Troubleshooting Severe Airflow Obstruction With a Pressure-Limited Transport Ventilator: Lessons From Two Cases

Abstract

Presentations of status asthmaticus or severe chronic obstructive pulmonary disease exacerbation can present a formidable challenge to effective invasive ventilation. The optimal ventilation strategy targets low respiratory rates and high inspiratory flow rates to prolong the expiratory time and minimize dynamic hyperinflation. Although the resulting high peak pressures can usually be accommodated by ICU ventilators, some ventilators have a relatively limited peak pressure capacity as determined by the turbine. Here, we describe two cases of severe airflow obstruction where the desired ventilation strategy required a peak pressure over the capacity of the Hamilton T1 transport ventilator. Changing to a pressure regulated strategy, maximizing the driving pressure, and titrating the inspiratory time overcame the limitation. But, this strategy comes at a cost. Clinicians should be made aware of the possibility of a pressure limitation in their ventilator and understand how to adjust their ventilation strategy appropriately during transitions.

KEY POINTS

Question: How do you manage severe airflow obstruction when the desired inspiratory pressure surpasses the ventilator’s capacity?

Findings: When working within a pressure-limited context, this case series outlines an approach of using a pressure regulated mode, maximizing driving pressure, and titrating the inspiratory time to achieve desired volumes while preserving expiratory time. Increased intrinsic positive end-expiratory pressure is a potential drawback to this approach and further decreases in respiratory rate may be needed to provide an adequate expiratory time.

Meaning: Clinicians should be aware of a possible pressure limitation with their ventilator, particularly with transport ventilators, and be prepared to adapt their ventilation strategy appropriately.

Severe airflow obstruction, dynamic hyperinflation, and intrinsic positive end-expiratory pressure (PEEPi) are the hallmarks of life-threatening chronic obstructive pulmonary disease (COPD) and status asthmaticus presentations. The ventilation strategy for these patients requires a specialized approach, utilizing low respiratory rates (RRs) and high inspiratory flow rates to prolong the expiratory time (Te) and minimize gas trapping (1). Conversely, the shortened inspiratory time (Ti), along with increases in airway resistance, result in higher peak pressures (Ppeak) (2). Although the Ppeak required to ventilate across high airway resistance can be easily accommodated by most ICU ventilators, some ventilators may have a relatively limited Ppeak capacity as determined by the turbine. Here, we describe two cases of severe airflow obstruction where the desired ventilation strategy required a Ppeak over the limit of the Hamilton T1 transport ventilator (Hamilton Medical AG, Bonaduz, Switzerland). Encountering such extreme pressures is a rare event, and transportation of these patients for essential diagnostic imaging or destination therapy requires careful planning. We discuss the ventilator strategy used in these cases, and outline other potential approaches to sustain ventilation in this pressure-limited context. Informed consent was obtained from the patient or substitute decision maker for publication of this report. This case was prepared according to the CAse REporting guidelines for consensus-based clinical case reporting.

Case 1 is a 23-year-old female who presented to the emergency department with status asthmaticus. Bronchodilators, magnesium sulfate, and steroids were given with minimal effect. Her treatment was escalated with IV epinephrine. Despite trials of high-flow nasal oxygen and noninvasive ventilation, she experienced progressive dyspnea and worsening hypercapnic acidosis (pH 7.19, Co₂ 57 mm Hg, bicarbonate [Hco₃] 22 mmol/L). She was intubated using ketamine and rocuronium.

Her arterial blood gas post intubation showed worsening hypercapnic respiratory failure (pH 7.07, Co₂ 71 mm Hg, Hco₃ 20 mmol/L). Ventilator settings were volume-control ventilation with a tidal volume (Vt) of 300 mL (6.5 mL/kg), PEEP 0 cm H₂O, Fio₂ 40%, RR 12, and an inspiratory flow rate of 80 L/min, which resulted in an inspiratory to expiratory ratio (I:E) of approximately 1:4 to 5. These settings resulted in a Ppeak of 89 cm H₂O, plateau pressure (Pplat) of 17 cm H₂O, and oxygen saturation of 94%. An end-expiratory hold revealed a PEEPi of 10 cm H₂O.

The ventilator was disconnected and manual pressure was applied intermittently. She was deeply sedated with neuromuscular blockade. Intravenous ketamine, salbutamol, and epinephrine infusions were initiated. Ppeak improved to 65–70 cm H₂O with Pplat remaining at 17 cm H₂O for the same volume. The endotracheal tube position was confirmed with chest radiograph, there was no pneumothorax, and a suction catheter was noted to pass easily. Given the refractory nature of her status asthmaticus, she was accepted to the off-site regional extracorporeal membrane oxygenation (ECMO) service.

On arrival, the critical care transport service attempted to switch the patient over to the Hamilton T1 transport ventilator on the aforementioned settings. The volumes achieved were only 100–110 mL despite maximizing the pressure limit to 60 cm H₂O. The patient was then switched to pressure-control ventilation with the inspiratory pressure set to 60 cm H₂O and PEEP to 0 cm H₂O to maximize the driving pressure. The Ti was then adjusted to match the prior Vt. With a Ti of 0.5 seconds, 100–110 mL was achieved (Fig. 1, point A). Lengthening Ti to 0.8 seconds (I:E of 1:5.25) resulted in a Vt of 300 mL at a RR of 12 (Fig. 1, point B). The patient was then able to tolerate the 60 minutes ambulance journey to the ECMO center, although disconnection and manual decompression was performed four times for rising end-tidal carbon dioxide (ETco₂) levels accompanied by falling Vt presumed to be due to gas trapping. Of note, end-tidal waveform capnography was used to titrate the compressions to effect. The average pre-compression ETco₂ was 95–100 mm Hg, and after 60–90 seconds of compression, was down to 40–45 mm Hg. On arrival at the ECMO center, she had clinically improved. She did not require cannulation and was eventually repatriated to her presenting hospital on post-admission day 6. She was extubated the same day, and then discharged home in stable condition on post-admission day 10.

Figure 1.

Expiratory time (Te; y-axis) vs. inspiratory to expiratory (I:E) ratio (x-axis, reversed so that the highest I:E ratios are on the left) for various respiratory rates (RRs). Time points from case 1 are shown with an inspiratory time (Ti) of 0.5 s (point A) and Ti 0.8 s (point B). Notice that the increase in Ti and I:E ratio causes only a small decrease in Te. Notice also that, within physiologic ranges commonly used in mechanical ventilation, the RR has the largest effect on Te. An increase in RR of 60% (from 12 to 20, analogous to our Ti increase of 60% from 0.5 to 0.8) would decrease Te by the same proportion. We have also included the equation relating Te to RR and I:E ratio overlayed on the plot.

Case 2 was a 61-year-old female who presented with a severe COPD exacerbation. She had known COPD (with possible asthma overlap) and frequent admissions over the past year including prior intubation. She received bronchodilators, steroids and a trial of noninvasive ventilation, but failed due to increased work of breathing and worsening blood gas measurements (pH 7.15, Pco₂ 92 mm Hg, Hco₃ 33 mmol/L). She was intubated with ketamine and rocuronium and had manual compression applied before being invasively ventilated with the following settings: volume-control ventilation 400 mL (9 cc/kg), Fio₂ 30%, PEEP 0 cm H₂O, RR 8, and I:E approximately 1:9. On these settings, she demonstrated a Ppeak of 65–70 cm H₂O, Pplat of 24 cm H₂O, and PEEPi of 8 cm H₂O. When the RR was increased to 12 to assess respiratory mechanics, her PEEPi was 11–12 cm H₂O. The rate was then decreased back to eight. Chest radiograph confirmed endotracheal tube position without evidence of pneumothorax. The suction catheter was noted to pass easily.

A CT scan of the head was requested. However, on switching to the Hamilton T1 for transport on the aforementioned settings, volumes fell substantially to less than 100 mL. The patient was then switched to pressure-control ventilation, with an inspiratory pressure of 60 cm H₂O and PEEP 0 cm H₂O. The Ti was then increased until the prior Vt was achieved. The patient was then transported safely to the CT scanner and back without complication. Although the CT was unremarkable, she experienced a prolonged admission in the ICU. Her stay was complicated by failure to wean from mechanical ventilation, ventilator associated pneumonia, invasive aspergillosis, and end-stage renal disease requiring dialysis. She died approximately 3 weeks after her initial presentation.

We describe two cases of severe airflow obstruction where the Ppeak required to deliver Vt at the desired rate were above the manufacturer’s limit for the Hamilton T1 ventilator. To our knowledge, the specific approach to ventilation in this context has not been previously discussed in the literature. Changing to a pressure regulated strategy, maximizing the driving pressure, and increasing Ti to achieve desired volumes can overcome this limitation. Small incremental changes on Ti will have a relatively low impact on Te if the respiratory cycle is of adequate length (Fig. 1). Increased PEEPi is a potential downside of this strategy. In cases where PEEPi is worsening by these changes, RR should be further decreased to increase Te through lengthening the entire respiratory cycle. This could have been attempted in case 1. It must be emphasized that decreasing the RR has a proportionally greater impact on Te, and unresolved worsening PEEPi will progressively diminish the limited driving pressure available for lung inflation in pressure-limited ventilation.

The Hamilton T1 is a commonly used transport ventilator worldwide (3), and this limitation may extend to other transport ventilators. We encourage education and simulation of these challenging case scenarios. Clinicians should be made aware of the possibility of pressure limitation in transport ventilators to adjust their ventilation strategy appropriately during transitions.