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 worseashen 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, ChildrensMedical 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 & WomensHospital, 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 doesnt seem right to you

There is no clear blood pressure definition ofhypotension. Instead, blood pressure must beplaced in the context of the patients 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 thepatients 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 persons 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 thepatients 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 thepatients 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 patients 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, thepatients 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 Parkinsons diseasewho may have primary autonomic dysfunction whichcan easily be exacerbated by dehydration orpolypharmacy.

Determination of orthostasis should be directed bythe patients 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 patients 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 patients 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 vesselspush 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.

EBMedicine.net November 2007 5 Emergency Medicine Practice

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 termedexposures. 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 physicians 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 Korotkoffs 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 thepatients 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 patients 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 Willebrands 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 RBCs 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 mans 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 RBCs) 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 (LFTs)Transaminases measure hepatocellular integrity.Albumin and PT/PTT reflect the livers syntheticfunction; alkaline phosphatase and bilirubin reflectthe livers 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 patients 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 recommendsaggressive 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 ringers 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 patients 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 BPs 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 patients 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 Medicines 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 patients 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 bodys 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 patientsclinical 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 betwee