What is Shock?
In its most basic form, shock is a state where observed oxygen consumption (oVOâ‚‚) is insufficient to meet the body's minimum required oxygen demands (dVOâ‚‚) to maintain whole-body homeostasis. This can occur either because oxygen delivery is insufficient, or because of ineffective oxygen metabolism by cells (EROâ‚‚).
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Shock due to ineffective oxygen delivery (DOâ‚‚)
Oxygen delivery can be defined by the following equation:
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Where:
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Hb = hemoglobin concentration (g/dL)
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SaOâ‚‚ = arterial oxygen saturation (%)CO = cardiac output (L/min)
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As shown by the solid green line in the graphic above, oxygen consumption remains independent of oxygen delivery over a broad range of values. This is partly explained by the peripheral tissues' ability to increase their oxygen extraction ratio (ERO₂, brown line) which is often reflected by a decrease in central (ScvO₂, blue line) or mixed (SvO₂) venous oxygen saturation. ​Under normal conditions, DO₂ exceeds VO₂ by a wide margin. But as DO₂ decreases, a critical threshold is eventually crossed where VO₂ is limited by both limited DO₂ (dashed green line) and by a relative inability to extract further oxygen from hemoglobin (dashed brown line.) This shift may be evidenced by a concurrent drop in the saturation of central venous O₂ (ScvO₂) and a rise in arterial lactate levels.
In cases where the observed DOâ‚‚ (oDOâ‚‚) is below the needed DOâ‚‚ for homeostasis (oDOâ‚‚:nDOâ‚‚ <1), shock is present due to a state of ineffective DOâ‚‚, often referred to as circulatory failure. In these cases, efforts to reverse shock should be focused toward improving DOâ‚‚ to vital organs and tissues.
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Shock due to ineffective oxygen extraction or utilization (EROâ‚‚)
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In some cases, oVOâ‚‚ is inadequate to meet the body's dVOâ‚‚, despite adequate DOâ‚‚ to the peripheral vasculature. In these cases, the decrease in VO2 is related to inadequate oxygen extraction within the body's cells (EROâ‚‚). Even if recognized early, this type of shock can be challenging to address, hence why the majority of efforts related to resuscitation of shock are targeted to improving DOâ‚‚, and not to improving EROâ‚‚.
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So, in its most basic form, shock is a state in which there is inadequate cellular oxygen utilization (VOâ‚‚) to maintain homeostasis in the human body. The management of shock largely rests on the assumption that optimizing macrohemodynamics and oxygen convective transport/delivery (DO2), will restore -or maintain- microcirculatory function, thereby restoring normal cellular respiration.
At the bedside: Recognizing signs of DO2/VO2 mismatch
Exact measurements of VOâ‚‚ (oxygen consumption) are not readily obtainable at the bedside, yet the entire rationale behind hemodynamic evaluation is based on identifying whether a state of inadequate oVOâ‚‚ exists and why. Paradigms for resuscitating shock are largely focused on improving oxygen delivery (DOâ‚‚) to ensure sufficient oxygen is present at the cellular level to meet the demands of nVOâ‚‚. Certain clinical signs may suggest a low DOâ‚‚, low VOâ‚‚ state and can help alert clinicians to recognize shock and begin resuscitative efforts.
In critically ill patients, even these low-tech indicators of perfusion can be challenging to interpret. Physical examination findings are often unreliable as patients may be anuric or on dialysis, under warming blankets, or sedated, all of which limit the utility of mental status, urine output, and temperature as perfusion markers. Pharmacologic and mechanical interventions, such as vasopressors, IV fluids, and positive pressure ventilation, can further distort physiological norms, making bedside assessment even more complex. Given these limitations, finding alternative and reliable surrogates to evaluate oxygen delivery (DOâ‚‚) becomes essential.