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Blood pressure, CVP, and CO serve as macro-hemodynamic parameters. To assess tissue oxygenation or perfusion, venous oxygen saturation, serum lactate level, and tissue oxygenation provide further guidance during resuscitation.
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CENTRAL VENOUS OXYGEN SATURATION
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Venous oxygen saturation monitoring is a method to assess the relationship between tissue oxygen extraction, oxygen delivery, and oxygen consumption. A normal oxygen extraction ratio of 25% to 35% results in a venous oxygen delivery (reflected in venous oxygen saturation) of approximately 70% of arterial oxygen delivery. Venous oxygen saturation (SVO2) is ideally measured in the pulmonary artery as a mixed venous sample (SmVO2); this access point is generally not practical in the ED. Clinically, venous oxygen saturation reflects the balance between oxygen delivery and oxygen consumption, with low values reflecting inadequate delivery and/or excessive consumption.
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Central venous oxygen saturation (ScVO2) measurement only requires placement of a central venous catheter in the jugular or subclavian vein, making it an attractive alternative to SmvO2. ScvO2 can be easily measured by drawing a standard venous blood gas from the distal port of the central line and obtaining a measured oxygen saturation. Also, a special catheter allows continuous measurement if desired.
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In healthy individuals, ScvO2 is 2% to 3% less than SmvO2; in shock states, ScvO2 is typically 5% to 10% higher than SmvO2 as blood flow is redistributed from the abdominal vascular beds to the cerebral and coronary circulation.27 Although absolute values of ScvO2 and SmvO2 may be different, low values of either measurement reflect an imbalance in oxygen transport and portend worse outcomes. Most important, the two measures typically change in parallel and thus trends in SCVO2 closely reflect trends in SmvO2.28
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Clinical Use of Central Venous Oxygen Saturation
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The principal value of ScvO2 is its ability to detect occult inadequate oxygen delivery. During initial management, low ScvO2 points to global tissue hypoxia despite normal vital signs and urine output. Left untreated, tissue hypoxia can lead to organ failure and death. Thus, regardless of the underlying pathophysiologic state (e.g., heart failure, septic shock, trauma), a low ScvO2 value represents inadequate oxygen delivery relative to oxygen consumption. Troubleshooting a low ScvO2 then focuses on the determinants of oxygen delivery (Is the patient hypoxic? Anemic? Is CO impaired, and if so, why? For example, low contractility, hypovolemia, or tamponade.). On the demand side, is oxygen consumption increased due to heightened metabolic demand such as from fever, pain, or seizure (Table 32-7)? Clinically, hypoxia and anemia are generally easily diagnosed and treated. A low ScvO2 can detect occult low CO, prompting further investigation and therapy.
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Normal (approximately 70%) or high ScvO2 values do not necessarily mean that the patient is hemodynamically stable. ScvO2 is a global measure of oxygen transport, and regional areas of tissue hypoperfusion can be present even with normal ScvO2 values, particularly in the lower half of the body. In several disease states (e.g., hypothermia, terminal shock, cyanide poisoning), the ability of the tissues to extract oxygen from the blood is impaired, leading to "arterialization" of the venous blood with high ScvO2.
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Using ScvO2 monitoring in a treatment protocol—targeting CVP 8 to 12 mm Hg, MAP >65 mm Hg, and ScvO2 >70%—for septic shock patients early after arrival to the ED (or early goal-directed therapy) decreased mortality in single-center studies.12,29,30,31,32 However, new data showed this invasive approach had no improved outcome compared to usual care in a multicenter study enrolling patients after early recognition, fluid boluses, and antibiotics have occured.33 These results show that CVP and ScvO2-guided care may be an appropriate option in patients where shock is failing to resolve despite efforts to identify.
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In critical illness, an oxygen debt develops when oxygen delivery is inadequate to meet tissue oxygen demand and compensatory mechanisms are exhausted. This results in global tissue hypoxia, anaerobic metabolism, and lactate production. High lactate is a well-established prognostic marker in critically ill patients with various forms of shock, a fact identified in the 1800s.34
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In addition to shock, causes of elevated lactate include seizure, diabetic ketoacidosis, malignancy, thiamine deficiency, malaria, human immunodeficiency virus infection, carbon monoxide or cyanide poisoning, and mitochondrial myopathies. Commonly used drugs, such as metformin, simvastatin, lactulose, antiretrovirals, niacin, isoniazid, and linezolid, can also cause a lactate elevation.35
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Blood lactate concentrations also reflect the interaction between its production and elimination. During critical illness, a patient with hepatic dysfunction may have a higher lactate level compared with another patient without liver disease due to impaired hepatic clearance. However, lactate elevation in a patient with chronic liver disease still portends a poor prognosis, because patients with liver disease do not commonly have a high lactate level in the absence of shock.36
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Clinical Use of Lactate
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Hyperlactatemia is not always accompanied by hypotension or a low bicarbonate level and/or elevated anion gap; thus, the lactate level must be separately measured. Venous lactate levels correlate well with arterial lactate levels.37 However, repeat any elevated venous lactate level if inconsistent with the clinical condition, preferably with an arterial measurement.
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A lactate level ≥4 mmol/L in normotensive patients requires further attention, because this cutoff is associated with increased intensive care unit admission rates and mortality. Furthermore, persistent elevation in lactate for >24 hours is associated with increased mortality as high as 90%.38 Lactate clearance (or the ability to decrease serum lactate levels) as early as 6 hours in patients with septic shock improves 60-day survival.39 When included in a treatment protocol, lactate clearance is noninferior to ScvO2-guided care in the ED.40 However, targeting both lactate clearance and optimal ScvO2 may result in better outcomes than either alone.41
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TISSUE OXYGEN SATURATION
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Tissue oxygen saturation (StO2) can be measured by near-infrared spectroscopy, a noninvasive technique capable of continuous measurement using the varying light absorption properties of deoxygenated and oxygenated blood. Near-infrared light (680 to 800 nm) is largely transparent to biologic tissue, absorbed primarily by hemoglobin, and minimally affected by skin blood flow. Importantly, the near-infrared spectroscopy signal primarily reflects hemoglobin in the small end vessels and approximates the oxygen saturation of venous blood. Near-infrared spectroscopy StO2 measurements correlate and trend with SmvO2 and ScvO2 and can detect occult regional hypoxia even when SmvO2 and vital signs have normalized.42 However, darkly pigmented skin may impair measurement accuracy.
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Clinical Use of Tissue Oxygen Saturation
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StO2 values reflect resuscitation adequacy and the magnitude of traumatic injury, as well as organ failure in critically ill patients.43 An StO2 <75% measured at the thenar eminence distinguishes severe shock patients from healthy volunteers. Dynamic measurements using a brief vascular occlusion test to measure changes in StO2 may offer greater value than static StO2 measurements.44
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Changes in StO2 during the vascular occlusion test are associated with the need for emergency operation or transfusion within the first 24 hours of hospitalization in trauma patients.45 However, StO2 as a hemodynamic goal incorporated in an ED treatment protocol is still investigative.