Describing hemodynamic states: a plea for systematic terminology

Abstract

A clear and systematic terminological framework is essential for exactly describing a patient’s hemodynamic state. After assessing absolute values of hemodynamic variables and considering the specific clinical context, the absolute values should be classified as ‘normal’, ‘higher than normal’, or ‘lower than normal’ – or as being ‘inside the target range’ or ‘outside the target range’. The acuity and dynamics of changes in the hemodynamic variables should be described. The alterations should then be assigned semiological names reflecting the corresponding ‘clinical sign’. Finally, it should be determined whether the alteration in the hemodynamic variable results in a state of acute circulatory failure or shock.

Hemodynamic management is a core component of care for surgical and critically ill patients [1, 2]. The ultimate goal of hemodynamic management is to provide adequate tissue perfusion and oxygenation to preserve or restore organ function [3]. In this context, the terms ‘hemodynamics’ and ‘cardiovascular dynamics’ refer to the interplay of multiple variables that are physiologically interdependent or mathematically derived from one another—including heart rate, stroke volume, cardiac output, and arterial blood pressure.

Both in clinical practice and in research, it is essential to describe a patient’s hemodynamic state precisely. Yet many terms commonly used to describe hemodynamic problems are vague and insufficiently differentiated. For example, the term ‘hemodynamic instability’ is often used interchangeably with ‘hypotension’, even though the two terms may reflect entirely different pathophysiological states. In fact, the term ‘hemodynamic instability’ should be avoided altogether because it is vague and does not allow for a precise characterization of hemodynamic alterations [4]. To harmonize hemodynamic terminology, we would like to encourage clinicians and researchers to use a systematic terminological framework to characterize a patient’s hemodynamic state (Fig. 1).

Fig. 1.

Framework for terminology describing haemodynamic states

Hemodynamic monitoring primarily provides absolute values of hemodynamic variables, such as heart rate or blood pressure. Therefore, characterizing a patient’s hemodynamic state should begin with the basic assessment of absolute hemodynamic variables—for example, a heart rate of 32 beats per minute or a mean arterial pressure of 50 mmHg. Importantly, absolute values of hemodynamic variables must be interpreted in the context of both factors that directly influence them and the clinical situation. Factors that directly influence hemodynamic variables include vasopressors as well as chronotropic and inotropic drugs. For example, a heart rate of 90 beats per minute has different clinical implications when it occurs spontaneously compared with when it is generated by a cardiac pacemaker. Likewise, a mean arterial pressure of 72 mmHg must be interpreted differently when achieved without pharmacologic support versus with a continuous norepinephrine infusion at 0.5 µg/kg/min. The clinical situation is also important for contextualizing absolute values of hemodynamic variables. Low mean arterial pressure may be physiological (e.g., during sleep) [5], non-physiological but not harmful (e.g., in a young low-risk patient under general anesthesia) [6, 7], or non-physiological and harmful (e.g., in an old patient with severe carotid artery stenosis having surgery in a sitting position) [8].

Based on the assessment of absolute values and clinical contextualization, values of hemodynamic variables should first be classified as ‘normal’, ‘higher than normal’, or ‘lower than normal’. However, the inherently context-dependent nature of hemodynamic variables makes clear distinctions between ‘normal’ and ‘abnormal’ values based on established physiological reference ranges debatable. Therefore, emphasis should be placed on individualized ‘target ranges’ that reflect the adequacy of tissue perfusion and oxygenation to meet metabolic demands in a given clinical situation.

Additionally, the acuity and dynamics of changes in hemodynamic variables should be described—for example, a “decline in heart rate from 78 to 42 beats per minute within 15 min following induction of general anesthesia” or a “sudden decline in mean arterial pressure from 98 to 40 mmHg due to an anaphylactic reaction after antibiotic administration”. Describing the acuity and dynamics of changes in hemodynamic variables provides important insights into underlying pathophysiology and supports timely and appropriate therapeutic decision-making.

As a next step, the absolute values of the hemodynamic variables should be assigned semiological names reflecting the corresponding ‘clinical sign’—for example ‘bradycardia’ or ‘arterial hypotension’. These terms describe clinical signs and do not, per se, imply that changes in the corresponding hemodynamic variable necessarily compromise tissue perfusion and oxygenation. To stay with this example, bradycardia or arterial hypotension may—but do not necessarily—result in inadequate tissue perfusion and oxygenation. Whether alterations in hemodynamic variables result in critically reduced tissue perfusion and oxygenation depends on the magnitude and duration of the alterations as well as the clinical context.

When alterations in hemodynamic variables result in critically reduced tissue perfusion and oxygenation such that metabolic demands can no longer be met and organ function becomes impaired, the cardiovascular system fails to fulfil its physiological function. This condition can be referred to as ‘circulatory failure’. When these alterations occur acutely, the term ‘acute circulatory failure’ is appropriate. Circulatory failure may manifest through clinical signs of organ dysfunction (such as oliguria, altered mental status, or mottled skin) and surrogate markers of hypoperfusion (such as rising lactate levels). Acute circulatory failure is potentially reversible but may also represent an evolving process progressing to shock – defined as “a life-threatening acute circulatory failure characterized by decreased tissue perfusion, leading to inadequate oxygen delivery and/or oxygen utilization to meet cellular metabolic demands” [2]. Accordingly, shock always represents acute circulatory failure, whereas not all acute circulatory failure constitutes shock.

In conclusion, a clear and systematic terminological framework is essential for exactly describing a patient’s hemodynamic state. The term ‘hemodynamic instability’ should be avoided because it is vague and does not allow for a precise characterization of hemodynamic alterations. Instead, after assessing absolute values of hemodynamic variables and considering the specific clinical context, the absolute values should be classified as ‘normal’, ‘higher than normal’, or ‘lower than normal’ – or as being ‘inside the target range’ or ‘outside the target range’. The acuity and dynamics of changes in the hemodynamic variables should be described. The alterations should then be assigned semiological names reflecting the corresponding ‘clinical sign’. Finally, it should be determined whether the alteration in the hemodynamic variable results in a state of acute circulatory failure or shock. This systematic terminological framework allows an unambiguous characterization of hemodynamic states and improves clarity in both clinical practice and research.

Authors’ contributions

Conception and draft: BS, KL. Drafting of manuscript: BS, KL. Critical revision of manuscript for important intellectual content: BS, KL. Final approval of the version to be published: BS, KL. Agreement to be accountable for all aspects of the work thereby ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved: BS, KL.

Funding

None.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Competing interests

BS is a consultant for Edwards Lifesciences (Irvine, CA, USA), Philips North America (Cambridge, MA, USA), GE Healthcare (Chicago, IL, USA), Vygon (Aachen, Germany), Masimo (Neuchâtel, Switzerland), Retia Medical (Valhalla, NY, USA), Maquet Critical Care (Solna, Sweden), Pulsion Medical Systems (Feldkirchen, Germany), Dynocardia (Cambridge, MA, USA), RDS (Strasbourg, France). BS has received institutional restricted research grants from Edwards Lifesciences, Baxter (Deerfield, IL, USA), GE Healthcare, Masimo, Philips Medizin Systeme Böblingen (Böblingen, Germany), CNSystems Medizintechnik (Graz, Austria), Pulsion Medical Systems, Vygon, Retia Medical, Osypka Medical (Berlin, Germany). BS has received honoraria for giving lectures from Edwards Lifesciences, Philips Medizin Systeme Böblingen, Baxter, GE Healthcare, Masimo, CNSystems Medizintechnik, Getinge (Gothenburg, Sweden), Pulsion Medical Systems, Vygon, Ratiopharm (Ulm, Germany). BS is an Editor of the British Journal of Anaesthesia. KL received consulting fees from Philips (a manufacturer of oscillometric NIBP devices) since 2024. Over the past three years, KL has received honoraria for delivering a lecture from Vygon, as well as congress registration and travel support from Advanz Pharma/Correvio (once in 2024 and once in 2025) and AOP Health (once in 2024). KL is a member of the editorial board of the Journal of Clinical Monitoring and Computing.