Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 9e

Chapter 12: Approach to Nontraumatic Shock Bret A. Nicks; John P. Gaillard

FIGURE 12-1.

EPIDEMIOLOGY

Using a systolic blood pressure <90 mm Hg as criteria, 0.4% to 1.3% of patients presenting to EDs are in shock.1 Mortality depends

on the inciting event. Septic shock has an estimated hospital mortality of 26%.2 Cardiogenic shock has an estimated hospital

mortality of 39% to 48%.3,4 Neurogenic shock occurs in <20% of spinal cord injuries (cervical, 19.3%; thoracic, 7%; lumbar, 3%).5

The definition of and treatment approach to shock continue to evolve, but the initial approach to a patient in shock follows similarprinciples, regardless of the inciting factors or cause.

Patients present to the ED in varying stages of critical illness and shock. These stages are confounded by age, comorbidities, anddelays in presentation. A focus on early recognition, rapid diagnosis, and empiric resuscitation is essential. Therapy and patientstabilization may need to occur simultaneously with evaluation.

PATHOPHYSIOLOGY

Shock is a state of circulatory insu�iciency that creates an imbalance between tissue oxygen supply (delivery) and demand(consumption), resulting in end-organ dysfunction. Reduction in e�ective perfusion may be due to a local or global delivery

deficiency or utilization deficiency with suboptimal substrate at the cellular or subcellular level.6-8 The mechanisms that can resultin shock are frequently divided into four categories: (1) hypovolemic, (2) distributive, (3) cardiogenic, and (4) obstructive.

CATEGORIES OF SHOCK

The four categories of shock can be described in terms of their respective physiologic changes and common causes, recognizing

that a single etiology may manifest the clinical findings of more than one shock type (Table 12-1).9,10 Hypovolemic shock occurswhen decreased intravascular fluid or decreased blood volume causes decreased preload, stroke volume, and cardiac output (CO).Severe blood loss (hemorrhage) can cause decreased myocardial oxygenation, which decreases contractility and CO. This actionmay lead to an autonomic increase in the systemic vascular resistance (SVR). Hypovolemic shock can also occur due to volume lossfrom other etiologies. In distributive shock, there is relative intravascular volume depletion due to marked systemic vasodilatation.

This is most commonly seen in septic shock.6 Compensatory responses to decreased SVR may include increased CO (increasedcontractility and heart rate) and tachycardia. The concurrent decreased SVR results in a decreased preload and may hinder COoverall. In sepsis, up to 40% of patients may have a transient cardiomyopathy characterized by decreased contractility and

increased mortality.6 Anaphylaxis, adrenal insu�iciency, and neurogenic shock are additional causes of distributive shock. Incardiogenic shock, the le� ventricle fails to deliver oxygenated blood to peripheral tissues due to variances in contractility, as well

as preload, a�erload, and right ventricular function.8 Myocardial infarction is the most common cause of cardiogenic shock.Dysrhythmias are another common cause because they can lead to a decreased CO. Bradyarrhythmias result in low CO, andtachyarrhythmias can result in decreased preload and stroke volume. Patients with cardiogenic shock may soon develop clinicallyevident infection (up to 46%) and/or demonstrate an inflammatory response similar to but less pronounced than with septic

shock.9 Obstructive shock is uncommon (1%) and is due to a decrease in venous return or cardiac compliance due to an increasedLoading [Contrib]/a11y/accessibility-menu.js

*Percentage of patients presenting to the ED; percentages will vary depending on hospital type and population.

†Etiologies may demonstrate findings of more than one type of shock.

Abbreviations: CO = cardiac output; MI = myocardial infarction; PE = pulmonary embolism; PTX = pneumothorax; SVR = systemic vascular

resistance.

le� ventricular outflow obstruction or marked preload decrease. Cardiac tamponade, pulmonary embolism, and tensionpneumothorax are causes of obstructive shock.

TABLE 12-1

Categories of Shock

Type Percentage* Hemodynamic Changes Etiologies†

Distributive 33%–50% Decreased preload, decreased SVR, mixed CO Sepsis, neurogenic shock, anaphylaxis

Hypovolemic 31%–36% Decreased preload, increased SVR, decreased CO Hemorrhage, capillary leak, GI losses,

burns

Cardiogenic 14%–29% Increased preload, increased a�erload, increased SVR,

decreased CO

MI, dysrhythmias, heart failure, valvular

disease

Obstructive 1% Decreased preload, increased SVR, decreased CO PE, pericardial tamponade, tension PTX

FACTORS AFFECTING CARDIAC OUTPUT

CO is determined by heart rate and stroke volume. Stroke volume is dependent on preload, a�erload, and contractility. The meanarterial pressure is dependent on CO and the SVR. This is important because there is a mean arterial pressure threshold belowwhich oxygen delivery is decreased. SVR directly impacts mean arterial pressure, but also impacts a�erload and thus CO. Patients inshock may initially have normal blood pressures (cryptic shock), yet have other objective signs of shock (see later section “ClinicalFeatures”). Tissue oxygenation is predicated on CO being su�icient enough to deliver oxygenated hemoglobin to the tissues. CO isdependent on the interplay of cardiac inotropy (speed and shortening capacity of myocardium), chronotropy (heart contractionrate), and lusitropy (ability of heart muscle to relax and heart chambers to fill). Determinants of inotropy include autonomic inputfrom sympathetic activation, parasympathetic inhibition, circulating catecholamines, and short-lived responses to an increase ina�erload (Anrep e�ect) or heart rate (Bowditch e�ect). Increases in the inotropic state help to maintain stroke volume at high heart

rates.11 During shock states, higher levels of epinephrine will be produced and reinforce adrenergic tone. Epinephrine levels aresignificantly elevated during induced hemorrhagic shock, but these levels subsequently reduce to almost normal levels a�er

adequate blood pressure is restored.12 An acidotic milieu, which is common in shock, further compromises ventricular contractile

force and blood pressure.13 Chronotropy and lusitropy are both influenced by sympathetic input. Norepinephrine interacts withcardiac β1-receptors, resulting in increased cyclic adenosine monophosphate. This leads to a process of intracellular signaling with

an increased chronotropy and sequestration of calcium, leading to myocardial relaxation.11

LACTIC ACID

When compensatory mechanisms fail to correct the imbalance between tissue supply and demand, anaerobic metabolism occursand results in the formation of lactic acid. Lactic acid is rapidly bu�ered, resulting in the formation of measured serum lactate.Normal venous lactate levels are <2.0 mmol/L. Most cases of lactic acidosis are a result of inadequate oxygen delivery, but lacticLoading [Contrib]/a11y/accessibility-menu.js

acidosis occasionally can develop from an excessively high oxygen demand (e.g., status epilepticus). In other cases, lactic acidosisoccurs because of impaired tissue oxygen utilization (e.g., septic shock or the postresuscitation phase of cardiac arrest). Elevatedlactate is a marker of impaired oxygen delivery or utilization and correlates with short-term prognosis of critically ill patients in the

ED.12 Serial lactate assessments may be indicated because lactate clearance is associated with improved outcomes in septic shock

and may assist with resuscitation.14

COMPENSATORY MECHANISMS AND THEIR FAILURE

Shock provokes a myriad of autonomic responses to maintain perfusion pressure to vital organs. Stimulation of the carotidbaroreceptor stretch reflex activates the sympathetic nervous system, triggering (1) arteriolar vasoconstriction, resulting inredistribution of blood flow from the skin, skeletal muscle, kidneys, and splanchnic viscera; (2) an increase in heart rate andcontractility that increases CO; (3) constriction of venous capacitance vessels, which augments venous return; (4) release of thevasoactive hormones epinephrine, norepinephrine, dopamine, and cortisol to increase arteriolar and venous tone; and (5) releaseof antidiuretic hormone and activation of the renin-angiotensin axis to enhance water and sodium conservation to maintain

intravascular volume.13

These compensatory mechanisms attempt to maintain oxygen delivery to the most critical organs (heart and brain), but blood flowto other organs, such as the kidneys and GI tract, may be compromised. The cellular response to decreased oxygen delivery(adenosine triphosphate depletion) leads to ion-pump dysfunction, influx of sodium, e�lux of potassium, and reduction inmembrane resting potential. As shock progresses, the loss of cellular integrity and the breakdown in cellular homeostasis result incellular death. These pathologic events give rise to a cascade of metabolic features including hyperkalemia, hyponatremia,azotemia, hyper- or hypoglycemia, and lactic acidosis.

Inflammation plays an important role in several di�erent types of shock, especially in septic shock, but also in shock associated

with anaphylaxis, burns, trauma, and cardiogenic causes.15 Previously, the systemic inflammatory response syndrome was part of

the definition of sepsis, but that changed with a revised definition of sepsis, Sepsis-3, in 2016.16 See Chapter 151, “Sepsis,” fordetailed discussion.

As global tissue hypoxia progresses, shock ensues, followed by the multiorgan dysfunction syndrome, which is manifested by renalfailure, respiratory failure, myocardial depression, liver failure, and then disseminated intravascular coagulation. The fulminantprogression from global tissue hypoxia to multiorgan dysfunction syndrome is determined by the severity of inadequate tissueperfusion and the balance of anti-inflammatory and proinflammatory mediators (Figure 12-1).

FIGURE 12-1.

The pathophysiology of shock, the inflammatory response, and multiorgan dysfunction.

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CLINICAL FEATURES

HISTORY AND COMORBIDITIES

Although the clinical presentation of a patient in shock and the underlying cause may be quite apparent (e.g., acute myocardialinfarction, anaphylaxis, or hemorrhage), it may be di�icult to obtain a history from patients in shock. Assistance with medicalhistory from EMS, family, or other sources may help determine the cause of shock. Some patients in shock may have few symptomsother than generalized weakness, lethargy, or altered mental status. If the patient is unresponsive, consider trauma as a primary orsecondary complication.

PHYSICAL EXAMINATION

Shock is usually associated with systemic arterial hypotension—systolic blood pressure <90 mm Hg. Blood pressure may not drop ifthere is an increase in peripheral vascular resistance in the presence of decreased CO with inadequate tissue hypoperfusion. For thisreason, blood pressure is an insensitive marker for global tissue hypoperfusion. Shock may occur with a normal blood pressure, andhypotension may occur without shock. No single vital sign is diagnostic of shock, and blood pressure is particularly insensitive inthe presence of peripheral vascular disease, tachycardia with a small pulse pressure, or cardiac dysrhythmias. Composite physicalfindings are useful in the assessment of shock (Table 12-2).

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TABLE 12-2

Composite Physical Examination Findings in Shock

Temperature Hyperthermia or hypothermia may be present. Endogenous hypothermia (hypometabolic shock) must be

distinguished from exogenous environmental hypothermia.

Heart rate Usually elevated; however, paradoxical bradycardia can be seen in shock states due to hypoglycemia, β-blocker use,

and preexisting cardiac disease.

Systolic blood

pressure

May actually increase slightly when cardiac contractility increases in early shock and then fall as shock advances.

Diastolic blood

pressure

Correlates with arteriolar vasoconstriction and may rise early in shock and then fall when cardiovascular

compensation fails.

Pulse pressure Increases early in shock and decreases before systolic pressure begins to drop.

Mean arterial

blood pressure

O�en low, <65 mm Hg.

CNS Acute delirium, restlessness, disorientation, confusion, and coma secondary to a decrease in cerebral perfusion

pressure.

Skin/capillary

refill

Pallor, pale, dusky, clammy, cyanosis, sweating, cool, and capillary refill time >2–3 s.

Cardiovascular Neck vein distention or flattening depending on the type of shock. Tachycardia and arrhythmias. An S3 may result

from high-output states. Decreased coronary perfusion pressures can lead to ischemia, decreased ventricular

compliance, increased le� ventricular diastolic pressure, and pulmonary edema.

Respiratory Tachypnea, increased minute ventilation, increased dead space, bronchospasm, and hyper- or hypocapnia with

progression to respiratory failure.

Splanchnic

organs

Ileus, GI bleeding, pancreatitis, and mesenteric ischemia can occur due to low-flow states.

Renal Reduced glomerular filtration rate. Renal blood flow redistributes from the renal cortex toward the renal medulla

leading to oliguria.

Metabolic Lactic acidosis, hyperglycemia, hypoglycemia, and hyperkalemia. As shock progresses, metabolic acidosis occurs

with concurrent respiratory compensation.

DIAGNOSIS

LABORATORY EVALUATION

No single laboratory value is sensitive or specific for shock. Laboratory studies are driven by the clinical presentation and thepresumptive cause. Common studies are listed in Table 12-3. Arterial blood gases are useful to assess acid-base status and

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*Ordering of tests should be individualized by patient presentation and history (see also Chapter 151, “Sepsis”).

ventilation and oxygenation concerns, whereas a venous blood gas is limited to acid-base information. A rise in serum lactate

correlates with mortality in many shock states12; typically this is due to anaerobic metabolism, but nonhypoxic causes of lacticacidosis due to cellular dysfunction occur in shock states. A wide range of laboratory abnormalities may be encountered in shock.The incidence of adrenal dysfunction can be as high as 30% in this subset of patients. Most abnormal values merely point to theparticular organ system that is contributing to, or being a�ected by, the shock state.

TABLE 12-3

Initial Diagnostic Studies to Evaluate a Patient in Shock*

CBC with di�erential

Electrolytes, glucose, calcium, magnesium, phosphorus

BUN, creatinine

Serum lactate

ECG

Urinalysis

Chest radiograph

Coagulation studies: prothrombin time, PTT, INR

Arterial blood gas (pH, carbon dioxide and oxygen levels, base deficit)

Hepatic function panel

Cultures: blood, urine, suspicious wounds, quantitative sputum culture

Cortisol level

Pregnancy test

CT of chest/abdomen/pelvis as indicated by history, physical exam

IMAGING

Chest Radiograph

The portable anteroposterior view chest radiograph is o�en used in the evaluation of unstable patients to avoid transporting thepatient during resuscitation. While limitations exist, evaluation of the heart size, presence of pulmonary edema, free air under thediaphragm, pneumothorax, infiltrates, or e�usions may provide useful clinical information.

US

Bedside US assessment is an important tool for developing a di�erential diagnosis, assessing volume status, defining cardiacfunction, and assisting with procedures. Various US methods are described to determine overall volume status by assessing right-sided filling pressures, including measuring inferior vena cava respiratory variation or end-expiratory vena cava respiratoryvariation, and other methods.

Bedside cardiac US to assess le� ventricular ejection fraction can assist with determining the cause of shock. Emergency physicians

trained in focused bedside cardiac US can provide an estimated ejection fraction with high relative correlation to cardiologists.17

US may also be used to assess for vascular emergencies. Identifying an abdominal aortic aneurysm on US may lead to furtherevaluation. Findings of a deep vein thrombosis may increase the suspicion for a pulmonary embolism.

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Additional US protocols, such as the Abdominal and Cardiac Evaluation with Sonography in Shock protocol and the Rapid

Ultrasound in Shock protocol, have been formulated using many of the aforementioned concepts.17-20 The Abdominal and CardiacEvaluation with Sonography in Shock protocol looks at cardiac function, inferior vena cava dynamics, pulmonary congestion, lungsliding and consolidation, abdominal free fluid, abdominal aortic aneurysm, and leg venous thrombosis to assist in di�erential

diagnosis generation or narrowing.17,18 The Rapid Ultrasound in Shock exam involves a three-part bedside physiologic assessment

simplified as the pump (cardiac), the tank (volume status), and the pipes (arterial and venous).19-21 However, as with any USintervention, operator competency is essential.

CT

Although CT is an accurate and noninvasive approach for detecting internal pathology, patients must travel from the ED to theradiology suite, which may be unadvisable in unstable shock. The potential benefits of CT must be weighed against the associatedrisks, including concerns about renal function due to hypovolemia and contrast-induced nephropathy. CT scans without IV contrastwill add some information to the clinical picture, although not to the degree of a scan with IV contrast.

HEMODYNAMIC MONITORING

Hemodynamic monitoring helps assess the severity of shock and the response to treatment. Monitoring capabilities should initiallyinclude pulse oximetry, ECG monitoring, and noninvasive blood pressure monitoring. In the critical care arena, intra-arterial bloodpressure monitoring, end-tidal carbon dioxide monitoring, central venous pressure, and central venous oxygen saturation from thesuperior vena cava (ScvO2) monitoring are frequently used. When obtaining central access, the average access time, number of

attempts, and mechanical complications are reduced when a US-assisted approach is used.22

TREATMENT

See Chapter 151, “Sepsis,” for treatment of sepsis. Comprehensive and timely ED care can significantly decrease the predicted

mortality of critically ill patients in as little as 6 hours of treatment.23 Application of an algorithmic approach to optimizehemodynamic end points with early goal-directed therapy in the ED reduced mortality by 16% in patients with severe sepsis or

septic shock in 2001.24 That original study, the Surviving Sepsis Campaign that followed,25 and other algorithmic e�orts26 havechanged 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.27,28 However, we attempt to present below themost beneficial aspects of shock care demonstrated by the medical progress of the past 15 years. The ABCDE tenets of shockresuscitation are establishing airway, controlling the work of breathing, optimizing the circulation, ensuring adequate oxygen

delivery, and achieving end points of resuscitation.29

ESTABLISHING THE AIRWAY

Airway control is best obtained through endotracheal intubation. Sedatives used to facilitate intubation may cause arterialvasodilatation, venodilation, or myocardial suppression and may result in hypotension. Positive-pressure ventilation reducespreload and CO. The combination of sedative agents and positive-pressure ventilation will o�en lead to hemodynamic collapse. Toavoid this unwanted situation, initiate volume resuscitation and vasoactive agents before intubation and positive-pressureventilation.

CONTROLLING THE WORK OF BREATHING

Control of breathing is required when significant work of breathing accompanies shock. Respiratory muscles are significantconsumers of oxygen during shock and contribute to lactate production. Mechanical ventilation and sedation allow for adequateoxygenation, improvement of hypercapnia, and assisted, controlled, synchronized ventilation. All of these treatments decrease thework of breathing and improve survival. When starting mechanical ventilation on a patient, it is essential to consider the patient’sLoading [Contrib]/a11y/accessibility-menu.js

compensatory minute ventilation prior to intubation to ensure appropriate initial settings are selected. A�er a patient is placed onmechanical ventilation, obtain an arterial blood gas to evaluate acid-base status, oxygenation, and ventilation. Neuromuscularblocking agents should be considered to further decrease respiratory muscle oxygen consumption and preserve oxygen delivery to

vital organs, especially if patients are severely hypoxemic due to acute respiratory distress syndrome.30

OPTIMIZING THE CIRCULATION

Fluids

Circulatory or hemodynamic stabilization begins with intravascular access through large-bore peripheral venous lines. TheTrendelenburg position does not improve cardiopulmonary performance compared with the supine position. It may worsenpulmonary gas exchange and predispose to aspiration. Passive leg raising above the level of the heart with the patient supine may

be e�ective. If passive leg raising results in an increase in blood pressure or CO, fluid resuscitation is indicated.31

Fluid resuscitation should begin with isotonic crystalloid.32 Balanced crystalloids, such as lactated Ringer’s solution, may o�er a

small mortality advantage over normal saline solution (14.3% vs. 15.4% in a large trial of 15,802 critically ill patients).33 The amountand rate of infusion are determined by an estimate of the hemodynamic abnormality. Most patients in shock have either anabsolute or relative volume deficit. The exception is the patient in cardiogenic shock with pulmonary edema. Administer fluidrapidly (over 5 to 20 minutes), in set quantities of 500 or 1000 mL of normal saline, and reassess the patient a�er each bolus.Patients with a modest degree of hypovolemia usually require an initial 20 to 30 mL/kg of isotonic crystalloid, and current Centersfor Medicare and Medicaid Services sepsis guidelines require 30 mL/kg; however, there are few data to support this uniform

recommendation.34 More fluids may be needed for profound volume deficits. It is common for patients in septic shock to receive 6 Lof crystalloid in the first 24 hours of hospital care. For large fluid volumes, consider using lactated Ringer’s or Plasma-Lyte® to avoid

hyperchloremic metabolic acidosis associated with 0.9% sodium chloride solution35,36 (see later section “Controversies ofTreatment”). In clinical situations where hypochloremia can be predicted, such as from GI losses due to vomiting or from urinaryexcretion due to diuretics, there may be an advantage to 0.9% sodium chloride rehydration.

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.26

Vasopressors

Vasopressors are used when there has been an inadequate response to volume resuscitation or if there are contraindications to

volume infusion.33 Vasopressors are most e�ective when the vascular space is “full” and least e�ective when the vascular space isdepleted. 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 mean arterial pressure above the 65 to 70 mm Hg range.37,38

Vasopressor agents have variable e�ects on the α-adrenergic, β-adrenergic, vasopressin, and dopaminergic receptors (Table 12-4).Although vasopressors improve perfusion pressure in the large vessels, they may decrease capillary blood flow in certain tissuebeds, especially the GI tract and peripheral vasculature. If multiple vasopressors are used, they should be simplified as soon as thebest therapeutic agent is identified. In addition to a vasopressor, an inotrope may be needed to directly increase CO by increasingcontractility and stroke volume. Careful vasopressor infusion initially through a peripheral IV is unlikely to result in tissue injury and

will improve the time to achieve hemodynamic stability.39,40

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TABLE 12-4

Commonly Used Vasoactive Agents (all vasopressors increase myocardial oxygen demand; most should be titrated to desired e�ect)

Drug Dose ActionCardiac

ContractilityVasoconstriction Vasodilation

Cardiac

Output

Dobutamine 2.0–20.0

micrograms/kg/min

β1, some β2

and α1 in

large dosages

++++ + ++ Increases

Side e�ects and

comments

Inotrope only; causes tachydysrhythmias, GI distress, hypotension in volume-depleted patients; less peripheral

vasoconstriction than dopamine; fewer arrhythmias than isoproterenol

Dopamine 0.5–20

micrograms/kg/min

α, β, and

dopaminergic

++ at 2.5–5

micrograms/kg/min

++ at 5–20

micrograms/kg/min

+ at 0.5–2.0

micrograms/kg/min

Usually

increases

Side e�ects and

comments

Tachydysrhythmias; a cerebral, mesenteric, coronary, and renal vasodilator at low doses; Surviving Sepsis Campaign

second line, lot of overlap with α/β/dopaminergic receptors and dose

Epinephrine 2–10

micrograms/min

α and β ++++ at 0.5–8

micrograms/kg/min

++++ at >8

micrograms/kg/min

+++ Increases

Side e�ects and

comments

Causes tachydysrhythmia, leukocytosis; increases myocardial oxygen consumption; may increase lactate; no real

maximum dose

Isoproterenol 0.01–0.1

microgram/kg/min

β1 and some

β2

++++ 0 ++++ Increases

Side e�ects and

comments

Inotrope; causes tachydysrhythmia, facial flushing, hypotension in hypovolemic patients; increases myocardial oxygen

consumption

Norepinephrine 0.5–50

micrograms/min

Primarily α1,

some β1

++ ++++ 0 Slightly

increases

Side e�ects and

comments

Useful when loss of venous tone predominates; first-line agent for most situations

Phenylephrine 10–200

micrograms/min

Pure α 0 ++++ 0 Decreases

Side e�ects and

comments

Reflex bradycardia, headache, restlessness, excitability, rarely arrhythmias; used on patients in shock with tachycardia or

supraventricular arrhythmias; not good comparatively for septic shock

Vasopressin 0.01–0.04 units/min Directly

stimulates V1

receptor on

smooth

muscle

0 ++++ 0 0

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Note: 0 = no e�ect; + = mild e�ect; ++ = moderate e�ect; +++ = marked e�ect; ++++ = very marked e�ect.

Drug Dose ActionCardiac

ContractilityVasoconstriction Vasodilation

Cardiac

Output

Side e�ects and

comments

Primarily vasoconstriction; usually started at max dose and not titrated, typically added to norepinephrine

ENSURING ADEQUATE OXYGEN DELIVERY

Control of oxygen consumption is important in restoring the balance of oxygen supply and demand to the tissue (oxygenconsumption equation). A hyperadrenergic state results from the compensatory response to shock, physiologic stress, pain, coldtreatment rooms, and anxiety. Pain further suppresses myocardial function, impairing oxygen delivery and increasing consumption.Providing analgesia, muscle relaxation, warm covering, anxiolytics, and even paralytic agents, when appropriate, decreases thisinappropriate systemic oxygen consumption.

Once blood pressure is stabilized through optimization of preload and a�erload, oxygen delivery can be assessed and furthermanipulated. Restore arterial oxygen saturation to ≥91%. In shock states, consider a transfusion of packed red blood cells to

maintain hemoglobin ≥7 grams/dL.34 If CO can be assessed, it should be increased using volume infusion or inotropic agents inincremental amounts until venous oxygen saturation (mixed venous oxygen saturation [SvO2] or ScvO2) and lactate are normalized.

Sequential examination of lactate and SvO2 or ScvO2 is a method to assess adequacy of a patient’s resuscitation. Continuous

measurement of SvO2 or ScvO2 can be used in the ED, although results from the ProCESS trial question the need for this in

resuscitation management.28 A variety of technologic tools may be used to assess tissue perfusion during resuscitation.41-47 Thesetechnologies may be available in some EDs, but are more o�en found 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.23,47

END POINTS OF RESUSCITATION

The goal of resuscitation is to use hemodynamic and physiologic values to guide therapy in order to maximize survival andminimize morbidity. No therapeutic end point is universally e�ective, and only a few have been tested in prospective trials, with

mixed results.28,37,38 Hypotension at ED presentation is associated with poor outcomes.48 Noninvasive parameters, such as bloodpressure, heart rate, and urine output, may underestimate the degree of remaining hypoperfusion and oxygen debt, so the use of

additional physiologic end points may be informative.28,37,38,48 A goal-directed approach of mean arterial pressure >65 mm Hg,central venous pressure of 8 to 12 mm Hg, ScvO2 >70%, and urine output >0.5 mL/kg/h during ED resuscitation of septic shock has

been shown to decrease mortality, but which of the metrics accounts for the mortality decrease remains in question.24,27,28,34

Source control, whether with infection, hemorrhage, or other state of shock, is essential in the initial stages of management. Ifshock or hypotension persists, reassessment at the patient’s bedside is essential while considering the important issues in Table 12-5.

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TABLE 12-5

Questions to Answer If There Is Persistent Shock or Hypotension

Equipment and monitoring

Is the patient appropriately monitored?

Is there an equipment malfunction, such as dampening of the arterial line or disconnection from the transducer?

Is the IV tubing into which the vasopressors are running connected appropriately?

Are the vasopressor infusion pumps working?

Are the vasopressors mixed adequately and in the correct dose?

Patient assessment

Do mentation and clinical appearance match the degree of hypotension?

Is the patient adequately volume resuscitated?

Does the patient have a pneumothorax a�er placement of central venous access?

Has the patient been adequately assessed for an occult penetrating injury?

Is there hidden bleeding from a ruptured spleen, large-vessel aneurysm, or ectopic pregnancy?

Does the patient have adrenal insu�iciency?

Is the patient allergic to the medication just given or taken before arrival?

Is there cardiac tamponade in the dialysis patient or cancer patient?

Is there associated acute myocardial infarction, aortic dissection, or pulmonary embolus?

CONTROVERSIES OF TREATMENT

Fluid Therapy

Rapid restoration of fluid deficits modulates inflammation and, if the condition progresses to shock, decreases the need forsubsequent vasopressor therapy, steroid administration, and invasive monitoring (e.g., pulmonary artery catheterization and

arterial line placement).33,46 Although there is general agreement that volume therapy is an integral component of earlyresuscitation, there is a lack of consensus for the type of fluid, standards of volume assessment, and end points despite care

mandates that dictate otherwise.49 Table 12-6 compares the most commonly used fluid therapies.50-54

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TABLE 12-6

Fluid Therapy

Crystalloids

Normal

saline (NS)

Slightly hyperosmolar containing 154 mEq/L of both sodium and chloride.

Risk of inducing hyperchloremic metabolic acidosis when given in large amounts due to relatively high chloride

concentration.

Lactated

Ringer’s (LR)

Sodium 130 mEq/L, potassium 4 mEq/L, calcium 3 mEq/L, chloride 109 mEq/L, lactate 28 mEq/L. Lactate can accept a

proton and subsequently be metabolized to carbon dioxide and water by the liver, leading to release of carbon dioxide

in the lungs and excretion of water by the kidneys. LR results in a bu�ering of the acidemia that is advantageous over

NS.

Theoretical risk of inducing hyperkalemia in patients with renal insu�iciency or renal failure due to small potassium

content (very small amount).

Plasma-Lyte® Balanced pH 7.4, sodium 140 mEq/L, chloride 98 mEq/L, potassium 5 mEq/L, magnesium 3 mEq/L, gluconate 23

mEq/L, acetate 27 mEq/L.

Colloids

Albumin Derived from human plasma.

Available in varying strengths from 4% to 25%.

Multiple studies have shown that there is no outcome di�erence whether colloids or crystalloids are used. Colloids cost

significantly more than crystalloids. One study actually showed an increase in mortality in trauma patients with head

injury.

Hydroxyethyl

starch

Synthetic colloid derived from hydrolyzed amylopectin.

These agents should be avoided in sepsis. Many harmful e�ects: renal impairment at recommended doses and

impairment of long-term survival at high doses, coagulopathy and bleeding complications from reduced factor VIII and

von Willebrand factor levels, impaired platelet function.

Colloids are high-molecular-weight solutions that increase plasma oncotic pressure. Colloids can be classified as either natural(albumin) or artificial (starches, dextrans, and gelatins). Due to their higher molecular weight, colloids stay in the intravascularspace significantly longer than crystalloids. The intravascular half-life of albumin is 16 hours versus 30 to 60 minutes for normal

saline and lactated Ringer’s solution.32,50-54

Resuscitation with crystalloids requires two to four times more volume than colloids.32,49,50 The outcome advantage between

crystalloid and colloids continues to remain unresolved in sepsis, despite multiple studies.32,49-52 Due to the equivalency and thehigher cost of colloids, crystalloids would seem to be a better choice for resuscitation in the ED.

Crystalloid type a�ects acid-base status and may have an e�ect on mortality, acute kidney injury, and the need for renal

replacement therapy.35,36,55-58 Two large, single-center, randomized controlled trials compared normal saline to balanced saltsolutions (lactated Ringer’s or Plasma-Lyte®) in the resuscitation of patients in the ED prior to admission and found fewer major

adverse events (persistent renal dysfunction, new renal replacement therapy, or mortality) in the balanced salt group.55,56 Thedi�erence favoring fewer adverse e�ects in the balance salt group was small (10.3% vs. 11.1% in those admitted to the intensive

care unit and 4.7% vs. 5.6% in those admitted to the floor).55,56 Since then, a meta-analysis including those two studies, plus fourprior randomized controlled trials, totaling 19,332 patients, found no significant di�erences in the outcome measures of intensive

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1. 

2. 

care unit mortality, acute kidney injury, and new renal replacement therapy when comparing 0.9% normal saline to balanced salt

solutions.59 Several ongoing randomized controlled trials comparing IV resuscitation fluids are pending completion.57,60,61 Arandomized controlled trial of 157 patients receiving IV hydration with 2 L of 0.9% normal saline versus lactated Ringer’s solution

before presumed discharge from ED found no di�erence in outcomes.62 The majority of the patients were healthy, with

hypovolemia from vomiting or diarrhea.62 Most consistent in all the cited trials is a hyperchloremic acidosis associated with large-volume resuscitation with normal saline and, as of yet, no measured adverse e�ects of resuscitation with balanced salt solutions,despite a theoretical potential for metabolic alkalosis, hypotonicity from fluids with lactate, and cardiotoxicity from fluids with

acetate.63

Sodium Bicarbonate

Bicarbonate administration shi�s the oxygen-hemoglobin dissociation curve to the le�, impairs tissue unloading of hemoglobin-bound oxygen, and may worsen intracellular acidosis. However, despite no definitive clinical trials supporting benefit but perhaps

harm, many clinicians remain uncomfortable withholding bicarbonate if the pH is <7.00.64,65 Animal studies of profound acidosis

demonstrate decreased ventricular contractility and systolic blood pressure.13 If bicarbonate is given, recognize the risk ofparadoxical intracerebral intracellular acidosis in the process. Consider situations, such as end-stage renal disease and renal tubularacidosis, that cannot reclaim bicarbonate through normal renal processes and whether bicarbonate may be indicated.

DISPOSITION

TRANSITION TO THE INTENSIVE CARE UNIT

Early recognition, treatment, and subsequent transfer of critically ill patients to the intensive care unit improves patient outcomes

and improves ED throughput.23,47 Communicate and document all ED resuscitative e�orts to the critical care team. Even whenresuscitation is systematic and thoughtful, miscommunication can undo the benefits of initial ED treatment. Ideally, before transfer,verbally communicate and document a system-oriented problem list with an assessment and plan, including all procedures andcomplications. For prolonged or “boarded” ED stays, constantly reassess the critically ill patient, ensure that care plans arecontinuing, and consider creating a critical care patient checklist. O�en, this will entail ordering tests that are not commonlyperformed on ED patients or ordering subsequent doses of medicines, particularly antibiotics.

PROGNOSIS

Some clinical variables are associated with poor outcome, such as severity of shock, temporal duration, underlying cause,preexisting vital organ dysfunction, and reversibility. Early recognition, intervention, source control, and smooth care transitionsoptimize outcomes. While associated morbidity and mortality remain high for patients with shock, integration of protocol-based

care pathways with ongoing refinement in response to new information may lead to continued reductions over time.23,28,34,47

Additional outcome predictions related to physiologic scoring systems, ED-based shock interventions, and the balance between

invasive and noninvasive or minimally invasive strategies are still being studied.23,66,67

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