A 66-year-old woman presents tothe emergency department(ED) with exertional dyspnea, generalizedweakness, and orthostaticdizziness; the symptoms startedabout 1 week earlier and have progressedinsidiously. The patient alsoreports diaphoresis and nausea withoutvomiting. She has no chest pain,palpitations, cough, or hemoptysis;she has not had a recent respiratorytract infection. While she is waitingto be admitted, she has an episode ofsyncope.
A 66-year-old woman presents tothe emergency department(ED) with exertional dyspnea, generalizedweakness, and orthostaticdizziness; the symptoms startedabout 1 week earlier and have progressedinsidiously. The patient alsoreports diaphoresis and nausea withoutvomiting. She has no chest pain,palpitations, cough, or hemoptysis;she has not had a recent respiratorytract infection. While she is waitingto be admitted, she has an episode ofsyncope.History.
The patient hassmoked one and a half packs of cigarettesa day for more than 50 years.Her medical history includes hypertension,type 2 diabetes mellitus,peripheral vascular disease, congestiveheart failure, chronic obstructivepulmonary disease, and hyperlipidemia.There is no history of stroke,pulmonary embolism, or deepvenous thrombosis. She underwentan aortofemoral bypass graft 5 yearsearlier.Examination.
Blood pressure is 132/77 mm Hg;heart rate, 120 beats per minute and regular; respirationrate, 20 breaths per minute; temperature, 36.1C (97F).The patient is alert but apprehensive. She has no signs ofexternal trauma. Head, eyes, ears, nose, and throat arenormal. Her neck is supple with bilateral jugular venousdistention at 45 degrees. No carotid bruits are audible.Bibasilar rales are present but not wheezing. Heartsounds are markedly muffled and diminished. No murmurs,gallops, or friction rubs are audible. Cranial nervesare intact; no sensory or motor deficits are noted. Reflexesare bilaterally symmetric.Laboratory and imaging studies.
The ECG showsno evidence of ischemia, abnormal intervals, or electricalalternans.Abnormal laboratory values include a white blood cellcount of 16,800/L; hemoglobin, 10.6 g/dL; and hematocrit,33.3%. A basic metabolic panel is normal except forblood urea nitrogen, 31 mg/dL, and sodium, 126 mEq/L.Her troponin-I, creatine kinase-MB, and brain natriureticpeptide levels are normal.The patient experiences orthostatic syncope whenshe attempts to stand for a chest radiograph.What abnormalities on the film suggest the cause ofher symptoms?PERICARDIAL TAMPONADE:AN OVERVIEWEtiology. Pericardial tamponade is rare but life-threatening.Penetrating chest trauma is the most commoncause of rapidly developing pericardial tamponade; however,chronic diseases, such as long-standing renal failure,rheumatoid arthritis, systemic lupus erythematosus, pericarditis,and malignancy, can result in large pericardial effusionsthat may progress to pericardial tamponade.The development of tamponade depends on the rateof the rise in intrapericardial pressure. A small amount ofintrapericardial fluid rapidly introduced into the pericardialspace can result in tamponade. In contrast, if the fluid increaseoccurs slowly, the pericardial sac can stretch to accommodateincreasing fluid volumes, which produces a"water-bottle" appearance of the cardiac silhouette on achest radiograph. Tamponade occurs only when the limitsof pericardial distensibility have been exceeded.Pathophysiology. The primary pathophysiology ofpericardial tamponade is the increase in intrapericardialpressure and volume. As the volume of effusion increasesin the relatively fixed space of the pericardial sac, it encroacheson the capacity of the atria and ventricles to filladequately. As a result, ventricular filling is mechanicallylimited and stroke volume is reduced. These changes resultin decreased cardiac output and finally produce diminishedarterial systolic blood pressure and decreased pulsepressure. Central venous pressure (CVP) also rises to exceed15 cm of water pressure because of the backup ofblood into the vena cava. In a hypotensive patient, a risingCVP indicates that the normal compensatory responsesare failing.1The circulatory system responds by an increase inheart rate and total peripheral resistance in an attempt tomaintain adequate cardiac output and blood pressure.The smooth muscle in the walls of the vena cava also constricts,resulting in increased venomotor tone and agreater rise in CVP-which may be recognized clinicallyas neck vein distention in some patients.A simultaneous fall in both CVP and blood pressure-which can occur precipitously and without warning-signals decompensation and imminent cardiac arrest.This patient's syncope was the clinical manifestationof the fall in CVP and blood pressure that marked theonset of tamponade.Diagnosis. Physical findings in pericardial tamponadeconsist of hypotension, distended neck veins and,rarely, distant or muffled heart sounds. These 3 findingsconstitute the Beck triad, which is present in a minority ofpatients with tamponade. The most reliable sign of pericardialtamponade is an elevated CVP in association withhypotension and tachycardia.When pericardial tamponade is suspected, a portableultrasound machine enables rapid, accurate, and noninvasivediagnosis at the patient's bedside. The characteristicsonographic feature of pericardial tamponade is the simultaneouspresence of pericardial fluid and diastolic collapseof the right ventricle or atrium. An indirect sonographicsign of tamponade is the demonstration of a dilated inferiorvena cava in a hypotensive patient.Cardiac ultrasonography performed in the ED usingsubcostal and long parasternal views has a reported sensitivityof 98.1% and specificity of 99.9% for the detection ofpericardial effusion.2 The presence of effusion in a hypotensivepatient points to tamponade.The ECG may be helpful when tamponade starts todevelop in a patient with chronic pericardial effusion. Electricalalternans is an ECG change in which the morphologyand amplitude of the QRS complex alternate everyother beat. The postulated cause is the mechanical oscillation of the heart in the pericardial fluid, which is calledthe "swinging heart phenomenon." The heart swingsfreely in pericardial fluid in chronic effusion, but whentamponade ensues, the frequency of cardiac oscillation decreasesto half the heart rate. The cardiac position thereforealternates, with a return of the heart to its originalposition every other beat.When electrical alternans is present, it is pathognomonicfor tamponade. Alternans is rarely seen in acutetamponade, such as that which results from chest trauma;it is more common in larger, chronic effusions that allowthe swinging heart phenomenon to occur. The reason forthe absence of electrical alternans in this patient is unclear.It may be related to the recurrent nature of the pericardialeffusion and the possible presence of adhesionsthat stopped the swinging heart phenomenon, or perhapsthe volume of the effusion had an effect.Radiography is not helpful in the identification ofacute tamponade associated with trauma; however, inchronic pericardial effusion, the cardiac silhouette mayhave a water-bottle appearance. This patient's chest filmdisplayed a transitional stage of the cardiac silhouette,which was progressing toward a water-bottle pattern.Treatment. Emergency treatment of pericardial tamponadeentails rapid volume expansion with crystalloid.Placement of a CVP catheter is helpful for monitoring.Although not a risk-free procedure, pericardiocentesisis useful for diagnostic and therapeutic reasons. Aspirationof as little as 5 to 10 mL of pericardial fluid may producedramatic clinical improvement, because intrapericardialvolume reduction to slightly below the critical levelallows compensatory mechanisms to maintain adequatehemodynamics. Whenever possible, pericardiocentesisshould be performed under sonographic guidance toavoid laceration of the heart or coronary vessels and tominimize stimulation of dysrhythmia.If pericardiocentesis is unsuccessful and the patient'scondition deteriorates into cardiac arrest, emergency thoracotomymay be indicated. Under most circumstances,there is time to perform a pericardial window procedureto manage the pericardial effusion definitively and to precludeits redevelopment.
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