Authors: Mugleton E et al.
Source: Anesthesiology, 2026, Letter to the Editor
Summary:
This commentary challenges the assumption that hemodynamic stability can serve as a surrogate for anesthetic depth and critiques overreliance on minimum alveolar concentration (MAC)–based frameworks when interpreting anesthetic adequacy. The author responds to prior work examining factors influencing MAC ratios, arguing that cardiovascular measurements alone fail to reflect the true central nervous system effects of anesthesia.
The letter emphasizes that anesthetic depth is fundamentally a brain-based phenomenon and that hemodynamic variables primarily reflect downstream physiologic consequences rather than direct anesthetic action on neural substrates. Advances in electroencephalography (EEG)-based monitoring provide more direct insight into anesthetic effects at the cortical level, offering superior alignment with the primary therapeutic target of anesthetic agents.
Through illustrative clinical examples, the author highlights how patients with preserved cardiac function may tolerate deeper anesthetic states without hemodynamic compromise, while patients with limited cardiac reserve may manifest hypotension at relatively low anesthetic doses. In such cases, reliance on blood pressure or heart rate as proxies for anesthetic depth risks both underdosing and overdosing, potentially increasing morbidity.
The commentary further argues that MAC values reflect population averages and do not adequately account for individual patient variability, particularly in atypical or vulnerable populations. The author cautions that physiologic responses to anesthesia are heterogeneous and that individualized monitoring strategies are necessary to optimize patient safety and outcomes.
Overall, the letter calls for a reevaluation of anesthetic monitoring paradigms, advocating for broader integration of neural monitoring techniques alongside traditional physiologic measures. The author concludes that anesthesiology should move beyond equating anesthetic depth with hemodynamic stability and instead adopt monitoring approaches that more directly assess anesthetic effects on the brain.
Key Points:
• Hemodynamic stability does not reliably indicate anesthetic depth
• MAC values represent population averages and are not individualized metrics
• Cardiovascular responses reflect downstream effects, not central anesthetic action
• EEG-based monitoring more directly measures brain anesthetic effects
• Reliance on physiologic surrogates may lead to under- or overdosing
• Patient-specific variability limits the utility of MAC-centric assessment
• Anesthetic monitoring should prioritize neural targets alongside physiology
Thank you to Anesthesiology for allowing us to summarize and discuss this letter.