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From the Departments of *Surgical, and
Medical Sciences, University Hospital, Uppsala, Sweden,
Department of Anesthesiology and Critical Care Medicine, University Hospital Freiburg, Germany,
Department of Anesthesiology and Critical Care Medicine, Klinikum Augsburg, Augsburg, Germany
Address correspondence and reprint requests to Rafael Kawati, MD, DEAA, Department of Surgical Sciences/Anesthesiology & Intensive Care, Uppsala University Hospital, SE-75185, Uppsala, Sweden. Address e-mail to r.kawati{at}telia.com.
| Abstract |
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) rate. Although the impact of narrowing on low inspiratory
is small, its decelerating effect on the high expiratory
is pronounced and, hence, easily detectable. Dividing the volume-flow curve of a passive expiration into five consecutive segments (slices) and calculating the time constants (
E) of these slices allows for analyzing whether and how expiratory
is impeded by a partial obstruction. In nine piglets, during volume-controlled ventilation, three grades of ETT obstruction were created with an external clamp. In all animals the
E increased with ETT obstruction (mean for the first slice: 550 ms with unobstructed ETT; grade 1: 661; grade 2: 877; and grade 3: 1563 ms, respectively) and this increase was significant with grade 2 and 3 obstruction. Ppeak, by contrast, did not increase significantly (base: 13, grade 1: 14, grade 2: 15 cm H2O) until the most severe (grade 3: 20 cm H2O) obstruction was created. We conclude that partial obstruction of the ETT can be reliably monitored with the expiratory
signal and has the potential of monitoring ETT narrowing in ventilator-dependent patients independent of the inspiratory
pattern applied. | Introduction |
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) gets turbulent and hence, disproportionately more pressure is required for driving gas, would Ppeak reach a clinically relevant level. A potential alternative to Ppeak is monitoring the
signal of passive expiration (2). Any obstruction acts as a brake on expiratory
, increasing the time required for emptying the lung. This can be described in terms of the expiratory time constants (
E) of consecutive segments of the expiratory
-volume plot (3). The decelerating effect of an ETT obstruction is most pronounced with the high
of early expiration, increasing
E during early expiration and yielding a typical
E over expiratory volume pattern that is easy to recognize and independent of the inspiratory
pattern applied.
To test these assumptions, we calculated
E with three degrees of ETT obstruction in anesthetized, mechanically ventilated piglets. We hypothesized that the increasing emptying time of the lung, corresponding to increasingly higher
E, would indicate increasing grades of obstruction. The increase in Ppeak was assumed to be less pronounced and of clinical relevance at the most severe grade of obstruction only.
| Methods |
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E at a 2-sided 5% significance level (assuming that the true difference is
200 ms and the sd, as inferred from pilot studies, is 100 ms). To safeguard against potential experimental loss, we planned for 10 animals; however, one animal died before the experiment was finished and was excluded from the analysis. After preparation and a recruitment procedure (tidal volume [Vt] doubled, positive end-expiratory pressure [PEEP] 10 cm H2O for 60 s), the lungs of the anesthetized piglets were ventilated (Servo 300; Siemens-Elema, Solna, Sweden) in volume-controlled mode (PEEP of 4 cm H2O, Fio2 0.4), and baseline measurements with the unobstructed ETT were performed. Thereafter, the ETT was stepwise obstructed with a graded external clamp (3 levels, defined as 2, 4, and 6 turns of the screw, respectively.
The expiratory volume-flow (V-
) curve was analyzed as described in detail previously (3). The V-
curve was divided into 5 slices of equal volume, assuming a linear slope within each particular slice. To eliminate the effects of inertia and the opening and closing of the ventilator valves on the
E analysis, we excluded the first 5% and the last 5% of the data points. The slope of a straight line fitted to the expiratory V-
curve within a slice (least squares fit) is equal to the derivative dV/d
, which has the dimension of time and can be directly read as the expiratory
E of that particular slice. The model assumes that the
-dependent resistance of the ETT is reasonably linear for narrow segments (slices) of the V-
curve. The narrower the slices, the better this assumption is fulfilled, but the more pronounced is the impact of cardiogenic oscillations on the determination of
E. The choice of five slices is, therefore, a compromise dictated by the model assumption.
Ppeak and end-expiratory pressures were also recorded. Intrinsic PEEP was estimated from the difference between set PEEP and the pressure after a 5-s end-expiratory hold (4,5), and end-inspiratory pause pressure was determined also after a 5-s hold. Compliance of the respiratory system (Crs) was calculated from Vt divided by the end-inspiratory/end-expiratory pressure difference (intrinsic PEEP considered). Resistance was calculated according to the method described by Milic-Emili et al. (6).
Compressing a plastic ETT with a clamp creates a nonconcentric obstruction. With exactly the same setup used in the animal experiments, we therefore studied the impact of nonconcentric narrowing on the pressure-
(P-
) curve in a physical model at Fio2 0.21 and 0.4. The resulting P-
curves were compared to those of native ETTs with known inner diameter (ID) (7), which allowed for testing the assumption that the external compression, despite being nonconcentric, would render the P-
curve more curvilinear, thus simulating the effects of a strictly concentric ETT narrowing.
The expiratory
curves were assessed for intrapulmonary flow limitation with the method described by Lourens et al. (8) comparing two subsequent
curves. If, with an added external obstruction, the second
did not decrease, flow limitation was assumed to be present during the first condition. When
differed by <5% during >50 ms (the time during which cardiogenic oscillations impacted on the
curve), the respective segment of the
curve was considered flow limited (8).
With the animals in the prone position the lungs were ventilated via an ETT (No. 8; Mallinckrodt, Athlone, Ireland) connected by a rigid 60-cm tubing system to a Servo 300 ventilator. Ventilatory frequency was 1820 breaths/min, inspiration-to-expiration ratio was 1:1, and Vt was between 10 to 12 mL/kg, resulting in an Paco2 close to 5.5 kPa.
Anesthesia was induced with 100200 mg ketamine and 1 mg/kg morphine and maintained with ketamine infusion (30 mg · kg1 · h1) plus morphine infusion (2 mg/h). Neuromuscular block was produced by continuous infusion of pancuronium 0.26 mg · kg1 · h1. Animals received sodium chloride 4.5 g/L with glucose 25 g/L at 10 mL · kg1 · h1 and a 5 mL/kg bolus of dextran-70 (Macrodex 70, Pharmacia Infusion AB, Uppsala, Sweden) to insure normovolemia.
Airway pressures were measured with a side port at the site of the pneumotachograph and fed to a pressure transducer.
was measured with a heated Fleisch pneumotachograph placed between the ETT and the Y-piece. Signals were sampled at 200 Hz and fed to a data acquisition system (Acqknowledge, version 3.2.7, BioPac Systems, Inc, Goleta, CA).
All values are expressed as mean and 95% (lower to upper) confidence interval. Differences in variables within the groups were assessed using repeated-measures analysis of variance. Significant differences were evaluated using the Student-Newman-Keuls test. Statistical significance was assumed with P
0.05.
| Results |
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curve almost indistinguishable from an ETT with ID of 7.5 mm, grade 2 corresponded to an ID 7 mm, and grade 3 to an ID of 5 mm.
In the unobstructed tube and with grade 1 and 2 obstruction,
E was significantly higher in early and mid-expiration (slices 13), compared with late expiration (Table 1). With grade 2 and grade 3 obstruction,
E increased in early expiration (slices 1 and 2; P
0.05), whereas in late expiration (slice 5)
E increased significantly only in grade 3 obstruction (Table 1, Figure 1).
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While
E increased with obstruction in all animals, Ppeak did not increase at all in 3 of 9 animals with grade 1 and 2 obstruction and by not more than 1.0 cm H2O in another 2 animals.
Ppeak did not increase significantly from its native level of 13 cm H2O (12.1 to 13.1) with grade 1 and 2 obstruction (Table 1, last column). With grade 3 obstruction, it increased to 20 cm H2O (16.7 to 23.2; P
0.05). Intrinsic PEEP was 2 cm H2O (0.5 to 3.5) in grade 3 obstruction.
Compared with the unobstructed tube, Crs decreased from 43 mL/cm H2O (38.847.8) to 37 mL/cm H2O (34.340.6), 38 mL/cm H2O (34.241.5), and 38 mL/cm H2O (32.442.8) in grade 1, 2, and 3 obstruction, respectively (P
0.05 to native ETT, Table 2, last column). Total effective resistance of the respiratory system (ETT included) did not increase significantly from its native level of 11 cm H2O · s · L1 (9.312.6) with grade 1 and 2 obstruction. With grade 3 obstruction it increased to 29 cm H2O · s · L1 (23.134.7; P
0.05).
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Intrapulmonary flow limitation was not detected under any conditions, or in any animals Figure 2 shows a representative animal.
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| Discussion |
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E increased in all individual animals with ETT obstruction. The mean increase in
E was statistically significant for grade 2 and 3 obstruction. Ppeak increased with grade 3 obstruction, but with grade 1 and 2 the increase was not significant or, in individual animals, even absent.
Although the clamp created a nonconcentric narrowing, the resulting P-
curve did not differ in shape from the one recorded from native ETTs with decreasing ID, the latter corresponding to a strictly concentric narrowing across the total ETT length. Therefore, grade 1 obstruction corresponded to an ID 7.5 mm, grade 2 to ID 7 mm, and grade 3 to ID 5 mm, suggesting that whatever the geometry of the narrowing, the P-
curve will not differ in any fundamental aspect from the P-
curve of a strictly concentric narrowing.
It was difficult to standardize the screwing of the clamp to obtain identical obstruction levels in all animals. We therefore cannot exclude that the levels of obstruction differed slightly from animal to animal. Grade 3 obstruction created an intrinsic PEEP of 2 cm H2O (0.5 to 3.5), which increased Ppeak in parallel. We assume that Ppeak would have performed even worse had intrinsic PEEP not been present.
The decrease in Crs from the unobstructed baseline level of 43 mL/cm H2O to 37 mL/cm H2O with all grades of obstruction was probably caused by the recruitment maneuver before the baseline measurement. Recruitment effects on Crs fade rapidly in healthy animals. In retrospect, it would have been better to repeat the recruitment before each level of obstruction to eliminate this time-related decrease in Crs.
The inspiratory pressure that is necessary to overcome the resistance of the ETT predominantly depends on the ID of the ETT and
. A critical
threshold (
crit) can be roughly estimated (9,10), below which
through a tube is laminar. The narrower the ETT, the lower is
crit. Not until narrowing comes down to an ID at which a new
crit is arrived at and
gets turbulent, is a sudden and pronounced increase in Ppeak observed. From the equation used to calculate the Reynolds number (9,10) it can be derived that, assuming a
of 9 L/min, the cross-sectional area of an ETT with ID 8 mm can be reduced by 36% or, with a
of 6 L/min, by 72%, respectively, before
gets turbulent. In the current study the ventilator delivered an inspiratory
of 0.17 L/s (10.2 L/min) corresponding to the
crit for an ETT with an ID of 7 mm (9,10). In other words, Ppeak would not increase to any clinically detectable level until the ID is narrowed to 7 mm. Even with high turbulent
, pronounced obstruction is necessary to increase Ppeak to a clinically relevant level. Assuming a tube-related increase in inspiratory pressure of 3 cm H2O being the intervention threshold of the clinician, this threshold is only reached at a reduction in cross-sectional area of 61% at a
of 300 mL/s or of 44% at 600 mL/s or of 23% at 900 mL/s, respectively.
Although a substantial degree of narrowing is required for the low
of constant flow inspiration to reach
crit, the situation is different during expiration.
Expiratory
exceeds by far the
of constant flow inflation (0.90 L/s versus 0.17 L/s in this study) (Figure 2) and, thus, makes expiration relatively more sensitive to the decelerating effects of ETT obstruction. Actually, high
also prevails during the inflation with a decelerating
profile (pressure controlled ventilation, PCV). Monitoring Ppeak is, however, not meaningful with PCV because airway pressures are preset. Expiratory
, by contrast, is independent of any inspiratory
pattern applied.
Moreover, our findings support the assumption that
E detects ETT obstruction earlier and more reliably than Ppeak. With grade 1 and 2 obstruction, Ppeak did not increase at all in 3 of 9 animals and by not more than 1.0 cm H2O in another 2 animals. The average Ppeak increase (Table 1) would probably escape clinical observation, whereas with grade 3 obstruction the pressure increase was very much amplified by the intrinsic PEEP.
Are there implications for the ventilator-dependent patient despite obviously quite different experimental conditions? Smaller Vts as used in the respiratory treatment of patients (1012 mL/kg) require smaller
than in the current experiment. The lower the actual
, the broader the range for the inspiratory
to increase before becoming turbulent. Short tracheostomy tubes would reduce resistance, and the
crit would be arrived at later. Changing length or the ID of the ETT or inspiratory
(by changing Vt, inspiration to expiration ratio, or frequency), all change either the threshold for
to become turbulent or the difference between the actual
and
crit. To avoid depending on the inspiratory
pattern we suggest to analyze and compare subsequent expiratory
curves. Expiratory
is driven by the alveolarmouth pressure difference and also depends on intrapulmonary resistance. Before concluding that ETT is partially obstructed, compliance and intrapulmonary airway resistance (assessing the
curve for flow limitation) must therefore be determined. To minimize potential increases in intrapulmonary resistance ketamine, which is recognized as a potent bronchodilator, was used in the current study.
Kinking of tubings or blocking of the ETT by thick secretions or similar emergencies would certainly not go undetected with Ppeak monitoring (11). Lower grades of obstruction that develop slowly and progressively might, however, be overlooked. This is of little importance during controlled ventilation because the respirator provides the pressure for overcoming the resistive forces of the respiratory system, ETT, and circuit. With any type of assisted spontaneous breathing, however, a low-grade obstruction already imposes a resistive load on the patient (12) and this extra tube-related work of breathing is difficult to detect. We regard the current study as one step toward developing a noninvasive tool for assessing the patency of the ETT as it relates to spontaneous breathing, which is crucial.
We conclude that analyzing the expiratory
signal during passive expiration detects partial obstruction of the ETT more reliably, earlier, and independently of the inspiratory
pattern applied than does the Ppeak. The expiratory
E over volume plot has, therefore, the potential to serve as a monitoring tool during controlled mechanical ventilation.
| References |
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This article has been cited by other articles:
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R. Kawati, L. Vimlati, J. Guttmann, G. Hedenstierna, U. Sjostrand, S. Schumann, and M. Lichtwarck-Aschoff Change in expiratory flow detects partial endotracheal tube obstruction in pressure-controlled ventilation. Anesth. Analg., September 1, 2006; 103(3): 650 - 657. [Abstract] [Full Text] [PDF] |
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