A structured therapeutic algorithm combining rapid escalation and early de-escalation of antihypertensive treatment helps harmonize practices and shorten hospital stays in acute aortic syndromes.
A structured, three-step protocol for antihypertensive management in acute aortic syndromes provides a pragmatic approach to standardize care and facilitate transition to oral therapy.
Objective: Acute aortic syndromes (AAS) encompass a group of life-threatening emergencies involving the thoracic and/or abdominal aorta, requiring rapid and multidisciplinary management, with mortality reaching 1–2% per hour in the absence of treatment. Poorly controlled hypertension (HTN) is the main risk factor, present in more than 70% of cases. Rapid and effective blood pressure (BP) control is essential to limit disease progression and prevent fatal complications. We present our experience at the Georges Pompidou European Hospital in developing a simple and reproducible decision-making protocol to standardize antihypertensive management in AAS, with the goal of reducing intensive care unit length of stay and optimizing the transition to safe outpatient management. Design and method: A collaborative effort was conducted, involving anesthesiologists, cardiac and vascular surgeons, emergency physicians, pharmacists, and hypertension specialists. The analysis was based on international guidelines (ESC, AHA, ESH), a systematic literature review, and internal data. Key challenges included inconsistent antihypertensive use, delays in treatment escalation, and prolonged ICU stays. These findings led to the development of a stepwise protocol to standardize drug choice, dosing, and monitoring. Results: The protocol is based on a three-step strategy: Acute phase: immediate initiation of an IV beta-blocker (esmolol or labetalol), targeting dual BP (SBP <= 120 mmHg) and heart rate (HR<= 60 bpm) goals. In case of contraindication, a non-dihydropyridine calcium channel blocker (CCB) is proposed. Therapeutic escalation: if targets are not achieved, addition of a rapidly acting and titratable vasodilator (nicardipine, sodium nitroprusside, or urapidil), always after HR control has been achieved, to avoid sympathetic activation. De-escalation phase: gradual transition to oral therapy, favoring beta-blockers, ACE inhibitors/ARBs, and CCB, with individualized adjustment according to hemodynamic tolerance and comorbidities. This user-friendly scheme specifies, for each drug, dosing regimens, dilution procedures, and escalation steps, to guide clinicians’ step by step. Conclusions: Our experience shows that a structured therapeutic algorithm, combining rapid escalation and early de-escalation of treatment, helps harmonize practices, secure the IV-to-oral transition, and shorten hospital stays. In the absence of specific recommendations, this protocol provides a pragmatic and reproducible approach that may improve patient outcomes.
Abdallah et al. (Fri,) conducted a other in Acute aortic syndromes. Structured therapeutic algorithm for antihypertensive management was evaluated. A structured therapeutic algorithm combining rapid escalation and early de-escalation of antihypertensive treatment helps harmonize practices and shorten hospital stays in acute aortic syndromes.