November 2007Volume 9, Number 11

Authors

Anthony J. Weekes, MD, RDCS, RDMS, FAAEMEmergency Ultrasound Program Director, Montefiore MedicalCenter; Assistant Professor of Emergency Medicine, AlbertEinstein College of Medicine, Bronx, NY

Ryan J. Zapata, MD, FACEPAttending Physician, Montefiore Medical Center; AssistantProfessor of Emergency Medicine, Albert Einstein College ofMedicine, Bronx, NY

Antonio Napolitano, MD, FACEPAttending Physician, Montefiore Medical Center; AssistantProfessor of Emergency Medicine, Albert Einstein College ofMedicine, Bronx, NY

Peer Reviewers

Corey M. Slovis, MD, FACP, FACEP, FAAEMProfessor and Chair, Department of Emergency Medicine,Vanderbilt University Medical Center, Nashville, TN

Scott D. Weingart, MDDirector, Division of Emergency Critical Care, Department ofEmergency Medicine, Mount Sinai School of Medicine, NewYork, NY

CME Objectives

Upon completion of this article, you should be able to:

1. Identify the common and life-threatening causes ofhypotension.

2. Understand the clinical approach to the rapid identificationof dangerous causes of hypotension.

3. Explain the emerging role of goal-directed bedside sonog-raphy in the rapid non-invasive diagnosis and manage-ment of hypotensive patients.

4. Appreciate the importance of early intervention in the man-agement of hypotension, including the role of intravenousfluids, inotropes, and vasopressors.

5. Decide the practical and evidence-based advantages anddisadvantages of various point-of-care tests, imagingmodalities, and treatments in hypotension.

Date of original release: November 1, 2007Date of most recent review: October 18, 2007

Termination date: November 1, 2010Time to complete activity: 4 hours

Medium: Print & onlineMethod of participation: Print or online answer form

and evaluationSee “Physician CME Information” on back page.

Symptomatic Hypotension: EDStabilization And The EmergingRole Of SonographyYou just performed an easy endotracheal intubation on an elderly womanbrought in by EMS. She was alert during transport but arrived diaphoreticand lethargic with a BP of 82/45 mmHg, an irregular pulse at 120, a rectaltemperature of 100.8° F, and she was tachypneic at 32 breaths per minute.Surprisingly, her oxygen saturation, which was initially 82%, decreasespostintubation to 76%. Portable chest x-ray shows proper ET tube place-ment, no infiltrates, no pneumothorax, and a normal cardiac silhouette. Thepatient is anuric. Labs show a creatinine of 2.1, a WBC count of 18,000, ahematocrit of 22%, and elevated lactate and transaminase levels. Heartsounds and breath sounds are normal, the abdomen is soft, and both legs areswollen. The patient is sick and you realize the key to her survival is findingthe cause of her hypotensive state…

Before an answer is found, two new patients arrive, both with end-stagerenal disease, diabetes mellitus, hypertension, and coronary artery disease.You begin to wonder why you ever took a job with single cliniciancoverage…

Patient #2 looks worse—ashen and diaphoretic, with a blood pressure of60/40 mmHg. He is afebrile and has a pulse of 100 in the arm without theAV fistula. He has a history of non compliance with his medications. Hedescribes the sudden onset of non radiating chest pain that has persisted forthe past two hours. Three sublingual nitroglycerin tablets given by EMSdid not make the chest pain any better and potentially contributed to hishypotension. On lung examination, you hear rales. You order fluids for thehypotension but realize this might be a mistake…

Patient #3 has a blood pressure of 100/60 mmHg and appears to be inno distress. She took her regular morning dose of clonidine and states thatshe completed hemodialysis yesterday and felt “woozy” afterwards. Sheappears well hydrated. She has no jugular venous distension but there are

Editor-in-ChiefAndy Jagoda, MD, FACEP,

Professor and Vice-Chair ofAcademic Affairs, Department ofEmergency Medicine; Mount SinaiSchool of Medicine; MedicalDirector, Mount Sinai Hospital,New York, NY.

Associate EditorJohn M. Howell, MD, FACEP,

Clinical Professor of EmergencyMedicine, George WashingtonUniversity, Washington, DC;Director of Academic Affairs, BestPractices, Inc, Inova FairfaxHospital, Falls Church, VA.

Editorial BoardWilliam J. Brady, MD, Associate

Professor and Vice Chair,Department of EmergencyMedicine, University of Virginia,Charlottesville, VA.

Peter DeBlieux, MDProfessor of Clinical Medicine,LSU Health Science Center, NewOrleans, LA.

Wyatt W. Decker, MD, Chair andAssociate Professor ofEmergency Medicine, Mayo ClinicCollege of Medicine, Rochester,MN.

Francis M. Fesmire, MD, FACEP,Director, Heart-Stroke Center,Erlanger Medical Center;Assistant Professor, UT College ofMedicine, Chattanooga, TN.

Michael J. Gerardi, MD, FAAP,FACEP, Director, PediatricEmergency Medicine, Children’sMedical Center, Atlantic HealthSystem; Department ofEmergency Medicine, MorristownMemorial Hospital, NJ.

Michael A. Gibbs, MD, FACEP,Chief, Department of EmergencyMedicine, Maine Medical Center,Portland, ME.

Steven A. Godwin, MD, FACEP,Assistant Professor andEmergency Medicine ResidencyDirector, University of FloridaHSC/Jacksonville, FL.

Gregory L. Henry, MD, FACEP,CEO, Medical Practice Risk

Assessment, Inc; ClinicalProfessor of EmergencyMedicine, University of Michigan,Ann Arbor.

Keith A. Marill, MD, Instructor,Department of EmergencyMedicine, Massachusetts GeneralHospital, Harvard Medical School,Boston, MA.

Charles V. Pollack, Jr, MA, MD,FACEP, Professor and Chair,Department of EmergencyMedicine, Pennsylvania Hospital,University of Pennsylvania HealthSystem, Philadelphia, PA.

Michael S. Radeos, MD, MPH,Associate Research Director,Department of EmergencyMedicine, New York HospitalQueens, Flushing, NY; AssistantProfessor of EmergencyMedicine, Weill Medical college ofCornell University, New York, NY.

Robert L. Rogers, MD, FAAEM,Assistant Professor andResidency Director, CombinedEM/IM Program, University ofMaryland, Baltimore, MD.

Alfred Sacchetti, MD, FACEP,Assistant Clinical Professor,Department of EmergencyMedicine, Thomas JeffersonUniversity, Philadelphia, PA.

Corey M. Slovis, MD, FACP,FACEP, Professor and Chair,Department of EmergencyMedicine, Vanderbilt UniversityMedical Center, Nashville, TN.

Jenny Walker, MD, MPH, MSW,Assistant Professor; DivisionChief, Family Medicine,Department of Community andPreventive Medicine, Mount SinaiMedical Center, New York, NY.

Ron M. Walls, MD, Professor andChair, Department of EmergencyMedicine, Brigham & Women’sHospital, Boston, MA.

Research EditorsNicholas Genes, MD, PhD, Mount

Sinai Emergency MedicineResidency.

Beth Wicklund, MD, RegionsHospital Emergency MedicineResidency, EMRA Representative.

International EditorsValerio Gai, MD, Senior Editor,

Professor and Chair, Dept of EM,University of Turin, Italy.

Peter Cameron, MD, Chair,Emergency Medicine, MonashUniversity; Alfred Hospital,Melbourne, Australia.

Amin Antoine Kazzi, MD, FAAEM,Associate Professor and ViceChair, Department of EmergencyMedicine, University of California,Irvine; American University, Beirut,Lebanon.

Hugo Peralta, MD, Chair ofEmergency Services, HospitalItaliano, Buenos Aires, Argentina.

Maarten Simons, MD, PhD,Emergency Medicine ResidencyDirector, 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 financialinterest 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.

Emergency Medicine Practice® 2 November 2007 • EBMedicine.net

bibasilar rales. Heart sounds are distant but there are norubs or murmurs. You suspect orthostatic hypotension.CXR shows no pulmonary congestion and the heartsilhouette is slightly enlarged. The ECG shows no obvioussigns of AMI. Repeat blood pressure is 96/58 mmHg andsomething doesn’t seem right to you…

There is no clear blood pressure definition ofhypotension. Instead, blood pressure must be

placed in the context of the patient’s age and currentclinical and baseline physiologic states. For example,what appears to be a “normal” blood pressure mayactually be a dangerously low blood pressure in thepatient who is generally hypertensive. Hypotensionis a sign, not a diagnosis, and it is not pathognomonicof any specific condition by itself. It can be found inboth acute critical conditions and in chronic steadystate conditions. The emergency physician mustdetermine which is present and tailor the aggressive-ness of interventions based on the underlyingetiology.

In critically ill patients, the first hours of treatmenthave a direct impact on morbidity and mortality. Inthese cases, the approach to hypotension is sometimesunstructured, with a focus on “correcting the num-bers” while investigating the cause. Less emergentbut equally challenging are those patients with lowblood pressures who are in a steady state but are notcritically ill (e.g., patients with end-stage congestiveheart failure). Trying to raise the blood pressure inthis group of patients is not generally indicated andmay be harmful.

The cases presented at the beginning of this articleillustrate the challenge posed by patients withhypotension and demonstrate the need for the emer-gency physician to accurately narrow the differentialdiagnosis. Management involves a three prongedapproach that simultaneously includes stabilization,diagnostic testing, and therapy. Because the differen-tial diagnosis is so broad, most guidelines are diagno-sis specific and do not provide a systematic approachto managing hypotension. This issue of EmergencyMedicine Practice is designed to provide an evidence-based, algorithmic approach to the management anddiagnosis of conditions causing hypotension. Specificattention will be given to the role of ultrasound in theclinical decision making involved in caring for thesepatients.

Terminology

General medical teaching cites normal blood pressure(BP) as 120/80 mmHg as measured over the brachialartery using auscultatory methods. Populationstudies have shown these numbers to range between109-137 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 and107-137 mmHg SBP and 61-78 mmHg DBP in

women.2 Keep in mind these numbers vary with thepatient’s size and ideal body weight.

Mean arterial pressure (MAP) is more reflective ofthe actual pressure in the arterioles and smallervessels than the standard blood pressure measure-ments and may be more helpful in the evaluation ofhypotension. MAP calculations are as follows:

MAP = 2/3 DBP + 1/3 SBP - or -

MAP = DBP + (SBP-DBP)/3 - or -

[ (2xDBP) + SBP ]/3

The standard definition of hypotension in an adultincludes the findings of: a SBP < 90 mmHg, a MAP< 60 mmHg, a decrease of more than 40 mmHg belowthe person’s baseline, or any combination of theaforementioned parameters.3 In some studies, thedefinition of hypotension uses a SBP < 100 mmHg.4,5

A healthy adult will have natural variations inblood pressure readings during a routine 24-hourperiod.6,7 A numerical blood pressure reading takes onclinical significance when the MAP is below thepatient’s usual regulated pressures for organ perfu-sion. For example, a blood pressure reading of140/90 mmHg may provoke symptoms of organhypoperfusion (such as dizziness and fatigue) if thepatient’s chronic blood pressure readings have beenconsistently much higher. Such a patient should beconsidered ‘acutely clinically hypotensive.’ Shock canoccur with “normal” blood pressure readings.8-10

Refractory hypotension refers to persistentlyhypotensive readings after the administration of anintravenous crystalloid fluid bolus of 20-40 mL/kg.

Pseudohypotension refers to the underestimationof the patient’s true BP secondary to arterial occlusionor other abnormalities. If the unaffected extremity hasadequate perfusion, the true blood pressure reading isnoticeably higher than in the affected extremity. Pulsedeficits or pseudohypotension can be a strong indica-tor of aortic side branch occlusions and thus raise thesuspicion of a vascular emergency.

Shock refers to a state of organ dysfunction oreven organ failure due to inadequate tissue perfusion.Multiple etiologies of shock are described and morethan one type may be present in a single patient. Thevarious types of shock are listed below:

• Cardiogenic – results from loss of cardiac output• Hypovolemic – results from decreased intravascu-

lar volume• Obstructive – results from intrinsic (e.g., pul-

monary embolus) or extrinsic (e.g., pericardialtamponade) vascular outflow obstruction

• Distributive – results from disruption of vasomo-tor regulation (e.g., anaphylactic, septic, andneurogenic shock)

Shock is the most feared cause of hypotension; it isnot a diagnosis but a final common pathway by whichmany disease processes produce multi-organ failure

EBMedicine.net • November 2007 3 Emergency Medicine Practice®

and death. The healthy adult is able to compensatefor normal changes in organ perfusion. In shock, theinsult is of such magnitude that normal compensatorymechanisms are overwhelmed and organ hypo-perfusion and dysfunction develop. This leads toirreversible end organ failure if resuscitation is notinitiated and achieved in time. The important thing torealize is that the development of hypotension is a latemanifestation of shock, and the rapidity of progres-sion through the spectrum of pre-shock, shock, andmulti-organ dysfunction stages depends on manyfactors. The severity of the inciting insult, thepatient’s preexisting medical conditions (especiallycardiopulmonary function), and their immune andnutritional status all play a role.

Orthostatic HypotensionStanding or sitting with the legs dangling can causeup to 1 L of blood volume to pool in the venouscirculation of the legs. The immediate result oflowering intrathoracic blood volume is a reduction inboth cardiac output and blood pressure. Through thenormal autonomic response, an increase in heart rateby as much as 25 beats/minute and an increase insystemic vascular resistance should keep bloodpressure at normal levels. A 5-10 mmHg drop in BPcan be seen in normal individuals within threeminutes of the position change. This change isclinically insignificant.

The symptomatic lowering of blood pressure uponstanding is called postural or orthostatic hypotension.Symptoms are usually due to an impaired autonomicresponse. Traditionally, orthostatic blood pressurereadings and heart rate are measured in the supinepatient then repeated with the patient in a standingposition. A decrease in the SBP of 20 mmHg or in theDBP of 10 mmHg after standing for three minutesdefines orthostatic BP.11 Parameters for abnormalorthostatic increases in heart rate are not well definedbut many have a HR greater than 20-30 beats perminute. Patients with a hypertensive blood pressurewhen supine can be symptomatically orthostatic witha large enough decrease in BP upon standing.

A similar blood pressure drop associated witheating is called postprandial hypotension.

Volume depletion can compound the symptomsfrom an abnormal sympathetic neurocirculatoryresponse but can also be an independent factorcausing orthostasis. Up to 20% of patients over theage of 65 can have orthostatic hypotension. Ofparticular note is the patient with Parkinson’s diseasewho may have primary autonomic dysfunction whichcan easily be exacerbated by dehydration orpolypharmacy.

Determination of orthostasis should be directed bythe patient’s clinical presentation. If symptomatic atrest and supine, orthostatic vital signs are not neces-sary as the patient is already “hypotensive” regardlessof the numbers. If history suggests near syncope orsimilar symptoms with position change prior to ED

presentation, orthostasis is already diagnosed andvital signs after treatment may be more helpful.

Critical Appraisal Of The Literature

Literature searches were performed using OvidMEDLINE and PubMed in the National Library ofMedicine for diagnosis and management recommen-dations as well as updates regarding conditionsinvolving hypotension. In addition, the CochraneDatabase of Systemic Reviews was searched forreviews on similar topics. This search provided anenormous number of studies, though few welldesigned, prospective studies. Another source ofinformation was the National Guideline Clearing-house™ which provided guidelines for sepsis man-agement and ultrasound-guided central line place-ment.

Difficulties arose in finding studies specific on themanagement of undifferentiated hypotension as thistopic covers a clinical sign that manifests in manydifferent clinical situations (including sepsis, dehydra-tion, heart disease, trauma, and many other diseasestates). Sub-topics of fluid management, sepsismanagement, pressor support, ultrasound applica-tions, Advanced Cardiac Life Support (ACLS),Advanced Trauma Life Support (ATLS), and otherswere reviewed and combined to produce recommen-dations for diagnosis and treatment, especially inearly stages of hypotension.

Epidemiology

While it is difficult to determine with accuracy theincidences of hypotension in a general population oreven in a select population of ED or hospitalizedpatients, studies have examined data on critically illpatients and effects of hypotension on outcome.

The duration of hypotension after trauma, sepsis,anaphylaxis, and cardiogenic sources are criticaldeterminants of morbidity, prognosis, and survival inthese groups of hypotensive patients.3

Jones et al performed a secondary analysis of dataaccrued from a randomized, controlled trial of rapidversus delayed bedside goal-directed ultrasound ofpatients with symptomatic, non-traumatic shock. Inthis study, hypotension was defined as an initial EDsystolic blood pressure reading of less than100 mmHg. Shock was defined by the presence ofhypotension with one or more predetermined signs orsymptoms. The hospital mortality of the 190 EDshock patients in this study was 15%. Adversehospital outcomes included organ failure, the need forintensive care admission, and in-hospital mortality.Fifty percent of the patients with a SBP < 80 mmHghad an adverse hospital outcome. Forty percent of thepatients with an adverse outcome had blood pressurereadings that were consistently below 100 mmHg formore than 60 minutes.13

The one month mortality rate after the onset of

Emergency Medicine Practice® 4 November 2007 • EBMedicine.net

hypovolemic shock is dependent on the underlyingcause and the patient’s co-morbidities. A 2002 studyby Moore et al of ED patients with atraumatichypotension (defined as a SBP < 100 mmHg) showedan in-hospital mortality rate of 18%.4 In a recentlyreleased prospective cohort study by Jones et al, EDpatients with a SBP < 80 mmHg had a six-foldincreased incidence of in-hospital death. Patients witha SBP < 100 mmHg for more than 60 minutes hadnearly three times the incidence of in-hospital death.14

Within one month of the diagnosis of septic shock, theoverall mortality rate can be as high as 40%. Mortal-ity for cardiogenic shock can be as high as 60%.15,16

Use of the presence of hypotension alone as apredictor of ED patient mortality is incomplete andrisks ignoring the importance of the associated clinicalcontext. In certain well-defined disease entities (suchas aortic dissection and cardiac failure), hypotensionis associated with sicker patients; thus, there arehigher mortality rates of 50-80%.17 Hypotension inpatients with end-stage renal disease (ESRD) and/oratherosclerotic cardiovascular disease is also associ-ated with higher mortality rates. Consequently, rapididentification of the etiology of the hypotensive statehas a potentially critical impact on the patient’s shortand long term clinical outcome.

Hypotension In TraumaThe ATLS protocols support the practice of usinghypotension as only a late marker of shock because ofits low sensitivity. Prior to 1989, ATLS guidelinestaught that the absence or presence of the carotid,femoral, and radial pulses could be correlated tosystolic blood pressures. When compared to inva-sively obtained arterial blood pressure measurements,however, it was discovered that the correlationspreviously made were overestimations.19 ATLS nolonger teaches pulse and SBP correlations in thecontext of clinical decision making.

The National Trauma Data Bank (n = 115,830),where hemorrhagic shock was the main cause ofhypotension, reports that SBP correlates with serumbase deficits (considered to be a marker of circulatoryshock). The mean and median SBP decreased to lessthat 90 mmHg when the base deficits were worse than-20.20 The Data Bank supports the conclusion thatSBP is a late marker for mortality and that, in thesetting of hemorrhagic shock, SBP should not be usedas a primary decision point in choosing which patientshould receive resuscitation efforts. Patients withhypotension and significant base deficits had amortality rate of 65%.

Pathophysiology

Normal BP results from a balance between the periph-eral vascular resistance and the cardiac output (CO),with total blood volume affecting both. Cardiacoutput is a product of the stroke volume (SV) and theheart rate (HR):

CO = SV x HR

Hypotension results when either the stroke volume orthe heart rate is decreased. In addition, blood volumeprovides the “substrate” that the resistance vessels“push” against in order to regulate BP. Thus, evenmaximal vasoconstriction will be ineffective if volumestatus is inadequate. This key point resurfaces inmanaging many hypotensive patients.

The peripheral vascular resistance (PVR) is regu-lated by a variety of mechanisms. Only a smallproportion of the blood volume is involved in perfus-ing tissues at any given time. Most of the total bloodvolume is contained in the venous system. The veinsserve as blood reservoirs that are mobilized by theneuroendocrine system in time of need. Certainorgans, such as the heart and brain, are autoregulated.Their perfusion is influenced by metabolic factors andnot by the neuroendocrine system. Thus, blood flowis preserved and can actually be enhanced in earlyvolume loss.

Adrenergic receptors are located in organs basedon their function in the “fight or flight” response tostress. Non essential organs in acute stress events(such as the gastrointestinal tract) have high concen-trations of vasoconstrictive alpha-1 (A1) receptors,while those essential to survival in acute stress (theheart, lung, and skeletal muscles) have high con-centrations of vasodilatory beta-2 (B2) receptors.Cardiac beta-1(B1) receptors produce increasedchronotropy and inotropy with consequent increasedoxygen demand. Dopaminergic receptors are prima-rily located in the splanchnic and the renal beds.

These receptors are stimulated by mediator releasefrom nerve endings (norepinephrine) and the endo-crine system (epinephrine). Mediator release isstimulated by the vasomotor centers located in themedulla and hypothalamus. Inhibitory outputs fromcardiac, renal, and blood vessel baroreceptors affectthese centers. Pathological drops in blood pressurecause decreased outputs to be sent from the barore-ceptors, disinhibiting the vasomotor centers. Sympa-thetic nervous system output or tone is thus aug-mented; “vagal tone” is conversely decreased.

In low pressure states, like hypovolemia, there isless baroreceptor stimulation which leads to ADHrelease. The release of ADH leads to: 1) An increase inwater absorption in the distal renal tubules and thenan increase in vascular blood volume; and 2) Periph-eral vasoconstriction. Other mediators that increaseadrenergic tone include carbon dioxide and hydrogenions.

The kidney plays a role in the regulation of bloodpressure through the following mechanisms:

• Glomerular filtration rate (GFR) decreases inhypotension which decreases sodium transittime in the tubules and increases its absorption.In turn, this increases the absorption of water.

• Increased water absorption mediated by ADH inthe distal tubule.

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• Renin release from granular cells of the afferentarteriole stimulated by adrenergic output,macula densa output, and direct action of lowblood pressure on the granular cells themselves.Renin catalyzes angiotensinogen to angiotensin-1 in the liver which is converted to angiotensin-2in the lung by angiotensin converting enzyme(ACE). Angiotensin-2 is a direct vasoconstrictorbut also stimulates the renal cortex to releasealdosterone, further promoting sodiumretention.

• Hypotension causes a decrease in the release ofatrial natriuretic peptides which decreasessodium and water loss in the urine.

Differential Diagnosis

The differential diagnosis of hypotension is vast.Table 1 provides a framework to use when approach-ing these patients.

Prehospital Care

The detection of hypotension prompts urgent trans-port to the nearest or most appropriate ED withconcomitant intravenous access and fluid administra-tion if possible. Advance notification places the EDon alert and facilitates expedited care when thepatient arrives. Patients should receive oxygen, anoxygen saturation monitor should be put in place, andelectrocardiogram (ECG) monitoring begun. If at allpossible, a 12-lead ECG should be performed in anyhypotensive patient who is at risk for acute coronarysyndrome. A cardiac monitor tracing and repeatedvital signs should be recorded clearly and exchangedbetween prehospital and ED personnel.

Jones et al conducted a cross sectional risk assess-ment study of non-traumatic ambulance transports inthe U.S. and Canada.5 Patients experiencing hypoten-sive episodes (a single reading of less than 100mmHg) with one or more predetermined symptoms

or signs of circulatory insufficiency were termed‘exposures.’ ‘Non-exposures’ were those patients withsymptoms of circulatory insufficiency but whoseblood pressure readings were always above100 mmHg. In the U.S. venue, there were 395exposures and 395 non-exposures; the in-hospitalmortality was 26% for exposures and 8% for non-exposures. In the multi-center Canadian venue, thein-hospital mortality rate was 32% for exposurescompared to 11% for non-exposures. This datasupports the association of out of hospital hypoten-sion with in-hospital mortality.

One of the highest risk groups of patients withhypotension are those with an acute myocardialinfarction. 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 ofcare was made available.21 Heightened ED readinesscuts vital minutes off of door-to-ECG to needle orballoon times. Medical control should be notified ofpatients with ischemic ECG findings and considera-tion should be given to transporting these patients toa center with percutaneous interruption capabilities.

The trauma literature is replete with studiesadvocating for ambulance notification and activationof the ED and trauma teams in cases of hypotension oruncontrolled hemorrhage. Trauma team activation hasbeen shown to improve outcomes in patients withpenetrating trauma. In a retrospective study of 180patients, Hooker et al showed that 61% of patientswith prehospital hypotension (defined in this study asSBP < 100 mmHg) required transfusion versus 11% ofpatients without a hypotensive reading in the field.22

Franklin et al showed that not only ED hypotensionbut prehospital hypotension was a bona fide indicatorto activate the trauma team.23 More than half of thepatients with hypotension required urgent operativehemorrhage control. Another study showed that anisolated prehospital hypotensive reading, even withnormal BP readings in the ED, marked the traumapatient for increased mortality and the need foroperative intervention for chest and abdominalinjuries.24

An interesting area of prehospital diagnostics isthe use of portable ultrasound devices to evaluatecardiac output and internal bleeding. Acquiredimages may be transmitted to the receiving hospital.Garrett et al recently showed the transmission ofwireless images to be effective in allowing a hospital-based cardiologist to do a preliminary assessment ofleft ventricular function and the presence or absenceof pericardial effusion.25 Successful transmission ofsonographic images occurred 88% of the time. Thepotential in trauma assessments and abdominal aortascreening in symptomatic patients en route topertinent tertiary care centers is an area of ongoingresearch.

Table 1. Differential Diagnosis Of Hypotension

HypovolemicHemorrhagic DehydrationLow oncotic intravascular pressure (third spacing)

CardiogenicAcute myocardial infarctionArrhythmiasLower stroke volumeInadequate cardiac output

Distributive Septic shockAnaphylaxic and anaphylactoid reactions Blood product transfusions (usually during the transfusion)Drug interactionsDrug overdoses Neurogenic impairment of sympathomimetic responsesAdrenal insufficiency

Emergency Medicine Practice® 6 November 2007 • EBMedicine.net

ED Evaluation

Hypotension is a predictor of negative outcomesregardless of the underlying etiology. Consequently, itis the emergency physician’s responsibility to quicklyidentify and treat underlying causes. A large,prospective study of 6303 patients conducted acrossfive hospital wards in Australia identified hypoten-sion (BP < 90 mmHg), a two or more point decrease ofthe Glasgow Coma Scale, the onset of coma, respira-tory rate less than 6 per minute, oxygen saturation< 90%, and bradycardia for more than 30 minutes aspredictors of mortality.26 Of these predictors,hypotension and oxygen desaturation were identifiedas the most common occurrences prior to cardiacarrest, with hypotension being associated with nearlya seven-fold increase in mortality.

In general, patients with hypotension should beplaced in the critical area of the ED. Oxygenationshould be maximized by placing the patient on 100%oxygen by nonrebreather face mask. Large boreintravenous access should be established, usingcentral access if necessary. An accurate set of vitalsigns should be obtained and frequently repeatedwhile the history, physical, and diagnostic tests areperformed.

The most common causes of hypotension —hypovolemia, cardiogenic shock and sepsis — mayoverlap. Noninvasive measures should be used earlyand frequently to assess oxygen debt, cardiac per-formance, and the overall flow state; see the followingdiscussions. Equally important is the need to monitorthe cardiac and flow state response to the therapiesinitiated. Given the insensitivity of blood pressure toevaluate cardiac output, the correction of bloodpressure is not the only goal.27

Vital SignsBlood pressure is a “vital sign” and must be measuredaccurately. The standard blood pressure is measuredover the brachial artery at the antecubital fossa. Caremust be taken in selecting an appropriate size cuff forthe patient and to ensure proper positioning of thecuff bladder over the brachial artery. When the cuffpressure drops below the SBP, blood audibly passeswith each systole, producing Korotkoff’s sounds.Once pressure drops below the DBP, these soundsdisappear because blood can now pass during bothsystole and diastole.

Blood pressures are often recorded with auto-mated cuffs, and a malpositioned cuff bladder willgive a falsely low reading which may lead to misman-agement if it goes unrecognized.6 Any low BP thatimpacts clinical care should be confirmed with amanual BP measurement. Automated cuff measure-ments have been tested against manual sphygmo-manometer readings and against direct intra-arterialblood pressure measurements. Varied results havebeen obtained.28,29 In a study by Lehman et al,

automated BP readings were compared with centralarterial blood pressure recordings in 120 patients.29

There were clinically significant inaccuracies(± 10 mmHg) in 24% of the automated device record-ings and severe inaccuracies (± 20 mmHg) in 3.2% ofthe automated device recordings. More recent studieshave demonstrated these devices to be of acceptableaccuracy when used correctly. Cavalcanti et alstudied manual cuff readings compared to automatedcuff readings in 92 patients; there was high correlation(within 10 mmHg) in all of the patients.30 Greaterinaccuracies have been found with cuffs that are toosmall, leading to erroneously high BP readings.31-34

Some studies have also examined differences in bloodpressure readings with respect to body position, armposition, and relative resting state of the patient.35-38

Unfortunately, these studies are based on monitoringof hypertension and only very loose inferences can bemade to the hypotensive patient. The best availableevidence suggests that blood pressure measurementsbe taken with the patient in a recumbent position withthe antecubital fossa at the level of the right atriumand that subsequent measurements remain consistentwith this position.

Other vital signs will offer clues to the extent andsource of hypotension and provide a baseline formonitoring the patient. Heart rate will likely beincreased in a hypotensive patient but may be affectedby body position, activity prior to measurement, ormedications (e.g., beta blockers). Orthostatic vitalsigns are rarely needed or indicated in the alreadyhypotensive patient. Respiratory rate, rectal tempera-ture, and pulse oximetry are fundamental to thepatient’s assessment. Of note, hypoperfusion mayinterfere with an accurate assessment of oxygensaturation.

Despite the importance of obtaining accurate vitalsigns, it is important to note that vital signs alonehave limitations in identifying shock states. Ander etal examined the use of lactic acid level and continuouscentral venous oxygen saturation in identifying thedisease severity of patients with acute decompensa-tion of severe chronic congestive heart disease (ejec-tion fraction [EF] < 30%).10 The vital signs did nothelp distinguish the patients with hidden shock states(defined as high lactic acid levels and low centralvenous oxygen saturations) from those with mildlydecompensated or stable CHF. The patients in theshock state required more aggressive treatment forCHF with resultant decrease in lactic acid levels andincreased central venous oxygen saturation.

History The evaluation of the patient with hypotension mustbe comprehensive. Ideally, the patient’s baselineblood pressure must be determined as well as theoverall clinical status. Symptoms that indicate acardiopulmonary cause include but are not limited toprodromal symptoms (such as chest pain, palpita-tions, and dyspnea). Nausea, vomiting, diarrhea, or

EBMedicine.net • November 2007 7 Emergency Medicine Practice®

abdominal pain, as well as hematemesis and melenamay indicate a gastrointestinal etiology. Fever, cough,or dysuria may point to an infectious etiology. Thepotential for an allergic reaction must be assessed aswell as the pregnancy status of women of childbear-ing age. A mental health screening will assess for thelikelihood of drug overdose as the etiology. SeeTables 2 and 3 for possible symptoms and key histori-cal questions.

Searching through medical records for the ‘base-line’ BP and finding multiple low blood pressurereadings during prior hospitalizations or ED visitsshould not lower the concern. These patients weresick enough to need frequent care and hospitaliza-tions. Routine clinic visits are a better source forestablishing a baseline.

Physical Due to the broad differential diagnosis, a thoroughand comprehensive physical examination is necessaryfor the evaluation of the hypotensive patient. Generalnutritional and hydration status should be assessed.During the head and neck examination, signs such assunken eyes, bitemporal wasting, and moisture of themucous membranes should be noted.

Neck examination can reveal the presence orabsence of jugular venous distention (JVD) and givesan early clue to pre-load status. The presence of JVDon a patient with hypotension is a serious finding thatmust be aggressively investigated. Neck vein disten-tion is usually caused by an impaired return ofvenous blood to the right side of the heart or bysignificantly elevated right heart pressures.Conditions that may cause this include pericardialtamponade, constrictive pericarditis, tension pneu-mothorax, right ventricular infarction, massivepulmonary embolism, and air trapping with mechani-cal ventilation. Tracheal deviation with dyspnea canpoint to pneumothorax.

During the chest examination, note the presence orabsence of breath sounds, crackles, wheezes, and areasof dullness or tympany to percussion. The heartexamination can reveal tachycardia, flow murmursindicating cardiac hyperactivity, diastolic and systolicmurmurs which may indicate valve dysfunction, ormuffled heart sounds indicating pericardial effusion.

The abdominal examination may reveal abnormalbowel sounds, bruits, ascites, palpable masses, disten-tion, rigidity, and areas of tenderness pointing topathology that indicates dehydration, sepsis, thirdspacing, or intra-abdominal bleeding.

Extremities may be cool and clammy and exhibitpoor capillary refill or peripheral pulses. Edema mayindicate third spacing or endocrinopathies such ashypothyroidism or adrenal pathology. A careful skinexamination may reveal petechiae, suggesting plateletdysfunction (as seen in a vasculitis) or purpura (asseen in disorders of coagulation).

The neurological examination will be most signifi-cant for arousability and abnormal mental status, butother more focal signs may be present as watershedareas in the brain are affected by decreased cerebralperfusion pressure. Rectal and pelvic exams arerecommended based on clinical suspicion.

Diagnostic Tests

Complete Blood Count (CBC)

White Blood Cell Count (WBC) The WBC rarely contributes to the acute managementof pathologic hypotension. Although high and lowWBC counts can suggest infection, they can alsomerely relate the severity of the insult resulting inhypotension. In 1992, the American College of ChestPhysicians (ACCP) and the Society of Critical Care

Table 2. Potential Symptoms Of Organ Hypoperfusion

Weakness DizzinessFatigue SyncopeAnxiety ThirstSense of doom DyspneaChest discomfort (any description)Confusion (reported by patient or otherwise witnessed)

Table 3. Quick Critical Questions: Key Historical Pointers

Events Immediately Preceding Call for helpEMS evaluation and course

Prior Hypotensive EpisodesNone DehydrationMedication-related GI bleedSepsis CardiacAllergic

Known Medical DiseasesCardiac PulmonaryRenal HepaticCerebrovascular accident PregnancyTransplant recipients HIV/AIDSAutoimmune disease CancerPsychiatric Cognitively impaired

Medication ExposurePrescribedNot prescribed, including herbal medicationsAlterations to medication regimenMedication overdoses (intentional or accidental)Illicit drugsEMS or ED administered (e.g., rapid sequence intubation,

sedation)

Allergy HistoryRecent or suspected exposure (food, medications, latex, etc.)

Coagulopathic StatesWarfarin (after trauma or spontaneous bleeding due to drug

toxicity)Hemophilia A and BThrombocytopenia < 20 KPlatelet dysfunction syndromes: von Willebrand’s disease,

uremia, etc.

Emergency Medicine Practice® 8 November 2007 • EBMedicine.net

Medicine (SCCM) introduced definitions for thesystemic inflammatory response syndrome (SIRS).15

Hypotension and the presence of WBC counts above12,000 or below 4000 were two of the four clinicalfindings used to diagnose the presence of this syn-drome, and both can be present in non-infectiousetiologies (e.g., polytrauma). A single white blood cellcount that is within the normal range does notexclude an infection-related cause of hypotension.The presence of extremely high or extremely lowwhite counts can also reflect the presence of hemato-logic, oncologic, and immune disease. The presenceof neutropenia (absolute neutrophil cell count of lessthan 1000) not only indicates the above, but also theneed for empiric antibiotic treatment when fever ispresent.

Hemoglobin/Hematocrit (H/H) In the setting of suspected hemorrhage, the finding ofa low value helps to make the clinician more confi-dent of his or her diagnosis. However, in the settingof massive rapid hemorrhage, the H/H may appearnormal even though the patient is in extremis. Ifclinical suspicion is high, the test needs to be repeatedover time. The H/H is also helpful in managementdecisions in that transfusion becomes a considerationwhen the hematocrit is less than 30 and you suspectthe patient has sepsis or myocardial ischemia.

Red blood cell (RBC) indices that may be helpfulinclude the mean corpuscular volume (MCV), rangedistribution width (RDW), and reticulocyte count.The MCV is a measure of the average size of redblood cells in the circulation. High or low valuesreflect nutritional deficiencies, drug effects, or red cellhematopoietic dysfunction. When present, thisabnormality does not eliminate the possibility of anacute event; it only suggests the presence of a chronicproblem having been present before the acute one.When many cell lines of different sizes are present, theMCV can erroneously be normal; in which case, theRDW becomes helpful. The RDW is a measure of therange of different sizes of RBC’s present in the bloodstream; its elevation suggests pathology even in theface of a normal MCV. The reticulocyte count ishelpful in determining whether an anemia is hyper-proliferative (high count) or hypoproliferative (lowcount).

Platelet Count (PLT)Platelet count and function must also be assessed inhypotensive patients. Thrombocytosis is rarely ofimmediate clinical concern in that platelet elevationsare commonly seen in many inflammatory or infec-tious diseases, leading to its nickname amongrheumatologists as the poor man’s sedimentation rate.It is also elevated in iron deficient anemia.

Thrombocytopenia is associated with severalserious diseases and is an ominous sign when presentwith hypotension. Thrombocytopenia in the setting ofanemia requires evaluation of the peripheral smear to

detect whether it is actually low and if schistocytes(peripherally shredded RBC’s) are present; a microan-giopathic hemolytic anemia (MAHA) should besuspected in these cases. When MAHA is not due to aconsumptive coagulopathy (discussed later), it is dueto pathologically activated platelets adhering in thecapillary bed with resulting RBC hemolysis andanemia. Toxins elaborated in sepsis and in thromboticthrombocytopenia purpura (TTP) can cause this.

Coagulation ProfileThere are three main reasons to send the InternationalNormalised Ratio (INR) with Prothrombin Time (PT)and Partial Thromboplastin Time (PTT) tests.

• To document the presence of a consumptivecoagulopathy, use INR/PT and PTT plus D-dimer, fibrin split products, and fibrinogenlevels.

• To evaluate coagulation function in the face ofanticoagulants 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 theclotting system. The fibrin produced settles in thecapillary beds and destroys RBCs and PLT's. After-wards, pathologic activation of the fibrinolytic systemproduces the purpura, hemorrhage, and PT/PTTabnormalities that are diagnostic of the condition.Other tests (such as fibrin split products, D-dimer, andfibrinogen levels) are sent when the condition ishighly suspected even in the face of a normal PT andPTT 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 deficienciesIncreased 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 congeni-tal factor deficiencies.

• Screen for the presence of hypo or dysfibrino-genemia, disseminated intravascular coagula-tion, liver failure, and vitamin K deficiency.

D-dimer is very specific for disseminatedintravascular coagulation.

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

EBMedicine.net • November 2007 9 Emergency Medicine Practice®

water balance than actual sodium concentration.Hyponatremia in the absence of diuretics or raresodium wasting nephropathies reflects the retention ofwater in excess of sodium, whatever the cause. It canbe chronic (such as in the syndrome of inappropriateantidiuretic hormone [SIADH]) or acute (as seen whenthere is volume loss of 10% or more). Hypernatremiaalmost always reflects severe dehydrations but withloss of water exceeding salt losses. Potassium eleva-tions reflect either increased or decreased intake orexcretion of potassium or sudden release of intracellu-lar potassium from massive tissue damage.

Bicarbonate and chloride are useful mainly in thecalculation of the anion gap, which can be used togenerate the differential of high anion gap acidosis ornon-anion gap acidosis.

Glucose Serum glucose levels tend to rise in pathologicallyhypotensive patients secondary to excessive cate-cholamine levels. Elevated serum glucose has beenidentified as a prognostic marker in severe illness.39-41

Hypoglycemia without a drug-induced cause isominous and denotes the presence of endocrinopathyor very severe hepatic gluconeogenic dysfunction. Itis a preterminal event in end-stage liver disease.

Liver Function Tests (LFT’s)Transaminases measure hepatocellular integrity.Albumin and PT/PTT reflect the liver’s syntheticfunction; alkaline phosphatase and bilirubin reflectthe liver’s excretory function. It is important to beaware of co-morbidities (e.g., history of hepatitis)when interpreting these tests.

Lactic Acid Normal values for serum lactic acid are usually below0.7 mmol/dL. Lactate levels above 2.1 mmol/dLpoint to severely inadequate multi-organ or extensive

single organ system ischemia (e.g., mesentericischemia).42,43

It does not matter whether the serum lactate is avenous or an arterial sample. In a study of 48 EDpatients, Younger et al showed that venous lactatelevels of 1.6 mmol/dL and higher had a 100% sensi-tivity and an 86% specificity in determining elevatedarterial lactate levels.44,45 A recent study by Jones et alalso determined that venous lactate levels are unaf-fected whether drawn with or without the use of atourniquet or sent to the laboratory on or off ice aslong as the sample is run within 15 minutes.46 Rapidlactate clearance is associated with improved mortal-ity rates and clinical improvement.47

Lactate levels rise in the early stages of sepsisbecause of increased glycolysis and later on because ofdecreased clearance by the liver and the kidneys.Prolonged organ hypoperfusion leads to increasinghypoxia and increased lactate production. Elevatedlactate levels suggest poor organ perfusion and alertthe clinician of impending organ failure. In a studyby Ander et al, vital signs and clinical impressionwere not able to distinguish patients with stable Killipclass IV congestive heart failure (CHF) from thosewith mild versus acute decompensations; however,lactate levels were able to stratify the patients’ sever-ity of illness.10

Electrocardiogram (ECG)An ECG and cardiac monitoring are fundamental tomanaging the patient with hypotension. Table 4 listspossible etiologies of hypotension that may berevealed by the ECG.

Radiologic Testing Plain films (such as the chest x-ray) are useful asscreening tools to confirm already suspected diag-noses of pneumonia or free air and to confirm pasthistory (such as heart failure). CT scanning and other

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, Arrhythmias (primary electrophysiologic cause)sinus rate abnormalities, ventricular arrhythmias, supraventricular

arrhythmias, pacemaker function and malfunction

ST segment elevation morphology (may be similar to non-ischemic Acute myocardial infarction or ischemia stigmatacauses of ST elevation such as benign early repolarization), ST segment depression, T wave depressions

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 Drug toxicity/exposure AV nodal blocking agents, terminal R wave in tricyclic antidepressant overdose, sinus tachycardia or tachyarrhythmia

Wide QRS complexes becoming sinusoidal Hyperkalemia

Emergency Medicine Practice® 10 November 2007 • EBMedicine.net

studies are warranted based on the disease process inquestion. See “Bedside Sonography” on page 15 for adiscussion of ultrasound in the evaluation of thehypotensive patient.

Emergency Department Management

The severity of hypotension is not solely based on thedepth of the numerical reading. The presence of signsand symptoms of organ hypoperfusion and thenumber of organs affected are critical features thatshould be recognized early by the treating physician.Despite our desire to make the correct final diagnosisand initiate definitive treatment, there are situationswhere the time consumed waiting for that diagnosiswould present a danger to the patient’s outcome.Thus, aggressive treatment of the hypotension mustoccur in tandem with its diagnostic work-up. Beyondthe recognition of symptomatic hypotension, there isthe issue of adequacy of treatment. In the Shoemakerstudy cited previously, 76% of patients had meanarterial pressures below 80 mmHg after admission.12

Twenty-four percent of patients that were admittedwere normotensive but subsequently had recurrenceof hypotension. Treatment of the patients was con-sidered suboptimal in most instances because:

• The underlying disease entity associated withthe hypotension was not yet identified

• The underlying disease was erroneously attrib-uted to another etiology

• The resuscitation efforts were late or not suffi-ciently aggressive

Certain basic steps in the treatment of the sympto-matic hypotensive patient are required and areoutlined in Figure 1.

FluidsThe mainstay of early treatment of hypotensionremains intravenous fluid management. Decreasedvascular tone can arise from a myriad of factors, butthe initial attempt at correction should be to increaseintravascular volume in the majority of cases, withexceptions typically stemming from cardiac decom-pensation (such as in left heart failure). Intravenouschallenges of at least 1-1.5 liters or 20-40 mL/kg 48-50

should be given as a bolus and the response moni-tored. The “Surviving Sepsis” protocol recommends“aggressive” use of IV fluids without a specificvolume, highlighting the fact that each patientrequires individualized therapy.51 Adequacy ofhydration can be assessed subjectively withapproximation of CVP via extent of JVD (measured at8-12 cm above the right atrium) or objectively with acentral venous pressure. The caveat to this guidelineis that CVP goals are not always clearly defined. Inthe Early Goal-Directed Therapy (EGDT) article byRivers et al, the CVP target of 8-12 mmHg for patientsin sepsis was not prospectively evaluated. Mostpatients in both the control and treatment groups

reached CVP readings that were higher than the targetrange. Preload assessment is offered by CVP readingsand does not speak accurately to adequate or optimalperfusion of organs in all patients with sepsis.Patients with invasively measured CVP readings ofmore than 8 mmHg may still have signs or directevidence of hypoperfusion. Sepsis patients with CVPreadings that are within the ‘target range’ used in theoften quoted EGDT study may still be hypoperfusedand responsive to fluids; they should not be deprivedof fluid repletion.

The fluid of choice remains an isotonic crystalloidsolution (normal saline or ringer’s lactate).48 Thoughonce in vogue, current evidence does not support theroutine use of colloidal solutions (albumin or het-astarch) in acute resuscitation.49,52-54 Although aplethora of literature exists regarding the use ofhypertonic saline in the management of the trauma orburn patient, advantages over normal saline in themanagement of the medical patient have not beendemonstrated. In a meta-analysis of 14 trials of 956trauma and burn patients and those undergoingsurgery, it was unclear that any benefits existed withthe administration of hypertonic saline.55

TraumaIn bleeding patients with blunt trauma, there is recentevidence that suggests lower volumes of crystalloidshould be used to prevent overdilution of blood andcoagulation factors.56,57 While tamponade of thebleeding may occur in a closed space, there is a fearthat bleeding may increase later if overdilution occurs.Although the data is not conclusive, packed red bloodcells and fresh frozen plasma should be consideredearly in the patient’s treatment in these cases.

In penetrating trauma, terms like “permissivehypotension” or “hypotensive resuscitation” haverecently been advocated.58-62 In essence, numericallylow blood pressures (approximately 70-80 mmHgsystolic) are preferred during early resuscitation ofthese patients so as to not “pop the clot” prior tosurgical intervention. Whether this is due to pureintravascular pressure or to dilution of clottingfactors, a preference for lower intravascular fluidinfusion is established. Care should be taken, how-ever, since target BP’s are not an accurate measure ofend-organ perfusion and any signs of such should stillbe treated aggressively. Additionally, timely transferto the operating room for definitive treatment isneeded in these cases as compensatory mechanismsmay have an effect on the patient’s clinical status andcould collapse with delays in treatment.

PressorsIf fluid resuscitation fails to correct hypotension,pressors become a consideration. The hemodynamiceffects of these agents come from their differentaffinity for the various endogenous catecholaminereceptors. Drug action can also vary from patient to

EBMedicine.net • November 2007 11 Emergency Medicine Practice®

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Emergency Medicine Practice® 12 November 2007 • EBMedicine.net

patient, and various doses of the same medication canhave different actions. The physician must be vigilantin monitoring patients on these agents. Improvementin overall organ perfusion (as determined by clinicalimprovement in symptoms, urine output, centralvenous pressure, lactate clearance, and tissue oxygensaturation) should be the primary goal of therapyrather than merely raising the blood pressure. Thereceptor affinities and actions of these drugs on thevarious hemodynamic parameters are listed inTable 5.

Current critical care and sepsis treatment guide-lines recommend the use of norepinephrine ordopamine as first line vasopressor agents, with aslight bias towards norepinephrine so as to avoidunwanted sinus tachycardia and arrhythmias.63-70 Ifthe hypotension is associated with relative bradycar-dia or primarily a cardiac etiology, then dopaminemay be the preferred pressor. Dobutamine may beadded if cardiac support is necessary (e.g., inotropicsupport) but may worsen peripheral vascular toneand hypotension. If further support is needed in thesetting of cardiogenic shock, the use of an intra-aorticballoon pump may be necessary.

Continuous vasopressin infusion is gainingsupport as an adjunct to other pressor agents specifi-cally in sepsis. A relative vasopressin deficiency hasbeen shown to exist in septic patients, although thisphenomenon may not actually be present until 24-48hours into the clinical course.71-75 Malay et al con-ducted a double blinded, placebo-controlled study of10 septic shock patients receiving either low dosevasopressin or placebo in addition to standard use offluid and other vasopressors and inotropes.57 Thepatients in the vasopressin arm of the study hadincreases in cardiac index and MAP which allowed forthe discontinuation of the other vasopressors andinotropes in that order. The MAP, cardiac index, andSVR were not statistically affected in the placebogroup. Two of the five patients in the placebo arm ofthe study died before 24 hours, but all the patients inthe vasopressin arm survived beyond 24 hours andwere able to maintain MAP above 70 mmHg solely onvasopressin infusions. Landry et al studied 19patients with vasodilatory septic shock and 12patients with cardiogenic shock.76 In 10 of thepatients with low SVR shock states, the mean bloodpressure increased from 92/52 to 146/66 mmHg; the

EBMedicine.net • November 2007 13 Emergency Medicine Practice®

SVR increased from 644 to 1187. Six patients receivinglow dose vasopressin infusion alone had a return tohypotension upon vasopressin withdrawal and animprovement to normotensive state when vasopressinwas restarted. When a vasopressin infusion of 0.04U/min was added to the shock treatment, reactivity toother pressor agents was enhanced; the authorsconcluded that the replenishment of vasopressinallows for the discontinuation of other pressors.Acute use of vasopressin in the ED is still controver-sial but can be considered.

Phenylephrine is also a peripherally acting vaso-pressor but there is limited support for its use and it isnot considered a first line agent. Epinephrine has areputation for potentially worsening vital organperfusion and is not a first line agent, though it doesremain the drug of choice in the treatment of anaphy-laxis. An abstract recently presented by Annane at theSociety of Critical Care Medicine’s 36th Critical CareCongress compared epinephrine to norepinephrine forthe treatment of hypotension. In contrast to tradi-tional thinking, no significant differences were foundin beneficial outcomes or adverse events after 28 days.So-called “renal dose” dopamine is no longer recom-mended as it has been shown to be ineffective inimproving renal function, and improvements in urineoutput are likely due to higher flow states and not tospecific renal bed effects.

Other Adjunctive TreatmentsOther pharmacologic agents for use in sepsis includestress dose steroids and activated protein C. Both arerecommended in current sepsis protocols.51,77 Consul-tation and cooperation with critical care medicine willfacilitate the use of these agents.

Adrenal insufficiency is found in more than half ofpatients in septic shock. Adrenal insufficiency isdefined as non-response to the 250 microgram corti-cotropin test (cortisol increase of less than 9 micro-grams/deciliter). Cortisol maintains vascular sensitiv-ity to catecholamines and helps blunt the endotoxineffect on the heart.

Only a few decades ago, high dose steroidadministration was commonly given to patients withseptic shock. Now, low dose steroids are thought toincrease arterial pressures and decrease the durationof shock. However, most randomized, controlledtrials do not point to any decrease in mortality rates ofseptic shock patients receiving stress dose steroids.78

That being said, no harm has been brought to lighteither. The low dose of glucocorticoids that is recom-mended by sepsis treatment guidelines is 300 mg ofhydrocortisone.51 In a study by Kortgen et al, therewas a significantly improved mortality rate when asepsis bundle that employed an even lower dose ofsteroids (hydrocortisone 150 mg) was used.79 At thecurrent time, based on the best available evidence,hydrocortisone 150-300 mg is indicated in patients inpresumed septic shock that remain hypotensivedespite adequate fluid and vasopressor

administration. In the ED, using dexamethasoneinstead of hydrocortisone offers the advantage of notinterfering with corticotropin stimulation testing afteradmission.

The role of activated protein C (APC) (Xigris®) inthe treatment of septic shock is controversial. Thiscompound has antithrombotic, profibrinolytic, andanti-inflammatory properties. A multi-center, random-ized, placebo-controlled trial of more than 1600patients showed that patients with septic shock whounderwent treatment with APC had a relative reduc-tion in the risk of death, but a statistically significantincreased risk of bleeding.80 APC has been FDAapproved for treatment in patients with severe sepsis,defined as an APACHE II score ≥ 25 or with refractoryorgan/multi-organ dysfunction. (APACHE scorecalculator:http://www.icumedicus.com/icu_scores/apacheIV.php [Lastaccessed June 9, 2007])

Special Situations In ED Management

AnaphylaxisAnaphylaxis is a true pure distributive shock withmediators causing end capillary damage and subse-quent leakage of fluid into the extravascular space.These mediators are responsible for the uncontrolled,uncoordinated vasodilatation seen in anaphylaxis. Apatient in cardiovascular collapse from truly life-threatening anaphylaxis can sequester the equivalentof 50% of their effective blood volume into theirextravascular space within minutes of onset.Treatment of an allergic reaction usually involves theuse of histamine blocking agents and steroids, but inthe setting of anaphylactic shock, the early adminis-tration of epinephrine (1:1000 dilution 1 mg/mL) isnecessary. Intramuscular injections (0.2-0.5 mL) ofthis solution into the thigh every five minutes asneeded is the preferred route, but it can also be givensubcutaneously. If circulatory collapse persists, anepinephrine infusion at 1-4 mcg/min should bestarted. If IV access is unavailable or delayed and thepatient is in extremis, epinephrine may also beadministered via the endotracheal tube with a dosetwo to three times greater than the IV dose (1:10,000solution). If the initial response to epinephrine istransient, repeat bolus dosing may be necessary or thedescribed IV drip at 1-4 mcg/min can be started.

Cardiogenic ShockCardiogenic shock occurs acutely when themyocardium suddenly loses 40% of its function in thepreviously normal heart or when the already diseasedheart loses a lesser percentage over time. Clinicalcriteria for the diagnosis of cardiogenic shock include:

• Systolic blood pressure < 90 mmHg (higher ifchronically hypertensive)

• A urine output < 0.5 cc/kg/hr• Evidence of end organ dysfunction manifesting

Emergency Medicine Practice® 14 November 2007 • EBMedicine.net

as renal failure, confusion, or peripheralhypoperfusion

• Pulmonary capillary wedge pressure > 18 • Cardiac index < 1.8 L/min/m2

Brain natriuretic peptide (BNP) levels are oftenmarkedly elevated in severe cardiogenic hypotensionand the elevations correlate with severity and progno-sis, though treatment in the ED setting rarely relies onthese levels.

Management focuses on relieving fluid overloadon the overworked heart and hemodynamic interven-tions to enhance myocardial pump function (bothpharmaceutical and mechanical when necessary). In ahypotensive patient, small fluid boluses (on the orderof 250-500 cc) are acceptable when the diagnosis isquestionable or to maintain perfusion as a bridge toother interventions.

When hypoxia from respiratory failure is present,early endotracheal intubation is a key intervention.The hypotension in cardiogenic shock precludes theuse of standard congestive heart failure meds (e.g.,lasix and nitrates). In addition to its obvious respira-tory benefits, endotracheal intubation has distincthemodynamic benefits. Positive pressure ventilationdecreases intrathoracic venous return and decreasespreload. With the decrease in right ventricularchamber size, left ventricular expansion is enhancedand forward pump function is enhanced. Myocardialoxygen demand is thus decreased. Intubation alonecan improve cardiac performance by as much as 30%.Ventilatory features such as positive end-expiratorypressure (PEEP), while removing fluid from thealveoli in the lungs, can also relieve hypoxia. Thepositive intrathoracic pressures from these interven-tions may worsen hypoxia.

Pressor support in cardiogenic shock can cause adilemma in treatment. Using dopamine or norepi-nephrine to maintain peripheral pressures may causedangerous increases in heart rate at a time whendecreasing myocardial workload is a key endpoint.Administering other medications that are beneficial tocardiac function (e.g., beta blockers, ACE inhibitors,diuretics) may worsen the hypotension. Inotropes(such as dobutamine or the phosphodiesteraseinhibitors inamrinone and milrinone) used to supportcardiac function may cause peripheral vasodilationand also worsen hypotension. A combination ofpressors and inotropes may be necessary to treat thesepatients and bridge the gap while definitive treatmentis initiated.

Airway And Post-Intubation ConsiderationsEarly intubation in a critically ill patient is a mainstayof ED practice. While providing airway protection,respiratory support, and blood oxygenation, thispractice can have deleterious effects on peripheralblood pressures through medication administrationand side-effects of positive pressure ventilation.Previously normotensive patients who are intubated

may subsequently develop hypotension. One large urban ED study associated subsequent

hypotension with 29% of 84 patients requiring med-ical intubation.81 Though mortality was not increased,13% of these patients required vasopressors and onepatient experienced cardiac arrest. Specific associa-tions were not found to correlate with medications,but hypercarbic COPD and hypoxemic respiratoryfailure showed statistical correlations. These soberingstatistics put the onus on ED physicians to be vigilantfor the occurrence of post-intubation hypotension andto take appropriate steps to prevent it.

Wide acceptance of rapid sequence intubation(RSI) protocols in the ED have greatly facilitated safeand successful airway management. The danger inthe hypotensive patient is the possible arbitrary use ofmedications, as this may worsen the patient’s hemo-dynamic status. For example, induction with benzo-diazepines, propofol, or barbiturates can contribute tohypotension and are not recommended in this patientpopulation. Two useful induction agents are etomi-date and ketamine. Etomidate produces a strongsedative-hypnotic effect but its effects on cardiac andother hemodynamic parameters are less significantthan with many other agents. Unfortunately, etomi-date suppresses cortisol release which may havesignificant repercussions in critically ill patients.82-84

Ketamine presents a very good option in thesepatients. As a dissociative anesthetic agent, thedepressant effects of other RSI medications areavoided while its adrenergic activity may help in BPsupport. Though current recommendations for intu-bation support the use of etomidate plussuccinylcholine, a trial directly comparing the morbid-ity associated with the use of etomidate versusketamine is underway.85

The post-intubation management is criticallyimportant in resuscitating the hypotensive patient.Patients who are marginally compensated mayprecipitously crash during this period. This isbecause intubation can further compromise preloaddue to high intrathoracic pressures associated withmechanical positive pressure ventilation. Positiveend-expiratory pressure (PEEP) can further increaseintrathoracic pressure, and in patients with obstruc-tive pulmonary disease, “auto-PEEP” can climb todangerously high levels. If air-trapping becomes anissue, allowing the lungs to decompress by temporar-ily disconnecting the ventilator can result in a dra-matic improvement in blood pressure. Be aware thatsimilar pathophysiology may occur even in non-invasive ventilatory modalities such as continuouspositive airway pressure and bilevel non-invasiveventilation.

EndocrinopathiesEndocrinopathies can have a profound effect both onthe rapid onset of hypotension and in its treatmentonce it occurs. Thyroxine and cortisol play importantroles in regulating the body’s basal metabolic rate. At

EBMedicine.net • November 2007 15 Emergency Medicine Practice®

the vascular level in the hypotensive patient, thismanifests as a failure of vascular smooth muscle torespond to sudden stresses, producing early cardio-vascular collapse. The problem continues duringtherapy as these patients show impaired responses totherapeutic interventions such as fluids and cate-cholamine infusion. Therapy focuses on vigilance insuspecting an underlying endocrinopathy, whichprompts the ordering of diagnostic tests (e.g., cortisoland thyroid function tests) and/or instituting earlyreplacement therapy. Treatment of severe hypothy-roidism (myxedema coma) not only includes givingthyroid hormone but also stress dose glucocorticoids.Beware of the patient on chronic steroid therapy orwho is adrenally suppressed. Exogenous administra-tion of stress dose steroids is imperative in these cases.As mentioned earlier, septic patients may be relativelyadrenally insufficient and should also receive stressdose steroids.

Bedside Sonography Use In The EmergencyDepartmentThe concept of the “golden hour” is built on strongevidence that the rapid identification of life-threaten-ing conditions and early initiation of time-sensitiveand specific treatments are critical to the patient’sclinical outcome.3-5,13,14,23,51,86-98 This section exploresthe emerging role of ultrasound in diagnosing andmanaging patients with hypotension.

Ultrasound In Hypotension ProtocolUltrasound has been used by physicians to detect lowintravascular volume states, to evaluate cardiacfunction, to evaluate the aorta, and to detect peri-toneal and pleural free fluid accumulations. In onestudy, an average of six minutes (+/- two minutes)was needed to perform a bundle of goal-directedultrasound applications to determine unexplainedhypotension.99 Indeed, the utilization of ultrasound isbecoming more widespread and is being extended tocode response teams in the hospital or to prehospitalteams performing ACLS care.100

Differentiating whether hypotension with orwithout pulmonary edema findings is caused by acardiac (pump) or non-cardiac (non pump) problem isone of the first major steps toward a careful tailoringof the medical treatment during a resuscitation. Theinvasive method of pulmonary artery catheter (PAC)placement and monitoring was compared to informa-tion obtained by performing noninvasive cardiacsonography in a 1994 study by Kaul et al.101 Forty-nine consecutive patients presenting with hypotensionand/or pulmonary edema were evaluated. Earlytransthoracic cardiac sonography data was comparedwith that of pulmonary catheter readings obtainedwithin two hours of each other. Two to three blindedobservers were used for each study. Completeagreement between PAC and cardiac sonography

information was found in 36 (86%) of the 42 patients.There was complete agreement in patients withhypotension alone and 90% of the 20 patients withpulmonary edema alone. The time taken for pul-monary artery catheter placement was 63 +/- 45minutes compared to 19 +/- 7 minutes for compre-hensive two-dimensional echocardiography.

Studies in hypotensive patients support thediagnostic role of ultrasonographic evaluation of theinferior vena cava (IVC) as an indicator of volumestatus. A prospective study of 50 patients by Adler etal identified hypovolemia, unrecognized right heartfailure, and high volume states based on the longitu-dinal views of the IVC using ultrasound.102 Bylooking at the anteroposterior diameter of the IVC andthe respiratory variation in size, one could reliablyestimate central venous pressure. Another studyevaluated the correlation between sonographically-measured proximal IVC diameters, the respirophasicvariations of the IVC size (caval index), and thecentral venous pressures (CVP) that were measuredinvasively. This study showed a definite correlationbetween caval index and central venous pressure.103

An IVC respiratory collapse of more than 50% repre-sents a caval index above 0.5. Eighty-nine percent ofpatients with a caval index above 0.5 had RA pressurereadings above 10 mmHg. Eighty-six percent ofpatients with a caval index below 50% had RApressure readings less than 10 mmHg (Figure 2).

Figure 2. (A) Schematic Of Subcostal Longitudinal View OfInferior Vena Cava. (B) IVC Size And Respiratory VariationCorrelation To Central Venous Pressure Measurements

A B

Using a convenience sample, Randazzo et al foundthat despite good agreement amongst physicians onthe left ventricular ejection fraction (LVEF), there waspoor agreement on patients with low CVP categoriesand strong agreement on the high CVP group.104 Inthis study, CVP was recorded and then the findingwas compared to formal echocardiograms performedwithin a few hours. Bendjelid et al studied 20mechanically ventilated patients having IVC sono-graphic measurements obtained while right atrialpressures (RAP) were measured at the same time; IVCdiameter at end expiration had a linear correlationwith the RAP readings.105,106

Moreno et al studied IVC diameter and respiratoryvariations in 175 subjects; there were 80 controls, 65patients with documented right heart cardiac disease,and 30 patients with cardiac disease but no right heartabnormality.107 The patients with right heart

Emergency Medicine Practice® 16 November 2007 • EBMedicine.net

abnormalities/disease had greater average IVCdiameters and much less respiratory collapsibilitythan the normal subjects or the ones with cardiacdisease without right heart involvement. Eventhough 30 patients were in atrial fibrillation, theauthors found no correlation between IVC size anddynamics and the sex, body surface area, age, andcardiac rhythm of the patients. The size of the IVCwas helpful in the further stratification of CVPmeasurements. The combination of small size andgreater collapse confirmed a low CVP. The combina-tion of an IVC diameter above 2.5 cm and a very low

caval index (barely any respiratory variation) istermed IVC plethora. In this study, plethora of theIVC was associated with CVP readings over 15 mmHg(Figure 3, 4, and 5).

Elevated right atrial pressures, determined byinvasive methods, are associated with a poor progno-sis in patients with pulmonary hypertension, conges-tive heart failure, congenital heart disease, and hearttransplantation. Sonographic findings of IVC plethorawere also associated with poor survival in a study of4385 stable male patients in an outpatient setting. Itwas determined to be an important prognostic findingin the one-year survival rate of patients but less so forthe 90-day survival rate. This was independent of theventricular function, a history of heart failure, otherillnesses, and pulmonary artery pressure readings.108

The prognostic impact of IVC plethora in the unstablepatient with hypotension remains to be determined.IVC plethora should spur a rapid search for a cause ofthe elevated RAP in the hypotensive patient.

In addition to using sonographic IVC diameter as

Note the pericardial effusion (short arrow) between the right atrialwall and the diaphragm. The hepatic veins (cross) branching off ofthe proximal IVC are dilated.

Figure 3. Enlarged IVC With Barely Any Respiratory VariationIn Size: IVC Plethora

Figure 4. Hypovolemia—Small IVC Diameter With LargeRespiratory Variations

Subcostal longitudinal view of IVC. The proximal IVC was amaximum of 0.5 cm with complete collapse with the patient’sinspiratory efforts. The caval index is suggestive of low right atrialpressures or central venous pressures. The pericardial effusion canbe seen between the diaphragm and the atrial myocardialcontractions.

Make measurements about 4 cm away from the IVC/diaphragmjuncture. The liver serves as an acoustic window for the IVC.Distinguish the IVC from the adjacent aorta. Firm transducerpressure is usually needed to displace the bowel gas interferenceof a view of the abdominal aorta but it is important to reducetransducer pressure on the abdomen to avoid compression ofthe IVC.

There is a small pericardial effusion (arrows), but the clinicallysignificant sonographic finding is that the heart chambers aredifficult to distinguish because the endocardial surfaces are veryclose together. This is due to severe hypovolemia. The heart wasable to become hyperdynamic but the poor filling volumes lead to avery low cardiac output. Fluid loss may be evident by history cluesor physical signs, but further goal-directed sonography can be usedto determine if there were any significant internal fluid accumula-tions in the thoracic, peritoneal, or pericardial spaces or potentialsources of cardiovascular hypovolemia (such as finding anabdominal aortic aneurysm or a ruptured ectopic tubal pregnancy).In this case, the patient had severe gastrointestinal bleedingcompounded by warfarin toxicity.

Figure 5. Cardiac Features Of Hypovolemia: Subcostal FourChamber View

Table 6. Estimation Of Left Ventricular Ejection Fraction

Cardiac Ultrasound 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

EBMedicine.net • November 2007 17 Emergency Medicine Practice®

a determinant of volemic status, it has also beenshown to assist in gauging response to therapy.Barbier et al conducted a prospective study of 23mechanically ventilated patients with sepsis-relatedcirculatory failure in an ICU setting.109 The presenceof respiratory variations in IVC diameter at baselineand after fluid boluses demonstrated that IVC disten-sibility could dichotomize fluid responders and fluidnon-responders with a 90% sensitivity and a 90%specificity.

The visual estimation of LVEF can be reportedqualitatively and quantitatively as increased, normal,or decreased (mildly, moderately, or severely)

(Table 6). Estimation of LVEF in the ED has beenshown to be useful in a number of studies.4,99,104

Pericardial effusion detection is best performed byechocardiography as it provides dynamic real-timeinformation on myocardial motion and physiology.Most pericardial effusions are not loculated. The rateof fluid accumulation, the size of the fluid buildup,and the compliance of the pericardial sac will alldetermine when intra-pericardial pressure (IPP)exceeds the right atrial wall pressure. Rapid pericar-dial fluid accumulations will lead to tamponade at alower fluid volume (e.g., stab wounds) than slowaccumulations over months (e.g., uremic effusions).When the IPP exceeds the RAP, it will provoke RAwall invagination or, even worse, right ventricularwall collapse during diastole (tamponade physiology)(Figure 6 and 7).

In summary, some of the Class I recommendationsfor echocardiography by the American College ofCardiology/American Heart Association Task Force onPractice Guidelines for the Clinical ApplicationEchocardiography apply to the patient being cared forin the ED, see Table 7. These indications include, butare not limited to:

• Patients with unexplained hypotension • Patients with dyspnea and clinical signs of

elevated central venous pressure when a cardiacetiology is possible or when a central venouspressure reading cannot be obtained or inter-preted with confidence, especially when cardiacdisease is suspected clinically

• Patients with suspected effusion, tamponade,and/or constrictive physiology

• The assessment of LV size and function withsuspected cardiomyopathy or the suspicion ofheart failure

Applied ED Bedside Ultrasonography

Abdominal Aortic Aneurysm (AAA) When hypotension is present in preoperative patientswith ruptured AAA, there is usually high mortality.110

Suspicion for AAA is heightened when the presentingsymptoms include sudden abdominal pain and

This image was taken in the systolic phase. There is also moderateto low overall left ventricular ejection fraction (determined by visualestimation). This patient has two causes for the symptomatichypotensive state: an effusion with tamponade and poor myocardialcontractility. Though the right sided preload is compromised by thepericardial effusion, it is unlikely that hypotension is due tohypovolemia (the ventricular volume seems adequate). A look at thesubcostal long view may provide more patient specific information;there may be a low IVC diameter and exaggerated respiratoryvariations to a high IVC diameter and poor respiratory variation.

Note the fluid in the pericardial sac that tapers at the atrioventricu-lar sulcus. The heart has a mild swing within the pericardial sacwhich did not show up as electrical alternans on the electrocardio-gram. There is no tamponade physiology.

Figure 6. Apical View Of A Heart With An Effusion AndTamponade

Figure 7. Moderately Sized Pericardial Effusion

Table 7. Key Clinical Questions Addressed by Sonography inthe Severely Hypotensive Patient

Sonographic Clinical Question Answer

Is a pericardial effusion present? Yes or NoIf yes, is it with tamponade? 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® 18 November 2007 • EBMedicine.net

radiation to the back, syncope, or other signs ofclinical shock. The presence of an aortic aneurysm isreliably detected sonographically (Figure 8 and 9).Indeterminate studies are possible due to interferenceby bowel gas. The sonographer can apply firm,steady pressure to the abdomen to displace bowel gasso that the posterior lying aorta can be seen. Thepresence of aortic rupture or leak is not determined byultrasound except if the rupture occurs into theperitoneal 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 DissectionsThe most lethal area of aortic dissection is the thoracicaorta. Involvement in the ascending thoracic aorta canextend through the adventitial layer with rapidaccumulations of blood into the pericardial sac withearly tamponade. Aortic root dilation can lead tosevere aortic insufficiency. Dissections involving theabdominal aorta or the proximal iliac arteries areeasier to detect. Intimal flaps are seen as echogeniclines that move independent of the aortic wall pulsa-tions (Figure 10).

The thoracic aorta (TA) presents a difficult chal-lenge in performing a thorough sonographic evalua-tion. The presence of lungs, ribs, and the naturallyvarying anterior-posterior create impediments toperforming complete studies. The parasternaltransthoracic approach offers a very limited view of aportion of the descending aorta; the left ventricularoutflow tract views provide clues of the most proxi-mal 1-2 cm portion of the ascending TA; the apicaltwo-chamber view may provide a longitudinal viewof a small portion of the descending TA; the supraster-nal views show the aortic arch. Transesophagealechocardiography is the preferred modality forimaging the thoracic aorta.

Pulmonary Embolism: Role Limited To MassivePulmonary Embolism (MPE)In the patient with shock, bedside transthoracicechocardiography evaluation is used to determine ifthere are signs of acute right heart strain; the mostlikely causes are massive pulmonary embolism orright ventricle infarction.111-113 Right ventricularcavity dilation is the right heart’s initial compensation

In this patient, free fluid was detected between the kidney and thecirrhotic shrunken liver. This scan is performed using the sameprinciples as the Focused Applications of Sonography in Trauma. Inthis apparent atraumatic setting, this hypotensive patient—with aknown history of mild ascites—had a more distended, painful, andtender abdomen (both new). Upon further questioning, he men-tioned falling three days earlier. Hemoperitoneum was the cause ofhis hypotension.

The history on this patient was notable for the abrupt onset ofabdominal pain, diaphoresis and near syncope. The cardiacultrasound revealed a partially empty heart, normal cardiaccontractions, and no pericardial effusion. It was very likely thathypovolemic shock was the etiology and evidence of hemorrhagewas sought. The pleural and peritoneal cavities did not reveal anyfree fluid. The abdominal ultrasound study found an abdominalaortic aneurysm. A thrombus was attached to the inner anterior andlateral walls. After urgent vascular surgical notification, the patientwas in the operating suite 12 minutes after the ED arrival time.

Figure 8. Free Fluid In The Abdomen

Figure 9. Abdominal Aortic Aneurysm With Thrombus

The diameter of the abdominal aorta in this patient is less than2 cm. There is no thrombus, but note the thin mobile echogenicintimal flap extending from the 12 o’clock to the 6 o’clock position.Such a finding should prompt the physician to image the thoracicaorta with either echocardiography and/or CT to verify if the moreurgent cardiothoracic surgery intervention is required.

Figure 10. Transverse View Of The Abdominal Aorta

EBMedicine.net • November 2007 19 Emergency Medicine Practice®

to severe pulmonary artery occlusion. The rightventricle is distended and also hypokinetic. The apexof the inner normal right ventricle is usually sharp,but with acute RV strain, it will become blunted. Theright ventricle is usually 60% of the diameter of theleft ventricle when measured in diastole. When theRV diameter to LV diameter ratio approaches orexceeds 1.0, the diagnostic certainty of acute RV strainis increased. The McConnell sign (hypomotility of RVfree wall with apical sparing) has been used as arelatively unique sonographic feature of significant PE(Figure 11).

The buildup of right ventricular pressures mayexceed that of the left ventricle, provoking a bulge ofthe septal wall into the LV cavity. True pressureoverload is distinguished from RV volume overloadby evaluating the septal distortion during systole anddiastole. In RV volume overload, the septal wall isflattened during diastole, but the greater LV systolicpressure returns the septal wall to its normalappearance. In RV pressure overload, the intraven-tricular septal wall may be flattened or pushed intothe LV during diastole. During systole, the intraven-tricular septum remains flattened or deviated into theLV. High RV wall stress eventually compromisescoronary blood flow to the inner RV myocardium andendocardium. The RV myocardial ischemic insultsfurther compromise the already weakened RV output.Diastolic filling of the left ventricle is reduced by theleftward bulge of the ventricular septal wall. Thereduced volume of already poorly oxygenated bloodleads to poor perfusion and oxygen delivery tomultiple organs.

RV dysfunction by cardiac ultrasound is not spe-cific for PE in that it can also be found in primarypulmonary hypertension, RV infarction, acute

exacerbations of COPD, and in certain cardiomy-opathies. In addition, RV dysfunction has beenreported by cardiac ultrasound in 40% of patientswith PE but no significant hemodynamic stability.Twenty percent of cases of diagnostically confirmedPE have normal echocardiographic findings. Sono-graphic RV dilation and hypokinesis in a patient thatis unstable suggests PE and drives the need fordefinitive study.114,115 Performing bedside ultrasoundcan be difficult in patients with obesity, hyperinflatedlung states, and those who are immobile and onmechanical ventilator support.

The hypotension that results in pulmonaryembolus is usually responsive to preload increasesand the use of vasopressors to augment coronaryperfusion of the myocardium. The best treatmentoccurs with a reduction of the pulmonary artery

This frame shows the right ventricle (arrow) size compared to theleft ventricle (measured at the level where mitral leaflets touch)during systole. The RV is dilated and larger than the LV. The free RVwall barely moved while the LV contracted; the ventricular endsystolic diameter and volume decrease shows strong LV perform-ance. Hypomotility of the RV is caused by right sided pressureincreases and/or a right ventricular infarction. Though a pulmonaryembolism was not definitively detected, acute right heart strainwithout signs of preexisting right or left heart strain is caused byvery few entities. Courtesy of Sarah Stahmer, MD.

Figure 11. Right Ventricular Dilation

A sterile probe cover and gel allow direct sonographic guidance ofvascular access and cannulation. The short axis view of the targetvessels allows needle placement. A long axis approach is anotheroption. Vascular access with sonographic guidance may also beused for peripheral vein cannulation, arterial and venous bloodsampling, and transvenous pacemaker line insertion and positioning.

In this cross sectional view of the internal jugular vein (and thecarotid just behind it), the anterior aspect of the internal jugular veinis indented. Reverberation artifact, caused by the metallic needle asit crosses the US beam, shoots down the monitor’s screen.Courtesy of Resa Lewiss, MD, RDMS.

Figure 12. Vascular Access With Sonographic Guidance

Figure 13. Cross Sectional View Of The Internal Jugular Vein

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occlusion by inherent thrombolysis, prevention offurther thromboembolic events with heparin, and —most effectively — the use of thrombolytic agents orpulmonary thromboendarterectomy.

Vascular AccessWell designed, randomized, controlled trials havecompared ultrasound-guided vascular cannulation tothe traditional anatomic landmark based vascularaccess.116 Vascular access is particularly more difficultin the patient with hypotension or cardiac arrest.117

Arterial pulsations may already be too faint toprovide guidance. In addition, the anatomic relation-ships of the femoral and neck vessels may vary thuscompounding the potential for errors. Prolonged andmultiple attempts, the development of complications,and failure to attain access will delay the administra-tion of time-sensitive medications and fluids. Ultra-sound-guided peripheral vascular access may bebetter and safer than central venous cannulation,especially in patients with coagulopathies wherevessel compression may be critically important(Figure 12 and 13).

Controversies / Cutting Edge

Hemodynamic MonitoringThe resuscitation literature points towards earlyaggressive management as being key to alteringoutcomes in patients with pathologic hypotension.This awareness has resulted in increased pressure toinitiate therapy in the ED and provide close monitor-ing. Static hemodynamic reports do not accuratelypredict the patient’s responsiveness to fluid adminis-tration or their actual clinical improvement.119 Forexample, while most patients with sepsis are discov-ered to be in a hyperdynamic state, this may be anearly compensatory response.99 The patient withseptic shock with a hyperdynamic LV on bedsideultrasound can have LV dysfunction several hourslater, especially if the patient has pre-existing cardiacdisease. RV dysfunction can also be present in asmany as one-third of patients with sepsis. Continu-ous monitoring of RV function is extremely helpful forthe assessment of cardiac and respiratory function andin response to treatments and interventions.

Measurement of cardiac filling pressures andpulmonary artery occlusion pressures are generallyused in more intensive care settings and requirehighly invasive procedures (e.g., central venouspressure readings and right heart catheterization).With normal CVP readings between 6-12 cm H2O, lowor high readings can help differentiate betweenhypovolemic states, cardiac failure, obstructiveetiologies, and/or hypervolemic states.

Right heart catheterization (RHC) and pulmonaryartery catheters (PAC) are more complicated and areused for occlusive pressure measurements. Furtherdata can be obtained with this modality, especially

when determining if pump failure primarily involvesthe left heart (e.g., decompensated CHF) or the rightheart (e.g., right ventricular MI or other obstructivepathology). A meta-analysis of several randomized,controlled trials showed that early (prophylactic) useof PAC-directed therapy aimed at tissue perfusionresulted in a marked improvement in patient out-come.120 Other RCT studies in the meta-analysis,however, showed that there were no outcomeimprovements when PAC-directed therapy was usedin ICU patients after organ failure and sepsis had setin. This was corroborated in other studies.121 In aprospective cohort study of 5735 critically ill patients,there was no patient group in which RHC demon-strated improved patient outcome. However, RHCwas associated with increased mortality, length ofstay, cost of care, and resource utilization.122 In a busyED, the practicality of using invasive monitoring isseverely limited by patient flow, inordinate amount ofprocedure time, and staffing issues; thus, it is notrecommended.

Fortunately, some noninvasive techniques showpromise; as they become more readily available, thesetechniques will allow the emergency physician tomore easily deliver goal-oriented treatment. Bioim-pedance monitors for cardiac output, transcutaneousoximetry, and capnometry for tissue perfusion inconjunction with pulse oximetry and blood pressuremeasurement have been shown to be accurate whencompared to the same information typically obtainedthrough a right heart catheter.8,123-125

Shoemaker et al studied the use of noninvasivemethods in 151 severely injured patients using thecontinuous monitoring of certain cardiac pulmonaryexchange and tissue perfusion parameters. Cardiacindex and tissue oxygenation measured in thismanner were significantly higher and well above“optimal” levels (as defined in the study) in survivorsas compared to non-survivors.126

Further support for the more expansive and earlieruse of non-invasive hemodynamic monitoring wasprovided by a study of 680 critically ill patients. Newbioimpedance methods for estimating cardiac outputcombined with arterial BP, pulse oximetry, andtranscutaneous PO2 and PCO2 were equivalent tothermodilution invasive data. The bioimpedancemonitor was able to detect low flow states and poortissue oxygenation early. Lower tissue oxygenationand higher tissue CO2 levels were significantly moreprevalent in the non-survivors.124

Limitations of the thoracic bioimpedance instru-ments may include improper lead positioning, motionartifacts due to tremors, restless patient movements,and patient disease-related conditions like pulmonaryedema, pleural effusions, valvular disease, andarrhythmias. With proper implementation of theseinstruments, however, better outcomes can be accom-plished through earlier diagnosis and treatment ofindividuals at risk for developing hypotension andshock before late effects on the vital signs are seen. As

EBMedicine.net • November 2007 21 Emergency Medicine Practice®

this technology becomes more widespread, additionaltraining in this monitoring will be necessary foremergency physicians, nurses, and other healthproviders in the ED.

Algorithmic Treatment Of Hypotension And ShockWith accurate monitoring of hemodynamic parame-ters and tissue perfusion, algorithms can be developedto directly address sub-clinical signs of poor tissueperfusion. The use of algorithms in managinghypotension is not a new concept. In 1983, a retro-spective study of fluid resuscitation in 603 patientswith hypotension was identified.12 This was a caseseries of patients with hypotension who were resusci-tated with either a fluid administration algorithm or

on the individual physician’s preferences. A chartreview showed that even with this specific clinicalguideline, compliance with the algorithm was subop-timal. There were significant delays in the start offluid challenges and many steps in the algorithm werenot followed. There were 114 deaths (19% mortality)in the study group. Significant comorbidities werepresent in 265 (44%) of the hypotensive patients.Forty-four patients in this subgroup developed severeshock-related organ dysfunction. These patients had ahigher mortality rate, more severe hypotension (lowermean arterial pressures), and more challenging andprolonged resuscitations. They also seemed to havenoticeably more delayed starts to the resuscitationefforts after hypotension was recognized. The authors

Risk Management Pitfalls For Hypotension

1. Assuming that an ashen, lethargic patient is nothypotensive because he has a good bloodpressure of 120/80 mmHg.Treating the number rather than the patient cancause you to miss the hypotensive state. Treatthe patient; this patient is hypotensive. The BP iswell below baseline and he looks terrible for now.It might get worse. Cardiac dysfunction andtissue ischemia can persist despite normalizationof BP, heart rate, and CVP.

2. Inadequate workup of the underlying etiology.Establishing adequate urine output with fluidboluses won’t stop bleeding from a gastric ulceror ruptured aorta. Giving antibiotics for a feverwon’t be effective if a gangrenous gallbladderremains undiagnosed.

3. Inadequate fluid loading.Look for low CVP signs, evaluate urine output,and monitor cardiac output response to fluidadministration. Tissue perfusion is your goaland cardiac output is usually the key to achiev-ing this. A hyperdynamic heart is attempting tocompensate for a low ventricular volume.

4. Delaying ventilator assistance.Improved ventilation and oxygen delivery to thelungs and ultimately the organs puts lessdemand on the heart and reduces the oxygendebt.

5. Overaggressive resuscitation without factoringin the wishes of the patient or family.A respectful and cost-effective treatment planmay hinge on getting these important pieces ofinformation.

6 . Discontinuing monitoring after a “good bloodpressure” is reached.

The BP is a single and imperfect parameter inassessing the patient’s volume and circulatorystate. Multiple tools may be necessary to assesstissue perfusion and changes in cardiac output.In some patients, there is an improvement in theblood pressure, a normalized pulse rate, and nomore postural dizziness after fluid administra-tion for self-limited diarrheal illness. Anotherpatient may have an improvement in the BP to120/80 but still feel weak and short of breathbecause the LVEF is 20%, or the pericardialeffusion remains undiagnosed, or the tissueoxygen debt state remains unpaid.

7. Allowing slow tests to guide management.Do not wait for the creatinine and D- dimer tocome back before getting the CT; do not wait forthe CXR to see if the mediastinum is wide or ifthe heart is large.

8. Discounting the possibility of orthostatichypotension as the primary etiology in theelderly patient with supine hypertensivereadings.

9. Ignoring the role and use of bedsidesonography in hypotension resuscitation.The rote use of fluid then vasopressors andinotropic agents may not help and can worsensome clinical processes. Hypotension is not adisease or even a syndrome to be fixed. It is asign that something is going wrong. You justhave to figure it out quickly and carefully. Goal-directed sonography accurately addresses manydangerous and time sensitive clinical questions.

10. Not re-evaluating hemodynamic profiles.RV, LV function, and preload status can changeeven when you do the right things.

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concluded that in circumstances where there were lessdeviations (or more compliance) from the fluidresuscitation guideline, the resuscitation efforts wereshorter and there were fewer shock-related problems.Improved clinical outcomes included lowered mortal-ity, shorter intensive care unit (ICU) length of stay(LOS), and less total time spent in the hospital. Thepatients with severe comorbid conditions were morelikely to succumb to death and complications. Invarious other studies, better outcomes in terms ofduration of hypotension, ICU and hospital stays, andoverall mortality were also achieved with the use ofalgorithms.50,127-129

Recombinant Factor VIIaThere has been recent study of the use of rFactor VIIato control bleeding during surgery. Of particular noteto emergency physicians is its use in bleeding traumapatients. This medication is used to induce clottingspecifically at the bleeding site and has particular usein blunt trauma and intracerebral hemorrhage, twoentities that are not so rare in an ED setting. Currentusage is recommended only in refractory bleedingand most case reports show its use as a “last-ditch”effort to control bleeding.130-133 Because of its pro-

coagulant properties and the relative lack of com-pleted randomized, controlled trials in its use, it canonly be recommended with a Class III designationuntil further information is received.134 There is nosignificant literature to support its use in medicallybleeding patients and it may actually be contraindi-cated because of the typical multi-system disease inthese patients.

Cost- And Time-Effective Strategies In The Workup Of Unexplained Hypotension

1. Keep bedside ultrasound available to answerfocused questions on global heart function andvolume status. Signs of vascular catastrophes,massive pulmonary embolism, and tension pneu-mothorax can also be sought without interruptingresuscitation efforts.

• Don’t use the CXR to rule out aortic dissection,pericardial effusion/tamponade, or cardiomyopa-thy based on a mere silhouette.

• Don’t wait for the CT and the serum creatinine todetermine if a high suspicion AAA is present orabsent.

1. It is necessary to use/acquire the bedside tools thatnoninvasively and accurately assess cardiac output,CVP, and tissue oxygenation as part of the resusci-tation in the hypotensive patient. Ultrasonographyis the ideal modality—it only takes a few minutesto get crucial accurate information on heart func-tion and major vascular integrity. It also allowssafer and quick access for medication administra-tion and guidance of invasive procedures.

2. Consider it a ‘red flag’ when patients have pre-hospital episodes of hypotension.

3. Improving multi-organ tissue oxygenation is yourmain goal. Monitor for signs of oxygen debt:hypoxia, metabolic acidosis, transcutaneousoxygen deficits, and elevated lactate levels. Thehemoglobin level may need supplementation ifinadequate.

4. Patients with hypotension do not usually fitexclusively in one category of etiology of hypoten-sion or shock. Therefore, the treatment is multi-pronged.

5. Time is of the essence. Hypotension is a latefinding and fixing it does not mean you correctedthe state of organ dysfunction that set in.

6. Repeat hemodynamic profiles regularly and in

response to changes, especially deteriorations, andafter major therapeutic interventions are put intoeffect (including fluid boluses).

7. Finding the source of hemorrhage or infection isthe first management step:

a. Thoracic: consider chest tube, endobronchialtamponade, interventional radiology involve-ment for vessel identification, embolization,etc., and surgical intervention if lobectomy isindicated.

b. Gastrointestinal: consider endoscopic varicealtamponade.

c. Consider surgery for aortic rupture, splenicrupture, and massive colonic bleeding.

d. Reverse bleeding tendencies.

8. Oxygen delivery in the critically ill patient withhypotension often requires intubation. Usemedications such as etomidate and fentanyl thatdo not cause hemodynamic deterioration. Con-sider ketamine for SBP improvement. Carefullyadminister induction agents (consider loweringthe dose) in any patient with a tenuoushemodynamic profile.

Key Points For Hypotension

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2. Assess cardiac dynamics and CVP estimates before,during, and after fluid and catecholamine support.Well designed studies support the use of goal-directed echocardiography in the hypotensive EDpatient.

3. Use crystalloid solutions for fluid resuscitation. Nooutcome improvements are in the current literaturethat justify the use of more expensive colloidalsolutions in the USA. Goals may include: CVPimprovement, cardiac index improvement, ade-quate urine output, and lactate clearance.

4. Organ hypoperfusion can be occult; aggressivelyseek to get clues using noninvasive monitoring suchas tissue oxygen saturation, central venous oxime-try, and lactate levels.

5. Use hypotension as a threshold point, not as a goal.Address multiple factors that may impact hypoten-sion and, more importantly, organ hypoperfusion.

Disposition

Because of the high morbidity and mortality associ-ated with hypotension regardless of etiology, thereshould be a low threshold for admission. Ultrasoundmay be a useful tool in directing the disposition. TheFocused Assessment of Sonography in Trauma (FAST)application allows the direct triage of hypotensivetrauma patients with positive FAST findings totherapeutic laparotomy without the use of CTimaging.135

In the new age of ED over-overcrowding (not atypo) the solution to high patient acuity and volumeshould not prolong critical care in the ED. Step downunits and expanding ICU’s help redirect resources andEM expertise to the next patient demanding answersfor their unexplained hypotension. The Acute Physi-ology and Chronic Health Evaluation (APACHE) II,the Simplified Acute Physiology Score (SAPS), and theHypotension Score were all created as prognosticatorsof patient outcome or severity of disease and have thepotential to guide ICU care.136

Case Conclusion

The first patient had deepening hypoxia (despite properendotracheal intubation) and was given antibiotics becauseof the fever and the elevated serum leukocyte count. Noobvious infectious source was evident. Bedside cardiacultrasound showed no pericardial effusion but did revealincreased left ventricular function, a distended thin walledright ventricle, and leftward septal wall deviation. The IVCwas distended and showed poor respiratory motion. Therewas no obvious IVC or intracardiac mass or clot. The bloodpressure was refractory to 2 L of IV crystalloids, and afterdiscussion with the critical care team, pulmonary embolismwas considered to be the likely cause of the acute right heartstrain. TEE confirmed the finding of pulmonary artery

thrombus, and thrombolytic agents were given.The second patient had rales and fluid administration

that led to more shortness of breath and yet anotherendotracheal intubation. Furosemide did not help and thedialysis center did not respond. The ECG was unimpres-sive and the patient, who was paralyzed and sedated,remained hypotensive and tachycardiac. You consideredinotropic or vasopressor support but then remembered thatthe new ultrasound was delivered yesterday. Theabdominal aorta appeared to be no more than 2 cm indiameter but you noticed an intimal flap. The heart alsohad a small pericardial effusion and an intimal flap next tothe aortic valve. The patient was taken to the OR where hesurvived a thoracic aorta repair.

The third patient also had rales. The heart wasenlarged on CXR. The lungs were mildly congested.Ultrasound showed a small pericardial fluid and barely anymyocardial activity overall with an ejection fraction of 10%at most. The IVC was thick and stayed the same after thepatient took in a quick and deep breath. She was quicklyput on dobutamine and fell asleep an hour later for the firsttime in weeks. A repeat echo showed an EF of 20% and thepatient appeared remarkably better—you left the shiftexhausted but a confirmed believer in the value of bedsideultrasound.

Summary

In an age when we are held to a higher standard ofbeing “Better, Faster, and Surer,” the sheer volume,increasing complexity, and higher acuity of EDpatients make the management of patients morechallenging than ever before. The early recognition ofclinical hypotension, the rapid initiation of goal-directed resuscitation, and the early use of accuratediagnostic tools remain the cornerstone to reducingmorbidity and mortality of hypotensive patients.Rapid identification of clinical hypotension should befollowed by the rapid and confident diagnosis of theprimary and contributory etiologies. The correction ofthe primary disorders must occur in parallel to thediagnostic workup to avoid adverse patient out-comes—a rather tall order for the EM physician.Using the tools that are available to us early, beforefurther deterioration of the critically ill patient, putsus one step closer to achieving that goal.

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Evidence-based medicine requires a critical appraisalof the literature based upon study methodology andnumber of subjects. Not all references are equallyrobust. The findings of a large, prospective, random-ized, and blinded trial should carry more weight thana case report.

To help the reader judge the strength of eachreference, pertinent information about the study, suchas the type of study and the number of patients in thestudy, will be included in bold type following thereference, where available.

Emergency Medicine Practice® 24 November 2007 • EBMedicine.net

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38. Netea RT, Smits P, Lenders JW, Thien T. Does it matter whetherblood pressure measurements are taken with subjects sitting orsupine? 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 prospec-tive 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 traumapatients. J Trauma. May 2004;56(5):1058-1062. (Prospective; 516patients)

41. Sung J, Bochicchio GV, Joshi M, Bochicchio K, Tracy K, Scalea TM.Admission hyperglycemia is predictive of outcome in critically illtrauma patients. J Trauma. Jul 2005;59(1):80-83. (Prospective; 1003patients)

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45. Lavery RF, Livingston DH, Tortella BJ, Sambol JT, Slomovitz BM,Siegel JH. The utility of venous lactate to triage injured patients inthe 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, andtourniquet use on whole blood venous point-of-care lactate concen-trations. Acad Emerg Med. Jul 2007;14(7):587-591. (Prospectivestudy, 80 patients)

47. Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance isassociated with improved outcome in severe sepsis and septicshock. Crit Care Med. Aug 2004;32(8):1637-1642. (Prospective obser-vational 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) inpediatric 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. [Comparisonof the effects of colloid and crystalloid solution for volume pre-loading on maternal hemodynamics and neonatal outcome inspinal anesthesia for cesarean section]. Masui. Sep 2004;53(9):1019-1024. (Randomized controlled trial; 32 patients)

50. Trzeciak S, Dellinger RP, Abate NL, et al. Translating research toclinical practice: a 1-year experience with implementing early goal-directed 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 SepsisCampaign guidelines for management of severe sepsis and septicshock. Crit Care Med. Mar 2004;32(3):858-873. (Consensus state-ment; Practice guideline)

52. Sand IC, Jagoda A, Vukich D. Maintenance fluids in prehospitalcare: crystalloid versus dextrose solutions—is there a difference? JEmerg 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 illpatients. Cochrane Database Syst Rev. 2004(4):CD000567. (Meta-analysis)

54. Alderson P, Bunn F, Lefebvre C, et al. Human albumin solution forresuscitation 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 iso-tonic crystalloid for fluid resuscitation in critically ill patients.Cochrane Database Syst Rev. 2004(3):CD002045. (Meta-analysis)

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65. Holmes CL. Vasoactive drugs in the intensive care unit. Curr OpinCrit Care. Oct 2005;11(5):413-417. (Review)

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74. Hall LG, Oyen LJ, Taner CB, et al. Fixed-dose vasopressin com-pared with titrated dopamine and norepinephrine as initial vaso-pressor therapy for septic shock. Pharmacotherapy. Aug2004;24(8):1002-1012. (Comparative study; 150 patients)

75. Lim TW, Lee S, Ng KS. Vasopressin effective in reversing cate-cholamine-resistant vasodilatory shock. Anaesth Intensive Care. Jun2000;28(3):313-317. (Case report)

76. Landry DW, Levin HR, Gallant EM, et al. Vasopressin deficiencycontributes to the vasodilation of septic shock. Circulation. Mar 41997;95(5):1122-1125. (Comparative, clinical observation; 19patients)

77. Annane D, Bellissant E, Bollaert PE, Briegel J, Keh D, Kupfer Y.Corticosteroids for treating severe sepsis and septic shock. CochraneDatabase Syst Rev. 2004(1):CD002243. (Review; Meta-analysis)

78. Prigent H, Maxime V, Annane D. Clinical review: corticotherapy insepsis. Crit Care. Apr 2004;8(2):122-129. (Review)

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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; 2640patients)

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81. Franklin C, Samuel J, Hu TC. Life-threatening hypotension associ-ated with emergency intubation and the initiation of mechanicalventilation. 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 corti-sol response to ACTH in the critically ill: a retrospective cohortstudy. Crit Care. May 24 2007;11(3):R61. (Retrospective; 405patients)

83. Mohammad Z, Afessa B, Finkielman JD. The incidence of relativeadrenal insufficiency in patients with septic shock after the admin-istration of etomidate. Crit Care. 2006;10(4):R105. (Retrospective;152 patients)

84. Zhang Y, Luo A, An G, Huang Y. [Effect of propofol and etomidatefor 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 SequenceIntubation: Consequences on Hospital Morbidity (KETASEDstudy). 2007. (Study in phase IV- patient enrollment)

86. Wood KE. The presence of shock defines the threshold to initiatethrombolytic 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 pathophysio-logic approach to the golden hour of hemodynamically significantpulmonary embolism. Chest. Mar 2002;121(3):877-905. (Review)

88. Sharma VK, Dellinger RP. Recent developments in the treatment ofsepsis. Expert Opin Investig Drugs. Feb 2003;12(2):139-152. (Review)

89. Schwartz B, Vermeulen MJ, Idestrup C, Datta P. Clinical variablesassociated with mortality in out-of-hospital patients with hemody-namically significant bradycardia. Acad Emerg Med. Jun2004;11(6):656-661. (Retrospective; 247 patients)

90. Kumar A, Roberts D, Wood KE, et al. Duration of hypotensionbefore initiation of effective antimicrobial therapy is the criticaldeterminant of survival in human septic shock. Crit Care Med. Jun2006;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 PulmonaryEmbolism Registry (ICOPER). Lancet. Apr 24 1999;353(9162):1386-1389. (Prospective outcome; 2454 patients)

92. Ginde AA, Rhee SH, Katz ED. Predictors of outcome in geriatricpatients with urinary tract infections. J Emerg Med. Aug2004;27(2):101-108. (Retrospective; 284 patients)

93. Farooq MM, Freischlag JA, Seabrook GR, Moon MR, AprahamianC, Towne JB. Effect of the duration of symptoms, transport time,and length of emergency room stay on morbidity and mortality inpatients with ruptured abdominal aortic aneurysms. Surgery. Jan1996;119(1):9-14. (Retrospective; 124 patients)

94. Chan L, Bartfield JM, Reilly KM. The significance of out-of-hospitalhypotension in blunt trauma patients. Acad Emerg Med. Aug1997;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 strokeis associated with brain injury and poor stroke outcome. Stroke. Feb2004;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. Apr2005;33(4):780-786. (Randomized control trial; 28 patients)

97. Fine MJ, Smith MA, Carson CA, et al. Prognosis and outcomes ofpatients with community-acquired pneumonia. A meta-analysis.Jama. Jan 10 1996;275(2):134-141. (Meta-analysis)

98. 2005 American Heart Association Guidelines for CardiopulmonaryResuscitation and Emergency Cardiovascular Care. Circulation. Dec13 2005;112(24 Suppl):IV1-203. (Clinical guideline; Consensusstatement)

99. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy ofleft ventricular function for identifying sepsis among emergencydepartment patients with nontraumatic symptomatic undifferenti-ated hypotension. Shock. Dec 2005;24(6):513-517. (Randomized con-trol trial; 103 patients)

100. Niendorff DF, Rassias AJ, Palac R, Beach ML, Costa S, GreenbergM. Rapid cardiac ultrasound of inpatients suffering PEA arrest per-formed by nonexpert sonographers. Resuscitation. Oct2005;67(1):81-87. (Comparative study; 5 patients)

101. Kaul S, Stratienko AA, Pollock SG, Marieb MA, Keller MW, SabiaPJ. Value of two-dimensional echocardiography for determiningthe basis of hemodynamic compromise in critically ill patients: aprospective study. J Am Soc Echocardiogr. Nov-Dec 1994;7(6):598-606. (Prospective, comparative study; 49 patients)

102. Adler C, Buttner W, Veh R. [Relations of the ultrasonic image of theinferior vena cava and central venous pressure]. Aktuelle Gerontol.Nov 1983;13(6):209-213. (Prospective, comparative study; 50patients)

103. Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation ofright atrial pressure from the inspiratory collapse of the inferiorvena 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 emer-gency physician assessment of left ventricular ejection fraction andcentral 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 thescale to measure the central venous pressure swing? Intensive CareMed. 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 andright atrial pressure depends on the echocardiographic methodused in patients who are mechanically ventilated. J Am SocEchocardiogr. 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 venacava as an index of right-sided cardiac function. Am J Cardiol. Feb 11984;53(4):579-585. (Prospective study; 175 patients)

108. Nath J, Vacek JL, Heidenreich PA. A dilated inferior vena cava is amarker 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 infe-rior vena cava diameter are helpful in predicting fluid responsive-ness in ventilated septic patients. Intensive Care Med. Sep2004;30(9):1740-1746. (Prospective; 23 patients)

110. Gloviczki P, Pairolero PC, Mucha P, Jr., et al. Ruptured abdominalaortic aneurysms: repair should not be denied. J Vasc Surg. May1992;15(5):851-857; discussion 857-859. (Retrospective; 231patients)

111. Schuster ME, Fishman JE, Copeland JF, Hatabu H, Boiselle PM.Pulmonary embolism in pregnant patients: a survey of practicesand 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 ofadult patients presenting with suspected pulmonary embolism.Ann Emerg Med. Feb 2003;41(2):257-270. (Clinical policy; Practiceguideline)

113. Daniels LB, Krummen DE, Blanchard DG. Echocardiography inpulmonary vascular disease. Cardiol Clin. Aug 2004;22(3):383-399,vi. (Review)

114. Pruszczyk P, Bochowicz A, Torbicki A, et al. Cardiac troponin Tmonitoring identifies high-risk group of normotensive patientswith 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 ofsuspected severe pulmonary embolism: transesophageal echocar-diography vs spiral CT. Chest. Sep 1997;112(3):722-728.(Comparative study; 49 patients)

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118. Cheitlin MD, Armstrong WF, Aurigemma GP, et al.ACC/AHA/ASE 2003 guideline update for the clinical applicationof echocardiography: summary article: a report of the AmericanCollege of Cardiology/American Heart Association Task Force onPractice Guidelines (ACC/AHA/ASE Committee to Update the1997 Guidelines for the Clinical Application of Echocardiography).Circulation. Sep 2 2003;108(9):1146-1162. (Practice guideline)

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120. Kern JW, Shoemaker WC. Meta-analysis of hemodynamic opti-mization in high-risk patients. Crit Care Med. Aug 2002;30(8):1686-1692. (Meta-analysis)

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123. Shoemaker WC. Temporal physiologic patterns of shock and circu-latory dysfunction based on early descriptions by invasive andnoninvasive monitoring. New Horiz. May 1996;4(2):300-318.(Review)

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127. Velmahos GC, Demetriades D, Shoemaker WC, et al. Endpoints ofresuscitation of critically injured patients: normal or supranormal?A prospective randomized trial. Ann Surg. Sep 2000;232(3):409-418.(Randomized control trial; 75 patients)

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CME Questions

1. The most definitive test in ruling out pulmonaryembolism as the cause of a patient’s hypotensionand dyspnea is:a. Bedside echocardiographyb. D-dimerc. Chest x-rayd. Contrast-enhanced CT of the thoraxe. Lower extremity venous compression ultra-

sound

2. Which of the following diagnostic tools suggestsprimary cardiogenic causes of the hypotension?a. Brain natriuretic peptide elevationsb. WBC count elevationsc. Lactate level of 1.0d. Urinary output of less than 10 cc/hr

3. What factors interact to produce a normal bloodpressure?a. Stroke volume and heart rateb. Systemic vascular resistance c. Peripheral vascular vasoreceptors and central

nervous system vasomotor centersd. The patient’s volume statuse. All of the above

4. Besides a systolic BP < 90 mmHg, which factor isthe most common occurrence prior to cardiacarrest in hospitalized patients?a. Dyspneab. Oxygen saturation < 90%c. Bradycardia for more than 30 minutesd. A decrease in GCS

5. In a patient presenting with hypotension andclear lungs without jugular venous distension,the most likely diagnosis is: a. Acute hemorrhageb. Cardiogenic shockc. Massive pulmonary embolismd. Cardiac tamponade

6. What is true about the use of vasopressor agents?a. Norepinephrine is the drug of choice for

anaphylaxisb. Dopamine is the drug of choice for sepsisc. Phenylephrine is primarily an alpha agonistd. Dobutamine is indicated for those patients

with an initial systolic blood pressure < 70mmHg

7. Which of the following statements about bedsidegoal-directed ultrasound is true?a. It allows the differentiation of the causes of

obstructive hypotensionb. It allows for rapid assessment of ventricular

function, wall motion, and valvularabnormalities

c. It can be used to facilitate vascular accessd. It is rapid, cost effective, and doesn’t require

the patient to leave the EDe. All of the above

8. Some factors contributing to hypotension inpatients intubated and ventilated in the EDinclude:a. Initiation of intubation with inadequate IV

accessb. Failure to consider metabolic derangements

likely present at the time of intubationc. The use of medications likely to cause

hypotension for intubation and sedationd. The inappropriate use of ventilatory modali-

ties (such as PEEP) that lower blood pressure e. All of the above

9. Which of the following diagnoses must beconsidered in a hypotensive patient with dyspneaand jugular venous distention?a. Tension pneumothoraxb. Acute pulmonary edemac. Pericardial tamponaded. Right ventricular infarctione. Pulmonary embolismf. All of the above

10. First line pressor agents in the treatment ofvarious causes of shock include all of the follow-ing EXCEPT:a. Norepinephrine use in the setting of pneumo-

nia, good left ventricular systolic function, andhypotension refractory volume resuscitation

b. Dobutamine use in a patient with severelydepressed left ventricular function and a bloodpressure of 80/40 mmHg

c. Epinephrine use in a patient with anaphylacticshock

d. Phosphodiesterase inhibitor use in the patientwith hypotension with pulmonary edema andpoor cardiac systolic function

e. Vasopressin use in the dehydrated patientwith suspected urosepsis

Emergency Medicine Practice® 28 November 2007 • EBMedicine.net

Physician CME InformationDate 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 ContinuingMedical Education (ACCME) through the joint sponsorship of Mount SinaiSchool of Medicine and Emergency Medicine Practice. The Mount Sinai Schoolof Medicine is accredited by the ACCME to provide continuing medicaleducation for physicians.

Credit Designation: The Mount Sinai School of Medicine designates thiseducational activity for a maximum of 48 AMA PRA Category 1 Credit(s)™ peryear. Physicians should only claim credit commensurate with the extent of theirparticipation in the activity.

ACEP Accreditation: Emergency Medicine Practice is approved by the AmericanCollege of Emergency Physicians for 48 hours of ACEP Category 1 credit perannual subscription.

AAFP Accreditation: Emergency Medicine Practice has been reviewed and isacceptable for up to 48 Prescribed credits per year by the American Academyof Family Physicians. AAFP Accreditation begins August 1, 2006. Term ofapproval is for two years from this date. Each issue is approved for 4Prescribed credits. Credits may be claimed for two years from the date of thisissue.

AOA Accreditation: Emergency Medicine Practice has been approved for 48Category 2B credit hours per year by the American Osteopathic Association.

Needs Assessment: The need for this educational activity was determined by asurvey of medical staff, including the editorial board of this publication; reviewof morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; andevaluation of prior activities for emergency physicians.

Target Audience: This enduring material is designed for emergency medicinephysicians, 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 maybe presenting investigational information about pharmaceutical products that isoutside Food and Drug Administration approved labeling. Information presentedas part of this activity is intended solely as continuing medical education and isnot intended to promote off-label use of any pharmaceutical product.Disclosure of Off-Label Usage: Vasopressin use in septic shock and for cardiacarrest are off-label. Hydrocortisone use as an adjunct in sepsis and septicshock is off-label.

Faculty Disclosure: It is the policy of Mount Sinai School of Medicine to ensureobjectivity, balance, independence, transparency, and scientific rigor in all CME-sponsored educational activities. All faculty participating in the planning orimplementation of a sponsored activity are expected to disclose to theaudience any relevant financial relationships and to assist in resolving anyconflict of interest that may arise from the relationship. Presenters must alsomake a meaningful disclosure to the audience of their discussions of unlabeledor unapproved drugs or devices.

In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty forthis CME activity were asked to complete a full disclosure statement. Theinformation received is as follows: Dr Weekes, Dr. Zapata, Dr. Napolitano, Dr.Slovis, and Dr. Weingart report no significant financial interest or otherrelationship with the manufacturer(s) of any commercial product(s) discussed inthis 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 EmergencyMedicine Practice six-month testing period, complete the post-test and theCME Evaluation Form distributed with the December and June issues, andreturn it according to the published instructions are eligible for up to 4 hours ofCME credit for each issue. You must complete both the post test and CMEEvaluation Form to receive credit. Results will be kept confidential. CMEcertificates will be delivered to each participant scoring higher than 70%.

• Online Single-Issue Program: Current, paid subscribers with current and validlicenses in the United States who read this Emergency Medicine Practice CMEarticle and complete the online post-test and CME Evaluation Form atEBMedicine.net are eligible for up to 4 hours of Category 1 credit toward theAMA Physician’s Recognition Award (PRA). You must complete both the post-test and CME Evaluation Form to receive credit. Results will be keptconfidential. CME certificates may be printed directly from the Web site to eachparticipant scoring higher than 70%.

Hardware/Software Requirements: You will need a Macintosh or PC to accessthe online archived articles and CME testing. Adobe Reader is required to viewthe PDFs of the archived articles. Adobe Reader is available as a freedownload at www.adobe.com.

CEO: Robert Williford President and Publisher: Stephanie Williford Director of Member Services & Continuing Education: Liz Alvarez

Direct all editorial or subscription-related questions to EB Medicine: 1-800-249-5770 • Fax: 1-770-500-1316 • Non-U.S. subscribers, call: 1-678-366-79335550 Triangle Parkway, Suite 150 • Norcross, GA 30092

E-mail: ebm@ebmedicine.net • Web Site: EBMedicine.net

Emergency Medicine Practice (ISSN Print: 1524-1971, ISSN Online: 1559-3908) is published monthly (12 times per year) by EB Practice, LLC, 5550 Triangle Parkway, Suite 150,Norcross, GA 30092. Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intendedas a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for makingspecific medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. Emergency Medicine Practice is a trademark of EBPractice, LLC. Copyright © 2007 EB Practice, LLC. All rights reserved. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC.Individual subscription price: $299, Institutional subscription price: $899 U.S. funds. (Call for international shipping prices.)

Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.

Now Available: The 2008 LLSA Study Guide

Save Time & Money Preparing For The ABEM Exam With:• 35 AMA/ACEP Category 1 CME credits• A full reprint of the original articles.• A handy summary of key points so you can get the

“must-know” information for each article.• A more in-depth discussion to clarify and elaborate on

the key points.• Sample questions to help you quiz yourself on your

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Class Of Evidence DefinitionsClass I: Conditions for which there is evidence for and/or general agreement

that the procedure or treatment is useful and effectiveClass II: Conditions for which there is conflicting evidence and/or a

divergence of opinion about the usefulness/efficacy of a procedure ortreatment

Class IIa: The weight of evidence or opinion is in favor of theprocedure or treatment

Class IIb: Usefulness/efficacy is less well established by evidence oropinion

Class III: Conditions for which there is evidence and/or general agreementthat the procedure or treatment is not useful/effective and in some casesmay be harmful