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Comprehensive and timely ED care can significantly decrease the predicted mortality of critically ill patients in as little as 6 hours of treatment.15 Application of an algorithmic approach to optimize hemodynamic end points with early goal-directed therapy in the ED reduced mortality by 16% in patients with severe sepsis or septic shock in 2001.16 That original study, the Surviving Sepsis Campaign that followed,17 and other algorithmic efforts18 have changed the approach to sepsis and shock care on a worldwide basis. Two large, multicenter, randomized controlled trials published in 2014 failed to show additional benefits to a rigid algorithmic approach.19,20 However, we attempt to present below the most beneficial aspects of shock care demonstrated by the medical progress of the last 15 years. The ABCDE tenets of shock resuscitation are establishing airway, controlling the work of breathing, optimizing the circulation, assuring adequate oxygen delivery, and achieving end points of resuscitation.21
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ESTABLISHING THE AIRWAY
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Airway control is best obtained through endotracheal intubation. Sedatives used to facilitate intubation may cause arterial vasodilatation, venodilation, or myocardial suppression and may result in hypotension. Positive-pressure ventilation reduces preload and CO. The combination of sedative agents and positive-pressure ventilation will often lead to hemodynamic collapse. To avoid this unwanted situation, initiate volume resuscitation and vasoactive agents before intubation and positive-pressure ventilation.
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CONTROLLING THE WORK OF BREATHING
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Control of breathing is required when significant tachypnea accompanies shock. Respiratory muscles are significant consumers of oxygen during shock and contribute to lactate production. Mechanical ventilation and sedation allow for adequate oxygenation, improvement of hypercapnia, and assisted, controlled, synchronized ventilation. All of these treatments decrease the work of breathing and improve survival. When starting mechanical ventilation on a patient, it is essential to consider the patient's compensatory minute ventilation prior to intubation to ensure appropriate initial settings are selected. After a patient is placed on mechanical ventilation, obtain an arterial blood gas to evaluate acid–base status, oxygenation, and ventilation. Neuromuscular blocking agents should be considered to further decrease respiratory muscle oxygen consumption and preserve Do2 to vital organs, especially if patients are severely hypoxemic due to acute respiratory distress syndrome.22
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OPTIMIZING THE CIRCULATION
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Circulatory or hemodynamic stabilization begins with intravascular access through large-bore peripheral venous lines. The Trendelenburg position does not improve cardiopulmonary performance compared with the supine position. It may worsen pulmonary gas exchange and predispose to aspiration. Passive leg raising above the level of the heart with the patient supine may be effective. If passive leg raising results in an increase in blood pressure or CO, fluid resuscitation is indicated.23
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Fluid resuscitation should begin with isotonic crystalloid.24 The amount and rate of infusion are determined by an estimate of the hemodynamic abnormality. Most patients in shock have either an absolute or relative volume deficit. The exception is the patient in cardiogenic shock with pulmonary edema. Administer fluid rapidly (over 5 to 20 minutes), in set quantities of 500 or 1000 mL of normal saline, and reassess the patient after each bolus. Patients with a modest degree of hypovolemia usually require an initial 20 to 30 mL/kg of isotonic crystalloid, as is suggested in the 2012 Surviving Sepsis Campaign Guidelines; however, there are few data to support this uniform recommendation, and fluid volume should be individualized to each patient.25 More fluids are needed for profound volume deficits. It is common for patients in septic shock to receive 6 L of crystalloid in the first 24 hours of hospital care. For large fluid volumes, consider using lactated ringer's or plasmalyte to avoid hyperchloremic metabolic acidosis.26,27
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Central venous access may aid in assessing volume status (preload) and monitoring Scvo2. It is also the preferred route for the long-term administration of certain vasopressor therapy. However, there is no need for universal central access in patients with septic shock, and the need for central access should be individually determined.20
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Vasopressors are used when there has been an inadequate response to volume resuscitation or if there are contraindications to volume infusion.25 Vasopressors are most effective when the vascular space is "full" and least effective when the vascular space is depleted. Patients with chronic hypertension may be at greater risk of renal injury at lower blood pressures; however, in others, there appears to be no mortality benefit in raising MAP above the 65 to 70 mm Hg range.28,29
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Vasopressor agents have variable effects on the α-adrenergic, β-adrenergic, vasopressin, and dopaminergic receptors (Table 12–7). Although vasopressors improve perfusion pressure in the large vessels, they may decrease capillary blood flow in certain tissue beds, especially the GI tract and peripheral vasculature. If multiple vasopressors are used, they should be simplified as soon as the best therapeutic agent is identified. In addition to a vasopressor, an inotrope may be needed to directly increase CO by increasing contractility and stroke volume.
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ASSURING ADEQUATE OXYGEN DELIVERY
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Control of oxygen consumption (V̇o2) is important in restoring the balance of oxygen supply and demand to the tissue (oxygen consumption equation). A hyperadrenergic state results from the compensatory response to shock, physiologic stress, pain, and anxiety. Shivering frequently results when a patient is unclothed for examination and then left inadequately covered in a cold resuscitation room. The combination of these variables increases V̇ o2. Pain further suppresses myocardial function, further impairing Do2 and V̇ o2. Providing analgesia, muscle relaxation, warm covering, anxiolytics, and even paralytic agents, when appropriate, decreases this inappropriate systemic oxygen consumption.
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Once blood pressure is stabilized through optimization of preload and afterload, Do2 can be assessed and further manipulated. Restore arterial oxygen saturation to ≥91%. In shock states, consider a transfusion of packed red blood cells to maintain hemoglobin ≥7 to 9 grams/dL.25 If CO can be assessed, it should be increased using volume infusion or inotropic agents in incremental amounts until venous oxygen saturation (mixed venous oxygen saturation [Smvo2] or Scvo2) and lactate are normalized.
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Sequential examination of lactate and Smvo2 or Scvo2 is a method to assess adequacy of a patient's resuscitation. Continuous measurement of Smvo2 or Scvo2 can be used in the ED, although recent literature questions the need for this in resuscitation management.20 A variety of technologic tools may be used to assess tissue perfusion during resuscitation.30,31,32,33,34,35 These technologies may be available in some EDs, but it is essentially standard of care in intensive care units. Transfer of the patient to the intensive care unit should not be delayed so that monitoring devices can be placed in the ED.15,36