admission diagnosis was angina and COPD exacerbation. Mrs. S had minimal response to I.V. steroids and bronchodilator therapy. She became progressively dyspneic with worsening arterial blood gas (ABG) results. Despite bi-level positive airway pressure therapy with FiO2 at 40%, her ABG results were: pH, 7.14; PaCO2, 74 mm Hg; PaO2, 107 mm Hg; HCO3–, 25 mEq/L; and SaO2, 96%. She received neuromuscular blockade and was electively endotracheally intubated. Soon thereafter, Mrs. S became profoundly hypotensive, requiring fluid resuscitation and vasopressor support. An ECG revealed new anterolateral ST segment elevation with marked inferior T-wave inversion. An echocardiogram showed left ventricular dysfunction with significant apical hypokinesis. Her diagnosis was cardiogenic shock.

Mrs. S was transferred to a tertiary hospital, an intra-aortic balloon pump was placed, and she underwent emergent cardiac catheterization. Angiography demonstrated normal coronary arteries and left ventriculography showed hypokinesis of the apex and mid-ventricle with basal hyperkinesis. The ejection fraction (EF) was measured at 25% (normal, 50% to 75%). At that time, she was diagnosed with heart failure, which responded to I.V. furosemide. Lisinopril and metoprolol were also administered. Mrs. S was successfully extubated and did well the remainder of her hospital course. Three weeks later outpatient echocardiography revealed normal left ventricular function with an EF of 55%. The final diagnosis was Takotsubo cardiomyopathy.

By Hope Padilla, BSN, RN, PCCN; Brendon Paltoo, MD; Renee Edsall, MSN, RN, CCRN; and Nancy Hettling, RN

Recognizing and treating

Takotsubo cardiomyopathy

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Mrs. S, 74, arrived in the ED with complaints of midsternal chest heaviness and difficulty breathing for the previous 2 to 3 days. Her history included hypertension, dyslipidemia, and chronic obstructive pulmonary disease (COPD). Her medications included atenolol, atorvastatin, nifedipine, and albuterol. One week earlier, her daughter had been hospitalized with a massive stroke. On presentation her vital signs were: temperature, 97.8º F (36.5º C); pulse, 141; respiratory rate, 40; BP, 195/113 mm Hg; and SpO2, 53% on room air. The initial ECG showed sinus tachycardia with nonspecific ST segment/T wave changes. Initial serum cardiac biomarkers were within normal limits. Physical assessment findings were normal with the exception of bilateral expiratory wheezing on auscultation. Her

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ALSO KNOWN AS stress cardiomyopathy or apical ballooning syndrome, Takotsubo cardiomyopathy (TCM) was first described in Japanese patients in 1990.1 The name refers to the peculiar shape of the left ventricle (LV), which resembles an octopus-fishing pot called a takotsubo, which has a round bottom and narrow neck. Acute emotional or physiologic stressors such as the death or illness of a loved one generally precede symptoms, so TCM is often called broken heart syndrome. The incidence of TCM is thought to be 1% to 2% of cases that present with suspected acute coronary syndromes (ACS).2,3 This article will review the pathophysiology, signs and symptoms, diagnosis, and treatment of TCM and discuss how to differentiate it from ACS. What causes TCM? The cause of TCM remains unclear, but studies indicate that catecholamine surges may play a significant role.4,5 Excessive sympathetic nervous system (SNS) stimulation may have an effect on the vascular wall, microcirculation, and myocardial cells, leading to a form of myocardial

stunning. Also, the apical myocardium may have an enhanced responsiveness to SNS stimulation.5 Other possible mechanisms include coronary artery vasospasm or an occlusive coronary artery thrombosis that spontaneously lyses before being detected during coronary angiography.6 Most patients (90%) with TCM are women, with most being postmenopausal.7 One reason may be that although men have higher catecholamine levels than women, women may have a more exaggerated response to increased levels. Postmenopausal women may be more vulnerable because of the reduced level of cardioprotective estrogens after menopause.8 A significant emotional or physical stressor typically precedes the development of TCM. Stressors include: • a loved one’s death • bad financial news • legal problems • natural disasters • motor vehicle collisions • exacerbation of a chronic medical illness • a newly diagnosed, significant medical condition • surgery

• an ICU stay • use of or withdrawal from illicit drugs.9 Signs and symptoms On initial presentation, TCM may be difficult to distinguish from ACS. Patients with TCM most commonly present with dyspnea and chest pain, mimicking ACS but without obstructive coronary artery disease.2,8 (See Absence of coronary artery disease.) Patients may also have ST-segment elevation and elevated cardiac biomarkers consistent with a myocardial infarction (MI).2,8,10 Because TCM involves the LV, anterior wall ST segment elevations in leads V2 to V4 are typical.11 In some cases, ECG is normal at presentation.7 When seen on ECG, TCM progresses in four stages: • Stage 1: immediate ST elevation • Stage 2: initial T-wave inversion from days 1 to 3 • Stage 3: transient improvement in T-wave inversion from days 2 to 6 • Stage 4: a second, deeper T-wave inversion with QT prolongation persisting for at least 2 months.12 Cardiac catheterization reveals characteristic LV systolic apical ballooning with a hypercontractile base and no evidence of obstructive

Absence of coronary artery disease Normal left and right coronary angiography in a patient with TCM.

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Recognizing apical ballooning As shown during systole at left, apical ballooning is characteristic of TCM. Normal systolic LV wall motion is shown at right.

coronary artery disease (see Recognizing apical ballooning). LV wall motion abnormalities in acute MI are often more localized. Progressive ECG changes as well as elevated cardiac biomarkers (serum creatine kinase and troponins) may be similar to changes seen in patients presenting with ST elevation MI (STEMI). In TCM, cardiac biomarkers may elevate minimally and peak at a concentration near the initial values, or may not increase at all in some cases. In contrast, patients with a STEMI experience a dramatic increase in cardiac biomarkers. Patients with TCM also have plasma levels of catecholamines (specifically epinephrine and norepinephrine) that are usually 2 to 3 times higher than in patients with MI and 7 to 34 times higher than normal.4,7,13,14 Hypotension can occur from a reduction in stroke volume because of acute LV systolic dysfunction or outflow tract obstruction. Cardiac murmurs and pulmonary crackles may be present on auscultation, indicating acute pulmonary edema.9 Accurate patient assessment is crucial for determining whether signs and symptoms indicate transient cardiac dysfunction or permanent

myocardial damage. Consideration of atypical causes in someone presenting with signs and symptoms of ACS could lead to an accurate diagnosis and timely treatments. Obtaining a thorough health history, especially for postmenopausal women, can help determine if the patient experienced a recent significant emotional and/or physiological stressor. TCM often involves postmenopausal women without severe coronary artery disease and often without the classic risk factors.15,16 Treating TCM Because patients with TCM present with the same clinical manifestations as someone having an MI, they should be immediately assessed and transferred to a cardiac catheterization lab to confirm diagnosis and receive appropriate treatment. To date, no treatments or interventions specific to TCM have been developed. Pharmacologic therapy usually proceeds along the same pathway as for patients with post-MI LV systolic dysfunction, including beta blockers, angiotensin-converting enzyme inhibitors, and diuretics as needed for volume overload.7 Most pharmacologic treatment starts after

the diagnosis is confirmed, but aspirin and beta blockers may be initiated before the patient’s arrival in the catheterization lab.2,9 Patients with significant hypotension who don’t have significant outflow tract obstruction may benefit from I.V. inotropes such as dopamine. However, inotropic agents should be avoided in patients with hypotension and moderate-to-severe LV outflow tract obstruction because they can worsen the degree of obstruction.7 The apical portions of the LV have the highest sympathetic innervation found in the heart, which may explain why excess catecholamines seem to selectively affect its function.17 An echocardiogram is indicated to further guide therapy and to evaluate for any other structural abnormalities. In patients with heart failure, supportive care with diuretics for volume overload has been used.7 Some patients with TCM require insertion of an intra-aortic balloon pump (IABP) to decrease left ventricular workload, decrease afterload, improve contractility, and increase stroke volume.11 Potential acute complications of TCM include cardiogenic shock, August l Nursing2014 l 53

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ventricular dysfunction syndrome (tako-tsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest. 2007;132(3):809-816.

ventricular dysrhythmias, heart failure, and mitral regurgitation. Inpatient care Patients with TCM should be admitted to a unit where they can be closely monitored for dysrhythmias. Goals of nursing care are similar to those for patients with ACS: controlling pain and BP, reducing anxiety, maintaining adequate oxygenation, preserving myocardial function, preventing cardiac decompensation, and avoiding and treating complications.16 Closely monitor vital signs and lab results in patients with TCM. Patients in acute congestive heart failure may require diuretics, and those with cardiogenic shock may require resuscitation with I.V. fluids and cautious use of inotropic agents. Beta blockers or calcium channel blockers may also be beneficial.9 Monitor patients for hypotension, shortness of breath, angina or anginal equivalent, dysrhythmias, or development of a new murmur. Carefully monitor fluid and electrolyte balance, particularly if patients are receiving diuretics.16 Because TCM is usually preceded by a significant emotional or physical stressor, provide patients with stress management resources to control and reduce the tension that occurs in stressful situations. Encourage patients to eat a healthy diet because a poor diet weakens the immune system. Ask about support systems (friends, family) that they can rely on during stressful situations. Promote daily physical activity and advise them to get 7 to 8 hours of sleep every night and incorporate ways to relax (yoga, hobbies, sports) into their daily lives to help them cope with stress.18 Positive outcomes The prognosis of TCM is usually favorable, with most patients experiencing complete recovery of left ventricular function in as little as a week to a few months.2,4,15 Advise patients to have a follow-up

4. Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med. 2005;352(6):539-548. 5. Abraham J, Mudd JO, Kapur NK, Klein K, Champion HC, Wittstein IS. Stress cardiomyopathy after intravenous administration of catecholamines and beta-receptor agonists. J Am Coll Cardiol. 2009; 53(15):1320-1325. 6. Mori H, Ishikawa S, Kojima S, et al. Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli. Cardiovasc Res.1993; 27(2):192-198. 7. Reeder GS, Prassad A. Stress (takotsubo) cardiomyopathy. UpToDate. 2014. http://www. 8. Akashi YJ, Goldstein DS, Barbaro G, Ueyame T. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation. 2008;118(25):2754-2762.

Patients with TCM most commonly present with dyspnea and chest pain, mimicking ACS but without obstructive coronary artery disease. echocardiogram in 4 to 6 weeks as directed by their healthcare provider.15 Referral to a cardiac rehabilitation program may be beneficial. Psychological support is essential for patients in emotional distress, and referrals can be made to help with coping strategies and/or bereavement counseling. TCM should be considered in patients with normal coronary arteries on angiography and left ventricular apical ballooning present on the left ventriculogram. Left ventricular dysfunction resolves in most patients regardless of medical treatment. Because the exact pathophysiology of TCM hasn’t been fully described, optimal management continues to evolve. ■ REFERENCES 1. Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol. 1991;21(2):203-214. 2. Nykamp D, Titak JA. Takotsubo cardiomyopathy, or broken-heart syndrome. Ann Pharmacother. 2010; 44(3):590-593. 3. Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left

9. Tomich EB, Brown DFM, Luerssen E, et al. Takotsubo cardiomyopathy. Medscape 2012. 10. Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol. 2001;38(1):11-18. 11. McCulloch B. Transient left ventricular apical ballooning. Crit Care Nurse. 2007;27(6):20-27. 12. Mitsuma W, Kodama M, Ito M, et al. Serial electrocardiographic findings in women with Takotsubo cardiomyopathy. Am J Cardiol. 2007;100(1):106-109. 13. Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol. 2004;94(3):343-346. 14. Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005;111(4):472-479. 15. Derrick D. The “broken heart syndrome”: understanding Takotsubo cardiomyopathy. Crit Care Nurse. 2009;29(1):49-57. 16. O’ Donovan, K. Broken heart syndrome. WIN. 2010;18(8):41-43. 17. Dorfman TA, Iskandrian AE. Takotsubo cardiomyopathy: state-of-the-art review. J Nucl Cardiol. 2009;16(1):122-134. 18. Zieve D, Eltz DR, Berger FK. Stress management. 2012. medlineplus/ency/article/001942.htm.

Hope Padilla is critical care staff nurse at University of Maryland Shore Medical Center at Dorchester; Brendon Paltoo is a board-certified invasive, noninterventional cardiologist in Cambridge, Md.; Renee Edsall is clinical nurse specialist for emergency center services at University of Maryland Shore Regional Health in Cambridge, Md.; and Nancy Hettling is per diem staff nurse at University of Maryland Shore Regional Health.

The authors have disclosed that they have no financial relationships related to this article.


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Recognizing and treating Takotsubo cardiomyopathy.

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