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. 2026 Jan 20;29(4):114746. doi: 10.1016/j.isci.2026.114746

Precise perioperative assessment and anesthesia strategy for painless gastrointestinal endoscopy in high-risk cardiovascular disease patients

Yanhong Li 1,4, Huili Xiao 2, Hong Zheng 2, Rurong Wang 1,3,∗
PMCID: PMC12995693  PMID: 41858632

Summary

Patients with cardiovascular disease (CVD) are at substantially increased risk during painless gastrointestinal endoscopy (PGE). Cardiopulmonary comorbidities, bowel preparation-related hypovolemia, and procedural stressors contribute to hemodynamic and respiratory instability. The conventional American Society of Anesthesiologists (ASA) physical status classification incompletely captures these dynamic risk factors and may fail to identify up to 42% of high-risk patients, contributing to a markedly increased incidence of anesthesia-related adverse events. We propose a bundled, physiology-driven perioperative strategy to improve safety in high-risk CVD patients undergoing PGE. This approach incorporates four key components. First, dynamic risk stratification using nomogram-based models (c-statistic up to 0.79) integrates cardiopulmonary and end-organ reserve (CPER), procedural variables, and biomarker trajectories, outperforming static ASA classification. Second, cardiovascular risk-adapted pharmacologic strategies prioritize hemodynamically stable regimens, favoring dexmedetomidine-ketamine over propofol-opioid combinations in patients with reduced left ventricular ejection fraction, and applying albumin-adjusted dosing in hepatic dysfunction (e.g., remimazolam ED95 = 0.107 mg/kg in Child-Pugh B cirrhosis). Third, precision intraoperative monitoring, including invasive arterial pressure, stroke volume variation, and capnography, enables early identification and targeted management of hypotension and hypoxemia. Finally, physiology-based discharge criteria emphasizing hemodynamic stability, respiratory adequacy, and neurologic recovery reduce delayed complications and unplanned readmissions. Transitioning from static preprocedural assessment to dynamic physiologic management substantially enhances perioperative safety in high-risk cardiovascular patients undergoing PGE. Integrating predictive risk models, tailored pharmacology, advanced monitoring, and physiology-based discharge protocols is associated with meaningful reductions in cardiopulmonary complications. Future randomized trials are needed to validate pharmacogenomic-guided dosing and closed-loop sedation systems, but maintaining hemodynamic stability (mean arterial pressure ≥ 65 mmHg) remains a central priority for improving outcomes in this vulnerable population.

Subject areas: Health sciences

Health sciences

Background

The global demand for painless gastrointestinal endoscopy (PGE) continues to rise, particularly among elderly individuals and patients with cardiovascular disease (CVD).1 These populations face a substantially elevated perioperative risk. Cardiovascular complications, including hypotension and arrhythmias, together with respiratory adverse events such as hypoxemia and aspiration, represent the leading contributors to PGE-related morbidity.2,3,4 Preexisting cardiopulmonary disease increases the likelihood of such complications by nearly 3-fold.2 Although anesthesiologists play a central role in preprocedural risk mitigation,5 current assessment strategies often fail to address the unique and evolving pathophysiology associated with PGE.

The American Society of Anesthesiologists (ASA) physical status classification remains the cornerstone of preoperative evaluation6; however, it exhibits important limitations when applied to high-risk cardiovascular patients undergoing PGE. Its static nature does not account for the dynamic physiological perturbations induced by bowel preparation and prolonged fasting.5,7,8 As a result, clinically relevant hypovolemia and electrolyte disturbances-affecting more than 17% of patients-are frequently underrecognized,9 particularly in individuals with multiple comorbidities.10,11 Although higher ASA classes are associated with an increased incidence of adverse events, the system still fails to identify up to 42% of at-risk patients, including those with occult gastric fluid retention, a known predictor of aspiration-related morbidity.9,12 Moreover, the ASA framework does not incorporate procedure-specific risk modifiers. Sedation depth is not standardized, and positional risks are not considered, despite evidence that prone positioning impairs cardiopulmonary function in as many as 89% of elderly patients with CVD.5,9 These deficiencies may lead to severe clinical consequences, exemplified by a 3.2-fold increase in anesthesia-related mortality among cirrhotic patients with an ASA class of 4 or higher, even when conventional preoperative evaluation appears adequate.12 Collectively, these limitations underscore the need to move beyond categorical risk scores toward integrated, dynamic models that incorporate real-time fluid status, drug-disease interactions, and procedure-specific physiological stressors.

To address these gaps, we propose an evidence-based peri-anesthesia framework tailored for high-risk CVD patients undergoing PGE. This framework aims to reduce cardiopulmonary complications through four complementary strategies. First, it overcomes key limitations of the ASA classification by incorporating dynamic assessments of intravascular volume status and occult gastric retention-factors that are strongly associated with adverse outcomes, including a 3.2-fold increase in mortality among cirrhotic patients with ASA class ≥4.9,12 Second, it introduces a triaxial risk stratification model that integrates patient-specific characteristics such as cardiopulmonary reserve, procedure-related risk modifiers including fasting duration and prone positioning, and biomarker trajectories, particularly electrolyte and lactate levels.8 Third, it applies a tiered pharmacologic strategy, favoring hemodynamically stable sedative combinations (e.g., etomidate-propofol regimens) in severe CVD, individualized adjuvant selection, and predefined rescue protocols for hypotension or hypoxemia.12 Finally, the framework enhances post-procedural safety through risk-adjusted discharge criteria and systematic monitoring for delayed complications. Together, this integrated approach shifts peri-anesthesia care from static risk assessment toward dynamic, point-of-care physiologic management, with the goal of mitigating the approximately 40% burden of CVD-related morbidity associated with PGE.6,12 To facilitate a clearer understanding of this bundled management pathway and its underlying pathophysiologic mechanisms, a central schematic illustration is provided (Figure S1).

The pathophysiological triad: Autonomic storm, oxygen debt, and fluid crisis in high-risk PGE

Endoscopy-induced vagal hyperactivation can precipitate severe autonomic cascades in patients with preexisting CVD. Bowel distension, in particular, has been shown to trigger profound bradycardia (heart rate <40 beats per minute) and hypotension (mean arterial pressure <55 mmHg) in approximately 25% of patients with ischemic heart disease, frequently culminating in myocardial ischemia.2 Concurrently, sedative-induced respiratory depression exacerbates ventilation–perfusion mismatch, resulting in procedural hypoxemia (SpO2 <88%) in 37%–42% of patients with chronic obstructive pulmonary disease (COPD) or obesity.2,8,9,13

In parallel, preprocedural fluid depletion caused by bowel preparation, together with third-spacing, leads to a synergistic reduction in cardiac preload and cardiac index, exceeding 35% in patients with heart failure. Point-of-care ultrasound studies assessing intravascular volume status have demonstrated significant reductions in both the maximum and minimum inferior vena cava diameters (IVCDmax and IVCDmin), accompanied by increased IVC collapsibility following standard bowel preparation, consistent with acute hypovolemia.14,15 In addition, electrolyte disturbances-most notably hypokalemia, with reported incidences of 17%–23%-are frequently observed as a consequence of osmotic cathartics and repeated purgative-induced losses. Peri-operative blood glucose fluctuations may also occur, with transient hyperglycemia triggered by catecholamine surges and anxiety-related sympathetic activation showing a significant positive correlation with in-hospital mortality and intensive care unit mortality in patients with critical cardiomyopathy. Although this review does not present original patient-level data, these well-documented peri-intervention physiologic changes are critical contributors to hemodynamic instability in high-risk cardiovascular patients undergoing PGE.16,17,18

Conversely, aggressive or poorly titrated fluid resuscitation may precipitate flash pulmonary edema, particularly in cirrhotic patients with ascites, thereby further complicating cardiopulmonary stability and anesthetic pharmacokinetics.12 Collectively, these converging insults constitute what we propose as the “PGE critical triangle”-a conceptual framework integrating vagally mediated coronary hypoperfusion, oxygen supply-demand mismatch, and the transition from hypovolemia to hydrostatic hemodynamic collapse. This triad likely underlies the 3.2-fold increase in cardiac events observed in cirrhotic patients with ASA class ≥4, reported across both planned transjugular intrahepatic portosystemic shunt (TIPS) and re-TIPS cohorts, regardless of pre-anesthesia screening results or standard medical management. Together, these observations underscore the need for perioperative strategies that prioritize sustained physiologic stability and long-term patient safety rather than short-term procedural success.

Advanced preprocedural risk stratification and optimization

Accurate perioperative risk assessment and targeted prevention are essential for high-risk CVD patients undergoing PGE. Addressing these challenges requires a three-pronged precision strategy that extends beyond the inherent limitations of the traditional ASA Physical Status classification.

First, patient-specific baseline characteristics and periprocedural physiologic perturbations exert a disproportionate influence on perioperative risk. Advanced age (>75 years) is associated with a 2.4-fold increase in adverse events compared with patients younger than 66 years.9 A body mass index (BMI) ≥27 increases the risk of respiratory complications by a factor of 3.1.9,19 Published evidence further indicates that bowel preparation and prolonged fasting reduce IVC diameter by approximately 10%–25%, a change that correlates strongly with induction-related hypotension in susceptible cardiovascular patients. Similarly, serum potassium levels often decline by 0.3–0.6 mmol/L in the hours following bowel preparation, while blood glucose concentrations may rise by 10–25 mg/dL as a result of sympathetic activation. These physiologic shifts underscore the importance of targeted correction during the pre-intervention window. CVD itself is closely associated with vagally mediated hypotension, with a reported prevalence of 28% in patients with ischemic heart disease.2 COPD further increases the likelihood of oxygen desaturation (SpO2 <88%) by 37%–42% during sedation.2,8 In addition, modifiable periprocedural factors substantially influence hazard profiles, including fasting durations exceeding 12 h,19 inpatient status (associated with a 40% increase in adverse events),9 and agitation or restlessness (sedation-agitation scale >4).19

Importantly, the timing of bowel preparation exerts a direct effect on peri-procedural physiology in high-risk cardiovascular patients. Changes in autonomic nervous activity during colonoscopy play an important role in precipitating cardiovascular events, such as arrhythmias, hypotension, hypertension, and myocardial infarction.20 Bowel cleansing induces fluid loss, electrolyte disturbances, and autonomic imbalance, with intravascular volume depletion typically peaking 6–12 h after completion of preparation. During this interval, patients demonstrate heightened susceptibility to induction-related hypotension, arrhythmias, and impaired oxygen delivery. Accordingly, preprocedural optimization-including volume assessment, electrolyte correction, and aspiration risk evaluation using gastric ultrasound-should be conducted after bowel preparation is completed but before anesthesia induction, ideally within 1–2 h prior to the procedure. This timing enables identification of occult hypovolemia or delayed gastric emptying, facilitates adjustment of sedative dosing, and allows proactive implementation of fluid or vasopressor strategies. Failure to align intervention timing with these physiologic changes likely accounts for a substantial proportion of hemodynamic instability observed during PGE in cardiovascular patients.

Second, optimization of comorbid conditions should be guided by predefined, quantifiable physiologic targets rather than subjective clinical impressions. Pulmonary hypertension requires preprocedural stabilization to a mean pulmonary artery pressure (mPAP) < 40 mmHg and a tricuspid annular plane systolic excursion (TAPSE)≥17 mm to preserve right ventricular function.8,21 In patients with COPD, bronchodilator therapy should achieve a forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC) ratio >0.7, sustained for at least two weeks before the procedure.13 Hepatic insufficiency warrants correction to a serum albumin level≥32 g/L, a strategy shown to reduce perioperative fluid-shift-related events by approximately 35%.12

Third, nomogram-based dynamic prediction models outperform the low-discriminative capacity of the ASA classification (c-statistic 0.62).7 Prospectively validated models incorporating high-impact variables-such as age≥75 years, established CVD, and prolonged fasting-demonstrate markedly improved sensitivity for predicting complications, with a reported c-statistic of 0.79.19 Beyond biochemical markers, bedside gastric ultrasound offers an objective assessment of aspiration risk by identifying retained gastric solids in approximately 6% of ostensibly fasted patients, prompting immediate reassessment of sedation depth or airway protection strategies.22 Building on this, point-of-care ultrasound (POCUS) provides a comprehensive physiologic evaluation that extends beyond gastric content assessment and directly supports dynamic risk stratification. Gastric antral cross-sectional area measurements and the Perlas qualitative grading scale facilitate identification of retained solids or gastric volumes exceeding 1.5 mL/kg.23 Intravascular volume status can be quantitatively assessed using IVC ultrasonography, including maximum and minimum IVC diameters (IVCDmax and IVCDmin) and the collapsibility index (>50% indicating hypovolemia), which correlates strongly with induction-related hypotension.24 When clinically indicated, focused cardiac ultrasound enables rapid estimation of left ventricular systolic function (e.g., visual ejection fraction assessment and left ventricular outflow tract velocity-time integral trends) and helps predict hemodynamic intolerance to sedative agents. Collectively, integration of these parameters into a dynamic prediction framework enables actionable, risk-adapted clinical decision-making: a predicted complication probability >40% supports arterial line placement and full hemodynamic rescue protocols; probabilities between 20% and 40% justify stroke volume variation-guided resuscitation strategies; and probabilities <20% are compatible with standard monitoring.

Targeted pharmacological optimization for high-risk PGE

Building on the individualized risk stratification described in advanced preprocedural risk stratification and optimization-particularly nomogram-identified high-risk cohorts with a predicted adverse event probability exceeding 40%-this section summarizes evidence-based pharmacological strategies aimed at maintaining hemodynamic stability during PGE.

Cardiovascular risk-adapted sedative selection

According to major international guidelines, including those from the American Society for Gastrointestinal Endoscopy (ASGE), the British Society of Gastroenterology (BSG), and the European Society of Gastrointestinal Endoscopy (ESGE), propofol remains the most widely used and globally accessible sedative agent for gastrointestinal endoscopy. Its widespread adoption is primarily attributable to its rapid onset, predictable recovery profile, broad availability, and cost-effectiveness. Although newer agents-such as remimazolam, esketamine, and dexmedetomidine-based combinations-have demonstrated favorable hemodynamic characteristics and potential advantages in selected high-risk cardiovascular populations, their uptake remains heterogeneous across regions because of differences in regulatory approval, drug availability, and economic constraints. Consequently, the pharmacological strategies discussed further reflect evidence from published clinical studies rather than universal practice recommendations.

Propofol remains superior when rapid recovery is desired, achieving awakening approximately 15 min earlier than midazolam.25,26 However, it is less suitable in patients with depressed systolic function (ejection fraction <40%), in whom significant hypotension occurs in up to 28% of cases.27 In such populations, remimazolam-metabolized by tissue esterases with hepatic organ-independent clearance and a short elimination half-life (approximately 0.75 h)−has been associated with markedly reduced respiratory depression (relative risk 0.46 compared with propofol) and hypotension, alongside a 22% increase in endoscopist satisfaction.28,29 For patients with moderate to severe systolic dysfunction (LVEF<35%), dexmedetomidine-ketamine regimens reduce the incidence of severe hypotension by 47% and apnea by 82% compared with propofol-fentanyl combinations.30 In elderly cardiovascular patients, dexmedetomidine has also demonstrated superior hemodynamic stability relative to midazolam and a lower risk of post-procedural cognitive impairment.22

Adjunctive agent synergy for dose optimization

Pharmacokinetic tailoring further enhances sedative safety in high-risk populations. In patients older than 75 years, propofol clearance is reduced by approximately 18%, while obesity increases the volume of distribution. When these adjustments are combined with low-dose esketamine (0.2 mg/kg), overall propofol requirements decrease by 18.76%, without compromising procedural conditions. Importantly, NMDA receptor antagonism provided by esketamine results in a 32% reduction in movement responses during endoscopy.31 Etomidate plus propofol TCI can significantly reduce propofol consumption, which is followed by fewer cardiovascular adverse events and respiratory depression32 Additionally, continuous lidocaine infusion (2 mg kg−1 h−1) reduces anesthetic requirements by 23%. These adjunctive strategies are also associated with a 24% reduction in recovery time and a more than 40% increase in patient-reported postoperative comfort and sleep quality.33 When applied in combination, such dose-sparing approaches reduce adverse event rates in nomogram-defined high-risk patients to levels comparable with intermediate-risk cohorts (Δ −38%).34

Pharmacokinetic adaptation in hepatic cirrhosis

Patients with hepatic cirrhosis require customized sedation regimens because of altered drug metabolism and protein binding. Albumin-guided dosing favors remimazolam over propofol in Child-Pugh B patients, with an ED95 of 0.107 mg/kg, whereas propofol often requires dose reductions exceeding 40% in hypoalbuminemic states, assuming an increase in the unbound drug fraction of more than 40% when serum albumin falls below 30 g/L.28 In contrast, midazolam is not recommended in Child-Pugh C cirrhosis because of a 52% reduction in CYP3A4-mediated clearance.25 Optimal peri-procedural management in this population also includes correction of coagulation parameters (international normalized ratio <1.5), prophylaxis against hepatic encephalopathy, preprocedural gastric ultrasound screening to exclude solid gastric contents, and continuous hemodynamic monitoring in patients with portal venous pressures exceeding 12 mmHg. Despite these pharmacokinetic advantages, remimazolam is not universally available, and its higher acquisition cost in some healthcare systems limits routine use. As a result, propofol continues to serve as the standard sedative agent in many regions worldwide.

Overall, risk stratification directly informs pharmacological decision-making. Advanced age (>75 years) favors adjunctive lidocaine use.33 baseline systolic dysfunction (EF <40%) discourages propofol monotherapy in favor of dexmedetomidine-based ketamine combinations27,30; Child-Pugh classification supports precision dosing of remimazolam where available28; and preexisting respiratory compromise (FEV1/FVC <0.7) mandates preference for respiratory-sparing agents,29 a strategy associated with a 65% reduction in cardiac arrest.12 Application of this integrated, risk-adapted pharmacological framework nearly eliminates outcome disparities between high-risk and low-to-intermediate-risk patients.34 Thus, while novel agents may enhance safety in specific patient subsets, propofol-based strategies remain the global mainstay, and individualized sedative selection should account for patient risk profiles alongside local availability and cost considerations.

Precision intraoperative management in high-risk PGE

Continuous physiologic monitoring is a cornerstone of intraoperative safety in high-risk cardiovascular patients undergoing PGE. In individuals with pulmonary hypertension or cardiomyopathy, invasive arterial pressure (IAP) monitoring-and, when clinically indicated, central venous pressure (CVP) assessment-provides real-time hemodynamic information essential for early detection of instability during sedation.8,35,36,37 Beyond hemodynamic surveillance, capnography plays a critical role in the early recognition of respiratory depression, particularly during administration of sedative agents with known respiratory suppressive effects. Elevations or abrupt changes in end-tidal carbon dioxide (PetCO2), rather than absolute thresholds alone, serve as sensitive indicators of hypoventilation and impending apnea.5,12 As with other highly vulnerable populations-such as recipients of left ventricular assist devices (LVADs)-the application of monitoring modalities should be individualized according to underlying physiology and procedural risk (Table S1).38

Fluid management requires precise titration, as both liberal (approximately 20 mL/kg) and restrictive (approximately 2 mL/kg) replacement strategies have been associated with comparable risks of peri-procedural hypotension in clinical studies. Continuous assessment of volume responsiveness is therefore essential to minimize cardiac complications, particularly in patients with limited myocardial reserve. In addition, maintenance of normothermia-defined as a core temperature ≥36°C-is recommended during prolonged procedures to prevent temperature-related hemodynamic and metabolic derangements.39,40,41

Management of intraoperative complications should follow physiology-driven principles rather than protocolized dosing alone. In hypotensive episodes, initial assessment and correction of intravascular volume should precede pharmacologic intervention. When vasopressor support is required, a pureα1-adrenergic agonist such as phenylephrine (50–100 μg intravenously) is preferred, whereas mixed or combination vasopressors should be avoided in patients with coronary artery disease (CAD) because of their potential to exacerbate myocardial oxygen imbalance.9 Bradycardia resulting from vagal stimulation should be managed with intravenous atropine (0.5 mg) and, if necessary, temporary interruption of the endoscopic stimulus. Hypoxemia should prompt stepwise escalation of respiratory support, ranging from supplemental oxygen to assisted ventilation, recognizing that propofol exerts a dose-dependent depressant effect on respiratory drive.27

Alternative sedative combinations may further enhance intraoperative stability in selected high-risk patients. Dexmedetomidine-ketamine regimens have been shown to reduce hypotension by 47% compared with propofol-fentanyl while providing comparable analgesia.30 Similarly, propofol combined with esketamine decreases total propofol requirements by 18.76%, a benefit that may be particularly advantageous when advanced physiologic monitoring is employed.31 Collectively, these findings reinforce the principle that intraoperative management should integrate preprocedural risk stratification with tailored pharmacologic selection and adaptive monitoring strategies, allowing clinicians to dynamically respond to patient-specific physiologic responses during PGE.

Postprocedural optimization in high-risk endoscopy

Postprocedural optimization in high-risk cardiovascular patients undergoing gastrointestinal endoscopy should be guided by physiology-based discharge criteria rather than time-dependent recovery alone. Discharge readiness can be evaluated across three domains, listed here in order of clinical importance: (1) hemodynamic stability, defined as systolic blood pressure maintained within 20% of baseline without orthostatic hypotension1,25; (2) respiratory adequacy, indicated by oxygen saturation ≥92% (or return to pre-procedural baseline) on room air with a normal capnography waveform2; and (3) neurologic recovery, reflected by return to baseline mental status (Aldrete score ≥9) and the ability to ambulate independently.25 Among these domains, attainment of physiologic stability is a stronger determinant of clinical outcomes than the elapsed time since sedative discontinuation. This principle is particularly relevant for propofol-based sedation, given its rapid pharmacokinetic clearance, which renders physiologic criteria more clinically meaningful than time-based discharge thresholds.25

Aspiration pneumonia remains an important post-endoscopic complication, with a reported incidence of 1.9% (95% CI, 1.2%–2.7%), underscoring the necessity of structured postprocedural observation following endoscopic submucosal dissection (ESD). Risk factors include propofol induction (odds ratio 2.3) and prolonged procedural duration exceeding 90 min (p < 0.001).42 Clinical manifestations may persist for 3–4 weeks. During early recovery, sustained oxygen desaturation (SpO2<90%) should prompt evaluation for aspiration-related lung injury or ischemic hypoxemia, with continued pulse oximetry monitoring as indicated. If respiratory compromise persists after initial recovery, escalation according to the institutional noninvasive monitoring and support (NMS) protocol is warranted. When aspiration is clinically suspected, prompt chest radiography and initiation of empiric antimicrobial therapy, such as piperacillin-tazobactam (4.5 g intravenously), are recommended.42

Cardiovascular complications frequently occur in parallel with pulmonary events and are most prevalent within the first postoperative hour. Accordingly, continuous electrocardiographic monitoring and high-sensitivity cardiac troponin testing are recommended in patients with ischemic symptoms or elevated baseline cardiovascular risk. Among cirrhotic patients, 18% of those who develop severe post-endoscopic electrolyte and hemodynamic-mediated perioperative syndrome (eHMPS) experience cardiac complications (p < 0.05). An ASA classification >III and procedural duration exceeding 60 min have been identified as independent risk factors for these events.9,12

Multimodal, opioid-sparing analgesia plays a critical role in postprocedural recovery. Holst et al. demonstrated that perioperative lidocaine infusion (2 mg kg−1 h−1) reduces postoperative carprofen requirements by 23%, lowers pain intensity (mean visual analog scale reduction of 4.2 points), and decreases fatigue (relative risk 0.61).33 Importantly, patient satisfaction is inversely correlated with opioid exposure (r = −0.73) rather than the specific anesthetic technique employed, emphasizing the value of non-opioid analgesic strategies. Patient-reported satisfaction further increases by approximately 40% when discharge is accompanied by procedure-specific analgesia protocols and access to a dedicated postprocedural complication hotline.27 Collectively, these findings highlight that optimal recovery in high-risk endoscopy depends on coordinated pharmacologic management, continuous physiologic assessment, and risk-adapted postprocedural surveillance.

Multidisciplinary protocols and technological integration in high-risk endoscopy

Institutionalized multidisciplinary frameworks are essential for the safe and effective perioperative management of high-risk cardiovascular patients undergoing PGE. Coordinated collaboration among gastroenterology, anesthesiology, and cardiology teams has been shown to reduce delayed discharge rates by 32%, largely through optimized timing of preprocedural assessment and intervention windows.1,8 Standardized interdepartmental communication protocols further decrease consultant response times by an average of 18.7 min (p = 0.002). The value of such coordination is particularly evident in complex endocrine procedures, such as pheochromocytoma resection, where immediate multidisciplinary consultation mitigates intraoperative hemodynamic crises (Table S2).35

Sustained educational initiatives are equally critical to ensure procedural proficiency in hemodynamic rescue. Simulation-based training programs reduce sedation-related complications by approximately 41%, primarily by reinforcing vasopressor titration strategies and advanced airway management algorithms.1,43 In parallel, quality improvement programs require the establishment of procedure-specific key performance indicators (KPIs), including mandatory documentation of hypotension (defined as systolic blood pressure <90 mmHg for more than 3 min), hypoxemia (SpO2<85% for more than 60 s), and protocol compliance.44 Even in centers conducting quarterly multidisciplinary audit cycles, adherence to British Society of Gastroenterology sedation standards is 54% higher than in non-audited settings.1,44

Future advances in high-risk endoscopy will increasingly rely on predictive analytics and automation. Integrated point-of-care assessment-combining frailty indices, bedside laboratory testing, and point-of-care ultrasound (POCUS)-based volumetric analysis-substantially enhances perioperative decision-making. Ultrasonographic parameters such as an inferior vena cava maximum diameter (IVCDmax) < 1.25 cm or an IVC collapsibility index >50% reliably predict induction-related hypotension and guide targeted preprocedural fluid optimization. When combined with gastric ultrasound screening to identify high-risk gastric content patterns, these tools provide actionable physiologic data that support safer sedation strategies and reduce aspiration-related complications in high-risk cardiovascular patients.22 Artificial intelligence-based nomograms incorporating echocardiographic parameters (e.g., right ventricular systolic pressure >60 mmHg, tricuspid annular plane systolic excursion <16 mm) demonstrate excellent predictive performance for intraoperative hemodynamic instability, with a reported negative predictive value of 94.1%.19,45 Closed-loop sedation systems integrating processed electroencephalography (bispectral index 40–60) with noninvasive cardiac output monitoring reduce propofol overdosing by 62% while maintaining hemodynamic stability (mean arterial pressure >65 mmHg).8

Technological innovation continues to expand beyond sedation monitoring. Robotic-assisted platforms have demonstrated clinical benefit in thoracic surgery, where video-assisted thoracoscopic surgery (VATS) reduces pulmonary vein thrombosis rates from 4.4% to 0.9% compared with open procedures.46,47 Emerging robotic endoscopic systems similarly offer enhanced precision and improved maneuverability in anatomically complex regions.48 In parallel, next-generation γ-aminobutyric acid (GABA)-ergic modulators currently in phase II trials exhibit approximately 40% less hypotension than propofol, without concomitant respiratory depression, highlighting their potential role in future high-risk sedation paradigms.

Successful implementation of these advances depends on system-level integration. Consensus-based protocols must define thresholds for AI-assisted decision support, credentialing standards for robotic platforms, and pharmacovigilance frameworks for novel sedative agents. The trajectory of care is shifting toward protocolized, patient-specific pathways that integrate the pharmacological strategies outlined in targeted pharmacological optimization for high-risk PGE with the physiologic monitoring frameworks described in precision intraoperative management in high-risk PGE, all embedded within unified clinical informatics architectures.

Accumulating evidence suggests that optimal outcomes in high-risk PGE are achieved through protocol-driven care pathways encompassing eight essential domains:(1) risk stratification using nomogram-based prediction models incorporating echocardiographic and serum biomarkers45,49; (2) pharmacodynamic optimization favoring hemodynamically neutral sedative classes30,31; (3) precision hemodynamic monitoring using IAP, CVP, or validated dynamic thresholds8,35; (4)standardized rescue algorithms for cardiorespiratory complications9,27; (5) temperature-controlled fluid stewardship46,50; (6) physiology-based discharge criteria1,25; (7) structured multidisciplinary coordination protocols4,35; and (8) integration of big data analytics and AI-enhanced clinical decision support systems.19,45

Despite these advances, substantial knowledge gaps remain. The efficacy of novel sedative regimens in patients with decompensated heart failure, the cost-effectiveness of robotic endoscopic platforms,48,51 and the external validation of machine learning-based risk models across diverse healthcare systems are yet to be fully established. Moreover, widespread adoption of new technologies is constrained by interoperability limitations and insufficient operator training.43,44 Addressing these challenges will require multicenter prospective trials focusing on:(1) pharmacogenetic dosing strategies in advanced cardiomyopathy (ejection fraction <35%); (2) the impact of closed-loop sedation systems on hemodynamic stability, with time spent below a mean arterial pressure of 65 mmHg as a primary endpoint; and (3) long-term cardiovascular outcomes following endoscopy in patients with valvular heart disease. Until such evidence matures, institutional success will depend on audited quality frameworks that mandate compliance with the monitoring standards outlined in precision intraoperative management in high-risk PGE and the discharge parameters detailed in postprocedural optimization in high-risk endoscopy, ensuring that the continuum from preprocedural stratification to postprocedural surveillance remains grounded in physiologic specificity and multidisciplinary accountability.1,8,35,46

Conclusion

Our review confirms that reducing mediastinitis and stroke in high-risk cardiovascular patients undergoing PGE requires shifting from static risk assessment to dynamic physiologic management. Recent evidence highlights four key strategies: (1) precision risk stratification via nomogram-derived models (c-statistic = 0.79), which surpass the ASA system by integrating cardiopulmonary fitness, procedural stress, and biomarker trends. (2) Cardiovascular pharmacology optimization: use pharmacodynamically neutral agents (e.g., dexmedetomidine-ketamine combination, reducing hypotension incidence by 47%) and albumin-adjusted dosing in cirrhosis. (3) Protocolized escalation with real-time hemodynamic monitoring (IAP/SVV) and closed-loop ventilation to prevent autonomic crises. (4) Discharge based on hemodynamic stability (>20% baseline SBP), neurological recovery (Aldrete≥9), and aspiration surveillance-lowering delayed complications by 32%. These strategies form part of selected eight-domain quality models (encompassing risk prediction, multidisciplinary coordination, and AI-supported decisions), which reduce adverse events by 38%–65% in validated cohorts. However, gaps persist between preclinical data/hypotheses and clinical application of CMP technologies (e.g., new sedatives for decompensated heart failure, cost-effectiveness of robotic endoscopic platforms). Until large studies validate pharmacogenomic dosing in advanced cardiomyopathy (EF<35%) and closed-loop system efficacy (MAP>65 mmHg), continuous hemodynamic monitoring and physiologic discharge criteria remain essential to reduce residual morbidity (40%) in these fragile patients.

Data and code availability

Data sharing is not applicable to this article as no new data were created or analyzed in this study.

Acknowledgments

We thank Professor Wang and Professor Zheng for their guidance and revision of this manuscript.

Author contributions

Conceptualization, Yanhong Li. and Huili Xiao; writing—original draft, Yanhong Li; writing—review & editing, Hong Zheng and Rurong Wang; supervision, Hong Zheng.

Declaration of interests

The authors declare no competing interests.

Footnotes

Supplemental information can be found online at https://doi.org/10.1016/j.isci.2026.114746.

Supplemental information

Document S1. Figure S1 and Tables S1 and S2
mmc1.pdf (263KB, pdf)

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Associated Data

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Supplementary Materials

Document S1. Figure S1 and Tables S1 and S2
mmc1.pdf (263KB, pdf)

Data Availability Statement

Data sharing is not applicable to this article as no new data were created or analyzed in this study.

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