Blood Pressure Targets Alone Fail Patients: Why Surgeons Must Watch Perfusion, Not Just Numbers

Anesthesiologists have long treated a single number as the guardian of the organs during surgery: keep mean arterial pressure above roughly 60–65 mmHg, and the kidneys, heart, and brain should be safe. A new Perspective published in Anesthesiology and Perioperative Science argues that this comfortable assumption is quietly failing patients, and that the future of perioperative care lies not in chasing thresholds but in reading the physiology behind every pressure reading.

The article, authored by Wanzhuo Xu, Jinjun Bian, and Lulong Bo, lays out why mean arterial pressure, or MAP, earned its central place in the operating room in the first place. MAP can be measured continuously or intermittently, is familiar to every clinician, and is physiologically more closely related than systolic pressure to the pressure component of organ perfusion. Those practical strengths, however, have encouraged what the authors call a conceptual shortcut: the belief that hitting a numerical MAP target is the same thing as restoring blood flow to tissue. Mounting evidence, they contend, shows that pressure correction alone is an incomplete therapeutic concept.

Contemporary consensus statements from the PeriOperative Quality Initiative and the European Society of Anaesthesiology and Intensive Care already frame an intraoperative MAP of approximately 60–65 mmHg as a pragmatic lower safety boundary rather than a universal endpoint that guarantees organ perfusion. The Perspective pushes one step further, proposing a transition from universal MAP thresholds, to static individualized targets based on preoperative blood pressure, and ultimately to dynamic, physiology-guided perfusion support. In this framework, MAP serves as an upstream warning signal that prompts clinicians to assess the underlying mechanism: cardiac output, vascular tone, venous congestion, tissue oxygenation, and organ vulnerability.

The observational evidence behind the safety floor remains solid. Intraoperative MAP below approximately 60–65 mmHg, particularly when sustained or recurrent, has been consistently associated with postoperative myocardial and kidney injury. But association is not prescription. The authors point to a series of randomized trials, including the Hypotension-Avoidance versus Hypertension-Avoidance trial, BP-CARES, IMPROVE-multi, and PRETREAT, which collectively suggest that simply intensifying perioperative blood pressure targets, managing antihypertensive medications by broad strategy, or assigning risk-stratified MAP goals does not reliably improve major clinical or patient-centered outcomes.

Those neutral or mixed findings should not be read as evidence that hypotension is harmless, the authors caution. Instead, they expose the limits of pressure-only interventions. A higher MAP may shorten the numerical duration of hypotension yet fail to improve oxygen delivery if cardiac output is low, venous pressure is elevated, or microcirculatory flow is impaired. Conversely, a moderate drop in MAP may be tolerated by a patient with preserved cardiac output, intact autoregulation, and no signs of tissue hypoperfusion. Earlier randomized trials using personalized pressure targets showed feasibility and hinted at benefit in selected contexts, but larger recent trials demonstrate that static individualization based on preoperative awake or nighttime blood pressure does not capture the shifting physiology of anesthesia, surgical stress, blood loss, inflammation, analgesia, and recovery.

The practical answer, according to the Perspective, is to ask why the pressure is low before deciding how to treat it. The authors organize perioperative hypotension into five overlapping hemodynamic profiles: vasodilatory, hypovolemic or preload-responsive, low-output or myocardial dysfunction, bradycardic or rhythm-related, and venous-congestive or perfusion-mismatch. The same MAP can represent very different biological states. Reflexively treating all hypotension with vasopressors can raise pressure while worsening afterload or regional vasoconstriction; treating it all with fluids can aggravate venous congestion and tissue edema.

The pathophysiology is straightforward but often ignored at the bedside. Global arterial pressure is commonly approximated as cardiac output multiplied by systemic vascular resistance, yet organ oxygen delivery also depends on hemoglobin concentration, arterial oxygen content, regional vascular distribution, diffusion distance, capillary recruitment, and cellular metabolic capacity. Vasoactive drugs may restore macrocirculatory pressure while reducing regional flow, the essence of macrocirculation–microcirculation decoupling. Crucially, organ perfusion pressure is set by the arteriovenous pressure gradient, not MAP alone: renal perfusion pressure, for example, can be approximated as MAP minus central venous pressure. Positive-pressure ventilation, high PEEP, fluid overload, increased intra-abdominal pressure, and right ventricular dysfunction can all reduce effective renal or splanchnic perfusion despite apparently adequate MAP, making venous congestion an active hemodynamic threat rather than a secondary observation.

The Perspective also highlights a postoperative monitoring blind spot. After surgery, patients often move to wards where intermittent vital-sign checks, residual anesthetic effects, occult bleeding, inflammatory vasodilation, and fluid shifts obscure deterioration. Prospective studies show postoperative blood pressure perturbations are common, persist for clinically meaningful periods, and are easily missed, while continuous non-invasive monitoring detects more hypotension than intermittent measurement. The authors identify the first 48 postoperative hours as the most relevant window for intensified surveillance, since many early myocardial, renal, and hemodynamic complications emerge then. A postoperative MAP below 65 mmHg should be treated as a pragmatic warning threshold, not an automatic mandate for fluids or vasopressors, and should trigger structured reassessment of heart rate, rhythm, oxygen saturation, urine output, hemoglobin trends, and organ injury markers.

The proposed management framework is deliberately pragmatic. MAP thresholds retain value as safety alerts and quality metrics, but once pressure crosses a clinically relevant boundary, clinicians should shift from numerical correction to phenotype-guided perfusion support: confirm the measurement and context, assess whether organ perfusion is impaired, identify the dominant hemodynamic phenotype, and select therapy by mechanism, whether fluids and hemorrhage control, vasopressors, chronotropic support, inotropes, or decongestion. Future trials, the authors argue, should test algorithms combining threshold alerts with hemodynamic phenotyping, perfusion markers, and postoperative surveillance, with organ-specific and patient-centered endpoints alongside treatment-related harm.

The central question, the authors conclude, is no longer whether MAP matters; it clearly does. The question is how MAP can be integrated with blood flow, venous pressure, microcirculatory function, and patient vulnerability to support tissue perfusion in real time. For a specialty built on vigilance, the message is provocative: the number on the monitor is only the beginning of the story.

Subject of Research: Perioperative arterial pressure management and physiology-guided perfusion support

Article Title: Perioperative arterial pressure management: from fixed thresholds to physiology-guided perfusion support

Article References: Xu, W., Bian, J., & Bo, L. (2026). Perioperative arterial pressure management: from fixed thresholds to physiology-guided perfusion support. Anesthesiology and Perioperative Science, 4(1), Article 38. https://doi.org/10.1007/s44254-026-00187-w

Image Credits: AI Generated

DOI: 10.1007/s44254-026-00187-w

Keywords: mean arterial pressure, perioperative care, organ perfusion, hypotension, hemodynamic phenotypes, venous congestion, acute kidney injury, cardiac output, microcirculation, postoperative monitoring, anesthesiology, randomized trials