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Symptomatic Hypotension ED Stabilization and the Emerging Role of Sonography Emergency Medicine Practice

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  November 2007  Volume 9, Number 11  Authors Anthony J. Weekes, MD, RDCS, RDMS, FAAEM Emergency Ultrasound Program Director, Montefiore MedicalCenter; Assistant Professor of Emergency Medicine, AlbertEinstein College of Medicine, Bronx, NY Ryan J. Zapata, MD, FACEP  Attending Physician, Montefiore Medical Center; AssistantProfessor of Emergency Medicine, Albert Einstein College ofMedicine, Bronx, NY  Antonio Napolitano, MD, FACEP  Attending Physician, Montefiore Medical Center; AssistantProfessor of Emergency Medicine, Albert Einstein College ofMedicine, Bronx, NY Peer ReviewersCorey M. Slovis, MD, FACP, FACEP, FAAEM Professor and Chair, Department of Emergency Medicine, Vanderbilt University Medical Center, Nashville, TN Scott D. Weingart, MD Director, Division of Emergency Critical Care, Department 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 srcinal release: November 1, 2007 Date 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 Sonography You 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%, decreases postintubation to 76%. Portable chest x-ray shows proper ET tube place-ment, no infiltrates, no pneumothorax, and a normal cardiac silhouette. The patient is anuric. Labs show a creatinine of 2.1, a WBC count of 18,000, 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 of 60/40 mmHg. He is afebrile and has a pulse of 100 in the arm without the AV fistula. He has a history of non compliance with his medications. 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-Chief  Andy Jagoda, MD, FACEP, Professor and Vice-Chair of Academic Affairs, Department ofEmergency Medicine; Mount SinaiSchool of Medicine; MedicalDirector, Mount Sinai Hospital,New York, NY.  Associate Editor John M. Howell, MD, FACEP, Clinical Professor of EmergencyMedicine, George WashingtonUniversity, Washington, DC;Director of Academic Affairs, BestPractices, Inc, Inova FairfaxHospital, Falls Church, VA. Editorial Board William J. Brady, MD,  AssociateProfessor and Vice Chair,Department of EmergencyMedicine, University of Virginia,Charlottesville, VA. Peter DeBlieux, MD Professor of Clinical Medicine,LSU Health Science Center, NewOrleans, LA. Wyatt W. Decker, MD, Chair and Associate 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 Editors Nicholas Genes, MD, PhD, MountSinai Emergency MedicineResidency. Beth Wicklund, MD, RegionsHospital Emergency MedicineResidency, EMRA Representative. International Editors  Valerio Gai, MD, Senior Editor,Professor and Chair, Dept of EM,University of Turin, Italy. Peter Cameron, MD, Chair,Emergency Medicine, 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 toprovide 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 MedicinePractice does not accept any commercial support.  Emergency Medicine Practice ® 2November 2007 ã 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… T here is no clear blood pressure definition of hypotension. Instead, blood pressure must beplaced 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 in both 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 emergent but equally challenging are those patients with low blood 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 Emergency Medicine 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 BPto range from 116-145 mmHg SBPand 66-84 mmHg DBPin men and107-137 mmHg SBPand 61-78 mmHg DBPinwomen. 2 Keep in mind these numbers vary with thepatient’s size and ideal body weight. Mean arterial pressure (MAP) is more reflective of the actual pressure in the arterioles and smallervessels than the standard blood pressure measure-ments and may be more helpful in the evaluation of hypotension. MAPcalculations 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 Ahealthy adult will have natural variations in blood pressure readings during a routine 24-hourperiod. 6,7 Anumerical blood pressure reading takes onclinical significance when the MAPis below thepatient’s usual regulated pressures for organ perfu-sion. For example, a blood pressure reading of 140/90mmHg 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 BPsecondary 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:ã Cardiogenic – results from loss of cardiac output ã Hypovolemic – results from decreased intravascu-lar volume ã Obstructive – results from intrinsic (e.g., pul-monary embolus) or extrinsic (e.g., pericardialtamponade) vascular outflow obstruction ã 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 ã November 20073 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 Hypotension Standing or sitting with the legs dangling can causeup to 1 Lof blood volume to pool in the venouscirculation of the legs. The immediate result of lowering intrathoracic blood volume is a reduction in both cardiac output and blood pressure. Through thenormal autonomic response, an increase in heart rate by as much as 25 beats/minute and an increase insystemic vascular resistance should keep bloodpressure at normal levels. A5-10 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. Adecrease in the SBPof 20 mmHg or in theDBPof 10 mmHg after standing for three minutesdefines orthostatic BP. 11 Parameters for abnormalorthostatic increases in heart rate are not well defined but many have a HR greater than 20-30 beats perminute. Patients with a hyper tensive blood pressurewhen supine can be symptomatically orthostatic witha large enough decrease in BPupon standing.Asimilar 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. Of particular 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 EDpresentation, 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 of Medicine 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 of information 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 of patients with symptomatic, non-traumatic shock. Inthis study, hypotension was defined as an initial EDsystolic blood pressure reading of less than100mmHg. Shock was defined by the presence of hypotension 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 ® 4November 2007 ã EBMedicine.net hypovolemic shock is dependent on the underlyingcause and the patient’s co-morbidities. A2002 study by 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 incidenceof 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 Trauma The ATLS protocols support the practice of usinghypotension as only a late marker of shock because of its 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 SBPcorrelations in thecontext of clinical decision making . The National Trauma Data Bank (n = 115,830),where hemorrhagic shock was the main cause of hypotension, reports that SBPcorrelates with serum base deficits (considered to be a marker of circulatoryshock). The mean and median SBPdecreased to lessthat 90 mmHg when the base deficits were worse than-20. 20 The Data Bank supports the conclusion thatSBPis a late marker for mortality and that, in thesetting of hemorrhagic shock, SBPshould 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 BPresults 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: ã 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.ã Increased water absorption mediated by ADH inthe distal tubule.

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