratory system pressures (airway pressure minus tank pressure) during CENPV were similar at inspiration and 1 to iv cmH_twoO higher at expiration (Table 3) as a result of a brusk peak of endotracheal airway pressure at the beginning of expiration (Figure 3).

Table 2

Lung volume and intraabdominal pressure level during continuous positive-force per unit area ventilation and continuous external negative-pressure ventilation^a

	Tidal volume (ml)		Minute volume (L/minute)			Lung volume at end expiration (ml)		Intraabdominal pressure (mmHg)

Patient	CPPV	CENPV	CPPV	CENPV	Respiratory rate (breaths/minute)	CPPV	CENPV	CPPV	CENPV
1	583	578	x.5	10.4	eighteen	612	623	22	four
ii	411	417	vii.iv	7.five	18	623	607	28	5
3	550	559	12.ane	12.three	22	937	927	12	-6
4	494	506	eight.4	8.6	17	710	722	thirty	5
five	437	426	8.3	eight.i	19	545	530	13	-two
6	560	568	14	xiv.2	25	667	650	19	-7
Mean ± SD	506 ± 70	509 ± 72	ten.ane ± two.6	10.ii ± 2.6	19.viii ± 3.one	682 ± 137	677 ± 138	21 ± eight	0 ± 6*

^aCENPV, continuous external negative-pressure ventilation; CPPV, continuous positive-force per unit area ventilation. Patient half-dozen had an open abdomen. *P = 0.03 compared to CPPV.

Table 3

Ventilatory pressures during continuous positive-force per unit area ventilation and continuous external negative-pressure ventilation at inspiration and expiration^a

	Airway force per unit area (cmH₂O)		Tank force per unit area (cmH₂O)	Transrespiratory pressure (cmH_twoO)	Oesophageal pressure (cmH_twoO)		Transpulmonary pressure level (cmH_twoO)

Patient	CPPV	CENPV	CENPV	CENPV	CPPV	CENPV	CPPV	CENPV
ane
Inspiration	33	-3 (27)	-30	27	20	-9 (21)	13	6
Expiration	16	v (20)	-15	xx	15	4 (19)	i	1
ii
Inspiration	36	-two (31)	-33	31	22	-9 (24)	14	7
Expiration	16	five (20)	-15	twenty	xv	v (20)	1	0
3
Inspiration	thirty	0 (31)	-31	31	19	-8 (23)	11	8
Expiration	16	2 (17)	-15	17	xv	2 (17)	i	0
iv
Inspiration	33	-ane (31)	-32	31	25	-9 (23)	8	eight
Expiration	xvi	4 (19)	-15	19	16	four (xix)	0	0
five
Inspiration	39	-2 (38)	-40	38	23	-ten (30)	sixteen	8
Expiration	xvi	4 (19)	-15	19	16	3 (eighteen)	0	1
6
Inspiration	47	0 (43)	-43	43	32	-10 (33)	15	ten
Expiration	23	5 (24)	-19	24	22	five (24)	i	0
Mean ± SD
Inspiration	36 ± half dozen	-ane.iii ± i.2* (33.5 ± 5.9)	-35 ± v	34 ± half dozen	24 ± 5	-ix ± 0.8* (25.vii ± 4.7)	13 ± 3	8 ± i.3^†
Expiration	17 ± 3	4.ii ± one.two* (19.five ± 2.3)	-xvi ± 1.6	twenty ± 2*	17 ± iii	4 ± i.2* (19.5 ± ii.4)	1 ± 0.5	0 ± 0.5

^aIn parentheses, both airway and oesophageal pressures are shown in reference to tank pressure to enable calculation of transpulmonary pressures (airway pressure - oesophageal pressure) in reference to both atmospheric and body surface pressure inside the tank. Transrespiratory organisation pressures during CENPV (airway force per unit area - tank pressure) were compared to airway pressures during CPPV. CENPV, continuous external negative-pressure ventilation; CPPV, continuous positive-pressure ventilation. *P = 0.03 and ^† P = 0.04 compared to the corresponding inspiratory or expiratory value during CPPV.

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Original polygraph recordings during a change from continuous positive-pressure ventilation (CPPV) to continuous negative-force per unit area ventilation (CENPV) in patient six. The pressure-time profiles of endotracheal pressure (AWP) during CPPV and tank pressure were similar during inspiration and expiration. During CENPV, endotracheal airway pressure level increased during inspiration and decreased after a brusque initial peak. This patient had high intraabdominal pressure despite an open abdomen that decreased impressively during CENPV. (To convert pressure values from millimetres of mercury to centimetres of water, multiply past 1.33.) ECG, electrocardiogram; AWP, airway pressure (measured in the trachea); CVP, central venous pressure; AP, arterial force per unit area; IAP, intraabdominal pressure, exp. CO₂, expired carbon dioxide.

Haemodynamics

Primal venous pressures decreased more than arterial pressures during CENPV (Figure 4). Simultaneously, the intrathoracic blood book index increased past 15% and the cardiac alphabetize increased past xx%, whereas no differences were plant after 1 and 2 hours (Figure 4). After 2 hours of CENPV, the centre rate ranged between 57 and 126 beats/minute (median = 89 beats/minute), and the extravascular lung water index varied between vi and 14 ml/kg (median = 9.5 ml/kg), and these parameters also did non differ betwixt CPPV and CENPV. During the recruitment manoeuvre, no relevant impairments were observed and all changes returned to baseline immediately.

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Haemodynamics during continuous positive-force per unit area ventilation (CPPV) and continuous external negative-pressure level ventilation (CENPV). Measurements were taken at time 0 (5 minutes after the recruitment manoeuvre) immediately later starting the two-hr ventilatory period of CPPV or CENPV. The changes in intravascular force per unit area effects were more permanent in contrast to the more transient effects on intrathoracic blood volume and cardiac index. *P < 0.05 compared to corresponding values at 1 or 2 hours during CPPV.

Word

CENPV improved gas exchange considerably compared to CPPV, which was achieved at matched tidal and end-expiratory lung volumes with lower airway, intraabdominal and transpulmonary pressures, and at least initially improving haemodynamics. Values for inspiratory airway pressures during CPPV were similar compared with tank pressures during CENPV, although negative inspiratory tank pressures were reached only at finish inspiration. The matching of end-expiratory lung volumes was obtained with an end-expiratory negative force per unit area of -15 cmH_twoO, which corresponded to a PEEP value of 16 cmH₂O in five of six patients. This constancy was surprising and probably indicates very like degrees of lung injury. Concordantly, the patients had very similar PaO₂/FiO_twovalues at a PEEP of 16 cmH₂O immediately before the measurement period. With less efficient cuirass or poncho wrap systems, higher pressure values were necessary to attain the aforementioned end-expiratory lung volumes compared to positive pressures [11,12]. Concordantly, when these systems were used to apply continuous negative pressure during IPPV in patients with lung injury, gas commutation either did not better [11,12] or even deteriorated when end-expiratory lung volumes were not matched [thirteen]. We matched lung volumes, and the PaO₂/FiO_iiratio increased impressively during CENPV, which may indicate alveolar recruitment with a decrease in pulmonary shunting.

On the contrary, even relatively high PEEP values used in the present written report were apparently all the same insufficient to maintain recruited lung volumes during CPPV. In surfactant-depleted rabbits, Grasso et al. also matched end-expiratory lung volumes and observed better oxygenation during CENPV than during CPPV [7]. This upshot was associated both with more aerated lung tissue and less lung injury subsequently 2.5 hours with the utilise of high tidal volumes of 12 ml/kg [7]. In our pilot study, nosotros measured neither aerated lung tissue nor FRC and we did not appraise markers of lung injury. However, we speculate that, similarly to the observations of Grasso et al. [vii], the improved oxygenation during CENPV observed in the present report could also be associated with alveolar recruitment and an increase in FRC. Increased FRC during CENPV would reduce alveolar strain (ratio between tidal volume inflated and FRC) [21], and improved lung recruitability during CENPV might exist associated with less injurious intratidal alveolar opening and closing of lung tissue [22]. Grasso et al. assumed that CENPV might be more effective and less injurious because of more homogeneous distension of the lung as negative pressure level is distributed across a broad surface of the chest wall and belly [7].

Concordantly, at given levels of transpulmonary pressure, Grasso et al. observed greater end-expiratory volumes, and transpulmonary pressures were lower when corresponding positive and negative pressure level values were compared [7]. Our data seem to confirm their observations, although we did not measure transpulmonary pressures under static conditions. Therefore, and because nosotros did not measure changes in transpulmonary pressure at 0 cmH₂O at expiration as described by Chiumello et al. [21], we did not assess the global average lung stress in the present pilot study. Similarly to other experimental data [7], nonetheless, transpulmonary pressures were lower during CENPV at end inspiration; therefore, nosotros speculate that lung stress could be lower every bit well in comparing to CPPV. Concordantly with the observations made by Grasso et al. [7], our data also suggest that the development of transpulmonary distending pressures may substantially differ during CENPV compared to CPPV. This may be associated with different regional pleural force per unit area gradients throughout the lungs that are poorly represented on the basis of just ane value of transpulmonary force per unit area [7].

During CENPV, transrespiratory system pressures (TRP) (airway pressure minus tank force per unit area) were about 3 cmH₂O lower at inspiration and about 3 cmH₂O higher at expiration every bit endotracheal airway pressures became positive during CENPV, probably due to the expiratory resistance of the endotracheal tube. These slightly higher TRP values at expiration may be sufficient to explain the improved oxygenation observed during CENPV.

The TRP differences between CENPV and CPPV, which varied considerably at inspiration and expiration, might be cause past different distributions of positive and negative pressures, depending on individual differences in pulmonary mechanics. Despite our study design, in which we used matched tidal volumes and randomization of ventilatory modes, we found the aforementioned TRP value of 31 cmH₂O in 3 patients, which may also reverberate very similar degrees of lung injury.

The high intraabdominal pressures [19] decreased past 20 mmHg during CENPV. This may counteract the effects of high intraabdominal pressures such equally cranial shifts of the diaphragm with consequent lung volume reduction, reduced lymphatic flow and lung oedema germination [23]. Intraabdominal perfusion pressure improved every bit the mean arterial pressure decreased only by 10 mmHg, which could exist beneficial, especially when visceral claret flow is impaired.

In comparison to arterial pressures, the quite elevated central venous pressures decreased more extensively during CENPV, indicating the relatively greater impact on the venous circulation than on the arterial circulation, where the vessel tone is stronger. When central venous pressures decreased during CENPV, the high intrathoracic blood book indices further increased past xv%, reflecting improved venous render, and the cardiac index improved considerably past 20%. Compared to CPPV, this improved venous render may upshot in less amending of mixed venous oxygen content and therefore may contribute to maintaining college levels of arterial oxygen content during CENPV.

In the present written report, the heart charge per unit too remained unchanged, indicating that the greater transpulmonary blood menstruum during CENPV apparently resulted from higher stroke volumes. Borrelli et al. observed very similar increases in cardiac output at lower intrathoracic blood volumes when a poncho was used to apply continuous negative pressure during IPPV [12]. The greater preload in the nowadays written report outweighed the effects on afterload, which increased when intrathoracic pressures decreased. During CENPV, both central venous and intraabdominal pressures decreased, which could event in similar pressure gradients for venous return compared to CPPV. In agreement with this finding, Grasso et al. did not observe changes in cardiac output when a whole-trunk device was used, but they did when negative pressure was practical to the chest but [7].

CENPV has been suspected to increase extravascular lung water compared to CPPV as a result of more negative pleural and interstitial pressures and because of higher left ventricular filling afterward enhanced venous render [24,25]. In our present study, extravascular lung water indices did non differ during CENPV compared to CPPV, which has also been observed in experimental studies [7,24,25]. Lung water tin increase with PEEP past decreasing lung lymph flow, which has been attributed to compressed pulmonary lymphatic vessels [26]. These compressions practice not occur under CENPV and may outweigh other effects, resulting in lung water values similar to those associated with CPPV.

The very pocket-size number of patients in this report represents its primary limitation and primary source of errors. In four of the six patients, pulmonary aspiration of gastric content was either the main or one contributory predisposing gene in the evolution of ARDS. Extrapolating this ascertainment to patients with other predisposing factors must be done with caution. In whatever case, the considerable variation in PaO₂/FiO₂responses to CENPV was apparently independent of the underlying illness, the efficiency of the prior lung recruitment manoeuvre or the severity of lung injury. Interestingly, increased oxygenation in response to placement in the prone position also was not related to lung recruitability in response to positive pressures [27]. Finally, at this phase the reasons for the different individual responses to CENPV remain unclear.

Equally a perchance less injurious and more effective fashion of ventilation, CENPV appears especially bonny when the potential to eliminate endotracheal intubation is taken into consideration. Tank respirators were used decades agone to apply continuous external negative pressure in three patients with astringent pneumonia who were not intubated [8-ten]. This improved oxygenation and enabled maintenance of spontaneous animate in severe lung injury.

Conclusions

Our results demonstrate for the offset time that CENPV is applicative and constructive, even in severely critically ill patients in a mod intensive care setting. The present study confirms recent experimental data and encourages consideration of further studies of the physiological effects and clinical effectiveness of CENPV in patients with ARDS.

Key letters

• CENPV differs substantially from CPPV and improves oxygenation under more physiologic conditions in patients with ARDS.

Abbreviations

ARDS: acute respiratory distress syndrome; CENPV: continuous external negative-pressure level ventilation; CPPV: continuous positive-pressure ventilation; FiO_ii: fraction of inspired oxygen; FRC: functional residual capacity; ECG: electrocardiogram; IPPV: intermittent positive-force per unit area ventilation; paO_ii: arterial oxygen tension; paCO₂: carbon dioxide tension; PEEP: positive end-expiratory pressure level; PiCCO: Pulse Contour Cardiac Output; SAPS: Simplified Acute Physiology Score; TRP: trans-respiratory arrangement pressure level.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

KR, UM, MC, WK and AC participated in the design of the study; KR, UM and MC participated in the collection and the associates of the data; KR and TD performed the statistical analysis; BS, JA, CW and Air conditioning gave technical or logistical support; KR, UM, TD, JA, CW and AC helped to draft the manuscript and, all authors read and approved the last manuscript.

Acknowledgements

Back up for the publication fee was granted by the High german Research Foundation (DFG). The authors thank Dr Horst Rückoldt, Prof Dr Jörn Heine, Dr Ljiljana Verner and Prof Dr Siegfried Piepenbrock for their administrative support.

References

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