By a News Reporter-Staff News Editor at Journal of Mathematics — According to news reporting originating from Alexandria, Virginia, by VerticalNews journalists, a patent by the inventors Mulqueeny, Qestra Camille (Balmoral, AU); Nava, Stefano (Pavia, IT), filed on October 20, 2005, was published online on December 10, 2013.
The assignee for this patent, patent number 8603006, is ResMed Limited (Bella Vista, AT).
Reporters obtained the following quote from the background information supplied by the inventors: “The invention relates to a method for the determination, and ultimately correction, of patient-ventilator asynchrony, e.g., asynchrony between ventilators that are assistive and are inclusive of patient triggered breaths, including but not limited to PSV, AC, AMV, and bilevel PS, and patients that can protect their airway and show some attempt to spontaneously breathe, including predominantly COPD, restrictive, mixed pathology and in general patients that require ventilatory assistance.
“Problem Description
“Patients with respiratory disorders or illness, and especially those with acute exacerbation, may have insufficient respiratory strength to maintain spontaneous breathing and require mechanical ventilatory assistance. The role and type of chosen ventilator is case specific, and varies in degree of respiratory participation, from Controlled Mechanical Ventilation (CMV) where the patient is completely passive, to forms of assisted ventilation which all share inspiratory effort with the patient after an active trigger of mechanical breath by the patient.
“Forms of assisted ventilation vary by mode, e.g., parameter control (flow/volume/pressure), and amount of introduced assistance to the spontaneous breath, and include but are not limited to: assist control ventilation (AMV), synchronized intermittent mandatory ventilation (SIMV), and Pressure-Support Ventilation (PSV). Therapeutic efficacy is reliant upon synchrony between variable pressure/flow delivery and the patient’s spontaneous respiratory cycle. Crucial to this is the ability of the ventilator to recognize when the patient initiates inspiratory effort (the trigger mechanism), and this is commonly achieved when the patient reaches either a positive flow threshold or minimal pressure threshold. In the case where patients fail to achieve this trigger threshold, patient-ventilator synchrony breaks down and may counteract any intended benefits otherwise seen using a ventilator. Otherwise known as ineffective triggering, this phenomenon has been observed in a variety of pathologies, however is most common in COPD. (‘When receiving high levels of pressure support or assist control ventilation, a quarter to a third of a patient’s inspiratory efforts may fail to trigger the machine.’ Tobin, et al. (Tobin M, Jubran A, Laghi F. Patient-Ventilator Interaction. American Journal of Respiratory and Critical Care Medicine. 163: 1059-1063, 2001.)).
“A major cause of this asynchrony is expiratory flow limitation, dynamic hyperinflation of the lungs and concomitant intrinsic PEEP. Dynamic hyperinflation can result from either gas trapping behind closed airways, mismatching of mechanical vs. neural expiration, or a combination of the above. This has been well studied in COPD and to a lesser degree in other pathologies, however it has been observed in a variety of patients. The mechanisms follow: 1) Obstruction to the airway in COPD is caused by pathological effects such as airway secretions, bronchospasm, and mucosal edema. In all cases airflow resistance increases, and forces muscle recruitment to aid expiration resulting in dynamic compression of the airways. 2) In the case of emphysema also, respiratory system compliance may increase. The rate of lung emptying becomes impeded and the normal expiratory duty cycle time available (as determined by respiratory negative feedback control) is insufficient for complete mechanical expiration to occur. 3) In restrictive patients breathing occurs at low lung volumes and so promotes airway closure and gas trapping, especially if respiratory rate is high. In all cases, the end-expiratory lung volume (EELV) is not allowed to return to the elastic equilibrium volume of the respiratory system, and extraneous gas is trapped within the lung, namely dynamic hyperinflation.