Tidal Volume Range Research Articles

High Flow Through a Nasal Cannula and CPAP Effect in a Simulated Infant Model

Limited data are available to describe the CPAP effects that can be expected when using high flow with a traditional nasal cannula. To describe the relationship between the pressure generated at the airway opening and flow through a nasal cannula using a simulated infant model. We hypothesized that positive pressure generated by a standard cannula at flows > 2 L/min would be minimal and clinically unimportant. Nares were simulated with holes drilled in a plastic fixture. A nares template for CPAP prongs served as a sizing template for the holes. Small, medium, and large nares fixtures were constructed and connected to a lung simulator that simulated spontaneous breathing. Respiratory muscle pressure was simulated by setting a waveform and adjusting the amplitude to deliver a range of tidal volumes (V(T)) from 3 mL to 12 mL. Lung compliance and resistance were set at 0.5 mL/cm H(2)O and 125 cm H(2)O/L/s, respectively. Nasal cannulas were inserted in the model nares. We assured that the prong occlusion of the nares did not exceed 50%. Cannula flow was adjusted from 2-6 L/min in 1-L/min increments. Data were averaged over 20 breaths. Mean airway pressure and percent change in V(T) were recorded. The greatest effect on V(T) (mean ± SD 0.16 ± 0.10 mL) and pressure change (mean ± SD 0.7 ± 0.5 cm H(2)O) occurred with the premature cannula. The least effect on pressure (mean ± SD 0.3 ± 0.22 cm H(2)O) and V(T) change (mean ± SD 0.01 ± 0.02 mL) occurred with the infant cannula. Clinically important pressures were not generated by high flows with a standard nasal cannula. The differences in spontaneous V(T) across all flows were negligible.

Adaptive Support Ventilation: An Inappropriate Mechanical Ventilation Strategy for Acute Respiratory Distress Syndrome?

We thank Drs. Dongelmans and Schultz for their letter expressing interest in our recent publication on adaptive support ventilation (ASV).1They correctly describe how ASV works but indicate that the ability of ASV to vary tidal volume in response to a changing clinical presentation is of concern especially if the tidal volume is allowed to exceed 6 ml/kg.First, it is important to remember that the tidal volumes used by the Acute Respiratory Distress Syndrome Network2in its landmark study varied between 4 and 8 ml/kg. Indeed, as we showed in our study, even though the average tidal volume delivered to patients in the low-tidal volume arm was about 6 ml/kg, tidal volume did vary between 4 and 8 ml/kg in many patients.We believe that allowing tidal volume to increase while keeping plateau pressure at a minimum setting (<28 cm H2O in our study) is the major concern of Drs. Dongelmans and Schultz, and they reference Hager et al. 3to demonstrate their point. However, they failed to acknowledge the subsequent letter from Shiu and Rozen4who determined from Hager's data that no significant change in mortality was observed regardless of tidal volume once plateau pressure was less than 28 cm H2O. Drs. Dongelmans and Schultz also referred to the article by Gajic et al .,5which was a retrospective review with plateau pressures available on only a few patients to illustrate the potential of large tidal volumes causing acute lung injury. The tidal volume range applied by ASV is essentially within the range of the lowest risk group (≤9 ml/kg) in the article by Gajic et al .5In addition, there are numerous articles in the surgical literature that indicate that at least short-term application of large tidal volume does not result in lung injury6–10in patients without existing lung injury. As we noted in our discussion, the upper and lower limits on ASV may need to be adjusted, and we believe that the upper limit should be set for patients with acute lung injury or acute respiratory distress syndrome at 8 ml/kg. However, the concept of ASV is sound because if practitioners are left on their own to adjust tidal volume, even centers who participated in the Acute Respiratory Distress Syndrome Network trial do not always appropriately select low tidal volumes and plateau pressures.11Where we believe the concept of ASV is most critical is in the patient where in spite of tidal volume being set at 6 ml/kg, plateau pressure exceeds 28 cm H2O. It is very clear that in these patients, the risk of increased mortality is real.3,12ASV does in these patients what the clinician should do and that is to reduce the tidal volume to avoid overdistension. ASV may not have the absolute limits correct, but the concept of closed loop control of ventilation is the future!*Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts. rkacmarek@partners.org

A Slightly Different Tune: The Multipart Harmony of Noisy Life Support

University of Manitoba, Winnipeg, Manitoba, Canada. amutch@cc.umanitoba.caI would like to bring to the attention of readers of Anesthesiology some inaccuracies in the Editorial View “Noisy Mechanical Ventilation: Listen to the Melody” by Drs. Shimabukuro and Gropper.1This article provided an overview of the research published in the journal by Spieth et al., 2“Effects of different levels of pressure support variability in experimental lung injury.” As stated by the editorialists, “Using variability in breathing patterns is not a completely new concept. It was probably first elucidated by Suki et al. 3in Nature in 1998.” In fact such an approach, subsequently called biologically variable ventilation, was first elucidated in 1996 in work done in my laboratory by Lefevre et al .4Careful reading of the article in Nature indicates that stochastic resonance was advanced as an explanation for the improvement in compliance and oxygenation with a noisy end-inspiratory pressure based on analysis of data from our publication. We have since extended these observations to more generally indicate where noisy ventilation will be efficacious and where it may be detrimental.5This analysis is based on Jensen’s inequality–a mathematical proof stating that a variable input will enhance an output when a smoothly continuous curvilinear function is convex.6In contrast, if the function describing a relationship is concave, the addition of noise can diminish output and potentially be detrimental. Noisy ventilation is especially advantageous with tidal volume protocols according to the Acute Respiratory Distress Syndrome Network trial because the volume-pressure curve is convex curvilinear in the range of low tidal volumes.7The lone negative animal study examining noisy ventilation in an acute respiratory distress syndrome model may be a consequence of large tidal volumes administered over the concave region of the sigmoidal volume-pressure curve—the portion of the static compliance curve where it may be deleterious to provide positive pressure ventilation based on modeling using Jensen’s inequality.8The editorial further raises the question of the use of noisy ventilation in normal lungs. My laboratory has examined the use of noisy ventilation in the experimental setting of baseline anesthesia without lung injury9and during ventilation of the dependent lung during one-lung anesthesia (an article published in Anesthesiology).10Colleagues published, again in Anesthesiology, the first clinical trial examining the application of variable ventilation during abdominal aneurysmectomy.11In each of these studies better gas exchange and respiratory mechanics were seen with noisy ventilation, as compared with conventional monotonous control mode ventilation, similar to the findings by Spieth et al. I do concur with the editorialists that “The importance of variability, whether referring to the respiratory system or DNA, in biologic systems should not be underestimated.” Based on the nonlinear amplification of output in convex curvilinear systems as outlined above, we have shown that noisy perfusion can improve cerebral oxygenation,12diminish renal injury,13and enhance delivery of cardioplegia14during cardiopulmonary bypass. These improvements are likely a consequence of better flow with noisy perfusion pressure over the convex curvilinear flow-pressure curve manifest by the microvasculature. An overview of some of these issues is discussed in a short review.15I also concur that “the time is here to translate these studies to the bedside.” The article by Spieth et al. reinforces prior work by this European group, the group in Boston, and the group in Canada, all demonstrating the advantage of adding noise to life support systems.University of Manitoba, Winnipeg, Manitoba, Canada. amutch@cc.umanitoba.ca

Bymixer system can measure O2 uptake and CO2 elimination in the anesthesia circle circuit

The ability to measure carbon dioxide elimination (Vco(2)), oxygen uptake (Vo(2)), and R (respiratory exchange ratio, Vco(2)/Vo(2)) during anesthesia may help the non-invasive detection of critical events (e.g., abrupt decrease in cardiac output) and metabolic upset (e.g., onset of anaerobic metabolism). We have developed a new clinical bymixer (inline mixing chamber) that can measure mixed inspired and expired gas fractions in the anesthesia circle circuit. The addition of a standard anesthesia gas analyzer and flowmeter, and a new airway temperature and humidity sensor, allow determinations of Vco(2) and Vo(2) at the airway opening of the circle circuit. Over a range of tidal volume and frequency, Vco(2) and Vo(2) were compared to reference values generated by the combustion of metered liquid ethanol in a new metabolic lung simulator. By linear regression, bymixer-flow measurements of Vco(2) (slope = 1.02, Y-intercept = -5.31, coefficient of determination, R(2) = 0.998) and Vo(2) (slope = 1.05, Y-intercept = -4.34, R(2) = 0.993) correlated closely to the reference values generated by the metabolic lung simulator. Limits of agreement analysis generated percent errors (mean +/- 1.96 SD) of -1.2 +/- 7.2% for Vco(2) and 2.5 +/- 9.8% for Vo(2). The new clinical bymixer is compact, lightweight, disposable, inexpensive, and has a fast and adjustable response time (time constant about 14 sec). Anesthesia circle circuit integrity is maintained. Bymixer-flow measurements of Vco(2) and Vo(2) are accurate and may add to clinical monitoring under anesthesia and surgery.

Weak link in the lung

The transition from peripheral airway disease to COPD is characterized by three sequential stages: stage I, during which the closing volume (CV) eventually exceeds the FRC; stage II, during which tidal expiratory flow limitation (EFL) is eventually exhibited; and stage III, during which dynamic hyperinflation (DH) progressively increases leading to dyspnoea and exercise limitation. Smoking is a condition which accelerates the age-related impairment of lung function. Indeed, McCarthy et al.1 who studied 35 smokers with FEV and FEV/FVC within normal limits, found that in almost all instances CV was higher than predicted normal both sitting and supine. More importantly, while in all 66 control non-smokers whose age was less than 65 years the FRC exceeded the CV in the sitting position, this was not the case in eight of the 35 smokers. In the supine position, the age-corrected prevalence of peripheral airway closure during tidal breathing was even higher in the smokers. Thus, during stage I the extent of peripheral airway closure increases progressively in smokers until tidal EFL is present not only supine but also sitting. Tidal FL implies sequential closure of the peripheral airways during expiration and reopening during inspiration, with concurrent risk of peripheral airway injury, which is characterized by denuded epithelium in the respiratory and membranous bronchioles. Furthermore, there is rupture of the airway-alveolar attachments.2–4 Thus, the peripheral airways represent a weak link in the lung because airway closure in the tidal volume range is a common phenomenon reflecting either a decreased FRC (e.g. obesity, left heart failure) or an increased CV (e.g. smoking, asthma). The smoking-related increase of CV accelerates the age-related decrease of maximal flow (Vmax) at low lung volume.5 Indeed, such a pattern is exhibited by all COPD patients and is due to the combined effect of age and smoke on gas trapping. As a result of gas trapping the RV increases. Peripheral airway closure is usually found in the dependent lung zones where the transpulmonary pressure is lowest. Thus, airway closure is a regional phenomenon, whose extent and location varies with body posture. Most normal subjects do not exhibit tidal EFL even during maximal exercise. In contrast, in many COPD patients EFL may be present even at rest.6 Two main mechanisms promote the occurrence of tidal EFL, namely a reduction of available flow and/or an increase in ventilatory requirements. Since smoking causes a progressive reduction of Vmax in the tidal volume range of susceptible subjects, tidal EFL eventually occurs even in the sitting position. Tidal EFL implies heterogeneous sequential dynamic compression of the peripheral airways during expiration and re-expansion during inspiration, with concurrent risk of peripheral airway injury.7 During stage II, both tidal EFL and peripheral airway closure may concur in eliciting airway injury. In stage II, EFL during tidal breathing occurs initially at local levels but it eventually extends to all pulmonary airways, that is, the tidal expiratory flow rates are maximal even during quiet breathing. Thus, during stage II, EFL progresses from a local to a generalized phenomenon. Both promote DH because, in order to generate an adequate pulmonary ventilation, subjects with tidal EFL must breathe at a higher volume than the relaxed FRC. In normal individuals at rest, the end-expiratory lung volume (FRC) corresponds to the relaxation volume (Vr) of the respiratory system, that is, the lung volume at which the elastic recoil pressure of the respiratory system is zero. Pulmonary hyperinflation, which is defined as an increase in FRC above the predicted normal range, maybe due to increased Vr as a result of loss of lung recoil (e.g. emphysema) or dynamic pulmonary hyperinflation, which is said to be present when the FRC exceeds Vr. DH exists when the duration of expiration is insufficient to allow the lungs to deflate to Vr before the next inspiration. This may occur when expiratory flow is impeded (e.g. increased airway resistance) and/or expiratory time is shortened (e.g. increased breathing frequency). In COPD patients DH is common and is mainly due to tidal EFL.6 It is the main factor causing dyspnoea and exercise limitation.8

AnaConDa?? Reflection Filter: Bench and Patient Evaluation of Safety and Volatile Anesthetic Conservation

The AnaConDa filter permits administration of volatile anesthetic without the use of an anesthesia machine. It is intended for use in the intensive care unit. We studied the AnaConDa reflection filter on the bench and in anesthetized patients. The bench analysis used a test lung, a gas analyzer, an intensive care ventilator, the AnaConDa filter, and a syringe pump. We studied a range of tidal volume, respiratory rate, and positive end-expiratory pressure values. We simulated errors during syringe refilling and patient transportation. In 15 anesthetized patients, we used the AnaConDa with constant ventilation variables, a constant sevoflurane infusion rate (4-5 mL/h), and two consecutive fresh gas flow levels. In the bench study, the expired volatile anesthetic fraction decreased linearly with respiratory frequency at constant minute ventilation, and decreased markedly in a hyperbolical manner when tidal volume increased at a constant respiratory rate. Changing the positive end-expiratory pressure level and inspiration/expiration ratio did not modify the AnaConDa's performance. Several safety failures were observed: refilling caused a transient change in AnaConDa output because of a pumping effect, and a standard Luer lock made it possible to connect the halogenate syringe on an IV infusion line. In anesthetized patients, reducing fresh gas flow from 8 to 1 L/min led to a median 40% increase in the expired volatile anesthetic fraction. This study shows that the device is generally reliable, but that there are several conditions under which it might deliver more anesthetic than intended.

Noninvasive monitoring of chest wall movement in infants using laser

Traditionally, non-invasive monitoring of tidal volume in infants has been performed using impedance plethysmography analyzed using a one or two compartment model. We developed a new laser system for use in infants, which measures antero-posterior movement of the chest wall during quiet sleep. In 24 unsedated or sedated infants (11 healthy, 13 with respiratory disease), we examined whether the analysis of thoracoabdominal movement based on a three compartment model could more accurately estimate tidal volume in comparison to V(T) measured at the mouth. Using five laser signals, chest wall movements were measured at the right and left, upper and lower ribcage and the abdomen. Within the tidal volume range from 4.6 to 135.7 ml, a three compartment model showed good short term repeatability and the best agreement with tidal volume measured at mouth (r(2) = 0.86) compared to that of a single compartment model (r(2) = 0.62, P < 0.0001) and a two compartment model (r(2) = 0.82, P < 0.01), particularly in the presence of respiratory disease. Three compartment modeling of a 5 laser thoracoabdominal monitoring permits more accurate estimates of tidal volume in infants and potentially of regional differences of chest wall displacement in future studies.

Respiratory function in morbidly obese subjects

Morbidly obese subjects are characterized by important changes in respiratory function both during spontaneous breathing as well as during general anesthesia and mechanical ventilation. The most characteristic abnormalities consist of decreased functional residual capacity (FRC), reduced expiratory reserve volume, decreased compliance and increased resistance of the respiratory system. Breathing at low lung volume promotes airway closure in the dependent lung zones with consequent gas exchange abnormalities. Furthermore, the decreased expiratory reserve as a result of decreased FRC and the higher ventilatory requirements of these patients due to increased metabolic demands may promote expiratory flow limitation (EFL) in the tidal volume range. The presence of peripheral airway closure and EFL during tidal breathing promotes peripheral airway injury and may accelerate the abnormalities of lung function. The risk of injury is expected to be higher during mechanical ventilation due to the high-pressure transients, which develop under this condition. Consequently, external positive end-expiratory pressure (PEEP) must be applied to these subjects in order to increase the end-expiratory lung volume above the closing volume as well as the flow limitation volume and thus decrease the risk of peripheral airway injury.

Respiratory function in morbidly obese subjects

AbstractMorbidly obese subjects are characterized by important changes in respiratory function both during spontaneous breathing as well as during general anesthesia and mechanical ventilation. The most characteristic abnormalities consist of decreased functional residual capacity (FRC), reduced expiratory reserve volume, decreased compliance and increased resistance of the respiratory system. Breathing at low lung volume promotes airway closure in the dependent lung zones with consequent gas exchange abnormalities. Furthermore, the decreased expiratory reserve as a result of decreased FRC and the higher ventilatory requirements of these patients due to increased metabolic demands may promote expiratory flow limitation (EFL) in the tidal volume range. The presence of peripheral airway closure and EFL during tidal breathing promotes peripheral airway injury and may accelerate the abnormalities of lung function. The risk of injury is expected to be higher during mechanical ventilation due to the high-pressu...

Measurement of Forced Expiratory Flows and Lung Volumes

After completing this article, readers should be able to: 1. Describe the information that measurements of forced expiratory flow can provide in spontaneously breathing and mechanically ventilated infants. 2. Delineate how lung volume can be measured. The measurements of forced expiratory flows and lung volumes are important to the evaluation of patients who have respiratory symptoms. Until recently, measurements have been restricted to adults and children old enough to cooperate with testing maneuvers. Newer techniques have enabled such measurements to be made in infants and led to improved understanding of normal lung and airway growth during infancy and early childhood, when dramatic changes occur. The measurements have had important clinical uses in the evaluation and treatment of infants who have respiratory disease, but their use has been limited because they require specialized equipment and expertise as well as sedation of the infant. In this article, we discuss the techniques required for measurement of forced expiratory flows and lung volumes, their limitations, and applications in clinical practice. Detection of airflow obstruction, by physical examination or by quantitative measurement techniques, is facilitated by increasing expiratory flow rates. Measurement of forced expiratory flows is useful because flow rates are inversely proportional to the fourth power of the radius of the airway and, therefore, are indicative of airway size when flow is limited. Disease states affecting the airways, including asthma, bronchopulmonary dysplasia (BPD), or congenital lesions such as pulmonary hypoplasia or vascular airway compression, are expected to decrease expiratory flow. Infants typically are sedated for testing to maintain relaxed breathing with a face mask placed over the mouth and nose. This sedation often is perceived by parents and physicians as one of the barriers to such testing. (1) However, sedation can be achieved safely using oral chloral hydrate at a dose of 80 to 100 mg/kg. …

Does Mechanical Injury of the Peripheral Airways Play a Role in the Genesis of COPD in Smokers?

In the present account it is proposed that in smokers the transition from peripheral airway disease to COPD is characterized by three sequential stages: Stage I, during which the closing volume eventually exceeds the functional residual capacity; Stage II, during which tidal expiratory flow limitation (EFL) is eventually exhibited; and Stage III, during which dynamic hyperinflation progressively increases leading to dyspnea and exercise limitation, which may be considered as markers of overt disease. Presence of airway closure (Stage I) and EFL (Stage II) in the tidal volume range may promote peripheral airway injury and accelerate the abnormalities of lung function. It is such injury that may determine which smoker is destined to develop COPD.

直角分岐管内振動流の数値解析(G02-6 流体,G02 バイオエンジニアリング部門)

To clarify flow phenomena in avian lung, oscillatory flow in a right angle branch was numerically studied in the range of dimensionless tidal volume, v_γ/a^3, of 10 to 80, and dimensionless frequency, α^2, of 8 to 40. The results show that the pressure drop caused by separation vortex at the entrance of side-daughter tube in the inspiratory phase drives unidirectional (circular) flow from the side-daughter tube to the daughter tube. Due to convective inertia, the unidirectional flow persists even in the expiratory phase, in which no vortex exists at the entrance of the side-daughter tube. By visualizing the streaming of fresh gas inspired from the mother tube, it is also shown that the unidirectional flow strongly enhances axial gas transportation in the process of avian respiration.

Orthopnea and Tidal Expiratory Flow Limitation in Patients With Euthyroid Goiter

Nontoxic goiters can cause extrathoracic upper airway obstruction and, if large, may extend into the thorax, causing intrathoracic airway obstruction. Although patients with goiter often report orthopnea, there are few studies on postural changes in respiratory function in these subjects. The aim of this study was to investigate the postural changes in respiratory function and the presence of flow limitation (FL) and orthopnea in patients with nontoxic goiter. In 32 patients with nontoxic goiter, respiratory function was studied in seated and supine position. Expiratory FL was assessed with the negative expiratory pressure method. Goiter-trachea radiologic relationships were arbitrarily classified as follows: grade 1, no evidence of tracheal deviation; grade 2, tracheal deviation present in lateral and/or anteroposterior plane but with tracheal compression < 20%; and grade 3, tracheal deviation present with compression > 20%. Subgroups were considered according to this classification and occurrence of orthopnea and FL. In all three groups of patients, the average maximal expiratory flow at 50% of FVC/maximal inspiratory flow at 50% of FVC ratios were > 1.1, suggesting the presence of upper airway obstruction. Grade 3 patients had a significantly lower expiratory reserve volume and maximal expiratory flow at 25% of FVC and higher airway resistance and 3-point FL score than patients with grade 1 and grade 2. The prevalence of orthopnea was highest in patients with grade 3 (75%, as compared to 18% in the grade 1 group). In patients with orthopnea, the prevalence of intrathoracic goiter was also higher (78%, vs 21% in patients without orthopnea). There is a high prevalence of orthopnea in patients with goiter, especially when the location is intrathoracic and causes a reduction of end-expiratory lung volume and flow reserve in the tidal volume range, promoting FL especially in supine position. Obesity is a factor that increases the risk of orthopnea in patients with goiter.

The kinetic spectrum of APD.

A generalized kinetic model to quantify the efficiency of cycler (CPD) and tidal peritoneal dialysis (TPD) is used to examine the relative efficiency of these techniques over a wide range of tidal volumes, drain profile characteristics, and hourly dialysate flow rates. In the patient with good catheter function, there is little difference in efficiency between CPD and TPD. In patients with long drain times or nonlinear drain profiles, greatly improved efficiency may theoretically be achieved with small tidal volume TPD. A generalized solution of the continuous flow PD (CFPD) kinetic model is used to demonstrate and contrast the kinetics of automated PD (APD) and CFPD.

Comparison of Subjective and Objective Measures in Recurrently Wheezy Infants

Objectives: The aim of this study was to compare subjective measures (overall health assessment both by the study physician and the child’s mother) with objective measurements of forced expiratory volumes (FEV_t) and maximal flow at functional residual capacity v̇_maxFRC) in recurrently wheezy infants. Methods: Sixteen wheezy infants (12 boys) aged 8–26 months were studied. A clinical assessment at visit 1 was followed by the run-in period during which day- and nighttime asthma symptom scores were obtained. The actual study period consisted of 2 visits when patient’s lung function was assessed. The first of which was during an acute exacerbation (visit 2), while the second was when the infant was asymptomatic (visit 3). FEV_t were obtained by the raised volume rapid thoracic compression technique (RVRTC) and v̇_maxFRC by the tidal volume rapid thoracic compression technique (TVRTC). Results: Mean FEV_t but not mean v̇_maxFRC were significantly lower at visit 2 compared to visit 3 (FEV_0.5: p = 0.005, and FEV_0.75: p = 0.002; v̇_maxFRC: p = 0.15) and correlated well with overall health assessment by the study physician (FEV_0.5: r = 0.82, and FEV_0.75: r = 0.84), but not with the overall health assessment by the mother. Conclusions: We have shown in the present study that objective measurements of FEV_t from a raised lung volume correlate well with the overall health assessment by the study physician; this was in contrast to measurements of v̇_maxFRC in the tidal volume range. We therefore conclude that the RVRTC technique is a feasible method to assess and monitor obstructive lung disease in infancy.

Impact of Mechanical Ventilation on the Developing Airway

After completing this article, readers should be able to: 1. Explain why immature infants are at a greater risk for mechanical ventilation-induced airway damage than are more mature infants. 2. Describe the effect of ventilatory pressures on components of the airway. 3. Delineate how mechanical ventilation disrupts airway mechanics. 4. Characterize how mechanical ventilation affects immature airway smooth muscle. 5. Describe techniques of optimizing ventilation to minimize respiratory damage. Although the air passages take on a mature appearance well before a fetus is viable, they undergo significant maturational changes in late gestation. During development, the airways are more susceptible to damage. In fact, although controversy still surrounds the pathogenesis of bronchopulmonary dysplasia (BPD) and other neonatal airway complications, it appears that the duration and higher pressures of mechanical ventilation, along with the use of oxygen, are related to the development of airway-related problems in preterm infants. As a result, because of their greater need for ventilatory assistance, very preterm infants are at substantially increased risk of airway damage. With recent and continuing advancements in neonatal care, a growing number of immature infants survive premature births. One of the primary hurdles that must be overcome in these infants is respiratory system immaturity. In this context, an understanding of the embryologic development and physiologic maturation of the respiratory system is imperative. The respiratory system can be subdivided grossly into the airways and the lung parenchyma. Developmental changes in the mechanical properties of these two components predispose the immature airway to injury. The immature lung is a relatively noncompliant structure. During neonatal development, lung compliance increases with lung maturity. However, the opposite is true for airways. Immature airways are relatively more compliant than their mature counterparts, with airway maturation resulting in a decrease in airway compliance. This produces an interesting predicament when contemplating the administration of mechanical ventilation …

Visual Validation of the Mechanical Stabilizing Effects of Positive End-Expiratory Pressure at the Alveolar Level

Background. Positive end-expiratory pressure (PEEP) reduces ventilator-induced lung injury (VILI), presumably by mechanically stabilizing alveoli and decreasing intrapulmonary shear. Although there is indirect support for this concept in the literature, direct evidence is lacking. In a surfactant depletion model of acute lung injury we observed unstable alveolar mechanics referred to as repeated alveolar collapse and expansion (RACE) as measured by changes in alveolar area from inspiration to expiration (I − EΔ). We tested the hypothesis that over a range of tidal volumes PEEP would prevent RACE by mechanically stabilizing alveoli.Materials and methods. Yorkshire pigs were randomized to three groups: control (n = 4), Tween (surfactant-deactivating detergent) (n = 4), and Tween + PEEP (7 cm H2O) (n = 4). Using in vivo video microscopy individual alveolar areas were measured with computer image analysis at end inspiration and expiration over consecutive increases in tidal volume (7, 10, 15, 20, and 30 cc/kg.) I − EΔ was calculated for each alveolus.Results. Surfactant deactivation significantly increased I − EΔ at every tidal volume compared to controls (P < 0.05). PEEP prevented this change, returning I − EΔ to control levels over a spectrum of tidal volumes.Conclusions. RACE occurs in our surfactant deactivation model of acute lung injury. PEEP mechanically stabilizes alveoli and prevents RACE over a range of tidal volumes. This is the first study to visually document the existence of RACE and the mechanical stabilizing effects of PEEP at the alveolar level. The ability of PEEP to stabilize alveoli and reduce shear during mechanical ventilation has important implications for therapeutic strategies directed at VILI and acute respiratory distress syndrome.

Is pulmonary resistance constant, within the range of tidal volume ventilation, in patients with ARDS?

When managing patients with acute respiratory distress syndrome (ARDS), respiratory system compliance is usually considered first and changes in resistance, although recognized, are neglected. Resistance can change considerably between minimum and maximum lung volume, but is generally assumed to be constant in the tidal volume range (VT). We measured resistance during tidal ventilation in 16 patients with ARDS or acute lung injury by the slice method and multiple linear regression analysis. Resistance was constant within VT in only six of 16 patients. In the remaining patients, resistance decreased, increased or showed complex changes. We conclude that resistance within VT varies considerably from patient to patient and that constant resistance within VT is not always likely.

Volume and time dependence of respiratory system mechanics in normal anaesthetized paralysed humans.

The purpose of the present investigation was to assess the effect of large tidal volumes and mean lung volumes on the viscoelastic properties of the respiratory system in normal humans; and to verify if in this case the results could be satisfactorily described by a simple linear viscoelastic model of the respiratory system. Twenty-eight subjects (7 females), aged 14-28 yrs, were studied before orthopaedic surgery on the lower limbs. None were obese, or had clinical evidence of cardiopulmonary disease. The interrupter conductance and the viscoelastic constants of the respiratory system were assessed using the rapid end-inspiratory airway occlusion method during mechanical ventilation with tidal volumes up to 3 L and applied end-expiratory pressures up to 23 cmH2O. It was found that the interrupter conductance increased linearly with lung volume over a larger range than used previously; and the viscoelastic resistance and time constant did not change over the entire range of tidal volumes and end-expiratory pressures studied. In conclusion, in normal anaesthetized, paralysed subjects a simple linear viscoelastic model satisfactorily described the viscoelastic behaviour of the respiratory system over the whole range of volume studied.

A new sensor for monitoring chest wall motion during high-frequency oscillatory ventilation

The recently developed technique of fibre optic respiratory plethysmography (FORP) has been modified to monitor the rapid, small amplitude movements of the chest wall during high-frequency oscillatory ventilation (HFOV). The FORP sensor is an expandable belt encircling the chest, in which is housed a fibre optic loop that alters its radius of curvature as a function of chest perimeter. These curvature changes cause variations in macrobending losses of light transmitted through the fibre, which are proportional to the chest perimeter. Dynamic measurement of transmitted light intensity can hence be used to monitor chest wall motion (CWM). For application to HFOV, the design of the FORP belt was altered to increase sensitivity and the materials were chosen to maximise macrobending effects induced by the CWM. FORP was tested in four piglets ventilated with HFOV, both in the normal and surfactant-deficient lung. Measurement of CWM was possible over the full range of tidal volumes and ventilation frequencies used during HFOV. In all cases, the measured frequency of the CWM fell within 3% of the applied ventilation frequency. In addition, the technique was sufficiently sensitive to detect changes in the amplitude of CWM in response to changes in applied tidal volume. It is anticipated that application of this new non-invasive measurement device will lead to an increased understanding of the dynamics of chest and abdominal wall motion during HFOV.