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The Journal of Emergency Medicine, Vol. 31, No. 1, pp. 87–90, 2006Copyright © 2006 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/06 $–see front matter

Case Presentations of the HarvardEmergency Medicine Residency

SYNCOPE WITH EXERTIONAL DYSPNEA

Scott B. Murray, MD,*† Adam Z. Barkin, MD,*‡ and Leon D. Sanchez, MD,*‡

*Division of Emergency Medicine, Harvard Medical School, Boston, Massachusetts, †Harvard Affiliated Emergency MedicineResidency, Beth Israel Deaconess Medical Center, Boston, Massachusetts, and ‡Department of Emergency Medicine, Beth Israel

Deaconess Medical Center, Boston, MassachusettsReprint Address: Leon D. Sanchez, MD, Department of Emergency Medicine, Beth Israel Deaconess Medical Center, One Deaconess

Road, West CC2, Boston, MA 02215

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r. Scott Murray: Today’s case is that of a 53-year-oldoman with a history of hypertension, treated with val-

artan, who presented to the Emergency DepartmentED) with two episodes of witnessed syncope. She ar-ived via Emergency Medical Services (EMS) after fall-ng out of bed and striking her head. The patient deniedhest pain, shortness of breath, palpitations, nausea,omiting, or lightheadedness preceding this syncopalvent or afterwards. There was no report of seizure-likectivity and there was neither a post-ictal period, incon-inence, nor tongue laceration. A pre-hospital fingersticklucose was 110 mg/dL. On review of systems, theatient denied recent trauma, headaches, abdominal pain,evers, chills, blood in the stool, leg swelling, recentravel, or focal neurologic complaints. Four weeks beforehis presentation, she was seen in the ED with a chiefomplaint of exertional dyspnea. The chest radiographCXR) at that time demonstrated a small pulmonarynfiltrate and hyperinflation. She was diagnosed with anxacerbation of chronic obstructive pulmonary diseaseCOPD) and community-acquired pneumonia, and wasreated with steroids, albuterol, ipratropium and azithro-ycin. The resting oxygen saturation at that time was

9%; however, this fell to 78% with ambulation. Inpa-ient hospitalization was recommended to the patient, buthe signed out against medical advice (AMA). She statedhat she was very anxious to reestablish contact withamily members who were in the path of Hurricaneatrina.

Case Presentations of the Harvard Emergency M

Eric S. Nadel, MD, of Harvard University Medical School

87

Dr. Peter Rosen: I would be leery about allowing aatient to refuse medical care who has any abnormalital sign, including hypoxia. Hypoxia may impair herudgment. Before allowing this patient to leave AMA, Iould be certain the patient is not hypoxic at rest when

he decision is being made. In addition, your documen-ation must be impeccable in this type of situation. Iould also make sure her anxiety and distress do not

mpair her decision-making capacity. Even when a pa-ient signs out AMA and the physician carefully docu-ents the decision, the physician is not free from liabil-

ty. Can you tell us about the patient’s physicalxamination at this presentation?

Dr. Murray: The temperature was 36.5°C (97.7°F),eart rate 88 beats/min, blood pressure 116/64 mm Hg,espiratory rate 20 breaths/min, and oxygen saturation9% on room air. In general, the patient appeared com-ortable, sitting up in the gurney. Examination of theead and neck was unremarkable. There was no evidencef trauma, the pupils were equal and reactive, and ex-raocular movements were intact. The neck was supple,on-tender and without jugular venous distension. Theungs had diminished breath sounds throughout. Theardiovascular examination revealed a regular rate andhythm without murmurs, rubs or gallops. The abdomenas soft, non-tender, non-distended, and with normoac-

ive bowel sounds. Stool was negative for occult blood.he extremities had no clubbing, cyanosis or edema.eripheral pulses were normal throughout. The cranial

e Residency are coordinated by David F. M. Brown, MD, and

edicin , Boston, Massachusetts

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88 S. B. Murray et al.

erve examination was normal and the motor and sen-ory examinations were equal throughout.

Dr. Carlo Rosen: You mentioned the patient hadeen treated for COPD. Did she carry this diagnosis? Iould be hesitant to attribute the degree of hypoxia thisatient demonstrated at her previous visit to COPD.

Dr. Murray: The patient had never been diagnosedith COPD nor been on steroids. Nevertheless, she

moked 1.5 packs of cigarettes per day for 30 years andad intermittently been on an albuterol inhaler when shead upper respiratory infection symptoms.

Dr. Jonathan Edlow: With the degree of hypoxiahis patient has demonstrated, you must consider theiagnosis of pulmonary embolism (PE). Patients with PEan have abnormal CXR findings including atelectasis,nfiltrates, elevated hemi-diaphragm, and other non-pecific findings. Had she been evaluated for PE in theast?

Dr. Murray: After leaving AMA from the ED 4eeks prior, the patient had followed up with her pri-ary care doctor who ordered a computed tomography

CT) angiogram of the chest. This was a normal studyithout evidence of PE.Dr. Shamai Grossman: Her exertional dyspnea

ould also be consistent with congestive heart failureCHF). Has she had any chest pain in the past 2 monthshat might suggest a recent myocardial infarction (MI)?

hat were her cardiac risk factors and did you have aXR on this visit?

Dr. Murray: She denied any history of chest pain.er risk factors for cardiovascular disease included hy-ertension, smoking cigarettes, and a family history of arother who suffered a myocardial infarction at age 42.he chest X-ray study did not demonstrate CHF or anyther significant disease (Figure 1).

Dr. Richard Wolfe: You mentioned that the patientad no chest pain, palpitations, gastrointestinal bleeding,

igure 1. Chest X-ray at second ED visit.

r murmur, but was dyspneic and hypoxic on exertion. F

an you describe her other risk factors for syncope?hat did the electrocardiogram (EKG) show at the first

nd second visit?Dr. Murray: She had no history of dysrhythmia,

rior episodes of syncope, nor any family history ofudden death. She was postmenopausal. During the firstisit, she refused to stay for an EKG as she was veryervous about contacting her family. The EKG at theecond visit showed a left atrial abnormality with QTcrolongation, poor R wave progression in the anterioreads with ST depressions and T wave inversions in thenferolateral leads (Figure 2). There was no prior EKGvailable for comparison.

Dr. Edward Ullman: There are other reasons to haven EKG like this besides ischemic heart disease. With aistory of syncope I would be concerned about centralervous system (CNS) disease, particularly a subarach-oid hemorrhage. Other possibilities include myocardialontusion and PE. However, given the normal neurologicxamination, lack of headache, and no major chestrauma, myocardial contusion and intracranial processesre less likely. An ultrasound study will determine ifhere is a pericardial effusion that could be from myo-ericarditis.

Dr. Murray: Based on the abnormal EKG, the patientas given an aspirin. There was concern for pericarditis

nd a bedside ED ultrasound study (US) was performed.his US demonstrated marked wall motion abnormali-

ies, but no effusion. A head CT scan did not revealntracranial hemorrhage or other acute abnormalities.ecause of the concern for acute ischemic coronary

yndrome and pulmonary embolism, intravenous heparinas started after the head CT scan and US were obtained.he troponin T was elevated at 0.33 ng/mL; creatineinase (CK), CK-MB, complete blood cell count, elec-rolytes, and renal function were all normal. The emer-ency physicians were concerned about ongoing silentyocardial ischemia, and a formal cardiology consult

igure 2. EKG from second ED visit.

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nd echocardiogram were obtained. The echocardiogramhowed left ventricular apical akinesis and ballooning.

Dr. Edlow: Although the echocardiogram revealedocal wall abnormality and possibly ischemic heart dis-ase, it should be noted that ventricular strain from a PEan cause an elevated troponin in a patient with undif-erentiated chest pain or dyspnea.

Dr. Ryan Friedberg: Although rare, focal myocar-itis can present this way. Patients will have focal wallotion abnormalities on echocardiogram, corresponding

o regionalized ischemic changes seen on an EKG, andositive cardiac biomarkers. The ballooning seems un-sual, though.

Dr. Ullman: This sounds like the “broken heart syn-rome,” a reversible cardiomyopathy associated withevere emotional stress, which clearly she has. It presentsike cardiac ischemia, sometimes with chest pain, anKG pattern that looks ischemic, a positive serum tro-onin, and a classic wall motion abnormality similar tohat described here. It’s a diagnosis of exclusion afterschemic causes are ruled out.

Dr. Murray: The patient was taken to cardiac cath-terization shortly after the echocardiogram and wasound to have normal coronary arteries with an ejectionraction of 35%. There was akinesis of the apical, distalnferior, and distal anterior walls, and apical ballooningFigure 3). Provocative testing for Prinzmetal’s anginand myocardial biopsy were not performed. Based on theeculiar wall motion abnormalities, the patient was di-gnosed with Takotsubo cardiomyopathy, also known ashe “broken heart syndrome.”

Takotsubo is Japanese for octopus bottle. During sys-ole, the heart’s akinetic apex balloons outward as thease of the heart contracts and it resembles the roundottle with a narrow neck that is used to trap octopi inapan (Figure 4). This cardiomyopathy occurs in thebsence of coronary artery disease. The etiology is un-nown, but one hypothesis is that vasospasm of the

igure 3. Cardiac catheterization showing the left ventricle iniastole (D) and systole (S). Note the apical akinesis andallooning of left ventricle in systole.

icrovasculature occurs due to elevated circulating cat-tE

cholamines from a stressful event and the myocardiums stunned. It differs from the vasospam of Prinzmetal’sngina in that large vessel spasm cannot be provokedith ergonovine or acetylcholine. It is not clear why the

ardiomyopathy is regionalized to the apex. Women areffected more often than men, particularly over the agef 60 years [6]. In Japan, it has been estimated to accountor 1% to 2% of patients provisionally diagnosed withT elevation myocardial infarctions before catheteriza-

ion, but is infrequently reported outside Japan (1). Sig-ificant emotional stress often involving loved ones usu-lly precedes presentation, leading to the term “brokeneart syndrome.” Increasingly, medical stressors are rec-gnized as precipitants: surgery, medical procedures,cute abdominal pain, stroke, asthma flare, and severelcohol abuse or withdrawal are the most commonlydentified precursors (1–3). The presenting symptomay be chest pain, dyspnea, or syncope.Patients initially have regional ST elevations that

rogress over time to Q waves and inverted T waves.ne small retrospective case series suggests that EKG

riteria alone can distinguish between infarction andakotsubo cardiomyopathy (4). Lack of inferior recipro-al changes, and ST segment elevation greater in leads4–V6 than leads V1–V3 suggests Takotsubo cardio-yopathy. However, EKG criteria do not distinguishakotsubo cardiomyopathy from infarction when theulprit lesion is distal to the left anterior descending

igure 4. A takotsubo. Reprinted from American Heart Jour-al, 143, Kurisu S, Inoue I, Kawagoe T, et al. Takotsubo-like

eft ventricular dysfunction with ST-segment elevation: aovel cardiac syndrome mimicking acute myocardial infarc-

ion, Pages 448–55 (8), Copyright 2002, with permission fromlsevier.

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rtery, and no criteria distinguish Takotsubo from myo-arditis (5). It is important to remember that this is aiagnosis of exclusion. Most patients will have elevatederum troponin, but fewer will have elevated serumreatinine kinase (6). Patients are at risk for ventricularupture, dysrhythmia (polymorphic or monomorphicentricular tachycardia, and ventricular fibrillation), andeft ventricular mural wall thrombus formation and em-olization (6,7). The mortality during the acute phaseanges between 2% and 4% (3). The EKG and echocar-iogram completely normalize within 10–50 days.

Management focuses on the treatment of left ventric-lar failure, and hemodynamic support when necessary.his patient was started on a beta-blocker for suspectedysrhythmia, presumed to be the cause of the syncope,nd placed on warfarin to prevent thrombus formation athe akinetic apex. Four weeks after the patient’s secondD visit, the echocardiogram and EKG had completelyormalized. The patient is doing well and has contacteder family displaced by the hurricane. As exemplified byhis case, patients with Takotsubo cardiomyopathy gen-rally have an excellent outcome if supported through

he acute phase of their disease (8).

REFERENCES

. Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Koike H, SasakaK. The clinical features of takotsubo cardiomyopathy. QJM 2003;96:563–73.

. Suzuki K, Osada N, Akasi YJ, et al. An atypical case of “Takotsubocardiomyopathy” during alcohol withdrawal: abnormality in thetransient left ventricular wall motion and a remarkable elevation inthe ST segment. Intern Med 2004;43:300–5.

. Ishikawa K. “Takotsubo” cardiomyopathy: a syndrome character-ized by transient left ventricular apical ballooning that mimics theshape of a bottle used for trapping octopus in Japan. Intern Med2004;43:275–6.

. Ogura RO, Hiasa Y, Takashi T, et al. Specific findings of thestandard 12-lead ECG in patients with Takotsubo cardiomyopathy:comparison with the findings of acute anterior myocardial infarc-tion. Circ J 2003;67:687–90.

. Inoue M, Shimizu M, Ino H, et al. Differentiation between patientswith takotsubo cardiomyopathy and those with anterior myocardialinfarction. Circ J 2005;69:89–94.

. Bybee KA, Kara T, Prasad A, et al. Systematic review: transient leftventricular apical ballooning: a syndrome that mimics ST-segmentelevation myocardial infarction. Ann Intern Med 2004;141:858–65.

. Akashi YJ, Tejima T, Sakurada H, et al. Left ventricular ruptureassociated with Takotsubo cardiomyopathy. Mayo Clin Proc 2004;79:821–4.

. Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventriculardysfunction with ST-segment elevation: a novel cardiac syndromemimicking acute myocardial infarction. Am Heart J 2002;143:

448–55.