scholarly journals Assessment of continuous ventilation during tracheal dilatation using a novel, non-occlusive balloon in an ovine model

Author(s):  
R Hofmeyr ◽  
J McGuire ◽  
P Marwick ◽  
K Park ◽  
M Proxenos ◽  
...  

Introduction: Balloon dilatation is frequently used in the management of tracheal stenosis. Traditional dilatation balloons cause complete occlusion of the tracheal lumen when deployed, limiting duration of dilatation due to development of hypoxia and increasing the risk of barotrauma. We assessed a novel, non occlusive airway dilatation balloon to determine whether it would allow continuous oxygenation and ventilation. Methods: This was a prospective, descriptive, interventional trial undertaken in the animal research laboratory using a healthy ovine model. Eight anaesthetised adult Dohne Merino sheep underwent placement and inflation of the study device in the trachea via an endotracheal tube with multiport adaptor. Airway pressures, ventilatory parameters, end-tidal capnography and peripheral oxygen saturations were monitored continuously and measured before insertion, before inflation and during balloon inflation. Results: All subjects could be ventilated continuously. At no time during balloon deployment and inflation was there a loss of capnograph waveform or peripheral arterial desaturation. While there was a slight trend to increased pressures and decreased tidal volumes after balloon insertion and inflation, these changes were not clinically relevant. The median (range) at each time point were tidal volume of 565 (370–780), 560 (330–830) and 550 (320–830) ml, peak airway pressure of 11(9–22), 14 (11–17) and 14 (13–17) cmH2O, and plateau pressure of 9 (7–17), 11 (9–14) and 11 (9–14) cmH2O respectively. Conclusion: Continuous oxygenation and ventilation through the study device during tracheal dilatation is possible, effective and practical.

1982 ◽  
Vol 52 (1) ◽  
pp. 245-253 ◽  
Author(s):  
C. E. Juratsch ◽  
B. J. Whipp ◽  
D. J. Huntsman ◽  
M. M. Laks ◽  
K. Wasserman

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5–2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5–2.0 min) of acute maldistribution of VA/Q.


BMC Genetics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
S. A. Woolley ◽  
S. E. Hayes ◽  
M. R. Shariflou ◽  
F. W. Nicholas ◽  
C. E. Willet ◽  
...  

Abstract Background Brachygnathia, cardiomegaly and renal hypoplasia syndrome (BCRHS, OMIA 001595–9940) is a previously reported recessively inherited disorder in Australian Poll Merino/Merino sheep. Affected lambs are stillborn with various congenital defects as reflected in the name of the disease, as well as short stature, a short and broad cranium, a small thoracic cavity, thin ribs and brachysternum. The BCRHS phenotype shows similarity to certain human short stature syndromes, in particular the human 3M syndrome-2. Here we report the identification of a likely disease-causing variant and propose an ovine model for human 3M syndrome-2. Results Eight positional candidate genes were identified among the 39 genes in the approximately 1 Mb interval to which the disease was mapped previously. Obscurin like cytoskeletal adaptor 1 (OBSL1) was selected as a strong positional candidate gene based on gene function and the resulting phenotypes observed in humans with mutations in this gene. Whole genome sequencing of an affected lamb (BCRHS3) identified a likely causal variant ENSOARG00000020239:g.220472248delC within OBSL1. Sanger sequencing of seven affected, six obligate carrier, two phenotypically unaffected animals from the original flock and one unrelated control animal validated the variant. A genotyping assay was developed to genotype 583 animals from the original flock, giving an estimated allele frequency of 5%. Conclusions The identification of a likely disease-causing variant resulting in a frameshift (p.(Val573Trpfs*119)) in the OBSL1 protein has enabled improved breeding management of the implicated flock. The opportunity for an ovine model for human 3M syndrome and ensuing therapeutic research is promising given the availability of carrier ram semen for BCRHS.


Author(s):  
Jan Hau Lee ◽  
Ira M. Cheifetz

This chapter on respiratory failure and mechanical ventilation provides essential information about how to support children with severe respiratory disorders. The authors discuss multiple modes of respiratory support, including high-flow nasal cannula oxygen, noninvasive ventilation with continuous positive airway pressure and bilevel positive airway pressure, as well as conventional, high-frequency, and alternative modes of invasive ventilation. The section on invasive mechanical ventilation includes key information regarding gas exchange goals, modes of ventilation, patient–ventilator interactions, ventilator parameters (including tidal volume, end-expiratory pressure, and peak plateau pressure), extubation readiness testing, and troubleshooting. The authors also provide the new consensus definition of pediatric acute respiratory distress syndrome. Also included are multiple figures and indispensable information on adjunctive therapies (inhaled nitric oxide, surfactant, prone positioning, and corticosteroids) and respiratory monitoring (including capnography and airway graphics analysis).


1998 ◽  
Vol 85 (5) ◽  
pp. 1929-1940 ◽  
Author(s):  
Sonia Meza ◽  
Manuel Mendez ◽  
Michele Ostrowski ◽  
Magdy Younes

Assisted ventilation with pressure support (PSV) or proportional assist (PAV) ventilation has the potential to produce periodic breathing (PB) during sleep. We hypothesized that PB will develop when PSV level exceeds the product of spontaneous tidal volume (Vt) and elastance (Vt sp ⋅ E) but that the actual level at which PB will develop [PSV(PB)] will be influenced by the[Formula: see text] (difference between eupneic[Formula: see text] and CO2 apneic threshold) and by ΔRR [response of respiratory rate (RR) to PSV]. We also wished to determine the PAV level at which PB develops to assess inherent ventilatory stability in normal subjects. Twelve normal subjects underwent polysomnography while connected to a PSV/PAV ventilator prototype. Level of assist with either mode was increased in small steps (2–5 min each) until PB developed or the subject awakened. End-tidal [Formula: see text], Vt, RR, and airway pressure (Paw) were continuously monitored, and the pressure generated by respiratory muscle (Pmus) was calculated. The pressure amplification factor (PAF) at the highest PAV level was calculated from [(ΔPaw + Pmus)/Pmus], where ΔPaw is peak Paw − continuous positive airway pressure. PB with central apneas developed in 11 of 12 subjects on PSV. [Formula: see text]ranged from 1.5 to 5.8 Torr. Changes in RR with PSV were small and bidirectional (+1.1 to −3.5 min−1). With use of stepwise regression, PSV(PB) was significantly correlated with Vt sp( P = 0.001), E ( P = 0.00009),[Formula: see text]( P = 0.007), and ΔRR ( P = 0.006). The final regression model was as follows: PSV(PB) = 11.1 Vt sp + 0.3E − 0.4 [Formula: see text] − 0.34 ΔRR − 3.4 ( r = 0.98). PB developed in five subjects on PAV at amplification factors of 1.5–3.4. It failed to occur in seven subjects, despite PAF of up to 7.6. We conclude that 1) a[Formula: see text] apneic threshold exists during sleep at 1.5–5.8 Torr below eupneic[Formula: see text], 2) the development of PB during PSV is entirely predictable during sleep, and 3) the inherent susceptibility to PB varies considerably among normal subjects.


Author(s):  
Carl Waldmann ◽  
Neil Soni ◽  
Andrew Rhodes

Pulmonary function tests in critical illness 90End-tidal CO2 monitoring 92Pulse oximetry 94Pulmonary function test results in critically ill patients can be important prognostically and guide ventilatory and weaning strategies. However, they are not straightforward to measure in mechanically ventilated patients and remain limited to dynamic volumes. Fortunately, most modern mechanical ventilators are able to calculate and display static and dynamic lung volumes, together with derived values for airway resistance, compliance and flow/volume/time curves. The ability to monitor these changes after altering ventilatory parameters has enabled more sophisticated adjustments of ventilation, to prevent potentially damaging mechanical ventilation....


1981 ◽  
Vol 50 (3) ◽  
pp. 552-560 ◽  
Author(s):  
J. A. Hirsch ◽  
B. Bishop

We have analyzed the effects of 4-6 min of 5, 10 and 15 cmH2O continuous negative airway pressure breathing (NPB) on steady-state end-expiratory lung volume (delta VR) and breathing pattern. Fourteen healthy adults, seated in a full body box, breathed via a mouthpiece on a bag-in-box. Pressure in the body box was elevated to the desired pressure level. Inspiratory (TI) and expiratory (TE) durations, tidal volume (VT), minute ventilation (VI), mean inspiratory flow (VT/TI), and mean expiratory flow (VT/TE) were calculated from pneumotachometer recordings. The effects of NPB are decreases in delta VR, VT, and VT/TI and increases in VT/TE. The responses to NPB are an increase in breathing frequency, due to a shortened TE, and an increase in inspiratory activity. The decrease in delta VR and the increase in VT/TE are limited by an active retardation of expiratory flow. End-tidal CO2 and VI were not altered significantly during NPB, suggesting no alveolar hyperventilation. Thus multiple components of the human response to NPB are not all engaged at the same levels of NPB. The changes in the timing of respiratory events occur at -5 cmH2O, whereas VT compensation is not seen until -15 cmH2O.


1995 ◽  
Vol 79 (2) ◽  
pp. 575-580 ◽  
Author(s):  
C. A. Harms ◽  
J. M. Stager

Is inadequate hyperventilation a cause of the exercise-induced hypoxemia observed in some athletes during intense exercise? If so, is this related to low chemoresponsiveness? To test the hypothesis that exercise-induced hypoxemia, inadequate hyperventilation, and chemoresponsiveness are related, 36 nonsmoking healthy men were divided into hypoxemic (Hyp; n = 13) or normoxemic (Nor; n = 15) groups based on arterial oxygen saturation (SaO2; Hyp < or = 90%, Nor > 92%) observed during maximum O2 uptake (VO2max). Men with intermediate SaO2 values (n = 8) were only included in correlation analysis. Ventilatory parameters were collected at rest, during a treadmill maximal oxygen consumption (VO2max) test, and during a 5-min run at 90% VO2max. Chemoresponsiveness at rest was assessed via hypoxic ventilatory response (HVR) and hypercapnic ventilatory response (HCVR). VO2max was not significantly different between Nor and Hyp. SaO2 was 93.8 +/- 0.9% (Nor) and 87.7 +/- 2.0% (Hyp) at VO2max. End-tidal PO2 and the ratio of minute ventilation to oxygen consumption (VE/VO2) were lower while PETCO2 was higher for Hyp (P < or = 0.01). End-tidal PO2, end-tidal PCO2, and VE/VO2 correlated (P < or = 0.05) to SaO2 (r = 0.84, r = -0.70, r = 0.72, respectively), suggesting that differences in oxygenation were due to differences in ventilation. HVR and HCVR were significantly lower for Hyp. HVR was related to VE/VO2 (r = 0.43), and HCVR was related to the ratio of VE to CO2 production at VO2max (r = 0.61)


2002 ◽  
Vol 13 (4) ◽  
pp. 355-359 ◽  
Author(s):  
Niels Zorger ◽  
Christoph Manke ◽  
Markus Lenhart ◽  
Thomas Finkenzeller ◽  
Behrus Djavidani ◽  
...  

2019 ◽  
Vol 161 (3) ◽  
pp. 458-467 ◽  
Author(s):  
Victoria Pepper ◽  
Cameron A. Best ◽  
Kaila Buckley ◽  
Cynthia Schwartz ◽  
Ekene Onwuka ◽  
...  

Objectives Humans receiving tissue-engineered tracheal grafts have experienced poor outcomes ultimately resulting in death or the need for graft explantation. We assessed the performance of the synthetic scaffolds used in humans with an ovine model of orthotopic tracheal replacement, applying standard postsurgical surveillance and interventions to define the factors that contributed to the complications seen at the bedside. Study Design Large animal model. Setting Pediatric academic research institute. Subjects and Methods Human scaffolds were manufactured with an electrospun blend of polyethylene terephthalate and polyurethane reinforced with polycarbonate rings. They were seeded with autologous bone marrow–derived mononuclear cells and implanted in sheep. Animals were evaluated with routine bronchoscopy and fluoroscopy. Endoscopic dilation and stenting were performed to manage graft stenosis for up to a 4-month time point. Grafts and adjacent native airway were sectioned and evaluated with histology and immunohistochemistry. Results All animals had signs of graft stenosis. Three of 5 animals (60%) designated for long-term surveillance survived until the 4-month time point. Graft dilation and stent placement resolved respiratory symptoms and prolonged survival. Necropsy demonstrated evidence of infection and graft encapsulation. Granulation tissue with signs of neovascularization was seen at the anastomoses, but epithelialization was never observed. Acute and chronic inflammation of the native airway epithelium was observed at all time points. Architectural changes of the scaffold included posterior wall infolding and scaffold delamination. Conclusions In our ovine model, clinically applied synthetic tissue-engineered tracheas demonstrated infectious, inflammatory, and mechanical failures with a lack of epithelialization and neovascularization.


1980 ◽  
Vol 49 (4) ◽  
pp. 708-714 ◽  
Author(s):  
S. M. Lewis ◽  
E. P. Hill

Recent studies suggest pH sampled by arterial chemoreceptors may not equal that sampled by external pH electrodes, because the uncatalyzed hydration of CO2 in plasma is a slow reaction (t 1/2 approximately 9 S). The importance of this reaction rate to ventilatory control (particularly during exercise) is not known. We studied the effect of catalyzing the CO2-pH reaction in three awake exercising dogs with chronic tracheostomies and carotid loops; the dogs were trained to run on a treadmill. Respiration frequency, tidal volume, total ventilation, and end-tidal partial pressure of CO2 (PCO2) were continuously monitored. Periodically, carotid artery blood was drawn and analyzed for partial pressure of O2 (PO2), PCO2, pH, and plasma carbonic anhydrase (CA) activity. Measurements were made during steady-state exercise (3 mph and 10% grade), during a control period, after injection of a 5 ml bolus of saline, and after injection of 5 mg/kg of bovine CA dissolved in 5 ml of saline. This dose of CA increased the reaction rate by more than 80-fold. Neither the control nor the CA injections significantly altered the ventilatory parameters. Saline and CA date differed by less than 5% in ventilation, 1 Torr in arterial PCO2, 0.01 in pH units, and 1.5 Torr in end-tidal PCO2. Thus the of CO2 hydration in plasma is not a significant factor in ventilatory control.


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