Physiological comparison of hemorrhagic shock and V˙ O2max: A conceptual framework for defining the limitation of oxygen delivery

Abstract

Disturbance of normal homeostasis occurs when oxygen delivery and energy stores to the body's tissues fail to meet the energy requirement of cells. The work submitted in this review is important because it advances the understanding of inadequate oxygen delivery as it relates to early diagnosis and treatment of circulatory shock and its relationship to disturbance of normal functioning of cellular metabolism in life-threatening conditions of hemorrhage. We explored data from the clinical and exercise literature to construct for the first time a conceptual framework for defining the limitation of inadequate delivery of oxygen by comparing the physiology of hemorrhagic shock caused by severe blood loss to maximal oxygen uptake induced by intense physical exercise. We also provide a translational framework in which understanding the fundamental relationship between the body's reserve to compensate for conditions of inadequate oxygen delivery as a limiting factor to $\dot{V}$ O₂max helps to re-evaluate paradigms of triage for improved monitoring of accurate resuscitation in patients suffering from hemorrhagic shock.

Keywords: Oxygen deficit; blood lactate; blood pH; compensatory reserve; oxygen extraction reserve.

Figure 1.

Conceptual model to illustrate the cascade coupling of ventilation, circulation, tissue metabolism, and energy balance in the mitochondria to cell function that defines common pathways to hemorrhagic shock and V̇O₂max. VI: inspiratory volume; TV: tidal volume; Rf: respiratory frequency; DO₂: oxygen delivery; CO: cardiac output; CaO₂: oxygen carrying capacity; V̇O₂: oxygen uptake; OER: oxygen extraction ratio; StO₂: tissue oxygen saturation; PCr: phosphocreatine. Conceptually adopted from Wasserman. (A color version of this figure is available in the online journal.)

Figure 2.

Conceptual comparison of normal circulating blood volume (normovolemia) with absolute and relative hypovolemia. Orange indicates circulating blood volume; Pink indicates capacitance of vascular space. Adopted from M.N. Sawka with permission. (A color version of this figure is available in the online journal.)

Figure 3.

Conceptual representation of the continuum of metabolic relationship of oxygen delivery (DO₂) to utilization (V̇O₂) responses from hemorrhagic shock (left of Normal Resting State) to exertion at V̇O₂max (right of Normal Resting State). OER: oxygen extraction ratio; SvO₂: venous oxygen saturation; StO₂: tissue oxygen saturation; PCr: phosphocreatine; DO_2crit: critical oxygen delivery. Responses to progressive hemorrhage modified from Hooper et al. See text for explanations.

Figure 4.

Time course of responses of systemic oxygen delivery (DO₂; Panel A), systemic oxygen uptake (V̇O₂; Panel B), tissue oxygen saturation (StO₂; Panel C), and oxygen extraction ratio (Panel D) during progressive central hypovolemia induced by lower body negative pressure (LBNP). Data are means ± SD; n = 18. Modified from Ward et al.

Figure 5.

Linear regression of the relationship between systemic oxygen delivery (DO₂) and compensatory reserve measurement (CRM) expressed by DO₂ (mL O₂·kg⁻¹ ·min⁻¹) = 0.08 × CRM (%) + 5.3. Open circles represent extension of the regression line to 0% and 100% CRM. Data, collected from non-human primates, are expressed as mean ± SEM; N = 12. Modified from Koons et al.

Figure 6.

Relationship between tissue oxygen saturation and compensatory reserve. Symbols are average (±95% CI) values generated from 55 healthy volunteer subjects exposed to 0, −15, −30, −45, −60, −70, −80 and −90 mmHg LBNP. Amalgamated r² = 0.965. Modified from Convertino and Sawka.