Download Undifferentiated Shock - American College of Emergency Physicians

March 2015 • Volume 29 • Number 3
Undifferentiated Shock
Lesson 6
Scott A. Goldberg, MD, and Patrick Liu, MD
■ Objectives
On completion of this lesson, you
should be able to:
1. Explain the pathophysiologic basis of
shock.
2. List the common causes of shock.
3. Discuss the initial evaluation and
stabilization of a patient with
undifferentiated shock.
4. Explain the diagnostic strategies
employed in the evaluation of
undifferentiated shock.
5. Discuss treatment algorithms for the
management of various shock states.
■From the EM Model
1.0 Signs, Symptoms, and Presentations
1.3.42 Shock
Shock occurs when the circulatory
system is unable to meet the body’s
metabolic demand, ultimately leading
to dysfunction of the vital organs
and death. Despite recent medical
advances, mortality for shock remains
extremely high (50% in cardiogenic
shock and 35% in septic shock),1,2 and
untreated shock is almost uniformly
fatal.3 The only variable consistently
shown to improve outcomes in
its management, regardless of
cause, is time to identification
and intervention. Shorter door-toballoon times following myocardial
infarction are associated with a
decreased incidence of cardiogenic
shock;4 early aggressive resuscitation
and antibiotics are among the few
interventions that can improve
outcomes in patients with septic
shock;5 and national standards stress
the importance of the first hour of
trauma management.6 The adept
emergency physician must, therefore,
be facile with the rapid recognition,
diagnosis, and management of the
multiple causes of the shocked state.
Case Presentations
■ Case One
A 59-year-old man is brought in by
EMS. He awoke from sleep with chest
pressure and shortness of breath.
The emergency medical technician
administered 325 mg of aspirin and
a sublingual nitroglycerin tablet en
route. The patient has a history of
hypertension, a 10-pack/year history
of smoking, and no allergies. On
arrival, he is tachypneic, has coarse
rales throughout both lungs, and has
jugular venous distention (JVD) above
the angle of the mandible. His skin
is cool and diaphoretic; vital signs
are blood pressure 85/42, heart rate
120, respiratory rate 32, and oxygen
saturation 82%.
■ Case Two
A 64-year-old woman presents
because of shortness of breath and
fatigue. She awoke this morning
with a feeling of suffocation and
was unable to ambulate. She was
recently diagnosed with breast cancer,
but had been previously well. On
arrival, she appears ill and is pale
and diaphoretic. She has clear lung
sounds, normal heart sounds, and no
JVD. Her skin is cool to the touch,
with weak distal pulses. Vital signs
are blood pressure 84/56, heart rate
132, respiratory rate 26, temperature
of 37.9°C (100.2°F), and oxygen
saturation 88%. An ECG shows sinus
tachycardia but is otherwise normal.
■ Case Three
A 32-year-old woman with no
known medical history arrives
via EMS following a motor vehicle
collision. The patient was a restrained
passenger in a vehicle traveling
approximately 55 miles per hour
when it hit a tree head on. The patient
arrives on a stretcher with a cervical
spine collar in place. Additional
medical history is unobtainable.
She is awake but confused, with a
Glasgow Coma Scale score of 9 (EVM
2-3-4). Breath sounds are shallow but
clear to auscultation bilaterally, and
distal pulses are intact. Vital signs are
blood pressure 78/46, heart rate 65,
9
Critical Decisions in Emergency Medicine
Critical Decisions
∙∙ What are the key components of a patient’s history
in the evaluation of undifferentiated shock?
∙∙ What additional evaluations, including laboratory studies
and imaging, assist in differentiating the cause of shock?
∙∙ What are the critical physical examination maneuvers
in the differentiation of various shock states?
∙∙ What are the important management principles
in treating the various etiologies of shock?
respiratory rate 8, and pulse oximetry
reading 98% on 4 liters of oxygen via
nasal cannula.
Shock
Shock is a systemic circulatory
insufficiency that results in an
imbalance of tissue oxygen supply and
demand. When circulating oxygen
content does not meet tissue demand,
a cascade of metabolic sequelae is
triggered that ultimately results in
cellular injury. This cellular cascade
causes an ion imbalance, resulting in
an overload of intracellular calcium.
Toxic levels of cellular calcium induce
free radical oxidative damage and
impede mitochondrial ATP synthesis,
muscle relaxation, and cardiac
myocyte contractility.7 Acidification
of the serum from anaerobic
metabolism, lactic acid production,
and renal failure further increase this
calcium overload. In addition, acidosis
independently diminishes skeletal
and cardiac muscle contractility,
decreases the effectiveness of
circulating catecholamines, increases
interstitial edema, and eventually
results in cell membrane disruption
and death.8 In specific types of shock,
pro-inflammatory cytokine release
causes cellular dysfunction and
endothelial cell activation, producing
nitric oxide and leading to generalized
vasodilation.9
The primary compensatory
mechanism for the shock state is
an increase in cardiac output via
catecholamine and cortisol release.
Selective arteriolar vasoconstriction
diverts blood away from the skin,
skeletal muscles, kidneys, and
splanchnic organs, while constriction
of venous capacitance vessels
increases cardiac preload and focuses
oxygen delivery to the heart and
10
brain. The release of antidiuretic
hormones and activation of the reninangiotensin axis increase sodium
and water reabsorption in an attempt
to optimize intravascular volume.
However – given sufficient stress –
the system fails, resulting in acidosis,
coagulopathy, inflammatory mediator
release, and ultimately multiple organ
dysfunction and death.7,9
The differential diagnosis for
undifferentiated shock can be broken
down into four broad classifications:
hypovolemic, cardiogenic,
obstructive, and distributive.
Understanding the pathophysiologic
differences between these groups
is critical to proper and timely
management.
Hypovolemic shock results from
a physiologic fluid status that is
insufficient to adequately perfuse
the body. This fluid deficit most
commonly is caused by hemorrhage,
ruptured abdominal aortic aneurysm,
or ectopic pregnancy. However,
hypovolemia also can result from
gastrointestinal losses, as seen
in severe vomiting and diarrhea.
Although septic shock generally
occurs through the distributive
mechanism described below, it is
important to note that cytokine
release can cause capillary leakage
into the interstitial space, resulting
in a relative decrease in intravascular
volume.7
When shock occurs because of an
intrinsic defect of the heart itself, it is
classified as cardiogenic. Cardiogenic
shock, defined as hypotension in the
setting of a decreased cardiac index
(<1.8 L·min-1·m-2) and increased
left heart filling pressures,10 occurs
when there is insufficient cardiac
output to adequately maintain
blood pressure and tissue perfusion.
Myocardial infarction; cardiac
contusion; myocarditis; arrhythmia;
heart failure; and toxins, including
certain medications, can all result
in cardiogenic shock. Mechanical
causes such as valvular rupture
or ventricular wall rupture are
particularly devastating.
Obstructive shock occurs as a
result of the physical obstruction of
the heart or great vessels. Although
obstructive shock often is categorized
as a subset of cardiogenic shock,
it is useful to think of the two as
distinct entities. Obstructive shock
occurs as the direct result of impaired
diastolic filling or significantly
increased cardiac afterload. Both
cardiac tamponade and tension
pneumothorax directly compromise
diastolic filling, albeit by different
mechanisms. Massive pulmonary
artery embolism can impede right
ventricular output, resulting in a
significant increase in afterload; and
right ventricular bowing into the left
ventricle impedes left ventricular
diastolic filling. Both result in
decreased cardiac output.
Distributive shock occurs
when there is normal circulating
intravascular volume, but the
capacity of the vascular system has
increased secondary to generalized
vasodilation.7 In the case of septic
shock, a severe systemic inflammatory
response is triggered, leading to
diffuse peripheral vasodilation
and a drop in cardiac afterload.
Anaphylactic shock is the result of
uncontrolled mast cell degranulation
and vasodilatory cytokine release.
Neurogenic shock occurs when a
traumatic high spinal cord injury
disrupts the sympathetic chain
of the autonomic nervous system,
resulting in a loss of vascular tone.
March 2015 • Volume 29 • Number 3
This type of shock often presents with
a paradoxical bradycardia due to the
now unopposed vagal stimulation of
the heart.7
Finally, it should be understood
that a clinical presentation of
undifferentiated shock can be
associated with multiple categories of
shock. For example, a trauma patient
with massive hemothorax might have
a combination of obstructive shock
from tamponade and the mechanics
of thoracic tension, in addition to
hypovolemic shock secondary to
hemorrhage.
CRITICAL DECISION
What are the key components of a
patient’s history in the evaluation of
undifferentiated shock?
In patients with undifferentiated
shock, attention should immediately
focus on stabilization of the patient’s
airway, breathing, and circulation.
Although a thorough history can
provide important information, this
should occur only after, or in tandem
with, initial stabilization.
Collateral history from EMS
personnel or family members can be
invaluable, especially in an altered
or confused patient. A complete
medication history should be
obtained, including information on
any new or changed medications.
Particular attention should be given to
any anticoagulants, diuretics, drugs of
abuse, antihypertensive medications,
or antiarrhythmic agents. A history of
allergies also should be obtained.
Often, symptoms such as
lightheadedness, weakness,
palpitations, fatigue, and decreased
urine output are associated with
impending shock, but many of these
findings are nonspecific. Recent
profuse vomiting, diarrhea, or
decreased oral intake can indicate
hypovolemia. The patient should be
questioned regarding recent melena,
hematochezia, or hematemesis.
Chest pain, increased dyspnea on
exertion, orthopnea, and worsening
volume overload should raise concern
for a cardiac cause. Risk factors
for pulmonary embolus should
be elicited and any recent trauma
should be addressed. Additionally,
elicit any exposure to potential
toxins, including but not limited to
home medications, pesticides, toxic
alcohols, and cyanide.
Patients in early sepsis can present
with vague symptoms, including
fevers, chills, and myalgias. They
should be questioned further
about symptoms such as cough
or abdominal pain, which can
help pinpoint infection. It also is
important to gather information on
any indwelling catheters, new rashes,
retained tampons or other foreign
bodies, recent operations, or other
immunocompromising conditions.
CRITICAL DECISION
What are the critical physical
examination maneuvers in the
differentiation of various shock
states?
Vital Sign Evaluation
Even though vital signs cannot
consistently identify shock, it is
essential to evaluate them early.
Tachycardia is an appropriate
compensatory response to the
shocked state, but significant
tachycardia, including cardiac
arrhythmias, can itself result in
decreased end diastolic volumes and
decreased cardiac output. Likewise,
significant bradycardia also can result
in decreased cardiac output and
systemic hypoperfusion. It should
be noted that while vital signs can
be useful in the initial identification
of shock, there often is a poor
correlation between blood pressure,
heart rate, and cardiac output in
severely hypotensive patients.11
Hypotension frequently is a late
and concerning finding in shock.
Blood pressures should be measured
often using an appropriately sized
blood pressure cuff. Although
hypotension is commonly found, it
is not always present, particularly
in early shock.3 In the case of
hemorrhagic shock, there seems
to be significant variability in the
relationship between blood loss and
the clinical signs of hypoperfusion;12
and the clinical utility of the
often-cited ATLS classification of
hemorrhagic shock table6 has been
disputed.13 The shock index, defined
as heart rate divided by systolic blood
pressure, might be of more help in
predicting disease severity.12,14,15
A shock index of 0.9 or greater is
concerning and should prompt
aggressive management.
A point-of-care blood glucose
analysis often is included in the initial
set of vital signs. Hyperglycemic
crises and severe hypoglycemia
should be identified and addressed
promptly. Pulse oximetry (Spo2)
monitoring, providing an estimate of
circulating oxygen, also is a routine
practice in the emergency department.
A low Spo2 generally indicates
hypoxemia or hypoventilation,
which should be promptly addressed.
Alternative devices, including
transcutaneous oxygen and carbon
dioxide monitoring16 and infrared
spectroscopy17 have become
increasingly available. However, while
these devices show promise, existing
data is insufficient to recommend
their routine use.
The patient’s core body
temperature also can yield valuable
information. Both hyperthermia
and hypothermia suggest a
systemic inflammatory response.
Environmental factors leading to
either can, in and of themselves,
lead to shock. Both hypothermia
and hyperthermia have been shown
to result in significantly increased
mortality,18 and steps should be
taken to re-establish a normal body
temperature immediately. Taken
together, a temperature higher than
38°C (100.4°F) or lower than 36°C
(96.8°F), a heart rate faster than 90
beats per minute, and a respiratory
rate of more than 20 breaths per
minute make up three of the four
clinical parameters defining the
systemic inflammatory response
syndrome (SIRS). The fourth, a white
blood cell count above 12,000 or less
than 4,000 per mm 3 or with more
than 10% bands, often is measured in
the patient’s laboratory evaluation.
11
Critical Decisions in Emergency Medicine
The Physical Examination
The early diagnosis of shock
is critical in reducing patient
morbidity; however, recognition
can be particularly difficult in its
earliest stages. As with any patient
who presents to the emergency
department, a primary survey
should be performed immediately
on presentation. After evaluating
patency and integrity of the
airway, the primary survey should
include auscultation of the lungs
for appropriate ventilation and the
presence of bilateral lung sounds. Any
signs of overt hemorrhage should be
immediately addressed, and bleeding
controlled. Direct pressure should
be applied if possible. In patients
with severe limb hemorrhage, a
tourniquet can be used if direct
pressure is impossible or impractical.
Tourniquets should be placed
proximal to the injury and should be
tightened to a pressure sufficient to
stop hemorrhage. Tourniquet times of
up to 2 hours are considered safe.19,20
After the primary survey, the
physician should perform a diligent
head-to-toe physical examination.
Mental status often is diminished
in shock because of cerebral
hypoperfusion. This can range from
mild disorientation to a profoundly
altered mental state and loss of
airway reflexes. Conjunctival pallor
can indicate anemia from internal
hemorrhage, and dry mucous
membranes indicate hypovolemia.
The neck veins should be examined
for jugular venous distention,
indicating increased right atrial
pressures. The Kussmaul sign, a
paradoxical increase in jugular venous
pressure during inspiration, can
indicate obstructive or cardiogenic
shock.
Findings such as absent breath
sounds over one lung suggest a
tension pneumothorax, and a new
cardiac murmur raises the possibility
of valvular rupture or septic shock
from infective endocarditis. Pulsus
paradoxus, a paradoxical decrease in
blood pressure during inspiration, or
muffled heart sounds might indicate
12
cardiac tamponade, but these findings
are not of sufficient sensitivity to
make a definitive diagnosis.21
The abdomen should be carefully
palpated for signs of peritonitis, and
the abdominal wall inspected for any
signs of ecchymosis. An abdominal
seatbelt mark should be searched for
in cases of motor vehicle collisions.
Edema and bruising surrounding the
umbilicus (Cullen sign) or ecchymosis
of the flanks (Grey Turner sign)
might indicate an intra-abdominal
catastrophe such as hemorrhagic
pancreatitis, ruptured spleen,
ruptured ectopic pregnancy, or a
ruptured aneurysm of the abdominal
aorta.22 Although a palpable mass
in the mid-abdomen can suggest
an aortic aneurysm, this finding is
difficult to recognize in most patients.
The extremities also should
be evaluated. Extremity paralysis
can indicate a neurogenic etiology.
Unilateral leg swelling, indicating
venous thrombosis, can suggest
obstructive shock from a pulmonary
embolus. Delayed capillary refill
time can indicate hypoperfusion, but
typically is not an early finding in
shock and can be found at baseline in
the elderly and those with peripheral
vascular disease. Bilateral peripheral
edema might suggest a cardiogenic
cause of shock. Cool peripheral skin
temperature can indicate shock;
however, there is poor correlation
between peripheral temperature and
cardiac index or systemic vascular
resistance.23 Further, patients with
distributive shock frequently will
present with normally perfused
extremities. A passive leg raise,
transiently increasing venous return,
is an easy bedside maneuver that can
predict fluid responsiveness.24
CRITICAL DECISION
What additional evaluations,
including laboratory studies and
imaging, assist in differentiating the
cause of the shocked state?
In addition to the physical
examination, additional diagnostic
measures help to differentiate
the etiology of shock. These
include the laboratory evaluation,
ECG, radiographic imaging,
ultrasonography, and advanced
hemodynamic monitoring.
Laboratory Investigations
Serum analysis can yield valuable
information about the cause and
severity of the shock state. A point-ofcare blood glucose analysis should be
performed immediately in all patients
presenting with undifferentiated
shock, and a pregnancy test should be
obtained in all women of childbearing
age. In addition, a metabolic profile
and CBC should be obtained. Cardiac
biomarkers can prove useful, and
blood cultures should be drawn
if there is suspicion of a systemic
infection. Likewise, a urine analysis
and culture should be obtained. If
a toxic ingestion for which a serum
assay exists is suspected, this should
also be tested. Blood should be tested
for type and crossmatch in the case
of suspected hemorrhagic shock.
A coagulation profile should be
considered, particularly if the patient
is taking anticoagulants, and can have
a role in estimating the severity of
illness. Specific serum markers also
should be considered and targeted
to specific suspected endocrine
emergencies, including a cortisol
level in suspected adrenal crisis
and thyroid stimulating hormone
and T3 and T4 levels in suspected
thyrotoxicosis or myxedema.
If the patient is in respiratory
distress, a blood gas analysis can be
useful. Venous blood gas analysis
– less invasive than arterial blood
gas analysis – provides an excellent
correlation to arterial values for pH,
bicarbonate, and partial pressure of
carbon dioxide (Pco2)25,26 and is the
preferred initial technique, especially
if the patient does not have any acute
oxygenation or ventilation issues.
The mixed-venous oxygen
saturation (Svo2), obtained via a
central venous catheter, or central
venous oxygen saturation (Scvo2),
obtained via a pulmonary artery
catheter, also can help guide
resuscitative therapy in septic shock.27
March 2015 • Volume 29 • Number 3
An Scvo2 value above 70% or an Svo2
value above 65% is desirable; failure
to meet these goals despite adequate
fluid resuscitation should prompt the
consideration of vasoactive agents or
blood transfusion.27 However, such
analysis requires the placement of
an invasive catheter that otherwise
might not be indicated. Further,
recent studies have suggested that
improvement in serum lactate levels
might be equivalent to invasive
measures in guiding resuscitative
efforts in septic shock.28
An elevated serum lactate indicates
an overall shock state, and a higher
lactate level suggests a sicker patient
with a higher risk of death.29,30 A
serum lactate level can be useful as
an indicator of overall illness severity,
but its use in septic shock has been
the most extensively evaluated.
Lactate should be measured, and
any result above normal should
be aggressively addressed, with
particular concern for patients with
a level above 4 mmol/L.27 Although
guidelines recommend reducing
lactate to normal levels within 6
hours, a reduction of 10% in 2 hours
is an alternative strategy.28 The
approach to achieving this target
will depend on specific patient
parameters, but will generally include
fluid resuscitation and administration
of vasoactive agents or blood
products, as discussed below.
Electrocardiography
The ECG can provide important
information regarding the cause
of shock. ST-segment elevations
indicate complete coronary artery
occlusion and resultant cardiogenic
shock. Evidence of right heart strain,
including negative T waves in the
lateral precordial leads or right
bundle-branch blocks, or the finding
of an S1Q3T3 or S1S2S3 pattern can
indicate pulmonary artery obstruction
from pulmonary embolism or
critical pulmonary hypertension.
Electrical alternans, despite having
a low sensitivity,21 suggests cardiac
tamponade. The ECG also can
help identify toxic or metabolic
derangements. A wide QRS complex
with a terminal R wave is suggestive
of a sodium channel-blocker overdose
such as with cyclic antidepressants.31
Bradycardia in the setting of a wide
QRS or a long QT suggests electrolyte
abnormalities, and a new heart block
suggests myocardial infarction or
ingestion of an atrioventricular nodal
blocking agent.
Plain Radiography
Plain radiography can be useful
in certain situations, but should
not delay empiric intervention in a
hemodynamically unstable patient.
Chest radiographs can reveal a
pneumothorax or hemothorax;
pulmonary edema is suggestive
of cardiogenic shock. A wide
mediastinum (generally wider than
8 cm) suggests an aortic dissection,
and evidence of pneumonia suggests a
source of septic shock.
Ultrasonography
Ultrasonography is a fast, simple,
and effective means of obtaining vital
information at the bedside.32
Two protocols developed to
aid in the differentiation of the
shock state are the abdominal and
cardiac evaluation with sonography
in shock (ACES) examination33
and the rapid ultrasonography for
shock and hypotension (RUSH)34
examination. These protocols take
slightly different approaches, but
focus on the same general principles.
The heart is evaluated for adequate
wall motion; right ventricular
bowing, suggesting elevated right
ventricular pressures from an
obstructive pathology; and evidence
of diastolic right ventricular collapse,
suggesting cardiac tamponade. A
hyperdynamic left ventricle generally
is seen in hypovolemia or in the
setting of vasoactive medications.
A hypodynamic ventricle often
points to a cardiac cause of shock,
toxins, or sepsis. The inferior vena
cava (IVC) is evaluated for diameter
and collapse as an indicator of fluid
tolerance. The IVC diameter is
measured at 2 to 3 cm from the right
atrial border on both inspiration and
expiration; collapse of 50% or more
suggests fluid tolerance.35 Then, the
abdomen is evaluated for free fluid.
Although as little as 200 mL of intraabdominal free fluid can be seen
using ultrasonography,36 the ability
of ultrasound to identify free fluid in
the retroperitoneal space is limited.
The aorta should be scanned along
its course to the bifurcation, and
measurements taken in both long and
short axis. A diameter of more than
3 cm is concerning for aneurysm.37
Finally, the lungs are examined for
pneumothorax or pleural fluid.
This series of evaluations easily can
be remembered with the pneumonic
HIMAP – heart, IVC, Morison
pouch, aorta, and pneumothorax.34
The RUSH examination38 adds an
evaluation for deep vein thrombosis
and groups the examinations into
three domains – the “tank,” the
“pump,” and the “pipes,” which refer
to volume status, the heart, and
vascular tone, respectively.
Ultrasonography of the lungs also
can be a useful adjunct by identifing
B-lines that indicate pulmonary
edema, which suggests cardiogenic
shock. If seen during empiric
fluid loading of the hypotensive
patient, B-lines can indicate that
the patient is no longer fluid
tolerant.39 Lung ultrasonography is
superior to plain films in identifying
pneumothoraces.40
In cases of suspected trauma,
the focused abdominal sonography
for trauma (FAST) examination is
useful in identifying intra-abdominal
hemorrhage.41 This examination
includes views of the Morison pouch
in the right upper quadrant, the
splenorenal space in the left upper
quadrant, suprapubic views of the
pelvis, and a subxyphoid cardiac
view. Although the FAST examination
is useful in the evaluation of
hypotensive trauma patients, the
protocols outlined above offer a more
complete evaluation in the case of
undifferentiated shock.
13
Critical Decisions in Emergency Medicine
Advanced Hemodynamic
Monitoring
Intravascular volume status,
cardiac output, tissue perfusion,
and overall hemodynamic status
can be assessed using advanced
hemodynamic monitoring,
although many of these methods
are controversial. The gold standard
of hemodynamic monitoring is the
Swan-Ganz catheter; however, its use
should be restricted to experienced
practitioners in ICUs and in highly
selected populations.42
Invasive blood pressure
monitoring should be considered
in the management of severe shock,
particularly with concomitant
vasopressor use or at the extremes
of blood pressure measurements.43
Invasive blood pressure monitoring
also should be considered if
peripheral blood pressure readings
are inaccurate or difficult to obtain.
Central venous pressure (CVP),
obtained via pressure transduction
from a central venous catheter,
also is frequently monitored in the
critically ill. Recently, however,
CVP has fallen out of favor as an
accurate estimate of fluid status in
the emergency department.44 The
use of ultrasonography to measure
the diameter and collapsibility of
the inferior vena cava provides an
alternative method for assessing
intravascular fluid status and fluid
responsiveness,32 particularly
at the extremes of distention or
collapsibility. Sonography also can be
used to estimate fluid responsiveness
through the measurement of brachial
artery peak velocity, in which the
peak velocity of blood flow through
the brachial artery is measured by
Doppler ultrasound during inspiration
as compared to expiration. However,
accurate measurement requires a
mechanically ventilated patient.45
CRITICAL DECISION
What are the important principles
in treating the various etiologies of
shock?
A patient with suspected shock
should undergo a primary survey
immediately on arrival, including
evaluation of the airway and
hemodynamic status. The patient
should be promptly moved to the
resuscitation area and placed on
Table 1.
Recommended Empiric Antibiotic Regimens for Patients with Severe Sepsis and Septic Shock55-5
14
Source
Skin and soft tissue
(Impetigo, cellulitis,
erysipelas,
necrotizing fasciitis)
Typical pathogens
Empiric antibiotic regimens*
∙ S . aureus, S. pyogenes, Strep
species
∙ Consider Vibrio vulnificus,
Aeromonas hydrophila,
anaerobic streptococci,
clostridia, polymicrobial for
necrotizing infections
∙ Strep and MSSA coverage:
∙ Nafcillin, 2 g IV q 24 hrs
∙ Cefazolin, 1 g IV q 8 hrs
∙ Ceftriaxone, 1-2 g IV q 24 hrs
∙ Cefotaxime, 1-2 g IV q 8 hrs
∙ Clindamycin, 600 mg IV q 8 hrs
∙ MRSA coverage:
∙ Clindamycin, 600 mg IV q 8 hrs
∙ Linezolid, 600 mg IV q 12 hrs
∙ Vancomycin, 15 mg/kg IV q 12 hrs
∙ Necrotizing infections:
∙ Imipenem-cilastatin, 1g IV q 6-8 hrs
∙ Meropenem, 1g IV q 8 hrs
∙ Ertapenem, 1g IV q 24 hrs
∙ Ampicillin-sulbactam, 1.5-3g IV q 6-8 hrs OR piperacillin-tazobactam
3.375g IV q 6-8 hrs PLUS clindamcin, 600 mg IV q 8 hrs PLUS
ciprofloxacin, 400 mg IV q 12 hrs
∙ Cefotaxime, 2 g IV q 6 hrs PLUS metronidazole 50 mg IV q 6 hrs OR
clindamycin, 600 mg IV q 8 hrs
Note: All necrotizing infections must include MRSA coverage.
Pneumonia
[Communityacquired
pneumonia (CAP),
healthcareassociated
pneumonia (HCAP)]
∙ C AP: S. pneumoniae,
Mycoplasma pneumoniae,
Haemophilus influenzae,
Chlamydophila pneumoniae,
Legionella, viruses
∙ HCAP: Pseudomonas, E.coli,
Klebsiella pneumoniae,
Acinetobacter, MRSA
∙ CAP coverage:
∙ Respiratory fluoroquinolone
∙ Beta-lactam PLUS macrolide
∙ Beta-lactam PLUS doxycycline
∙ HCAP coverage:
∙A
ntipseudomonal cephalosporin OR antipseudomonal carbapenem
OR beta-lactam/beta-lactamase inhibitor
PLUS
ntipseudomonal fluoroquinolone OR aminoglycoside
∙A
PLUS
∙ MRSA coverage (linezolid or vancomycin)
March 2015 • Volume 29 • Number 3
a cardiac monitor. Intravenous
access should be obtained rapidly
with large-bore catheters (14- to
18-gauge). Intraosseous access is
a viable alternative if intravenous
access is unobtainable. Although the
tibial insertion site might be more
familiar, a humeral insertion provides
an alternative location with similar
infusion capability; infusion rates of
more than 5 liters per hour in an
adult patient are possible.46,47
Ventilatory support might be
necessary in the event of significant
respiratory distress or arrest.
Noninvasive positive-pressure
ventilation has been used successfully
for a variety of conditions, particularly
in cardiogenic pulmonary edema.48
However, invasive ventilation via
endotracheal tube might become
necessary in the hypotensive patient,
especially in cases of decreased
mental status. It should be noted,
however, that increased intrathoracic
pressures in mechanical ventilation
can decrease cardiac output and
potentially worsen hypotension,
particularly in patients requiring high
end-expiratory pressures.
The choice of medication used
for intubation in the shocked patient
also warrants consideration. In a
patient with suspected septic shock,
etomidate can cause a decrease in
circulating cortisol levels, although
this has not been shown to have a
measurable effect on mortality rates
and should not preclude the use of
etomidate as a sedative agent.49 In
the hypotensive patient, a decreased
dose of sedative should be used, and
strong consideration should be given
to the use of ketamine because of its
sympathetic stimulation.50 The chosen
paralytic dose should be increased
(time to onset of action escalates in
the setting of hypoperfusion).
After initial stabilization, the
patient often requires empiric
management before a definitive
Table 1 (Continued).
Recommended Empiric Antibiotic Regimens for Patients with Severe Sepsis and Septic Shock55-5
CNS
(Meningitis,
encephalitis)
∙ 0 -3 month: E.coli, Group B
Strep, Listeria
∙ Adult: S. pneumococcus, N.
meningitidis, Listeria (>50 yo)
Genitourinary
E. coli, Proteus mirabilis,
(UTI, pyelonephritis) Klebsiella pneumoniae,
Staphylococcus saprophyticus
∙ 0-3 months:
∙ Cefotaxime ,50 mg/kg q 8 hrs PLUS ampicillin, 50 mg/kg q 8 hrs
∙ Adult:
∙ Ceftriaxone, 2 g IV q 12 hrs PLUS vancomycin, 500-750 mg IV q 6 hrs
∙ Ampicillin, 2 g IV q 4 hrs for listeria coverage if >50 years old
∙ Consider acyclovir
∙ Ciprofloxacin, 400 mg IV q 12 hrs
∙ Levofloxacin, 750 mg IV q 24 hrs
∙ Ampicillin, 2 g IV q 6 hrs PLUS Gentamicin 2 mg/kg load THEN 1.7-2
mg/kg q 8 hrs
∙ Ampicillin-sublactam, 3 g IV q 6 hrs
∙ Extended spectrum cephalosporin
∙ Carbapenem
Intra-abdominal
∙ E. coli, Strep species, Klebsiella ∙ Single agent:
(Biliary,
species, Pseudomonas,
∙ Imipenem-cilastatin 250-500 mg IV q 6-8 hrs
appendicitis,
Proteus, Clostridium species,
∙ Meropenem
1g IV q 8 hrs
diverticulitis,
Acinetobacter, Staphylococcus
∙ Piperacillin-tazobactam 4.5 g IV q 8 hrs
colitis, abscess,
aureus, Enterobacteriaceae,
∙ Combination therapy:
spontaneous
Bacteroides fragilis, anaerobes
∙ Ciprofloxacin, 400 mg IV q 12 hrs
bacterial peritonitis) ∙ Enterococcus: coverage
∙ Levofloxacin, 750 mg IV q 24 hrs
recommended for severe
∙ Cefepime, 2 g IV q 8 hrs
infections
∙ Ceftazidime, 2 g IV q 8 hrs
PLUS
∙ Metronidazole 500 mg IV q 6-8 hrs
∙ Add vancomycin if concern for MRSA
Without an obvious ∙ Children >3 months: S.
∙ Children >3 months:
source
pneumonia, N. meningitidis, S.
∙ Ceftriaxone, 75-100 mg/kg IV q 24 hrs
∙ Neutropenic adults:
∙ Vancomycin, 1 g IV q 12 hrs PLUS
∙ Imipenem, 1 g IV q 8 hrs OR cefepime, 2 g IV q 8 hrs OR ceftazidime,
3 g IV q 6 hrs
∙ +/- aminoglycoside
*Dosing is based on a typical 70-kg patient with normal renal function.
aureus, H. influenza
∙ Adults: Gram-negative bacilli,
S. aureus, streptococci, others
15
Critical Decisions in Emergency Medicine
diagnosis is made. Interventions
should be made based on the
likelihood of the particular cause of
shock. When the history, physical,
examination, or ancillary testing
suggests a specific toxidrome, targeted
antidotes should be provided.
Suspected adrenal insufficiency
initially should be treated with
dexamethasone, as it does not
interfere with subsequent evaluation.
In the case of known adrenal
insufficiency, dexamethasone or
hydrocortisone can be administered.
Patients with a cardiac cause of
shock require treatment depending
upon the suspected condition. If
the ECG demonstrates ST-segment
elevations consistent with STEMI, the
patient should be taken immediately
for cardiac revascularization or given
thrombolytic therapy.10 Emergency
department interventions should not
delay revascularization. If a massive
pulmonary embolus is suspected,
immediate thrombolysis is warranted
in a hemodynamically unstable
patient,51 although a definitive
diagnosis is preferred if the patient’s
clinical condition allows. The most
well-described adult dosing regimen
is alteplase, 10-mg bolus, followed
by 90 mg over the subsequent 100
minutes, in addition to heparin;51
however, other agents and dosing
regimens have been used.
If there is evidence of significant
ongoing hemorrhage, blood products
should be promptly transfused
in accordance with institutional
protocol.52 Hypotensive resuscitation
has demonstrated benefits in patients
with hemorrhagic shock.53 Patients
should receive blood and blood
products to maintain physiologic
parameters of adequate perfusion,
but should not be resuscitated to
normal arterial blood pressures.
Although typed and crossmatched
blood products are preferred,
uncrossmatched blood should be
administered until crossmatched
products are available. If the patient is
taking any anticoagulant medications,
these agents should be reversed.
Some circumstances require
prompt invasive or surgical
interventions. Needle thoracostomy
can provide temporary decompression
of a tension pneumothorax. When
pleural space cannot be reached with
standard catheters, tube thoracostomy
should be performed in all patients
with suspected tension physiology.54
Pericardiocentesis is indicated when
cardiac tamponade is confirmed
by bedside echocardiography.
Bradycardia can necessitate
transcutaneous pacing or placement
of a transvenous cardiac pacing
wire, depending on the cause. An
identifiable, surgically correctable
source of septic shock should be
addressed promptly, including
incision or débridement of soft tissue
infections, laparotomy for bowel
perforation or ischemia, and washout
of infected joints.
In a patient with presumed sepsis,
broad-spectrum antibiotics should
be administered as early as possible,
preferably within the first hour
(Table 1).27 Empiric treatment should
be initiated against all suspected
pathogens – be they bacterial, viral, or
fungal. Combination drug therapy is
strongly encouraged for patients who
Table 2.
A Summary of Cardio- and Vasoactive Medications60
16
Agent
Receptor of
Action
Dosing
Notes
Dobutamine
β1 >> β2
5 - 40 mcg/kg/min
Dopamine
Low: DA
Moderate: β1
High: α1
2 – 20 mcg/kg/min
Epinephrine
Low: β1, β2
High: α1
Isoproterenol
β1, β2
1 - 10 mcg/min
Push dose:
5 – 20 mcg every 2 – 5 min
2 – 10 mcg/min
Strong inotropy, moderate chronotropy; mild
vasodilation; increased myocardial oxygen demand.
Arrhythmogenic.
Norepinephrine precursor; positive inotropy and
chronotropy at low to moderate doses; vasoconstriction
at higher doses
Strong inotropy and chronotropy; potential to induce
myocardial infarction
Norepinephrine
α1 >> β1, β2
2 - 30 mcg/min
Phenylephrine
α1
Vasopressin
V1, V2
40-200 mcg/min
Push dose:
50 – 200 mcg every 2 – 5 min
0.01 - 0.04 units/min
Strong inotropy and chronotropy with minimal effect
on vasculature; some decrease in systemic vascular
resistance; neutral cardiac output
Significant vasoconstriction, minimal chronotropy;
possible reflex bradycardia; potential to induce
tachyarrhythmia and myocardial infarction
Vasopressor with minimal cardiac effect; potential to
cause significant reflex bradycardia
Minimal coronary and cerebral vasoconstriction; dosedependent increase in systemic vascular resistance;
preservation of effect in acidosis
March 2015 • Volume 29 • Number 3
are critically ill or neutropenic, or if
there is a possibility for multidrugresistant pathogens. At least two sets
of blood cultures should be obtained
prior to antimicrobial administration,
provided the testing does not delay
treatment. Anti-infective therapy
should be narrowed as soon as
susceptible pathogens are isolated.27
Fluids should be administered
liberally, guided by appropriate
measures of fluid responsiveness as
discussed above. Although limited
data supports the preferential use
of either Ringer’s lactate or normal
saline, large volumes of normal
saline can cause a hyperchloremic
(nonanion gap) metabolic acidosis.
In the case of hemorrhagic shock,
packed red blood cells should be
administered in lieu of crystalloid.
The use of colloid solutions offers
no additional benefit and should be
avoided.58
Vasoactive agents might be
necessary based on the hemodynamic
profile of the presumed cause of the
shock state (Table 2). In the case of
anaphylactic shock, for example, the
drug of choice is epinephrine; and
in cardiogenic shock, the addition
of dobutamine to agents such as
norepinephrine can be beneficial.
Dopamine has an increasingly limited
role in the management of shock
and should be used with caution.59
The lowest possible vasopressor
dose should be used to maintain
adequate perfusion. Patients with
neurogenic shock often will require
blood pressure support; however, the
associated bradycardia need not be
treated.
Case Resolutions
■ Case One
Immediately on arrival, the patient
who awoke with chest pressure
and shortness of breath was placed
on noninvasive positive-pressure
ventilation, and a cardiac monitor was
applied. An ECG showed ST-segment
elevations in the inferior leads with
reciprocal depressions. The cardiac
catheterization team was activated;
and while the cardiac lab was being
prepared, bedside echocardiography
was performed, showing focal
hypokinesis and poor contractility.
Despite some improvement in oxygen
saturation, the patient ultimately
required endotracheal intubation.
A central line was placed, and the
patient was started on norepinephrine
and dobutamine. In the cardiac
catheterization lab, a right coronary
artery occlusion was identified and
stented. An intra-aortic balloon
pump temporarily was placed for
hemodynamic support. The patient
recovered well in the ICU and was
discharged several days later.
■ Case Two
The patient in this case received
supplemental oxygen via nasal
cannula, and her oxygen saturation
improved to 94%. She was placed
on a cardiac monitor, intravenous
access was obtained, and a bolus
of normal saline was administered.
Bedside ultrasonography revealed a
distended IVC without respiratory
variation. No free fluid was seen in
the abdomen, and the abdominal
aorta was of normal caliber. No
appreciable pneumothorax was
identified. Echocardiography
demonstrated no pericardial effusion,
but the right ventricle was noted
to be distended with a bowed
septum and there was poor cardiac
contractility. Repeat blood pressure
was 60/42, and the patient’s mental
status began to deteriorate. A central
venous catheter was placed and
norepinephrine was administered.
After discussion with the family and
an evaluation for contraindications,
systemic thrombolytic agents were
given. The patient’s hemodynamic
status eventually improved and
thoracic computed tomography (CT)
angiography confirmed the diagnosis
of pulmonary embolus.
■ Case Three
In the case of the woman injured
in a motor vehicle collision, a second
large-bore intravenous line was
placed and the institutional massive
transfusion protocol was initiated
for presumed internal hemorrhage.
The patient remained difficult to
arouse and was intubated for airway
protection. Bedside ultrasonography
revealed no evidence of
pneumothorax, pericardial effusion,
or free fluid in the peritoneum.
Blood was transfused with a goal
mean arterial pressure of 55 to 65,
while preparations were made to
transport her to radiology for a CT
scan. ECG, chest radiograph, and
pelvis radiograph in the trauma bay
were all unremarkable. The patient
maintained her blood pressure
through the CT scan, which revealed
an unstable C3-C4 cervical spinal
fracture. The patient remained
persistently hypotensive despite fluid
resuscitation. Bedside ultrasound of
the IVC did not show any respiratory
variation in vessel diameter, and she
was given a vasopressor infusion prior
to being taken to the operating room
for neurosurgical intervention.
Summary
Shock is a common presentation
that is associated with high morbidity
and mortality. Undifferentiated shock
requires rapid identification and
management, often empirically, and
treatment should be tailored to the
suspected cause. Several diagnostic
tools can help determine the cause
of the shocked state, complementing
the history and physical examination.
Limited bedside ultrasonography
has an ever-increasing role in the
emergency department and should
be used liberally. Serum lactate
levels have shown continued utility,
while noninvasive measures of fluid
responsiveness and tolerance are
rapidly usurping the use of central
venous pressure measurements.
Undifferentiated shock can provide
a substantial diagnostic dilemma,
but diligent evaluation and careful
utilization of appropriate diagnostic
measures and interventions can
help the astute emergency physician
improve clinical outcomes.
17
Critical Decisions in Emergency Medicine
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The Critical ECG
A 67-year-old woman with the sensation of a rapid heart beat
Atrial fibrillation, rate 140, aberrant ventricular conduction. When the rhythm is irregularly irregular, the most common
causes are atrial fibrillation, multifocal atrial tachycardia, and atrial flutter with variable AV conduction. Distinct P waves
or flutter waves are absent, excluding the latter two possibilities. The QRS complexes are wide, suggesting aberrant
ventricular conduction. Aberrant conduction can be the result of a bundle branch block, metabolic abnormality (eg,
hyperkalemia), accessory pathway (eg, WPW), or a non-specific intraventricular conduction delay. In the absence of a full
12-lead ECG, it is difficult to specify the exact cause of the aberrant conduction in this case.
Feature Editor: Amal Mattu, MD, FACEP. From: Mattu, A, Brady W. ECGs for the Emergency Physicians 2. London: BMJ
Publishing; 2008:14,23-24. Reprinted with permission.
19