Male patient of 89 years-of-age, with history of smoking and arterial hypertension, and the following cardiovascular background: complete right branch bundle block, bilateral pulmonary embolism resulting in anticoagulation, atrial fibrillation, and heart failure with preserved ejection fraction. As mentioned before, he also had melanoma in current treatment with a checkpoint inhibitor (Pembrolizumab), and chronic renal disease (creatinine 2.2 mg/dL).

He was admitted in the emergency department because of chest pain of intensity 5/10 with palpitations and dyspnea. The physical examination revealed signs of left sided heart failure, and the patient exhibited no fever. Moreover, he remained lucid with no apparent neurological impairments. The following routine exams were carried out: Electrocardiogram: AF rhythm, 60 bpm, complete right bundle-brunch blockade; Chest X-ray cardiothoracic index increased/cardiomegaly, redistribution of pulmonary flow, and broad vascular pedicle. He had a high sensitive troponin T at admission of 554 ng/L and creatinine of 3 mg/dL. Echocardiogram showed right chambers dilated, left ventricle with global hypokinesia, increased left ventricle filling pressures and pulmonary hypertension. Ejection fraction was estimated in 40%.

Coronary artery disease was initially considered as a potential diagnosis; however, given the patient's medical history, and the temporal relationship with the administration of pembrolizumab, a drug related to the occurrence of myocarditis, that became the primary suspicion, leading to the initiation of high-dose steroid treatment. To determine the etiology of the suspected myocarditis, an endomyocardial biopsy was performed. Unfortunately, an intraprocedural complication arose: pleural effusion resulting in iatrogenic cardiac tamponade, leading to hemodynamic instability. The patient had a blood pressure (BP) of 70/40 mmHg and a heart rate (HR) of 130 bpm, with poor peripheral perfusion and mental confusion requiring volume and inotrope support with noradrenaline. Clinical manifestations raised suspicion of tamponade, prompting a bedside echocardiogram that confirmed diagnosis. It required immediate pericardial drainage via subxiphoid puncture, obtaining a 550 mL hematic debit. After pericardiocentesis, patient improved hemodynamically (BP 140/80 HR 100 bpm), but this did not last more than two or three minutes. The pericardial fluid was drained and re-generated rapidly. A catheter for pericardial drainage was placed and more than 1 L of blood drained in the first hour. He received three units of platelets as treatment since he had been on aspirin therapy for the past 48 h. Additionally, prothrombin complex 600 IU was administered due to the history of apixaban use more than 48 hs before. Aminocaproic acid (10 g in 100 mL) was administered, and four units of red blood cells were transfused. Despite these efforts, the patient remained hemodynamically unstable, and due to the elevated surgical risk, intrapericardial thrombin (600 UI of thrombin in 1 mL of saline) was employed, administered as a bolus, to achieve successful hemostasis. Echocardiograms (Fig. 1): the initial 2D echocardiogram before thrombin injection shows pericardial fluid and right ventricular collapse, indicative of cardiac tamponade. This goes along with the second image that shows the mitral peak E wave that has more than 25–40% of variation within inspiration, also consistent with cardiac tamponade. Contrarily, the resting images show no pericardial fluid accumulation after the intervention has been made, and the mitral peak E waves velocity within normal variation.

A 2D Echocardiogram: Subxiphoid view showing pericardial fluid with right ventricular collapse consistent with cardiac tamponade (arrow); B Doppler echocardiography: variation in mitral peak E velocity more than 25–40% with inspiration; C 2D Echocardiogram: Subxiphoid view showing no pericardial effusion (arrow); D Doppler echocardiography: mitral peak velocity without abnormal variation