The effect of acute ventilation-perfusion mismatch on respiratory heat exchange in a porcine model

Background Respiratory heat exchange is an important physiological process occurring in the upper and lower respiratory tract and is usually completed when inspired gases reach the alveoli. Animal and human studies demonstrated that heat exchange can be modulated by altering pulmonary ventilation and perfusion. The purpose of this study was to examine the effect of acute ventilation-perfusion (V/Q) mismatch on respiratory heat exchange. In clinical practice, monitoring respiratory heat exchange might offer the possibility of real-time tracking of acute V/Q-mismatch. Methods In 11 anesthetized, mechanically ventilated pigs, V/Q-mismatch was established by means of four interventions: single lung ventilation, high cardiac output, occlusion of the left pulmonary artery and repeated whole-lung lavage. V/Q-distributions were determined by the multiple inert gas elimination technique (MIGET). Respiratory heat exchange was measured as respiratory enthalpy using the novel, pre-commercial VQm™ monitor (development stage, Rostrum Medical Innovations, Vancouver, CA). According to MIGET, shunt perfusion of low V/Q compartments increased during single lung ventilation, high cardiac output and whole-lung lavage, whereas dead space and ventilation of high V/Q compartments increased during occlusion of the left pulmonary artery and whole-lung lavage. Results Bohr dead space increased after pulmonary artery occlusion and whole-lung lavage, venous admixture increased during single lung ventilation and whole-lung lavage, PaO2/FiO2 was decreased during all interventions. MIGET confirmed acute V/Q-mismatch. Respiratory enthalpy did not change significantly despite significant acute V/Q-mismatch. Conclusion Clinically relevant V/Q-mismatch does not impair respiratory heat exchange in the absence of additional thermal stressors and may not have clinical utility in the detection of acute changes.

Clinical and functional featuresof respiratory heat exchange and cold airway hyperresponsiveness in patients with bronchial asthma and chronic polypous rhinosinusitis

The aim of the study was to investigate airway conditioning function and cold hyperresponsiveness in patients with bronchial asthma (BA) and nasal polyps. One hundred and eleven asthma patients with or without chronic polypous rhinosinusitis (CPR) were examined. Respiratory heat exchange and cold airway hyperresponsiveness were assessed using thermometry of expired air during quiet breathing and isocapnic hyperventilation with cold air in comparison with a group of healthy persons. The conditioning nasal function was worsened in BA patients with CPRS. Disorders of nasal heat exchange led to decreased temperature of the exhaled air during quiet breathing and cold hyperventilation. These disorders were closely related to increased frequency and severity of cold airway hyperresponsiveness.

The particularities of cold-induced bronchial hyperreactivity in patients with chronic respiratory diseases

Prevalence and clinical and physiological features of coldinduced bronchial hyperreactivity in patients with respiratory diseases were shown. In patients with chronic bronchitis, coldinduced bronchial hyperreactivity was associated with worsening of lung ability to condition the inspired air. Disorders of respiratory heat exchange in patients with bronchial asthma were not the leading cause of coldinduced bronchoconstriction, which was associated with high sensitivity of airway receptors and IgEdependent mechanisms. A set of diagnostic criteria allowing detection of the dominant mechanism of airway cold hyperreactivity was proposed.

A Microcomputer-Based Respiratory Heat Exchange Facility for Use in the Diagnosis of Thermally Induced Asthma

Exercise-induced asthma is prevalent in many asthmatics and during the winter months can be exacerbated by cold air inhalation. A laboratory facility was required to permit early diagnosis of cold air sensitivity in these patients. This paper describes the development of a modular air conditioning system to produce a range of inhalative thermal burdens and the microcomputer interfacing to measure the rate of airway heat loss imposed. A single-stage refrigerator was built capable of cooling 150 1/min air to —25°C. This was also used to generate dry ambient temperature air by rewarming the chilled air supply. An air humidifier was developed based upon natural convection and evaporation. It was capable of raising 150 1/min ambient air to 37°C, 100 per cent relative humidity. In two pilot studies of 18 asthmatics it was found that the rate of respiratory heat exchange could be correlated with the magnitude of post exertional bronchoconstriction (lung dysfunction) and that exercise-induced asthma could be minimized by attenuating the rate of airway heat loss.

A graphic analysis of respiratory heat exchange

A new graphic representation of respiratory heat exchange is proposed using the concept of equivalent temperatures directly related to enthalpy values. On such a diagram it is possible to 1) compute the value of the heat exchange (delta H) knowing the inspired temperature (TI) and the partial pressure of water vapor (PIH2O) [or the relative humidity (rhI)] of inspired gas; 2) estimate the variation in delta H following a given variation in TI and PIH2O or, inversely, to choose the variation in TI and PIH2O necessary to obtain a given variation in delta H; 3) dissociate inspiratory and expiratory exchanges and to evaluate the efficiency of the respiratory heat exchange process in different environmental situations; and 4) easily compare the results of different studies published on respiratory heat exchanges in humans or other animal species.