Patient-ventilator asynchrony results from an imbalance between a patient’s respiratory drive and the output from the mechanical ventilator.
Patient-ventilator asynchrony is associated with poor patient outcomes including mortality. Postulated mechanisms include excessive work of breathing and lung overdistension.
Ventilator waveform analysis is a no-cost and easily employed method to detect patient-ventilator asynchrony and monitor the effectiveness of strategies to mitigate asynchronies.
Attempts to normalize arterial blood gas values often increase patient-ventilator asynchrony.
Increases in set minute ventilation—ventilator overdrive—decrease respiratory drive and improve synchrony, often with low but acceptable PaCO2.
Mechanical ventilation is a crucial intervention for critically ill patients with respiratory failure. Controlled ventilation delivers breaths of set volumes or pressures and does not allow for variation due to patient efforts, potentially leading to disuse atrophy of respiratory muscles and myriad adverse effects of excessive sedation. Support or assist modes allow patient efforts to affect ventilation and are more commonly used. Advantages of support modes include preservation of respiratory muscle function and decreased need for sedation and paralysis. However, even with the use of support modes, the ventilator flows and timing may not be matched to those dictated by the patient’s respiratory drive. Patient-ventilator asynchrony, or a mismatch between ventilator output and patient respiratory drive, risks increased energy expenditure, respiratory muscle fatigue and injury, and lung overdistension, leading to lung injury. Accordingly, critical care clinicians must be skilled at recognizing asynchrony, elucidating its underlying causes, and implementing strategies to reduce asynchrony.
CAUSES OF PATIENT-VENTILATOR ASYNCHRONY
Determinants of Respiratory Drive in Critical Illness
A patient’s respiratory drive is one-half of the balance necessary for synchrony. While the determinants of respiratory drive are quite complex,1 an understanding of how critical illness affects respiratory drive is vital to the success of mechanical ventilation. The respiratory center within the brainstem receives inputs from numerous sources in response to chemical, mechanical, and brain cortical functions (see Fig. 49-1). The arterial partial pressure of carbon dioxide, PaCO2, and subsequent pH, are perhaps the most recognized mediators of respiratory drive. Critical illnesses that increase metabolic rates increase CO2 production, and thus increase respiratory requirements to maintain eucapnia and a neutral pH. Indeed, increasing PaCO2 leads to increasing respiratory effort by the patient,2 while decreasing PaCO2 decreases ventilation.3,4 Similarly, albeit to a lesser degree, both hypoxemia and hyperoxia affect respiratory drive through inputs from carotid bodies.5,6 Critical illness often augments the hyperventilatory responses to changes in blood gases.6 However, most critically ill patients possess a heightened respiratory drive despite normalization of blood gases. Decreased lung compliance and lung protective (low tidal volume) ventilation activate thoracic stretch receptors that stimulate the respiratory center, as do airway irritation receptors that are stimulated by endotracheal tubes and airway secretions. Inflammation, present to some degree ...