Peak Tracheal Pressure Research Articles

A new perspective during laryngo-tracheal surgery: the use of an ultra-thin endotracheal tube (Tritube®) and flow-controlled ventilation—a retrospective case series and a review of the literature

BackgroundUpper airway surgery often poses a challenge to both anesthesiologists and surgeons, as airway access, mechanical ventilation, and surgical difficulties may occur in a tricky combination. To fulfill the need for a tubeless surgery, techniques such as apneic oxygenation or jet ventilation may be used, which carry the risk of several complications. The ultrathin cuffed endotracheal tube Tritube can be used with flow-controlled ventilation (FCV) to provide adequate surgical field and ventilation. To assess the feasibility, safety, and effectiveness of this technique, we describe a series of 21 patients, with various lung conditions, undergoing laryngo-tracheal surgery with FCV delivered via Tritube. Moreover, we perform a narrative systematic review to summarize clinical data on the use of Tritube during upper airway surgery.ResultsAll patients were successfully intubated in one attempt with Tritube. The median (interquartile range [IQR]) tidal volume was 6.7 (6.2–7.1) mL/kg of ideal body weight, the median end-expiratory pressure was 5.3 (5.0–6.4) cmH2O, and the median peak tracheal pressure was 16 (15–18) cmH2O. The median minute volume was 5.3 (5.0–6.4) L/min. Median global alveolar driving pressure was 8 (7–9) cmH2O. The median maximum level of end-tidal CO2 was 39 (35–41) mmHg. During procedures involving laser, the maximum fraction of inspired oxygen was 0.3, with the median lowest peripheral oxygen saturation of 96% (94–96%). No complications associated with intubation or extubation occurred. In one patient, the ventilator needed to be rebooted for a software issue. In two (10%) patients, Tritube needed to be flushed with saline to remove secretions. In all patients, optimal visualization and accessibility of the surgical site were obtained, according to the surgeon in charge. Thirteen studies (seven case reports, two case series, three prospective observational studies, and one randomized controlled trial) were included in the narrative systematic review and described.ConclusionsTritube in combination with FCV provided adequate surgical exposure and ventilation in patients undergoing laryngo-tracheal surgery. While training and experience with this new method is needed, FCV delivered with Tritube may represent an ideal approach that benefits surgeons, anesthesiologists, and patients with difficult airways and compromised lung mechanics.

Physiological effects of high-flow oxygen in tracheostomized patients

BackgroundHigh-flow oxygen therapy via nasal cannula (HFOTNASAL) increases airway pressure, ameliorates oxygenation and reduces work of breathing. High-flow oxygen can be delivered through tracheostomy (HFOTTRACHEAL), but its physiological effects have not been systematically described. We conducted a cross-over study to elucidate the effects of increasing flow rates of HFOTTRACHEAL on gas exchange, respiratory rate and endotracheal pressure and to compare lower airway pressure produced by HFOTNASAL and HFOTTRACHEAL.MethodsTwenty-six tracheostomized patients underwent standard oxygen therapy through a conventional heat and moisture exchanger, and then HFOTTRACHEAL through a heated humidifier, with gas flow set at 10, 30 and 50 L/min. Each step lasted 30 min; gas flow sequence during HFOTTRACHEAL was randomized. In five patients, measurements were repeated during HFOTTRACHEAL before tracheostomy decannulation and immediately after during HFOTNASAL. In each step, arterial blood gases, respiratory rate, and tracheal pressure were measured.ResultsDuring HFOTTRACHEAL, PaO2/FiO2 ratio and tracheal expiratory pressure slightly increased proportionally to gas flow. The mean [95% confidence interval] expiratory pressure raise induced by 10-L/min increase in flow was 0.2 [0.1–0.2] cmH2O (ρ = 0.77, p < 0.001). Compared to standard oxygen, HFOTTRACHEAL limited the negative inspiratory swing in tracheal pressure; at 50 L/min, but not with other settings, HFOTTRACHEAL increased mean tracheal expiratory pressure by (mean difference [95% CI]) 0.4 [0.3–0.6] cmH2O, peak tracheal expiratory pressure by 0.4 [0.2–0.6] cmH2O, improved PaO2/FiO2 ratio by 40 [8–71] mmHg, and reduced respiratory rate by 1.9 [0.3–3.6] breaths/min without PaCO2 changes. As compared to HFOTTRACHEAL, HFOTNASAL produced higher tracheal mean and peak expiratory pressure (at 50 L/min, mean difference [95% CI]: 3 [1–5] cmH2O and 4 [1–7] cmH2O, respectively).ConclusionsAs compared to standard oxygen, 50 L/min of HFOTTRACHEAL are needed to improve oxygenation, reduce respiratory rate and provide small degree of positive airway expiratory pressure, which, however, is significantly lower than the one produced by HFOTNASAL.

Effects of Condensate in the Exhalation Limb of Neonatal Circuits on Airway Pressure During Bubble CPAP

Bubble CPAP is frequently used in spontaneously breathing infants with lung disease. Often bubble CPAP systems lack pressure alarms and pressure-release valves. We observed a large volume of condensate in the exhalation limb of a patient circuit and conducted a series of experiments to test the hypothesis that accumulated condensate could affect delivered pressures. An anatomically accurate nasal airway model of a preterm infant was attached to a spontaneously breathing lung model. A bubble CPAP system was attached to the nasal airway with bi-nasal short prongs, and the rate of fluid condensation was measured. Next, tracheal pressures were monitored digitally to detect changes in airway pressure related to condensate accumulation. Measurements were obtained with volumes of 0, 5, 10, 15, and 20 mL of water in the exhalation limb, at flows of 4, 6, 8, and 10 L/min. Measurements with 20 mL in the exhalation limb were recorded with and without a pressure-relief valve in the circuit. The rate of condensate accumulation was 3.8 mL/h. At volumes of ≥ 10 mL, noticeable alterations in the airway pressure waveforms and significant increases in mean tracheal pressure were observed. The pressure-relief valve effectively attenuated peak tracheal pressure, but only decreased mean pressure by 0.5-1.5 cm H2O. Condensate in the exhalation limb of the patient circuit during bubble CPAP can significantly increase pressure delivered to the patient. The back and forth movement of this fluid causes oscillations in airway pressure that are much greater than the oscillations created by gas bubbling out the exhalation tube into the water bath. We recommend continuously monitoring pressure at the nasal airway interface, placing an adjustable pressure-relief valve in the circuit, set to 5 cm H2O above the desired mean pressure, and emptying fluid from the exhalation limb every 2-3 hours.

Depression of cough reflex by microinjections of antitussive agents into caudal ventral respiratory group of the rabbit

We have previously shown that the caudal nucleus tractus solitarii is a site of action of some antitussive drugs and that the caudal ventral respiratory group (cVRG) region has a crucial role in determining both the expiratory and inspiratory components of the cough motor pattern. These findings led us to suggest that the cVRG region, and possibly other neural substrates involved in cough regulation, may be sites of action of antitussive drugs. To address this issue, we investigated changes in baseline respiratory activity and cough responses to tracheobronchial mechanical stimulation following microinjections (30-50 nl) of some antitussive drugs into the cVRG of pentobarbital-anesthetized, spontaneously breathing rabbits. [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) and baclofen at the lower concentrations (0.5 mM and 0.1 mM, respectively) decreased cough number, peak abdominal activity, and peak tracheal pressure and increased cough-related total cycle duration (Tt). At the higher concentrations (5 mM and 1 mM, respectively), both drugs abolished the cough reflex. DAMGO and baclofen also affected baseline respiratory activity. Both drugs reduced peak abdominal activity, while only DAMGO increased Tt, owing to increases in expiratory time. The neurokinin-1 (NK(1)) receptor antagonist CP-99,994 (10 mM) decreased cough number, peak abdominal activity, and peak tracheal pressure, without affecting baseline respiration. The NK(2) receptor antagonist MEN 10376 (5 mM) had no effect. The results indicate that the cVRG is a site of action of some antitussive agents and support the hypothesis that several neural substrates involved in cough regulation may share this characteristic.

Tracheal pressure and endotracheal tube obstruction can be detected by continuous cuff pressure monitoring: in vitro pilot study

To evaluate whether the degree of endotracheal tube (ETT) obstruction can be predicted by changes of ETT cuff pressure (P (c)) as a function of peak inspiratory pressure. The study was conducted in three phases: phase I evaluated the correlation between peak tracheal pressure (P (tr)) and P (c); phase II evaluated the relation between P (c) versus ventilator pressure (P (v)) and ETT obstruction (range of obstruction 0-58%). In phase III the analytical model developed in phase II was used to predict the degree of obstruction of five ETTs removed from intensive care unit (ICU) patients. All measurements were conducted on a tracheal-lung simulator. In phases I and II it was found that P (c) correlates significantly with P (tr). The gradient (dP (c)/dP (v)) reflects the degree of ETT obstruction according to the formula: obstruction (%) = -553 x (dP (c)/dP (v))(2) + 672.5 x (dP (c)/dP (v)) - 142.81. Using this formula, the degree of obstruction of the ETTs could be predicted in ICU patients during controlled mechanical ventilation (r (2) = 0.98, p < 0.001). This study proposes a new method to predict the degree of ETT obstruction based on differences between P (c) and P (v). The method was proved accurate on simulator, and further studies are needed on intubated patients.

Cough reflex responses during pulmonary C-fibre receptor activation in anesthetized rabbits

We investigated the changes induced by pulmonary C-fibre receptor activation in the cough reflex evoked by mechanical stimulation of the tracheobronchial tree in pentobarbitone anesthetized, spontaneously breathing rabbits. Phrenic nerve and abdominal muscle activities were monitored along with tracheal and arterial blood pressures. The activation of pulmonary C-fibre receptors by means of right atrial injection of phenylbiguanide (PBG) caused the pulmonary chemoreflex characterized by tachypnea, bradycardia and hypotension. During the pulmonary chemoreflex, the time components (total cycle duration, inspiratory and expiratory times) of the cough motor pattern significantly decreased, whereas no consistent changes in peak phrenic and abdominal activity, peak tracheal pressure and number of coughs evoked by each stimulation trial were observed. At variance with previous findings in cats and dogs, the results show that tracheobronchial cough is not significantly reduced in the rabbit during PBG-induced chemoreflex. This study is the first to provide evidence supporting the hypothesis that the time components of the cough motor pattern are, to some extent, dependent upon the timing characteristics of the ongoing respiratory activity and suggests a novel mechanism leading to cough depression.

Bilateral vagotomy differentially alters the magnitude of hypoglossal and phrenic long-term facilitation in anesthetized mechanically ventilated rats

Acute intermittent hypoxia elicits long-term increases in respiratory motor output (long-term facilitation, LTF). Most investigators study LTF in mechanically ventilated, bilaterally vagotomized, and anesthetized animals. Vagotomy blocks inhibitory lung-volume feedback that could diminish the magnitude of LTF. However, the effects of vagotomy on LTF may not be so straight forward. In cats, vagotomy increases LTF of upper airway muscles but may decrease LTF of accessory pump muscles. The effects of vagotomy on LTF in rats are unknown. We hypothesized that the magnitude of hypoglossal and phrenic LTF would be differentially regulated by vagal afferent feedback in anesthetized and mechanically ventilated rats. Hypoglossal and phrenic motor outputs were recorded from vagotomized and vagally intact anesthetized mechanically ventilated adult Sprague-Dawley rats before, during, and up to 60-min after intermittent hypoxia. Ventilator frequency (f), pump volume, and peak tracheal pressure were not different between groups. The effects of vagotomy on the magnitude of LTF depended on the motoneuron population in question. The magnitude of hypoglossal LTF increased after vagotomy (vagi intact, -5+/-10%; vagotomy, 66+/-11% above baseline; p<0.05); whereas, the magnitude of phrenic LTF decreased after vagotomy (vagi intact, 135+/-24%; vagotomy, 40+/-13% above baseline; p<0.05). These data support previous work in anesthetized cats, and suggest that the expression of hypoglossal and phrenic respiratory motor plasticity is differentially regulated by vagal afferent feedback.

Modulation of the cough reflex by antitussive agents within the caudal aspect of the nucleus tractus solitarii in the rabbit

We have previously shown that ionotropic glutamate receptors in the caudal portion of the nucleus tractus solitarii (NTS), especially in the commissural NTS, play a prominent role in the mediation of tracheobronchial cough and that substance P potentiates this reflex. This NTS region could be a site of action of some centrally acting antitussive agents and a component of a drug-sensitive gating mechanism of cough. To address these issues, we investigated changes in baseline respiratory activity and cough responses to tracheobronchial mechanical stimulation following microinjections (30-50 nl) of centrally acting antitussive drugs into the caudal NTS of pentobarbitone-anesthetized, spontaneously breathing rabbits. [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO) and baclofen decreased baseline respiratory frequency because of increases in the inspiratory time only at the higher concentration employed (5 mM and 1 mM, respectively). DAMGO (0.5 mM) and baclofen (0.1 mM) significantly decreased cough number, peak abdominal activity, peak tracheal pressure, and increased cough-related total cycle duration. At the higher concentrations, these agents suppressed the cough reflex. The effects of these two drugs were counteracted by specific antagonists (10 mM naloxone and 25 mM CGP-35348, respectively). The neurokinin-1 (NK1) receptor antagonist CP-99,994 (10 mM) abolished cough responses, whereas the NK2 receptor antagonist MEN 10376 (5 mM) had no effect. The results indicate that the caudal NTS is a site of action of some centrally acting drugs and a likely component of a neural system involved in cough regulation. A crucial role of substance P release in the mediation of reflex cough is also suggested.

Cardiorespiratory failure in rat induced by severe inspiratory resistive loading

The mechanisms underlying acute respiratory failure induced by respiratory loads are unclear. We hypothesized that, in contrast to a moderate inspiratory resistive load, a severe one would elicit central respiratory failure (decreased respiratory drive) before diaphragmatic injury and fatigue. We also wished to elucidate the factors that predict endurance time and peak tracheal pressure generation. Anesthetized rats breathed air against a severe load ( approximately 75% of the peak tracheal pressure generated during a 30-s occlusion) until pump failure (fall in tracheal pressure to half; mean 38 min). Hypercapnia and hypoxemia developed rapidly ( approximately 4 min), coincident with diaphragmatic fatigue (decreased ratio of transdiaphragmatic pressure to peak integrated phrenic activity) and the detection in blood of the fast isoform of skeletal troponin I (muscle injury). At approximately 23 min, respiratory frequency and then blood pressure fell, followed immediately by secondary diaphragmatic fatigue. Blood taken after termination of loading contained cardiac troponin T (myocardial injury). Contrary to our hypothesis, diaphragmatic fatigue and injury occurred early in loading before central failure, evident only as a change in the timing but not the drive component of the central respiratory pattern generator. Stepwise multiple regression analysis selected changes in mean arterial pressure and arterial Pco(2) during loading as the principal contributing factors in load endurance time, and changes in mean arterial pressure as the principal contributing factor in peak tracheal pressure generation. In conclusion, the temporal development of respiratory failure is not stereotyped but depends on load magnitude; moreover respiratory loads induce cardiorespiratory, not just respiratory, failure.

Effect of bronchial artery blood flow on cardiopulmonary bypass-induced lung injury.

Cardiovascular surgery requiring cardiopulmonary bypass (CPB) is frequently complicated by postoperative lung injury. Bronchial artery (BA) blood flow has been hypothesized to attenuate this injury. The purpose of the present study was to determine the effect of BA blood flow on CPB-induced lung injury in anesthetized pigs. In eight pigs (BA ligated) the BA was ligated, whereas in six pigs (BA patent) the BA was identified but left intact. Warm (37 degrees C) CPB was then performed in all pigs with complete occlusion of the pulmonary artery and deflated lungs to maximize lung injury. BA ligation significantly exacerbated nearly all aspects of pulmonary function beginning at 5 min post-CPB. At 25 min, BA-ligated pigs had a lower arterial Po(2) at a fraction of inspired oxygen of 1.0 (52 +/- 5 vs. 312 +/- 58 mmHg) and greater peak tracheal pressure (39 +/- 6 vs. 15 +/- 4 mmHg), pulmonary vascular resistance (11 +/- 1 vs. 6 +/- 1 mmHg x l(-1) x min), plasma TNF-alpha (1.2 +/- 0.60 vs. 0.59 +/- 0.092 ng/ml), extravascular lung water (11.7 +/- 1.2 vs. 7.7 +/- 0.5 ml/g blood-free dry weight), and pulmonary vascular protein permeability, as assessed by a decreased reflection coefficient for albumin (sigma(alb); 0.53 +/- 0.1 vs. 0.82 +/- 0.05). There was a negative correlation (R = 0.95, P < 0.001) between sigma(alb) and the 25-min plasma TNF-alpha concentration. These results suggest that a severe decrease in BA blood flow during and after warm CPB causes increased pulmonary vascular permeability, edema formation, cytokine production, and severe arterial hypoxemia secondary to intrapulmonary shunt.

Preload changes by positive pressure ventilation can be used for assessment of left ventricular systolic function.

Assessment of preload independent left ventricular function with conductance volumetry is traditionally accomplished by inflating a balloon in the inferior caval vein. Our aim was to investigate if a similar change in preload could be achieved by positive pressure ventilation with large tidal volume. Conductance volumetry generating left ventricular pressure-volume loops was used in seven pentobarbital-anesthetized pigs. Changes in preload recruitable stroke work were studied, comparing the effects of inferior vena cava occlusion (IVCO) or large tidal volume (LTV). Cardiodepression was induced by halothane anesthesia and halothane + phenylephrine, and stimulation by epinephrine infusion. Although the decreasis in left ventricular end diastolic volume was slightly less with LTV (16.5 +/- 1.7 ml, mean +/- SEM) than with IVCO (22.4 +/- 1.7 ml) (P < 0.0001) the PRSW-slopes showed a high degree of correlation (r=0.80, P < 0.0001). Although peak tracheal pressures increased significantly to 27.8 +/- 0.9 mmHg during LTV, esophageal pressures (used as an indicator of pericardial pressure) were unchanged. Positive pressure ventilation with LTV is similar to IVCO in creating transient changes in preload, necessary for assessment of left ventricular systolic function. This observation was valid also during drug-induced cardiac depression and stimulation. The preload recruitable stroke work used for this validation was shown to be a reliable and stable method.

Binding the Abdomen Can Improve Speech in Men With Phrenic Nerve Pacers

Two men with high cervical spinal cord injuries and phrenic nerve pacers were studied with and without an elastic binder around the abdomen. Speech improved with the binder, as determined by listener preference ratings provided by 10 judges and by the subjects themselves. Improvement was substantial in one subject and slight in the other. The subject with the greater improvement exhibited higher peak tracheal pressure, higher sound pressure level, and longer utterance duration with the binder in place. Speech improvement was attributed primarily to augmentation of tidal volume associated with the use of the binder. An abdominal binder can be an effective intervention to improve speech in certain individuals with spinal cord injuries and phrenic nerve pacers. Speech may be further improved by using behavioral strategies, such as neck muscle activation, glossopharyngeal breathing, and pharyngeal or buccal speech production.

Effect of topical anesthesia of the laryngeal mucosa on upper airway mechanics in exercising horses.

To determine the effect of desensitization of the laryngeal mucosal mechanoreceptors on upper airway mechanics in exercising horses. 6 Standardbreds. In study 1, videoendoscopic examinations were performed while horses ran on a treadmill with and without topical anesthesia of the laryngeal mucosa. In study 2, peak tracheal and nasopharyngeal pressures and airflows were obtained from horses during incremental treadmill exercise tests, with and without topical anesthesia of the laryngeal mucosa. A nasal occlusion test was performed on each horse while standing during an endoscopic examination for both trials. In study 1, horses had nasopharyngeal collapse while running on the treadmill when the laryngeal mucosa was anesthetized. In study 2, inspiratory upper airway and nasopharyngeal impedance were significantly higher, and peak tracheal inspiratory pressure, respiratory frequency, and minute ventilation were significantly lower in horses when the laryngeal mucosa was anesthetized, compared with values obtained when horses exercised without topical anesthesia. Peak inspiratory and expiratory airflows were lower in horses when the laryngeal mucosa was anesthetized, although differences did not quite reach significance (P = 0.06 and 0.09, respectively). During a nasal occlusion test, horses had episodes of nasopharyngeal collapse and dorsal displacement of the soft palate when the laryngeal mucosa was anesthetized. Upper airway function was normal in these horses without laryngeal mucosal anesthesia. Receptors within the laryngeal mucosa may be important in maintaining upper airway patency in exercising horses.

Diaphragm muscle fiber injury after inspiratory resistive breathing.

Five awake previously tracheotomized mongrel dogs were challenged with inspiratory resistive breathing (IRB). The mean peak tracheal pressure = -35.4 +/- 1.1 cmH2O, ETCO2 = 39.8 +/- 1.5 mmHg was sustained for 2 h/d over 4 consecutive d. On the fourth day, following IRB, the dogs were placed under general anaesthesia, and the diaphragm was perfused via the internal mammary artery with a low molecular weight fluorescent tracer (Procion orange, FW = 631), to which normal muscle fibers are impermeable. Muscle fiber membrane damage was identified on tissue sections by using fluorescent microscopy showing the presence of the tracer in the cytoplasm. Four dogs undergoing the same protocol (except IRB) served as control. The dye was seen in 7.6 +/- 2.6% and in 0.3 +/- 0.1% of fibers in the IRB and control groups, respectively (p < 0.05). Via ATPase staining, it was found that fibers of type I were predominantly affected as compared to type II (p < 0.05). In addition, an increased area fraction of fibers demonstrating sarcomere disruption was found after IRB (2.4 +/- 0.5%) compared to pre-IRB (0.4 +/- 0.1%; p < 0.05). We conclude that resistive breathing of a magnitude similar to that seen in some respiratory diseases, or used in respiratory muscle training programs induces muscle membrane and sarcomere injury.

Simple Adjustments Can Improve Ventilator-Supported Speech

Six subjects who were tracheostomized and chronically ventilator-supported because of neuromuscular disease or injury were studied to determine if their speech could be improved. Using subjects' own portable ventilators, adjustments were made that reduced inspiratory flow and added positive end-expiratory pressure (PEEP). These adjustments resulted in increases in speaking time per ventilator cycle, increases in number of syllables produced per cycle, and decreases in peak tracheal pressure. Improvements in speech were perceptible to listeners in 3 of the 6 subjects. Listeners preferred speech produced under the ventilator-adjusted condition primarily because the quantity of speech produced per ventilator cycle increased, loudness fluctuation decreased, and voice quality improved. The only subject who showed no perceptible benefit from the adjustments had a substantial air leak around her tracheostomy tube. Importantly, gas exchange was not compromised in any of the subjects. We believe that adjustments such as prolonging inspiration and adding PEEP, when implemented in collaboration with appropriate health-care professionals, represent a simple, inexpensive, and safe intervention for improving speech in certain ventilator-supported individuals.

Sidestream smoke exposure enhances rapidly adapting receptor responses to substance P in young guinea pigs.

We determined the effect of sidestream tobacco smoke (SS) exposure on responses of lung rapidly adapting receptors (RARs), peak tracheal pressure (Ptr), and arterial blood pressure (ABP) to substance P in young guinea pigs. Guinea pigs were exposed to SS or filtered air from day 8 to days 41-45 of life. They were then anesthetized and given three doses of intravenous substance P (1.56-4.94 nmol/kg). SS exposure augmented substance P-evoked increases in RAR activity (P = 0.029 by analysis of variance) but not substance P-evoked increases in peak Ptr or decreases in ABP. Neurokinin 1-receptor blockade (CP-96345, 400 nmol/kg) attenuated substance P-evoked increases in RAR activity (P = 0.001) and ABP (P = 0.009) but not in peak Ptr (P = 0.06). This chronic exposure to SS in young guinea pigs exaggerates RAR responsiveness to substance P. The findings may help explain the increased incidence of airway hyperresponsiveness and cough in children chronically exposed to environmental tobacco smoke.

Effect of nasal occlusion on tracheal and pharyngeal pressures in horses

Abstract Objective To compare tracheal and pharyngeal inspiratory and expiratory pressures achieved during 60 seconds of nasal occlusion in standing horses with pressures achieved in horses during intense exercise. Animals 5 Standardbreds. Procedure Tracheal and pharyngeal inspiratory and expiratory pressures were obtained from 5 horses during 60 seconds of nasal occlusion and compared with tracheal and pharyngeal pressures achieved during incremental treadmill exercise tests in which horses ran at 50, 75, and 100% of the speed that resulted in maximal heart rate ( HRmax) Results Significant difference was not detected between peak tracheal inspiratory pressure during nasal occlusion and peak tracheal inspiratory pressure at HRmax. Peak pharyngeal inspiratory pressure was sig nificantly more negative, and peak tracheal and peak pharyngeal expiratory pressures were sig nificantly more positive during 60 seconds of nasal occlusion than those observed in horses running at HRmax. Conclusion During upper airway endoscopy in standing horses, 60-second nasal occlusion induced tracheal and pharyngeal inspiratory pressures that equaled or exceeded pressures achieved during high-intensity exercise. Clinical Relevance Nasal occlusion is useful to simulate upper airway pressures achieved during high-intensity exercise. (Am J Vet Res 1996;57:1258–1260)

Mechanism of atrial natriuretic peptide release with increased inspiratory resistance

Elevated plasma atrial natriuretic peptide (ANP) levels and concomitant increases in renal sodium and water excretion are often encountered in respiratory diseases associated with increased airway resistance such as obstructive sleep apnea. The present study utilized an anesthetized rat model to determine the principal mechanism(s) responsible for stimulation of ANP release in this clinical syndrome. A 10-minute increase in external resistive loading, which reduced peak tracheal pressure to −15 to −17 mm Hg produced a significant increase in both central venous pressure and right atrial transmural pressure. This maneuver subsequently resulted in significant transient increases in glomerular filtration rate; urine flow; urinary Na +, K +, and Cl − excretion; and urinary cyclic guanosine monophosphate (cGMP) excretion, which was taken as an index of increased circulating levels of ANP. Similar changes in renal function and cGMP excretion occurred when arterial PO 2 was lowered to a degree equivalent to that seen with increased resistive loading. Lowering arterial PO 2 also significantly increased mean central venous pressure and right atrial transmural pressure. Conversely, the resistive loading-induced changes in renal function and cGMP excretion did not occur when the reduction in arterial PO 2 was prevented by breathing a high PO 2 gas mixture during the resistive loading. Additionally, O 2 supplementation prevented the increases in both mean central venous pressure and right atrial transmural pressure caused by increased resistive loading. These data indicate that the elevated ANP release that results from an acute increase in external resistive loading is not caused by a decrease in intrathoracic pressure but rather suggest that the elevated ANP release is primarily caused by an increased right atrial transmural pressure resulting from hypoxia-induced pulmonary vasoconstriction.

Substance P contributes to rapidly adapting receptor responses to pulmonary venous congestion in rabbits.

1. This study tested the hypothesis that substance P stimulates rapidly adapting receptors (RARs), contributes to the increase in RAR activity produced by mild pulmonary congestion, and evokes an augmented response from RARs when combined with near-threshold levels of pulmonary congestion. 2. RAR activity, peak tracheal pressure, arterial blood pressure and left atrial pressure were measured in paralysed, anaesthetized and ventilated rabbits. Substance P was given i.v. in one-half log incremental doses to a maximum of 3 micrograms kg-1. Mild pulmonary congestion was produced by inflating a balloon in the left atrium to increase left atrial pressure by 5 mmHg. Near-threshold levels of pulmonary congestion were produced by increasing left atrial pressure by 2 mmHg. 3. Substance P produced dose-dependent increases in RAR activity. The highest dose given increased the activity from 1.3 +/- 0.5 to 11.0 +/- 3.1 impulses bin-1. Increases in left atrial pressure of 5 mmHg increased RAR activity from 3.8 +/- 1.4 to 14.7 +/- 3.9 impulses bin-1. Blockade of NK1 receptors with CP 96345 significantly attenuated RAR responses to substance P and to mild pulmonary congestion. 4. Doses of substance P, which alone had no effect, stimulated the RARs when delivered during near-threshold levels of pulmonary congestion. 5. The findings suggest that substance P augments the stimulatory effect of mild pulmonary congestion on RAR activity, most probably by enhancing hydraulically induced microvascular leak.

Effect of a mask and pneumotachograph on tracheal and nasopharyngeal pressures, respiratory frequency, and ventilation in horses

Abstract Objective To investigate the effect of a mask and pneumotachograph on ventilation, respiratory frequency, and tracheal and nasopharyngeal pressures in horses running on a treadmill. Design Six horses ran at 50, 75, and 100% of the speed that resulted in maximum oxygen consumption, with and without a mask and pneumotachograph. Tracheal and pharyngeal inspiratory and expiratory pressures, respiratory frequency, and arterial blood gases were measured. Animals Six Standardbred horses. Procedure Oxygen consumption was measured during an incremental exercise test to determine the speed that resulted in maximal oxygen consumption for each horse. Tracheal and pharyngeal pressures were measured, using transnasal tracheal and pharyngeal side-hole catheters connected to differential pressure transducers. Carotid arterial blood samples were collected and PaO2, PaCO2, and pH were measured with a blood gas analyzer. Results Peak tracheal and pharyngeal inspiratory pressures were significantly more negative, peak tracheal and pharyngeal expiratory pressures were significantly more positive and respiratory frequency was significantly lower (all P &lt; 0.05) at all speeds when horses wore a mask The PaCO2, was higher and arterial pH and PaO2, were lower (P &lt; 0.05) when horses wore a mask. Conclusions The mask and pneumotachograph altered upper airway pressures, respiratory frequency, and ventilation in horses running on a treadmill.(Am J Vet Res 1996; 57: 250-253)