There are three main forms of interaction between the patient and the ventilator: Asynchrony related to breath initiation and phase duration (i.e. trigger asynchrony, phase asynchrony), and mismatching related to ventilator settings of inspiratory flow and/or tidal volume.
Trigger asynchrony occurs when the patient attempts to trigger a breath but is unable to, either because of inspiratory muscle weakness, inappropriate trigger sensitivity set on the ventilator or dynamic hyperinflation (auto-PEEP or intrinsic PEEP). Phase “cycle” asynchrony occurs when the inspiratory phase of the ventilator-delivered breath does not match the patient’s neural impulse for ventilation (respiratory rate or inspiratory time). To initiate a breath the patient’s respiratory effort must exceed a threshold (trigger) set in the machine. When this fails to happen this can be due to three factors:
- Inspiratory muscle insufficiency
- Inappropriate trigger sensitivity set on the ventilator
- The presence of “intrinsic PEEP” (also known as “auto-PEEP” or dynamic hyperinflation)
- In VCV mode, trigger asynchrony without dynamic hyperinflation is shown by breath c below, indicated by a patient respiratory effort unrelated to the mandatory breath. (Breath a is a “passive” time cycled controlled breath, breath b is a synchronous patient-triggered “assisted” breath)
- Trigger asynchrony with dynamic hyperinflation is shown with breath d, where flow has not returned to zero prior to patient respiratory effort
- First ask: Does expiratory flow reach zero before a failed trigger attempt occurs?
- If yes: increase trigger sensitivity setting (typical settings are 1–2 cmH2O below set PEEP for pressure triggered breaths or 2–5 L/min for flow triggered breaths).
- If trigger settings are appropriate, investigate possible neuromuscular sources.
- If no: suspect air-trapping from two possible sources: 1) primary dynamic hyperinflation, or 2) prolonged expiration due to advanced primary airways disease (evidenced by prolonged expiratory phase, I:E ratio of ~1:4). To distinguish between these, observe the expiratory flow waveforms:
- Primary dynamic hyperinflation is identified by a relatively high peak expiratory flow interrupted by the subsequent inspiration before reaching zero (Fig. 1, Breath d).
- To treat primary dynamic hyperinflation: 1) lower MV demand when possible (e.g. control of fever, pain and anxiety), 2) decrease inspiratory time (0.7–0.85 sec), and/or 3) decrease RR slowly to the point when each patient effort results in a triggered breath. Prevent undetected hypoventilation by keeping the set rate ~2 breaths below the patient’s spontaneous RR.
- Advanced primary airways disease is identified by a relatively blunted peak expiratory flow that quickly falls to near-zero and continues at a very low steady rate until interrupted by the subsequent inspiration (see figure below with (a) denoting prolonged expiration with continuous low expiratory flow and (b) denoting ineffective efforts manifesting as corresponding “divots” in both Paw and expiratory flow waveforms).
- To treat severe primary airways disease: 1) target inspiratory time <1 sec, RR <10, and I:E ratio ~1:4, and/or 2) carefully increase external PEEP (not to exceed 10 cmH2O) to approximate intrinsic PEEP. If intrinsic PEEP cannot be readily measured, then a simple technique is to slowly increase external PEEP until patient efforts are “captured” by the ventilator (or the advised safety limit of 10 cmH2O is reached).Note: do not use external PEEP strategy in severe bronchoconstriction or obstruction (i.e. status asthmaticus).
Phase “cycle” asynchrony occurs when the inspiratory phase of the ventilator does not match the patient’s neural impulse for inspiration, such as when:
- The set RR exceeds the spontaneous rate (without suppressing respiratory drive)
- The set inspiratory time is either too long or too brief
Phase “cycle” asynchrony can be detected by the following (in VCV mode, where constant flow (Breaths a–e) or decelerating flow pattern (Breaths f & g) are used. Breaths a & f demonstrate “passive,” time-cycled controlled breaths in each flow pattern.):
- Premature termination of breath (Breath b) by pressure spikes during patient expiration due to respiratory rate mismatch. Note: other common sources are when patients tense their chest wall (“bearing down,” coughing), biting the endotracheal tube or tube occlusion from secretions)
- Pressure spikes near end of inspiration (Breaths c & g) or during end-inspiratory pause (Breath d) generated by patient expiration if set inspiratory time is too long
- Inspiratory effort during an end-inspiratory pause (Breath e) due to tachypnea.
- Scenarios depicted by Breaths d & e above can lead to erroneous measurements of Pplat and compliance.
Phase “cycle” asynchrony can cause the following two triggering patterns:
- “Double triggering” especially when set inspiratory time ≤0.6 sec (see below)
- “Reverse triggering” when mandatory breaths trigger inspiratory efforts denoted by Paw spikes and esophageal pressure (Pes) drops.
- Treat underlying conditions (e.g. sedation, analgesia, antipyretics, and buffering)
- If tachypneic, set RR 1 breath above spontaneous RR which may reduce dyspnea
- If minute ventilation >12 L/min, decrease inspiratory time to 0.7–0.85 sec
- If double triggering, decrease “expiratory flow trigger” to lengthen inspiratory time (only a feature of pressure support mode: standard setting of 25% should eliminate the problem)
- If reverse triggering, briefly trial reducing RR to attempt “re-synchronization”
Flow mismatching occurs in 3 conditions:
- When the peak inspiratory flow rate is below patient peak flow.
- Transient flow discrepancies between ventilator and patient flow pattern.
- When the set flow rate greatly exceeds patient flow demand.
Flow mismatching is indicated by convex or concave inspiratory Paw waveforms:
- Ventilator flow exceeding patient’s flow demand (Breath b) (ie.minimal patient work of breathing)
- Patient’s flow demand exceeding delivered flow (Breath c)
- Inspiratory effort involving active recruitment of the abdominal muscles (evidenced by abdominal wall contractions) which creates a pressure spike. (Breath d)
Uptitrate inspiratory flow until concavity disappears (breath b represents ideal).
Tidal volume mismatching occurs when ventilator VT < patient VT and is most commonly encountered during lung-protective ventilation. It also may occur as a patient undergoes changes in activity/metabolism and/or response to pain, discomfort, regardless of ventilation strategy.
VT mismatching frequently coincides with or causes asynchrony and/or flow mismatching. Prominent features in VCV mode include:
- Low Ppeak and/or a sawtooth Paw waveform (Breath a).
- Spontaneous flow and VT waveforms (red dash lines) illustrate points where VT mismatching coincides with either the absence of ventilator inspiratory flow (Breath a) or mismatching flow pattern at specific points during inspiration(Breath b).
- Reverse triggering and double triggering can arise from VT mismatching due to failure of circuit pressurization during inspiration (see above).
To treat VT mismatching in VCV mode, increase the set VT to match demand. Treating VT mismatching is an “either/or” situation. Matching VT demand in VCV may exceed lung-protective targets and changing to pressure control or pressure support presents the same problem. Because the only other alternative is sedation or perhaps neuromuscular blockade, clinicians must balance competing issues to find a balance. Assessing the causes as either “transient” (e.g. undertreated pain, fever, breathlessness following suctioning or other procedures) or “sustained” (e.g. maximizing lung-protection during the acute phase of illness when gas exchange and hemodynamic instability are prominent problems) should guide treatment.