Respiratory Dead Space Research Articles

Ventilatory control during exercise with increased respiratory dead space in goats

Our objectives were to determine 1) the effects of increased respiratory dead space (VD) on the ventilatory response to exercise and 2) whether changes in the ventilatory response are due to changes in chemoreceptor feedback (rest to exercise) vs. changes in the feedforward exercise stimulus. Steady-state ventilation (VI) and arterial blood gas responses to mild or moderate hyperoxic exercise in goats were compared with and without increased VD. Responses were compared using a simple mathematical model with the following assumptions: 1) steady state, 2) linear CO2 chemoreceptor feedback, 3) linear feedforward exercise stimulus proportional to CO2 production (VCO2) and characterized by an exercise gain (Gex), and 4) additive exercise stimulus and CO2 feedback producing the system gain (Gsys = delta VI/delta VCO2). Model predictions at constant Gex [assuming VD-to-tidal volume (VT) ratio independent of VCO2] are that increased VD/VT will 1) increase arterial PCO2 (PaCO2) and VI at rest and 2) increase Gsys via changes in chemoreceptor feedback due to a small increase in the PaCO2 vs. VCO2 slope. Experimental results indicate that increased VD increased VD/VT, PaCO2, and VI at rest and increased Gsys during exercise. However, measurable changes in the PaCO2 vs. VCO2 slope occurred only at high VD/VT or running speeds. Gex was estimated at each VD for each goat by using the model in conjunction with experimental measurements. With 0.2 liter VD, Gex increased 40% (P less than 0.01); with 0.6 liter VD, Gex increased 110% between 0 and 2.4 km/h and 5% grade (P less than 0.01) but not between 2.4 and 4.8 km/h. Thus, Gex is increased by VD through a limited range. In goats, increases in Gsys with increased VD result from increases in both Gex and CO2 chemoreceptor feedback. These results are consistent with other experimental treatments that increase the exercise ventilatory response, maintaining constant relative PaCO2 regulation, and suggest that a common mechanism linked to resting ventilatory drive modulates Gex.

End-tidal CO 2 pressure in the monitoring of cardiac output during canine hemorrhagic shock

The value of end-Tidal CO 2 pressure (PETCO 2) in monitoring circulatory status has been recently established in cardiac arrest. In an effort to extend its usefulness to other low-flow states, we studied the changes of PETCO 2 during progressive hemorrhage in anesthetized, mechanically ventilated dogs. PETCO 2 correlated with cardiac index (CI) in a logarithmic way ( r = .95, P < .001), not only in the whole group but in any individual experiment as well. Venoarterial and arterial-end-tidal CO 2 gradients also correlated with CI ( r = .85, P < .001 and r = .63, P < .001, respectively). These results suggest that cardiac output reductions are followed by increments in respiratory dead space, so CO 2 accumulates in venous blood and its pulmonary excretion is decreased. In this way, sequential changes in PETCO 2 during mechanical ventilation could noninvasively contribute to hemodynamic evaluation in hemorrhagic shock.

Serial distribution of bronchoconstriction in normal subjects. Methacholine versus histamine.

We compared the relative sites of airway responses to methacholine and histamine aerosols in normal subjects by simultaneous assessment of respiratory resistance (Rrs) and anatomic dead space (VD). Methacholine (12.5 mg/ml) or histamine (12.5 mg/ml) was continuously inhaled during tidal breathing until a nearly twofold increase in Rrs was observed. Large airway response was determined by VD, and overall airway response was determined by Rrs. Small airways response was inferred from Rrs when the change in VD was slight. Inhalation of methacholine and histamine increased Rrs with decreased VD, but the decrease in VD was significantly greater with methacholine than with histamine for an equivalent change in Rrs (p less than 0.01). Inhalation of atropine (5 mg/ml) decreased Rrs with a simultaneous increase in VD. After inhalation of atropine, time required for a twofold increase in Rrs by histamine inhalation was prolonged, and histamine did little decrease VD. These results suggest that the predominant site of cholinergically mediated constriction is the large airways, and that histamine constricts the large airways in part via a cholinergic reflex mechanism and constricts the small airways via its direct action in normal subjects.

Invasive and Noninvasive Measurement of the Respiratory Deadspace in Anesthetized Children with Cardiac Disease

To compare the magnitude of the different "invasive" and "noninvasive" dead space variables and the effect on them of ventilator setting, CO2 single breath tests (SBT-CO2) were obtained using an on-line computerized system based on the Servo ventilator and CO2 Analyzer 930, in 50 children anesthetized for cardiac surgery. The variables were the airway deadspace (VDaw), Bohr's deadspace (VDBohr) obtained noninvasively using end-tidal PCO2 (PETCO2) for alveolar PCO2 in the deadspace equation, and the physiologic deadspace, VDphys. In 42 children with normal single breath tests, VDaw was two-thirds of VDBohr; in 9 children in whom phase III of SBT-CO2 (the "alveolar plateau") was steeper than normal, it was only half of VDBohr. Steeper slopes of phase III were seen particularly in the present of left-right (LR) shunting. VDphys was very similar in magnitude to VDBohr in all children, except those with right-left (RL) shunts. VDaw was the major component of VDphys only in children with normal arterial-end-tidal PCO2 differences, i.e., those without RL shunts. When two ventilator frequencies giving the same alveolar ventilation were compared in children with normal gas exchange, VDBohr as a fraction of tidal volume was least at the lower frequency, as it also is in adults. The data confirm that noninvasive CO2 monitoring and measurement of deadspace gives useful indexes of the adequacy of ventilation in all children except those with RL shunts.

Effects of cromolyn in horses with chronic obstructive pulmonary disease.

The effect of disodium cromoglycate (cromolyn) in preventing the pulmonary dysfunction caused by the inhalation of barn and hay dust was studied in 5 horses with confirmed chronic obstructive pulmonary disease (COPD). The horses were studied before (Con) and after exposure to hay and dust allergens (Expos) and after pretreatment with cromolyn followed by exposure (Cr-Expos). There was a significant reduction in PaO2 from 86.8 +/- 8.3 to 73.1 +/- 8.8 when the horses were exposed to hay and dust allergens. The PaO2 after pretreatment with cromolyn and exposures was 78.1 +/- 5.5. There were no significant changes in PaCO2, FRC, pH and A-aDO2 when the Con, Expos, and Cr-Expos periods were compared. There were significant increases in VE from a control value of 77.9 +/- 18.2 to 128.7 +/- 55.1 and 133.7 +/- 17.1 L/min during the exposures, which was due primarily to increases in respiratory frequency. Respiratory dead space (VD/VT) increased from 0.55 +/- 0.10 to 0.71 +/- 0.07 and 0.65 +/- 0.05, and alveolar ventilation (VA) remained constant. Pulmonary resistance (RL) and transpulmonary pressure (Ptr) increased from a control of 0.77 +/- 0.28 cm H2O/L/sec and 7.73 +/- 3.38 cm H2O to 2.93 +/- 1.01 and 20.17 +/- 4.81 during the Expos period and tidal volume (VT) fell from 7.5 +/- 1.0 to 5.7 +/- 1.3 L. The pre-treatment with cromolyn before exposures significantly reduced the increase in RL and Ptr and returned VT to Con levels.

A method for direct measurement of systemic uptake and elimination of volatile organics in small animals

A method was developed which was suitable for toxicokinetic studies requiring direct, repetitive sampling of blood and breath during exposures of small animals to volatile chemicals. Anesthetized male Sprague-Dawley rats were tracheostomized, and a specially fabricated one-way breathing valve was inserted directly into the trachea, in order that the inhaled and exhaled breath streams could be separated and independently sampled. The desired concentration of 1,1,1-trichloroethane was generated in a gas sampling bag, which was connected to the inlet side of the valve for inhalation exposures. Rats dosed with 1,1,1-trichloroethane by gavage inhaled ambient air through the valve. A pneumotachograph was positioned in the influent air stream to measure respiration. Respiratory rate, minute volume, and core temperature were continuously recorded on a physiograph. Samples of inspired and expired air were periodically collected from sampling ports immediately adjacent to the breathing valve and were analyzed for their 1,1,1-trichloroethane content by gas chromatography. Using this system, it was possible to determine percentage systemic uptake at any given time and to monitor cumulative uptake (i.e., total dose received) over the course of inhalation exposures. Alveolar concentrations were calculated by taking into account the respiratory indexes and dead space volume. A femoral vein was cannulated, so that concentrations of the chemical in the blood and breath could be measured concurrently. Data from rats dosed orally and by inhalation with 1,1,1-trichloroethane are presented to illustrate the applicability of the method in kinetics studies of volatile chemicals.

Analysis Of Respiratory Pattern During Panting In Fowl, Gallus Domesticus

ABSTRACT When exposed to hot environments, birds depend mostly on respiratory evaporative cooling in order to maintain body temperature since cutaneous evaporation is limited for most species because they lack sweat glands. As well as serving this thermoregulatory function the respiratory system must also accommodate the obligatory requirement of adequate gaseous exchange. The hyperthermic bird must increase ventilation rates over evaporative surfaces in the respiratory system and buccopharynx for cooling purposes and yet avoid a severe blood hypocapnia and alkalosis (Calder &amp; Schmidt-Nielsen, 1968). Recently Bech, Johansen &amp; Maloiy (1979) showed that flamingoes, Phoenicopterus ruber, avoid hypocapnia during panting by restricting hyperventilation to the respiratory dead-space. This is achieved by increasing respiratory frequency, f, but reducing tidal volume, VT, to a value which closely matches the tracheal dead-space volume, VD. AS a result of the diminished VT, carbon dioxide accumulated within the respiratory system and rapid, shallow panting was periodically interrupted by bursts of 1–3 deeper breaths which served to flush out the excess carbon dioxide. A similar pattern of breathing has been observed in domestic fowl by Gleeson &amp; Brackenbury (1983). These authors showed that the carbon dioxide accumulated during rapid shallow breathing in the posterior (abdominal) air sacs as a result of the increase in the VD/VT ratio. Other authors have reported an increased f and reduced VT in the panting fowl (Kassim &amp; Sykes, 1982; Arad &amp; Marder, 1983) but the diphasic pattern of breathing during panting has not been adequately described or quantified although its presence is apparent from earlier records of breathing movements in the panting fowl (Romijn &amp; Lokhorst, 1961). Some forms of diphasic panting also occur in other species of bird, although there is considerable variation in the frequency and regularity of the alternating patterns of breathing between species (for a review see Bech et al. 1979).

Ventilation by external high-frequency oscillation in cats.

Eight anesthetized tracheostomized cats were placed in an 8.2-liter airtight chamber with the trachea connected to the exterior. Thirty-two combinations of high-frequency oscillations (HFO) (0.5-30 Hz; 25-100 ml) were delivered for 10 min each in random order into the chamber. Arterial blood gas tensions during oscillation were compared with control measurements made after 10 min of spontaneous breathing without oscillation when the mean arterial PCO2 (PaCO2) was 30.1 Torr. Ventilation due to spontaneous breathing (Vs) and oscillation (Vo) were derived from the chamber pressure trace and a pneumotachograph, respectively. As the oscillation frequency increased, oscillated tidal volume (Vo) decreased from a mean of 39 (0.5 Hz) to 3.3 ml (30 Hz) when 100 ml was delivered to the chamber. From 6-25 Hz, apnea occurred with Vo less than estimated respiratory dead space (VD); the minimum effective Vo/VD ratio was 0.37 +/- 0.05. Although Vo was maximal at 10 Hz at each oscillation volume, the lowest PaCO2 occurred at 2-6 Hz, and arterial PO2 rose as expected during hypocapnia. Above 10 Hz, PaCO2 was determined by Vo and was independent of frequency, whereas at lower frequencies, PaCO2 was related to Vo; below 6 Hz, PaCO2 varied inversely with the calculated alveolar ventilation. As oscillations became more effective, both PaCO2 and Vs fell progressively and were highly correlated; apnea occurred when PaCO2 was reduced by a mean of 4.5 Torr. Mean chamber pressure remained near zero up to 15 Hz, indicating functional residual capacity did not change. We conclude that externally applied HFO can readily maintain gas exchange in vivo, with Vo less than VD at frequencies over 2 Hz.

Physiological responses of birds to flight and running.

Summary1. The energy required for sustained physical activity in flying and running birds is obtained from fatty acids mobilized from adipose stores under the influence of hormones. There is some evidence that glucagon, insulin and growth hormone may be involved in this process.2. Energy expenditure can increase up to 14 times and 12 times resting values in flying and running birds, respectively. Energy expenditure varies only slightly over the normal range of flight speeds in individual species, but in running birds there is a linear correlation between oxygen consumption and speed. The slope of this relationship is an inverse function of body weight and indicates the energy cost of transport in ml O2.kg‐1.m‐1.3. Increased oxygen demands by the working muscles are met by increased ventilation and circulation. Increased oxygen delivery by the blood is achieved by rises in cardiac output and oxygen extraction. Cardiac stroke volume changes relatively little and the increased cardiac output results mainly from an increase in heart rate. Regional blood distribution during exercise may be determined not only by the demands of the locomotory muscles but also by the need to increase heat loss from the skin and respiratory tract.4. Ventilatory movements during flight are frequently synchronized in a I:I fashion with wing movements. Increased ventilation during flight and running may be stimulated, not only by the need for increased gas exchange, but also in order to raise heat loss by respiratory evaporation. Thermal hyperventilation carries a risk of CO, washout from the lungs and consequent blood alkalosis. The risk is minimized in some species by appropriate alterations in the rate and depth of breathing, which help to confine excess ventilation to the respiratory dead space.5. Metabolic heat produced during exercise is either lost from the respiratory linings and the skin, or stored by the body with a resultant rise in body temperature. Changes in peripheral blood perfusion and active regulation of the feathers may assist cutaneous heat loss. Respiratory evaporation usually accounts for less than 30% of the total heat loss, even at high air temperatures, and becomes progressively less efficient at higher exercise intensities. At high air temperatures and high exercise intensities, most of the metabolic heat is stored, and exercise duration is limited as the body temperature approaches the upper lethal limit.

Effects of respirators under heat/work conditions.

Physiological responses and perceived strain of five unacclimatized male subjects were studied. The subjects were exposed to heat during an exercise task and were evaluated while wearing half and full facepiece, cartridge-type, air-purifying respirators, and without a respirator. The exercise consisted of walking on a treadmill for a period of 1 hour in a controlled environmental chamber at each of two different energy expenditure levels (200 and 400 Kcal/hr) (approximately equal to 58 and 116 Watts) and two different heat exposures (air temperatures of 25 degrees C and 43.3 degrees C). The results indicated that wearing a full facepiece respirator imposed significant physiological strain added to that caused by the heat and workloads used in the study. Five of the six physiological measures show this increased physiological strain: heart rate; minute ventilation; oxygen consumption; energy expenditure; and oral temperature. There was no detectable effect on sweat rate. Although subjective ratings indicated more discomfort with increasing physiological strain, the observed correlations between such measures were low (Tb less than .60). The net consequence of the significant effects indicates that workers' tolerance to moderate or higher levels of work under hot conditions while wearing a respirator is reduced. The reduction is more pronounced when wearing a full mask than when wearing a half mask. Changes in respirator design which minimize respiratory dead space are suggested to alleviate this problem. Otherwise, prevention of excessive physiological strain from respirator use when working at moderate or higher levels at hot job sites could necessitate more rest breaks or limiting work time under such conditions.

The renal response to acute asphyxia in spontaneously breathing newborn lambs

The effects of acute asphyxia on neonatal renal function were examined in spontaneously breathing newborn lambs. 25 min of asphyxia were induced by addition of a respiratory dead space to reduce PaO 2 to 41 ± 3 mm Hg, pH to 7.03 ± 0.05 and increase PaCO 2 to 68 ± 5 mm Hg (mean ± S.E.M.). Glomerular filtration rates did not change significantly during or after asphyxia. Immediately following asphyxia significant (P < 0.05) increases over the baseline were found in urinary flow rates, fractional sodium excretion, absolute sodium excretion and osmolar clearances. These changes were in part secondary to significant (P < 0.05) increases in plasma glucose concentrations associated with increases (P < 0.05) in circulating arterial catecholamine concentrations. The percentage of tubular reabsorption of glucose decreased significantly (P < 0.05) and urinary glucose excretion increased significantly. Renal blood flow was unchanged. Therefore, asphyxia induced significant hyperglycemia which contributed to the concomitant natriuresis and osmotic diuresis in these newborn lambs.

Cardiovascular and pulmonary effects of recumbency in two conscious ponies.

Respiratory dead-space, tidal volume, respiratory rate, blood gases, cardiac output, heart rate and arterial and pulmonary arterial blood pressures were measured in two conscious, trained ponies in the standing position and in left lateral recumbency. The ponies were reluctant to remain lying down for more than about 20 mins but the reason for this did not become apparent. Tidal volume was reduced during recumbency but the respiratory rate increased, tending to maintain the minute volume at about that of the standing animal. Arterial carbon dioxide tension did not change significantly from standing values but the mean arterial oxygen tension values tended to decrease in both ponies during recumbency because of a slight increase in pulmonary venous admixture. Venous admixture in these two laterally recumbent conscious animals was considerably less than previously reported for anaesthetised subjects.

Interaction of series and parallel dead space in the lung

The volume of ventilation delivered to unperfused zones of the respiratory system (respiratory dead space) can be divided into the volume occupied by the conducting airways (series dead space) and the volume of unperfused alveolar space (parallel dead space). The effect of the interaction between these two components of dead space on steady-state gas exchange was first evaluate with a mathematical model. The response of both parallel and series dead space was predicted to underestimate the dead space measured by the inert gas elimination technique (V D IG). This error was largest when the volumes of parallel and series dead space were equal. The size of the parallel dead space in the model could be calculated from measurements of V D IG made before and after adding a series dead space of known volume. In 16 anesthetized dogs series and parallel dead space were quantitated using the multiple inert gas elimination technique with addition of known volumes of series daead space. In five normal dogs, the series and parallel dead space averaged 20% and 13% of the tidal volume, respectively. In eleven dogs with the left pulmonary artery occluded the parallel dead space averaged 26%. This method represents the first means of quantitating these two anatomically separate components of wasted ventilation.

Physiologic effects of respirator dead space and resistance loading.

Air-purifying respirators impose several loads on breathing. The effects of inspiratory flow resistance, respiratory dead space such as that of a full-face mask, and moderate exercise and maximal exercise were assessed alone and in combination in nine normal volunteers. There were significant effects on respiratory timing variables (e.g., inspiratory time, inspiratory: expiratory time ratio), peak mouth pressure and peak inspiratory flow rate. Only minimal effects on heart rate were noted. These results suggest that prospective workers who must utilize respirators should be observed during exercise as well as at rest and that a respirator dead space and inspiratory resistance should not produce a significant heart rate change but should lead to adaptation of the inspiratory: expiratory time ratio. Workers who show atypical responses should be assessed particularly carefully.

Dynamic Calibration of Apparatus to Measure Respiratory Dead Space

Dynamic Calibration of Apparatus to Measure Respiratory Dead Space

1350 EFFECTS OF RATE OF VOLUME EXPANSION ON BRAIN BLOOD FLOW AFTER ASPHYXIA AND HYPOTENSION IN THE PIGLET

The rate at which the systemic arterial blood pressure (SABP) is restored after asphyxial and hypotensive insults may be a factor in the pathogenesis of perinatal central nervous system lesions. To examine this, brain blood flow (BBF) was determined in 16 newborn piglets during asphyxia, superimposed hypotension and subsequent volume expansion (15 ml/kg, plasmanate). Asphyxia (A) was produced by a respiratory dead space and hypotension (H) by phelbotomy. Group 1 received plasmanate in 3 min., Group 2 in 30 min. and Group 3 received none. BBF (microsphere technique) was measured with each insult and at 5 and 30 min. after the start of the volume expansion and removal of the dead space. Results were (M±SEM):*p<.02 as compared to control, +p<.05 as compared to Group 3. SABP was reduced (p<.05) in Group 3 at 5 min. after A and H. All groups had significant reductions in hematocrit from control at the completion of the study. At autopsy, intracranial hemorrhage was not observed. The data indicate that 1) the rate of volume expansion did not influence the magnitude of BBF and 2) the higher BBF at the completion of volume expansion probably reflects compensation for anemia to achieve adequate oxygen delivery.

A computer program for calculating respiratory anatomic dead space

The Fowler technique for estimating anatomic dead space ( V D - the volume of the airway conducting system) on the basis of CO 2 changes in the expired air of a single breath was adapted to computer analysis. The areas above and below the sigmoid CO 2 curve in the region of transition from inspired to alveolar concentration were simultaneously integrated (forward and backward) on a time base until the sum of the two integrated values equalled the total area representing the transition. This point on the CO 2 curve was defined as the CO 2 midpoint. Expiratory flow was then integrated with time from its beginning to the CO 2 midpoint, and the resultant volume represented V D for that breath. The computer program was able to compensate for differences in response time between the gas monitor and the flow measuring device and was able to integrate the areas rapidly. The program provided a rapid calculation of V D , which compared well with values calculated by tedious, manual methods.

Air Sac Gases and Ventilation During Panting in Fowl, Gallus Gallus

BY J. H. BRACKENBURY, P. AVERY AND M. GLEESONDepartment of Biology, University of Salford, Salford M$ \WT(Received 7 July 1980)Exposure to elevated environmental temperatures i producen s large increasesventilation and respiratory evaporatio in birdn s (Calde rBouverot, Hildwein LeGoff & 1974, ; Richards, 1976). Some workers have reportedsevere blood alkalosi in pantins g bird dues t luno g hyperventilatio n Calder & Schmidt-Nielsen, 1968; Frankel & Frascella, 1968), othersonly a small decreas ien arterial Pcc> (Marder2 , Arad & Gafni, 1974; Marde & Aradr ,1975; Krausz, Bernstei & Mardern, 1977) It ha. oftes n been suggested, followingZeuthen (1942), that intrapulmonary valves may shunt air away from the parabronchiduring panting thus alleviatin the risgk of hypocapnic alkalosi bust such valves havenot yet been demonstrated in vivo.Recently Bech, Johansen & Maloiy (1979) showed that flamingoes Phoenicopterus,ruber, avoid hypocapnia during b pantiny restricting g hyperventilatio to then res-piratory dead space. Thi is achieves d by a 7-fold reductio of tidan l volume V,

An anaesthetic circuit to improve patient monitoring by gas analysis.

This circuit is designed to maximise the range of respiratory variables that can be monitored by a mass spectrometer either alone, or preferably in association with blood gas analysis. In particular, it permits monitoring of respiratory dead space, lung shunt, ventilation, and gas exchange, as well as inspired and end-expired gas concentrations. Laboratory and clinical data indicate satisfactory performance of the circuit both clinically and analytically. The circuit is most suitable for controlled ventilation where, by operating as a "minute volume divider", it confers stability of minute volume on the manual ventilation technique.

Cardiorespiratory simulation for the evaluation of recovery following coronary artery bypass surgery

The interpretation of a patient's status and recovery after coronary artery bypass surgery are difficult because of the complex interaction of many factors and because only relatively limited, non-specific measurements can be made. The objective of this study was to develop a simulation model of basic cardiorespiratory functions which would be useful as a clinical tool to obtain a refined characterization of a patient's cardiopulmonary interactions based on clinical measurements. The simulation was used to generate the same types of measurements obtained on patients. The basic approach was to adjust the simulation parameters so that the simulated measurements agreed with the patient's data. Thirty-five patients who had multiple coronary bypass surgery were simulated. The measurements agreed within clinical significance for a wide range of physiologic states. The resulting values of the simulation parameters provide functional indices of ventilation/perfusion disparity, diffusion gradients, venous-arterial pulmonary shunt, and respiratory dead space. The simulation model also offered a technique for estimating the efficacy of cardiorespiratory support maneuvers in changing blood gas and pH values in the critically ill post-coronary-bypass patient with an acute respiratory distress syndrome.