Particle removal by the respiratory system note on the removal of airborne particulates by the human respiratory tract with particular reference to the role of diffusion.
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Diffusion↗
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Normative aging of the respiratory system.
An absolute quantified normal rate of change and normal range of functions of the respiratory system applicable to all older adults as they age is elusive. Like life expectancy, which is dependent on a cohort effect, the norms of respiratory system function are related to the birth cohort to which a given individual belongs and the age at which the parameter is assessed. No single rate of change can express normal across all age ranges even for those individuals in apparently good health [29]. Analogous to defining risk factors for a disease, determining that a change in anatomy or physiology is not disease requires stringent prospective evaluation for the absence of occult disease and known risk factors for disease prior to concluding that the alteration is inevitable with the normal aging process [19,31]. Additional limitations in quantifying the norms of respiratory function with age are the lack of participation of the oldest adults in studies and the lack of precision and accuracy in these performance-based measurements. The data, although limited, do support a qualitative emphysematous change in lung histology and lung-thorax mechanics. This change plus altered lung volumes influence oxygenation and oxygen consumption. There is no evidence that the changes in the respiratory system with aging impact day-to-day function of older adults, but they may become evident under circumstances when physiologic demand reaches the limits of supply. Despite changes in cholinergic and adrenergic receptor functioning, there is no evidence to suggest altering prescribing these classes of medications for older people. Pioneer physiologists asked the original question "Is there a difference in this measurement for older people?" Researchers in pulmonary medicine, pathology, radiology, epidemiology, and public health have continued to revise the question toward the clinical implications while studying the aging process from their respective viewpoints. Clinicians who need to develop an integrated care plan should neither rely on formulas to "normalize" a measurement for age nor assume that a established predictive value of a diagnostic test done in young adults can be automatically applied to geriatric patients [4]. Rather, the clinical situation should consider that the variability in normal is greater with older age and that all diagnostic tests and care plans should be considered in the context of the patient's symptoms [5].
Aged↗
Pressure-volume relations of the respiratory system in healthy children.
Static pressure-volume (P-V) curves of the respiratory system were obtained in 48 healthy children (1 mo to 16 yr of age) during anesthesia and muscle paralysis. The lungs were inflated to a pressure of 25 to 40 cm H2O, and during the subsequent deflation an interrupter placed in the airway tubing opened and closed every 0.16 s. Airway flow was integrated to obtain the volume decrement between consecutive flow interruptions. Airway pressure was measured during interruptions, and a curve relating pressure to lung volume was plotted, assuming the lung volume at zero pressure to equal functional residual capacity (FRC). FRC was measured using tracer gas washout. The maximum slope of the P-V curve (maximum compliance = Crsmax, ml/cm H2O) was closely related to length (in centimeters) of the child: Crsmax = 7.7 x 10(-4) x length2.38; r = 0.97. The pressure coinciding with Crsmax was 6 +/- 1 cm H2O (mean +/- SD) in infants (1 to 6 mo of age) and 12 +/- 1 cm H2O in older children (> 1.5 yr of age). Total lung capacity (TLC) per kg body weight increased with age and was 52 +/- 13 ml/kg in infants and 87 +/- 11 mg/kg in older children. The FRC/TLC ratio was greater in infants (38 +/- 4%) than in older children (30 +/- 5%). The lung volume coinciding with Crsmax was nearly the same at all ages, when expressed as a percentage of TLC: 62 +/- 3%. Specific compliance of the respiratory system, that is, Crsmax/TLC, decreased with growth and was 0.044 +/- 0.006 cm H2O-1 in infants and 0.035 +/- 0.004 cm H2O-1 in older children. It is concluded that although the P-V relations of the respiratory system changed markedly with growth, especially during the first year of life, the lung volume (%TLC) at which maximum compliance occurred varied little.
Adolescent↗
[Check list of the helminths in the respiratory system of domesticated animals in Turkey].
Helminths of the respiratory system make up an important part of the parasitic diseases found in domestic animals. Therefore, many studies have been carried out on these helminths in Turkey. In this article, a check list and the prevalence rates of helminths of respiratory system found in domestic animals in Turkey has been given.
Animals↗
Atrial natriuretic factor (ANF) and ANF receptor C gene expression and localization in the respiratory system: effects induced by hypoxia and hemodynamic overload.
Atrial natriuretic factor (ANF) and ANF receptor C (ANF.RC) expression have been investigated in healthy and cardiomyopathic hamsters (CMPH) with widespread necrosis of the diaphragm and myocardium leading to respiratory and heart failure. ANF- and ANF.RC-producing cells were localized in different structures of the respiratory system, and the regulation of their expression by the individual and/or combined action of hypoxia and hemodynamic overload was analyzed. The study was performed in 20-, 90-, and 150-day-old animals using immunohistochemistry, in situ hybridization, Northern blot, and RIA analyses. ANF was shown to be expressed in the tracheo-bronchial epithelium and muscle and, to a lesser extent, in the alveolar wall and muscular media of the pulmonary arteries and extraparenchymal pulmonary veins in both healthy hamsters and CMPH. In 150-day-old CMPH, hypoxia (PaO2 < 50 mm Hg) induced a 10-fold increase in ANF messenger RNA accumulation and a 6-fold increase in the immunoreactive ANF (IR-ANF) concentration in lungs, as quantitated by RIA. As plasma IR-ANF concentrations were elevated in all CMPH age groups, it was most likely produced by the myocardium. ANF.RC messenger RNA was homogeneously distributed throughout the entire respiratory system and was increased 2-fold in hypoxic 150-day-old CMPH only. These results suggest that ANF originating in the respiratory system exerts only paracrine effects on different structures of the respiratory system in addition to the action of circulating ANF. Hemodynamic overload (left ventricular end-diastolic pressure, 17.20 +/- 3.80 mm Hg) might contribute to enhanced ANF gene expression only in extraparenchymal pulmonary vein walls of 150-day-old CMPH. We also propose that ANF.RC overexpression might be a protective mechanism operated via either ANF clearance or inhibition of adenylate cyclase activity to counteract exaggerated smooth muscle relaxation.
Animals↗
PANEL discussion; respiratory system.
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Humans↗
Dependencies of respiratory system resistance and elastance on amplitude and frequency in the normal range of breathing.
We calculated respiratory system resistance (Rrs) and elastance (Ers) from pressure and flow at the mouth in six seated subjects relaxed at FRC (cheeks tightly compressed) during sinusoidal volume forcing (250, 500, and 750 ml) at 0.2, 0.4, and 0.6 Hz. Dependencies of Rrs and Ers on frequency and tidal volume were generally the same in each subject; Rrs tended to decrease with frequency and tidal volume, whereas Ers tended to increase with frequency and decrease with tidal volume. Multiple linear regression of combined data indicated that the frequency and tidal volume effects on Rrs and Ers were significant (p less than 0.05), and that the effects on Rrs decreased at higher flows. Average Rrs was highest (4.43 cm H2O/L/s +/- 0.21 SE) at 0.2 Hz-250 ml, and lowest (3.07 cm H2O/L/s +/- 0.37) at 0.6 Hz-750 ml. Average Ers was highest (12.1 cm H2O/L +/- 1.1) at 0.6 Hz-250 ml, and lowest (7.1 cm H2O/L +/- 0.6) at 0.2 Hz-750 ml. We conclude that frequency and tidal volume dependencies in Rrs and Ers in the normal range of breathing should be considered when interpreting measurements of respiratory system impedance or developing models to describe the mechanical behavior of the respiratory system.
Airway Resistance↗
The mechanical properties of the respiratory system during anesthesia.
1. Static compliance of the total respiratory system is decreased during anesthesia, 2. The fall in total static compliance is probably caused by a fall in lung compliance. 3. It seems unlikely that the fall in lung compliance is the primary event. The change in pleural pressures at FRC before and during anesthesia would answer this question, but the data are conflicting. 4. It is more likely that the position of the chest wall pressure-volume curve shifts to the right as a consequence of anesthesia, so that the position of equilibrium for the lung and chest wall at FRC is at a lower volume. The alteration in the chest wall is possibly because of loss of respiratory muscle tone. 5. FRC is reduced. Gas trapping occurs as a secondary event if FRC falls to below CC. 6. Lung compliance falls as a consequence of the fall in FRC, but only if FRC drops below CC, and closure occurs. No data of the correlation of change in lung compliance to the relationship of FRC to CC have been published. 7. A-aDo2 increases because of an increase in the amount of lung where ventilation is reduced compared to perfusion. Areas of zero ventilation (shunt) will also be produced. 8. The changes in lung compliance, FRC, and A-aDo2 appear to have similar characteristics. They are not influenced by depth or type of general anesthesia or the presence of neuromuscular blockade. They appear as soon as anesthesia is induced and are not progressive with time during anesthesia. They are less in the sitting position and in taller, thinner subjects. They appear to be only transiently affected by hyperinflations. 9. The fall in total respiratory system compliance may contribute to the apparent depression of the ventilatory response to carbon dioxide.
Anesthesia, General↗
Alfentanil does not increase resistance of the respiratory system in ASA I patients ventilated mechanically during general anesthesia.
PURPOSE: Several experimental and clinical studies have demonstrated a direct bronchoconstrictor effect of opioids on smooth bronchial musculature following iv administration. The aim of this study was to evaluate the effects of alfentanil on respiratory system mechanics in a group of ASA I patients ventilated mechanically during general anesthesia. CLINICAL FEATURES: Twenty consecutive ASA I patients (ten men and ten women) scheduled for general surgery interventions were studied (mean age 45.4 +/- 9.9 yr, mean weight 61.9 +/- 6.7 kg). Exclusion criteria were a history of chronic obstructive pulmonary disease, asthma or other pulmonary disease, atopy, wheezes, smoking and age below 18 yr. Subjects were randomly divided in two groups: Group A, receiving alfentanil at a 15 microg x kg(-1) dose and Group B receiving alfentanil at a 30 microg x kg(-1) dose. Respiratory mechanic variables were acquired at baseline (T0) and after three, ten and 15 min (T1, T2 and T3, respectively). We compared the basal values to the values measured at each time interval; basal values, prior to drug administration, served as control for each patient. P values < 0.05 were considered statistically significant. RESULTS: We did not observe significant differences in respiratory mechanic variables after the administration of alfentanil, 15 and 30 microg x kg(-1). More specifically, respiratory system compliance and the different subcomponents of respiratory system resistances (i.e., maximum, minimum and delta resistance of respiratory system) were within normal limits and did not vary after alfentanil administration. CONCLUSION: No respiratory adverse effect was reported after alfentanil iv administration.
Adult↗
The low-frequency dependence of respiratory system resistance and elastance in normal dogs.
The resistance (R) and elastance (E) of the respiratory system were determined by fitting the equation: pressure = R x flow + E x volume to data obtained from normal anesthetized/paralyzed dogs during mechanical ventilation at different frequencies (5 to 50 breaths per min) and tidal volumes. R exhibited a 50% decrease with increasing frequency while E showed a less marked but still distinct increase with frequency. Volume-time profiles were also recorded in the same animals during passive expiration, and the frequency dependence of resistance and elastance from 0 to 1 Hz predicted from the bi-exponential curves fitted to the profiles. The way in which resistance and elastance were predicted to vary with frequency was similar to the variations determined from regular ventilation data. There were, however, some systematic differences between the actual values of resistance and elastance obtained by the two methods which may reflect certain nonlinear characteristics of the respiratory system such as static hysteresis. Nonlinearities were also evident in that both the resistances and the elastances at all frequencies showed a slight decrease with increasing tidal volume. We conclude that a large part of the mechanical behaviour of the normal canine respiratory system at low frequencies can be accounted for in terms of a two-compartment model describing a homogeneous alveolar region surrounded by viscoelastic tissue.
Airway Resistance↗
Primary care for women. Comprehensive assessment of the respiratory system.
This article reviews the anatomy and physiology of the respiratory system and provides techniques for the physical assessment and data collection for common respiratory complaints in women. The pertinent historical, physical examination, and laboratory data for asthma, pneumonia, bronchitis, cough, and tuberculosis are also presented. This article is the first of two articles on primary care for women with respiratory complaints; the subsequent article will address primary care management of common respiratory conditions.
Female↗
Chest wall and lung contribution to the elastic properties of the respiratory system in patients with chronic obstructive pulmonary disease.
Conflicting data are available on the relative contribution of the chest wall (cw) to the intrinsic positive end-expiratory pressure of the total respiratory system (PEEPi,rs) in patients with chronic obstructive pulmonary disease (COPD). In order to assess the chest wall and lung contribution to the elastic properties of the respiratory system in COPD patients during acute ventilatory failure, using the "interrupter technique", static inflation volume-pressure (V-P) curves of the total respiratory system (rs), lung (L) and cw were obtained in seven mechanically-ventilated COPD patients during application of zero end-expiratory pressure (ZEEP) and different levels (0-15 cmH2O) of PEEP. On ZEEP, PEEPi,rs was present in all patients (range 10.5-13.1 cmH2O), to which PEEPi,cw and PEEPi,L contributed 17 +/- 2 and 83 +/- 1%, respectively. The static V-P curves of the rs, L, and cw on ZEEP were concave toward the horizontal axis, indicating that elastance increased with inflating volume. Application of PEEP did not affect lung and chest wall mechanics until PEEP levels exceeding 90% of PEEPi,cw on ZEEP (critical value of PEEP (Pcrit)). At PEEP levels higher than Pcrit, and relative to the V-P curves on ZEEP, we observed that: 1) the V-P curve of the rs showed an initial shift along the curve on ZEEP followed by a downward displacement with inflating volume; 2) the V-P curve of the L was shifted along the curve on ZEEP throughout inflating volume; and 3) the V-P curve of the cw was initially displaced along the curve on ZEEP, whilst a downward displacement appeared at higher lung volume. In conclusion, our data show that, in chronic obstructive pulmonary disease patients with flow limitation, the increase in pleural pressure does not make a significant contribution to the intrinsic positive end-expiratory pressure of the total respiratory system. However, during tidal ventilation, a substantial increase in elastance of the chest wall is present. The critical values of positive end-expiratory pressure below which there are no changes in chest wall and lung mechanics amount to 90% of the total PEEPi,rs on ZEEP. Positive end-expiratory pressure levels higher than such critical value cause important alterations of the elastic properties of the lung and chest wall.
Aged↗
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.
Adolescent↗
Respiratory system simulations and modeling.
Simulators and models of the respiratory system range from simple mechanical devices to complex systems that include sophisticated computers. These systems have considerable utility in clinician education, guiding therapies, evaluating new devices and techniques, and in improving our understanding of the cardiorespiratory system. Simulators and models are of 3 types: signs-and-symptoms simulators, anatomic models, and physiologic models. Signs-and-symptoms simulators range from human actors to computer-controlled patient mannequins. Clinical scenarios, from minor abnormalities to catastrophic emergencies, can be simulated. As has been found with aircraft cockpit simulators, improved clinician performance in simulated emergencies should translate into improved performance in real patient-care situations. Anatomic modeling can simulate basic anatomy for training clinicians. Three-dimensional reconstruction of the airways, using real patient data, can help to plan therapy, understand the disease process, and warn of safety issues. Anatomic modeling with radiographs and magnetic resonance images, sometimes created using radiolabeled tracer gases, can create 3-dimensional images of regional lung anatomy and function. Physiologic signals such as carbon dioxide production, oxygen consumption, and washout/washin of various tracer gases can be used to model ventilation-perfusion and ventilation-volume relationships, and those models can improve understanding of disease processes and guide therapies.
Computer Graphics↗
Respiratory system compliance decreases after cardiopulmonary resuscitation and stomach inflation: impact of large and small tidal volumes on calculated peak airway pressure.
The purpose of the present study was to evaluate respiratory system compliance after cardiopulmonary resuscitation (CPR) and subsequent stomach inflation. Further, we calculated peak airway pressure according to the different tidal volume recommendations of the European Resuscitation Council (7.5 ml/kg) and the American Heart Association (15 ml/kg) for ventilation of an unintubated cardiac arrest victim. After 4 min of ventricular fibrillation, and 6 min of CPR, return of spontaneous circulation (ROSC) after defibrillation occurred in seven pigs. Respiratory system compliance was measured at prearrest, after ROSC, and after 2 and 4 l of stomach inflation in the postresuscitation phase; peak airway pressure was subsequently calculated. Before cardiac arrest the mean (+/- S.D.) respiratory system compliance was 30 +/- 3 ml/cm H2O, and decreased significantly (P < 0.05) after ROSC to 24 +/- 5 ml/cm H2O, and further declined significantly to 18 +/- 4 ml/cm H2O after 2 l, and to 13 +/- 3 ml/cm H2O after 4 l of stomach inflation. At prearrest, the mean +/- S.D. calculated peak airway pressure according to European versus American guidelines was 9 +/- 1 versus 18 +/- 3 cm H2O, after ROSC 12 +/- 2 versus 23 +/- 4 cm H2O, and 15 +/- 2 versus 30 +/- 5 cm H2O after 2 l, and 22 +/- 6 versus 44 +/- 12 cm H2O after 4 l of stomach inflation. In conclusion, respiratory system compliance decreased significantly after CPR and subsequent induction of stomach inflation in an animal model with a wide open airway. This may have a significant impact on peak airway pressure and distribution of gas during ventilation of an unintubated patient with cardiac arrest.
Airway Resistance↗
Clinical implications of respiratory system changes in aging.
Nurses must consider the many age-related respiratory system changes when assessing and managing respiratory-related symptoms of older individuals. This article reviews upper and lower respiratory tract changes and provides tips for clinical management of the older person. Pertinent respiratory symptom assessment scales are described. Smoking cessation and other health promotion counseling is discussed.
Aged↗
Nonspecific cellular defense of the avian respiratory system: a review.
The normal, steady-state, avian respiratory system has very low numbers of residing avian respiratory phagocytes (ARP). Birds must rely heavily on the influx of ARP to defend against infectious agents. The system is refractory to elicitation by inert stimulants, but responds efficiently to replicating bacteria, with very rapid influx of large numbers of activated ARP (polymorphonuclear neutrophils, heterophils, and macrophages) with increased phagocytic proportions and capacities. The numbers subside within a few a days. Activated ARP act in a non agent-specific manner: Pasteurella multocida-activated ARP can defend against a severe Escherichia coli airsacculitis. Parenteral routes of stimulation generally are not, respiratory routes are very, efficient in activating ARP. Heterophils are the most efficient in defensive reactions, such as oxidative burst, production of nitric oxide and killing of bacteria. Respiratory viruses may stimulate, but also may diminish some of the defensive functions of ARP. This is also true for attenuated, modified live virus vaccines. These vaccines must be used carefully in the presence of subclinical bacterial, mycoplasmal infections. Published literature on non-specific cellular defense of the avian respiratory system is very limited, particularly about interactions among multiple infectious agents and the system.
Animals↗