The main reasons for instituting mechanical ventilation are to decrease the work of breathing, support gas exchange, and buy time for other interventions to reverse the cause of respiratory failure.1 Mechanical ventilation can be applied in patients who are making or not making respiratory efforts, whereby assisted or controlled modes of support are used, respectively.1 In patients without respiratory efforts, the respiratory system represents a passive structure, and thus the ventilator is the only system that controls breathing. During assisted modes of ventilator support, the patient’s system of control of breathing is under the influence of the ventilator pump.2–4 In the latter instance, ventilatory output is the final expression of the interaction between the ventilator and the patient’s system of control of breathing. Thus, physicians who deal with ventilated patients should know the effects of mechanical ventilation on control of breathing, as well as their interaction. Ignorance of these issues may prevent the ventilator from achieving its goals and also lead to significant patient harm.
The respiratory control system consists of a motor arm, which executes the act of breathing, a control center located in the medulla, and a number of mechanisms that convey information to the control center.5,6 Based on information, the control center activates spinal motor neurons that subserve the respiratory muscles (inspiratory and expiratory); the intensity and rate of activity vary substantially between breaths and between individuals. The activity of spinal motor neurons is conveyed, via peripheral nerves, to respiratory muscles, which contract and generate pressure (Pmus). According to equation of motion, Pmus at time t during a breath is dissipated in overcoming the resistance (Rrs) and elastance (Ers) of the respiratory system (inertia is assumed to be negligible) as follows:
where ΔV(t) is instantaneous volume relative to passive functional residual capacity and (t) is instantaneous flow. Equation (1) determines the volume–time profile and, depending on the frequency of respiratory muscle activation, ventilation. Volume–time profile affects Pmus via neuromechanical feedback; inputs generated from other sources (cortical inputs) may modify the function of control center. Ventilation, gas-exchange properties of the lung, and cardiac function determine arterial blood gases, termed arterial oxygen tension (PaO2) and arterial carbon dioxide tension (PaCO2), which, in turn, affect the activity of control center via peripheral and central chemoreceptors (chemical feedback). This system can be influenced at any level by diseases or therapeutic interventions.
During mechanical ventilation, the pressure provided by the ventilator (Paw) is incorporated into the system.3 Thus, the total pressure applied to respiratory system at time t [PTOT(t)] is the sum of Pmus(t) and Paw(t). As a result, the equation of motion is modified as follows:
The relationships of Equation (2) determine the volume–time profile during mechanical ventilation, which via neuromechanical, chemical, and behavioral feedback systems affects the Pmus ...