Airway pressure release ventilation

Prolonging inspiratory time may recruit more slowly recruitable alveoli (24) and improve V/Q matching (24,25). The development of intrinsic PEEP from the short expiratory times can have similar effects to that of applied PEEP. Since long inspiratory times increase the total intrathoracic pressures, cardiac output may be affected. Finally, inspiratory-to-expiratory time ratio (I/E) > 1 1— known as inverse ratio ventilation—is uncomfortable, in the absence of airway pressure release ventilation (26,27). 

Inverse ratio ventilation (I/E >1 1) can increase PEEP and improve V/Q in severe respiratory failure (24—27). This setting is applied as airway pressure release ventilation (APRV) (Table 1), which, although appealing, lacks good outcome studies supporting its use. 

Stock MC, Downs JB, Frolicher DA. Airway pressure release ventilation. Crit Care Med 1987 15 462-466. 

If abnormal, these measurements mandate close observation and support at the intensive care level. If the measurements are normal, they all must be repeated 4 to 6 hours after the suspected exposure only then can an individual be released to a lower medical priority status. Abnormality of any one of those measures, in the absence of other explanation, should prompt institution of therapy for noncardiac pulmonary edema. At the early stages of treatment, therapy should include positive airway pressure with early application of the PEEP mask. Later application of positive pressure ventilation through intubation may be required if the PEEP mask fails to maintain adequate arterial Po2. 

Carbon dioxide is a rapid, potent stimulus to ventilation. Inhalation of 10% CO can produce minute volumes of 75 L/min in normal individuals. Carbon dioxide acts at multiple sites to stimulate ventilation. Elevated Pco causes bronchodilation, whereas hypocarbia causes constriction of airway smooth muscle these responses may play a role in matching pulmonary ventilation and perfusion. Circulatory effects of CO result from the combination of direct local effects and centrally mediated effects on the autonomic nervous system. The direct effects are diminished contractility of the heart and vascular smooth muscle (vasodilation). The indirect effects result from the capacity of CO to activate the sympathetic nervous system these indirect effects generally oppose the local effects ofCO. Thus, the balance of opposing local and sympathetic effects determines the total circulatory response to CO. The net effect of CO inhalation is an increase in cardiac output, heart rate, and blood pressure. In blood vessels, however, the direct vasodilating actions of carbon dioxide appear more important, and total peripheral resistance decreases when the Pco is increased CO also is a potent coronary vasodilator. Cardiac arrhythmias associated with increased Pco are due to the release of catecholamines. 

When outburst occurs in mine, airflow catastrophic will occur in intake airways connected with the source of outburst because of the great impact force produced by gas flow transiently released and of the gas pressure after the dynamic of outburst disappears, of which the most typical is airflow reverse of side branches. Therefore, this paper will use one dimensional unsteady-state flow momentum equation established above to analyze law of airflow reversalof side branches induced by gas pressure when upward ventilation airflow catastrophic occuring. 

Pressure-generating and cycled devices are not suitable for ventilation in toxic trauma. Because of their construction, these devices will cycle once a preset pressure has been released. Therefore, if there is airway resistance and reduced lung... 

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