Introduction
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Noninvasive ventilation (NIV) has recently emerged as a fundamental treatment for patients with acute exacerbation of obstructive lung disease or cardiogenic pulmonary edema, often avoiding intubation. However, some patients have difficulty tolerating this therapy due to anxiety. Dexmedetomidine (PRECEDEX) is an attractive sedative to manage this problem, since it may be titrated and doesn’t suppress respiratory drive.
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I've seen good results with the use of dexmedetomidine to facilitate NIV in patients with obstructive airway disease (asthma and COPD). There are some patients with obstructive physiology who seem to slip into a vicious cycle of anxiety, dyspnea, tachypnea, and autoPEEP (figure below). Intubated patients with severe asthma or COPD typically require lower respiratory rates in order to have adequate expiratory time and avoid autoPEEP. This concept is also true with non-intubated patients. By decreasing anxiety and respiratory rate, dexmedetomidine may reduce autoPEEP and work of breathing. Some patients with airway obstruction improve dramatically when treated with a combination of dexmedetomidine and NIV, with immediate anxiolysis, decreased respiratory rate, and reduced dyspnea. Dexmedetomidine causes bronchodilation in animal models, an effect of unclear significance in humans which could contribute as well.
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I must admit that I don’t have any experience using dexmedetomidine for acute cardiogenic pulmonary edema. Such patients often respond rapidly to aggressive afterload reduction with nitroglycerine infusion, so there may be less of a requirement for NIV if not well tolerated. Nonetheless, anxiety and sympathetic activation do play a role in the physiology of flash pulmonary edema, so dexmedetomidine could be uniquely helpful here as well (given both anxiolytic and sympatholytic activity).
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Prior randomized controlled trials of dexmedetomidine & noninvasive ventilation
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Senoglu 2010 performed a trial of 40 patients with COPD exacerbation and difficulty tolerating NIV who were randomized to midazolam (0.05 mg/kg loading dose followed by 0.1 mg/kg/hr infusion) or dexmedetomidine (1 ug/kg loading dose followed by 0.5 ug/kg/hr infusion). Outcomes were fairly similar between groups with equivalent blood gas results. In the midazolam group two patients were unable to be adequately sedated and one patient was oversedated, problems not encountered in the dexmedetomidine group. Fewer dose-adjustments were required to titrate the dexmedetomidine to target effect.
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Huang 2012 performed a trial of 62 patients with acute cardiogenic pulmonary edema and difficulty tolerating NIV randomized to midazolam (optional loading dose of up to 0.05 mg/kg followed by infusion starting at 0.05-0.1 mg/kg/hr) or dexmedetomidine (optional loading dose of up to 1 ug/kg followed by infusion starting at 0.2-0.7 ug/kg/hr). Patients in the dexmedetomidine group were significantly less likely to require mechanical ventilation (21% vs 45%) and had reduced ICU length of stay (averaging 5 vs. 9 days). The risk of vomiting and pulmonary infection were both significantly lower in the dexmedetomidine group. The dexmedetomidine group did have higher rates of bradycardia but no patient required intervention or interruption of the study drug.
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Devlin et al. study in June issue of CHEST
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Unlike the above studies that investigated the use of dexmedetomidine only for patients unable to tolerate NIV, Delvin et al. studied the use of early routinedexmedetomidine for all patients on NIV. The study involved a total of 33 patients, most of whom had respiratory failure due to pneumonia (55%), followed by COPD/asthma (30%), and pulmonary edema (9%). All patients received divided doses of midazolam as needed for sedation, fentanyl as needed for pain, and haloperidol as needed for delirium. Patients in the dexmedetomidine group additionally received a dexmedetomidine infusion started at 0.2 ug/kg/hr and titrated up by 0.1 ug/kg/hr every 30 minutes as needed to a maximal dose of 0.7 ug/kg/hr.
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The results? Dexmedetomidine was not associated with greater likelihood of tolerating NIV. Dexmedetomidine did increase the number of episodes of deep sedation (25% vs 0%, p = 0.04).
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There are many possible reasons that this was a negative study aside from the low sample size. Prior studies used dexmedetomidine as the sole sedative, whereas this study combined it with several other medications. Dexmedetomidine was started at a low dose and titrated up very gradually without an initial loading dose. Given that most patients remained at a low dose of dexmedetomidine (average dose 0.22 ug/kg/hr) and that there was no difference in as-needed midazolam or fentanyl consumption between the groups, many patients were likely on subtherapeutic doses of dexmedetomidine.
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The greater number of episodes of deep sedation in the dexmedetomidine group is concerning. This could reflect the synergistic combination of dexmedetomidine with other agents.
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Conclusions
- Although literature is sparse, there is evidence supporting dexmedetomidine for patients unable to tolerate NIV, especially among patients with cardiogenic pulmonary edema. It appears to have a good safety profile when used as the sole sedative agent.
- Devlin et al. argues against the routine use of dexmedetomidine among all patients on NIV, although this study has limitations.
- Until more is known about dexmedetomidine-facilitated NIV, these patients should probably receive close ICU-level monitoring with the capability to immediately intubate if needed. Additionally, it may be sensible to reserve dexmedetomidine for situations where NIV is likely to have substantial benefit (i.e., obstructive lung disease and cardiogenic pulmonary edema).
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Any exp outside the icu or ED with this patient population? My institution req icu for dex. Any exp with ketamine for same scenario?