1. science
2. medicine

November 2007
Symptomatic Hypotension: ED
Stabilization And The Emerging
Role Of Sonography
Volume 9, Number 11
Authors
Anthony J. Weekes, MD, RDCS, RDMS, FAAEM
Emergency Ultrasound Program Director, Montefiore Medical
Center; Assistant Professor of Emergency Medicine, Albert
Einstein College of Medicine, Bronx, NY
You just performed an easy endotracheal intubation on an elderly woman
brought in by EMS. She was alert during transport but arrived diaphoretic
and lethargic with a BP of 82/45 mmHg, an irregular pulse at 120, a rectal
temperature of 100.8° F, and she was tachypneic at 32 breaths per minute.
Surprisingly, her oxygen saturation, which was initially 82%, decreases
postintubation to 76%. Portable chest x-ray shows proper ET tube placement, no infiltrates, no pneumothorax, and a normal cardiac silhouette. The
patient is anuric. Labs show a creatinine of 2.1, a WBC count of 18,000, a
hematocrit of 22%, and elevated lactate and transaminase levels. Heart
sounds and breath sounds are normal, the abdomen is soft, and both legs are
swollen. The patient is sick and you realize the key to her survival is finding
the cause of her hypotensive state…
Before an answer is found, two new patients arrive, both with end-stage
renal disease, diabetes mellitus, hypertension, and coronary artery disease.
You begin to wonder why you ever took a job with single clinician
coverage…
Patient #2 looks worse—ashen and diaphoretic, with a blood pressure of
60/40 mmHg. He is afebrile and has a pulse of 100 in the arm without the
AV fistula. He has a history of non compliance with his medications. He
describes the sudden onset of non radiating chest pain that has persisted for
the past two hours. Three sublingual nitroglycerin tablets given by EMS
did not make the chest pain any better and potentially contributed to his
hypotension. On lung examination, you hear rales. You order fluids for the
hypotension but realize this might be a mistake…
Patient #3 has a blood pressure of 100/60 mmHg and appears to be in
no distress. She took her regular morning dose of clonidine and states that
she completed hemodialysis yesterday and felt “woozy” afterwards. She
appears well hydrated. She has no jugular venous distension but there are
Editor-in-Chief
Andy Jagoda, MD, FACEP,
Professor and Vice-Chair of
Academic Affairs, Department of
Emergency Medicine; Mount Sinai
School of Medicine; Medical
Director, Mount Sinai Hospital,
New York, NY.
Associate Editor
John M. Howell, MD, FACEP,
Clinical Professor of Emergency
Medicine, George Washington
University, Washington, DC;
Director of Academic Affairs, Best
Practices, Inc, Inova Fairfax
Hospital, Falls Church, VA.
Editorial Board
William J. Brady, MD, Associate
Professor and Vice Chair,
Department of Emergency
Medicine, University of Virginia,
Charlottesville, VA.
Peter DeBlieux, MD
Professor of Clinical Medicine,
LSU Health Science Center, New
Orleans, LA.
Wyatt W. Decker, MD, Chair and
Associate Professor of
Emergency Medicine, Mayo Clinic
College of Medicine, Rochester,
MN.
Francis M. Fesmire, MD, FACEP,
Director, Heart-Stroke Center,
Erlanger Medical Center;
Assistant Professor, UT College of
Medicine, Chattanooga, TN.
Michael J. Gerardi, MD, FAAP,
FACEP, Director, Pediatric
Emergency Medicine, Children’s
Medical Center, Atlantic Health
System; Department of
Emergency Medicine, Morristown
Memorial Hospital, NJ.
Michael A. Gibbs, MD, FACEP,
Chief, Department of Emergency
Medicine, Maine Medical Center,
Portland, ME.
Steven A. Godwin, MD, FACEP,
Assistant Professor and
Emergency Medicine Residency
Director, University of Florida
HSC/Jacksonville, FL.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc; Clinical
Professor of Emergency
Medicine, University of Michigan,
Ann Arbor.
Keith A. Marill, MD, Instructor,
Department of Emergency
Medicine, Massachusetts General
Hospital, Harvard Medical School,
Boston, MA.
Charles V. Pollack, Jr, MA, MD,
FACEP, Professor and Chair,
Department of Emergency
Medicine, Pennsylvania Hospital,
University of Pennsylvania Health
System, Philadelphia, PA.
Michael S. Radeos, MD, MPH,
Associate Research Director,
Department of Emergency
Medicine, New York Hospital
Queens, Flushing, NY; Assistant
Professor of Emergency
Medicine, Weill Medical college of
Cornell University, New York, NY.
Robert L. Rogers, MD, FAAEM,
Assistant Professor and
Residency Director, Combined
EM/IM Program, University of
Maryland, Baltimore, MD.
Ryan J. Zapata, MD, FACEP
Attending Physician, Montefiore Medical Center; Assistant
Professor of Emergency Medicine, Albert Einstein College of
Medicine, Bronx, NY
Antonio Napolitano, MD, FACEP
Attending Physician, Montefiore Medical Center; Assistant
Professor of Emergency Medicine, Albert Einstein College of
Medicine, Bronx, NY
Peer Reviewers
Corey M. Slovis, MD, FACP, FACEP, FAAEM
Professor and Chair, Department of Emergency Medicine,
Vanderbilt University Medical Center, Nashville, TN
Scott D. Weingart, MD
Director, Division of Emergency Critical Care, Department of
Emergency Medicine, Mount Sinai School of Medicine, New
York, NY
CME Objectives
Upon completion of this article, you should be able to:
1. Identify the common and life-threatening causes of
hypotension.
2. Understand the clinical approach to the rapid identification
of dangerous causes of hypotension.
3. Explain the emerging role of goal-directed bedside sonography in the rapid non-invasive diagnosis and management of hypotensive patients.
4. Appreciate the importance of early intervention in the management of hypotension, including the role of intravenous
fluids, inotropes, and vasopressors.
5. Decide the practical and evidence-based advantages and
disadvantages of various point-of-care tests, imaging
modalities, and treatments in hypotension.
Date of original release: November 1, 2007
Date of most recent review: October 18, 2007
Termination date: November 1, 2010
Time to complete activity: 4 hours
Medium: Print & online
Method of participation: Print or online answer form
and evaluation
See “Physician CME Information” on back page.
Alfred Sacchetti, MD, FACEP,
Assistant Clinical Professor,
Department of Emergency
Medicine, Thomas Jefferson
University, Philadelphia, PA.
Corey M. Slovis, MD, FACP,
FACEP, Professor and Chair,
Department of Emergency
Medicine, Vanderbilt University
Medical Center, Nashville, TN.
Jenny Walker, MD, MPH, MSW,
Assistant Professor; Division
Chief, Family Medicine,
Department of Community and
Preventive Medicine, Mount Sinai
Medical Center, New York, NY.
Ron M. Walls, MD, Professor and
Chair, Department of Emergency
Medicine, Brigham & Women’s
Hospital, Boston, MA.
Research Editors
Nicholas Genes, MD, PhD, Mount
Sinai Emergency Medicine
Residency.
Beth Wicklund, MD, Regions
Hospital Emergency Medicine
Residency, EMRA Representative.
International Editors
Valerio Gai, MD, Senior Editor,
Professor and Chair, Dept of EM,
University of Turin, Italy.
Peter Cameron, MD, Chair,
Emergency Medicine, Monash
University; Alfred Hospital,
Melbourne, Australia.
Amin Antoine Kazzi, MD, FAAEM,
Associate Professor and Vice
Chair, Department of Emergency
Medicine, University of California,
Irvine; American University, Beirut,
Lebanon.
Hugo Peralta, MD, Chair of
Emergency Services, Hospital
Italiano, Buenos Aires, Argentina.
Maarten Simons, MD, PhD,
Emergency Medicine Residency
Director, OLVG Hospital,
Amsterdam, The Netherlands.
Accreditation: This activity has been planned and implemented in accordance with the Essentials and Standards of the Accreditation Council for Continuing Medical Education
(ACCME) through the joint sponsorship of Mount Sinai School of Medicine and Emergency Medicine Practice. The Mount Sinai School of Medicine is accredited by the ACCME to
provide continuing medical education for physicians. Faculty Disclosure: Dr. Weekes, Dr. Zapata, Dr. Napolitano, Dr. Slovis, and Dr. Weingart report no significant financial
interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation. Commercial Support: Emergency Medicine
Practice does not accept any commercial support.
bibasilar rales. Heart sounds are distant but there are no
rubs or murmurs. You suspect orthostatic hypotension.
CXR shows no pulmonary congestion and the heart
silhouette is slightly enlarged. The ECG shows no obvious
signs of AMI. Repeat blood pressure is 96/58 mmHg and
something doesn’t seem right to you…
women.2 Keep in mind these numbers vary with the
patient’s size and ideal body weight.
Mean arterial pressure (MAP) is more reflective of
the actual pressure in the arterioles and smaller
vessels than the standard blood pressure measurements and may be more helpful in the evaluation of
hypotension. MAP calculations are as follows:
T
here is no clear blood pressure definition of
hypotension. Instead, blood pressure must be
placed in the context of the patient’s age and current
clinical and baseline physiologic states. For example,
what appears to be a “normal” blood pressure may
actually be a dangerously low blood pressure in the
patient who is generally hypertensive. Hypotension
is a sign, not a diagnosis, and it is not pathognomonic
of any specific condition by itself. It can be found in
both acute critical conditions and in chronic steady
state conditions. The emergency physician must
determine which is present and tailor the aggressiveness of interventions based on the underlying
etiology.
In critically ill patients, the first hours of treatment
have a direct impact on morbidity and mortality. In
these cases, the approach to hypotension is sometimes
unstructured, with a focus on “correcting the numbers” while investigating the cause. Less emergent
but equally challenging are those patients with low
blood pressures who are in a steady state but are not
critically ill (e.g., patients with end-stage congestive
heart failure). Trying to raise the blood pressure in
this group of patients is not generally indicated and
may be harmful.
The cases presented at the beginning of this article
illustrate the challenge posed by patients with
hypotension and demonstrate the need for the emergency physician to accurately narrow the differential
diagnosis. Management involves a three pronged
approach that simultaneously includes stabilization,
diagnostic testing, and therapy. Because the differential diagnosis is so broad, most guidelines are diagnosis specific and do not provide a systematic approach
to managing hypotension. This issue of Emergency
Medicine Practice is designed to provide an evidencebased, algorithmic approach to the management and
diagnosis of conditions causing hypotension. Specific
attention will be given to the role of ultrasound in the
clinical decision making involved in caring for these
patients.
MAP = 2/3 DBP + 1/3 SBP
- or MAP = DBP + (SBP-DBP)/3
- or [ (2xDBP) + SBP ]/3
The standard definition of hypotension in an adult
includes the findings of: a SBP < 90 mmHg, a MAP
< 60 mmHg, a decrease of more than 40 mmHg below
the person’s baseline, or any combination of the
aforementioned parameters.3 In some studies, the
definition of hypotension uses a SBP < 100 mmHg.4,5
A healthy adult will have natural variations in
blood pressure readings during a routine 24-hour
period.6,7 A numerical blood pressure reading takes on
clinical significance when the MAP is below the
patient’s usual regulated pressures for organ perfusion. For example, a blood pressure reading of
140/90 mmHg may provoke symptoms of organ
hypoperfusion (such as dizziness and fatigue) if the
patient’s chronic blood pressure readings have been
consistently much higher. Such a patient should be
considered ‘acutely clinically hypotensive.’ Shock can
occur with “normal” blood pressure readings.8-10
Refractory hypotension refers to persistently
hypotensive readings after the administration of an
intravenous crystalloid fluid bolus of 20-40 mL/kg.
Pseudohypotension refers to the underestimation
of the patient’s true BP secondary to arterial occlusion
or other abnormalities. If the unaffected extremity has
adequate perfusion, the true blood pressure reading is
noticeably higher than in the affected extremity. Pulse
deficits or pseudohypotension can be a strong indicator of aortic side branch occlusions and thus raise the
suspicion of a vascular emergency.
Shock refers to a state of organ dysfunction or
even organ failure due to inadequate tissue perfusion.
Multiple etiologies of shock are described and more
than one type may be present in a single patient. The
various types of shock are listed below:
• Cardiogenic – results from loss of cardiac output
• Hypovolemic – results from decreased intravascular volume
• Obstructive – results from intrinsic (e.g., pulmonary embolus) or extrinsic (e.g., pericardial
tamponade) vascular outflow obstruction
• Distributive – results from disruption of vasomotor regulation (e.g., anaphylactic, septic, and
neurogenic shock)
Shock is the most feared cause of hypotension; it is
not a diagnosis but a final common pathway by which
many disease processes produce multi-organ failure
Terminology
General medical teaching cites normal blood pressure
(BP) as 120/80 mmHg as measured over the brachial
artery using auscultatory methods. Population
studies have shown these numbers to range between
109-137 mmHg for the systolic blood pressure (SBP)
and 66-87 mmHg for the diastolic blood pressure
(DBP).1 Another study found BP to range from
116-145 mmHg SBP and 66-84 mmHg DBP in men and
107-137 mmHg SBP and 61-78 mmHg DBP in
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November 2007 • EBMedicine.net
presentation, orthostasis is already diagnosed and
vital signs after treatment may be more helpful.
and death. The healthy adult is able to compensate
for normal changes in organ perfusion. In shock, the
insult is of such magnitude that normal compensatory
mechanisms are overwhelmed and organ hypoperfusion and dysfunction develop. This leads to
irreversible end organ failure if resuscitation is not
initiated and achieved in time. The important thing to
realize is that the development of hypotension is a late
manifestation of shock, and the rapidity of progression through the spectrum of pre-shock, shock, and
multi-organ dysfunction stages depends on many
factors. The severity of the inciting insult, the
patient’s preexisting medical conditions (especially
cardiopulmonary function), and their immune and
nutritional status all play a role.
Critical Appraisal Of The Literature
Literature searches were performed using Ovid
MEDLINE and PubMed in the National Library of
Medicine for diagnosis and management recommendations as well as updates regarding conditions
involving hypotension. In addition, the Cochrane
Database of Systemic Reviews was searched for
reviews on similar topics. This search provided an
enormous number of studies, though few well
designed, prospective studies. Another source of
information was the National Guideline Clearinghouse™ which provided guidelines for sepsis management and ultrasound-guided central line placement.
Difficulties arose in finding studies specific on the
management of undifferentiated hypotension as this
topic covers a clinical sign that manifests in many
different clinical situations (including sepsis, dehydration, heart disease, trauma, and many other disease
states). Sub-topics of fluid management, sepsis
management, pressor support, ultrasound applications, Advanced Cardiac Life Support (ACLS),
Advanced Trauma Life Support (ATLS), and others
were reviewed and combined to produce recommendations for diagnosis and treatment, especially in
early stages of hypotension.
Orthostatic Hypotension
Standing or sitting with the legs dangling can cause
up to 1 L of blood volume to pool in the venous
circulation of the legs. The immediate result of
lowering intrathoracic blood volume is a reduction in
both cardiac output and blood pressure. Through the
normal autonomic response, an increase in heart rate
by as much as 25 beats/minute and an increase in
systemic vascular resistance should keep blood
pressure at normal levels. A 5-10 mmHg drop in BP
can be seen in normal individuals within three
minutes of the position change. This change is
clinically insignificant.
The symptomatic lowering of blood pressure upon
standing is called postural or orthostatic hypotension.
Symptoms are usually due to an impaired autonomic
response. Traditionally, orthostatic blood pressure
readings and heart rate are measured in the supine
patient then repeated with the patient in a standing
position. A decrease in the SBP of 20 mmHg or in the
DBP of 10 mmHg after standing for three minutes
defines orthostatic BP.11 Parameters for abnormal
orthostatic increases in heart rate are not well defined
but many have a HR greater than 20-30 beats per
minute. Patients with a hypertensive blood pressure
when supine can be symptomatically orthostatic with
a large enough decrease in BP upon standing.
A similar blood pressure drop associated with
eating is called postprandial hypotension.
Volume depletion can compound the symptoms
from an abnormal sympathetic neurocirculatory
response but can also be an independent factor
causing orthostasis. Up to 20% of patients over the
age of 65 can have orthostatic hypotension. Of
particular note is the patient with Parkinson’s disease
who may have primary autonomic dysfunction which
can easily be exacerbated by dehydration or
polypharmacy.
Determination of orthostasis should be directed by
the patient’s clinical presentation. If symptomatic at
rest and supine, orthostatic vital signs are not necessary as the patient is already “hypotensive” regardless
of the numbers. If history suggests near syncope or
similar symptoms with position change prior to ED
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Epidemiology
While it is difficult to determine with accuracy the
incidences of hypotension in a general population or
even in a select population of ED or hospitalized
patients, studies have examined data on critically ill
patients and effects of hypotension on outcome.
The duration of hypotension after trauma, sepsis,
anaphylaxis, and cardiogenic sources are critical
determinants of morbidity, prognosis, and survival in
these groups of hypotensive patients.3
Jones et al performed a secondary analysis of data
accrued from a randomized, controlled trial of rapid
versus delayed bedside goal-directed ultrasound of
patients with symptomatic, non-traumatic shock. In
this study, hypotension was defined as an initial ED
systolic blood pressure reading of less than
100 mmHg. Shock was defined by the presence of
hypotension with one or more predetermined signs or
symptoms. The hospital mortality of the 190 ED
shock patients in this study was 15%. Adverse
hospital outcomes included organ failure, the need for
intensive care admission, and in-hospital mortality.
Fifty percent of the patients with a SBP < 80 mmHg
had an adverse hospital outcome. Forty percent of the
patients with an adverse outcome had blood pressure
readings that were consistently below 100 mmHg for
more than 60 minutes.13
The one month mortality rate after the onset of
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hypovolemic shock is dependent on the underlying
cause and the patient’s co-morbidities. A 2002 study
by Moore et al of ED patients with atraumatic
hypotension (defined as a SBP < 100 mmHg) showed
an in-hospital mortality rate of 18%.4 In a recently
released prospective cohort study by Jones et al, ED
patients with a SBP < 80 mmHg had a six-fold
increased incidence of in-hospital death. Patients with
a SBP < 100 mmHg for more than 60 minutes had
nearly three times the incidence of in-hospital death.14
Within one month of the diagnosis of septic shock, the
overall mortality rate can be as high as 40%. Mortality for cardiogenic shock can be as high as 60%.15,16
Use of the presence of hypotension alone as a
predictor of ED patient mortality is incomplete and
risks ignoring the importance of the associated clinical
context. In certain well-defined disease entities (such
as aortic dissection and cardiac failure), hypotension
is associated with sicker patients; thus, there are
higher mortality rates of 50-80%.17 Hypotension in
patients with end-stage renal disease (ESRD) and/or
atherosclerotic cardiovascular disease is also associated with higher mortality rates. Consequently, rapid
identification of the etiology of the hypotensive state
has a potentially critical impact on the patient’s short
and long term clinical outcome.
CO = SV x HR
Hypotension results when either the stroke volume or
the heart rate is decreased. In addition, blood volume
provides the “substrate” that the resistance vessels
“push” against in order to regulate BP. Thus, even
maximal vasoconstriction will be ineffective if volume
status is inadequate. This key point resurfaces in
managing many hypotensive patients.
The peripheral vascular resistance (PVR) is regulated by a variety of mechanisms. Only a small
proportion of the blood volume is involved in perfusing tissues at any given time. Most of the total blood
volume is contained in the venous system. The veins
serve as blood reservoirs that are mobilized by the
neuroendocrine system in time of need. Certain
organs, such as the heart and brain, are autoregulated.
Their perfusion is influenced by metabolic factors and
not by the neuroendocrine system. Thus, blood flow
is preserved and can actually be enhanced in early
volume loss.
Adrenergic receptors are located in organs based
on their function in the “fight or flight” response to
stress. Non essential organs in acute stress events
(such as the gastrointestinal tract) have high concentrations of vasoconstrictive alpha-1 (A1) receptors,
while those essential to survival in acute stress (the
heart, lung, and skeletal muscles) have high concentrations of vasodilatory beta-2 (B2) receptors.
Cardiac beta-1(B1) receptors produce increased
chronotropy and inotropy with consequent increased
oxygen demand. Dopaminergic receptors are primarily located in the splanchnic and the renal beds.
These receptors are stimulated by mediator release
from nerve endings (norepinephrine) and the endocrine system (epinephrine). Mediator release is
stimulated by the vasomotor centers located in the
medulla and hypothalamus. Inhibitory outputs from
cardiac, renal, and blood vessel baroreceptors affect
these centers. Pathological drops in blood pressure
cause decreased outputs to be sent from the baroreceptors, disinhibiting the vasomotor centers. Sympathetic nervous system output or tone is thus augmented; “vagal tone” is conversely decreased.
In low pressure states, like hypovolemia, there is
less baroreceptor stimulation which leads to ADH
release. The release of ADH leads to: 1) An increase in
water absorption in the distal renal tubules and then
an increase in vascular blood volume; and 2) Peripheral vasoconstriction. Other mediators that increase
adrenergic tone include carbon dioxide and hydrogen
ions.
The kidney plays a role in the regulation of blood
pressure through the following mechanisms:
• Glomerular filtration rate (GFR) decreases in
hypotension which decreases sodium transit
time in the tubules and increases its absorption.
In turn, this increases the absorption of water.
• Increased water absorption mediated by ADH in
the distal tubule.
Hypotension In Trauma
The ATLS protocols support the practice of using
hypotension as only a late marker of shock because of
its low sensitivity. Prior to 1989, ATLS guidelines
taught that the absence or presence of the carotid,
femoral, and radial pulses could be correlated to
systolic blood pressures. When compared to invasively obtained arterial blood pressure measurements,
however, it was discovered that the correlations
previously made were overestimations.19 ATLS no
longer teaches pulse and SBP correlations in the
context of clinical decision making.
The National Trauma Data Bank (n = 115,830),
where hemorrhagic shock was the main cause of
hypotension, reports that SBP correlates with serum
base deficits (considered to be a marker of circulatory
shock). The mean and median SBP decreased to less
that 90 mmHg when the base deficits were worse than
-20.20 The Data Bank supports the conclusion that
SBP is a late marker for mortality and that, in the
setting of hemorrhagic shock, SBP should not be used
as a primary decision point in choosing which patient
should receive resuscitation efforts. Patients with
hypotension and significant base deficits had a
mortality rate of 65%.
Pathophysiology
Normal BP results from a balance between the peripheral vascular resistance and the cardiac output (CO),
with total blood volume affecting both. Cardiac
output is a product of the stroke volume (SV) and the
heart rate (HR):
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November 2007 • EBMedicine.net
• Renin release from granular cells of the afferent
arteriole stimulated by adrenergic output,
macula densa output, and direct action of low
blood pressure on the granular cells themselves.
Renin catalyzes angiotensinogen to angiotensin1 in the liver which is converted to angiotensin-2
in the lung by angiotensin converting enzyme
(ACE). Angiotensin-2 is a direct vasoconstrictor
but also stimulates the renal cortex to release
aldosterone, further promoting sodium
retention.
• Hypotension causes a decrease in the release of
atrial natriuretic peptides which decreases
sodium and water loss in the urine.
or signs of circulatory insufficiency were termed
‘exposures.’ ‘Non-exposures’ were those patients with
symptoms of circulatory insufficiency but whose
blood pressure readings were always above
100 mmHg. In the U.S. venue, there were 395
exposures and 395 non-exposures; the in-hospital
mortality was 26% for exposures and 8% for nonexposures. In the multi-center Canadian venue, the
in-hospital mortality rate was 32% for exposures
compared to 11% for non-exposures. This data
supports the association of out of hospital hypotension with in-hospital mortality.
One of the highest risk groups of patients with
hypotension are those with an acute myocardial
infarction. Interestingly, even in this high risk group,
one study reported a decrease in mortality from 69%
in the control phase to 10% when paramedic level of
care was made available.21 Heightened ED readiness
cuts vital minutes off of door-to-ECG to needle or
balloon times. Medical control should be notified of
patients with ischemic ECG findings and consideration should be given to transporting these patients to
a center with percutaneous interruption capabilities.
The trauma literature is replete with studies
advocating for ambulance notification and activation
of the ED and trauma teams in cases of hypotension or
uncontrolled hemorrhage. Trauma team activation has
been shown to improve outcomes in patients with
penetrating trauma. In a retrospective study of 180
patients, Hooker et al showed that 61% of patients
with prehospital hypotension (defined in this study as
SBP < 100 mmHg) required transfusion versus 11% of
patients without a hypotensive reading in the field.22
Franklin et al showed that not only ED hypotension
but prehospital hypotension was a bona fide indicator
to activate the trauma team.23 More than half of the
patients with hypotension required urgent operative
hemorrhage control. Another study showed that an
isolated prehospital hypotensive reading, even with
normal BP readings in the ED, marked the trauma
patient for increased mortality and the need for
operative intervention for chest and abdominal
injuries.24
An interesting area of prehospital diagnostics is
the use of portable ultrasound devices to evaluate
cardiac output and internal bleeding. Acquired
images may be transmitted to the receiving hospital.
Garrett et al recently showed the transmission of
wireless images to be effective in allowing a hospitalbased cardiologist to do a preliminary assessment of
left ventricular function and the presence or absence
of pericardial effusion.25 Successful transmission of
sonographic images occurred 88% of the time. The
potential in trauma assessments and abdominal aorta
screening in symptomatic patients en route to
pertinent tertiary care centers is an area of ongoing
research.
Differential Diagnosis
The differential diagnosis of hypotension is vast.
Table 1 provides a framework to use when approaching these patients.
Prehospital Care
The detection of hypotension prompts urgent transport to the nearest or most appropriate ED with
concomitant intravenous access and fluid administration if possible. Advance notification places the ED
on alert and facilitates expedited care when the
patient arrives. Patients should receive oxygen, an
oxygen saturation monitor should be put in place, and
electrocardiogram (ECG) monitoring begun. If at all
possible, a 12-lead ECG should be performed in any
hypotensive patient who is at risk for acute coronary
syndrome. A cardiac monitor tracing and repeated
vital signs should be recorded clearly and exchanged
between prehospital and ED personnel.
Jones et al conducted a cross sectional risk assessment study of non-traumatic ambulance transports in
the U.S. and Canada.5 Patients experiencing hypotensive episodes (a single reading of less than 100
mmHg) with one or more predetermined symptoms
Table 1. Differential Diagnosis Of Hypotension
Hypovolemic
Hemorrhagic
Dehydration
Low oncotic intravascular pressure (third spacing)
Cardiogenic
Acute myocardial infarction
Arrhythmias
Lower stroke volume
Inadequate cardiac output
Distributive
Septic shock
Anaphylaxic and anaphylactoid reactions
Blood product transfusions (usually during the transfusion)
Drug interactions
Drug overdoses
Neurogenic impairment of sympathomimetic responses
Adrenal insufficiency
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automated BP readings were compared with central
arterial blood pressure recordings in 120 patients.29
There were clinically significant inaccuracies
(± 10 mmHg) in 24% of the automated device recordings and severe inaccuracies (± 20 mmHg) in 3.2% of
the automated device recordings. More recent studies
have demonstrated these devices to be of acceptable
accuracy when used correctly. Cavalcanti et al
studied manual cuff readings compared to automated
cuff readings in 92 patients; there was high correlation
(within 10 mmHg) in all of the patients.30 Greater
inaccuracies have been found with cuffs that are too
small, leading to erroneously high BP readings.31-34
Some studies have also examined differences in blood
pressure readings with respect to body position, arm
position, and relative resting state of the patient.35-38
Unfortunately, these studies are based on monitoring
of hypertension and only very loose inferences can be
made to the hypotensive patient. The best available
evidence suggests that blood pressure measurements
be taken with the patient in a recumbent position with
the antecubital fossa at the level of the right atrium
and that subsequent measurements remain consistent
with this position.
Other vital signs will offer clues to the extent and
source of hypotension and provide a baseline for
monitoring the patient. Heart rate will likely be
increased in a hypotensive patient but may be affected
by body position, activity prior to measurement, or
medications (e.g., beta blockers). Orthostatic vital
signs are rarely needed or indicated in the already
hypotensive patient. Respiratory rate, rectal temperature, and pulse oximetry are fundamental to the
patient’s assessment. Of note, hypoperfusion may
interfere with an accurate assessment of oxygen
saturation.
Despite the importance of obtaining accurate vital
signs, it is important to note that vital signs alone
have limitations in identifying shock states. Ander et
al examined the use of lactic acid level and continuous
central venous oxygen saturation in identifying the
disease severity of patients with acute decompensation of severe chronic congestive heart disease (ejection fraction [EF] < 30%).10 The vital signs did not
help distinguish the patients with hidden shock states
(defined as high lactic acid levels and low central
venous oxygen saturations) from those with mildly
decompensated or stable CHF. The patients in the
shock state required more aggressive treatment for
CHF with resultant decrease in lactic acid levels and
increased central venous oxygen saturation.
ED Evaluation
Hypotension is a predictor of negative outcomes
regardless of the underlying etiology. Consequently, it
is the emergency physician’s responsibility to quickly
identify and treat underlying causes. A large,
prospective study of 6303 patients conducted across
five hospital wards in Australia identified hypotension (BP < 90 mmHg), a two or more point decrease of
the Glasgow Coma Scale, the onset of coma, respiratory rate less than 6 per minute, oxygen saturation
< 90%, and bradycardia for more than 30 minutes as
predictors of mortality.26 Of these predictors,
hypotension and oxygen desaturation were identified
as the most common occurrences prior to cardiac
arrest, with hypotension being associated with nearly
a seven-fold increase in mortality.
In general, patients with hypotension should be
placed in the critical area of the ED. Oxygenation
should be maximized by placing the patient on 100%
oxygen by nonrebreather face mask. Large bore
intravenous access should be established, using
central access if necessary. An accurate set of vital
signs should be obtained and frequently repeated
while the history, physical, and diagnostic tests are
performed.
The most common causes of hypotension —
hypovolemia, cardiogenic shock and sepsis — may
overlap. Noninvasive measures should be used early
and frequently to assess oxygen debt, cardiac performance, and the overall flow state; see the following
discussions. Equally important is the need to monitor
the cardiac and flow state response to the therapies
initiated. Given the insensitivity of blood pressure to
evaluate cardiac output, the correction of blood
pressure is not the only goal.27
Vital Signs
Blood pressure is a “vital sign” and must be measured
accurately. The standard blood pressure is measured
over the brachial artery at the antecubital fossa. Care
must be taken in selecting an appropriate size cuff for
the patient and to ensure proper positioning of the
cuff bladder over the brachial artery. When the cuff
pressure drops below the SBP, blood audibly passes
with each systole, producing Korotkoff’s sounds.
Once pressure drops below the DBP, these sounds
disappear because blood can now pass during both
systole and diastole.
Blood pressures are often recorded with automated cuffs, and a malpositioned cuff bladder will
give a falsely low reading which may lead to mismanagement if it goes unrecognized.6 Any low BP that
impacts clinical care should be confirmed with a
manual BP measurement. Automated cuff measurements have been tested against manual sphygmomanometer readings and against direct intra-arterial
blood pressure measurements. Varied results have
been obtained.28,29 In a study by Lehman et al,
Emergency Medicine Practice®
History
The evaluation of the patient with hypotension must
be comprehensive. Ideally, the patient’s baseline
blood pressure must be determined as well as the
overall clinical status. Symptoms that indicate a
cardiopulmonary cause include but are not limited to
prodromal symptoms (such as chest pain, palpitations, and dyspnea). Nausea, vomiting, diarrhea, or
6
November 2007 • EBMedicine.net
Physical
abdominal pain, as well as hematemesis and melena
may indicate a gastrointestinal etiology. Fever, cough,
or dysuria may point to an infectious etiology. The
potential for an allergic reaction must be assessed as
well as the pregnancy status of women of childbearing age. A mental health screening will assess for the
likelihood of drug overdose as the etiology. See
Tables 2 and 3 for possible symptoms and key historical questions.
Searching through medical records for the ‘baseline’ BP and finding multiple low blood pressure
readings during prior hospitalizations or ED visits
should not lower the concern. These patients were
sick enough to need frequent care and hospitalizations. Routine clinic visits are a better source for
establishing a baseline.
Due to the broad differential diagnosis, a thorough
and comprehensive physical examination is necessary
for the evaluation of the hypotensive patient. General
nutritional and hydration status should be assessed.
During the head and neck examination, signs such as
sunken eyes, bitemporal wasting, and moisture of the
mucous membranes should be noted.
Neck examination can reveal the presence or
absence of jugular venous distention (JVD) and gives
an early clue to pre-load status. The presence of JVD
on a patient with hypotension is a serious finding that
must be aggressively investigated. Neck vein distention is usually caused by an impaired return of
venous blood to the right side of the heart or by
significantly elevated right heart pressures.
Conditions that may cause this include pericardial
tamponade, constrictive pericarditis, tension pneumothorax, right ventricular infarction, massive
pulmonary embolism, and air trapping with mechanical ventilation. Tracheal deviation with dyspnea can
point to pneumothorax.
During the chest examination, note the presence or
absence of breath sounds, crackles, wheezes, and areas
of dullness or tympany to percussion. The heart
examination can reveal tachycardia, flow murmurs
indicating cardiac hyperactivity, diastolic and systolic
murmurs which may indicate valve dysfunction, or
muffled heart sounds indicating pericardial effusion.
The abdominal examination may reveal abnormal
bowel sounds, bruits, ascites, palpable masses, distention, rigidity, and areas of tenderness pointing to
pathology that indicates dehydration, sepsis, third
spacing, or intra-abdominal bleeding.
Extremities may be cool and clammy and exhibit
poor capillary refill or peripheral pulses. Edema may
indicate third spacing or endocrinopathies such as
hypothyroidism or adrenal pathology. A careful skin
examination may reveal petechiae, suggesting platelet
dysfunction (as seen in a vasculitis) or purpura (as
seen in disorders of coagulation).
The neurological examination will be most significant for arousability and abnormal mental status, but
other more focal signs may be present as watershed
areas in the brain are affected by decreased cerebral
perfusion pressure. Rectal and pelvic exams are
recommended based on clinical suspicion.
Table 2. Potential Symptoms Of Organ Hypoperfusion
Weakness
Dizziness
Fatigue
Syncope
Anxiety
Thirst
Sense of doom
Dyspnea
Chest discomfort (any description)
Confusion (reported by patient or otherwise witnessed)
Table 3. Quick Critical Questions: Key Historical Pointers
Events Immediately Preceding
Call for help
EMS evaluation and course
Prior Hypotensive Episodes
None
Medication-related
Sepsis
Allergic
Known Medical Diseases
Cardiac
Renal
Cerebrovascular accident
Transplant recipients
Autoimmune disease
Psychiatric
Dehydration
GI bleed
Cardiac
Pulmonary
Hepatic
Pregnancy
HIV/AIDS
Cancer
Cognitively impaired
Medication Exposure
Prescribed
Not prescribed, including herbal medications
Alterations to medication regimen
Medication overdoses (intentional or accidental)
Illicit drugs
EMS or ED administered (e.g., rapid sequence intubation,
sedation)
Diagnostic Tests
Complete Blood Count (CBC)
Allergy History
Recent or suspected exposure (food, medications, latex, etc.)
White Blood Cell Count (WBC)
The WBC rarely contributes to the acute management
of pathologic hypotension. Although high and low
WBC counts can suggest infection, they can also
merely relate the severity of the insult resulting in
hypotension. In 1992, the American College of Chest
Physicians (ACCP) and the Society of Critical Care
Coagulopathic States
Warfarin (after trauma or spontaneous bleeding due to drug
toxicity)
Hemophilia A and B
Thrombocytopenia < 20 K
Platelet dysfunction syndromes: von Willebrand’s disease,
uremia, etc.
EBMedicine.net • November 2007
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Emergency Medicine Practice®
Medicine (SCCM) introduced definitions for the
systemic inflammatory response syndrome (SIRS).15
Hypotension and the presence of WBC counts above
12,000 or below 4000 were two of the four clinical
findings used to diagnose the presence of this syndrome, and both can be present in non-infectious
etiologies (e.g., polytrauma). A single white blood cell
count that is within the normal range does not
exclude an infection-related cause of hypotension.
The presence of extremely high or extremely low
white counts can also reflect the presence of hematologic, oncologic, and immune disease. The presence
of neutropenia (absolute neutrophil cell count of less
than 1000) not only indicates the above, but also the
need for empiric antibiotic treatment when fever is
present.
detect whether it is actually low and if schistocytes
(peripherally shredded RBC’s) are present; a microangiopathic hemolytic anemia (MAHA) should be
suspected in these cases. When MAHA is not due to a
consumptive coagulopathy (discussed later), it is due
to pathologically activated platelets adhering in the
capillary bed with resulting RBC hemolysis and
anemia. Toxins elaborated in sepsis and in thrombotic
thrombocytopenia purpura (TTP) can cause this.
Coagulation Profile
There are three main reasons to send the International
Normalised Ratio (INR) with Prothrombin Time (PT)
and Partial Thromboplastin Time (PTT) tests.
• To document the presence of a consumptive
coagulopathy, use INR/PT and PTT plus Ddimer, fibrin split products, and fibrinogen
levels.
• To evaluate coagulation function in the face of
anticoagulants such as warfarin (Coumadin®),
use the INR/PT.
• To evaluate liver synthetic function (e.g.,
albumin, vitamin K-dependent clotting factors),
use PT.
Disseminated intravascular coagulopathy (DIC)
produces MAHA by inappropriate activation of the
clotting system. The fibrin produced settles in the
capillary beds and destroys RBCs and PLT's. Afterwards, pathologic activation of the fibrinolytic system
produces the purpura, hemorrhage, and PT/PTT
abnormalities that are diagnostic of the condition.
Other tests (such as fibrin split products, D-dimer, and
fibrinogen levels) are sent when the condition is
highly suspected even in the face of a normal PT and
PTT results.
Increased PT times may be due to:
• Liver disease (Bile duct obstruction, cirrhosis,
and hepatitis)
• Disseminated intravascular coagulation
• Vitamin K deficiency
• Warfarin (Coumadin®) therapy
• Factor I, II, V, VII, and X deficiencies
Increased PTT evaluates the intrinsic coagulation
system and can be used to:
• Monitor heparin therapy and to aid in detecting
classical hemophilia A and B and other congenital factor deficiencies.
• Screen for the presence of hypo or dysfibrinogenemia, disseminated intravascular coagulation, liver failure, and vitamin K deficiency.
D-dimer is very specific for disseminated
intravascular coagulation.
Hemoglobin/Hematocrit (H/H)
In the setting of suspected hemorrhage, the finding of
a low value helps to make the clinician more confident of his or her diagnosis. However, in the setting
of massive rapid hemorrhage, the H/H may appear
normal even though the patient is in extremis. If
clinical suspicion is high, the test needs to be repeated
over time. The H/H is also helpful in management
decisions in that transfusion becomes a consideration
when the hematocrit is less than 30 and you suspect
the patient has sepsis or myocardial ischemia.
Red blood cell (RBC) indices that may be helpful
include the mean corpuscular volume (MCV), range
distribution width (RDW), and reticulocyte count.
The MCV is a measure of the average size of red
blood cells in the circulation. High or low values
reflect nutritional deficiencies, drug effects, or red cell
hematopoietic dysfunction. When present, this
abnormality does not eliminate the possibility of an
acute event; it only suggests the presence of a chronic
problem having been present before the acute one.
When many cell lines of different sizes are present, the
MCV can erroneously be normal; in which case, the
RDW becomes helpful. The RDW is a measure of the
range of different sizes of RBC’s present in the blood
stream; its elevation suggests pathology even in the
face of a normal MCV. The reticulocyte count is
helpful in determining whether an anemia is hyperproliferative (high count) or hypoproliferative (low
count).
Platelet Count (PLT)
Platelet count and function must also be assessed in
hypotensive patients. Thrombocytosis is rarely of
immediate clinical concern in that platelet elevations
are commonly seen in many inflammatory or infectious diseases, leading to its nickname among
rheumatologists as the poor man’s sedimentation rate.
It is also elevated in iron deficient anemia.
Thrombocytopenia is associated with several
serious diseases and is an ominous sign when present
with hypotension. Thrombocytopenia in the setting of
anemia requires evaluation of the peripheral smear to
Emergency Medicine Practice®
Serum Chemistry Panel
Blood Urea Nitrogen (BUN) And Creatinine (Cr)
The BUN and Cr provide indicators of renal function.
A BUN/Cr ratio of > 1:20 suggests dehydration.
Electrolytes
Elevations in serum sodium more accurately reflect
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November 2007 • EBMedicine.net
water balance than actual sodium concentration.
Hyponatremia in the absence of diuretics or rare
sodium wasting nephropathies reflects the retention of
water in excess of sodium, whatever the cause. It can
be chronic (such as in the syndrome of inappropriate
antidiuretic hormone [SIADH]) or acute (as seen when
there is volume loss of 10% or more). Hypernatremia
almost always reflects severe dehydrations but with
loss of water exceeding salt losses. Potassium elevations reflect either increased or decreased intake or
excretion of potassium or sudden release of intracellular potassium from massive tissue damage.
Bicarbonate and chloride are useful mainly in the
calculation of the anion gap, which can be used to
generate the differential of high anion gap acidosis or
non-anion gap acidosis.
single organ system ischemia (e.g., mesenteric
ischemia).42,43
It does not matter whether the serum lactate is a
venous or an arterial sample. In a study of 48 ED
patients, Younger et al showed that venous lactate
levels of 1.6 mmol/dL and higher had a 100% sensitivity and an 86% specificity in determining elevated
arterial lactate levels.44,45 A recent study by Jones et al
also determined that venous lactate levels are unaffected whether drawn with or without the use of a
tourniquet or sent to the laboratory on or off ice as
long as the sample is run within 15 minutes.46 Rapid
lactate clearance is associated with improved mortality rates and clinical improvement.47
Lactate levels rise in the early stages of sepsis
because of increased glycolysis and later on because of
decreased clearance by the liver and the kidneys.
Prolonged organ hypoperfusion leads to increasing
hypoxia and increased lactate production. Elevated
lactate levels suggest poor organ perfusion and alert
the clinician of impending organ failure. In a study
by Ander et al, vital signs and clinical impression
were not able to distinguish patients with stable Killip
class IV congestive heart failure (CHF) from those
with mild versus acute decompensations; however,
lactate levels were able to stratify the patients’ severity of illness.10
Glucose
Serum glucose levels tend to rise in pathologically
hypotensive patients secondary to excessive catecholamine levels. Elevated serum glucose has been
identified as a prognostic marker in severe illness.39-41
Hypoglycemia without a drug-induced cause is
ominous and denotes the presence of endocrinopathy
or very severe hepatic gluconeogenic dysfunction. It
is a preterminal event in end-stage liver disease.
Liver Function Tests (LFT’s)
Electrocardiogram (ECG)
Transaminases measure hepatocellular integrity.
Albumin and PT/PTT reflect the liver’s synthetic
function; alkaline phosphatase and bilirubin reflect
the liver’s excretory function. It is important to be
aware of co-morbidities (e.g., history of hepatitis)
when interpreting these tests.
An ECG and cardiac monitoring are fundamental to
managing the patient with hypotension. Table 4 lists
possible etiologies of hypotension that may be
revealed by the ECG.
Radiologic Testing
Lactic Acid
Plain films (such as the chest x-ray) are useful as
screening tools to confirm already suspected diagnoses of pneumonia or free air and to confirm past
history (such as heart failure). CT scanning and other
Normal values for serum lactic acid are usually below
0.7 mmol/dL. Lactate levels above 2.1 mmol/dL
point to severely inadequate multi-organ or extensive
Table 4: Diagnoses In Hypotension That May Be Found On ECG
Potential ECG Findings Encountered
Diagnoses Considered
Conduction delays, varying degrees of atrio-ventricular blockade,
sinus rate abnormalities, ventricular arrhythmias, supraventricular
arrhythmias, pacemaker function and malfunction
Arrhythmias (primary electrophysiologic cause)
ST segment elevation morphology (may be similar to non-ischemic
causes of ST elevation such as benign early repolarization), ST
segment depression, T wave depressions
Acute myocardial infarction or ischemia stigmata
ST elevations with PR segment depression (relative to T-P segment)
Pericarditis (consider effusion or myocardial dysfunction)
Low voltage QRS complexes, electrical alternans
Tamponade
Atrial enlargement: suggests chronic pressure and/or volume overload
Cardiac valve dysfunction
Bradycardia or AV in the setting of hypotension due to use/overuse of
AV nodal blocking agents, terminal R wave in tricyclic antidepressant
overdose, sinus tachycardia or tachyarrhythmia
Drug toxicity/exposure
Wide QRS complexes becoming sinusoidal
Hyperkalemia
EBMedicine.net • November 2007
9
Emergency Medicine Practice®
reached CVP readings that were higher than the target
range. Preload assessment is offered by CVP readings
and does not speak accurately to adequate or optimal
perfusion of organs in all patients with sepsis.
Patients with invasively measured CVP readings of
more than 8 mmHg may still have signs or direct
evidence of hypoperfusion. Sepsis patients with CVP
readings that are within the ‘target range’ used in the
often quoted EGDT study may still be hypoperfused
and responsive to fluids; they should not be deprived
of fluid repletion.
The fluid of choice remains an isotonic crystalloid
solution (normal saline or ringer’s lactate).48 Though
once in vogue, current evidence does not support the
routine use of colloidal solutions (albumin or hetastarch) in acute resuscitation.49,52-54 Although a
plethora of literature exists regarding the use of
hypertonic saline in the management of the trauma or
burn patient, advantages over normal saline in the
management of the medical patient have not been
demonstrated. In a meta-analysis of 14 trials of 956
trauma and burn patients and those undergoing
surgery, it was unclear that any benefits existed with
the administration of hypertonic saline.55
studies are warranted based on the disease process in
question. See “Bedside Sonography” on page 15 for a
discussion of ultrasound in the evaluation of the
hypotensive patient.
Emergency Department Management
The severity of hypotension is not solely based on the
depth of the numerical reading. The presence of signs
and symptoms of organ hypoperfusion and the
number of organs affected are critical features that
should be recognized early by the treating physician.
Despite our desire to make the correct final diagnosis
and initiate definitive treatment, there are situations
where the time consumed waiting for that diagnosis
would present a danger to the patient’s outcome.
Thus, aggressive treatment of the hypotension must
occur in tandem with its diagnostic work-up. Beyond
the recognition of symptomatic hypotension, there is
the issue of adequacy of treatment. In the Shoemaker
study cited previously, 76% of patients had mean
arterial pressures below 80 mmHg after admission.12
Twenty-four percent of patients that were admitted
were normotensive but subsequently had recurrence
of hypotension. Treatment of the patients was considered suboptimal in most instances because:
• The underlying disease entity associated with
the hypotension was not yet identified
• The underlying disease was erroneously attributed to another etiology
• The resuscitation efforts were late or not sufficiently aggressive
Trauma
In bleeding patients with blunt trauma, there is recent
evidence that suggests lower volumes of crystalloid
should be used to prevent overdilution of blood and
coagulation factors.56,57 While tamponade of the
bleeding may occur in a closed space, there is a fear
that bleeding may increase later if overdilution occurs.
Although the data is not conclusive, packed red blood
cells and fresh frozen plasma should be considered
early in the patient’s treatment in these cases.
In penetrating trauma, terms like “permissive
hypotension” or “hypotensive resuscitation” have
recently been advocated.58-62 In essence, numerically
low blood pressures (approximately 70-80 mmHg
systolic) are preferred during early resuscitation of
these patients so as to not “pop the clot” prior to
surgical intervention. Whether this is due to pure
intravascular pressure or to dilution of clotting
factors, a preference for lower intravascular fluid
infusion is established. Care should be taken, however, since target BP’s are not an accurate measure of
end-organ perfusion and any signs of such should still
be treated aggressively. Additionally, timely transfer
to the operating room for definitive treatment is
needed in these cases as compensatory mechanisms
may have an effect on the patient’s clinical status and
could collapse with delays in treatment.
Certain basic steps in the treatment of the symptomatic hypotensive patient are required and are
outlined in Figure 1.
Fluids
The mainstay of early treatment of hypotension
remains intravenous fluid management. Decreased
vascular tone can arise from a myriad of factors, but
the initial attempt at correction should be to increase
intravascular volume in the majority of cases, with
exceptions typically stemming from cardiac decompensation (such as in left heart failure). Intravenous
challenges of at least 1-1.5 liters or 20-40 mL/kg 48-50
should be given as a bolus and the response monitored. The “Surviving Sepsis” protocol recommends
“aggressive” use of IV fluids without a specific
volume, highlighting the fact that each patient
requires individualized therapy.51 Adequacy of
hydration can be assessed subjectively with
approximation of CVP via extent of JVD (measured at
8-12 cm above the right atrium) or objectively with a
central venous pressure. The caveat to this guideline
is that CVP goals are not always clearly defined. In
the Early Goal-Directed Therapy (EGDT) article by
Rivers et al, the CVP target of 8-12 mmHg for patients
in sepsis was not prospectively evaluated. Most
patients in both the control and treatment groups
Emergency Medicine Practice®
Pressors
If fluid resuscitation fails to correct hypotension,
pressors become a consideration. The hemodynamic
effects of these agents come from their different
affinity for the various endogenous catecholamine
receptors. Drug action can also vary from patient to
10
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EBMedicine.net • November 2007
11
Emergency Medicine Practice®
Clear
Wet
STILL
HYPOTENSIVE?
See back page for Class Of Evidence Definitions.
In a bleeding patient, consider
early administration of blood and
blood products coupled with
somewhat limited use of
crystalloid infusion to avoid
potential dilution of hematocrit
and coagulation factors.
If CVP is inadequate, continue to
administer IV crystalloid to an
adequate CVP. Consider use of
pressors to “bridge the gap” until
full fluid resuscitation is achieved.
If CVP is adequate, use pressors as
indicated by underlying pathology.
Monitor for adequate CVP/right
atrial pressure (at least 8-12 cm
H2O) as a sign of adequate fluid
resuscitation. JVD observation,
bedside sonography, or direct
central venous pressure monitoring
may be utilized. (Class I)
Administer at least 20-40 mL/kg
(typically 1-2 liters) IV crystalloid
solution as a bolus/fluid challenge.
“Maintenance” rates are not
adequate. Crystalloid solution is
equal to colloid in terms of outcome
and significantly less expensive.
(Class I)
Absent
Treatment for
DECREASED
VASCULAR TONE
i.e., DISTRIBUTIVE
SHOCK
Pneumonia/ pneumonitis
Diagnoses to Consider:
Acute lung injury
(ARDS)
Initial treatment of non-cardiogenic
hypotension is FLUID
RESUSCITATION.
Distributive shock:
Sepsis
Spinal
Anaphylactic
Diagnoses to consider:
Hypovolemia
Lung sounds- clear or wet?
STILL
HYPOTENSIVE?
(despite maximum
dose of first agent)
YES
Is the patient septic?
First line agents- add norepinephrine or dopamine. (Class IIa)
-thenPhenylephrine 100-180 mcg/min then titrate to a maintenance
dose of 40-60 mcg/min. (Class IIa) Acts exclusively on alpha-1
receptors. Consider if severe tachycardia with other pressors
-thenEpinephrine 1-4 mcg/min. (Class IIb) Epinephrine is the drug
of choice in anaphylactic shock. (Class I)
May add other vasopressors:
Early goal-directed therapy
-andConsider if refractory hypotension:
Stress dose steroids dexamethasone preferred to
preserve later ACTH-stimulation
test (Class IIb)
-andVasopressin 0.04 units/min (range
0.01-0.04 units/min) May allow
other vasopressor agents to be
titrated down. (Class IIb)
Norepinephrine 8-12 mcg/min starting dose (12 mcg/min max)
and titrate to desired BP. Can titrate down to 2-4 mcg/min
when BP goal achieved. (Class I)
-orDopamine 10-20 mcg/kg/min and titrate up to 50 mcg/kg/min
max. (Class I) Consider more strongly if chronotropic and
inotropic cardiac support is desired as dopamine has greater
beta-1 receptor activity than norepinephrine. “Renal dose”
dopamine (i.e., strictly used for “preserving renal function”) is
no longer recommended (5 mcg/kg/min).
Vasopressor support: any large vein is acceptable for
emergency administration of these drugs, but central venous
access is preferred to decrease risk of extravasation. Bedside
sonography can improve procedure success and reduce
patient discomfort with use here. (Class I)
Step One:
Is JVD or sonographic
evidence of increased CVP
present?
CARDIOGENIC
SHOCK with left
heart failure
Wet
Lung sounds- clear or wet?
Decreased Cardiac
Output/Cardiac Index?
Treatment for
IMPAIRED CARDIAC
FUNCTION (may occur
in later stages of other
types of shock).
Clear
-Tension pneumothorax (Class IIa)
-Massive pulmonary embolus (Class IIb)
-Cardiac tamponade (Class I)
-Inferior wall MI with right ventricular infarct
(Class I)
-Post-intubation hypotension due to high
intrathoracic pressures and decreased venous
return
Consider OBSTRUCTIVE etiology and treat
accordingly; the use of bedside sonography is
particularly useful in diagnosis.
Dobutamine 0.5-1 mcg/kg/min, titrate to 40mcg/kg/min max.
Maintenance dose typically 2.5-20 mcg/kg/min. Has the greatest
arrhythmogenic potential as it is an adrenergic agent. (Class IIa)
-orInamrinone (formerly amrinone- renamed to avoid confusion with
amiodarone) (Class IIb) 0.75 mg/kg bolus over 2-3 minutes. May
repeat once then maintenance dose at 5-15 mcg/kg/min.
Phosphodiesterase (PDE) inhibitor- theoretically less
dsyrhythmogenic.
-orMilrinone 50 mcg/kg bolus over 10 minutes then maintenance
dose of 0.375-0.75 mcg/kg/min. (Class IIb) Newest PDE inhibitor
in the USA. May have least risk of peripheral vasodilation.
Inotropic Support of Cardiac Function:
Each of these medications can produce peripheral vasodilation
and thus could require peripheral vasopressor support during
administration in the already hypotensive patient.
Present
Initial stabilization of the patient includes airway support if necessary, immediate treatment of obvious causes of hypotension (e.g., frank bleeding, trauma, etc.), and ACLS protocols for arrhythmias or arrest.
Otherwise, some key physical exam findings (i.e., JVD and lung sounds) can help direct further diagnosis and management of hypotension in this patient.
Hypotensive patient defined as: Systolic BP < 90 -or- MAP < 60 -or- Decrease in Baseline BP (MAP) > 30% or 40 mmHg
Signs and symptoms of impaired tissue perfusion via physical exam, diagnostic testing, or invasive and non-invasive monitoring means SHOCK and aggressive treatment are necessary.
Figure 1. Algorithm For The Assessment and Treatment Of Hypotension
patient, and various doses of the same medication can
have different actions. The physician must be vigilant
in monitoring patients on these agents. Improvement
in overall organ perfusion (as determined by clinical
improvement in symptoms, urine output, central
venous pressure, lactate clearance, and tissue oxygen
saturation) should be the primary goal of therapy
rather than merely raising the blood pressure. The
receptor affinities and actions of these drugs on the
various hemodynamic parameters are listed in
Table 5.
Current critical care and sepsis treatment guidelines recommend the use of norepinephrine or
dopamine as first line vasopressor agents, with a
slight bias towards norepinephrine so as to avoid
unwanted sinus tachycardia and arrhythmias.63-70 If
the hypotension is associated with relative bradycardia or primarily a cardiac etiology, then dopamine
may be the preferred pressor. Dobutamine may be
added if cardiac support is necessary (e.g., inotropic
support) but may worsen peripheral vascular tone
and hypotension. If further support is needed in the
setting of cardiogenic shock, the use of an intra-aortic
balloon pump may be necessary.
Emergency Medicine Practice®
Continuous vasopressin infusion is gaining
support as an adjunct to other pressor agents specifically in sepsis. A relative vasopressin deficiency has
been shown to exist in septic patients, although this
phenomenon may not actually be present until 24-48
hours into the clinical course.71-75 Malay et al conducted a double blinded, placebo-controlled study of
10 septic shock patients receiving either low dose
vasopressin or placebo in addition to standard use of
fluid and other vasopressors and inotropes.57 The
patients in the vasopressin arm of the study had
increases in cardiac index and MAP which allowed for
the discontinuation of the other vasopressors and
inotropes in that order. The MAP, cardiac index, and
SVR were not statistically affected in the placebo
group. Two of the five patients in the placebo arm of
the study died before 24 hours, but all the patients in
the vasopressin arm survived beyond 24 hours and
were able to maintain MAP above 70 mmHg solely on
vasopressin infusions. Landry et al studied 19
patients with vasodilatory septic shock and 12
patients with cardiogenic shock.76 In 10 of the
patients with low SVR shock states, the mean blood
pressure increased from 92/52 to 146/66 mmHg; the
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November 2007 • EBMedicine.net
administration. In the ED, using dexamethasone
instead of hydrocortisone offers the advantage of not
interfering with corticotropin stimulation testing after
admission.
The role of activated protein C (APC) (Xigris®) in
the treatment of septic shock is controversial. This
compound has antithrombotic, profibrinolytic, and
anti-inflammatory properties. A multi-center, randomized, placebo-controlled trial of more than 1600
patients showed that patients with septic shock who
underwent treatment with APC had a relative reduction in the risk of death, but a statistically significant
increased risk of bleeding.80 APC has been FDA
approved for treatment in patients with severe sepsis,
defined as an APACHE II score ≥ 25 or with refractory
organ/multi-organ dysfunction. (APACHE score
calculator:
http://www.icumedicus.com/icu_scores/apacheIV.php [Last
accessed June 9, 2007])
SVR increased from 644 to 1187. Six patients receiving
low dose vasopressin infusion alone had a return to
hypotension upon vasopressin withdrawal and an
improvement to normotensive state when vasopressin
was restarted. When a vasopressin infusion of 0.04
U/min was added to the shock treatment, reactivity to
other pressor agents was enhanced; the authors
concluded that the replenishment of vasopressin
allows for the discontinuation of other pressors.
Acute use of vasopressin in the ED is still controversial but can be considered.
Phenylephrine is also a peripherally acting vasopressor but there is limited support for its use and it is
not considered a first line agent. Epinephrine has a
reputation for potentially worsening vital organ
perfusion and is not a first line agent, though it does
remain the drug of choice in the treatment of anaphylaxis. An abstract recently presented by Annane at the
Society of Critical Care Medicine’s 36th Critical Care
Congress compared epinephrine to norepinephrine for
the treatment of hypotension. In contrast to traditional thinking, no significant differences were found
in beneficial outcomes or adverse events after 28 days.
So-called “renal dose” dopamine is no longer recommended as it has been shown to be ineffective in
improving renal function, and improvements in urine
output are likely due to higher flow states and not to
specific renal bed effects.
Special Situations In ED Management
Anaphylaxis
Anaphylaxis is a true pure distributive shock with
mediators causing end capillary damage and subsequent leakage of fluid into the extravascular space.
These mediators are responsible for the uncontrolled,
uncoordinated vasodilatation seen in anaphylaxis. A
patient in cardiovascular collapse from truly lifethreatening anaphylaxis can sequester the equivalent
of 50% of their effective blood volume into their
extravascular space within minutes of onset.
Treatment of an allergic reaction usually involves the
use of histamine blocking agents and steroids, but in
the setting of anaphylactic shock, the early administration of epinephrine (1:1000 dilution 1 mg/mL) is
necessary. Intramuscular injections (0.2-0.5 mL) of
this solution into the thigh every five minutes as
needed is the preferred route, but it can also be given
subcutaneously. If circulatory collapse persists, an
epinephrine infusion at 1-4 mcg/min should be
started. If IV access is unavailable or delayed and the
patient is in extremis, epinephrine may also be
administered via the endotracheal tube with a dose
two to three times greater than the IV dose (1:10,000
solution). If the initial response to epinephrine is
transient, repeat bolus dosing may be necessary or the
described IV drip at 1-4 mcg/min can be started.
Other Adjunctive Treatments
Other pharmacologic agents for use in sepsis include
stress dose steroids and activated protein C. Both are
recommended in current sepsis protocols.51,77 Consultation and cooperation with critical care medicine will
facilitate the use of these agents.
Adrenal insufficiency is found in more than half of
patients in septic shock. Adrenal insufficiency is
defined as non-response to the 250 microgram corticotropin test (cortisol increase of less than 9 micrograms/deciliter). Cortisol maintains vascular sensitivity to catecholamines and helps blunt the endotoxin
effect on the heart.
Only a few decades ago, high dose steroid
administration was commonly given to patients with
septic shock. Now, low dose steroids are thought to
increase arterial pressures and decrease the duration
of shock. However, most randomized, controlled
trials do not point to any decrease in mortality rates of
septic shock patients receiving stress dose steroids.78
That being said, no harm has been brought to light
either. The low dose of glucocorticoids that is recommended by sepsis treatment guidelines is 300 mg of
hydrocortisone.51 In a study by Kortgen et al, there
was a significantly improved mortality rate when a
sepsis bundle that employed an even lower dose of
steroids (hydrocortisone 150 mg) was used.79 At the
current time, based on the best available evidence,
hydrocortisone 150-300 mg is indicated in patients in
presumed septic shock that remain hypotensive
despite adequate fluid and vasopressor
EBMedicine.net • November 2007
Cardiogenic Shock
Cardiogenic shock occurs acutely when the
myocardium suddenly loses 40% of its function in the
previously normal heart or when the already diseased
heart loses a lesser percentage over time. Clinical
criteria for the diagnosis of cardiogenic shock include:
• Systolic blood pressure < 90 mmHg (higher if
chronically hypertensive)
• A urine output < 0.5 cc/kg/hr
• Evidence of end organ dysfunction manifesting
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Emergency Medicine Practice®
may subsequently develop hypotension.
One large urban ED study associated subsequent
hypotension with 29% of 84 patients requiring medical intubation.81 Though mortality was not increased,
13% of these patients required vasopressors and one
patient experienced cardiac arrest. Specific associations were not found to correlate with medications,
but hypercarbic COPD and hypoxemic respiratory
failure showed statistical correlations. These sobering
statistics put the onus on ED physicians to be vigilant
for the occurrence of post-intubation hypotension and
to take appropriate steps to prevent it.
Wide acceptance of rapid sequence intubation
(RSI) protocols in the ED have greatly facilitated safe
and successful airway management. The danger in
the hypotensive patient is the possible arbitrary use of
medications, as this may worsen the patient’s hemodynamic status. For example, induction with benzodiazepines, propofol, or barbiturates can contribute to
hypotension and are not recommended in this patient
population. Two useful induction agents are etomidate and ketamine. Etomidate produces a strong
sedative-hypnotic effect but its effects on cardiac and
other hemodynamic parameters are less significant
than with many other agents. Unfortunately, etomidate suppresses cortisol release which may have
significant repercussions in critically ill patients.82-84
Ketamine presents a very good option in these
patients. As a dissociative anesthetic agent, the
depressant effects of other RSI medications are
avoided while its adrenergic activity may help in BP
support. Though current recommendations for intubation support the use of etomidate plus
succinylcholine, a trial directly comparing the morbidity associated with the use of etomidate versus
ketamine is underway.85
The post-intubation management is critically
important in resuscitating the hypotensive patient.
Patients who are marginally compensated may
precipitously crash during this period. This is
because intubation can further compromise preload
due to high intrathoracic pressures associated with
mechanical positive pressure ventilation. Positive
end-expiratory pressure (PEEP) can further increase
intrathoracic pressure, and in patients with obstructive pulmonary disease, “auto-PEEP” can climb to
dangerously high levels. If air-trapping becomes an
issue, allowing the lungs to decompress by temporarily disconnecting the ventilator can result in a dramatic improvement in blood pressure. Be aware that
similar pathophysiology may occur even in noninvasive ventilatory modalities such as continuous
positive airway pressure and bilevel non-invasive
ventilation.
as renal failure, confusion, or peripheral
hypoperfusion
• Pulmonary capillary wedge pressure > 18
• Cardiac index < 1.8 L/min/m2
Brain natriuretic peptide (BNP) levels are often
markedly elevated in severe cardiogenic hypotension
and the elevations correlate with severity and prognosis, though treatment in the ED setting rarely relies on
these levels.
Management focuses on relieving fluid overload
on the overworked heart and hemodynamic interventions to enhance myocardial pump function (both
pharmaceutical and mechanical when necessary). In a
hypotensive patient, small fluid boluses (on the order
of 250-500 cc) are acceptable when the diagnosis is
questionable or to maintain perfusion as a bridge to
other interventions.
When hypoxia from respiratory failure is present,
early endotracheal intubation is a key intervention.
The hypotension in cardiogenic shock precludes the
use of standard congestive heart failure meds (e.g.,
lasix and nitrates). In addition to its obvious respiratory benefits, endotracheal intubation has distinct
hemodynamic benefits. Positive pressure ventilation
decreases intrathoracic venous return and decreases
preload. With the decrease in right ventricular
chamber size, left ventricular expansion is enhanced
and forward pump function is enhanced. Myocardial
oxygen demand is thus decreased. Intubation alone
can improve cardiac performance by as much as 30%.
Ventilatory features such as positive end-expiratory
pressure (PEEP), while removing fluid from the
alveoli in the lungs, can also relieve hypoxia. The
positive intrathoracic pressures from these interventions may worsen hypoxia.
Pressor support in cardiogenic shock can cause a
dilemma in treatment. Using dopamine or norepinephrine to maintain peripheral pressures may cause
dangerous increases in heart rate at a time when
decreasing myocardial workload is a key endpoint.
Administering other medications that are beneficial to
cardiac function (e.g., beta blockers, ACE inhibitors,
diuretics) may worsen the hypotension. Inotropes
(such as dobutamine or the phosphodiesterase
inhibitors inamrinone and milrinone) used to support
cardiac function may cause peripheral vasodilation
and also worsen hypotension. A combination of
pressors and inotropes may be necessary to treat these
patients and bridge the gap while definitive treatment
is initiated.
Airway And Post-Intubation Considerations
Early intubation in a critically ill patient is a mainstay
of ED practice. While providing airway protection,
respiratory support, and blood oxygenation, this
practice can have deleterious effects on peripheral
blood pressures through medication administration
and side-effects of positive pressure ventilation.
Previously normotensive patients who are intubated
Emergency Medicine Practice®
Endocrinopathies
Endocrinopathies can have a profound effect both on
the rapid onset of hypotension and in its treatment
once it occurs. Thyroxine and cortisol play important
roles in regulating the body’s basal metabolic rate. At
14
November 2007 • EBMedicine.net
the vascular level in the hypotensive patient, this
manifests as a failure of vascular smooth muscle to
respond to sudden stresses, producing early cardiovascular collapse. The problem continues during
therapy as these patients show impaired responses to
therapeutic interventions such as fluids and catecholamine infusion. Therapy focuses on vigilance in
suspecting an underlying endocrinopathy, which
prompts the ordering of diagnostic tests (e.g., cortisol
and thyroid function tests) and/or instituting early
replacement therapy. Treatment of severe hypothyroidism (myxedema coma) not only includes giving
thyroid hormone but also stress dose glucocorticoids.
Beware of the patient on chronic steroid therapy or
who is adrenally suppressed. Exogenous administration of stress dose steroids is imperative in these cases.
As mentioned earlier, septic patients may be relatively
adrenally insufficient and should also receive stress
dose steroids.
information was found in 36 (86%) of the 42 patients.
There was complete agreement in patients with
hypotension alone and 90% of the 20 patients with
pulmonary edema alone. The time taken for pulmonary artery catheter placement was 63 +/- 45
minutes compared to 19 +/- 7 minutes for comprehensive two-dimensional echocardiography.
Studies in hypotensive patients support the
diagnostic role of ultrasonographic evaluation of the
inferior vena cava (IVC) as an indicator of volume
status. A prospective study of 50 patients by Adler et
al identified hypovolemia, unrecognized right heart
failure, and high volume states based on the longitudinal views of the IVC using ultrasound.102 By
looking at the anteroposterior diameter of the IVC and
the respiratory variation in size, one could reliably
estimate central venous pressure. Another study
evaluated the correlation between sonographicallymeasured proximal IVC diameters, the respirophasic
variations of the IVC size (caval index), and the
central venous pressures (CVP) that were measured
invasively. This study showed a definite correlation
between caval index and central venous pressure.103
An IVC respiratory collapse of more than 50% represents a caval index above 0.5. Eighty-nine percent of
patients with a caval index above 0.5 had RA pressure
readings above 10 mmHg. Eighty-six percent of
patients with a caval index below 50% had RA
pressure readings less than 10 mmHg (Figure 2).
Bedside Sonography Use In The Emergency
Department
The concept of the “golden hour” is built on strong
evidence that the rapid identification of life-threatening conditions and early initiation of time-sensitive
and specific treatments are critical to the patient’s
clinical outcome.3-5,13,14,23,51,86-98 This section explores
the emerging role of ultrasound in diagnosing and
managing patients with hypotension.
Figure 2. (A) Schematic Of Subcostal Longitudinal View Of
Inferior Vena Cava. (B) IVC Size And Respiratory Variation
Correlation To Central Venous Pressure Measurements
Ultrasound In Hypotension Protocol
Ultrasound has been used by physicians to detect low
intravascular volume states, to evaluate cardiac
function, to evaluate the aorta, and to detect peritoneal and pleural free fluid accumulations. In one
study, an average of six minutes (+/- two minutes)
was needed to perform a bundle of goal-directed
ultrasound applications to determine unexplained
hypotension.99 Indeed, the utilization of ultrasound is
becoming more widespread and is being extended to
code response teams in the hospital or to prehospital
teams performing ACLS care.100
Differentiating whether hypotension with or
without pulmonary edema findings is caused by a
cardiac (pump) or non-cardiac (non pump) problem is
one of the first major steps toward a careful tailoring
of the medical treatment during a resuscitation. The
invasive method of pulmonary artery catheter (PAC)
placement and monitoring was compared to information obtained by performing noninvasive cardiac
sonography in a 1994 study by Kaul et al.101 Fortynine consecutive patients presenting with hypotension
and/or pulmonary edema were evaluated. Early
transthoracic cardiac sonography data was compared
with that of pulmonary catheter readings obtained
within two hours of each other. Two to three blinded
observers were used for each study. Complete
agreement between PAC and cardiac sonography
EBMedicine.net • November 2007
A
B
Using a convenience sample, Randazzo et al found
that despite good agreement amongst physicians on
the left ventricular ejection fraction (LVEF), there was
poor agreement on patients with low CVP categories
and strong agreement on the high CVP group.104 In
this study, CVP was recorded and then the finding
was compared to formal echocardiograms performed
within a few hours. Bendjelid et al studied 20
mechanically ventilated patients having IVC sonographic measurements obtained while right atrial
pressures (RAP) were measured at the same time; IVC
diameter at end expiration had a linear correlation
with the RAP readings.105,106
Moreno et al studied IVC diameter and respiratory
variations in 175 subjects; there were 80 controls, 65
patients with documented right heart cardiac disease,
and 30 patients with cardiac disease but no right heart
abnormality.107 The patients with right heart
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Emergency Medicine Practice®
abnormalities/disease had greater average IVC
diameters and much less respiratory collapsibility
than the normal subjects or the ones with cardiac
disease without right heart involvement. Even
though 30 patients were in atrial fibrillation, the
authors found no correlation between IVC size and
dynamics and the sex, body surface area, age, and
cardiac rhythm of the patients. The size of the IVC
was helpful in the further stratification of CVP
measurements. The combination of small size and
greater collapse confirmed a low CVP. The combination of an IVC diameter above 2.5 cm and a very low
caval index (barely any respiratory variation) is
termed IVC plethora. In this study, plethora of the
IVC was associated with CVP readings over 15 mmHg
(Figure 3, 4, and 5).
Elevated right atrial pressures, determined by
invasive methods, are associated with a poor prognosis in patients with pulmonary hypertension, congestive heart failure, congenital heart disease, and heart
transplantation. Sonographic findings of IVC plethora
were also associated with poor survival in a study of
4385 stable male patients in an outpatient setting. It
was determined to be an important prognostic finding
in the one-year survival rate of patients but less so for
the 90-day survival rate. This was independent of the
ventricular function, a history of heart failure, other
illnesses, and pulmonary artery pressure readings.108
The prognostic impact of IVC plethora in the unstable
patient with hypotension remains to be determined.
IVC plethora should spur a rapid search for a cause of
the elevated RAP in the hypotensive patient.
In addition to using sonographic IVC diameter as
Figure 3. Enlarged IVC With Barely Any Respiratory Variation
In Size: IVC Plethora
Table 6. Estimation Of Left Ventricular Ejection Fraction
Note the pericardial effusion (short arrow) between the right atrial
wall and the diaphragm. The hepatic veins (cross) branching off of
the proximal IVC are dilated.
Clinical Diagnosis
Well filled hyperdynamic heart
Distributive shock:
sepsis, anaphylaxis
Well filled hypodynamic heart
Cardiogenic shock: sepsis,
metabolic/ischemic,
toxidrome
Barely filled hyperdynamic heart
Hypovolemia: hemorrhage,
dehydration
Figure 5. Cardiac Features Of Hypovolemia: Subcostal Four
Chamber View
Figure 4. Hypovolemia—Small IVC Diameter With Large
Respiratory Variations
There is a small pericardial effusion (arrows), but the clinically
significant sonographic finding is that the heart chambers are
difficult to distinguish because the endocardial surfaces are very
close together. This is due to severe hypovolemia. The heart was
able to become hyperdynamic but the poor filling volumes lead to a
very low cardiac output. Fluid loss may be evident by history clues
or physical signs, but further goal-directed sonography can be used
to determine if there were any significant internal fluid accumulations in the thoracic, peritoneal, or pericardial spaces or potential
sources of cardiovascular hypovolemia (such as finding an
abdominal aortic aneurysm or a ruptured ectopic tubal pregnancy).
In this case, the patient had severe gastrointestinal bleeding
compounded by warfarin toxicity.
Subcostal longitudinal view of IVC. The proximal IVC was a
maximum of 0.5 cm with complete collapse with the patient’s
inspiratory efforts. The caval index is suggestive of low right atrial
pressures or central venous pressures. The pericardial effusion can
be seen between the diaphragm and the atrial myocardial
contractions.
Make measurements about 4 cm away from the IVC/diaphragm
juncture. The liver serves as an acoustic window for the IVC.
Distinguish the IVC from the adjacent aorta. Firm transducer
pressure is usually needed to displace the bowel gas interference
of a view of the abdominal aorta but it is important to reduce
transducer pressure on the abdomen to avoid compression of
the IVC.
Emergency Medicine Practice®
Cardiac Ultrasound
16
November 2007 • EBMedicine.net
a determinant of volemic status, it has also been
shown to assist in gauging response to therapy.
Barbier et al conducted a prospective study of 23
mechanically ventilated patients with sepsis-related
circulatory failure in an ICU setting.109 The presence
of respiratory variations in IVC diameter at baseline
and after fluid boluses demonstrated that IVC distensibility could dichotomize fluid responders and fluid
non-responders with a 90% sensitivity and a 90%
specificity.
The visual estimation of LVEF can be reported
qualitatively and quantitatively as increased, normal,
or decreased (mildly, moderately, or severely)
(Table 6). Estimation of LVEF in the ED has been
shown to be useful in a number of studies.4,99,104
Pericardial effusion detection is best performed by
echocardiography as it provides dynamic real-time
information on myocardial motion and physiology.
Most pericardial effusions are not loculated. The rate
of fluid accumulation, the size of the fluid buildup,
and the compliance of the pericardial sac will all
determine when intra-pericardial pressure (IPP)
exceeds the right atrial wall pressure. Rapid pericardial fluid accumulations will lead to tamponade at a
lower fluid volume (e.g., stab wounds) than slow
accumulations over months (e.g., uremic effusions).
When the IPP exceeds the RAP, it will provoke RA
wall invagination or, even worse, right ventricular
wall collapse during diastole (tamponade physiology)
(Figure 6 and 7).
In summary, some of the Class I recommendations
for echocardiography by the American College of
Cardiology/American Heart Association Task Force on
Practice Guidelines for the Clinical Application
Echocardiography apply to the patient being cared for
in the ED, see Table 7. These indications include, but
are not limited to:
• Patients with unexplained hypotension
• Patients with dyspnea and clinical signs of
elevated central venous pressure when a cardiac
etiology is possible or when a central venous
pressure reading cannot be obtained or interpreted with confidence, especially when cardiac
disease is suspected clinically
• Patients with suspected effusion, tamponade,
and/or constrictive physiology
• The assessment of LV size and function with
suspected cardiomyopathy or the suspicion of
heart failure
Figure 6. Apical View Of A Heart With An Effusion And
Tamponade
This image was taken in the systolic phase. There is also moderate
to low overall left ventricular ejection fraction (determined by visual
estimation). This patient has two causes for the symptomatic
hypotensive state: an effusion with tamponade and poor myocardial
contractility. Though the right sided preload is compromised by the
pericardial effusion, it is unlikely that hypotension is due to
hypovolemia (the ventricular volume seems adequate). A look at the
subcostal long view may provide more patient specific information;
there may be a low IVC diameter and exaggerated respiratory
variations to a high IVC diameter and poor respiratory variation.
Applied ED Bedside Ultrasonography
Abdominal Aortic Aneurysm (AAA)
Figure 7. Moderately Sized Pericardial Effusion
When hypotension is present in preoperative patients
with ruptured AAA, there is usually high mortality.110
Suspicion for AAA is heightened when the presenting
symptoms include sudden abdominal pain and
Table 7. Key Clinical Questions Addressed by Sonography in
the Severely Hypotensive Patient
Note the fluid in the pericardial sac that tapers at the atrioventricular sulcus. The heart has a mild swing within the pericardial sac
which did not show up as electrical alternans on the electrocardiogram. There is no tamponade physiology.
EBMedicine.net • November 2007
17
Sonographic Clinical Question
Answer
Is a pericardial effusion present?
If yes, is it with tamponade?
Yes or No
Yes or No
What is the RV size?
Normal or dilated
What is the LV function?
Hyperdynamic/normal/
moderately weak/
very weak
What is the LV size?
Dilated/normal/small
Is there IVC collapse?
Yes or No
Is there an AAA?
Yes or No
Is there free intraperitoneal fluid?
Yes or No
Emergency Medicine Practice®
radiation to the back, syncope, or other signs of
clinical shock. The presence of an aortic aneurysm is
reliably detected sonographically (Figure 8 and 9).
Indeterminate studies are possible due to interference
by bowel gas. The sonographer can apply firm,
steady pressure to the abdomen to displace bowel gas
so that the posterior lying aorta can be seen. The
presence of aortic rupture or leak is not determined by
ultrasound except if the rupture occurs into the
peritoneal cavity, releasing free fluid. Most episodes
of abdominal rupture occur into the retroperitoneum;
this may contain and curtail the rate of blood leakage.
Bedside ultrasound does not detect the site of rupture.
Aortic Dissections
The most lethal area of aortic dissection is the thoracic
aorta. Involvement in the ascending thoracic aorta can
extend through the adventitial layer with rapid
accumulations of blood into the pericardial sac with
early tamponade. Aortic root dilation can lead to
severe aortic insufficiency. Dissections involving the
abdominal aorta or the proximal iliac arteries are
easier to detect. Intimal flaps are seen as echogenic
lines that move independent of the aortic wall pulsations (Figure 10).
The thoracic aorta (TA) presents a difficult challenge in performing a thorough sonographic evaluation. The presence of lungs, ribs, and the naturally
varying anterior-posterior create impediments to
performing complete studies. The parasternal
transthoracic approach offers a very limited view of a
portion of the descending aorta; the left ventricular
outflow tract views provide clues of the most proximal 1-2 cm portion of the ascending TA; the apical
two-chamber view may provide a longitudinal view
of a small portion of the descending TA; the suprasternal views show the aortic arch. Transesophageal
echocardiography is the preferred modality for
imaging the thoracic aorta.
Figure 8. Free Fluid In The Abdomen
In this patient, free fluid was detected between the kidney and the
cirrhotic shrunken liver. This scan is performed using the same
principles as the Focused Applications of Sonography in Trauma. In
this apparent atraumatic setting, this hypotensive patient—with a
known history of mild ascites—had a more distended, painful, and
tender abdomen (both new). Upon further questioning, he mentioned falling three days earlier. Hemoperitoneum was the cause of
his hypotension.
Pulmonary Embolism: Role Limited To Massive
Pulmonary Embolism (MPE)
In the patient with shock, bedside transthoracic
echocardiography evaluation is used to determine if
there are signs of acute right heart strain; the most
likely causes are massive pulmonary embolism or
right ventricle infarction.111-113 Right ventricular
cavity dilation is the right heart’s initial compensation
Figure 9. Abdominal Aortic Aneurysm With Thrombus
Figure 10. Transverse View Of The Abdominal Aorta
The history on this patient was notable for the abrupt onset of
abdominal pain, diaphoresis and near syncope. The cardiac
ultrasound revealed a partially empty heart, normal cardiac
contractions, and no pericardial effusion. It was very likely that
hypovolemic shock was the etiology and evidence of hemorrhage
was sought. The pleural and peritoneal cavities did not reveal any
free fluid. The abdominal ultrasound study found an abdominal
aortic aneurysm. A thrombus was attached to the inner anterior and
lateral walls. After urgent vascular surgical notification, the patient
was in the operating suite 12 minutes after the ED arrival time.
Emergency Medicine Practice®
The diameter of the abdominal aorta in this patient is less than
2 cm. There is no thrombus, but note the thin mobile echogenic
intimal flap extending from the 12 o’clock to the 6 o’clock position.
Such a finding should prompt the physician to image the thoracic
aorta with either echocardiography and/or CT to verify if the more
urgent cardiothoracic surgery intervention is required.
18
November 2007 • EBMedicine.net
to severe pulmonary artery occlusion. The right
ventricle is distended and also hypokinetic. The apex
of the inner normal right ventricle is usually sharp,
but with acute RV strain, it will become blunted. The
right ventricle is usually 60% of the diameter of the
left ventricle when measured in diastole. When the
RV diameter to LV diameter ratio approaches or
exceeds 1.0, the diagnostic certainty of acute RV strain
is increased. The McConnell sign (hypomotility of RV
free wall with apical sparing) has been used as a
relatively unique sonographic feature of significant PE
(Figure 11).
The buildup of right ventricular pressures may
exceed that of the left ventricle, provoking a bulge of
the septal wall into the LV cavity. True pressure
overload is distinguished from RV volume overload
by evaluating the septal distortion during systole and
diastole. In RV volume overload, the septal wall is
flattened during diastole, but the greater LV systolic
pressure returns the septal wall to its normal
appearance. In RV pressure overload, the intraventricular septal wall may be flattened or pushed into
the LV during diastole. During systole, the intraventricular septum remains flattened or deviated into the
LV. High RV wall stress eventually compromises
coronary blood flow to the inner RV myocardium and
endocardium. The RV myocardial ischemic insults
further compromise the already weakened RV output.
Diastolic filling of the left ventricle is reduced by the
leftward bulge of the ventricular septal wall. The
reduced volume of already poorly oxygenated blood
leads to poor perfusion and oxygen delivery to
multiple organs.
RV dysfunction by cardiac ultrasound is not specific for PE in that it can also be found in primary
pulmonary hypertension, RV infarction, acute
exacerbations of COPD, and in certain cardiomyopathies. In addition, RV dysfunction has been
reported by cardiac ultrasound in 40% of patients
with PE but no significant hemodynamic stability.
Twenty percent of cases of diagnostically confirmed
PE have normal echocardiographic findings. Sonographic RV dilation and hypokinesis in a patient that
is unstable suggests PE and drives the need for
definitive study.114,115 Performing bedside ultrasound
can be difficult in patients with obesity, hyperinflated
lung states, and those who are immobile and on
mechanical ventilator support.
The hypotension that results in pulmonary
embolus is usually responsive to preload increases
and the use of vasopressors to augment coronary
perfusion of the myocardium. The best treatment
occurs with a reduction of the pulmonary artery
Figure 12. Vascular Access With Sonographic Guidance
A sterile probe cover and gel allow direct sonographic guidance of
vascular access and cannulation. The short axis view of the target
vessels allows needle placement. A long axis approach is another
option. Vascular access with sonographic guidance may also be
used for peripheral vein cannulation, arterial and venous blood
sampling, and transvenous pacemaker line insertion and positioning.
Figure 11. Right Ventricular Dilation
Figure 13. Cross Sectional View Of The Internal Jugular Vein
This frame shows the right ventricle (arrow) size compared to the
left ventricle (measured at the level where mitral leaflets touch)
during systole. The RV is dilated and larger than the LV. The free RV
wall barely moved while the LV contracted; the ventricular end
systolic diameter and volume decrease shows strong LV performance. Hypomotility of the RV is caused by right sided pressure
increases and/or a right ventricular infarction. Though a pulmonary
embolism was not definitively detected, acute right heart strain
without signs of preexisting right or left heart strain is caused by
very few entities. Courtesy of Sarah Stahmer, MD.
EBMedicine.net • November 2007
In this cross sectional view of the internal jugular vein (and the
carotid just behind it), the anterior aspect of the internal jugular vein
is indented. Reverberation artifact, caused by the metallic needle as
it crosses the US beam, shoots down the monitor’s screen.
Courtesy of Resa Lewiss, MD, RDMS.
19
Emergency Medicine Practice®
occlusion by inherent thrombolysis, prevention of
further thromboembolic events with heparin, and —
most effectively — the use of thrombolytic agents or
pulmonary thromboendarterectomy.
when determining if pump failure primarily involves
the left heart (e.g., decompensated CHF) or the right
heart (e.g., right ventricular MI or other obstructive
pathology). A meta-analysis of several randomized,
controlled trials showed that early (prophylactic) use
of PAC-directed therapy aimed at tissue perfusion
resulted in a marked improvement in patient outcome.120 Other RCT studies in the meta-analysis,
however, showed that there were no outcome
improvements when PAC-directed therapy was used
in ICU patients after organ failure and sepsis had set
in. This was corroborated in other studies.121 In a
prospective cohort study of 5735 critically ill patients,
there was no patient group in which RHC demonstrated improved patient outcome. However, RHC
was associated with increased mortality, length of
stay, cost of care, and resource utilization.122 In a busy
ED, the practicality of using invasive monitoring is
severely limited by patient flow, inordinate amount of
procedure time, and staffing issues; thus, it is not
recommended.
Fortunately, some noninvasive techniques show
promise; as they become more readily available, these
techniques will allow the emergency physician to
more easily deliver goal-oriented treatment. Bioimpedance monitors for cardiac output, transcutaneous
oximetry, and capnometry for tissue perfusion in
conjunction with pulse oximetry and blood pressure
measurement have been shown to be accurate when
compared to the same information typically obtained
through a right heart catheter.8,123-125
Shoemaker et al studied the use of noninvasive
methods in 151 severely injured patients using the
continuous monitoring of certain cardiac pulmonary
exchange and tissue perfusion parameters. Cardiac
index and tissue oxygenation measured in this
manner were significantly higher and well above
“optimal” levels (as defined in the study) in survivors
as compared to non-survivors.126
Further support for the more expansive and earlier
use of non-invasive hemodynamic monitoring was
provided by a study of 680 critically ill patients. New
bioimpedance methods for estimating cardiac output
combined with arterial BP, pulse oximetry, and
transcutaneous PO2 and PCO2 were equivalent to
thermodilution invasive data. The bioimpedance
monitor was able to detect low flow states and poor
tissue oxygenation early. Lower tissue oxygenation
and higher tissue CO2 levels were significantly more
prevalent in the non-survivors.124
Limitations of the thoracic bioimpedance instruments may include improper lead positioning, motion
artifacts due to tremors, restless patient movements,
and patient disease-related conditions like pulmonary
edema, pleural effusions, valvular disease, and
arrhythmias. With proper implementation of these
instruments, however, better outcomes can be accomplished through earlier diagnosis and treatment of
individuals at risk for developing hypotension and
shock before late effects on the vital signs are seen. As
Vascular Access
Well designed, randomized, controlled trials have
compared ultrasound-guided vascular cannulation to
the traditional anatomic landmark based vascular
access.116 Vascular access is particularly more difficult
in the patient with hypotension or cardiac arrest.117
Arterial pulsations may already be too faint to
provide guidance. In addition, the anatomic relationships of the femoral and neck vessels may vary thus
compounding the potential for errors. Prolonged and
multiple attempts, the development of complications,
and failure to attain access will delay the administration of time-sensitive medications and fluids. Ultrasound-guided peripheral vascular access may be
better and safer than central venous cannulation,
especially in patients with coagulopathies where
vessel compression may be critically important
(Figure 12 and 13).
Controversies / Cutting Edge
Hemodynamic Monitoring
The resuscitation literature points towards early
aggressive management as being key to altering
outcomes in patients with pathologic hypotension.
This awareness has resulted in increased pressure to
initiate therapy in the ED and provide close monitoring. Static hemodynamic reports do not accurately
predict the patient’s responsiveness to fluid administration or their actual clinical improvement.119 For
example, while most patients with sepsis are discovered to be in a hyperdynamic state, this may be an
early compensatory response.99 The patient with
septic shock with a hyperdynamic LV on bedside
ultrasound can have LV dysfunction several hours
later, especially if the patient has pre-existing cardiac
disease. RV dysfunction can also be present in as
many as one-third of patients with sepsis. Continuous monitoring of RV function is extremely helpful for
the assessment of cardiac and respiratory function and
in response to treatments and interventions.
Measurement of cardiac filling pressures and
pulmonary artery occlusion pressures are generally
used in more intensive care settings and require
highly invasive procedures (e.g., central venous
pressure readings and right heart catheterization).
With normal CVP readings between 6-12 cm H2O, low
or high readings can help differentiate between
hypovolemic states, cardiac failure, obstructive
etiologies, and/or hypervolemic states.
Right heart catheterization (RHC) and pulmonary
artery catheters (PAC) are more complicated and are
used for occlusive pressure measurements. Further
data can be obtained with this modality, especially
Emergency Medicine Practice®
20
November 2007 • EBMedicine.net
this technology becomes more widespread, additional
training in this monitoring will be necessary for
emergency physicians, nurses, and other health
providers in the ED.
on the individual physician’s preferences. A chart
review showed that even with this specific clinical
guideline, compliance with the algorithm was suboptimal. There were significant delays in the start of
fluid challenges and many steps in the algorithm were
not followed. There were 114 deaths (19% mortality)
in the study group. Significant comorbidities were
present in 265 (44%) of the hypotensive patients.
Forty-four patients in this subgroup developed severe
shock-related organ dysfunction. These patients had a
higher mortality rate, more severe hypotension (lower
mean arterial pressures), and more challenging and
prolonged resuscitations. They also seemed to have
noticeably more delayed starts to the resuscitation
efforts after hypotension was recognized. The authors
Algorithmic Treatment Of Hypotension And Shock
With accurate monitoring of hemodynamic parameters and tissue perfusion, algorithms can be developed
to directly address sub-clinical signs of poor tissue
perfusion. The use of algorithms in managing
hypotension is not a new concept. In 1983, a retrospective study of fluid resuscitation in 603 patients
with hypotension was identified.12 This was a case
series of patients with hypotension who were resuscitated with either a fluid administration algorithm or
Risk Management Pitfalls For Hypotension
The BP is a single and imperfect parameter in
assessing the patient’s volume and circulatory
state. Multiple tools may be necessary to assess
tissue perfusion and changes in cardiac output.
In some patients, there is an improvement in the
blood pressure, a normalized pulse rate, and no
more postural dizziness after fluid administration for self-limited diarrheal illness. Another
patient may have an improvement in the BP to
120/80 but still feel weak and short of breath
because the LVEF is 20%, or the pericardial
effusion remains undiagnosed, or the tissue
oxygen debt state remains unpaid.
1. Assuming that an ashen, lethargic patient is not
hypotensive because he has a good blood
pressure of 120/80 mmHg.
Treating the number rather than the patient can
cause you to miss the hypotensive state. Treat
the patient; this patient is hypotensive. The BP is
well below baseline and he looks terrible for now.
It might get worse. Cardiac dysfunction and
tissue ischemia can persist despite normalization
of BP, heart rate, and CVP.
2. Inadequate workup of the underlying etiology.
Establishing adequate urine output with fluid
boluses won’t stop bleeding from a gastric ulcer
or ruptured aorta. Giving antibiotics for a fever
won’t be effective if a gangrenous gallbladder
remains undiagnosed.
7. Allowing slow tests to guide management.
Do not wait for the creatinine and D- dimer to
come back before getting the CT; do not wait for
the CXR to see if the mediastinum is wide or if
the heart is large.
3. Inadequate fluid loading.
Look for low CVP signs, evaluate urine output,
and monitor cardiac output response to fluid
administration. Tissue perfusion is your goal
and cardiac output is usually the key to achieving this. A hyperdynamic heart is attempting to
compensate for a low ventricular volume.
8. Discounting the possibility of orthostatic
hypotension as the primary etiology in the
elderly patient with supine hypertensive
readings.
9. Ignoring the role and use of bedside
sonography in hypotension resuscitation.
The rote use of fluid then vasopressors and
inotropic agents may not help and can worsen
some clinical processes. Hypotension is not a
disease or even a syndrome to be fixed. It is a
sign that something is going wrong. You just
have to figure it out quickly and carefully. Goaldirected sonography accurately addresses many
dangerous and time sensitive clinical questions.
4. Delaying ventilator assistance.
Improved ventilation and oxygen delivery to the
lungs and ultimately the organs puts less
demand on the heart and reduces the oxygen
debt.
5. Overaggressive resuscitation without factoring
in the wishes of the patient or family.
A respectful and cost-effective treatment plan
may hinge on getting these important pieces of
information.
10. Not re-evaluating hemodynamic profiles.
RV, LV function, and preload status can change
even when you do the right things.
6 . Discontinuing monitoring after a “good blood
pressure” is reached.
EBMedicine.net • November 2007
21
Emergency Medicine Practice®
concluded that in circumstances where there were less
deviations (or more compliance) from the fluid
resuscitation guideline, the resuscitation efforts were
shorter and there were fewer shock-related problems.
Improved clinical outcomes included lowered mortality, shorter intensive care unit (ICU) length of stay
(LOS), and less total time spent in the hospital. The
patients with severe comorbid conditions were more
likely to succumb to death and complications. In
various other studies, better outcomes in terms of
duration of hypotension, ICU and hospital stays, and
overall mortality were also achieved with the use of
algorithms.50,127-129
coagulant properties and the relative lack of completed randomized, controlled trials in its use, it can
only be recommended with a Class III designation
until further information is received.134 There is no
significant literature to support its use in medically
bleeding patients and it may actually be contraindicated because of the typical multi-system disease in
these patients.
Cost- And Time-Effective Strategies In The
Workup Of Unexplained Hypotension
1. Keep bedside ultrasound available to answer
focused questions on global heart function and
volume status. Signs of vascular catastrophes,
massive pulmonary embolism, and tension pneumothorax can also be sought without interrupting
resuscitation efforts.
Recombinant Factor VIIa
There has been recent study of the use of rFactor VIIa
to control bleeding during surgery. Of particular note
to emergency physicians is its use in bleeding trauma
patients. This medication is used to induce clotting
specifically at the bleeding site and has particular use
in blunt trauma and intracerebral hemorrhage, two
entities that are not so rare in an ED setting. Current
usage is recommended only in refractory bleeding
and most case reports show its use as a “last-ditch”
effort to control bleeding.130-133 Because of its pro-
• Don’t use the CXR to rule out aortic dissection,
pericardial effusion/tamponade, or cardiomyopathy based on a mere silhouette.
• Don’t wait for the CT and the serum creatinine to
determine if a high suspicion AAA is present or
absent.
Key Points For Hypotension
response to changes, especially deteriorations, and
after major therapeutic interventions are put into
effect (including fluid boluses).
1. It is necessary to use/acquire the bedside tools that
noninvasively and accurately assess cardiac output,
CVP, and tissue oxygenation as part of the resuscitation in the hypotensive patient. Ultrasonography
is the ideal modality—it only takes a few minutes
to get crucial accurate information on heart function and major vascular integrity. It also allows
safer and quick access for medication administration and guidance of invasive procedures.
7. Finding the source of hemorrhage or infection is
the first management step:
a. Thoracic: consider chest tube, endobronchial
tamponade, interventional radiology involvement for vessel identification, embolization,
etc., and surgical intervention if lobectomy is
indicated.
2. Consider it a ‘red flag’ when patients have prehospital episodes of hypotension.
3. Improving multi-organ tissue oxygenation is your
main goal. Monitor for signs of oxygen debt:
hypoxia, metabolic acidosis, transcutaneous
oxygen deficits, and elevated lactate levels. The
hemoglobin level may need supplementation if
inadequate.
b. Gastrointestinal: consider endoscopic variceal
tamponade.
c. Consider surgery for aortic rupture, splenic
rupture, and massive colonic bleeding.
d. Reverse bleeding tendencies.
4. Patients with hypotension do not usually fit
exclusively in one category of etiology of hypotension or shock. Therefore, the treatment is multipronged.
8. Oxygen delivery in the critically ill patient with
hypotension often requires intubation. Use
medications such as etomidate and fentanyl that
do not cause hemodynamic deterioration. Consider ketamine for SBP improvement. Carefully
administer induction agents (consider lowering
the dose) in any patient with a tenuous
hemodynamic profile.
5. Time is of the essence. Hypotension is a late
finding and fixing it does not mean you corrected
the state of organ dysfunction that set in.
6. Repeat hemodynamic profiles regularly and in
Emergency Medicine Practice®
22
November 2007 • EBMedicine.net
2. Assess cardiac dynamics and CVP estimates before,
during, and after fluid and catecholamine support.
Well designed studies support the use of goaldirected echocardiography in the hypotensive ED
patient.
thrombus, and thrombolytic agents were given.
The second patient had rales and fluid administration
that led to more shortness of breath and yet another
endotracheal intubation. Furosemide did not help and the
dialysis center did not respond. The ECG was unimpressive and the patient, who was paralyzed and sedated,
remained hypotensive and tachycardiac. You considered
inotropic or vasopressor support but then remembered that
the new ultrasound was delivered yesterday. The
abdominal aorta appeared to be no more than 2 cm in
diameter but you noticed an intimal flap. The heart also
had a small pericardial effusion and an intimal flap next to
the aortic valve. The patient was taken to the OR where he
survived a thoracic aorta repair.
The third patient also had rales. The heart was
enlarged on CXR. The lungs were mildly congested.
Ultrasound showed a small pericardial fluid and barely any
myocardial activity overall with an ejection fraction of 10%
at most. The IVC was thick and stayed the same after the
patient took in a quick and deep breath. She was quickly
put on dobutamine and fell asleep an hour later for the first
time in weeks. A repeat echo showed an EF of 20% and the
patient appeared remarkably better—you left the shift
exhausted but a confirmed believer in the value of bedside
ultrasound.
3. Use crystalloid solutions for fluid resuscitation. No
outcome improvements are in the current literature
that justify the use of more expensive colloidal
solutions in the USA. Goals may include: CVP
improvement, cardiac index improvement, adequate urine output, and lactate clearance.
4. Organ hypoperfusion can be occult; aggressively
seek to get clues using noninvasive monitoring such
as tissue oxygen saturation, central venous oximetry, and lactate levels.
5. Use hypotension as a threshold point, not as a goal.
Address multiple factors that may impact hypotension and, more importantly, organ hypoperfusion.
Disposition
Because of the high morbidity and mortality associated with hypotension regardless of etiology, there
should be a low threshold for admission. Ultrasound
may be a useful tool in directing the disposition. The
Focused Assessment of Sonography in Trauma (FAST)
application allows the direct triage of hypotensive
trauma patients with positive FAST findings to
therapeutic laparotomy without the use of CT
imaging.135
In the new age of ED over-overcrowding (not a
typo) the solution to high patient acuity and volume
should not prolong critical care in the ED. Step down
units and expanding ICU’s help redirect resources and
EM expertise to the next patient demanding answers
for their unexplained hypotension. The Acute Physiology and Chronic Health Evaluation (APACHE) II,
the Simplified Acute Physiology Score (SAPS), and the
Hypotension Score were all created as prognosticators
of patient outcome or severity of disease and have the
potential to guide ICU care.136
Summary
In an age when we are held to a higher standard of
being “Better, Faster, and Surer,” the sheer volume,
increasing complexity, and higher acuity of ED
patients make the management of patients more
challenging than ever before. The early recognition of
clinical hypotension, the rapid initiation of goaldirected resuscitation, and the early use of accurate
diagnostic tools remain the cornerstone to reducing
morbidity and mortality of hypotensive patients.
Rapid identification of clinical hypotension should be
followed by the rapid and confident diagnosis of the
primary and contributory etiologies. The correction of
the primary disorders must occur in parallel to the
diagnostic workup to avoid adverse patient outcomes—a rather tall order for the EM physician.
Using the tools that are available to us early, before
further deterioration of the critically ill patient, puts
us one step closer to achieving that goal.
Case Conclusion
The first patient had deepening hypoxia (despite proper
endotracheal intubation) and was given antibiotics because
of the fever and the elevated serum leukocyte count. No
obvious infectious source was evident. Bedside cardiac
ultrasound showed no pericardial effusion but did reveal
increased left ventricular function, a distended thin walled
right ventricle, and leftward septal wall deviation. The IVC
was distended and showed poor respiratory motion. There
was no obvious IVC or intracardiac mass or clot. The blood
pressure was refractory to 2 L of IV crystalloids, and after
discussion with the critical care team, pulmonary embolism
was considered to be the likely cause of the acute right heart
strain. TEE confirmed the finding of pulmonary artery
EBMedicine.net • November 2007
References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than
a case report.
To help the reader judge the strength of each
reference, pertinent information about the study, such
as the type of study and the number of patients in the
study, will be included in bold type following the
reference, where available.
23
Emergency Medicine Practice®
1. Weisser B, Grune S, Burger R, et al. The Dubendorf Study: a population-based investigation on normal values of blood pressure selfmeasurement. J Hum Hypertens. Apr 1994;8(4):227-231.
(Randomized control trial; Comparative study; 503 patients)
2. Rasmussen SL, Torp-Pedersen C, Borch-Johnsen K, Ibsen H.
Normal values for ambulatory blood pressure and differences
between casual blood pressure and ambulatory blood pressure:
results from a Danish population survey. J Hypertens. Oct
1998;16(10):1415-1424. (Randomized control trial; Comparative
study; Population study; 2656 patients)
3. Levy MM, Fink MP, Marshall JC, et al. 2001
SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions
Conference. Intensive Care Med. Apr 2003;29(4):530-538. (Consensus
statement; Review)
4. Moore CL, Rose GA, Tayal VS, Sullivan DM, Arrowood JA, Kline
JA. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad Emerg Med.
Mar 2002;9(3):186-193. (Prospective, observational trial; 51
patients)
5. Jones AE, Stiell IG, Nesbitt LP, et al. Nontraumatic out-of-hospital
hypotension predicts inhospital mortality. Ann Emerg Med. Jan
2004;43(1):106-113. (Multi-center; Retrospective chart review;
10,807 total patients)
6. Pickering TG, Hall JE, Appel LJ, et al. Recommendations for blood
pressure measurement in humans and experimental animals: part
1: blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public
Education of the American Heart Association Council on High
Blood Pressure Research. Circulation. Feb 8 2005;111(5):697-716.
(Practice guideline)
7. Zhao ZY, Zhao ZY, Wang YQ, Yan ZH, Cui J, Li YY. Quantitative
study of circadian variations of ambulatory blood pressure in
Chinese healthy, hypertensive, and diabetes subjects. Clin Exp
Hypertens. Feb-Apr 2005;27(2-3):187-194. (Comparative study;
Observational; 150 patients)
8. Van De Water JM, Dalton ML, Parish DC, Vogel RL, Beatty JC,
Adeniyi SO. Cardiopulmonary assessment: is improvement needed? World J Surg. 2005;29 Suppl 1:S95-98. (Controlled clinical trial;
186 patients)
9. McGee S, Abernethy WB, 3rd, Simel DL. The rational clinical examination. Is this patient hypovolemic? Jama. Mar 17
1999;281(11):1022-1029. (Meta-analysis)
10. Ander DS, Jaggi M, Rivers E, et al. Undetected cardiogenic shock
in patients with congestive heart failure presenting to the emergency department. Am J Cardiol. Oct 1 1998;82(7):888-891.
(Prospective, observational study; 44 patients)
11. Streeten DH. Variations in the clinical manifestations of orthostatic
hypotension. Mayo Clin Proc. Jul 1995;70(7):713-714. (Comment)
12. Shoemaker WC, Hopkins JA. Clinical aspects of resuscitation with
and without an algorithm: relative importance of various decisions.
Crit Care Med. Aug 1983;11(8):630-639. (Retrospective; Chart
review; 603 patients)
13. Jones AE, Aborn LS, Kline JA. Severity of emergency department
hypotension predicts adverse hospital outcome. Shock. Nov
2004;22(5):410-414. (Randomized control trial; 202 patients)
14. Jones AE, Yiannibas V, Johnson C, Kline JA. Emergency department hypotension predicts sudden unexpected in-hospital mortality: a prospective cohort study. Chest. Oct 2006;130(4):941-946.
(Prospective cohort study; 4790 patients)
15. Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ
failure and guidelines for the use of innovative therapies in sepsis.
The ACCP/SCCM Consensus Conference Committee. American
College of Chest Physicians/Society of Critical Care Medicine.
Chest. Jun 1992;101(6):1644-1655. (Consensus statement; Practice
guideline)
16. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic shock complicating acute myocardial infarction—etiologies, management and
outcome: a report from the SHOCK Trial Registry. Should we
emergently revascularize Occluded Coronaries for cardiogenic
shocK? J Am Coll Cardiol. Sep 2000;36(3 Suppl A):1063-1070.
(Review)
17. Hollenberg SM, Kavinsky CJ, Parrillo JE. Cardiogenic shock. Ann
Intern Med. Jul 6 1999;131(1):47-59. (Review article)
18. Johnson DR, Douglas D, Hauswald M, Tandberg D. Dehydration
and orthostatic vital signs in women with hyperemesis gravidarum. Acad Emerg Med. Aug 1995;2(8):692-697. (Prospective;
Observational; 23 patients)
Emergency Medicine Practice®
19. Deakin CD, Low JL. Accuracy of the advanced trauma life support
guidelines for predicting systolic blood pressure using carotid,
femoral, and radial pulses: observational study. Bmj. Sep 16
2000;321(7262):673-674. (Observational study)
20. Parks JK, Elliott AC, Gentilello LM, Shafi S. Systemic hypotension
is a late marker of shock after trauma: a validation study of
Advanced Trauma Life Support principles in a large national sample. Am J Surg. Dec 2006;192(6):727-731. (Database review; 115830
patients)
21. Pressley JC, Severance HW, Jr., Raney MP, et al. A comparison of
paramedic versus basic emergency medical care of patients at high
and low risk during acute myocardial infarction. J Am Coll Cardiol.
Dec 1988;12(6):1555-1561.(Comparative, prospective study)
22. Hooker EA, Miller FB, Hollander JL, Bukowski EM. Do all trauma
patients need early crossmatching for blood? J Emerg Med. Jul-Aug
1994;12(4):447-451. (Retrospective chart review; 180 patients;
Prospective clinical protocol; 136 patients)
23. Franklin GA, Boaz PW, Spain DA, Lukan JK, Carrillo EH,
Richardson JD. Prehospital hypotension as a valid indicator of
trauma team activation. J Trauma. Jun 2000;48(6):1034-1037; discussion 1037-1039. (Retrospective database analysis; 6976 patients)
24. Shapiro NI, Kociszewski C, Harrison T, Chang Y, Wedel SK,
Thomas SH. Isolated prehospital hypotension after traumatic
injuries: a predictor of mortality? J Emerg Med. Aug 2003;25(2):175179. (Retrospective; 545 patients)
25. Garrett PD, Boyd SY, Bauch TD, Rubal BJ, Bulgrin JR, Kinkler ES Jr.
Feasibility of real-time echocardiographic evaluation during
patient transport. J Am Soc Echocardiogr. Mar 2003;16(3):197-201.
(Comparative study)
26. Buist M, Bernard S, Nguyen TV, Moore G, Anderson J. Association
between clinically abnormal observations and subsequent in-hospital mortality: a prospective study. Resuscitation. Aug 2004;62(2):137141. (Prospective; Data collection; 564 patients)
27. Jones AE, Tayal VS, Sullivan DM, Kline JA. Randomized, controlled trial of immediate versus delayed goal-directed ultrasound
to identify the cause of nontraumatic hypotension in emergency
department patients. Crit Care Med. Aug 2004;32(8):1703-1708.
(Randomized control trial; 184 patients)
28. De Jong JR, Ros HH, De Lange JJ. Noninvasive continuous blood
pressure measurement during anaesthesia: a clinical evaluation of
a method commonly used in measuring devices. Int J Clin Monit
Comput. Feb 1995;12(1):1-10. (Controlled clinical trial; 15 patients)
29. Lehmann KG, Gelman JA, Weber MA, Lafrades A. Comparative
accuracy of three automated techniques in the noninvasive estimation of central blood pressure in men. Am J Cardiol. Apr 15
1998;81(8):1004-1012. (Randomized controlled trial; 120 patients)
30. Cavalcanti S, Marchesi G, Ghidini C. Validation of automated oscillometric sphygmomanometer (HDBPM) for arterial pressure measurement during haemodialysis. Med Biol Eng Comput. Jan
2000;38(1):98-101. (Controlled clinical trial; 92 patients)
31. Van Montfrans GA, Van der Hoeven GM, Karemaker JM, Wieling
W, Dunning AJ. Accuracy of auscultatory blood pressure measurement with a long cuff. Br Med J (Clin Res Ed). Aug 8
1987;295(6594):354-355. (Randomized controlled trial; 37 patients)
32. Gomez-Marin O, Prineas RJ, Rastam L. Cuff bladder width and
blood pressure measurement in children and adolescents. J
Hypertens. Oct 1992;10(10):1235-1241. (Comparative study; 1582
patients)
33. Banner TE, Gravenstein JS. Comparative effects of cuff size and
tightness of fit on accuracy of blood pressure measurements. J Clin
Monit. Oct 1991;7(4):281-284. (Comparative study; 6 patients)
34. Stolt M, Sjonell G, Astrom H, Rossner S, Hansson L. Improved
accuracy of indirect blood pressure measurement in patients with
obese arms. Am J Hypertens. Jan 1993;6(1):66-71. (Randomized controlled trial; 20 patients)
35. Sala C, Santin E, Rescaldani M, Magrini F. How long shall the
patient rest before clinic blood pressure measurement? Am J
Hypertens. Jul 2006;19(7):713-717. (Comparative study; 55 patients)
36. Lategola MT, Busby DE. Differences between seated and recumbent resting measurements of auscultative blood pressure. Aviat
Space Environ Med. Aug 1975;46(8):1027-1029. (Randomized controlled trial; 100 patients)
37. Netea RT, Bijlstra PJ, Lenders JW, Smits P, Thien T. Influence of the
arm position on intra-arterial blood pressure measurement. J Hum
Hypertens. Mar 1998;12(3):157-160. (Comparative study; 16
patients)
24
November 2007 • EBMedicine.net
38. Netea RT, Smits P, Lenders JW, Thien T. Does it matter whether
blood pressure measurements are taken with subjects sitting or
supine? J Hypertens. Mar 1998;16(3):263-268. (Comparative study;
245 patients)
39. Christiansen C, Toft P, Jorgensen HS, Andersen SK, Tonnesen E.
Hyperglycaemia and mortality in critically ill patients. A prospective study. Intensive Care Med. Aug 2004;30(8):1685-1688.
(Prospective)
40. Laird AM, Miller PR, Kilgo PD, Meredith JW, Chang MC.
Relationship of early hyperglycemia to mortality in trauma
patients. J Trauma. May 2004;56(5):1058-1062. (Prospective; 516
patients)
41. Sung J, Bochicchio GV, Joshi M, Bochicchio K, Tracy K, Scalea TM.
Admission hyperglycemia is predictive of outcome in critically ill
trauma patients. J Trauma. Jul 2005;59(1):80-83. (Prospective; 1003
patients)
42. Lange H, Jackel R. Usefulness of plasma lactate concentration in
the diagnosis of acute abdominal disease. Eur J Surg. Jun-Jul
1994;160(6-7):381-384. (Prospective; 85 patients)
43. Murray MJ, Gonze MD, Nowak LR, Cobb CF. Serum D(-)-lactate
levels as an aid to diagnosing acute intestinal ischemia. Am J Surg.
Jun 1994;167(6):575-578. (Prospective; 31 patients)
44. Younger JG, Falk JL, Rothrock SG. Relationship between arterial
and peripheral venous lactate levels. Acad Emerg Med. Jul
1996;3(7):730-734. (Comparative study; 48 patients)
45. Lavery RF, Livingston DH, Tortella BJ, Sambol JT, Slomovitz BM,
Siegel JH. The utility of venous lactate to triage injured patients in
the trauma center. J Am Coll Surg. Jun 2000;190(6):656-664.
(Comparative study; 375 patients)
46. Jones AE, Leonard MM, Hernandez-Nino J, Kline JA.
Determination of the effect of in vitro time, temperature, and
tourniquet use on whole blood venous point-of-care lactate concentrations. Acad Emerg Med. Jul 2007;14(7):587-591. (Prospective
study, 80 patients)
47. Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is
associated with improved outcome in severe sepsis and septic
shock. Crit Care Med. Aug 2004;32(8):1637-1642. (Prospective observational study; 111 patients)
48. Upadhyay M, Singhi S, Murlidharan J, Kaur N, Majumdar S.
Randomized evaluation of fluid resuscitation with crystalloid
(saline) and colloid (polymer from degraded gelatin in saline) in
pediatric septic shock. Indian Pediatr. Mar 2005;42(3):223-231.
(Prospective; Randomized; Open label; 60 patients)
49. Yokoyama N, Nishikawa K, Saito Y, Saito S, Goto F. [Comparison
of the effects of colloid and crystalloid solution for volume preloading on maternal hemodynamics and neonatal outcome in
spinal anesthesia for cesarean section]. Masui. Sep 2004;53(9):10191024. (Randomized controlled trial; 32 patients)
50. Trzeciak S, Dellinger RP, Abate NL, et al. Translating research to
clinical practice: a 1-year experience with implementing early goaldirected therapy for septic shock in the emergency department.
Chest. Feb 2006;129(2):225-232. (Retrospective; 32 total patients)
51. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis
Campaign guidelines for management of severe sepsis and septic
shock. Crit Care Med. Mar 2004;32(3):858-873. (Consensus statement; Practice guideline)
52. Sand IC, Jagoda A, Vukich D. Maintenance fluids in prehospital
care: crystalloid versus dextrose solutions—is there a difference? J
Emerg Med. Nov-Dec 1994;12(6):803-809. (Comparative study)
53. Roberts I, Alderson P, Bunn F, Chinnock P, Ker K, Schierhout G.
Colloids versus crystalloids for fluid resuscitation in critically ill
patients. Cochrane Database Syst Rev. 2004(4):CD000567. (Metaanalysis)
54. Alderson P, Bunn F, Lefebvre C, et al. Human albumin solution for
resuscitation and volume expansion in critically ill patients.
Cochrane Database Syst Rev. 2004(4):CD001208. (Meta-analysis)
55. Bunn F, Roberts I, Tasker R, Akpa E. Hypertonic versus near isotonic crystalloid for fluid resuscitation in critically ill patients.
Cochrane Database Syst Rev. 2004(3):CD002045. (Meta-analysis)
56. Kwan I, Bunn F, Roberts I. Timing and volume of fluid administration for patients with bleeding following trauma. Cochrane Database
Syst Rev. 2001(1):CD002245. (Meta-analysis; Review)
57. Kwan I, Bunn F, Roberts I. Timing and volume of fluid administration for patients with bleeding. Cochrane Database Syst Rev.
2003(3):CD002245. (Meta-analysis; Review)
EBMedicine.net • November 2007
58. Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation
during active hemorrhage: impact on in-hospital mortality. J
Trauma. Jun 2002;52(6):1141-1146.(Randomized controlled study;
110 patients)
59. Mapstone J, Roberts I, Evans P. Fluid resuscitation strategies: a systematic review of animal trials. J Trauma. Sep 2003;55(3):571-589.
(Meta-analysis)
60. Capone AC, Safar P, Stezoski W, Tisherman S, Peitzman AB.
Improved outcome with fluid restriction in treatment of uncontrolled hemorrhagic shock. J Am Coll Surg. Jan 1995;180(1):49-56.
(Animal study)
61. Owens TM, Watson WC, Prough DS, Uchida T, Kramer GC.
Limiting initial resuscitation of uncontrolled hemorrhage reduces
internal bleeding and subsequent volume requirements. J Trauma.
Aug 1995;39(2):200-207; discussion 208-209. (Animal study)
62. Bickell WH, Wall MJ, Jr., Pepe PE, et al. Immediate versus delayed
fluid resuscitation for hypotensive patients with penetrating torso
injuries. N Engl J Med. Oct 27 1994;331(17):1105-1109. (Prospective
study, 598 patients)
63. Cao L, Weil MH, Sun S, Tang W. Vasopressor agents for cardiopulmonary resuscitation. J Cardiovasc Pharmacol Ther. Jun 2003;8(2):115121. (Review)
64. Tran TP, Panacek EA, Rhee KJ, Foulke GE. Response to dopamine
vs norepinephrine in tricyclic antidepressant-induced hypotension.
Acad Emerg Med. Sep 1997;4(9):864-868. (Comparative study;
Retrospective; 26 patients)
65. Holmes CL. Vasoactive drugs in the intensive care unit. Curr Opin
Crit Care. Oct 2005;11(5):413-417. (Review)
66. Holmes CL, Patel BM, Russell JA, Walley KR. Physiology of vasopressin relevant to management of septic shock. Chest. Sep
2001;120(3):989-1002. (Review)
67. Beale RJ, Hollenberg SM, Vincent JL, Parrillo JE. Vasopressor and
inotropic support in septic shock: an evidence-based review. Crit
Care Med. Nov 2004;32(11 Suppl):S455-465. (Review)
68. Kellum JA, Pinsky MR. Use of vasopressor agents in critically ill
patients. Curr Opin Crit Care. Jun 2002;8(3):236-241. (Review)
69. Ogawa R. [Distributive shock and it’s therapy by cardio-vascular
acting drugs]. Nippon Geka Gakkai Zasshi. Oct 1999;100(10):679-682.
(Review)
70. Mullner M, Urbanek B, Havel C, Losert H, Waechter F, Gamper G.
Vasopressors for shock. Cochrane Database Syst Rev.
2004(3):CD003709. (Review; Meta-analysis)
71. Malay MB, Ashton RC, Jr., Landry DW, Townsend RN. Low-dose
vasopressin in the treatment of vasodilatory septic shock. J Trauma.
Oct 1999;47(4):699-703; discussion 703-695. (Randomized controlled trial; 10 patients)
72. Iwai A, Sakano T, Uenishi M, Sugimoto H, Yoshioka T, Sugimoto T.
Effects of vasopressin and catecholamines on the maintenance of
circulatory stability in brain-dead patients. Transplantation. Oct
1989;48(4):613-617. (Clinical trial; Comparative study; 25 patients)
73. Leone M, Albanese J, Delmas A, Chaabane W, Garnier F, Martin C.
Terlipressin in catecholamine-resistant septic shock patients. Shock.
Oct 2004;22(4):314-319. (Prospective; Open-label; 17 patients)
74. Hall LG, Oyen LJ, Taner CB, et al. Fixed-dose vasopressin compared with titrated dopamine and norepinephrine as initial vasopressor therapy for septic shock. Pharmacotherapy. Aug
2004;24(8):1002-1012. (Comparative study; 150 patients)
75. Lim TW, Lee S, Ng KS. Vasopressin effective in reversing catecholamine-resistant vasodilatory shock. Anaesth Intensive Care. Jun
2000;28(3):313-317. (Case report)
76. Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiency
contributes to the vasodilation of septic shock. Circulation. Mar 4
1997;95(5):1122-1125. (Comparative, clinical observation; 19
patients)
77. Annane D, Bellissant E, Bollaert PE, Briegel J, Keh D, Kupfer Y.
Corticosteroids for treating severe sepsis and septic shock. Cochrane
Database Syst Rev. 2004(1):CD002243. (Review; Meta-analysis)
78. Prigent H, Maxime V, Annane D. Clinical review: corticotherapy in
sepsis. Crit Care. Apr 2004;8(2):122-129. (Review)
79. Kortgen A, Niederprum P, Bauer M. Implementation of an evidence-based “standard operating procedure” and outcome in septic shock. Crit Care Med. Apr 2006;34(4):943-949. (Retrospective
cohort; 60 patients)
80. Abraham E, Laterre PF, Garg R, et al. Drotrecogin alfa (activated)
for adults with severe sepsis and a low risk of death. N Engl J Med.
Sep 29 2005;353(13):1332-1341. (Randomized controlled trial; 2640
patients)
25
Emergency Medicine Practice®
81. Franklin C, Samuel J, Hu TC. Life-threatening hypotension associated with emergency intubation and the initiation of mechanical
ventilation. Am J Emerg Med. Jul 1994;12(4):425-428. (Prospective;
Observational; 84 patients)
82. De Jong MF, Beishuizen A, Spijkstra JJ, et al. Predicting a low cortisol response to ACTH in the critically ill: a retrospective cohort
study. Crit Care. May 24 2007;11(3):R61. (Retrospective; 405
patients)
83. Mohammad Z, Afessa B, Finkielman JD. The incidence of relative
adrenal insufficiency in patients with septic shock after the administration of etomidate. Crit Care. 2006;10(4):R105. (Retrospective;
152 patients)
84. Zhang Y, Luo A, An G, Huang Y. [Effect of propofol and etomidate
for anesthesia induction on plasma total cortisol concentration].
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. Jun 2000;22(3):284-286.
(Prospective; 20 patients)
85. Adnet F. Ketamine Versus Etomidate During Rapid Sequence
Intubation: Consequences on Hospital Morbidity (KETASED
study). 2007. (Study in phase IV- patient enrollment)
86. Wood KE. The presence of shock defines the threshold to initiate
thrombolytic therapy in patients with pulmonary embolism.
Intensive Care Med. Nov 2002;28(11):1537-1546. (Review)
87. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant
pulmonary embolism. Chest. Mar 2002;121(3):877-905. (Review)
88. Sharma VK, Dellinger RP. Recent developments in the treatment of
sepsis. Expert Opin Investig Drugs. Feb 2003;12(2):139-152. (Review)
89. Schwartz B, Vermeulen MJ, Idestrup C, Datta P. Clinical variables
associated with mortality in out-of-hospital patients with hemodynamically significant bradycardia. Acad Emerg Med. Jun
2004;11(6):656-661. (Retrospective; 247 patients)
90. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension
before initiation of effective antimicrobial therapy is the critical
determinant of survival in human septic shock. Crit Care Med. Jun
2006;34(6):1589-1596. (Retrospective chart review; 2741 patients)
91. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism:
clinical outcomes in the International Cooperative Pulmonary
Embolism Registry (ICOPER). Lancet. Apr 24 1999;353(9162):13861389. (Prospective outcome; 2454 patients)
92. Ginde AA, Rhee SH, Katz ED. Predictors of outcome in geriatric
patients with urinary tract infections. J Emerg Med. Aug
2004;27(2):101-108. (Retrospective; 284 patients)
93. Farooq MM, Freischlag JA, Seabrook GR, Moon MR, Aprahamian
C, Towne JB. Effect of the duration of symptoms, transport time,
and length of emergency room stay on morbidity and mortality in
patients with ruptured abdominal aortic aneurysms. Surgery. Jan
1996;119(1):9-14. (Retrospective; 124 patients)
94. Chan L, Bartfield JM, Reilly KM. The significance of out-of-hospital
hypotension in blunt trauma patients. Acad Emerg Med. Aug
1997;4(8):785-788. (Retrospective; 104 patients)
95. Castillo J, Leira R, Garcia MM, Serena J, Blanco M, Davalos A.
Blood pressure decrease during the acute phase of ischemic stroke
is associated with brain injury and poor stroke outcome. Stroke. Feb
2004;35(2):520-526. (Prospective; 304 patients)
96. Bourgoin A, Leone M, Delmas A, Garnier F, Albanese J, Martin C.
Increasing mean arterial pressure in patients with septic shock:
effects on oxygen variables and renal function. Crit Care Med. Apr
2005;33(4):780-786. (Randomized control trial; 28 patients)
97. Fine MJ, Smith MA, Carson CA, et al. Prognosis and outcomes of
patients with community-acquired pneumonia. A meta-analysis.
Jama. Jan 10 1996;275(2):134-141. (Meta-analysis)
98. 2005 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation. Dec
13 2005;112(24 Suppl):IV1-203. (Clinical guideline; Consensus
statement)
99. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy of
left ventricular function for identifying sepsis among emergency
department patients with nontraumatic symptomatic undifferentiated hypotension. Shock. Dec 2005;24(6):513-517. (Randomized control trial; 103 patients)
100. Niendorff DF, Rassias AJ, Palac R, Beach ML, Costa S, Greenberg
M. Rapid cardiac ultrasound of inpatients suffering PEA arrest performed by nonexpert sonographers. Resuscitation. Oct
2005;67(1):81-87. (Comparative study; 5 patients)
Emergency Medicine Practice®
101. Kaul S, Stratienko AA, Pollock SG, Marieb MA, Keller MW, Sabia
PJ. Value of two-dimensional echocardiography for determining
the basis of hemodynamic compromise in critically ill patients: a
prospective study. J Am Soc Echocardiogr. Nov-Dec 1994;7(6):598606. (Prospective, comparative study; 49 patients)
102. Adler C, Buttner W, Veh R. [Relations of the ultrasonic image of the
inferior vena cava and central venous pressure]. Aktuelle Gerontol.
Nov 1983;13(6):209-213. (Prospective, comparative study; 50
patients)
103. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of
right atrial pressure from the inspiratory collapse of the inferior
vena cava. Am J Cardiol. Aug 15 1990;66(4):493-496. (Prospective,
comparative study; 83 patients)
104. Randazzo MR, Snoey ER, Levitt MA, Binder K. Accuracy of emergency physician assessment of left ventricular ejection fraction and
central venous pressure using echocardiography. Acad Emerg Med.
Sep 2003;10(9):973-977. (Observational study; 115 patients)
105. Bendjelid K. Predicting fluid responsiveness: should we adapt the
scale to measure the central venous pressure swing? Intensive Care
Med. Sep 2004;30(9):1847; author reply 1848. (Comment)
106. Bendjelid K, Romand JA, Walder B, Suter PM, Fournier G.
Correlation between measured inferior vena cava diameter and
right atrial pressure depends on the echocardiographic method
used in patients who are mechanically ventilated. J Am Soc
Echocardiogr. Sep 2002;15(9):944-949. (Prospective; 20 patients)
107. Moreno FL, Hagan AD, Holmen JR, Pryor TA, Strickland RD,
Castle CH. Evaluation of size and dynamics of the inferior vena
cava as an index of right-sided cardiac function. Am J Cardiol. Feb 1
1984;53(4):579-585. (Prospective study; 175 patients)
108. Nath J, Vacek JL, Heidenreich PA. A dilated inferior vena cava is a
marker of poor survival. Am Heart J. Mar 2006;151(3):730-735.
(Retrospective; 4383 patients)
109. Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med. Sep
2004;30(9):1740-1746. (Prospective; 23 patients)
110. Gloviczki P, Pairolero PC, Mucha P, Jr., et al. Ruptured abdominal
aortic aneurysms: repair should not be denied. J Vasc Surg. May
1992;15(5):851-857; discussion 857-859. (Retrospective; 231
patients)
111. Schuster ME, Fishman JE, Copeland JF, Hatabu H, Boiselle PM.
Pulmonary embolism in pregnant patients: a survey of practices
and policies for CT pulmonary angiography. AJR Am J Roentgenol.
Dec 2003;181(6):1495-1498. (Survey; Practice guidelines)
112. Clinical policy: critical issues in the evaluation and management of
adult patients presenting with suspected pulmonary embolism.
Ann Emerg Med. Feb 2003;41(2):257-270. (Clinical policy; Practice
guideline)
113. Daniels LB, Krummen DE, Blanchard DG. Echocardiography in
pulmonary vascular disease. Cardiol Clin. Aug 2004;22(3):383-399,
vi. (Review)
114. Pruszczyk P, Bochowicz A, Torbicki A, et al. Cardiac troponin T
monitoring identifies high-risk group of normotensive patients
with acute pulmonary embolism. Chest. Jun 2003;123(6):1947-1952.
(Comparative study; 60 patients)
115. Pruszczyk P, Torbicki A, Pacho R, et al. Noninvasive diagnosis of
suspected severe pulmonary embolism: transesophageal echocardiography vs spiral CT. Chest. Sep 1997;112(3):722-728.
(Comparative study; 49 patients)
116. Randolph AG, Cook DJ, Gonzales CA, Pribble CG. Ultrasound
guidance for placement of central venous catheters: a meta-analysis of the literature. Crit Care Med. Dec 1996;24(12):2053-2058.
(Meta-analysis)
117. Hilty WM, Hudson PA, Levitt MA, Hall JB. Real-time ultrasoundguided femoral vein catheterization during cardiopulmonary
resuscitation. Ann Emerg Med. Mar 1997;29(3):331-336; discussion
337. (Prospective, randomized, comparative study; 20 patients)
118. Cheitlin MD, Armstrong WF, Aurigemma GP, et al.
ACC/AHA/ASE 2003 guideline update for the clinical application
of echocardiography: summary article: a report of the American
College of Cardiology/American Heart Association Task Force on
Practice Guidelines (ACC/AHA/ASE Committee to Update the
1997 Guidelines for the Clinical Application of Echocardiography).
Circulation. Sep 2 2003;108(9):1146-1162. (Practice guideline)
119. Vieillard-Baron A, Prin S, Chergui K, Dubourg O, Jardin F.
Hemodynamic instability in sepsis: bedside assessment by Doppler
echocardiography. Am J Respir Crit Care Med. Dec 1
2003;168(11):1270-1276. (Review)
26
November 2007 • EBMedicine.net
120. Kern JW, Shoemaker WC. Meta-analysis of hemodynamic optimization in high-risk patients. Crit Care Med. Aug 2002;30(8):16861692. (Meta-analysis)
121. Boyd O, Hayes M. The oxygen trail: the goal. Br Med Bull.
1999;55(1):125-139. (Meta-analysis)
122. Connors AF, Jr., Speroff T, Dawson NV, et al. The effectiveness of
right heart catheterization in the initial care of critically ill patients.
SUPPORT Investigators. Jama. Sep 18 1996;276(11):889-897.
(Prospective cohort; 5735 patients)
123. Shoemaker WC. Temporal physiologic patterns of shock and circulatory dysfunction based on early descriptions by invasive and
noninvasive monitoring. New Horiz. May 1996;4(2):300-318.
(Review)
124. Shoemaker WC, Belzberg H, Wo CC, et al. Multicenter study of
noninvasive monitoring systems as alternatives to invasive monitoring of acutely ill emergency patients. Chest. Dec
1998;114(6):1643-1652. (Prospective, comparative study; 680
patients)
125. Shoemaker WC, Wo CC, Bishop MH, Thangathurai D, Patil RS.
Noninvasive hemodynamic monitoring of critical patients in the
emergency department. Acad Emerg Med. Jul 1996;3(7):675-681.
(Prospective, comparative study; 60 patients)
126. Shoemaker WC, Wo CC, Chan L, et al. Outcome prediction of
emergency patients by noninvasive hemodynamic monitoring.
Chest. Aug 2001;120(2):528-537. (Prospective, descriptive study;
151 patients)
127. Velmahos GC, Demetriades D, Shoemaker WC, et al. Endpoints of
resuscitation of critically injured patients: normal or supranormal?
A prospective randomized trial. Ann Surg. Sep 2000;232(3):409-418.
(Randomized control trial; 75 patients)
128. Hopkins JA, Shoemaker WC, Chang PC, Schluchter M, Greenfield
S. Clinical trial of an emergency resuscitation algorithm. Crit Care
Med. Aug 1983;11(8):621-629. (Comparative study; 603 patients)
129. Shoemaker WC, Fleming AW. Resuscitation of the trauma patient:
restoration of hemodynamic functions using clinical algorithms.
Ann Emerg Med. Dec 1986;15(12):1437-1444. (Prospective, comparative study)
130. Scarpelini S, Rizoli S. Recombinant factor VIIa and the surgical
patient. Curr Opin Crit Care. Aug 2006;12(4):351-356. (Review)
131. McMullin NR, Kauvar DS, Currier HM, Baskin TW, Pusateri AE,
Holcomb JB. The clinical and laboratory response to recombinant
factor VIIA in trauma and surgical patients with acquired coagulopathy. Curr Surg. Jul-Aug 2006;63(4):246-251. (Retrospective; 18
patients)
132. Tieu BH, Holcomb JB, Schreiber MA. Coagulopathy: Its
Pathophysiology and Treatment in the Injured Patient. World J
Surg. Mar 30 2007. (Review)
133. Howes DW, Stratford A, Stirling M, Ferri CC, Bardell T.
Administration of recombinant factor VIIa decreases blood loss
after blunt trauma in noncoagulopathic pigs. J Trauma. Feb
2007;62(2):311-315; discussion 314-315. (Randomized control trial;
Animal study)
134. Thomas GO, Dutton RP, Hemlock B, et al. Thromboembolic complications associated with factor VIIa administration. J Trauma. Mar
2007;62(3):564-569. (Retrospective; 285 patients)
135. Lee BC, Ormsby EL, McGahan JP, Melendres GM, Richards JR. The
utility of sonography for the triage of blunt abdominal trauma
patients to exploratory laparotomy. AJR Am J Roentgenol. Feb
2007;188(2):415-421. (Retrospective; 4029 patients)
136. Heidenreich PA, Foster E, Cohen NH. Prediction of outcome for
critically ill patients with unexplained hypotension. Crit Care Med.
Nov 1996;24(11):1835-1840. (Prospective cohort; 101 patients)
2. Which of the following diagnostic tools suggests
primary cardiogenic causes of the hypotension?
a. Brain natriuretic peptide elevations
b. WBC count elevations
c. Lactate level of 1.0
d. Urinary output of less than 10 cc/hr
3. What factors interact to produce a normal blood
pressure?
a. Stroke volume and heart rate
b. Systemic vascular resistance
c. Peripheral vascular vasoreceptors and central
nervous system vasomotor centers
d. The patient’s volume status
e. All of the above
4. Besides a systolic BP < 90 mmHg, which factor is
the most common occurrence prior to cardiac
arrest in hospitalized patients?
a. Dyspnea
b. Oxygen saturation < 90%
c. Bradycardia for more than 30 minutes
d. A decrease in GCS
5. In a patient presenting with hypotension and
clear lungs without jugular venous distension,
the most likely diagnosis is:
a. Acute hemorrhage
b. Cardiogenic shock
c. Massive pulmonary embolism
d. Cardiac tamponade
6. What is true about the use of vasopressor agents?
a. Norepinephrine is the drug of choice for
anaphylaxis
b. Dopamine is the drug of choice for sepsis
c. Phenylephrine is primarily an alpha agonist
d. Dobutamine is indicated for those patients
with an initial systolic blood pressure < 70
mmHg
7. Which of the following statements about bedside
goal-directed ultrasound is true?
a. It allows the differentiation of the causes of
obstructive hypotension
b. It allows for rapid assessment of ventricular
function, wall motion, and valvular
abnormalities
c. It can be used to facilitate vascular access
d. It is rapid, cost effective, and doesn’t require
the patient to leave the ED
e. All of the above
8. Some factors contributing to hypotension in
patients intubated and ventilated in the ED
include:
a. Initiation of intubation with inadequate IV
access
b. Failure to consider metabolic derangements
likely present at the time of intubation
c. The use of medications likely to cause
hypotension for intubation and sedation
d. The inappropriate use of ventilatory modalities (such as PEEP) that lower blood pressure
e. All of the above
CME Questions
1. The most definitive test in ruling out pulmonary
embolism as the cause of a patient’s hypotension
and dyspnea is:
a. Bedside echocardiography
b. D-dimer
c. Chest x-ray
d. Contrast-enhanced CT of the thorax
e. Lower extremity venous compression ultrasound
EBMedicine.net • November 2007
27
Emergency Medicine Practice®
Physician CME Information
9. Which of the following diagnoses must be
considered in a hypotensive patient with dyspnea
and jugular venous distention?
a. Tension pneumothorax
b. Acute pulmonary edema
c. Pericardial tamponade
d. Right ventricular infarction
e. Pulmonary embolism
f. All of the above
Date of Original Release: November 1, 2007. Date of most recent review:
October 18, 2007. Termination date: November 1, 2010.
Accreditation: This activity has been planned and implemented in accordance
with the Essentials and Standards of the Accreditation Council for Continuing
Medical Education (ACCME) through the joint sponsorship of Mount Sinai
School of Medicine and Emergency Medicine Practice. The Mount Sinai School
of Medicine is accredited by the ACCME to provide continuing medical
education for physicians.
Credit Designation: The Mount Sinai School of Medicine designates this
educational activity for a maximum of 48 AMA PRA Category 1 Credit(s)™ per
year. Physicians should only claim credit commensurate with the extent of their
participation in the activity.
ACEP Accreditation: Emergency Medicine Practice is approved by the American
College of Emergency Physicians for 48 hours of ACEP Category 1 credit per
annual subscription.
AAFP Accreditation: Emergency Medicine Practice has been reviewed and is
acceptable for up to 48 Prescribed credits per year by the American Academy
of Family Physicians. AAFP Accreditation begins August 1, 2006. Term of
approval is for two years from this date. Each issue is approved for 4
Prescribed credits. Credits may be claimed for two years from the date of this
issue.
AOA Accreditation: Emergency Medicine Practice has been approved for 48
Category 2B credit hours per year by the American Osteopathic Association.
Needs Assessment: The need for this educational activity was determined by a
survey of medical staff, including the editorial board of this publication; review
of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and
evaluation of prior activities for emergency physicians.
Target Audience: This enduring material is designed for emergency medicine
physicians, physician assistants, nurse practitioners, and residents.
Goals & Objectives: Upon completing this activity, you should be able to: (1)
demonstrate medical decision-making based on the strongest clinical evidence;
(2) cost-effectively diagnose and treat the most critical ED presentations; and
(3) describe the most common medicolegal pitfalls for each topic covered.
Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that is
outside Food and Drug Administration approved labeling. Information presented
as part of this activity is intended solely as continuing medical education and is
not intended to promote off-label use of any pharmaceutical product.
Disclosure of Off-Label Usage: Vasopressin use in septic shock and for cardiac
arrest are off-label. Hydrocortisone use as an adjunct in sepsis and septic
shock is off-label.
Faculty Disclosure: It is the policy of Mount Sinai School of Medicine to ensure
objectivity, balance, independence, transparency, and scientific rigor in all CMEsponsored educational activities. All faculty participating in the planning or
implementation of a sponsored activity are expected to disclose to the
audience any relevant financial relationships and to assist in resolving any
conflict of interest that may arise from the relationship. Presenters must also
make a meaningful disclosure to the audience of their discussions of unlabeled
or unapproved drugs or devices.
In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for
this CME activity were asked to complete a full disclosure statement. The
information received is as follows: Dr Weekes, Dr. Zapata, Dr. Napolitano, Dr.
Slovis, and Dr. Weingart report no significant financial interest or other
relationship with the manufacturer(s) of any commercial product(s) discussed in
this educational presentation.
Method of Participation:
• Print Subscription Semester Program: Paid subscribers with current and valid
licenses in the United States who read all CME articles during each Emergency
Medicine Practice six-month testing period, complete the post-test and the
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return it according to the published instructions are eligible for up to 4 hours of
CME credit for each issue. You must complete both the post test and CME
Evaluation Form to receive credit. Results will be kept confidential. CME
certificates will be delivered to each participant scoring higher than 70%.
• Online Single-Issue Program: Current, paid subscribers with current and valid
licenses in the United States who read this Emergency Medicine Practice CME
article and complete the online post-test and CME Evaluation Form at
EBMedicine.net are eligible for up to 4 hours of Category 1 credit toward the
AMA Physician’s Recognition Award (PRA). You must complete both the posttest and CME Evaluation Form to receive credit. Results will be kept
confidential. CME certificates may be printed directly from the Web site to each
participant scoring higher than 70%.
Hardware/Software Requirements: You will need a Macintosh or PC to access
the online archived articles and CME testing. Adobe Reader is required to view
the PDFs of the archived articles. Adobe Reader is available as a free
download at www.adobe.com.
10. First line pressor agents in the treatment of
various causes of shock include all of the following EXCEPT:
a. Norepinephrine use in the setting of pneumonia, good left ventricular systolic function, and
hypotension refractory volume resuscitation
b. Dobutamine use in a patient with severely
depressed left ventricular function and a blood
pressure of 80/40 mmHg
c. Epinephrine use in a patient with anaphylactic
shock
d. Phosphodiesterase inhibitor use in the patient
with hypotension with pulmonary edema and
poor cardiac systolic function
e. Vasopressin use in the dehydrated patient
with suspected urosepsis
Class Of Evidence Definitions
Class I: Conditions for which there is evidence for and/or general agreement
that the procedure or treatment is useful and effective
Class II: Conditions for which there is conflicting evidence and/or a
divergence of opinion about the usefulness/efficacy of a procedure or
treatment
Class IIa: The weight of evidence or opinion is in favor of the
procedure or treatment
Class IIb: Usefulness/efficacy is less well established by evidence or
opinion
Class III: Conditions for which there is evidence and/or general agreement
that the procedure or treatment is not useful/effective and in some cases
may be harmful
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the key points.
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November 2007 • EBMedicine.net