Tracheal Mucosal Blood Flow Research Articles

Evaluation of the Effect of the Endotracheal Tube Cuff Pressure Measurement on Postoperative Sore Throat

BACKGROUND
 Following general anaesthesia, up to 62% of patients experience postoperative sore throat. Despite the fact that it resolves on its own, efforts must be made to reduce it. We wanted to evaluate the difference between conventional method and instrumental measurement of cuff pressure in incidence and severity of postoperative sore throat in this study.
 METHODS
 A prospective observational study that included 150 adult patients aged < 50 years scheduled for elective surgical operation requiring general anaesthesia and endotracheal intubation. They were divided randomly into two groups: Group A included 75 patients and the adequacy of cuff inflation was generally assessed clinically and group B included 75 patients and the adequacy of cuff inflation was generally assessed by using a cuff manometer.
 RESULTS
 Incidence of postoperative sore throat in all times was significantly lower in Group B than in Group A. Prevalence of mild postoperative sore throat after one hr. was significantly higher in group B than that in group A (94.1% versus 61.4%, P= 0.001).
 CONCLUSIONS
 Impaired tracheal mucosal blood flow was an important factor in the incidence of postoperative sore throat associated with tracheal intubation and recommended that a cuff inflation pressure of 30 cmH2O should not be exceeded.

The Professional Experience of Anaesthesiologists in Proper Inflation of Laryngeal Mask and Endotracheal Tube Cuff.

Cuffs inflated to inappropriately high pressures cause ischemia, reducing tracheal mucosal blood flow, while cuffs inflated at lower pressure than necessary give rise to inadequate ventilation, aspiration of gastric contents, or extubation due to air leakage. In this study, we aimed to investigate the effect of the experience of anaesthesia staff on endotracheal tube and laryngeal mask airway cuff inflation. The study included 348 elective patients scheduled to undergo surgery under general anaesthesia, with 34 anaesthesia technicians, 16 anaesthesia residents, and 12 anaesthesiologists with different years of professional experience. The participants were told to inflate the cuff balloon with air to the level of the pressure that was appropriate for them. No information was provided to the participants about the values of the cuff pressure pending the completion of all measurements. After placement of the laryngeal mask airway and endotracheal tube, the success of the procedure was checked by monitoring square-wave capnograph tracing and thoracoabdominal motion. Each participant performed the procedures on three patients, and the mean cuff pressures were measured. There was no significant correlation between duration of experience of technicians, residents, and experts in using laryngeal mask airway pressure (r=-0.192/p=0.278, r=0.225/p=0.402, r=-0.476/p=0.118, respectively) and endotracheal tube (r=-0.306/p=0.079, r=-0.060/p=0.826, r=-0.478/0.116, respectively). It has been concluded that professional experience does not contribute to achieving normal cuff pressure without monitoring. Introduction of the cuff manometer into routine anaesthesia practice will be useful, irrespective of anaesthesiologists' experience.

Design and In Vitro Testing of a Pressure-Sensing Syringe for Endotracheal Tube Cuffs

Endotracheal intubation is a frequently performed procedure in the prehospital setting, intensive care unit, and for patients undergoing surgery. The endotracheal tube cuff must be inflated to a pressure that prevents air leaks without compromising tracheal mucosal blood flow. For simultaneous endotracheal tube cuff inflation and measurement, we designed and tested a novel pressure-sensing syringe in vitro. The prototype was developed using a standard 10-mL polycarbonate syringe body that houses a plunger and a silicone rubber bellows, the pressure-sensing element. Bellow feasibility was determined and modeled using finite element analysis. Repeatability testing at each pressure measurement for each bellows (pressure versus deflection) was within an average standard deviation of 0.3 cm to 1.61 cm (1%-5% error). Using an aneroid manometer for comparison, there was excellent linear correlation with a Spearman rank of 0.99 (P < 0.001), up to 30 cm H(2)O.

Microvascular blood flow in the airway mucosa modulates bronchoconstriction

in this issue of the Journal of Applied Physiology , Mazzone et al. ([4][1]) demonstrate the role of α-adrenergic control of airway vasculature tone, which in turn regulates the magnitude of airway smooth muscle response to bronchoconstrictive challenges. They demonstrate by intravital microscopy

An in vitro study of the compliance of paediatric tracheal tube cuffs and tracheal wall pressure

Cuff volume-pressure curves and cuff pressure-tracheal wall pressure relationships were investigated in eight brands of currently available cuffed, paediatric tracheal tubes with internal diameters of 5.0 mm. Cuff volume-pressure curves were measured with the cuff unrestricted and with the cuff placed within a tracheal model with wall pressure measurements. With the tracheal tube cuffs, unrestricted cuff compliance at 20 cmH(2)O cuff pressure varied between 0.06 and 0.3 ml x cmH(2)O(-1). With the cuff restricted within the model trachea, all tracheal tube cuffs became considerably less compliant (0.01-0.09 ml x cmH(2)O(-1)). We found tracheal wall pressure was similar to the cuff pressure as long as the resulting cuff diameter was sufficiently large freely to drape the inner tracheal wall. We found that, regardless of whether a higher or lower compliant tube cuff was used, cuff hyperinflation uniformly resulted in potentially compromised tracheal mucosal blood flow; cuff pressure monitoring using cuff pressure limitation is therefore strongly recommended.

Proseal Laryngeal Mask Airway for the Resection of a High Grade Upper Tracheal Stenosis: A case report

Laryngeal mask airways (LMAs) have several advantages compared with conventional endotracheal tube (ETT) in tracheal surgery. LMAs cannot penetrate the airway below the level of the glottis, but enable the access to the larynx and tracheobronchial tree while avoiding airflow impairment, tracheal stimulation, trauma, and the interference of tracheal mucosal blood flow. Moreover, LMAs have lower airway resistance than ETTs. We describe the use of a proseal laryngeal mask airway (PLMA) in patients with high grade upper tracheal stenosis. We suggest that PLMA might have advantages over the classic LMA by preventing aspiration and by allowing the evacuation of air from the stomach in high-grade upper tracheal stenosis.

Simple on-line endotracheal cuff pressure relief valve.

Ischemic injury of the tracheal mucosa in the endotracheally intubated patient is directly proportional to the tracheal tube cuff pressure. At a cuff pressure of 30 cm H2O, the tracheal mucosal blood flow becomes partially obstructed, and at a pressure of 45 cm H2O, the obstruction to the tracheal mucosal blood becomes total, leading to tracheal mucosal damage and subsequent complications. In our institute, we have developed a simple and very inexpensive method to gauge the cuff pressure. We use a regular 20-mL syringe attached in line with the connector of the endotracheal tube cuff. In this manner, we monitored the intracuff pressure in 120 patients who underwent ear or neck surgery. The syringe was connected to the tube cuff and inflated with 15 mL of air. The syringe was left constantly connected to the cuff. In addition, the cuff pressure was measured with the Mallinckrodt Hi-Lo aneroid pressure gauge at the beginning of surgery and hourly thereafter for the duration of surgery. At the same time, a check for leakage around the cuff was made by auscultation with a stethoscope above the sternal notch. Multiple comparisons between the repetitive intracuff pressure measurements revealed that there were no significant differences in the intracuff pressure values measured at the different times of surgery. These results indicate that there was an adequate venting of the excess intracuff pressure and also that there was no leakage around the cuff.

The Laryngeal Mask and High-Frequency Jet Ventilation for Resection of High Tracheal Stenosis

The Laryngeal Mask and High-Frequency Jet Ventilation for Resection of High Tracheal Stenosis

Reconstruction of trachea and carina with immediate or cryopreserved allografts in dogs

Grafting is required when primary reconstruction of a tracheocarinal defect is not feasible. To determine the viability of and the nature of the healing process occurring in the cryopreserved graft, we performed tracheocarinal transplantation in dogs. We performed 32 tracheocarinal reconstructions in dogs using autotransplanted, immediately transplanted, or cryopreserved allografts. The viability of each graft was evaluated serially by fiberoptic macroexamination and by measurement of the tracheal mucosal blood flow using a hydrogen clearance method. In group A (n = 8), the tracheal carina was removed and reimplanted immediately. In group B (n = 8), the tracheocarina was allotransplanted immediately after harvest. In group C (n = 8), allotransplantations were performed using grafts cryopreserved for 1 to 3 weeks by freeze-drying. In group D (n = 8), we attempted to achieve immunosuppression-free transplantation with the cryopreserved allografts. Sufficient viability and good healing (6/8, 75%) occurred in the dogs with cryopreserved tracheocarinal allotransplants. Three of 8 dogs (38%) with cryopreserved allotransplants survived for 25 to 57 days without immunosuppression. The cryopreservation of tracheocarinal allografts for 3 weeks without the use of a preservative solution was shown to be feasible. Cryopreservation prolonged the survival of nonimmunosuppressed allotransplants in dogs.

Evaluation of tracheal mucosal blood flow during an extended radical operation for esophageal carcinoma: clinical and experimental studies.

Using the hydrogen gas clearance method, a plate-type probe was attached to the surface of the cuff of an endotracheal tube in order to measure the ischemic changes in the tracheal mucosa produced by peritracheal lymph node dissection. In eight human subjects with intrathoracic esophageal carcinoma, the tracheal mucosal blood flow was 40.1 ml/100 g per minute after they had undergone a right thoracotomy and then decreased to 13.0 ml/100 g per minute after they had further received an extended radical operation preserving the right bronchial artery. No tracheal ulcers were seen. The same ischemic changes in the tracheal mucosa were also measured in dogs. The right bronchial artery contributes about one-third of the total blood flow to the trachea and this was thus calculated to be about 10-14 ml/100 g per minute.

Effect of endothelin-1 on canine airway blood flow.

The effect of endothelin-1 (ET-1) on the blood flow contributions of the pulmonary and systemic circulations to the trachea and main bronchi were measured in anesthetized dogs by injecting 15-microns radiolabeled microspheres into the right and left heart, respectively. After the microsphere injections the animals were killed, and the tracheal cartilage, tracheal muscle mucosa, and main bronchi were excised and collected for radioactive counting. The results of this study showed that under normal conditions tracheal blood flow was primarily systemic (> 95% of total tracheal blood flow) averaging 25-50 ml/min/100 g, whereas both the pulmonary (9-10 ml/min/100 g) and systemic circulations (19-20 ml/min/100 g) contributed substantially to main bronchi blood flow. Administration of ET-1 i.v. decreased systemic tracheal cartilage blood flow from 25.3 +/- 3.8 to 14.5 +/- 2.8 ml/min/100 g, systemic tracheal mucosal blood flow from 50.0 +/- 7.0 to 25.0 +/- 7.0 ml/min/100 g, and systemic main bronchi blood flow from 19.4 +/- 4.6 to 11.6 +/- 3.4 ml/min/100 g (p < 0.05). These results indicate that ET-1 is a potent constrictor of the airway circulation and may contribute to airway ischemia seen in different airway disease states.

Effects of inspiratory resistance, inhaled beta-agonists and histamine on canine tracheal blood flow

Tracheobronchial blood flow is potentially important in asthma as it could either influence the clearance of mediators from the airways, thus affecting the duration and severity of bronchospasm, or enhance oedema formation with a resultant increase in airflow obstruction. In anaesthetized dogs, spontaneously breathing via a tracheostomy, we investigated the effects of three interventions which are relevant to acute asthma attacks and could potentially influence blood flow and its distribution to the mucosa and remaining tissues of the trachea: 1) increased negative intrathoracic pressure swings (-25 +/- 1 cmH2O) induced by an inspiratory resistance; 2) variable inhaled doses of a beta-adrenoceptor-agonist (terbutaline); and 3) aerosolized histamine sufficient to produce a threefold increase in pulmonary resistance. Microspheres labelled with different radioisotopes were used to measure blood flow. Resistive breathing did not influence tracheobronchial blood flow. Following a large dose of terbutaline, mucosal blood flow (Qmb) increased by 50%. After inhaled histamine, Qmb reached 265% of the baseline value. We conclude that, whereas increased negative pressure swings do not influence tracheobronchial blood flow or its distribution, inhalation of aerosolized terbutaline, corresponding to a conventionally nebulized dose, increases mucosal blood flow. Our results also confirm that inhaled histamine, in a dose sufficient to produce moderate bronchoconstriction, increases tracheal mucosal blood flow in the area of deposition.

Changes in tracheal mucosal thickness and blood flow in sheep

Airway narrowing may be produced by increasing the blood volume of the airway mucosa. Here changes in tracheal mucosal thickness (MTtr) were measured in 10 anesthetized sheep. Arteries to the cervical trachea were isolated, and blood flow (Qtr) was measured with an electromagnetic flow probe. Simultaneous changes in MTtr were measured with a mechanical probe over a fixed cartilage. Arterial injections of phenylephrine produced dose-related falls in Qtr and MTtr with a maximum peak fall in MTtr of -104 +/- 18 (SE) microns. Methacholine, bradykinin, albuterol, and histamine produced dose-related increases in Qtr. The largest peak increase in MTtr of 308 +/- 121 microns was seen with bradykinin. For methacholine, albuterol, and histamine the largest increases in MTtr were 154 +/- 47, 45 +/- 10, and 153 +/- 31 microns, respectively. The increases in MTtr were not always closely dose related. The peak changes in MTtr occurred substantially later than those in Qtr for all the drugs and up to 120 s later for methacholine and bradykinin. Generally, changes in MTtr and Qtr persisted for less than 10 min; at the higher doses of bradykinin increases in MTtr lasted for up to 15 min. Changes in MTtr were most closely associated in time with changes in Qtr for the vasoconstrictor phenylephrine. These changes in MTtr would alter airway resistance little in the normal trachea and by substantially more in smaller airways such as the bronchi or in the narrowed trachea. Changes in mucosal thickness may be due not only to changes in tracheal blood volume but may also reflect the effects of tissue edema and mucus secretion.

Independent control of mucosal and total airway blood flow during hypoxemia

In the larger airways, the blood circulation forms a subepithelial (mucosal) and outer (peribronchial) microvascular network. This raises the possibility that blood flow in these two networks is regulated independently. We used hypoxemia as a stimulus to induce changes in tracheal mucosal blood flow normalized for systemic arterial pressure (Qtr n) measured with an inert soluble gas technique and total bronchial blood flow (Qbr) and normalized Qbr (Qbrn) measured with an electromagnetic flow probe in anesthetized sheep. Fifteen minutes of hypoxemia [PO2 40 +/- 7 (SD) Torr] decreased mean Qtr n from 1.1 +/- 0.4 to 0.8 +/- 0.4 ml.min-1.mmHg-1.10(2) (-27%; P less than 0.05; n = 7) and increased mean Qbr n from 12.1 +/- 3.2 to 17.1 +/- 5.4 ml.min-1.mmHg-1.10(2) (+41%; P less than 0.05; n = 6). The rise in Qbr correlated with cardiac output (r = 0.68; P less than 0.05). Phentolamine pretreatment (0.1 mg/kg iv) blunted the hypoxemia-related decrease of mean Qtr n (-8%; P = NS). Tyramine (2.5 mg) applied locally to the trachea decreased mean Qtr n significantly after 30 and 45 min by 31 and 19%, respectively (P less than 0.05). 6-Hydroxydopamine (0.2 mg 4 times for 1 h locally applied) prevented the hypoxemia-induced as well as local tyramine-induced decrease in mean Qtr n (0 and 0%).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Blood Flow Modifies Allergic Airway Smooth Muscle Contraction

We tested the hypothesis that airway perfusion modifies the contractile response of airway smooth muscle to allergen challenge by influencing the clearance of locally released spasmogens. In six intact, lightly sedated, sheep allergic to Ascaris suum, we measured tracheal mucosal blood flow (Qtr) with a soluble gas uptake method and tracheal dead space (Vtr), an index of airway smooth muscle tone, by helium dilution before and serially after local aerosol challenge with A. suum extract or ragweed extract (control). The former challenge was repeated during continuous intravenous infusion of either vasopressin or nitroglycerin, which by themselves had no effect on Vtr and decreased and increased Qtr, respectively. Ragweed had no effect on Qtr and Vtr, whereas A. suum increased mean (+/- SE) Qtr by 111 +/- 31% (p less than 0.05) and decreased mean Vtr by 15 +/- 2% (p less than 0.05) immediately after challenge, with Qtr returning to baseline by 40 min and Vtr by 80 min. Vasopressin infusion prevented the A. suum-induced increase in Qtr and prolonged the decrease in mean Vtr (p less than 0.05). During nitroglycerin infusion, A. suum failed to alter Qtr or Vtr. Vasopressin and nitroglycerin had no effect on the contractile responses of tracheal smooth muscle to A. suum in vitro. These results indicate that the effects of vasopressin and nitroglycerin on antigen-induced airway smooth muscle contraction in vivo were due to alterations in airway blood flow rather than to alterations in the release of or airway smooth muscle responsiveness to chemical mediators.

Effect of histamine on tracheal mucosal perfusion, water content and airway smooth muscle in sheep

We examined the response of tracheal mucosal blood flow normalized for systemic arterial pressure (Q̇trn), water content (V H 2O ) and luminal dead spac anesthetized sheep. Nebulized histamine produced rapid increases in mean Q̇trn ( + 84%) and V H 2O (+ 85%), and a decrease in mean Vtr(−17%)( P<0.05) within 5 min post completion of challenge. Mean Vtr rapidly returned to baseline, while mean Q ̇ trn and V H 2O remained elevated for 60 and 90 min after challenge, respectively. Pretreatment with chlorpheniramine (H 1-antagonist) blocked the changes in Vtr and V H 2O , and attenuated the increase in Q̇trn. Metiamide (H 2-antagonist) pretreatment abolished the increase in Q̇trn and blunted the increase in V H 2O , but had no effect on the decrease in Vtr. 2-methylhistamine (H 1-agonist) decreased mean Q̇trn and Vtr ( P<0.05) and dimaprit (H 2-agonist) increased mean Q̇trn ( P<0.05) without changing Vtr. Neither 2-methylhistamine nor dimapritsignificantly altered V H 2O Atropine blocked histamine induced decreases in Vtr and slightly attenuatedthe increases in Q̇trn and V H 2O . Thus, histamine increased airway smooth muscle tone and mucosal water content principally via H 1 receptors, and mucosal perfusion via H 2 receptors. The airway smooth muscle contraction involved muscarinic pathways.

Laser-Doppler measurement of tracheal mucosal blood flow: comparison with tracheal arterial flow

Blood flow in the tracheal mucosa (Qm) has been measured by laser-Doppler flowmetry in anesthetized sheep and dogs. The values have been compared with tracheal arterial inflow (Qtr) by use of an electromagnetic flow probe and with tracheal arterial perfusion pressure (Ptr) produced by mechanical perfusion. Changes in blood flow were caused by injections of methacholine, phenylephrine, and histamine into the perfusion circuit. These interventions produced a range of measurements for each animal. Correlations of Qm against Qtr were significant in two of five animals (R = 0.03-0.93); correlations of Qm against Ptr were significant in two of four animals (R = 0.56-0.96). Percent changes in Qtr were generally much larger than those of Qm, and there was considerable variability between Qm and either Qtr or Ptr. Qm reflected the same vascular changes as Ptr or Qtr in 28 interventions and showed an opposing change in 4 cases. In 11 interventions, changes measured by Ptr or Qtr were not reflected by any changes in Qm. Thus qualitative changes in tracheal perfusion measured with these methods were usually the same; quantitatively the three methods showed great differences. These differences may reflect different regulatory mechanisms in various components of the tracheal vasculature or different technical aspects of the methods used.

Tracheal mucosal blood flow responses to autonomic agonists.

In lightly anesthetized adult sheep, we determined tracheal mucosal blood flow (Qtr) by measuring the steady-state uptake of dimethyl ether from a tracheal chamber created by an endotracheal tube provided with two cuffs. Qtr normalized for carotid arterial pressure [Qtr(n)] was determined before and after the exposure of the tracheal mucosa to aerosolized phenylephrine (0.25-2.0 mg), isoproterenol (0.05-0.8 mg), and methacholine (2.5-20 mg). The same doses of methacholine were also administered during the intravenous infusion of vasopressin. The measurements were repeated after intravenous pretreatment with the respective antagonists phentolamine, propranolol, and atropine. Mean +/- SE base-line Qtr(n) was 1.2 +/- 0.1 ml.min-1.mmHg-1.10(2). The autonomic antagonists had no effect on mean Qtr(n). Phenylephrine produced a dose-dependent decrease in mean Qtr(n) (-70% at the highest dose), which was blunted by phentolamine, and isoproterenol produced a dose-dependent increase in mean Qtr(n) (40% at the highest dose), which was blocked by propranolol. Methacholine failed to alter mean Qtr(n) even when Qtr was first decreased by vasopressin. We conclude that in lightly anesthetized adult sheep 1) base-line Qtr(n) is not under adrenergic or cholinergic control, 2) a locally administered alpha-adrenergic agonist decreases and beta-adrenergic agonist increases Qtr(n) via specific receptor activation, and 3) a locally administered cholinergic muscarinic agonist has no effect on Qtr(n).

Measurement of airway mucosal perfusion and water volume with an inert soluble gas.

The purpose of this study was to develop and validate a new in vivo technique for the measurement of tracheal mucosal blood flow (Qtr) and tissue water volume (VH2O) with an inert soluble gas. The technique was based on the notion that the uptake of dimethyl ether (VDME) from an isolated tracheal segment is governed by VH2O (transient state) and Qtr (steady state). In lightly anesthetized sheep, an endotracheal tube with two cuffs placed 14.5-16.5 cm apart was placed to create a chamber into which dimethyl ether was introduced and from which VDMME into the mucosa was determined with a sensitive pneumotachograph. Mean Qtr was 1.20 ml/min (range 0.87-1.73), and mean VH2O was 1.67 ml (range 1.27-2.26). Qtr correlated with cardiac output but not with body weight or tracheal mucosal surface area determined by He dilution. VH2O did not show a correlation with any of these parameters. The response to selected pharmacological agents suggested that the measurements of Qtr and VH2O are independent of each other and from changes in tracheal diameter. Mean Qtr was 80% of mean tracheal mucosal blood flow measured with radiolabeled microspheres. We concluded that the inert soluble gas method is capable of measuring in vivo the perfusion and a water compartment of the intact tracheal mucosa.

Tracheobronchial and upper airway blood flow in dogs during thermally induced panting.

Tracheobronchial blood flow increases two- to fivefold in response to isocapnic hyperventilation with warm dry or cold dry air in anesthetized, tracheostomized dogs. To determine whether this response is governed by central nervous system thermoregulatory control or is a local response to the drying and/or cooling of the airway mucosa, we studied eight anesthetized spontaneously breathing dogs in a thermally controlled chamber designed so that inspired air temperature, humidity, and body temperature could be separately regulated. Four dogs breathed through the nose and mouth (group 1), and four breathed through a short tracheostomy tube (group 2). Dogs were studied under the following conditions: 1) a normothermic control period and 2) two periods of hyperthermia in which the dogs panted with either warm 100% humidified air or warm dry (approximately 10% humidified) air. Radiolabeled microspheres (15 +/- 3 micron diam) were injected into the left ventricle as a marker of nasal, lingual, and tracheobronchial blood flow. After the final measurements, the dogs were killed and tissues of interest excised. Results showed that lingual and nasal blood flow (ml.min-1.g-1) increased during panting (P less than 0.01) in both groups and were not affected by the inspired air conditions. In group 1, tracheal mucosal blood flow barely doubled (P less than 0.01) and bronchial blood flow did not change during humid and dry air panting. In group 2, there was a sevenfold increase in tracheal mucosal and about a threefold increase in bronchial blood flow (P less than 0.01), which was only observed during dry air panting.(ABSTRACT TRUNCATED AT 250 WORDS)