C H A P T E R 6 

Shock
Michael A. Puskarich  |  Alan E. Jones

PRINCIPLES Specific Causes

Background and Importance Hemorrhagic Shock

In philosophic terms, shock can be viewed as a transition between Hemorrhagic shock results from a rapid reduction in intravascu-
life and death. Whether shock results from hemorrhage, sepsis, or lar blood volume from any cause. Rapid hemorrhage generally
cardiac failure, mortality rates exceed 20%.1,2 In scientific lexicon, causes an increase in the strength of cardiac contraction and heart
shock results from the widespread failure of the circulatory system rate (HR), followed by baroreceptor activation and peripheral
to oxygenate and nourish the body adequately. At the cellular level, vasoconstriction. Typically, an initial slight increase in the dia-
shock alters mitochondrial energy transfer and evokes the produc- stolic blood pressure (BP) with a narrowing of the pulse pressure
tion and accumulation of toxic chemicals. The emergency clini- progresses to a decrease in ventricular filling and cardiac output,
cian identifies shock by linking the qualitative clinical impression, causing a reduction in systolic BP. This response varies consider-
synthesized from the patient’s history of present illness, age, health ably with cardiopulmonary status, age, and presence of vasoactive
status, and general appearance, to quantitative data, including medications. The responses of HR and BP are therefore notori-
vital signs, laboratory tests, urine output, and measurements ously variable in hemorrhage, so no firm conclusion can be made
of systemic oxygenation. When the clinical impression and quan- at the bedside about the presence, absence, or degree of hemor-
titative data suggest widespread organ hypoperfusion, emergent rhagic shock by simple evaluation of the HR and BP.
resuscitation is used to restore tissue oxygenation and substrate Even before the cardiac output begins to decline, blood flow is
delivery to prevent deterioration into a vicious cycle of systemic directed away from noncritical organs and tissues, and their cells
inflammation, organ dysfunction, and death. Anaphylaxis and its produce and release lactic acid. Consequently, acidemia often
treatment are discussed in Chapter 109. precedes any significant decrease in cardiac output. However,
For years, shock has been classified into four broad categories the blood contains bicarbonate ions that buffer the blood pH,
based on Blalock’s 1934 description—hematologic, vasogenic, keeping it near neutral, even as lactic acid accumulates. The base
cardiogenic, and neurologic. This basic organization scheme deficit—amount of strong base that would have to be added to
remains useful today for discussions of pathophysiology. For dis- 1 L of blood to normalize the pH—represents an index of how
cussions of management, a system based on the requisite treat- far the bloodstream has dipped into this reserve. A normal
ment response is more clinically useful. Box 6.1 outlines five base deficit is more positive than −2 mEq/L. The arterial and
categories of shock that generally have specific mechanisms and venous blood base deficit can become more negative early in
treatments. The epidemiology of shock in the emergency depart- hemorrhage, even while blood pH and BP remain normal. The
ment (ED) context is diverse and evolving. Traumatic, cardio- base deficit, therefore, crudely represents the physiologic endpoint
genic, or septic shock are diagnosed in fewer than 3% of ED that distinguishes trivial blood loss from clinically significant
patients. Our understanding of the metabolic, systemic, and hemorrhage. In addition to chemical buffering, the body responds
inflammatory responses that occur in all types of circulatory to small reductions in arterial pH by activating brainstem chemo-
shock and the specific pathophysiology of the major causes of receptors, which increase minute ventilation, leading to reduced
shock has led to dramatic increases in the early identification partial pressure of carbon dioxide in the arterial blood (Paco2),
and treatment of these states, with resultant improvement in providing an additional means of compensating for evolving
outcomes. acidosis.
With progressive blood loss, cardiovascular reflexes can no
Anatomy, Physiology, and Pathophysiology longer sustain adequate filling of the vasculature, and frank hypo-
tension supervenes. Arterial hypotension is generally and arbi-
At the subcellular level, shock first affects the mitochondria. Mito- trarily defined as an arterial BP less than 90 mm Hg. Usually
chondria function at the lowest oxygen tension in the body, but coincident with the development of hypotension, the compensa-
they consume almost all the oxygen used by the body. More than tory chemical and respiratory buffering mechanisms become
95% of aerobic chemical energy comes from mitochondrial com- overwhelmed, resulting in acidosis. The hypothalamic-pituitary-
bustion of fuel substrates (fats, carbohydrates, ketones) plus adrenomedullary axis is activated, releasing stress hormones and
oxygen into carbon dioxide (CO2) and water. Mitochondria have inducing glycogenolysis, lipolysis, and mild hypokalemia. Signifi-
therefore been referred to as the canaries in the coal mine because cant traumatic hemorrhage in otherwise normal ED patients,
they are affected first in conditions of inadequate tissue perfusion. therefore, will generally cause an arterial lactate concentration
When mitochondria have inadequate oxygen, the cell catabolizes greater than 4.0 mmol/L, Paco2 less than 35 mm Hg, mild
fuels to lactate, which accumulates and diffuses into the blood. In hyperglycemia (150–170 mg/dL) and mild hypokalemia (3.5–
the setting of hypoxia, mitochondria are unable to provide suffi- 3.7 mEq/L). Although hemorrhagic hypotension reduces lung
cient energy to maintain cellular processes and, at a certain point, perfusion, arterial hypoxemia should not be attributed simply to
an irreversible series of intracellular cascades leads to cellular blood loss, but instead should prompt investigation for aspiration,
dysfunction, organ failure, and ultimately death. airway obstruction, alveolar consolidation, or lung injury.
68
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 CHAPTER 6  Shock 69

BOX 6.1 

Five Categories of Shock According to Primary Treatment of Causes and Problems

PRIMARILY INFUSION OF VOLUME Septic shock with myocardial failure (hypodynamic shock)
Hemorrhagic shock Overdose of negative inotropic drug
Traumatic Beta blocker
Gastrointestinal Calcium channel antagonist
Body cavity Structural cardiac damage
Hypovolemia Traumatic (eg, flail mitral valve)
Gastrointestinal losses Ventriculoseptal rupture
Dehydration from insensible losses Papillary muscle rupture
Third-space sequestration from inflammation
IMMEDIATE RELIEF FROM OBSTRUCTION TO
VOLUME INFUSION AND VASOPRESSOR SUPPORT CARDIAC OUTPUT
Septic shock Pulmonary embolism
Anaphylactic shock Cardiac tamponade
Central neurogenic shock Tension pneumothorax
Drug overdose Valvular dysfunction
Acute thrombosis of prosthetic valve
IMPROVEMENT IN PUMP FUNCTION BY INFUSION OF Critical aortic stenosis
INOTROPIC SUPPORT OR REVERSAL OF THE CAUSE Congenital heart defects in newborn (eg, closure of patent ductus
OF PUMP DYSFUNCTION arteriosus, with critical aortic coarctation)
Myocardial ischemia Critical idiopathic subaortic stenosis (hypertrophic obstructive
Coronary artery thrombosis cardiomyopathy)
Arterial hypotension with hypoxemia
Cardiomyopathy SPECIFIC ANTIDOTES DUE TO CELLULAR OR
Acute myocarditis MITOCHONDRIAL POISONS
Chronic diseases of heart muscle (ischemic, diabetic, infiltrative, Carbon monoxide
endocrinologic, congenital) Methemoglobinemia
Cardiac rhythm disturbances Hydrogen sulfide
Atrial fibrillation with rapid ventricular response Cyanide
Ventricular tachycardia
Supraventricular tachycardia

The second phase of organ injury from hemorrhagic shock sepsis in hospitalized patients, indicating that the pathophysiology
occurs during resuscitation. The acute phase of hemorrhage initi- of sepsis cannot be explained simply by the response to LPS.
ates the inflammatory cascade, and resuscitation unleashes these Septic shock often causes three major effects that must be
volatile inflammatory mediators on the body, inducing organ addressed during resuscitation—hypovolemia, cardiovascular
injury. During resuscitation, neutrophils become more aggressive, depression, and induction of systemic inflammation. Septic shock
binding to the lung endothelium and causing capillary leakage produces relative and absolute hypovolemia, reducing right ven-
that characterizes acute respiratory distress syndrome (ARDS). tricular filling. Absolute hypovolemia results from gastrointestinal
Inflammatory cytokines are liberated, causing additional cellular volume loss, tachypnea, sweating, and decreased fluid intake
damage and compounded by persistent microischemia in numer- during development of the illness. Further relative hypovolemia
ous organs due to an imbalance between vasodilation by nitric results from increasing venous capacitance in conjunction with
oxide (NO) and vasoconstriction by endothelins. The liver dem- increased capillary leak and resultant loss of intravascular volume
onstrates centrilobular injury, demonstrated clinically by elevated into third spaces. Septic shock causes direct myocardial depres-
transaminase levels, whereas the kidney may manifest acute spasm sion. Measurements of cardiac contractility have shown that
of the preglomerular arterioles, with resultant acute tubular mechanical function becomes impaired early in the course of
necrosis. A growing body of evidence has suggested that resuscita- septic shock, even in the hyperdynamic stages. Circulating media-
tion from hemorrhage exerts greater injury on the heart than the tors, myocardial cellular injury from inflammation, and deranged
actual hypotensive insult. metabolism interact synergistically to injure the heart during
septic shock, and specific cytokines (most notably tumor necrosis
Septic Shock factor alpha [TNF-α] and interleukin-1 beta [IL-1β]), overpro-
duction of NO by inducible nitric oxide synthase (iNOS), and
Although historically presented as the archetype of vasogenic or possibly impairment in mitochondrial oxidative phosphorylation,
distributive shock, in reality the clinical course of septic shock is may all play a role. Similar to hemorrhagic shock, systemic inflam-
much more complex and varies over the course of the disease, mation causes capillary leak in the lung, resulting in ARDS. Wide-
with variables degrees of intravascular volume depletion, periph- spread systemic inflammation likely plays a role in the development
eral vasodialation, and impaired cardiac function. Septic shock and persistence of multisystem organ failure in sepsis through
can be produced by infection with any microbe, although in half microvascular and mitochondrial dysfunction. Clinical trials to
or more of cases of septic shock, no organism is identified. One date have yet to demonstrate the effectiveness of specific or general
well-known mediator of sepsis is lipopolysaccharide (LPS), con- antiinflammatory therapies in mitigating this response, and the
tained in the outer cell membrane of gram-negative bacteria; treatment of septic shock relies primarily on the reversal of shock,
however, gram-positive organisms are now the primary cause of supportive care, and source control.

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70 PART I  Fundamental Clinical Concepts  |  SECTION One  Critical Management Principles

Cardiogenic Shock medications are administered. BP and HR correlate poorly with

the cardiac index (CI) in shock and often underestimate the sever-
Cardiogenic shock results when more than 40% of the myocar- ity of systemic hypoperfusion. Moreover, children with hypovole-
dium becomes dysfunctional from ischemia, inflammation, mic shock frequently demonstrate a normal BP until they rapidly
toxins, or immune injury. Otherwise, cardiogenic shock essen- deteriorate.
tially produces the same circulatory and metabolic alterations as Urine output provides an excellent indicator of vital organ
those that are observed with hemorrhagic shock. Undoubtedly, perfusion and is readily available with insertion of a Foley cath-
impaired baseline cardiac function can contribute to the develop- eter. Measurement of urine output, however, requires 30 to 60
ment of circulatory shock secondary to infection, hemorrhage, or minutes for accurate determination of whether output is normal
vasodilatory drug overdose. However, when shock results from a (>1.0 mL/kg/h), reduced (0.5–1.0 mL/kg/h), or severely reduced
pure cardiac cause, severe left ventricular dysfunction will be (<0.5 mL/kg/h), and is of limited use in patients with preexisting
evident on echocardiography early in the course. Patients with renal disease. Arterial or venous lactate concentration and the base
severe underlying dysfunction are far more likely to have a car- deficit provide accurate assessment of global perfusion status. A
diogenic cause of shock than patients with normal or moderate lactate concentration greater than 4.0 mM or base deficit more
left ventricular dysfunction. negative than −4 mEq/L indicates circulatory insufficiency severe
enough to cause subsequent multiple organ failure.4 A downward
Neurogenic Shock trend of the serum lactate concentration or upward trend of the
base deficit, with correspondingly improving vital signs and urine
Neurogenic shock results from interrupted sympathetic and para- output, reliably gauge the adequacy of resuscitation and prognosis
sympathetic input from the spinal cord to the heart and periph- in shock from any cause. A rising lactate concentration (or refrac-
eral vasculature, typically resulting from acute traumatic injury. tory hypotension, with worsening base deficit), despite ongoing
Traditionally, it has been described as peripheral vasodilation in resuscitation, calls for more intensive measures. Once the empiri-
conjunction with bradycardia. However, ED patients with shock cal criteria for circulatory shock have been discovered, the next
from acute spinal injury actually manifest a range of heart rates step is to consider the cause of the shock. Fig. 6.1 shows a potential
and peripheral vascular resistance, most likely due to variable sequence of decisions to help arrive at a diagnosis in a patient with
location of injury and the balance between disrupted efferent undifferentiated shock.
sympathetic and parasympathetic tone.3 As a result, no single The history, vital signs, and physical examination documented
presentation adequately summarizes patients with neurogenic by prehospital providers can be useful in ED evaluation and
shock. It is likely that the downstream pathophysiologic conse- management. Patients with prehospital hypotension, whether
quences of persistently impaired perfusion mimic those of cardio- of medical or traumatic origin, have up to a fourfold higher
genic and hemorrhagic shock. in-hospital mortality rate than patients without hypotension.5
On physical examination, dry mucous membranes suggest
MANAGEMENT dehydration, whereas jugular venous distention suggests conges-
tive cardiac failure or right ventricular strain from pulmonary
Decision Making embolism (PE). Muffled heart sounds with jugular venous disten-
tion suggest cardiac tamponade, whereas a loud, machine-like,
Patients presenting to the the ED in shock frequently have no systolic murmur indicates acute rupture of a papillary muscle or
obvious cause. Rapid recognition of shock requires the integration interventricular septum. Diffuse rhonchi suggest bronchospasm,
of information from the immediate history and physical examina- cardiac failure, or PE. Abdominal tenderness may indicate perito-
tion and is strongly supported by the presence of a worsening base nitis, intestinal perforation, or occult trauma. The presence of
deficit or lactic acidosis. In general, patients with shock exhibit a melanotic stool on rectal examination indicates gastrointestinal
stress response; they are ill appearing, asthenic, pale, often sweat- hemorrhage. The neurologic examination documents responsive-
ing, usually tachypneic, and often have a weak and rapid pulse ness, cognition, and presence of any focal deficits and can be a
(Box 6.2). In all patients with shock, HR, BP, and oxyhemoglobin means of clinically assessing end-organ perfusion. In children,
saturation are continuously monitored. HR can be normal or low documentation should include response to parents, appropriate-
in shock, especially in cases complicated by prescribed drugs that ness of crying, symmetry of grimace, symmetry of extremity
depress HR. BP initially can be normal because of adrenergic movements, and motor tone.
reflexes. Noninvasive measurement of BP may be inaccurate in Laboratory, radiographic, and other ancillary data can be
severe hypotensive states, and insertion of an arterial pressure useful to assess tissue and vital organ perfusion and diagnose
monitoring line improves the ability to monitor the dynamic injury from trauma, find the source of infection with sepsis, or
response to therapy, which is particularly important if vasoactive identify the cause of cardiac failure. Chest radiography, electro-
cardiography, finger stick glucose measurement, complete blood
count (CBC), urinalysis, serum electrolyte levels, and kidney
and liver function tests are indicated for most patients with
BOX 6.2  suspected shock. Arterial blood gas determination provides the
base deficit and allows correlation of arterial gas tensions (Pao2
Empirical Criteria for Diagnosis of and Paco2) with those measured by pulse oximetry and capnog-
raphy. Serum lactate level measurement is performed as early as
Circulatory Shocka possible in patients with suspected shock; venous or arterial
lactate concentrations can be used. If the peripheral venous lactate
• Ill appearance or altered mental status level is used, the effect of time, storage temperature, and tourni-
• Heart rate > 100 beats/min quet use have no significant effect if the measurement is done
• Respiratory rate > 20 breaths/min or PaCO2 < 32 mm Hg within 15 minutes after the sample was obtained. Cardiac and
• Arterial base deficit < −4 mEq/L or lactate level > 4 mM/L
abdominal bedside ultrasound scanning can screen for inadequate
• Urine output < 0.5 mL/kg/h
central venous volume, occult hemoperitoneum, abdominal
• Arterial hypotension > 30 min duration, continuous
aortic aneurysm, left ventricular failure, and cardiac tamponade.
a
Regardless of cause. Four criteria should be met. A systematic ultrasound protocol can significantly improve the

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 CHAPTER 6  Shock 71

Search for: BOX 6.3 

Yes 1. Hemorrhagic shock
History
of trauma?
2. Tension pneumothorax
3. Cardiac tamponade
Definitions and Criteria for Septic,
No 4. Cardiac injury Hemorrhagic, and Cardiogenic Shock
SEPTIC SHOCK
Evidence of
Systemic Inflammatory Response Syndrome (SIRS)
gastrointestinal
Yes Two or more of the following:
hemorrhage, Volume resuscitate
vomiting, 1. Temperature > 38°C or < 36°C
or diarrhea? 2. Heart rate > 90 beats/min
3. Respiratory rate > 20 breaths/min or Paco2 < 32 mm Hg
No 4. White blood cell count > 12,000/mm3, < 4,000/mm3, or > 10%
1. Begin treatment for band neutrophilia
sepsis syndrome
Fever or Yes 2. Search for source
hypothermia? of infection Severe Sepsis
3. Consider thyroid SIRS with suspected or confirmed infection and associated with organ
No function tests dysfunction or hypotension; organ dysfunction may include presence of
lactic acidosis, oliguria, and/or altered mental status.
1. Treat for cardiogenic
Electrocardiographic shock from myocardial Septic Shock
evidence of ischemia Yes ischemia SIRS with suspected or confirmed infection with hypotension despite
or chest pain with major 2. Consider massive adequate fluid resuscitation requiring vasopressor support; septic shock
risk factors for coronary pulmonary embolism
artery disease? should still be diagnosed if vasopressor therapy has normalized blood
with right ventricular
pressure.
strain effect
No HEMORRHAGIC SHOCK
1. Evaluate or treat for
ingestion of negative
Simple Hemorrhage
inotropic drug Suspected bleeding with pulse rate < 100 beats/min, normal
Unexplained Yes respiratory rate, normal blood pressure, and normal base deficit
bradycardia with 2. Initiate thyroid function
hypotension? tests
3. Consider treatment for Hemorrhage with Hypoperfusion
No
addisonian crisis or Suspected bleeding with base deficit < −4 mEq/L or persistent pulse
steroid withdrawal rate > 100 beats/min

Unexplained Yes Rule out pulmonary Hemorrhagic Shock

hypoxemia? embolism Suspected bleeding, with at least four criteria listed in Box 6.2
No
1. Volume resuscitate CARDIOGENIC SHOCK
2. Emergent abdominal Cardiac Failure
Abdominal Yes computed tomography Clinical evidence of impaired forward flow of the heart, including
or low or surgical consultation presence of dyspnea, tachycardia, pulmonary edema, peripheral edema,
back pain? to evaluate for peritoneal and/or cyanosis
inflammation or vascular
No rupture
Cardiogenic Shock
Cardiac failure plus four criteria listed in Box 6.2
Wheezing Yes Treat for
with hives or
anaphylaxis
skin flushing?

Fig. 6.1.  Flow diagram to classify undifferentiated shock. 2. Septic shock. International consensus definitions distinguish
septic shock from its precursor conditions—systemic inflam-
matory response syndrome (SIRS), sepsis, and severe sepsis.9
SIRS is often a precursor of shock, but the nonspecific criteria
emergency clinician’s ability to accurately diagnose the cause of for SIRS are found in a large variety of conditions, many of
undifferentiated shock in ED patients, and the finding of hyper- which are benign, so the clinical context is vital to understand-
dynamic left ventricular function in patients with undifferentiated ing the significance of these physiologic variations. Although
shock strongly suggests sepsis.6,7 a consensus definition of septic shock requires persistent hypo-
Consensus definitions of shock show the spectrum of tension after fluid resuscitation, initiation of treatment for
hypoperfusion for the following three common causes of shock empirically diagnosed severe sepsis or septic shock should not
(Box 6.3): await the onset of hypotension. The incorporation of an indi-
1. Hemorrhagic shock. The American College of Surgeons has cator of tissue hypoperfusion (Box 6.4) into the clinical assess-
divided hemorrhagic shock into four stages, depending on the ment may improve identification of hypoperfusion, particularly
severity of blood loss and physiologic response to this loss, but in subtle cases.10
such arbitrary divisions are of little value and are not accurate 3. Cardiogenic shock. Cardiogenic shock should be thought to be
reflections of degree of hemorrhage in clinical practice.8 A present whenever cardiac failure (ischemic, toxic, or obstruc-
more useful approach defines hemorrhagic shock as being tive) causes systemic hypoperfusion that manifests as lactic
present when systemic hypoperfusion manifests as lactic acidosis with organ dysfunction.
acidosis or increasing base deficit with concomitant organ Box 6.5 presents the general treatment approach for these three
dysfunction. common causes of shock.

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72 PART I  Fundamental Clinical Concepts  |  SECTION One  Critical Management Principles

BOX 6.4  these measurements has been debated. However, a triple-lumen

catheter also allows for safe infusion of vasopressors in hypoten-
Variables Indicating Tissue Hypoperfusion sive patients unresponsive to an initial fluid bolus, as well as more
rapid simultaneous infusion of intravenous (IV) fluids and anti-
biotics in patients with limited IV access. In children, a 3- or 5-Fr
Hypotension
Tachycardia bilumen catheter can be placed in the femoral vein with few com-
Low cardiac output plications. If unable to attain adequate peripheral or central
Dusky or mottled skin venous access rapidly in patients with shock, intraosseous (IO)
Delayed capillary refill access should be established, because it is easy and can provide a
Altered mental state temporary method of administering fluid resuscitation and medi-
Low urine output cations to adults and children. However, IO access should be
Low central venous oxygen saturation considered a bridge to definitive IV access due to the risk of
Elevated lactate level complications with prolonged usage in the inpatient setting. If
vasoactive medications are administered, additional peripheral IV
catheters will be required for infusion of crystalloid and other
treatments. Many patients with renal disease or cancer have
indwelling catheters in place. In patients with empirical criteria
BOX 6.5  for shock, this catheter should be used for IV access, unless satis-
factory access has already been established at other anatomic sites.
Clinical Management Guidelines for Three In EDs where the standard practice is not to use these ports at the
Common Causes of Shock request of other emergency clinicians, a specific hospital policy
and training session should be developed to make an exception in
HEMORRHAGIC SHOCK the case of circulatory shock. In general, failure to administer
• Ensure adequate ventilation and oxygenation. fluids rapidly and in sufficient quantity outweighs considerations
• Provide immediate control of hemorrhage, when possible (eg, about preservation of the line for future therapy.
traction for long bone fractures, direct pressure), and obtain urgent
consultation as indicated for uncontrollable hemorrhage. Quantitative Resuscitation
• Initiate judicious infusion of isotonic crystalloid solution
(10–20 mL/kg). Quantitative resuscitation, also called goal-directed therapy, goal-
• With evidence of poor organ perfusion and 30-min anticipated oriented resuscitation, or hemodynamic optimization, was first
delay to hemorrhage control, begin packed red blood cell (PRBC) described in 1988 and refers to the practice of resuscitating
infusion (5–10 mL/kg). patients to predefined physiologic endpoints indicating that sys-
• With suspected massive hemorrhage, immediate PRBC transfusion temic perfusion and vital organ function have been restored. Since
may be preferable as the initial resuscitation fluid. that time, many studies have evaluated the efficacy of such a
• Treat coincident dysrhythmias (eg, atrial fibrillation with therapeutic approach to shock and have confirmed its benefit
synchronized cardioversion). for reducing mortality. For many years, in the intensive care
unit (ICU), clinicians have relied on the use of the pulmonary
CARDIOGENIC SHOCK artery catheter to help optimize left ventricular filling indices, but
• Ameliorate increased work of breathing; provide oxygen and data supporting the efficacy of this practice on patient-centered
positive end-expiratory pressure (PEEP) for pulmonary edema. outcomes such as mortality are lacking. There is insufficient evi-
• Begin vasopressor or inotropic support; norepinephrine (0.5 µg/
dence to support the use of pulmonary artery catheters for ED
min) and dobutamine (5 µg/kg/min) are common empirical agents.
patients, and their significant complication rate, in the context
• Seek to reverse the insult (eg, thrombolysis, percutaneous
transluminal angioplasty). of uncertain or no benefit, leads us to recommend against their
• Consider intraaortic balloon pump counterpulsation for refractory routine use.
shock. Lactate clearance refers to serial measurements of the venous
or arterial lactate level and is calculated according to the following
SEPTIC SHOCK formula:
• Ensure adequate oxygenation; remove work of breathing.
• Administer 20 mL of crystalloid/kg or 5 mL of colloid (albumin)/kg, ([Lactateinitial − lactatedelayed ] lactateinitial ) ×100
and titrate infusion based on dynamic indices, volume
responsiveness, and/or urine output. Lactate clearance has been shown to be equivalent to central
• Begin antimicrobial therapy; attempt surgical drainage or venous oxygen saturation as an endpoint of early septic shock
débridement. resuscitation.12 Lactate clearance measurements are easily obtained
• Begin PRBC infusion for hemoglobin level <7 g/dL. from peripheral venous blood and are a preferred endpoint of
If volume restoration fails to improve organ perfusion, begin resuscitation. If the lactate concentration has not decreased by
vasopressor support with norepinephrine, infused at 0.5 µg/min. 10% to 20% 2 hours after resuscitation has begun, additional steps
are undertaken to improve systemic perfusion. Resuscitation
should continue until the lactate concentration drops below
2 mM/L.13
Monitoring Perfusion Status Mixed venous oxygen saturation (SvO2) measurements reflect
the balance between oxygen delivery and oxygen consumption.
Patients with cardiac failure or renal failure may benefit from The SvO2 can be used as a surrogate for CI—targeting an SvO2 of
closer measurement of dynamic variables of fluid responsiveness 65% is equivalent to reaching a CI of 2.5–3.5 L/min/m2—as a
that can be measured from an arterial line (eg, stroke volume therapeutic endpoint in critically ill patients. Although SvO2
variation or stroke volume index) or a central venous line (central requires the use of a pulmonary artery catheter, the central venous
venous pressure [CVP]).11 A triple-lumen catheter allows for oxygen saturation (ScvO2 ) drawn from the central circulation has
accurate measurement of the CVP, although the clinical utility of been shown to parallel changes or trends over time and is the

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 CHAPTER 6  Shock 73

preferable method for pulmonary artery catheter placement in departmental, or individual preferences. Initial volume replace-
the ED. ment consists of the rapid infusion of 20 to 25 mL of isotonic
Quantitative resuscitation, which incorporates multiple indices crystalloid per kilogram.
of circulatory and oxygenation status, has been shown in meta-
analyses to reduce mortality and morbidity in ED patients with Colloids and Hypertonic Saline.  Colloids, including
severe sepsis or septic shock significantly when instituted as early albumin, have been used in patients with hemorrhage, but at
in the disease course as is practical. In such an approach, patients considerable increase in cost and without effect on morbidity
are resuscitated early, within the first 6 hours, to achieve normal- or mortality. Colloids offer the theoretic advantage of a high
ization of markers of volume status, perfusion, and adequate osmotic pressure, which should help maintain normal intravas-
oxygen delivery (Fig. 6-2). The first description of an ED-based cular volume. Initial resuscitation fluid treatment with hyper-
quantitative resuscitation strategy targeted specific volume, perfu- tonic saline or hypertonic saline and dextran, compared with
sion, and oxygen delivery endpoints and was termed early goal- normal saline, has not been found to result in superior 28-day
directed therapy (EGDT).14 Recently, three large multicenter trials survival.18
did not demonstrate a mortality advantage for patients receiving In the setting of septic shock, initial fluid resuscitation should
the complex and invasive physiologic interventions associated consist of serial boluses of IV isotonic crystalloid as long as
with EGDT as compared to the appropriate volume resuscitation the patient continues to demonstrate a positive hemodynamic
and targeted therapies that constitute the current usual care of response to fluid loading. Persistent hypotension, despite 30 mL/
shock.11,15,16 Patients in these studies received 2 to 4 L early volume kg of IV fluid, indicates the need to add vasopressors to the resus-
resuscitation and relatively prompt antibiotic administration, citation (see below). If patients require large volumes of crystal-
suggesting that early recognition and initiation of fluid and anti- loid (>4 L), we recommend adding 5- to 10-mL/kg boluses of a
biotic therapy, in conjunction with close monitoring and thought- natural colloid (eg, albumin), rather than additional isotonic crys-
ful care, may be more important than the use of invasive talloid alone, until volume responsiveness is achieved.19 We do not
measurements to attain the specific resuscitation goals suggested recommend use of synthetic colloids, such as hydroxyethyl hetas-
by earlier studies. tarch, which have recently been demonstrated to be associated
with a higher risk of renal failure.20 The infusion of hemoglobin-
Pharmacology based blood substitutes as alternatives to packed red blood cells
(PRBCs) for the resuscitation of hemorrhagic shock has been
Volume Replacement extensively studied and is associated with significant increased
risk of death and myocardial infarction; we recommend against
Most patients with shock can be fully resuscitated with peripheral their use.
venous access established with at least two 18-gauge two catheters.
The goal in volume replacement is slightly elevated left ventricular Blood Products.  In the setting of hemorrhage or a critically
end-diastolic volume, which is difficult to measure in the ED. low hemoglobin level (<7g/dL), if criteria for shock persist despite
Historically, CVP has been used to estimate right ventricular crystalloid infusion (see Box 6.2), we recommend transfusion of
filling pressure and is used in some quantitative resuscitation algo- PRBCs (1–2 units in adults or 5–10 mL/kg in children). Fully
rithms. However, CVP measurement does not accurately reflect crossmatched blood is safest and is always preferable unless the
left ventricular end-diastolic volume, and CVP poorly predicts the patient’s need is considered sufficiently urgent to justify the use
hemodynamic response to a fluid challenge. Thus, assessment of of type-specific or even uncrossmatched blood. Use of the latter
fluid responsiveness and fluid resuscitation should not be based is generally confined to patients with hemorrhagic shock with
solely on CVP. A better approach would include the use of the persistent, severe, arterial hypotension and massive or uncon-
clinical response to fluid resuscitation, such as increases in urine trolled hemorrhage. O-negative blood is used in women of child-
output, BP, and decreasing lactate concentrations, alone or in bearing age, and O-positive blood is used in all others (see Chapter
combination with CVP measurements. In patients for whom fluid 111). If patients require more than 2 units of PRBCs for hemor-
resuscitation may be associated with higher risk of harm (eg, rhage, we recommend a balanced resuscitation using PRBCs,
severe systolic heart failure), the use of dynamic variables of fluid fresh-frozen plasma, and platelets in a 1 : 1 : 1 ratio, which is associ-
responsiveness that can be measured from an arterial line (eg, ated with better hemostasis and lower death due to exsanguina-
stroke volume variation, stroke volume index, passive straight leg tion by 24 hours.1
raise) may be beneficial over empirical fluid boluses, but their use The goal hemoglobin target for patients with septic shock in
in the ED has not been studied. the acute resuscitation window, generally defined as the first 6
hours following presentation, remains controversial. A recent
Crystalloids.  Standard treatment for hemorrhagic shock his- large randomized controlled trial (RCT) in ICU patients with
torically consisted of rapidly infusing several liters of isotonic septic shock found similar rates of ischemic events, use of life
crystalloid in adults or three successive 20-mL/kg boluses in chil- support, and 90-day mortality among patients transfused at a
dren. Recent studies have endorsed the concept of delayed resus- threshold of 7 g/dL as compared to 9 g/dL.6 Thus, we recommend
citation or hypotensive resuscitation for hemorrhagic shock (see transfusion of PRBCs at a threshold of 7 g/dL in patients with
Chapter 33). No study to date has demonstrated the survival septic shock unless specific contraindications exist or patients
benefit of one type of crystalloid versus another; therefore, the refuse transfusion.
choice of fluids may be less important than scrupulous monitor-
ing for adequate tissue perfusion. Although a single Australian Vasopressors
study has suggested an association between use of chloride-rich
solutions and subsequent renal dysfunction in ICU patients, the The primary goal of vasopressor support is to increase cardiac
study solutions included colloids as well as crystalloids and were output and oxygen delivery to vital organs when crystalloid resus-
not randomized, so any causative inference is not justified.17 citation alone is inadequate. To reduce the potential for limb
Normal saline or lactated Ringer’s solution may be used for damage from extravasation from a peripheral IV injection, vaso-
volume replacement during resuscitation, with no evidence active medications are optimally administered through a central
clearly supporting one over the other. Accordingly, the selection venous catheter, although this is not always feasible in the acute
of isotonic crystalloid solution may be based on institutional, setting. Patients with septic shock who remain hypotensive after

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74 PART I  Fundamental Clinical Concepts  |  SECTION One  Critical Management Principles

Suspected or confirmed infection with

signs of systemic inflammation
Does patient have acute evidence of:
Yes  Lactate > upper limit of normal
 Urine output < 0.5 mL/kg/h
MAP < 65 or SBP < 90 mm Hg No  PaCO2/FiO2 < 250 in patients without or
after 30 ml/kg fluid bolus? < 200 in patients with pneumonia
 Creatinine > 2.0 mg/dL
 Bilirubin > 2.0 mg/dL
Yes  Platelet count < 100,000 cells/µL
 Coagulopathy (INR > 1.5)
Sepsis-induced
hypoperfusion Yes

___Cardiac monitoring, pulse oximetry

___Obtain blood cultures
___Initiate broad spectrum antibiotics
___IJ or SC central line placement if vasopressors required
___O2 or mechanical ventilation to keep Sat > 94%
___Measure lactate

Volume
responsive Crystalloid 500–1000-mL bolus
Volume
q15–30 min until unresponsive;
assessment
reassess regularly
Volume
nonresponsive
MAP < 65 mm Hg MAP < 65 mm Hg
Arterial line placement
MAP Norepinephrine (NE) drip @ Vasopressin drip @
5–40 µg/min And NE @ 0.04 U/min
40 µg/min
MAP 65–100

Reassess volume and perfusion status Crystalloid 500-mL Dobutamine drip @

(One or more of the following): bolus (2.5-20 µg/kg/min)
 Focused exam (vital signs, cardiopulmonary, capillary
refill, pulse, and skin assessment)
 Measure CVP Volume Volume
 Measure ScvO2 responsive nonresponsive
 Bedside cardiovascular ultrasound
 Dynamic assessment of fluid responsiveness
Abnormal Volume
Normal assessment

Remeasure lactate Lactate elevated

(if initially elevated)

Lactate normal

Early goals achieved

Reassess antibiotic coverage

Fig. 6.2.  Flow diagram outlining an example of a formalized resuscitation strategy. This figure illustrates
the sequential targeting of preload, afterload, oxygen supply, and demand matching for sepsis-induced
hypoperfusion. The protocol outlines specific hemodynamic and physiologic parameters that the emer-
gency clinician should seek to attain within the first 6 hours of care. This protocol is focused on resuscita-
tion and should be used in conjunction with standard clinical care for patients with suspected infection,
such as appropriate diagnostic studies, to determine the focus of infection and appropriate antimicrobial
agents to treat the infection. HCT, Hematocrit; ICU, intensive care unit; IJ, internal jugular; INR, interna-
tional normalized ratio; MAP, mean arterial pressure; NS, normal saline; PaCO2, partial pressure of carbon
dioxide, arterial; Sat, peripheral oxygen saturation; SBP, systolic blood pressure; SC, subclavian; ScvO2 ,
central venous oxygen saturation; SIRS, systemic inflammatory response syndrome; WBC, white blood cell
count.

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 CHAPTER 6  Shock 75

a 30-mL/kg fluid bolus generally require vasopressor support. fluoroquinolone and vancomycin, is a rational empirical choice.
Several randomized trials and a meta-analysis have suggested that One such regimen would include piperacillin-tazobactam, 4.5 g
norepinephrine (5–30 µg/min) is associated with improved effi- IV every 6 hours, plus levofloxacin, 750 mg IV every 12 hours,
cacy and lower rates of adverse effects, making norepinephrine the and vancomycin, 30 mg/kg (maximum dose, 2 g) given every
vasopressor of choice for correction of hypotension in septic 12 hours, adjusted as appropriate for trough levels and renal
shock.7 In patients who remain in shock after initial crystalloid failure.
boluses, norepinephrine should be initiated at a rate of 0.05 μg/ Patients with neutropenia and sepsis syndrome are at particu-
kg/min and titrated at 3- to 5-minute intervals until the mean lar risk for progressive sepsis, organ failure, and death. Neutrope-
arterial pressure is greater than 65 mm Hg or the systolic BP is nia can be suspected in patients who have recently undergone
greater than 90 mm Hg. There are no clear data regarding an chemotherapy, and these patients often know that they are neu-
absolute maximum dose, but generally there is little or no addi- tropenic. Antimicrobial administration is particularly urgent for
tional pressor effect once a dose of 30 µg/min has been reached. these patients and should occur rapidly after blood cultures are
Vasopressin can be added as a second vasopressor agent when obtained, in parallel with crystalloid administration. Antibiotic
norepinephrine reaches the maximum dose of 30 µg/min. Vaso- considerations for the neutropenic patient are discussed in
pressin should be administered at a fixed rate of 0.03 to 0.04 units/ Chapter 115. Chemotherapy patients with sepsis represent a
min and should not be titrated. A trial of vasopressin cessation special challenge because the pathophysiology may be compli-
can be attempted once the patient demonstrates improving hemo- cated by anemia, thrombocytopenia, dehydration from vomiting,
dynamics over at least a 6-hour period. Except in cases of a pro- and the effects of adjunctive steroid therapy. Chemotherapy
longed stay in the ED, vasopressors will not be stopped until the patients often have indwelling catheters, which predispose them
patient is in the ICU. Following vasopressor initiation, particularly to more unusual causes of sepsis, including gram-positive bacteria
in patients who require high or rapid upward titration of the and fungi (see Chapters 115 and 187).
vasopressor dose, patients should be reassessed for their respon-
siveness to additional fluid boluses through the use of dynamic Corticosteroids
variables or empirical 500-mL boluses, with careful attention to
the clinical response. Vasopressor support, along with crystalloid There is no evidence for high-dose, short-course corticosteroid
therapy, is continued until the patient can maintain the blood therapy in unselected patients with septic shock. Most current
pressures listed without vasopressor support, which can be tested guidelines recommend that low-dose hydrocortisone be adminis-
at the bedside by weaning the vasopressor agent at a rate of 2 to tered only to patients receiving chronic steroid replacement and
3 µg/min every 5 to 10 minutes. in patients with refractory shock, despite adequate fluid and vaso-
pressor support. Even this is only marginally supported, if at all,
Inotropes by scientific evidence. Corticotropin stimulation testing is no
longer considered of value.
Dobutamine may also be used with norepinephrine to increase
cardiac output and maintain adequate oxygen delivery in cardio- Special Cases
genic and septic shock. In the setting of cardiogenic shock, dobu-
tamine may be indicated by some combination of hypotension, Systemic thrombolytic therapy is indicated in patients with shock
cool extremities, poor urine output, and elevated lactate level. In from pulmonary embolism (see Chapter 78) without contraindi-
the setting of septic shock, if the lactate level does not decrease at cations.21 Specific treatments for shock as a result of poisoning
least 10% and/or the measured ScvO2 does not reach 70%, despite with vasoactive medications and other toxins are discussed in the
fluid resuscitation and vasopressor administration (see earlier), relevant chapters in this text.
dobutamine can be added at a dose of 2 µg/kg/min and titrated
every 5 to 10 minutes, to a maximum of 20 µg/kg/min. Due to Devices and Procedures
stimulation of vasodilating peripheral beta receptors, dobutamine
does have the potential to decrease the BP, so careful attention to Ventilation
a patient’s individual response is necessary. If simultaneous BP
and inotropic support is necessary for septic shock, epinephrine Rapid sequence intubation is the preferred method of airway
alone, 0.2 µg/kg/min starting dose, provides similar outcomes and control in most patients with refractory shock (see Chapter 1).
adverse event rates as a combination of norepinephrine plus Tissue hypoperfusion leads to increasing fatigue of the muscles of
dobutamine. When norepinephrine is the first pressor initiated respiration, and respiratory failure commonly supervenes in
and an inotrope is indicated, we recommend the addition of patients with persistent shock. Intubation prevents aspiration,
dobutamine, with the ability to titrate each agent individually. increases oxygenation, treats acute respiratory failure, provides
However, it is acceptable as an alternative to discontinue the nor- initial treatment for metabolic or hypercarbic acidemia, and pro-
epinephrine and initiate epinephrine infusion to provide vaso- tects the patient who will be sent to an uncontrolled environment
pressor and inotropic support via a single agent. (eg, for testing). Intubation also reduces the work of breathing,
which, in the patient with hypoperfusion, further exacerbates
Antimicrobial Therapy lactic acidemia. Strenuous use of accessory respiratory muscles
can increase oxygen consumption by 50% to 100% and decrease
Treatment of the infection with antimicrobial therapy and, where cerebral blood flow by 50%. More importantly, if the patient has
necessary, surgical drainage (see later, “Source Control”), should increased airway resistance (eg, bronchospasm with anaphylaxis)
be instituted as soon as practical in cases of septic shock.10 Current or a decrease in lung compliance (eg, pulmonary edema, ARDS),
evidence does not support an absolute time requirement for a more negative intrathoracic pressure must be generated to fill
administration but, when septic shock is the working diagnosis the lungs with each inspiration. The greater suction effect is
in the ED, we recommend initiation of appropriate antibiotics also exerted on the left ventricle, impeding its ability to eject
as soon as practical after the diagnosis is made, ideally within 4 and increasing functional afterload. Positive-pressure ventilation
hours of ED presentation. When there is no focus of infection removes this impedance and can improve ventricular function
identified in a patient with presumed septic shock, a semisynthetic and cardiac output up to 30%. The use of etomidate for patients
penicillin with a β-lactamase inhibitor, in combination with a with septic shock is discussed in Chapter 1.

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76 PART I  Fundamental Clinical Concepts  |  SECTION One  Critical Management Principles

Source Control Pericardiocentesis and Thrombectomy

Controlling hemorrhage remains the cornerstone of treating Shock caused by mechanical obstruction can be managed by
hemorrhagic shock, and evidence continues to support immedi- direct intervention. Large, acute pericardial effusions should be
ate surgery when direct vascular control cannot otherwise managed with pericardiocentesis. Surgical thrombectomy for
be obtained (see Chapters 33 and 41). Gastrointestinal bleeding massive pulmonary embolism is performed rarely. Direct throm-
may require urgent endoscopy, often in the ED or ICU, and bolysis via interventional radiology, however, has been gaining
aortic rupture requires emergency consultation by a vascular acceptance as a therapeutic option in patients with shock, particu-
surgeon. In septic shock related to an abscess, aggressive infection larly if systemic thrombolytics are contraindicated.
(eg, necrotizing fasciitis; see Chapter 129) or wound (eg, toxic
shock syndrome; see Chapter 130), removal of the infectious OUTCOMES
stimulus through surgical intervention should proceed as soon as
practical. Outcomes for patients with shock vary with the underlying cause
of the shock state and the premorbid or comorbid status of the
Intraaortic Balloon Pumps and Percutaneous patient. Outcomes have progressively improved, with emphasis on
Coronary Intervention early diagnosis and treatment. In general, persistent hypotension
(refractory shock) is associated with worse outcomes. Patients
The use of intraaortic balloon counterpulsation and percutaneous meeting consensus definitions for hemorrhagic shock have a mor-
coronary intervention in selected patients with cardiogenic shock tality rate of about 20%,1 whereas this exceeds 40% in septic and
or acute cardiovascular emergencies is discussed in Chapter 68. cardiogenic shock.2

KEY POINTS
• Circulatory shock can occur with normal arterial blood pressure, • A combination of a worsening base deficit, increasing lactate level,
and not all patients with arterial hypotension have circulatory and low urine output represents persistent or worsening circulatory
shock. shock.
• A base deficit more negative than −4 mEq/L or a serum lactate • Early initiation of fluid resuscitation, with pressor support as needed,
level greater than 4.0 mmol/L warrants a presumptive diagnosis and appropriate antimicrobial therapy improve the outcomes in
of shock. patients with septic shock.
• Urine output is a reliable index of vital organ perfusion in patients • The use of defined physiologic endpoints to measure systemic
with suspected shock. Normal urine output is 1.0 mL/kg/h. Output perfusion during resuscitation (quantitative resuscitation) improves
less than 0.5 mL/kg/h indicates severe renal hypoperfusion. outcomes for ED patients with shock.

The references for this chapter can be found online by accessing the accompanying Expert Consult website.

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 CHAPTER 6  Shock 76.e1

REFERENCES
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the PROPPR randomized clinical trial. JAMA 313:471–482, 2015. 12. Jones AE, Shapiro N, Trzeciak S, et al: Lactate clearance vs central venous oxygen
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shock among critically ill patients in Australia and New Zealand, 2000–2012. JAMA 746, 2010.
311:1308–1316, 2014. 13. Puskarich M, Trzeciak S, Shapiro N, et al: Whole Blood lactate kinetics in patients
3. Summers RL, Baker SD, Sterling SA, et al: Characterization of the spectrum of hemo- undergoing quantitative resuscitation for severe sepsis and septic shock. Chest
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535, 2013. 14. Rivers E, Nguyen B, Havstad S, et al: Early goal-directed therapy in the treatment of
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associated with increased mortality in blunt major trauma patients: multicentre 16. Mouncey PR, Osborn TM, Power GS, et al: Trial of early, goal-directed resuscitation
cohort study. Resuscitation 82:1202–1207, 2011. for septic shock. N Engl J Med 372:1301–1311, 2015.
6. Holst LB, Haase N, Wetterslev J, et al: Lower versus higher hemoglobin threshold for 17. Yunos NM, Bellomo R, Hegarty C, et al: Association between a chloride-liberal vs
transfusion in septic shock. N Engl J Med 371:1381–1391, 2014. chloride-restrictive intravenous fluid administration strategy and kidney injury in
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in the treatment of septic shock: a meta-analysis. Crit Care Med 40:725–730, 18. Bulger EM, May S, Kerby JD, et al: Out-of-hospital hypertonic resuscitation after
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CHAPTER 6: QUESTIONS & ANSWERS

6.1. Which of the following is considered one of the empirical mentioned may include the presence of lactic acidosis, oliguria,
criterion for the diagnosis of circulatory shock? and/or altered mental status. The diagnosis of SIRS is made when
A. Partial pressure of carbon dioxide (Paco2) < 40 mm Hg two or more of the following are present:
B. Partial pressure of oxygen (Pao2) < 55 mm Hg 1. Temperature > 38°C or < 36°C
C. Serum lactate level < 4 mM/L 2. Heart rate > 90 beats/min
D. Systolic blood pressure (SBP) < 100 mm Hg 3. Respiratory rate > 20 breaths/min or Paco2 < 32 mm Hg
E. Urine output < 0.5 mL/kg/h 4. White blood cell count > 12,000/mL, < 4,000/mL, or >
10% band neutrophilia
Answer: E. Four of the following criteria should be met for the
diagnosis of circulatory shock:
6.3. An 18-year-old unrestrained driver is transported to the
1. Ill appearing or altered mental status
emergency department (ED) after being thrown from his
2. Heart rate > 100 beats/min
vehicle during a motor vehicle collision. He was intubated
3. Respiratory rate > 20 breaths/min or Paco2 < 32 mm Hg
in the field and received an intravascular bolus of 3 L of
4. Arterial base deficit < −4 mEq/L or lactate level >
normal saline before arrival to the ED. His initial Glasgow
4 mM/L
Coma Score (GCS) is 7, and his blood pressure on arrival is
5. Urine output < 0.5 mL/kg/h
80/50 mm Hg. Which of the following would be the most
6. Arterial hypotension > 20 min duration
appropriate to initiate immediately on arrival to the ED?
A. Dobutamine
6.2. Which of the following, when present and in the setting of
B. Dopamine
suspected or confirmed infection, helps distinguish severe
C. Hetastarch
sepsis from systemic inflammatory response syndrome?
D. Norepinephrine
A. Heart rate > 90 beats/min
E. Packed red blood cell (PRBC) transfusion
B. Hypotension
C. Paco2 < 32 mm Hg Answer: E. In patients with signs of hemorrhagic shock and sus-
D. Temperature < 36°C pected central nervous system trauma or GCS < 9, immediate
E. >10% band neutrophilia PRBC transfusion should be initiated. This assists with volume
expansion and oxygen delivery to the brain. Pressors and positive
Answer: B. The diagnosis of severe sepsis is made in patients who
inotropes will be of little benefit before volume replacement, and
meet the criteria for systemic inflammatory response syndrome
hetastarch has no proven benefit for initial resuscitation in head
(SIRS) with suspected or confirmed infection and associated
injury patients.
with organ dysfunction or hypotension. The organ dysfunction

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