Matthew Van Ligten, Bryan Merte
A 52-year-old woman with epilepsy treated with levetiracetam and lamotrigine, hypertension, and non-Hodgkin lymphoma previously treated with chemotherapy and in remission presented after being found confused and incontinent of urine. Her daughter found her staring blankly after being unable to reach her by phone for approximately one hour.
As the patient remained postictal and was a limited historian, additional history was obtained from emergency medical services. Paramedics had been called for what appeared to be one of her typical seizures with prolonged confusion. They subsequently witnessed a second episode of blank staring in the ambulance followed by extensor posturing, which resolved prior to medication administration after approximately two minutes.
There was no reported head trauma or infectious prodrome and no known cardiopulmonary disease. Chart review showed an outside hospitalization several months earlier for sepsis secondary to pneumonia; her prior lymphoma treatment regimen was not available in the records, though a recent formal echocardiogram was unremarkable.
The patient was comfortable appearing and in no acute distress. Respiratory effort and breath sounds were normal, as were heart rate and rhythm. She was alert and oriented to person and place but not year, with impaired attention. She was drowsy but demonstrated no focal cranial nerve, motor, sensory, or coordination deficits.
| Test | Result |
| White blood cell count | 20.4 × 10³/µL |
| Absolute neutrophil count | 17.3 × 10³/µL |
| Hemoglobin | 14.1 g/dL |
| Platelets | 512 × 10³/µL |
| Sodium | 134 mmol/L |
| Creatinine | 1.01 mg/dL |
| Glucose | 299 mg/dL |
| Lactate | 2.5 mmol/L |

Approximately 60 minutes after ED arrival, the patient had another staring spell concerning for recurrent seizure. During the episode, her oxygen saturation fell into the low 70s with a reliable waveform and associated lip cyanosis. The episode resolved before benzodiazepine administration. Serial reassessments over the next 30 minutes showed progressive tachycardia, hypertension, and hypoxemia.
| Vital sign | Value |
| Blood pressure | 205/145 mm Hg |
| Heart rate | 146 beats/min |
| Respiratory rate | 26 breaths/min |
| Temperature | 36.7°C |
| Oxygen saturation | 93% on 2 L/min nasal cannula |
She appeared ill and agitated with mildly increased work of breathing. Electrocardiography demonstrated sinus tachycardia without ST-segment elevation or other acute ischemic changes. Initial troponin was 424 ng/L (reference <51 ng/L).
A bedside ultrasound of the heart and lungs was performed.

Emergency Department Course
The patient received intravenous levetiracetam while CT of the head, CT angiography of the head and neck, and CT pulmonary angiography were obtained to investigate structural, vascular, and cardiopulmonary causes. Because the history remained limited and the differential included recurrent pneumonia, aspiration, and central nervous system infection, a broad infectious and metabolic evaluation was initiated. Lumbar puncture was deferred because of clinical instability, and empiric vancomycin, ampicillin, and ceftriaxone were administered. Before cardiopulmonary decompensation, while her vital signs were normal, she received a total of 1 L of intravenous crystalloid.
After cardiac and lung POCUS raised concern for Takotsubo syndrome with cardiogenic pulmonary edema, no additional large-volume crystalloid was administered. Treatment included intravenous furosemide, nitroglycerin, supplemental oxygen, and metoprolol 5 mg IV ×2. Metoprolol was used for severe-range hypertension and tachycardia after clinically significant LV outflow tract obstruction was considered unlikely on POCUS. Heart rate and blood pressure improved without observed hypotension, bradycardia, or another adverse effect. Because nitroglycerin and other interventions were given concurrently, the improvement cannot be attributed to metoprolol alone.
Noninvasive positive-pressure ventilation was deferred because the oxygen requirement remained modest and airway protection was a concern during the postictal period. The patient was admitted to the intensive care unit for recurrent seizure or possible nonconvulsive status epilepticus, acute hypoxemic respiratory failure, and severe left ventricular systolic dysfunction.
Hospital Course and Outcome
During admission, NT-proBNP resulted at 19,459 pg/mL, and troponin peaked at 2,259 ng/L. Formal transthoracic echocardiography demonstrated an LVEF of 19%, regional wall-motion abnormalities consistent with Takotsubo syndrome, and a possible apical LV thrombus. Therapeutic anticoagulation was started empirically.
Coronary CT angiography showed moderate stenosis of the first diagonal branch with otherwise mild plaque burden. Lesion-specific CT-derived fractional flow reserve indicated a low likelihood of flow limitation. No LV thrombus was visualized on coronary CT angiography or subsequent contrast-enhanced echocardiography.
Serial imaging showed rapid recovery of systolic function: LVEF improved from 19% to 54% on early repeat echocardiography and to 66% within 48 hours. The characteristic wall-motion pattern, prior documentation of normal systolic function, absence of a flow-limiting coronary lesion, and rapid recovery strongly supported Takotsubo syndrome. Invasive coronary angiography was therefore deferred.
The neurologic presentation was characterized as possible nonconvulsive status epilepticus. EEG showed possible epileptiform discharges, although no further clinical seizure-like episodes occurred. Brain MRI demonstrated acute left parietal and left paramedian frontal infarcts. The stroke service considered the multifocal distribution most consistent with a cardioembolic mechanism in the setting of the suspected apical thrombus and initial LVEF of 19%.
Because the patient had recovery of her systolic function and neither contrast-enhanced echocardiography nor coronary CT angiography confirmed a persistent thrombus, therapeutic anticoagulation was discontinued in favor of antiplatelet therapy. The patient was discharged home on aspirin with family support at her neurologic baseline.
Discussion
Takotsubo syndrome is an acute heart failure syndrome characterized by transient regional LV dysfunction. The classic pattern consists of apical and midventricular hypokinesis or akinesis with relative basal hyperkinesis, though other variants occur. While regional dysfunction generally extends beyond a single coronary artery distribution, alternative causes of myocardial injury such as culprit coronary lesions must still be excluded before formal diagnosis.1,2
Acute neurologic disease is a recognized physical trigger, and seizures are among the most frequently reported neurologic precipitants. These patients may not report chest pain or dyspnea, so the diagnosis can be overlooked when the initial evaluation is dominated by altered mental status or seizure activity.3 In this case, the causation between seizure activity, multifocal ischemic stroke, and cardiac dysfunction could not be definitively established; therefore, the diagnosis is most accurately represented by seizure-associated Takotsubo syndrome.
POCUS cannot independently distinguish Takotsubo syndrome from acute coronary occlusion, and B-lines are not specific to cardiogenic edema. However, immediate recognition of severe LV dysfunction with a characteristic regional pattern, combined with diffuse B-lines, rapidly shifted the working diagnosis toward cardiogenic pulmonary edema. This led the team to withhold additional crystalloid, begin diuresis and afterload reduction, and advocate for the appropriate level of care for stabilization and definitive cardiac testing. The case does not establish that the initial liter of crystalloid caused the deterioration or that additional fluid would necessarily have caused harm.
Evidence for beta-blockers in Takotsubo syndrome remains observational and conflicting. Expert consensus considers beta-blockade reasonable in selected hemodynamically stable patients until LV recovery, with cautious use in acute severe heart failure, hypotension, bradycardia, and marked QTc prolongation.4 A recent registry analysis associated beta-blocker therapy at discharge with lower long-term mortality but not reduced recurrence or faster LVEF recovery.5 There is no randomized evidence establishing benefit from acute IV beta-blockade. The observed improvement after metoprolol in this case should therefore be reported as a clinical course observation rather than evidence of efficacy.
Severe apical dysfunction can promote LV thrombus formation and systemic embolization.6 The first formal echocardiogram raised concern for an apical thrombus and prompted empiric anticoagulation, while MRI showed multifocal cerebral infarcts. However, neither contrast echocardiography nor coronary CT angiography later confirmed the thrombus. The case therefore illustrates a suspected cardioembolic complication rather than a definitively demonstrated LV thrombus.
The rapid recovery from an LVEF of 19% to 66% within 48 hours, together with prior normal systolic function, favored the diagnosis of transient stress cardiomyopathy. Initial severe systolic dysfunction identified a high-risk phenotype, even though ventricular function recovered quickly.7,8
Bottom Line
In patients with seizure or altered mental status who develop unexplained tachycardia, hypoxemia, elevated cardiac biomarkers, or pulmonary edema, combined cardiac and lung POCUS can rapidly identify severe ventricular dysfunction and pulmonary congestion. The examination can guide early stabilization and level-of-care decisions while definitive coronary and cardiac evaluation proceeds. Severe transient apical dysfunction should also prompt evaluation for LV thrombus and systemic embolic complications.
References
1. Medina de Chazal H, Del Buono MG, Keyser-Marcus L, et al. Stress cardiomyopathy diagnosis and treatment: JACC state-of-the-art review. J Am Coll Cardiol. 2018;72(16):1955-1971. doi:10.1016/j.jacc.2018.07.072
2. Singh T, Khan H, Gamble DT, et al. Takotsubo syndrome: pathophysiology, emerging concepts, and clinical implications. Circulation. 2022;145(13):1002-1019. doi:10.1161/CIRCULATIONAHA.121.055854
3. Cammann VL, Scheitz JF, von Rennenberg R, et al. Clinical correlates and prognostic impact of neurologic disorders in Takotsubo syndrome. Sci Rep. 2021;11(1):23555. doi:10.1038/s41598-021-01496-9
4. Ghadri JR, Wittstein IS, Prasad A, et al. International expert consensus document on Takotsubo syndrome (part II): diagnostic workup, outcome, and management. Eur Heart J. 2018;39(22):2047-2062. doi:10.1093/eurheartj/ehy077
5. Raposeiras-Roubin S, Santoro F, Arcari L, et al. Beta-blockers and long-term mortality in Takotsubo syndrome: results of the multicenter GEIST Registry. JACC Heart Fail. 2025;13(5):815-825. doi:10.1016/j.jchf.2024.11.015
6. Ding KJ, Cammann VL, Szawan KA, et al. Intraventricular thrombus formation and embolism in Takotsubo syndrome: insights from the International Takotsubo Registry. Arterioscler Thromb Vasc Biol. 2020;40(1):279-287. doi:10.1161/ATVBAHA.119.313491
7. Citro R, Radano I, Parodi G, et al. Long-term outcome in patients with Takotsubo syndrome presenting with severely reduced left ventricular ejection fraction. Eur J Heart Fail. 2019;21(6):781-789. doi:10.1002/ejhf.1373
8. Almendro-Delia M, Lopez-Flores L, Uribarri A, et al. Recovery of left ventricular function and long-term outcomes in patients with Takotsubo syndrome. J Am Coll Cardiol. 2024;84(13):1163-1174. doi:10.1016/j.jacc.2024.05.075
















