Ventilation Output Research Articles

The effect of lower limb passive movement on lung function

This study examined the effects of ankle passive movement on lung function in healthy adults. A pre-test post-test experimental design was used. Passive plantar and dorsiflexion of the ankle were performed at 60 repetitions per minute on 60 healthy subjects in the supine position. Lung function at rest was compared to that during passive movements. The results indicated that all measured parameters including the breathing frequency, tidal volume, minute ventilation, oxygen consumption and carbon dioxide output, increased significantly during passive movements as compared to those at rest. The authors conclude that passive movements elicit a significant ventilatory increase in healthy human subjects. The effect of passive movements in the treatment of unconscious or diseased individuals should be investigated.

Intra-breath profiles of alveolar gas exchange and the initial limb-to-lung transit delay during exercise in humans: relevance for modeling the exercise hyperpnea.

Following the onset of constant load exercise, pulmonary ventilation (VE), 02 uptake (VO2) and CO2 output (VCO2) all increase exponentially as a function of time, subsequent to the limb-to-lung transit time which is termed phase I (ΦI). The onset of the exponential phase (ΦII) for Vol and VCO2 is “consequent” to the arrival of altered mixed venous gas tensions at the pulmonary capillary bed resulting from increased muscle metabolic rate1. It is not known, however, whether the onset of the ΦII V E coincides with that of VO2 and VCO2, suggestive of a ‘pulmonary’ mechanism of mediation, or whether its onset is delayed i.e. consistent with a transit delay to downstream sites of chemoreception (e.g. carotid bodies) - evidence that is crucial for assembling a mechanistic control model of the transient.

Transgenic approaches to the study of respiratory function

Genetically engineered mice have proven an invaluable tool for establishing linkages between individual genes and the generation of complex behaviors, including respiration. This presentation will focus on the use of mice carrying targeted gene deletions (gene knockouts) to elucidate the role of neuronal growth factors in the development of the neural respiratory controller and breathing behavior. In particular, I will focus on the role of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) in development of peripheral chemoafferent neurons and central respiratory output. Initial studies in my laboratory demonstrated that mice that are homozygous for a null mutation at the bdnf locus exhibit a severe developmental deficit in control of breathing, characterized by depressed and irregular ventilation and central respiratory output and a lack of hypoxic ventilatory drive [1,2]. These deficits are due at least in part to loss of peripheral chemoafferent neurons that require BDNF for survival during fetal development [1,3,4]. Surprisingly, null mutations in the gdnf gene result in a similar phenotype, despite the fact that BDNF and GDNF are structurally unrelated and signal through wholly different classes of receptors. However, we recently found that BDNF and GDNF are both required for survival of the same population of chemoafferent neurons and that null mutations in either gene results in chemoafferent cell loss [5]. This dual requirement for BDNF and GDNF appears to be related to the fact that both molecules are expressed in the fetal carotid body and act as target-derived survival factors for chemoafferent neurons [5,6]. Loss of chemoafferent input at fetal stages is particularly deleterious for maturation of ventilatory function, as chemoafferent drive is required for stabilization of central respiratory output after birth. Potential implications of these findings for human developmental disorders of breathing will be discussed.

Lesion or muscimol in the rostral ventral medulla reduces ventilatory output and the CO 2 response in decerebrate piglets

Developmental abnormalities have been described in the arcuate nucleus of sudden infant death syndrome (SIDS) victims. The arcuate nucleus has putative homologues in chemosensitive areas of the ventral medulla in animals. We refer to some of these areas collectively as the rostral ventral medulla (RVM). In the RVM of decerebrate piglets 2–15 days of age, we studied the effects of electrolytic lesions ( n=7) or microdialysis of muscimol ( n=15), a GABAa receptor agonist, on ventilatory output and the response to hypercapnia. Lesions caused a 66.7±17.3% reduction in eupneic phrenic minute activity (MA) and abolished the response to hypercapnia. Muscimol dialysis caused a 32.4±10.4% reduction in MA with a significant downward displacement of the response to hypercapnia with no significant effect on the slope. We conclude that the piglet RVM contains neurons of vital importance in the maintenance of normal breathing and the response to systemic CO 2. We hypothesize that dysfunction of homologous regions in the human infant could lead to impaired ability to respond to hypercapnia and could potentially be involved in the pathogenesis of SIDS.

Neurotransmitters in central respiratory control

A diverse group of processes are involved in central control of ventilation. Both fast acting neurotransmitters and slower acting neuromodulators are involved in the central respiratory drive. This review deals with fast acting neurotransmitters that are essential centrally in the ventilatory response to H +/CO 2 and to acute hypoxia. Data are reviewed to show that the central response to H +/CO 2 is primarily at sites in the medulla, the most prominent being the ventral medullary surface (VMS), and that acetylcholine is the key neurotransmitter in this process. Genetic abnormalities in the cholinergic system lead to states of hypoventilation in man and that knock out mice for genes responsible for neural crest development have none or diminished CO 2 ventilatory response. In the acute ventilatory response to hypoxia the afferent impulses from the carotid body reach the nucleus tractus solitarius (NTS) releasing glutamate which stimulates ventilation. Glutamate release also occurs in the VMS. Hypoxia is also associated with release of GABA in the mid-brain and a biphasic change in concentration of another inhibitory amino acid, taurine. Collectively changes in these amino acids can account for the ventilatory output in response to acute hypoxia. Future studies should provide more data on molecular and genetic basis of central respiratory drive and the role of neurotransmitter in this essential function.

Hypoxic and Hypercapnic Breathlessness in Patients With Type I Diabetes Mellitus

The putative role of the performance of inspiratory muscles and breathing pattern in inducing dyspnea has been recently assessed during hypoxic stimulation in patients with type I diabetes (IDDM). Compared to a hypoxic stimulus, a hypercapnic stimulus, which may differently affect the pattern of breathing, could therefore modulate the coupling between respiratory effort and ventilatory output, which is involved in dyspnea sensation. Eight stable patients aged 19 to 48 years old, with IDDM (duration of disease, 36 to 240 months) and no smoking history, cardiopulmonary involvement, or autonomic neuropathy; and an age- and sex-matched control group. Pulmonary volumes, diffusing capacity of the lung for carbon monoxide, time and volume components (tidal volume [VT] and respiratory frequency), dynamic elastance (Eldyn), and swings in pleural pressure (Pessw) were measured. Maximal inspiratory pleural pressure (Pes) during a maximal sniff maneuver (Pessn), respiratory muscle effort or output (Pessw%Pessn), tension time index (TTI) = TI/total breathing cycle time x Pessw(%Pessn), and swing in Pes during VT as a percentage of Pessn were also evaluated. Dyspnea sensation was assessed by a modified Borg scale. Subjects were studied at baseline and during hypoxic and hypercapnic rebreathing tests. Compared to control subjects, patients exhibited normal routine spirometric function and Pessn, but a higher Eldyn, indicating peripheral airway involvement. In patients, but not in control subjects, Eldyn increased during both chemical stimuli and increased more during hypoxia than during hypercapnia. Also, changes in both VT and Pessw(%Pessn) on changes in PCO(2) were lower, while changes in Pessw(%Pessn)/VT, an index of neuroventilatory dissociation (NVD) of the ventilatory pump, on changes in PCO(2) were greater. Changes in VT and NVD for unit change in arterial oxygen saturation were lower and higher, respectively. Changes in Borg scale per changes in NVD were greater during both stimuli. Furthermore, compared to hypoxic conditions, a greater VT for any level of both minute volume and Pessw(%Pessn), and lower changes in Borg scale on changes in Pessw(%Pessn) and Pessw(%Pessn)/VT were found in hypercapnia. Changes in NVD and Borg scale related to changes in Eldyn with both chemical stimuli. In IDDM, the greater perception of dyspnea is associated with changes in inspiratory effort being out of proportion to changes in VT. The greater increase in Eldyn and the lower increase in VT may, in part, account for the greater perception of breathlessness during hypoxia.

Lung deflation stimulates fictive ventilation in decerebrated and unidirectionally ventilated toads

We describe how the degree of lung inflation and hypercapnia influenced fictive ventilation in five toads ( Bufo marinus) that were decerebrated and paralysed with roccuronium. Both lungs were unidirectionally ventilated and the degree of lung inflation was determined by controlling the outflow resistance of these catheters, while ventilatory motor output was assessed on the basis of nervous activity in the mandibular branch of the Vth cranial nerve. The pattern of the recorded activity (‘fictive ventilation’) resembled the ventilatory patterns previously described for conscious toads. Increasing the fraction of CO 2 in the gas mixture used for unidirectional ventilation from 0.00 to 0.05 stimulated fictive breathing. fictive ventilation was also greatly stimulated, at all CO 2 levels, by reduced lung volume, while complete inflation of the lungs abated fictive ventilation at all levels of CO 2. Stimulation of CO 2 sensitive chemoreceptors and pulmonary stretch receptors appear to have interactive effects on the central generation of ventilatory output in toads.

TRH microdialysis into the RTN of the conscious rat increases breathing, metabolism, and temperature.

Thyrotropin-releasing hormone (TRH) injected into the retrotrapezoid nucleus (RTN) of anesthetized rats produces a large, prolonged stimulation of ventilatory output (C. L. Cream, A. Li, and E. E. Nattie. J. Appl. Physiol. 83: 792-799, 1997). Here we inject or dialyze TRH into the RTN of conscious rats. In 6 of 17 injections (200 nl, 3.1 +/- 1.7 mM), ventilation (VE) increased 31% by 10 min, with recovery by 60 min. With dialysis, each animal of one group (n = 5) received, in random order, 10 mM TRH, 10 mM TRHOH (a metabolite of TRH), and artificial cerebrospinal fluid (aCSF); each animal of a second group (n = 5) received aCSF and 1 mM TRH. TRHOH and aCSF had no sustained effects. TRH (1 mM) increased VE (32%, P < 0.02, by 10 min, with recovery by 60 min), O(2) consumption (VO(2); 19%, P < 0. 03), and body (rectal) temperature (T(re); 0.5 degrees C, P < 0.09). TRH (10 mM) increased VE (78%, P < 0.01, by 10 min, with no recovery at 60 min), VO(2) (48%, P < 0.01), and T(re) (1.0 degrees C, P < 0. 01). TRH also induced arousal. The tissue volume affected in dialysis, estimated by spread of dialyzed fluorescein (332.3 mol wt, mol wt of TRH = 362.4), was 1,580 +/- 256 nl for 10 mM (n = 5) and 590 +/- 128 nl for 1 mM (n = 5). We conclude that 1) the RTN is involved in the integration of VE, VO(2), T(re), and arousal and 2) TRH may establish the responsiveness of RTN neurons.

Effects of assisted mechanical ventilation on control of breathing

During spontaneous breathing, the respiratory muscle pressure (Pmus) waveform is determined by a complex system consisting of a motor arm, a control center, and various feedback mechanisms that convey information to the control center. During assisted mechanical ventilation, the pressure delivered by the ventilator (Paw) is incorporated into the system and may alter the Pmus waveform, which in turn modifies the function of the ventilator. Thus, the response of Pmus to Paw and the response of Paw to Pmus constitute the two components of patient-ventilator interaction as well as of control of breathing during assisted mechanical ventilation. The response of Paw to Pmus depends on: 1) the mode of ventilatory support; 2) the mechanics of the respiratory system, and 3) the characteristics of the Pmus waveform. On the other hand the response of Pmus to Paw is mediated through four feedback systems: 1) mechanical; 2) chemical; 3) reflex, and 4) behavioral. It follows that the system that controls the act of breathing may be considerably modified by mechanical ventilation. The physician dealing with a mechanically ventilated patient should take into account the interaction between the respiratory effort and the function of the ventilator and be aware that the ventilatory output may or may not reflect the various aspects of control of breathing.

Effects of chemical feedback on respiratory motor and ventilatory output during different modes of assisted mechanical ventilation.

The purpose of the study was to examine the effects of chemical feedback on respiratory motor and ventilatory output in conscious subjects ventilated on various modes of assisted mechanical ventilation. Seven subjects were connected to a ventilator and randomly ventilated on assist-volume control (AVC), pressure support (PS) or proportional assist ventilation (PAV). On each mode, the assist level was set to the highest comfortable level. Airway and oesophageal (Poes) pressures, tidal volume, respiratory frequency (fR) and end-tidal carbon dioxide tension (PET,CO2) were measured breath-by-breath. When the subjects were stable on each mode, the fraction of inspired carbon dioxide (FI,CO2) was increased stepwise, and changes in minute ventilation (V'E) and respiratory motor output, estimated by the pressure-time product of all the respiratory muscles per breath (PTPrm) and per minute (PTPminute), were observed. At zero FI,CO2, PTPminute/PET,CO2 did not differ between modes, while V'E/ PTPminute was significantly lower with PAV than that with PS and AVC. As a result V'E/PET,CO2 was significantly lower with PAV, preventing, unlike AVC and PS, a significant drop in PET,CO2. With PAV, independent of CO2, V'E/PTPminute remained constant, while it decreased significantly with increasing CO2 stimulus with PS and AVC. At high PET,CO2 respiratory effort was significantly lower with PAV than that with PS and AVC. In conclusion, the mode of mechanical ventilation modifies the effects of chemical feedback on respiratory motor and ventilatory output. At all carbon dioxide stimulus levels neuroventilatory coupling was better preserved with proportional assist ventilation than with pressure support and assist-volume control ventilation.

Equipment review: Mechanical effects of heat-moisture exchangers in ventilated patients

Although they represent a valuable alternative to heated humidifiers, artificial noses have unfavourable mechanical effects. Most important of these is the increase in dead space, with consequent increase in the ventilation requirement. Also, artificial noses increase the inspiratory and expiratory resistance of the apparatus, and may mildly increase intrinsic positive end-expiratory pressure. The significance of these effects depends on the design and function of the artificial nose. The pure humidifying function results in just a moderate increase in dead space and resistance of the apparatus, whereas the combination of a filtering function with the humidifying function may critically increase the volume and the resistance of the artificial nose, especially when a mechanical filter is used. The increase in the inspiratory load of ventilation that is imposed by artificial noses, which is particularly significant for the combined heat-moisture exchanger filters, should be compensated for by an increase either in ventilator output or in patient's work of breathing. Although both approaches can be tolerated by most patients, some exceptions should be considered. The increased pressure and volume that are required to compensate for the artificial nose application increase the risk of barotrauma and volutrauma in those patients who have the most severe alterations in respiratory mechanics. Moreover, those patients who have very limited respiratory reserve may not be able to compensate for the inspiratory work imposed by an artificial nose. When we choose an artificial nose, we should take into account the volume and resistance of the available devices. We should also consider the mechanical effects of the artificial noses when setting mechanical ventilation and when assessing a patient's ability to breathe spontaneously.

A system to simulate gas exchange in humans to control quality of metabolic measurements.

We have developed a gas exchange simulation system (GESS) to assess the quality control in measurements of metabolic gas exchange. The GESS simulates human breathing from rest to maximal exercise. It approximates breath-by-breath waveforms, ventilatory output, gas concentrations, temperature and humidity during inspiration and expiration. A programmable motion control driving two syringes allows the ventilation to be set at any tidal volume (VT), respiratory frequency (f), flow waveform and period of inspiration and expiration. The GESS was tested at various combinations of VT (0.5-2.51) and f(10-60 stroke x min(-1)) and at various fractional concentrations of expired oxygen (0.1294-0.1795); and carbon dioxide (0.0210-0.0690) for a pre-set flow waveform and for expired gases at the same temperature and humidity as room air. Expired gases were collected in a polyethylene bag for measurement of volume and gas concentrations. Accuracy was assessed by calculating the absolute and relative errors on parameters (error=measured-predicted). The overall error in the gas exchange values averaged less than 2% for oxygen uptake and carbon dioxide output, which is within the accuracy of the Douglas bag method.

New modes of mechanical ventilation

Clinical optimization of patient-ventilator interaction can be obtained only through continuous matching of the triggering, flow delivering, and cycling functions of the ventilator with patient's ventilatory drive, spontaneous inspiratory flow demand, and neural inspiratory time. Total patient-controlled mechanical support modes are designed to automatically interface physiologic respiratory parameters and mechanical support. The ventilator should therefore be able to analyze respiratory mechanics, respiratory drive and blood gases, and detect patient's flow requirements, instantaneously adapting ventilator output to patient needs requiring application of automatic control technology. The closed-loop technology currently applied are described. Based on available data, extended technologic and clinical research still has to be performed to introduce these new modes of mechanical ventilation into clinical practice successfully.

Analysis of respiratory mechanics during artificial ventilation.

Mechanical or artificial ventilation is the most important life-saving therapeutic instrument in modern intensive care medicine. The ventilator takes on the convective transport of the respiratory gas, i.e. delivery of oxygen and removal of carbon dioxide. The technical gas delivery system (ventilator, respiratory tubing system, gas humidifier) and the respiratory system (lungs and thorax) of the patients form a connected pneumatic system of high complexity. The respiratory system produces a mechanical impedance to ventilator output. Impedance is composed of an elastic, a non-elastic, i.e. resistive, and an inertive part. The corresponding indices describing respiratory mechanics are compliance, flow resistance and inertance. Based on the equation of motion of the respiratory system, several methods of analysing respiratory mechanics during mechanical ventilation are described. Quantitative analysis of respiratory system mechanics (a) is a prerequisite for the understanding of the complex patient-ventilator interaction, (b) provides important clinical information on pulmonary function and the course of disease, and (c) allows the physician at the bedside to adjust the ventilatory settings to the needs of the individual patient.

A comprehensive simulator of the human respiratory system: Validation with experimental and simulated data

A comprehensive model of oxygen (O2) and carbon dioxide (CO2) exchange, transport, and storage in the adult human is presented, and its ability to provide realistic responses under different physiological conditions is evaluated. The model comprises three compartments (i.e., lung, body tissue, and brain tissue) and incorporates a controller that adjusts alveolar ventilation and cardiac output dynamically integrating stimuli coming from peripheral and central chemoreceptors. A new realistic CO2 dissociation curve based on a two-buffer model of acid-base chemical regulation is included. In addition, the model explicitly considers relevant physiological factors such as buffer base, the nonlinear interaction between the O2 and CO2 chemoreceptor responses, pulmonary shunt, dead space, variable time delays, and Bohr and Haldane effects. Model simulations provide results consistent with both dynamic and steady-state responses measured in subjects undergoing inhalation of high CO2 (hypercapnia) or low O2 (hypoxia) and subsequent recovery. An analysis of the results indicates that the proposed model fits the experimental data of ventilation and gas partial pressures as some meaningful simulators now available and in a very large range of gas intake fractions. Moreover, it also provides values of blood concentrations of CO2, HCO3-, and hydrogen ions in good agreement with more complex simulators characterized by an implicit formulation of the CO2 dissociation curve. In the experimental conditions analyzed, the model seems to represent a single theoretical framework able to appropriately describe the different phenomena involved in the control of respiration.

Lung function and exercise gas exchange in chronic heart failure.

The ventilatory response to exercise in patients with chronic heart failure (HF) is greater than normal for a given metabolic rate. The objective of the present study was to determine the mechanism(s) for the high ventilatory output in patients with chronic HF. Centers in Germany, Italy, Japan, and the United States participated in this study. Each center contributed studies on patients and normal subjects of similar age and sex. One hundred thirty patients with chronic HF and 52 healthy subjects participated. Spirometric and breath-by-breath gas exchange measurements were made during rest and increasing cycle exercise. Arterial blood was sampled for measurement of pH, PaCO2, PaO2, and lactate during exercise in 85 patients. Resting forced expiratory volume in 1 second (FEV1) and vital capacity (VC) were proportionately reduced at all levels of impairment. Patients with more severe HF had greater tachypnea and a smaller tidal volume (VT) at a given exercise expired volume per unit time (VE). This was associated with an expiratory flow pattern characteristic of lung restriction. VE and VCO2 as a function of VO2 were increased during exercise in HF patients. The increases were greater the lower the peak VO2 per kilogram of body weight. The ratio of VD (physiological dead space) to VT and the difference between arterial and end tidal PCO2 at peak VO2 also increased inversely with peak VO2/kg. In contrast, the difference between alveolar and arterial PO2 and PaCO2 were both normal, on average, at peak VO2 regardless of the level of impairment. The more severe the exercise limitation, the higher the lactate and the lower the HCO3- at a given VO2, although pH was tightly regulated. The increase in VE in chronic HF patients is caused by an increase in VD/VT due to high ventilation/perfusion mismatching, an increase in VCO2 relative to VO2 resulting from HCO3- buffering of lactic acid, and a decrease in PaCO2 due to tight regulation of arterial pH. With regard to the excessive VE in HF patients, the increases in VD/VT and VCO2 relative to VO2 are more important as the patient becomes more exercise limited. Regional hypoperfusion but not hypoventilation typifies lung gas exchange in HF. This and other mechanisms might account for the restrictive changes leading to exercise tachypnea in HF patients.

Airway thermal volume in humans and its relation to body size.

The objective of this study was to investigate the influence of volume ventilation (VE) and cardiac output (Q) on the temperature of the expired gas at the distal end of the endotracheal tube in anesthetized humans. In 63 mechanically ventilated adults, we used a step decrease in the humidity of inspired gas to cool the lungs. After change from humid to dry gas ventilation, the temperature of the expired gas decreased. We evaluated the relationship between the inverse monoexponential time constant of the temperature fall (1/tau) and either VE or Q. When VE was increased from 5.67 +/- 1.28 to 7.14 +/- 1.60 (SD) l/min (P = 0. 02), 1/tau did not change significantly [from 1.25 +/- 0.38 to 1.21 +/- 0.51 min-1, P = 0.81]. In the 11 patients in whom Q changed during the study period (from 5.07 +/- 1.81 to 7.38 +/- 2.45 l/min, P = 0.02), 1/tau increased correspondingly from 0.89 +/- 0.22 to 1. 52 +/- 0.44 min-1 (P = 0.003). We calculated the airway thermal volume (ATV) as the ratio of the measured values Q to 1/tau and related it to the body height (BH): ATV (liters) = 0.086 BH (cm) - 9. 55 (r = 0.90).

Respiratory-related pharyngeal constrictor muscle activity in normal human adults.

Electromyographic activity of the superior, middle, and inferior pharyngeal constrictor (PC) muscles was examined in 10 normal adult humans during wakefulness and sleep. Wire electrodes were inserted close to the midline of the posterior pharyngeal wall at the level of the soft palate (superior PC), tip of the epiglottis (middle PC), and corniculate tubercle (inferior PC). In general, the three PC muscles exhibited similar patterns of activation. The PCs were activated during swallows, repetitive "pa" sounds, changes in head position, and the last portions of slow inspiratory and expiratory vital capacity maneuvers. Respiratory-related PC activity was infrequent during quiet breathing during wakefulness; variable and inconsistent phasic activation in expiration in one or more of the PCs was present in seven of the 10 subjects, particularly after a swallow. Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia were associated with recruitment of phasic PC activity, which was predominantly expiratory; however, variable discharge patterns were observed within a given muscle and a given subject. When phasic PC activity was present, preactivation during late inspiration was frequently observed. PC activity was absent in NREM sleep and exhibited sporadic, nonrespiratory-related bursts of activity during REM sleep. Passively induced hypocapnic hyperventilation in NREM sleep was not associated with PC activation. The results indicate that the PCs have very similar patterns of activation and exhibit phasic expiratory activity during relatively high ventilatory output states in wakefulness.

Exercise performance in children with asthma: is it different from that of healthy controls?

Exercise tolerance and possible limitation in work capacity of asthmatic children is still a matter of debate. The aim of this study was to compare ventilation and gas exchange response to exercise of asthmatic children with that of healthy controls. Exercise performance was evaluated in 80 children with mild-to-moderate asthma, aged 7-15 yrs, and in 80 healthy controls matched for age, height, weight and habitual level of physical activity. The children performed a maximal exercise test on a treadmill, during which oxygen uptake (V'O2), carbon dioxide output (V'CO2) and minute ventilation (V'E) were measured continuously. No premedication was given to the asthmatic children. Forced expiratory volume in one second (FEV1) at rest was 93+/-11% of predicted in asthmatic children and 95+/-9% pred in controls. After the run, the mean fall in FEV1 was 13.9% (range 0-57%) and 1.6% (0-9%), respectively (p<0.001). The two groups achieved similar maximum oxygen uptake (V'O2,max) ((mean+/-SD) 40.3+/-8.4 and 42.6+/-9.6 mL x min(-1) x kg(-1) in asthmatics and controls, respectively; NS) and maximum minute ventilation output (V'E,max) (42.9+/-14.8 and 45.7+/-14.9 L x min(-1) respectively; NS). The kinetics of V'O2, V'CO2 and V'E during the test revealed no differences between the two populations. Moreover, anaerobic threshold and oxygen pulse were the same in the two groups. Asthmatics showed a ventilatory pattern with lower respiratory frequencies and greater tidal volumes during the run. These results suggest that asthmatic children can achieve a level of exercise performance similar to that of healthy children, provided that they have a comparable level of habitual physical activity. The only difference found concerned the ventilatory pattern of the asthmatic children, which was characterized by a reduced respiratory frequency and greater tidal volume at the same minute ventilation. The level of physical conditioning was found to be the main determinant of exercise tolerance for children with controlled asthma.

Patient-ventilator interactions in the critically ill

Positive-pressure breaths can be categorized by three variables: the trigger, the limit, and the cycle. They interface the ventilator with the three variables of the breathing pattern: ventilatory drive, ventilatory requirements, and duration and ratio of inspiratory time to total breath cycle duration. The inspiratory effort necessary to trigger a breath is a significant part of the total inspiratory effort; optimization of the triggering mechanisms may improve patient to ventilator interaction. Setting ventilator flow as close as possible to patient's flow by appropriate setting of peak value and waveform profile will also improve patient to ventilator interactions. During pressure support ventilation, ineffective efforts and uncoupling between effort and ventilator output are due to the asynchrony between ventilator and patient's inspiratory time. They may be counterbalanced by adequate peak flow and flow threshold values. Proportional assist ventilation may optimize patient to ventilator interactions, but continuous monitoring of respiratory mechanics should be performed along with its definitive technologic implementation. Its clinical use should be continuously adapted to resistance and elastance measurements.