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Clinical Imperative
Circulatory Failure: Bringing Advanced Physiology to Clinical Practice
Over 50% of patients with shock do not survive. Circulatory failure is the main cause of multi-organ failure and death. Continuous blood pressure monitoring cannot detect early circulatory collapse when interventions are most effective.
CLINICAL CONSENSUS REFERENCE · EUROPEAN HEART JOURNAL: ACUTE CARDIOVASCULAR CARE (2026) 15, 634–648
Criteria for the Diagnosis of Cardiogenic Shock — European Perspective: A Clinical Consensus Statement of the ACVC, HFA, and EAPCI of the ESC
Hoong Sern Lim, Agnieszka Tycinska, Clement Delmas, Jacob Eifer Møller, Janine Pöss, Christian Stoppe, Christophe Vandenbriele, Holger Thiele, Kurt Huber, Ingo Ahrens, Christian Hassager, Ovidiu Chioncel, Marco Metra, Matteo Pagnesi, Wiktor Kuliczkowski, Maja Cikes, Linda W. van Laake, Alessandro Sionis, Mario Iannaccone, Stephane Manzo-Silberman, Federico Pappalardo, Susanna Price, Thomas F. Lüscher, Benedikt Schrage.
European Heart Journal: Acute CardioVascular Care (2026) 15, 634–648. DOI: 10.1093/ehjacc/zuag100.
Pivotal Physiological Principles from the Consensus Statement
- The Single-Value Fallacy: “The dilemma of whether to use SBP or MAP for the diagnosis of CS cannot be reconciled, due to the inherent physiologic limitations of arterial BP as a parameter... These limitations simply reflect the fact that the complexities of circulatory shock cannot be captured by a single parameter and certainly not by a single value. Therefore, arterial BP, be it SBP or MAP, must be interpreted in conjunction with other hemodynamic parameters and evidence of hypoperfusion.” (p. 641)
- Normotensive Shock & Occult Hypoperfusion: Preserved systolic blood pressure resulting from compensatory vasoconstriction (high systemic vascular resistance) is associated with severe organ hypoperfusion and short-term mortality comparable to patients with hypotensive shock.
- The Three Essential Pillars: Shock diagnosis requires (i) resting end-organ hypoperfusion, (ii) primarily caused by hemodynamic abnormalities, and (iii) underlying cardiac dysfunction commensurate with shock.
- Mandatory Right-Heart Assessment: Concomitant right heart dysfunction significantly worsens prognosis; central venous filling pressures, CVP waveforms, and right ventricular-arterial coupling must be evaluated.
The Inherent Limitations of Blood Pressure Monitoring
Continuous blood pressure monitoring is routinely used in critical care, cardiac intensive care units, and high-risk operative environments to detect circulatory failure and guide timely, effective interventions. However, there are inherent physiological limitations to relying solely on blood pressure:
1. Low Blood Pressure is a Late Marker of Shock
Compensatory physiological mechanisms vigorously "defend" systemic arterial blood pressure at the expense of regional and microvascular perfusion.
For example, the Advanced Trauma Life Support (ATLS) guidelines of the American College of Surgeons have long emphasized that a measurable decrease in blood pressure is expected to occur only when blood volume loss exceeds >30–40% (>1,500 mL in a 70-kg adult), when tissue perfusion is already severely compromised.
2. Blood Pressure Does Not Reveal the Etiology
Blood pressure monitoring does not tell us why the blood pressure is low or how to correct it. Blood pressure is tightly regulated by multiple complex mechanisms with feedback loops. Failure of any of these mechanisms—diminished myocardial contractility, arterial vasoplegia, loss of aortic compliance, or right-heart failure—can result in circulatory collapse. Continuous monitoring of pressure numbers alone cannot provide insight into the underlying mechanism, and by extension cannot guide targeted therapeutic correction.
The premise for conventional blood pressure monitoring is flawed: it cannot detect early circulatory failure when corrective interventions are most effective, and cannot guide appropriate, differentiated therapy to prevent multi-organ failure and death.
Data-Driven, Physiology-Guided Actionable Insights
There is an urgent clinical need for a hemodynamic monitoring system that can detect early signs of circulatory failure and guide appropriate, effective therapy tailored to the patient's individual physiology.
Our aim: To translate advanced physiological concepts directly into the clinical domain, combining these concepts with machine learning to provide a differentiated, precise assessment of the cardiovascular system for personalized therapeutic interventions.
Kymometrics: Beyond the Numbers. Into the Physiology.
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1. Unlocking the Reservoir Wave Model:
Utilizing existing continuous blood pressure monitoring systems to extract reservoir excess parameters derived from the reservoir-wave model. These parameters provide physiological insights into arterial compliance (τ = RC), characteristic impedance, and wave reflections to support informed therapeutic decisions.
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2. Advanced Central Venous Pressure (CVP) Waveform Analysis:
Central venous pressure becomes far more than just a single static number. Analysis of central venous pressure waveforms and phasic deflections provides direct insights into venous return, right-heart function, and volume responsiveness.
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3. Proprietary Statistical & Machine Learning Package:
Combining advanced cardiovascular physiology with modern analytical algorithms to transform raw waveform data into actionable, real-time clinical insights. Predictive analytics identify subtle patterns of clinical decline before they become critical emergencies.
Turning Hemodynamic Data into Physiological Insight
- Proactive, Not Reactive: Continuous characterization of cardiovascular physiology in real time to detect complex deterioration early and guide patient-specific therapy, reduce morbidity, shorten hospital stay, and save lives.
- Precision Medicine at the Bedside: Tailor patient-specific interventions based on advanced cardiovascular and hemodynamic profiling, ensuring optimal use of fluids, vasoactive drugs, and mechanical circulatory support.
- Streamlined Clinical Workflows: Reduce cognitive load on intensive care teams in high-risk environments by replacing data noise with clear, actionable physiological intelligence.
