At 0655, at the end of a 16-hour tour, you're dispatched on a call for "difficulty breathing." You and your partner are greeted at the door by the patient's daughter, who says, “My mom can’t breathe. I can’t believe this—my father’s funeral was yesterday.” She tells you her mother woke up from sleep about one hour prior to your arrival with severe difficulty breathing.
From the door of the patient’s room, you see a 77-year-old Caucasian female in the tripod position with frank pallor and diaphoresis. She is alert and able to answer with only a few words. As you begin your assessment, your partner obtains a baseline set of vitals and puts the patient on high-concentration oxygen. He tells you that when auscultating the patient’s blood pressure he didn’t hear anything, and your attempt to auscultate gets the same result. The patient does not have palpable radial pulses, and the pulse oximeter is not getting any readings. The fact that both you and your partner were unable to auscultate a blood pressure and the absence of radial pulses lead you to believe this patient is likely hypotensive. Auscultation of the lungs reveals rales in the mid and upper fields, with absent lung sounds at the bases. The patient's respirations are labored and shallow at a rate of 36 breaths per minute. The 3-lead EKG reveals sinus tachycardia at a rate of 138; the 12-lead EKG reveals symmetric T-wave inversion in the inferior leads. The patient’s only medical history is hyperlipidemia. IV access is established and the patient is moved to the ambulance, where you are finally able to auscultate a blood pressure of 70/40, which confirms your suspicion of hypotension, and you initiate transport.
Shortly after leaving the scene, you notice the patient is having more difficulty breathing. Normally, CPAP would be the first-line treatment for pulmonary edema, but due to hypotension, CPAP is contraindicated in this case. As you suspect the pulmonary edema is secondary to cardiogenic shock, you withhold fluids and quickly contact medical control for a dopamine drip. While on the phone with medical control, you attempt to initiate assisted ventilations with the BVM, which the patient doesn’t tolerate. Due to her anxiety and worsening hypoxia, you also request orders for sedation followed by intubation, only if needed. The patient’s mental status quickly deteriorates before you are able to administer the sedative and you initiate mechanical ventilations. Positive pressure ventilations are delivering adequate chest rise, and you are able to maintain a good mask seal, so you opt to hold off on intubation. After giving your hospital presentation via radio, you also opt to hold the dopamine drip due to your 90-second ETA to the hospital.
This appears to be a typical case of cardiogenic shock with hypotension and pulmonary edema. In cases of sudden-onset cardiogenic shock, acute myocardial infarction is usually the culprit, with infarcted myocardium leaving the patient’s heart an ineffective pump.
Stress cardiomyopathy (SCM), also known as broken heart syndrome or Takotsubo cardiomyopathy, is most common among post-menopausal women, and is characterized by transient ballooning of the apical portion of the left ventricle with normal contractility at the base. The apical region of the heart is “ballooning” due to normal contractility in the base with akinesia (lack of movement) in the apical region, making it appear as though the apical region is bulging or ballooning. The condition was originally described in Japan, where it got the name Takotsubo cardiomyopathy after “takotsubo"—a pot designed to trap octopus that has a wide base and narrow neck, resembling the left ventricle of patients with this cardiomyopathy.1 This condition is precipitated by intense emotional or physical stress. Due to the abnormal contractile pattern of the left ventricle, it is no surprise that this condition most commonly mimics acute myocardial infarction with chest pain and/or dyspnea as the most common chief complaints, although pulmonary edema, cardiogenic shock and/or dysrhythmias may be present. Those are often accompanied by various ST and/or T-wave changes, as well as elevated cardiac enzymes. Due to the fact that SCM so closely mimics myocardial infarction, many patients undergo coronary angioplasty, where the majority reveal normal to mildly occluded coronaries, a sentinel sign that the patient may be presenting with SCM rather than acute myocardial infarction (AMI).
Although SCM and AMI may present similarly, the long-term prognosis is very different between the two. SCM is a transient disorder in which cardiac function tends to return to normal within days to weeks following the episode. There is a low recurrence rate of approximately 10%,2 as well as a very low mortality rate of around 1%.3 In cases of myocardial infarction, the long-term prognosis is variable, depending on the time to reperfusion and the extent of infarcted tissue. Patients who have suffered from massive infarctions are often left with significant lifestyle changes.
Presently, the exact pathophysiology of the disorder has not been elucidated and is an active area of research. SCM has been associated with extremely elevated plasma catecholamine and neuropeptide levels, suggesting an exaggerated response from the sympathetic nervous system. The association with catecholamine levels and neuropeptides is clear, although it does not explain the mechanism by which the ventricular wall abnormalities occur or the reason for their much higher prevalence among post-menopausal females.
In the Field
Due to the fact that SCM presents very similarly to acute MI, diagnosis of stress cardiomyopathy will not take place in the field. Treatment should be based upon the patient’s symptoms; ischemic chest pain, difficulty breathing, etc., should be treated per local protocol. As most of these patients will mimic acute coronary syndrome, oxygen, aspirin, nitroglycerin and morphine will likely be the most common treatment modalities.
As healthcare professionals, it is imperative to do a thorough patient assessment. When eliciting a history from a patient, it’s important not to overlook things such as mental health and current stress level. Stress cardiomyopathy is another disease to add to your list of differential diagnoses. Your next STEMI alert patient may actually just have a broken heart.
Back to the Patient
One week after you brought in this patient, the ED attending tells you she developed ST-segment elevations and had positive cardiac enzymes. The physician tells you the coronary angiography revealed no significant occlusions and the patient was placed on an intra-aortic balloon pump for two days, but was just released and is doing fine. The doctor asks, “Ever heard of stress cardiomyopathy?”
1. Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 118:397–409, 2008.
2. Elesber AA, Prasad A, Lennon RJ, et al. Four-year recurrence rate and prognosis of the apical ballooning syndrome. J Am Coll Cardiol 50:448–528, 2007.
3. Gianni M, Dentali F, Grandi AM, et al. Apical ballooning syndrome or Takotsubo cardiomyopathy: A systematic review. Eur Heart J 27:1523–1529.26, 2006.
4. Wittstein IS, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 352:539–548, 2005.
Joshua Nackenson, NREMT-P, is a paramedic in New York City and Long Island, NY, working for the North Shore LIJ Health System and Wyandanch Wheatley Heights Ambulance Corps, and is a volunteer firefighter/paramedic with the Dix Hills Fire Department. He is also on the faculty for EMS education at the State University of New York at Stony Brook. Contact him at email@example.com.