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HOME > Acute Crit Care > Volume 41(2); 2026 > Article
Review Article
CPR/Resuscitation Beyond blood pressure: a comprehensive overview of clinical indices in shock and tissue hypoperfusion
Acute and Critical Care 2026;41(2):201-212.
DOI: https://doi.org/10.4266/acc.003425
Published online: May 28, 2026

Department of Critical Care Medicine, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Korea

Corresponding author: Sua Kim Department of Critical Care Medicine, Korea University Ansan Hospital, Korea University, College of Medicine, 123 Jeokgeum-ro, Danwon-gu, Ansan 15355, Korea Tel +82-31-412-4883 Fax +82-31-412-5588 Email: sua0047@gmail.com
• Received: August 22, 2025   • Revised: December 10, 2025   • Accepted: December 11, 2025

© 2026 The Korean Society of Critical Care Medicine

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Shock is a state of circulatory failure characterized by impaired tissue perfusion due to a mismatch between oxygen delivery and consumption (VO2). While macrocirculation serves as a conduit to sustain blood flow toward the microcirculatory networks, it is the microcirculation that ultimately ensures the delivery of oxygen and nutrients to maintain cellular and organ function. The maintenance of proper macrocirculation is essential, but it does not necessarily indicate adequate microcirculation or recovery from shock. Thus, assessment of the microcirculation is also required to confirm effective tissue oxygenation. A comprehensive evaluation of both circulatory levels is crucial for accurate diagnosis and prognostication in patients with shock. This review explores a diverse range of clinical, biochemical, and device-based indicators that reflect the perfusion status of patients in shock. By examining their physiological significance and clinical relevance, we aim to provide a comprehensive framework for the hemodynamic assessment of critically ill patients and support the use of multidimensional strategies in shock management.
  • Key Words: hypoperfusion; microcirculation; shock; systemic circulation
Shock is a clinical syndrome characterized by impaired tissue perfusion resulting from a critical imbalance between oxygen delivery (DO2) and consumption (VO2). Although hypotension has traditionally been considered a hallmark of shock, it is now recognized as insufficient to assess the severity of circulatory failure. Instead, shock is more accurately defined by the presence of global tissue hypoperfusion, which ultimately leads to cellular dysfunction, metabolic derangement, and organ failure [1-3].
Historically, clinical monitoring and resuscitation efforts in shock have focused on macrocirculatory variables such as mean arterial pressure (MAP), cardiac output (CO), and central venous pressure (CVP). These parameters reflect the global flow and pressure dynamics of the circulatory system, which are crucial for DO2. However, the adequate DO2 is defined by the effective transport to the microvascular beds, where cellular metabolism occurs. Restoration of macrocirculatory stability does not always guarantee sufficient microcirculatory perfusion, a dissociation referred to as hemodynamic incoherence or macro- and microcirculatory uncoupling [4,5].
The microcirculation, comprising arterioles, capillaries, and venules, plays a central role in gas exchange. It is tightly regulated by arteriolar tone, precapillary sphincters, and the endothelial surface layer, including the glycocalyx [6]. In states of shock, microcirculatory dysfunction is driven by inflammatory insults, ischemia-reperfusion injury, hypoxia, and endothelial barrier disruption. These changes can occur even in the presence of normalized macrocirculatory parameters, resulting in ongoing cellular hypoxia and tissue injury (Figure 1) [4].
Therefore, accurate assessment of shock should integrate both macrocirculatory and microcirculatory indices. This review aims to explore the range of clinical, biochemical, and device-derived parameters that can contribute to the diagnosis and monitoring of shock and tissue hypoperfusion. By categorizing these indices into conventional macrocirculatory parameters, downstream markers of tissue hypoperfusion, clinical signs of microcirculatory dysfunction, device-based microcirculatory monitoring, and emerging biomarkers of shock, this review proposes an integrated perspective on the comprehensive hemodynamic assessment of critically ill patients.
Macrocirculatory Shock
In the early phase of shock, compensatory mechanisms attempt to preserve the systemic arterial pressure and perfusion through increased sympathetic tone, tachycardia, and vasoconstriction. These responses aim to maintain the MAP and CO to ensure DO2 to vital organs [1]. At the macrocirculatory level, blood vessels primarily function as conduits, with flow and pressure determined by CO and vascular tone [7]. However, perfusion is not solely dependent on MAP. The perfusion pressure at the tissue level depends on the autoregulatory system of the smaller vessels, which modulates local vascular resistance according to metabolic demand. When MAP decreases, compensatory vasodilation may transiently preserve tissue perfusion. Nevertheless, once the MAP falls below the lower limit of autoregulatory threshold, the flow becomes pressure-dependent and collapses, a phenomenon observed in advanced shock [6].
Microcirculatory Shock
Microcirculatory alterations during shock involve both structural and functional changes. Ischemia, hypoxia, and systemic inflammation induce the degradation of the endothelial glycocalyx and direct endothelial injury. This disruption increases vascular permeability and promotes capillary leakage and tissue edema. Red blood cells exhibit impaired deformability and alignment [7]. Leukocyte adhesion and plasma extravasation further aggravate the endothelial dysfunction (Figure 2) [8]. These changes initiate a cascade that impairs DO2 at the cellular level. Autoregulation of the flow is lost, capillary recruitment is diminished, and perfusion becomes increasingly heterogeneous. In severe cases, microthrombosis and vasoconstriction contribute to the capillary obstruction. Consequently, even when the macrocirculatory targets are met, cellular hypoxia may persist, manifesting clinically as organ dysfunction [4]. This dissociation between macro- and microcirculatory recovery demonstrates the limitations of traditional resuscitation endpoints. Such discrepancy reinforces the need for integrative indices that connect global hemodynamics and tissue level perfusion.
Conventional Macrocirculatory Parameters
Macrocirculatory parameters play a key role in the initial assessment and management of shocks. These include vital signs and hemodynamic variables that reflect systemic perfusion pressure and CO. The most commonly used indicators are the MAP, heart rate, and CO, which are often complemented by stroke volume and CVP.
MAP remains a primary target during resuscitation. Clinical guidelines typically recommend maintaining a MAP of ≥65 mmHg to ensure adequate organ perfusion [9]. However, MAP alone is an inadequate surrogate for tissue perfusion, as systemic blood pressure may remain within target ranges even when regional or cellular DO2 is compromised [10]. CO and its derivatives, including stroke volume and cardiac index, are directly linked to global oxygen delivery (DO2 = CO × arterial oxygen content) and are therefore considered the core of hemodynamic resuscitation with blood pressure. However, no target value of CO exists during shock resuscitation. Although the adequacy of CO can be assessed in the context of delivery-consumption mismatch (DO2–VO2), it is difficult to use CO as a direct therapeutic target [11].
CVP has traditionally been used to assess preload and guide resuscitation endpoints. However, CVP-guided strategy results in over-resuscitation [12]. Instead, the CVP directly contributes to the determination of systemic perfusion pressure. Elevated CVP reduces the gradient between MAP and venous pressure, thereby impairing organ perfusion, particularly renal perfusion, and increasing the risk of subsequent organ dysfunction [13,14]. Although these macrocirculatory parameters are essential for the initial diagnosis and therapeutic targeting, they provide only a partial view of the patient’s perfusion status. Persistent tissue hypoxia may exist despite normalization of these indices, underscoring the need to incorporate tissue perfusion- and metabolism-oriented assessment tools for a more comprehensive evaluation of shock.
Downstream Markers of Tissue Hypoperfusion and Organ Dysfunction
Downstream markers provide insight into the metabolic consequences of impaired perfusion. These parameters reflect tissue hypoxia, anaerobic metabolism, and organ dysfunction, offering critical information about the adequacy of resuscitation beyond macro-level hemodynamics.
Serum Lactate is one of the most widely utilized biomarkers in the evaluation of shock, with a cutoff value of >2 mmol/L. Elevated lactate levels suggest a shift toward anaerobic metabolism, commonly indicating inadequate tissue perfusion. Importantly, lactate also serves as the primary marker for monitoring the adequacy of resuscitation and the response to shock management. However, lactate is considered a late marker, and its elevation may also reflect non-hypoxic processes such as increased glycolysis, impaired clearance, adrenergic stimulation, or local hypoxia [15,16]. Mixed or central venous oxygen saturation (SvO2 or ScvO2) reflects the balance between oxygen delivery and consumption, with normal values ranging from 65% to 80%. A low SvO2 suggests inadequate oxygen delivery relative to tissue demand, which reflects low CO, anemia, hypoxia, or increased oxygen consumption [15]. A high SvO2 also requires cautious interpretation because it may indicate impaired oxygen extraction or oxygen metabolism failure, as observed in severe sepsis [17]. Therefore, its proper assessment requires a contextual understanding of hemoglobin levels, arterial oxygen content, and metabolic state.
Venous-to-arterial carbon dioxide difference (P(v-a)CO2 gap) serves as a complementary tool for assessing the adequacy of CO [18]. A widened gap >6 mmHg suggests impaired CO2 washout, implying a reduced CO. Notably, the PCO2 gap may detect hemodynamic changes earlier than lactate because CO2 dynamics respond more rapidly to variations in perfusion [19]. However, a normal gap did not exclude the possibility of tissue hypoperfusion. As the PCO2 gap does not reflect aerobic or anaerobic metabolism, it should be interpreted in conjunction with lactate and SvO2 during resuscitation [20].
Clinical signs of organ dysfunction such as altered mental status and oliguria represent downstream manifestations of tissue hypoperfusion. While nonspecific, these signs often precede biochemical markers and may serve as early indicators of perfusion failure. Downstream markers complement macrocirculatory assessments by capturing the physiological and metabolic effects of hypoperfusion. They help identify ongoing tissue injury despite normalized vital signs and guide further therapeutic decisions.
Clinical Signs of Microcirculatory Dysfunction
Microcirculatory indicators assess tissue perfusion at the capillary level and are crucial for evaluating shock, particularly when conventional macrocirculatory parameters fail to detect ongoing tissue hypoxia. Given the central role of the microcirculation in delivering oxygen to parenchymal cells, assessing microvascular perfusion is essential.
Capillary refill time (CRT) is a simple and rapid bedside assessment of microcirculatory status and has been proposed as a clinical marker in patients with shock [21-23]. It measures the time required for skin color to return after blanching induced by brief pressure, typically applied to the fingertip. A prolonged CRT >3 s has been associated with increased mortality and correlates with other markers of hypoperfusion such as lactate and mottling. A Randomized Clinical Trial of Peripheral Perfusion-Targeted Resuscitation in Early Septic Shock (ANDROMEDA-SHOCK) trial highlighted CRT as a viable target for resuscitation, demonstrating its non-inferiority over lactate-guided therapy in terms of mortality [24]. And, CRT remained unchanged in patients without significant changes in CO or MAP after resuscitation, while its response was variable in patients with hemodynamic improvement, suggesting that CRT may reflect complex physiological mechanism beyond simple microcirculatory changes [25]. Although recent meta-analyses have shown that the prognostic performance of CRT for adverse outcomes is modest [26], it remains one of the most practical and physiologically meaningful bedside indicators of tissue perfusion. The ongoing ANDROMEDA-SHOCK-2 trial is designed to determine whether a CRT-guided resuscitation can translate microcirculatory optimization into improved survival [27], addressing the mortality effect that remained inconclusive in the original study. Given the growing use of CRT in both clinical practice and research, implementing a standardized protocol is essential to ensure consistency, enhance reproducibility, and strengthen applicability in patient care.
Skin mottling was first documented as patchy skin discoloration due to small-vessel vasoconstriction [28,29]. Ait-Oufella et al. [29] suggested a skin mottling score based on a semi-quantitative visual assessment of skin discoloration. It serves as an indicator of the cutaneous vasoconstriction associated with hypoperfusion. Higher mottling scores were independently associated with poor outcomes and were particularly useful in patients with septic shock or cardiogenic shock [30]. Mottling often precedes alterations in systemic hemodynamics, making it a sensitive and early marker [31]. Although it can be assessed through simple visual inspection, a standardized protocol for quantitative evaluation is lacking.
Core-Peripheral Temperature Gradients
Cold skin has been regarded as the result of low CO or vasoconstriction of microvasculature. Previous studies have reported that cold toes are associated with more severe forms of shock [32,33]. The difference between the central and toe or fingertip temperatures reflects peripheral vasoconstriction, and can be a surrogate for systemic vasomotor tone and perfusion. Decreased gradients often suggest improved perfusion, whereas widened gradients indicate ongoing shock [34]. The method remains promising, but further validation is needed particularly in establishing standardized procedures for skin temperature measurement before it can be reliably used to assess hemodynamic status.
Device-Based Microcirculation Monitoring
Technological advances have enabled bedside assessment of microcirculation, allowing clinicians to monitor capillary flow and tissue oxygenation in real-time. These devices are particularly valuable for guiding perfusion-targeted resuscitation strategies tailored to individual patients.
Handheld vital microscopy using Sidestream Dark Field or Incident Dark Field imaging provides direct visualization of the microcirculation, typically in the sublingual area, in a noninvasive manner at the patient’s bedside [35]. These devices quantify sublingual microcirculatory conditions using imaging-based quantification of vessel density, perfusion heterogeneity, and the proportion of perfused vessels, reflecting both the extent and functional integrity of capillary blood flow and tissue oxygenation. Impaired capillary recruitment and heterogenous microvascular flow distribution can be evaluated by perfused vessel density or a high heterogeneity index, parameters that have been linked to adverse outcomes in shock [36]. With recent advancements in automated quantification of these indicators using handheld vital microscopy [37,38], microcirculation-guided monitoring may emerge as a necessary component of shock resuscitation [39].
Near-infrared spectroscopy (NIRS) estimates tissue oxygen saturation (StO2) by analyzing the light-absorption properties of hemoglobin, providing an indicator of tissue hypoperfusion [40]. Continuous NIRS monitoring at the thenar eminence can reflect changes in regional perfusion [41]. Vascular occlusion tests, involving the compression of a proximal artery using pneumatic cuff, induce transient ischemia followed by reperfusion of the target site. StO2 values obtained during vascular occlusion test can provide dynamic information about microvascular reactivity and oxygen utilization [42,43]. While NIRS-based techniques have shown prognostic value, the clinical relevance remains limited by methodological complexity and lack of precision [44].
Contrast-enhanced ultrasound (CEUS) utilizes microbubble contrast agents to assess tissue perfusion at the organ level in ultrasound imaging allowing for real-time dynamic assessment, particularly in highly vascular organs such as the liver, kidneys, heart and brain [45,46]. Renal perfusion at the microvascular level has been correlated with clinical outcomes, including the development of acute kidney injury during shock resuscitation and encephalopathy and the alteration of brain regional microcirculation was related with survival in sepsis, as assessed using CEUS. These findings reveal the fact that improvements in macrocirculatory parameters do not necessarily translate into adequate regional microcirculatory perfusion. Although CEUS currently faces challenges related to operator dependence, contrast availability, and the lack of standardized quantitative protocols, it represents a promising tool for regional perfusion heterogeneity. While further methodological refinement is needed before widespread implementation in critical care practice, CEUS has already been successfully applied in other clinical fields, suggesting that its integration into hemodynamic monitoring could offer meaningful diagnostic and physiologic insights [47-49].
Emerging Biomarkers of Shock
In recent years, several novel biomarkers have emerged to aid in the assessment of shock, providing mechanistic insights beyond those offered by traditional hemodynamic and biochemical variables. These biomarkers reflect microvascular integrity, endothelial function, inflammatory responses, and neurohormonal activation−all key contributors to shock pathophysiology. However, as multiple factors can influence their levels, these biomarkers should be interpreted as adjunctive rather than definitive diagnostic indicators. A comprehensive understanding of the characteristics of each biomarker in different shock state is essential for their appropriate use in clinical and research settings.
Syndecan-1 and other endothelial and vascular biomarkers serves as indicators of endothelial glycocalyx degradation, which regulates vascular permeability, inflammation, and coagulation. In septic and hemorrhagic shock, glycocalyx disruption leads to increased vascular permeability and impaired capillary perfusion [8,50]. Syndecan-1 is a transmembrane proteoglycan and a core component of the endothelial glycocalyx; it is released into the circulation upon glycocalyx degradation [51]. Elevated plasma syndecan-1 levels have been associated with worse outcomes in patients with shock, suggesting its potential role as a biomarker of endothelial injury and microvascular dysfunction [52]. In addition to syndecan-1, other molecules such as heparan sulfate, hyaluronic acid, and soluble VE-cadherin reflect different aspects of endothelial glycocalyx degradation and junctional integrity [53]. Conversely, sphingosine-1-phosphate plays a protective role by stabilizing the glycocalyx [54]. Angiopoietins, particularly the ratio of angiopoietin-2 to angiopoietin-1, reflect endothelial activation and dysfunction. Angiopoietin-1 exerts endothelium-stabilizing effects, whereas angiopoietin-2 promotes vascular leakage and inflammation, and its elevation correlates with the severity of sepsis and mortality [55]. The angiopoietin balance is crucial in maintaining vascular quiescence and preventing increased permeability. Proadrenomedullin is a precursor of adrenomedullin (ADM) and serves as a surrogate marker for ADM. ADM is a peptide produced by endothelial and vascular smooth muscle cells, acting as a potent vasodilator and vasoactive mediator. Accordingly, it is recognized as a marker of endothelial dysfunction and inflammation, associated with vasoplegia, hypotension, and increased adverse outcomes in patients with shock [56].
Interleukin-6, interleukin-8, and tumor necrosis factor-α are proinflammatory cytokines that serve as key mediators in the inflammatory cascade that precipitates hemodynamic instability and tissue injury [57,58]. They are also widely recognized as important biomarkers of inflammation. Recently, the soluble urokinase-type plasminogen activator receptor has been identified as a marker of chronic immune activation that has prognostic utility in critically ill patients, correlating with multi-organ failure and mortality [59,60]. Inflammatory biomarkers offer insight into the host response to shock and may facilitate early prognosis when integrated with hemodynamic parameters and organ function scores.
Renin and the renin-angiotensin-aldosterone system (RAAS) play essential roles in blood pressure regulation and fluid homeostasis, influencing various organs, including the vasculature, kidneys, heart, brain, adrenals, and immune cells [61,62]. Plasma renin levels typically rise in response to hypoperfusion and sympathetic activation during shock. In septic conditions, this response is further amplified by metabolic mediators such as succinate and by the loss of feedback inhibition due to insufficient angiotensin II generation, resulting in markedly elevated renin levels [63]. Moreover, the renin/aldosterone ratio may help identify RAAS dysfunction and guide vasopressor or corticosteroid therapy [64]. Elevated renin concentrations have been associated with increased vasopressor requirements and poor outcomes [65,66].
Biomarkers reflecting end-organ damage have shown growing evidence for their prognostic value in various forms of shock. Organ-specific biomarkers allow for precise assessment of dysfunction in key systems commonly affected by impaired perfusion. For instance, troponin, creatinine, bilirubin, and transaminases provide important evidence when evaluating end-organ damage resulting from shock. Although these markers are not exclusive to shock states, abnormal laboratory findings in conjunction with hemodynamic instability suggest clinically significant hypoperfusion [67]. In addition to standard clinical chemistry results, emerging biomarkers offer deeper insights into organ injury during shock. Kidney injury biomarkers, such as neutrophil gelatinase-associated lipocalin and kidney injury molecule-1, provide early detection of acute kidney injury, a frequent complication of circulatory failure. Circulating dipeptidyl peptidase 3, released during cellular injury, has emerged as a valuable indicator of both vascular hemodynamic profiles and reflects the downstream consequences of shock-induced microvascular and metabolic disturbances. Liver-type fatty acid-binding protein serves as a sensitive indicator of hepatic ischemia and oxidative stress, often preceding rises in traditional liver enzymes in septic or hypoperfused state. Similarly, intestinal fatty acid-binding protein reflects early enterocyte injury due to splanchnic hypoperfusion, and elevated levels have been linked to intestinal barrier disruption and systemic inflammation.
Shock is a dynamic continuum of circulatory failure characterized by tissue hypoperfusion and organ dysfunction. Growing evidence supports the concept of macro- and microcirculatory uncoupling underscoring the need for complementary indices investigating perfusion at the tissue level. The assessment of tissue perfusion has evolved from global metabolic surrogates, such as lactate, and ScvO2, toward bedside clinical and imaging-based markers detecting early microvascular dysfunction.
Before ANDROMEDA-SHOCK trial [24], parameters formally endorsed by international guidelines, including the Survival Sepsis Campaign and American College of Cardiology / American Heart Association statements for cardiogenic shock, had been limited to lactate and ScvO2 for evaluating tissue hypoperfusion and guiding resuscitation. Since then, prolonged CRT (typically >2–3 seconds) has been acknowledged as a practical bedside marker of tissue hypoperfusion [9,68]. Although its measurement technique and threshold remain imperfectly standardized, its simplicity, low cost and rapid responsiveness to changes in peripheral flow make CRT an attractive complement to global macrocirculatory variables in contemporary shock assessment.
Emerging technologies have increased our understanding of microcirculatory alteration in shock. Tools such as hand-held vital microscopy and CEUS have enabled observation of flow heterogeneity and impairment directly or indirectly in diverse types of shock and provided important pathophysiologic insight. However, these techniques are not ready for routine clinical application. Biomarkers further complement these visual and physiologic assessments by capturing endothelial injury, inflammation, and neurohormonal stress. Nevertheless, clinical application of these markers remains limited by assay availability, cost, and lack of standardized threshold. While not actional in daily practice, integration of these markers into research framework can enhance mechanistic understanding and refine risk stratification models.
Taken together, these parameters span from conventional hemodynamic target to advanced microcirculatory monitoring tools and novel biomarkers, providing a multidimensional framework for the assessment of shock and tissue hypoperfusion. Table 1 summarizes the modalities, their physiological interpretation, clinical utility and limitations.
There is no currently accepted process defining the optimal sequence or combination of perfusion markers. A stepwise and comprehensive approach is recommended—first ensuring macrocirculatory targets, then reassessing tissue perfusion using bedside indicators such as CRT and mottling, and finally interpreting laboratory or imaging-based indices within the overall clinical condition. This aligns with recent Surviving Sepsis Campaign and ACC/AHA guidance, both emphasizing the importance of confirming tissue hypoperfusion.
Therefore, these markers represent complementary components of a multidimensional assessment. Traditional variables remain essential for maintaining global perfusion pressure, whereas tissue-level indices provide dynamic feedback on the adequacy of microcirculatory flow and DO2. Although many emerging modalities are not applicable for routine use, their contribution to elucidating the mechanisms of circulatory failure is significant. Integrating established and investigational markers within a physiology-guided framework, clinicians can better detect occult hypoperfusion, avoid over-resuscitation, and tailor interventions to the individual patient. Future research should aim to standardize measurement protocols, validate prognostic thresholds, and explore how real-time multimodal monitoring can improve outcomes across diverse populations.
▪ Conventional hemodynamic indices often fail to reflect regional or microcirculatory perfusion deficits. Incorporating direct and physiologic markers of tissue perfusion is essential to avoid limitations in diagnostic assessment during shock resuscitation.
▪ A careful interpretation of parameters reflecting macrocirculatory status, tissue oxygenation, and bedside clinical signs is critical to guide individualized hemodynamic interventions aligned with the patient’s physiologic and clinical circumstances.
▪ Novel biomarkers and perfusion-monitoring technologies may provide meaningful direction for future clinical integration, facilitating the detection of covert hypoperfusion and risk stratification as further evidence becomes available.

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING

None.

ACKNOWLEDGMENTS

None.

AUTHOR CONTRIBUTIONS

Conceptualization: SK. Methodology: SK. Writing – original draft: JK, SK, JHL, SK. Writing – review & editing: JK, SK, JHL, SK. All authors read and agreed to the published version of the manuscript.

Figure 1.
Persistent macro- and microcirculatory mismatch despite macrocirculatory restoration can drive further shock progression and organ failure. Redrawn based on Merdji et al. Ann Intensive Care 2023;13:38 [7], originally adapted from Chioncel and Mebazaa, in Microcirculation: from bench to bedside (2020).
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Figure 2.
Types of microvascular changes. (A) Heterogeneous distribution of red blood cells with perfused capillaries next to non-circulating capillaries. (B) Dilution of red blood cells can occur in hemorrhagic shock during fluid resuscitation. (C) Congestion due to increased venous pressure in cardiogenic shock. (D) Tissue edema with increased oxygen diffusion distances. Adapted from Duranteau et al. Crit Care 2023;27:190 [4].
acc-003425f2.jpg
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Table 1.
Summary of indices for the assessment of shock and tissue hypoperfusion
Modality/marker Interpretation Clinical use/strength Notes/limitations
MAP, SBP/DBP, CO, CI Systemic flow & pressure Initial hemodynamic target May not reflect microcirculation (hemodynamic incoherence)
CVP Assumption of perfusion pressure Used in fluid management as for safety margin Over-resuscitation risk, no fixed target
Lactate Anaerobic metabolism, local/systemic hypoperfusion Prognosis, resuscitation guide Nonspecific, lagging indicator
ScvO2, SvO2 Balance of DO2 and VO2 CO adequacy evaluation Interpretation context-dependent
P(v–a)CO₂ gap Adequacy of CO₂ washout CO adequacy evaluation Not reflective of metabolic state
Clinical signs (oliguria, mental change) Organ dysfunction Easily observable clue Nonspecific, variable sensitivity
Clinical signs of microcirculatory dysfunction
 Capillary refill time Peripheral perfusion Bedside dynamic test for microvascular function status Affected by temp, lighting, skin color
 Skin mottling score Cutaneous perfusion heterogeneity Sensitive early marker of systemic hemodynamic change Semi-subjective
 Temperature gradient Core-to-periphery flow difference Suggests vasoconstriction Variable by causes
 HVM (IDF/SDF imaging) Sublingual microcirculation Direct capillary flow imaging Automated quantification standard under development
 NIRS Regional tissue oxygen saturation Bedside monitoring of muscle perfusion Methodological complexity; limited specificity
 CEUS Organ perfusion (kidney/liver) Evaluates fluid responsiveness Contrast needed
Lack of standardization
 NGAL, KIM-1 Kidney injury Predict AKI early Not yet standard use, research stage markers
 I-FABP, L-FABP Gut, liver ischemia Intestinal or hepatic hypoperfusion
 Troponin Myocardial injury Cardiac shock severity
 Syndecan-1, cDPP3 Endothelium, cell necrosis Glycocalyx degradation, systemic injury

MAP: mean arterial pressure; SBP: systolic blood pressure; DBP: diastolic blood pressure; CO: cardiac output; CI: cardiac index; CVP: central venous pressure; ScvO2: central venous oxygen saturation; DO2: oxygen delivery; VO2: oxygen consumption; HVM: hand-held vital microscopy; IDF: Incident Dark Field; SDF: Sidestream Dark Field; NIRS: near infrared spectroscopy; CEUS: contrast-enhanced ultrasound; NGAL: neutrophil gelatinase-associated lipocalin; KIM-1: kidney injury molecule-1; I-FABP: intestinal fatty acid binding protein; L-FABP: liver-type fatty acid-binding protein; cDPP3: circulating dipeptidyl peptidase 3.

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        Beyond blood pressure: a comprehensive overview of clinical indices in shock and tissue hypoperfusion
        Acute Crit Care. 2026;41(2):201-212.   Published online May 28, 2026
        DOI: https://doi.org/10.4266/acc.003425
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      Beyond blood pressure: a comprehensive overview of clinical indices in shock and tissue hypoperfusion
      Image Image Image
      Figure 1. Persistent macro- and microcirculatory mismatch despite macrocirculatory restoration can drive further shock progression and organ failure. Redrawn based on Merdji et al. Ann Intensive Care 2023;13:38 [7], originally adapted from Chioncel and Mebazaa, in Microcirculation: from bench to bedside (2020).
      Figure 2. Types of microvascular changes. (A) Heterogeneous distribution of red blood cells with perfused capillaries next to non-circulating capillaries. (B) Dilution of red blood cells can occur in hemorrhagic shock during fluid resuscitation. (C) Congestion due to increased venous pressure in cardiogenic shock. (D) Tissue edema with increased oxygen diffusion distances. Adapted from Duranteau et al. Crit Care 2023;27:190 [4].
      Graphical abstract

      Figure 1.

      Figure 2.

      Graphical abstract

      Beyond blood pressure: a comprehensive overview of clinical indices in shock and tissue hypoperfusion
      Modality/marker Interpretation Clinical use/strength Notes/limitations
      MAP, SBP/DBP, CO, CI Systemic flow & pressure Initial hemodynamic target May not reflect microcirculation (hemodynamic incoherence)
      CVP Assumption of perfusion pressure Used in fluid management as for safety margin Over-resuscitation risk, no fixed target
      Lactate Anaerobic metabolism, local/systemic hypoperfusion Prognosis, resuscitation guide Nonspecific, lagging indicator
      ScvO2, SvO2 Balance of DO2 and VO2 CO adequacy evaluation Interpretation context-dependent
      P(v–a)CO₂ gap Adequacy of CO₂ washout CO adequacy evaluation Not reflective of metabolic state
      Clinical signs (oliguria, mental change) Organ dysfunction Easily observable clue Nonspecific, variable sensitivity
      Clinical signs of microcirculatory dysfunction
       Capillary refill time Peripheral perfusion Bedside dynamic test for microvascular function status Affected by temp, lighting, skin color
       Skin mottling score Cutaneous perfusion heterogeneity Sensitive early marker of systemic hemodynamic change Semi-subjective
       Temperature gradient Core-to-periphery flow difference Suggests vasoconstriction Variable by causes
       HVM (IDF/SDF imaging) Sublingual microcirculation Direct capillary flow imaging Automated quantification standard under development
       NIRS Regional tissue oxygen saturation Bedside monitoring of muscle perfusion Methodological complexity; limited specificity
       CEUS Organ perfusion (kidney/liver) Evaluates fluid responsiveness Contrast needed
      Lack of standardization
       NGAL, KIM-1 Kidney injury Predict AKI early Not yet standard use, research stage markers
       I-FABP, L-FABP Gut, liver ischemia Intestinal or hepatic hypoperfusion
       Troponin Myocardial injury Cardiac shock severity
       Syndecan-1, cDPP3 Endothelium, cell necrosis Glycocalyx degradation, systemic injury
      Table 1. Summary of indices for the assessment of shock and tissue hypoperfusion

      MAP: mean arterial pressure; SBP: systolic blood pressure; DBP: diastolic blood pressure; CO: cardiac output; CI: cardiac index; CVP: central venous pressure; ScvO2: central venous oxygen saturation; DO2: oxygen delivery; VO2: oxygen consumption; HVM: hand-held vital microscopy; IDF: Incident Dark Field; SDF: Sidestream Dark Field; NIRS: near infrared spectroscopy; CEUS: contrast-enhanced ultrasound; NGAL: neutrophil gelatinase-associated lipocalin; KIM-1: kidney injury molecule-1; I-FABP: intestinal fatty acid binding protein; L-FABP: liver-type fatty acid-binding protein; cDPP3: circulating dipeptidyl peptidase 3.

      Table 1.

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