Patient-Ventilator Dyssynchrony: Clinical Significance and Implications for Practice
Year: 2009
Type: article
Abstract: Nurses continue to face the challenge of preventing the consequences of patient-ventilator dyssynchrony, which is common yet underappreciated in critically ill patients.The cost of providing care to critically ill patients in the United States consumes roughly 15% of all health care dollars, or 1% of the gross national product.1 Contributing to this economic burden are patients admitted to the intensive care unit (ICU) who require mechanical ventilation and patients with complications from their dependence on this technology.2,3 In fact, 50% of ICU patients receive mechanical ventilation.4Often, sedation is required to increase patients’ tolerance of the endotracheal tube, reduce anxiety, and facilitate sleep. In particular, sedation is used frequently to reduce patient-ventilator dyssynchrony (PVD).5–9 Sassoon and Foster10 define PVD as a mismatching between the patient’s breaths (neural) and ventilator-assisted breaths (phase asynchrony), as well as the inability of the ventilator’s flow delivery to match the patient’s flow demand (flow asynchrony). This definition suggests a faulty interaction between the patient and ventilator that is commonly managed by sedation and advanced ventilator modes and adjustments. The correction of PVD is complex and multifaceted given the current capabilities of traditional ventilators. An imperfect solution exists because the sensitivity and responsiveness of both the patient and the ventilator during the interaction is confounded by factors related to the patient and the ventilator. However, in light of the most serious complications (hypoxemia, barotrauma, prolonged mechanical ventilation, and discomfort) of PVD, and an imperfect solution for the resolution of PVD at the current time, nurses continue to face the challenge of preventing the consequences of PVD as well as complications due to oversedation or undersedation.In this article, we discuss the factors contributing to PVD; the manifestations, measurement, types, and causes of PVD; nursing implications; and future directions for improvement, with nursing research questions proposed for consideration.Patient-ventilator interaction is influenced by factors related to the patient (respiratory center output, respiratory system mechanisms, disease states and conditions, artificial airway) and factors related to the ventilator (ventilator triggering, ventilator cycling off ).Achieving patient-ventilator synchrony during interactive modes of ventilation (assist control [AC] and synchronized intermittent mandatory ventilation [SIMV]) is a daunting task because patients’ ventilation is controlled by mechanical, chemical, behavioral, and reflex mechanisms that are highly dynamic. These factors can disrupt the patient-ventilator interface because the ventilator responds to the patient’s inspiratory and expiratory signals, which affect pressure and flow in the ventilator circuit.11 Given patients’ dynamic conditions during critical illness, patient-related factors such as respiratory center output, respiratory mechanics, disease states or conditions, and endotracheal tube type or size influence the patient-ventilator interaction (Table 1).The patient’s respiratory center output can produce a decreased or increased drive that may contribute to the development of PVD. Respiratory drive is dependent on both voluntary and autonomic control. Voluntary control is operationalized through the cerebral cortex (forceful inspiration/expiration, breath holding) and thalamus (emotional behaviors associated with intense feelings, fear, pain, anger, sorrow).21 Autonomic control is operationalized by the brainstem, with the pneumotaxic and apneustic respiratory centers in the pons and 2 neuronal groups, called the dorsal (inspiratory) and ventral (inspiratory/expiratory) respiratory groups, located in the medulla.21 Afferent neurotransmissions from the body are communicated to the medullary neuronal groups from multiple receptors throughout the body. Table 2 describes these receptors specifically and their influence on the autonomic control of respiratory drive. Once the medulla receives impulses, the inspiratory and expiratory centers respond by determining whether inspiration or expiration should be stimulated or inhibited. The pneumotaxic center of the pons fine-tunes the rhythmicity of the ventilatory drive, and the efferent message is sent to the phrenic and intercostal nerves to stimulate or inhibit ventilation.21If respiratory drive is decreased, the ventilator may not be able to respond to the reduced effort, especially if the clinician does not preset the ventilator’s sensitivity at a level that will detect the patient’s effort.10 A reduced drive can be caused by sedatives, opioids, and hypnotics. Sedatives, opioids, and sleep all increase the time delay between the start of the patient’s inspiratory effort and ventilator triggering.20 Metabolic states of alkalosis, sleep deprivation, severe hypothyroidism, and bilateral injury of the mid to lower medulla can decrease respiratory drive, thereby influencing the patient-ventilator interaction.12If a patient’s respiratory drive increases vigorously, however, the duration of inspiratory drive may become longer than ventilator inflation time, causing the ventilator to trigger more than once (double trigger).20 An increased respiratory drive can cause the patient to need more flow from the ventilator.12 If the preset flow does not meet patient demand, flow dyssynchrony can occur. An increased respiratory output can be caused by increased chemoreceptor stimulation, pain, psychogenic alteration, medications, and increased ventilatory demand, metabolic rate, and workload.A patient’s respiratory mechanics can contribute to dyssynchrony. The patient may have a prolonged inspiratory time. If inspiratory time is longer than the ventilator’s preset inspiratory time, the patient may take an additional breath because the need for ventilation has not been met, thereby causing double triggering.10On the other hand, the patient may have a shortened exhalation time that increases the amount of intrinsic positive pressure at the end of expiration (PEEPi, auto-PEEP) because all volume has not been exhaled. This leads to dynamic hyperinflation causing the patient to breathe with high lung volumes and high elastic recoil pressures.12 The excess pressure on the alveoli at the end of expiration (auto-PEEP) causes increased workload for the patient’s diaphragm. Auto-PEEP is a common cause of failure-to-trigger PVD because the patient must overcome excess auto-PEEP by dropping intrathoracic pressure through muscular effort of sufficient magnitude to be sensed by the ventilator.It is also important to consider the strength of the diaphragm and accessory muscles. Muscular strength may be decreased because of diaphragm deconditioning (prolonged ventilator assistance, physical immobility), malnutrition, and neuromuscular disease. Weakened respiratory muscles reduce the ability to meet the threshold necessary to initiate a ventilated breath during interactive modes.12Patients’ underlying diseases and conditions can lead to PVD. For example, patients with obstructive lung disease or high ventilatory demand and patients receiving inverse-ratio ventilation or airway pressure release ventilation can have dynamic hyperinflation.12 Dynamic hyperinflation moves the diaphragm to a flattened, less domelike configuration, which limits the patient’s ability to generate a forceful inspiration and creates a greater trigger threshold to overcome, leading to failed efforts.12 Pain and splinting from surgical or other sources may reduce a patient’s inspiratory effort and contribute to PVD.14In addition, psychogenic mechanisms from agitation,12 fear, and stress may contribute to PVD because of resulting tachypnea and reduced mental capacity from overriding anxiety. Disease and ventilator-related factors can also agitate patients (Table 1). Agitation in patients who are receiving mechanical ventilation can be exacerbated by many factors, such as disease states (pulmonary edema, pulmonary embolism, pneumothorax), body posture, abdominal distension, retained airway secretions, pain, and bronchospasm.13 Last, the environment can be the source of noxious stimuli such as excessive noise, light, or physical stimulation that may contribute to the patient’s stress response, thereby increasing anxiety and possible agitation.15Finally, the size and type of airway may contribute to PVD.14 An endotracheal tube of inadequate diameter may increase resistance and limit flow for a patient with high ventilatory demand. The internal diameter of the endotracheal tube can be reduced by accumulation of secretions and debris that can markedly increase airway resistance.16 The patient-ventilator interaction is dependent on the patient’s ability to overcome this resistance and the amount of ventilator assistance.12Synchronous patient-ventilator interaction requires a ventilator to be sensitive to respiratory efforts and responsive to airflow demand.11 Two major factors contributing to PVD are ventilator triggering (signal opens inspiratory valve) and cycling (signal opens expiratory valve at end inspiration).11,22The ventilator should ideally respond to a patient’s inspiratory effort immediately. The sensitivity trigger is typically set to be stimulated on the basis of pressure, flow, or time. Unfortunately, in some situations, the sensitivity level may be set too low to sense the patient’s effort. In this situation, the patient’s effort may be wasted and not trigger a breath, which may lead to increased respiratory muscle loading.22,23 A prolongation of the trigger phase may also occur because of errors in the ventilator’s pressure transducer, the ventilator’s delay in sampling pressure signals, the duration of time from onset of diaphragm contraction to actual decrease in airway pressure, the duration of time from decrease of airway pressure to be sensed by the ventilator, and the duration of time from when the valve is signaled to when flow reaches the airway circuit.11 These factors generate phase dyssynchrony.In phase dyssynchrony, a lag (termed delay time) occurs between the time when the ventilator first senses the trigger and the time when the ventilator responds by delivering gas flow.14 When the inspiration trigger is driven by a change in pressure (pressure trigger), the delay time by most commercial ventilators may reach 110 to 120 milliseconds before gas flows into the patient’s circuit.11 If the inspiratory trigger delay becomes too prolonged, the patient may try to increase his inspiratory efforts.11 Therefore to avoid trigger dyssynchrony, it is best for clinicians to set the shortest trigger delay time, which will minimize patients’ efforts to trigger an inspiration in interactive modes.11Traditional ventilators can only measure and respond to patient airway pressures at the airway opening and flow downstream on the expiratory limb of the ventilator circuit.24,25 The greater the distance from the central nervous system’s respiratory center that the ventilator senses the trigger drive, the greater the potential for PVD.11 New, experimental techniques offer different ways and sites to sense and respond to patients’ inspiratory signals. Proportional assist ventilation enhances synchrony by using a feedback mechanism to “amplify airway pressure proportionally to inspiratory flow and volume.”24(p26) This mechanism enables the ventilator to track changes in the patient’s ventilatory effort, thereby resulting in a more physiological breathing pattern.24 Other factors such as air leaks and water in the ventilator tubing can dampen the signal being sent from the patient to the ventilator during this interaction.11Neurally adjusted ventilatory assist senses the diaphragm’s electric stimulation signal through an esophageal probe on the end of a nasogastric tube that sits close to the diaphragm.26 The signal is amplified, filtered, and processed by the ventilator’s software to then generate adjusted ventilation pressures specific to the patient’s initiated diaphragmatic output.27Methods that are used less frequently may also be effective. Pdi-driven servoventilation adjusts ventilated pressure breaths in response to the patient’s transdiaphragmatic pressures (Pdi).27 This ventilator is triggered through the Pdi or a preset flow threshold, whichever is generated first. Inspiration ends when the inspiratory flow reaches a preset threshold.27 Shape-signal or flow-shape triggering28 depends on a distorted expiratory waveform that is generated when the patient initiates a breath in order to sense a patient’s inspiratory trigger. The ventilator algorithm generates a new flow signal that is offset from the patient’s actual flow by 0.25 L/s and delays it for 300 milliseconds, thereby allowing the signal to lag behind the patient’s actual flow rate so that, once the patient initiates a breath, the sudden decrease in expiratory flow will cross the generated shape signal to initiate a ventilated breath.20Cycling off terminates the mechanical breath harmoniously when the patient desires to end inspiration and begin exhalation.20 Moving from inspiration to expiration on the ventilator is operationalized through volume, pressure, flow, or time cycling. To achieve this, clinicians preset ventilator settings of (a) target volumes, (b) peak inspiratory peak flow shape or inspiratory time limit or changes in The settings to synchrony between the end of inspiration and of however, are not of ventilator flow occurs before or the patient inspiratory a mechanical breath is before the patient desires the patient to inspiratory allowing pressure to overcome elastic recoil and resulting in the ability to meet the trigger threshold and initiate a new breath, called double triggering.20 of ventilator flow causes excessive inspiratory muscle into and during the expiratory phase and an of respiratory Nurses should be able to double triggering on the ventilator’s waveform and that double triggering may be a cause of increased respiratory the other hand, if the mechanical breath does not when the patient’s muscular inspiration is the time for exhalation is and expiratory workload and auto-PEEP resulting in possible failed trigger on the causes patients to or ventilator flow by using their expiratory muscles. This resistance in increased expiratory and excessive thereby leading to possible barotrauma, and cerebral the be to a ventilator on the basis of a patient’s inspiratory time. a is not on ventilator, for the ventilator with the of adjusted ventilatory assist by that of in triggering the If triggering occurs during inspiratory muscles will be when be which has caused to muscle and reduced strength in not in muscle injury from triggering may interaction is complex and the interface the of interactive ventilator modes in greater of patients and of respiratory a is PVD. and that ventilators should be sensitive to the patient’s ventilatory effort and responsive to the patient’s a of respiratory cycling and flow of ventilation between the ventilator and the occurs frequently and is a high of dyssynchrony in patients longer than and patients with the most dyssynchrony a longer duration of mechanical of this a amount of PVD, which of The most triggering and double trigger with and patients with obstructive pulmonary disease more of sedation during mechanical ventilation may and influence the of PVD. the of sedation level is not oversedation and are A of such as of sedation or intermittent of and can reduce the of excessive However, the of may PVD as patients become more patients in for the other of the sedation a of patients receiving mechanical ventilation and that the of triggering with lower patients more on the Agitation This suggests that highly patients may reduce their respiratory drive so that become in an inspiratory trigger sufficient to initiate a ventilated synchrony is important for and that patient-ventilator interaction is a major in determining respiratory muscle can be by the and the most occurs when the patient and ventilator are synchrony during interactive ventilator modes requires ventilator sensitivity and responsiveness to the patient’s which is not possible with current ventilators. of patient-ventilator synchrony of decreased of reduced or wasted respiratory and reduced of breaths during In addition, prolonged mechanical ventilation and longer due to sedation may be resulting breathing from PVD can lead to increased workload on respiratory and In addition, that PVD may in respiratory muscle In patients with PVD a longer duration of mechanical ventilation, other have been Other specific and of PVD time are not well or these consequences may an critical and increase ventilator-related nurses should the of patient-ventilator To achieve these nurses must to for PVD, for of PVD such as in Table and possible causes of PVD, and with the to ventilator and to of of dyssynchrony may clinicians to PVD more and and major of PVD that can be the different of a patient’s ventilated breath (Table first phase of a ventilator-assisted breath is The factors that influence this patient factors an respiratory drive and inspiratory and ventilator factors responsiveness to detect the or flow, ability to reach a pressure set trigger delay time, and ability to the To avoid trigger dyssynchrony, these factors must be dyssynchrony is a common of PVD, and can from to trigger to to trigger occurs when the ventilator does not sense the pressure or flow trigger. This is the of a respiratory drive or excessive that the patient’s effort from being sent to the ventilator’s hyperinflation causes a pressure and the patient overcome the trigger the ventilator does not generate flow for the patient’s initiated This occurs in patients with obstructive pulmonary disease or when trigger are not adjusted by triggering is in triggering occurs when the patient is triggering the ventilator through an excess demand for flow or volume that the ventilator is not preset to that lead to this with change in or ventilator the cause of the double triggering is important in order to PVD. If the cause is a situation, such as excessive the ventilator may be for a duration the is If double triggering is nurses should with the to ventilator flow or volume settings to meet the patient’s demand is caused by a ventilator sensitivity level that other than the patient’s of a of that cause in the such as water leaks and from patients with output, and that a low respiratory drive and decreased respiratory rate when hyperinflation is Nurses should for causes of to and with the to the sensitivity level of inspiration is the demand for air dyssynchrony can occur when the ventilator is not set for the patient’s demand. the flow rate is set too low with the patient’s inspiratory demand. of flow dyssynchrony is the of auto-PEEP is when the expiratory flow waveform does not to before the breath and a increase in peak inspiratory pressure is dyssynchrony can occur in ventilated settings of or volume ventilation, the flow is and flow dyssynchrony can be by the of the during breathing and A of the pressure during flow in the of a breath is the end of inspiration and breath it is at this that dyssynchrony can this type of PVD occurs in all ventilator modes because clinicians set the expiratory time on the dynamic and patient’s initiated inspiratory time. and that the most important to consider with this type of PVD is the of time between the patient’s effort and the end of ventilator PVD can be or In the flow of air before the patient In the patient is as the to a the end of expiration is with the patient’s expiratory dyssynchrony can this time, expiration may be shortened or In the of shortened the can be air and a possible inability to reach the trigger threshold that leads to to the other hand, prolonged expiration does not cause for the the patient initiates a breath before the expiratory is expiration may cause patient-ventilator synchrony in critically ill patients is required to and excessive or inadequate to their with nurses and respiratory are the first to that a patient is PVD. may both detect changes in nurses and respiratory may different to the Nurses patients who are the respiratory may be more to PVD by changes in the can be by changes in the volume, pressure, and flow on the ventilator. PVD can be through waveform it is not whether nurses these or whether nurses from waveform in their that clinicians are in and the waveform at the the other hand, nurses may more of physiological and as well as patients’ behaviors in than to PVD. Table the and of patients with dyssynchrony. This the and with of PVD by patients in an to more and this complex forceful of accessory inspiratory intercostal and of accessory muscles in the may all such as and of airway pressures have also been In addition, patients’ behaviors such as or as well as ventilator pressure nurses to PVD. However, these behaviors and physiological of patients have not been as of most used and measure of PVD is the however, by nurses is not in the of of PVD, the of inadequate or excessive sedation may leading to physiological and which may in of of PVD a patient-ventilator synchrony is by the the patient’s ventilatory and is however, that increasing the level of the cause of PVD or ventilator may time receiving mechanical waveform has been for the the is This may be due to in and of a to airway pressures by using a system to the of the ventilator This to the on the ventilator and a of the patient’s pulmonary of dyssynchrony, and respiratory efforts when and are The of is the ability to and these allowing nurses time to and Therefore of and of PVD, the of to detect and sedation is used to the patient-ventilator interaction and reduce dyssynchrony, of PVD is for of However, of PVD have been and of ventilator synchrony has not been in commonly used for such as the the or the which is used to level of and have the need to and that all of sedation are being The of Nurses has called for to and to the of and of in In addition, the of that a sedation end using a sedation be with In a of for the level and of sedation in and ICU that many have been used to measure of sedation in ICU have been for their in change in sedation time and of clinicians sedation have to an of PVD, using of the patient-ventilator used groups of and to PVD to be in their to the sedation however, the have not been for of dyssynchrony, and has not been the to the a for of inspiratory phase of respiratory rate more than and of accessory muscles to ventilator it is not if the of factors is A the a that is on level of and it does a of as a for for the of Nurses has a sedation that the of This from best physiological response from patient-ventilator to dyssynchrony with physiological specific of physiological response are not for sedation are being that of PVD, to measure this of PVD is a for of however, sedation not it in the of sedation level or the proposed measure has not been from an future nursing research is to the of between and respiratory to PVD is a different in patient care and to the a of to the of PVD. Respiratory are in the of ventilator and of patients’ and of airway pressure are in these as well as disease of patients receiving mechanical Nurses are specifically in and to disease and the a in the of patient in the patients’ is that nurses for of which start by PVD. of airway pressure and flow for PVD in patients receiving mechanical ventilation by using airway pressure be a ventilator may consider for of for and of PVD, to the from used for techniques have been used in research to detect and double when these are clinicians and their patients will from the of Table describes to different of PVD, their and nursing for with the health care patients receiving mechanical ventilation to become to the ventilator is and that patients may is Nurses not the of the ventilator affect the of PVD; however, nurses should and with especially when other are in the may need to to patients a breath to assist with PVD the cause is and the critical care environment should be to the of conditions that be for the patient’s during PVD. or may affect the interaction between patient and ventilator. and of PVD will of and reduce duration of mechanical health care is contributing to the of in the of PVD. are with different and and respiratory are to detect PVD and on this are yet nurses have to to the of PVD, through and of rate, respiratory rate, and by using airway pressure to detect dyssynchrony. The is to that can be to detect PVD. questions PVD can be (Table clinicians are to PVD and it will the and of PVD.
Source: Critical Care Nurse
DOI: 10.4037/ccn2009612
Language: English
Subfield: Pulmonary and Respiratory Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2162400573