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Patient–ventilator interaction
Clinical management of patients with acute respiratory failure is based on the concept that significant changes in respiratory mechanics, respiratory muscle performance, and control of breathing are the underlying mechanisms responsible for acute respiratory failure. The effects of mechanical ventilation on gas exchange, respiratory muscle load, and dyspnea depend on the matching between the ventilator settings and the patient’s respiratory physiology. However, mechanical ventilation is rarely optimized, which would require ventilator settings based on accurate and reproducible measurements of lung and chest wall mechanics, respiratory muscle function, and respiratory drive.
Respiratory physiology
The goal of the intrinsic ventilatory control system is to integrate the timing and intensity of the phrenic nerve signal, inputs from chemoreceptors and pulmonary stretch receptors, and variations in metabolic demands. Contraction of the respiratory muscles leads to the generation of flow and volume to provide adequate alveolar ventilation with tolerable work of breathing. During spontaneous breathing, the respiratory muscles generate pressure (P mus ) to produce flow against the resistive properties (R RS ), deliver volume against the elastic properties (E RS ) of the respiratory system, and overcome any intrinsic positive end-expiratory pressure (PEEPi, known better clinically as auto-PEEP ). Under these circumstances, the act of spontaneous breathing can be described at any instant as follows:
where Pres represents the resistive pressure and is a function of flow (Pres = Flow × R RS ) and Pel represents the elastic recoil pressure generated by lung expansion and is a function of volume (Pel = Volume × E RS ). Assuming that R RS and E RS are linear, the equation becomes:
In patients with acute respiratory failure requiring ventilatory support, pressure generated by the ventilator (Pappl) is added to the pressure generated by the contraction of the respiratory muscles according to the following equation:
The complex interaction among all the variables in Equation 3 can be summarized by the concept of neuroventilatory coupling ( Fig. 54.1) . Under normal conditions, as well as at the onset of acute respiratory failure before mechanical assistance is delivered, the spontaneous contraction of the respiratory muscles suddenly generates flow and volume; the slope of the relationship between effort and ventilatory output is conditioned by the contractile properties of the respiratory muscles and the impedance of the respiratory system. When positive pressure is applied to assist the action of breathing using most modes of mechanical ventilation, the coupling between effort and output may be compromised.
During volume-targeted assist-control ventilation (ACV), flow and tidal volume remain unaffected by muscle contraction. During pressure-targeted flow-cycled (pressure support ventilation [PSV]) or time-cycled (assist-control pressure-targeted ventilation [AC/PCV]) ventilation, despite better coupling between inspiratory effort and the ventilator’s output, any increase in respiratory impedance decreases the amount of delivered flow and volume. During noninvasive ventilation (NIV), air leaks may further compromise the coupling between patient effort and ventilatory output.
Patient and ventilator variables
Patient variables
The patient interacts with the ventilator based on three physiologic variables , , :
- 1.
Respiratory drive
- 2.
Ventilatory requirements
- 3.
Timing of the breathing pattern
Ventilator variables
The ventilator interfaces with the patient’s physiology based on three technologic variables:
- 1.
Delivery mechanism (control variable); that is, the algorithm used by the ventilator to assist ventilation through the delivery of flow, volume, or pressure
- 2.
Inspiratory trigger (phase trigger variable), or the determinant of when the ventilator starts to deliver flow, volume, and pressure ,
- 3.
Cycle-off criterion (phase cycling variable), or the determinant of when the ventilator stops assisting inspiratory effort and opens the circuit to allow tidal deflation ,
Features of ventilators, such as blowers and inspiratory, expiratory, and positive end-expiratory pressure valves, influence the interaction between patient and ventilator.
To unload the respiratory muscles, restore adequate gas exchange, and relieve the patient from dyspnea, the clinician has two options: (1) total ventilator-controlled mechanical support or (2) partially patient-controlled support.
Total ventilator-controlled mechanical support
In this mode, flow, volume, and pressure are imposed by the ventilator, which thus totally replaces the patient’s breathing pattern. Any pressure generated by the respiratory muscles is silenced or ineffectual. Although this passive condition can be achieved in some conscious patients (i.e., patients with neuromuscular diseases), it usually requires sedation and/or paralysis. The risk of patient-ventilator asynchrony is abolished, but there are potential risks associated with sedation and paralysis, including respiratory muscle atrophy, lung damage caused by overdistention, patient discomfort, retention of airway secretions, and difficulty weaning after prolonged controlled mechanical ventilation.
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