Resuscitation from Circulatory Shock

Published on 26/03/2015 by admin

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91 Resuscitation from Circulatory Shock

Circulatory failure results in a decrease in oxygen delivery (DO2) associated with a decrease in cellular partial pressure of oxygen (PO2). When a critical PO2 value is reached, oxidative phosphorylation is limited and leads to a shift from aerobic to anaerobic metabolism. The result is a rise in cellular and blood lactate concentrations associated with a decrease in adenosine triphosphate (ATP) synthesis. Adenosine diphosphate (ADP) and hydrogen ions accumulate and together with the raised serum lactate level lead to metabolic lactic acidosis. This state is called dysoxia and can be accepted as a definition for “shock,” a state in which inadequate tissue oxygenation produces cellular injury. Shock often, but not only, results from circulatory failure and decreased DO2.

Resuscitation from “circulatory shock” requires an emergency and global approach that is based on limited clinical features for establishing diagnosis and probabilistic therapy. The efficacy of this initial therapeutic strategy then becomes part of the diagnostic approach: if the chosen therapy is successful, it confirms the diagnosis retrospectively. This initial diagnostic approach is essentially based on physician knowledge of global hemodynamics and oxygen-derived parameters. It can be helped by rapidly available oxygen-derived biological markers.

image Understanding Underlying Pathophysiology of Global Flow and Oxygen Delivery

Addressing Global Adequacy of Tissue Oxygenation

Adequacy of tissue oxygenation is defined as an adapted oxygen supply (or DO2) to oxygen demand.1 Oxygen demand varies according to tissue type and according to time. Although oxygen demand cannot be measured or calculated, oxygen uptake or consumption (image) and DO2 both can be quantified; they are linked by a simple relationship:

where ERO2 represents oxygen extraction ratio (ERO2 in %; image and DO2 in mL O2/kg/min). DO2 represents the total flow of oxygen in the arterial blood and is given as the product of cardiac output (image) by arterial oxygen content (CaO2):

with CaO2 being the product of hemoglobin (Hb, g/100 mL) by arterial oxygen saturation (SaO2, %) and Hb O2 capacity (1.39 mL O2/g Hb): CaO2 = Hb × SaO2 × 1.39.

Under physiologic control, oxygen demand equals image (≈2.4 mL O2/kg/min for a 12 mL O2/kg/min DO2, which corresponds to a 20% ERO2). The rate of oxygen delivered by blood is physiologically larger than the rate of image: DO2 is adapted to oxygen demand. When oxygen demand increases (e.g., during exercise), DO2 has to adapt and increase.

During circulatory shock and/or severe hypoxemia, as DO2 declines secondary to a decrease in image and/or a decrease in CaO2, image can be maintained by a compensatory increase in ERO2, image and DO2 remaining therefore independent. But as DO2 falls further, a critical point (DO2 crit) is reached; ERO2 can no longer compensate for this fall in DO2, and at this critical level, image becomes DO2 dependent (Figure 91-1). At this DO2 crit (4 mL/kg/min), for a image of about 2.4 mL/kg/min, ERO2 reaches its critical point (ERO2 crit) of 60%. When image is higher, DO2 crit is higher as well. Increase in oxygen extraction occurs via two fundamental adaptive mechanisms2: (1) redistribution of blood flow among organs via an increase in sympathetic adrenergic tone and central vascular contraction (this is responsible for a decreased perfusion in organs with low ERO2, such as the skin and splanchnic area, and a maintained perfusion in organs with high ERO2, such as heart and brain); and (2) capillary recruitment within organs responsible for peripheral vasodilation (opposite to central vasoconstriction).

Using Mixed Venous Oxygen Saturation to Assess Adequacy of Global Tissue Oxygenation

In the clinical setting, mixed venous oxygen saturation (SvO2) can be used for assessing whole-body image-to-DO2 relationships. Indeed, according to the Fick equation, tissue image is proportional to cardiac output:

where CvO2 is mixed venous blood oxygen content. To some extent, image is approximately equal to cardiac output × (SaO2 − SvO2) × Hb × 1.39, and SvO2 is approximately equal to SaO2image/(image × Hb × 1.39).

Four situations can be responsible for a decrease in SvO2: a decrease in SaO2 (hypoxemia), in Hb (anemia) or in cardiac output, or an increase in image (like in exercise). At DO2 crit, SvO2 is about 40% (SvO2 crit) with an ERO2 of 60% and a SaO2 of 100%. This SvO2 crit has been identified in humans.3 It is important to emphasize that for the same decrease in CaO2 (induced by a decrease of Hb or SaO2), the decrease in SvO2 will be more pronounced if cardiac output cannot adapt. Hence, SvO2 represents adequacy of global flow to CaO2 decrease. A 40% SvO2 can be taken as an imbalance between arterial blood oxygen supply and tissue oxygen demand with evident risk of dysoxia. In the clinical setting, a decrease of SvO2 of 5% from its normal value (77%-65%) is representative of a significant fall in DO2 and/or an increase in oxygen demand (Figure 91-2). If initial probabilistic treatment (fluid resuscitation and/or low-dose inotropes and/or red blood cell transfusion) does not allow SvO2 to be restored to a minimal 65%, Hb, SaO2, and cardiac output should then be individually measured to introduce the appropriate treatment.

Assessing Global Flow

Global flow (i.e., cardiac output) is dependent on preload, myocardial contractility, afterload, and heart rate. Regional flow distribution is not homogeneous and is dependent on central and peripheral vascular tone, which ultimately results in the composite systemic vascular resistances (SVR). As an oversimplification, mean arterial pressure (MAP) can be estimated as the product of cardiac output by SVR. When flow decreases, MAP remains stable when SVR increases; this corresponds to increased sympathetic adrenergic tone and central vascular contraction in low ERO2 organs, and preserved peripheral vasodilation in high ERO2 organs. Overall, ERO2 increases and SvO2 decreases.

Minimal data exist to guide selection of the threshold for blood pressure maintenance. Arbitrary values of a systolic blood pressure of 90 mm Hg or a MAP of 60 to 65 mm Hg have traditionally been chosen. Observation of an inappropriate tissue perfusion (e.g., raised blood lactate level, metabolic acidosis, SvO2 lower than 65%, decreased urinary flow) and its persistence despite probabilistic therapy (fluid, low-dose inotropes, red blood cells) should lead to optimizing flow according to the Frank-Starling curve. This can be assessed by invasive and noninvasive investigative procedures (see later).

During circulatory shock, image-to-DO2 dependency with a rise in blood lactate levels implies oxygen debt. Several authors have reported that oxygen debt is related to the likelihood of multiple organ failure and mortality in postoperative or polytrauma patients.4,5 Patients who survive multiple organ failure have been shown to have higher cardiac index, lower SVR, higher image, and higher SvO2 than nonsurvivors.6,7 Rixen and Siegel5 demonstrated that the degree of tissue oxygen debt is related to an enhanced inflammatory response, associated with an increased risk of acute respiratory distress syndrome and higher mortality rates.

Recent research has emphasized the potential interest of central venous oxygen saturation (ScvO2) for detecting global oxygenation impairment.7 Experimental studies reported that changes in SvO2 and ScvO2 closely reflect circulatory disturbances during periods of hypoxia, hemorrhage, and subsequent resuscitation (ScvO2 being approximately 5% higher than SvO2 in the critically ill). Fluctuations in these two parameters correlated relatively well, although absolute values differed.8 Finally, observational data found ScvO2 to be a useful parameter in detecting occult tissue hypoperfusion in both sepsis and cardiac failure.9,10 An important feature with ScvO2 monitoring is that ScvO2 can be continuously provided by central venous catheters equipped with optic fibers (e.g., PreSep oximetry catheter [Edwards Lifesciences, Irvine, California]). In initial resuscitation of circulatory shock, insertion of a central venous catheter is a standard, rapid, and easy approach, much easier than any other invasive hemodynamic monitoring, especially in patients who are not yet sedated, intubated, and ventilated.

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