Airborne Management of Acute Aortic Syndromes: Emerging Evidence for Antiemetic Use in Prehospital Care

Acute aortic syndromes (AASs), (eg acute aortic dissection, intramural hematoma, represent some of the most time-critical cardiovascular emergencies. Rapid transfer to an aortic center is essential to reduce mortality, particularly for Stanford Type A dissection, in which hourly mortality may increase by 1%–2% without surgical intervention. However, patients transported by a helicopter are exposed to physiological stressors that may worsen hemodynamic instability or precipitate complications. Among these, nausea and vomiting, common in air transport, pose a unique concern in individuals with fragile aortic pathology. Despite this risk, the role of antiemetic therapy in AAS transport remains poorly characterized in the literature, though emerging observational data provide an important starting point. A recent retrospective study by Muramatsu et al. examined 105 patients with acute aortic dissection transported by a physician-staffed helicopter over a 10-year period in Japan. Notably, 81.9% of patients received antiemetic medication during flight, making antiemetics one of the most frequently administered drug classes alongside analgesics and antihypertensives. Importantly, the authors reported no episodes of in-flight cardiac arrest, no cases of hemodynamic collapse, and an overall improvement in systolic blood pressure upon arrival when compared to departure.[1] Although the primary objective of the study was not to evaluate antiemetic efficacy, the absence of adverse outcomes provides preliminary reassurance regarding the safety of these agents in the context of prehospital aortic care. The pathophysiological rationale for antiemetic use in this population is important to understand. Vomiting leads to transient surges in intrathoracic and arterial pressure, which may theoretically exacerbate aortic wall stress or propagate dissection. In addition, uncontrolled nausea can worsen patient agitation and sympathetic activation, both undesirable in AAS, where blood pressure and heart rate control are critical therapeutic aims. Thus, preventive antiemetic therapy may contribute to stability during transport by reducing retching-associated hemodynamic fluctuations and by promoting patient comfort and cooperation. Evidence from other prehospital cohorts supports the potential benefit of antiemetic administration during transport. Suzuki et al., studying physician-staffed helicopter transport for seizure patients, observed that antiemetic use was associated with reduced need for endotracheal intubation and better neurological performance at hospital arrival, although mortality remained unchanged.[2] Although not directly related to aortic disease, this study highlights that antiemetics may mitigate secondary insults during flight by reducing vomiting-related aspiration risk or airway complications. Notably, the overall survival benefit of helicopter transport for AAS remains debated. A multicenter analysis comparing HEMS and ground transport for Stanford Type A dissection demonstrated no significant difference in mortality despite the expected time advantage of air transfer.[3] This finding underscores that transport mode alone does not determine outcomes; rather, the quality of care delivered during transit, including blood pressure control, analgesia, sedation, and potentially antiemetic therapy, may influence clinical trajectory. A recent study by Yanagawa et al. concluded that in patients, aortic disease prehospital administration of antiemetic agents was associated with lower heart rate, reduced need for tracheal intubation, and higher systolic blood pressure.[4] Within this framework, antiemetic therapy emerges as a small but potentially meaningful component of a larger stabilization strategy. Nevertheless, several limitations in current evidence must be acknowledged. First, no randomized or prospective studies have isolated the effect of antiemetic drugs on outcomes in aortic transport. The heavy reliance on retrospective data limits causal inference. Second, antiemetic administration was nearly universal in the Muramatsu study cohort, which precludes meaningful comparison between treated and untreated groups. Third, important clinical variables, such as severity of baseline nausea, choice of antiemetic agent, dosing strategies, and flight environmental factors, were not standardized or controlled. Finally, potential adverse effects of antiemetics, particularly QT-prolonging agents or those causing sedation or hypotension, have not been rigorously evaluated in this high-risk cardiovascular population. Given these gaps, there is a clear need for structured prospective research to evaluate antiemetic therapy in the prehospital management of AAS. Key areas include observational registries with detailed recording of antiemetic use, hemodynamic parameters, vomiting episodes, and transit complications. Other priority areas include outcomes in patients receiving versus not receiving antiemetic prophylaxis, type of aortic pathology, comorbidities, and transport conditions. Ultimately, well-designed studies could inform development of standardized HEMS protocols specifying agent selection (e.g., ondansetron vs. metoclopramide vs. droperidol), dosing intervals, monitoring requirements, and indications for prophylactic versus symptomatic administration. Incorporating evidence-based antiemetic therapy into transport protocols may help reduce physiological stress, minimize complications, and improve readiness for definitive intervention upon arrival. While current data suggest that antiemetic use is safe and potentially beneficial, rigorous scientific evaluation is needed before it can be formally recommended as a standard component of prehospital aortic care. In the interim, clinicians should continue to apply judicious clinical judgment, balancing patient comfort, hemodynamic goals, and drug risk profiles when managing nausea in high-risk aortic patients during helicopter transport.