Low-pressure tamponade due to hemothorax after transcatheter edge-to-edge repair of the mitral valve

Abstract

BACKGROUND

The use of percutaneous transcatheter edge-to-edge repair (TEER) for mitral regurgitation (MR) has increased, including an increased application to older, frailer, and higher risk patients.

CASE SUMMARY

A 74 year-old woman with severe MR, a left ventricular ejection fraction of 45%, and a small circumferential pericardial effusion underwent TEER of the mitral valve. After the placement of two MitraClips, the MR was assessed as mild to moderate. Within 10-20 minutes after the completion of the case, the patient was dyspneic and hypotensive despite volume resuscitation. Point-of-care ultrasound (POCUS) showed no changes in cardiac contractility, valve function, or the pericardial space. The right heart chambers appeared small with right atrial (RA) diastolic collapse. There was no evidence of venous congestion. Further exam showed a large right pleural fluid collection. Given the clinical scenario of dyspnea, hypotension, and diastolic RA collapse, low-pressure tamponade was suspected. A thoracentesis expelled 1200 mL of blood with immediate hemodynamic improvement. The patient made an uneventful recovery.

CONCLUSION

The application of POCUS is crucial for detecting, diagnosing, and properly managing cardiac dysfunction and procedural complications associated with TEER. While tamponade is classically associated with a pericardial effusion and vena caval plethora, their absence does not dismiss the suspicion or diagnosis of tamponade. This case highlights the value of POCUS in assessing low-pressure tamponade caused by a large, pressurized pleural effusion. Clinical suspicion, supported by POCUS findings, was confirmed by a thoracentesis that resulted in immediate hemodynamic improvement.

Key Words: Low-pressure tamponade; Pleural effusion; MitraClip; Echocardiography; Point of care ultrasound

Core Tip: In the case presented, the acute accumulation of blood in the right pleural space resulted in low-pressure tamponade, which was further confirmed by a thoracentesis that resulted in immediate improvement in hemodynamics. The case highlights varied presentation of tamponade and the value of periprocedural ultrasound to assess cardiopulmonary dysfunctions.

INTRODUCTION

The use of percutaneous transcatheter edge-to-edge repair (TEER) for mitral regurgitation (MR) has increased, including an increased application to older, frailer, and higher risk patients[1-6]. Despite its increasing application to a higher risk population, the incidence of adverse outcomes has declined from 15% in 2005 to ≤ 3.5% in 2020, reflecting improved device technology, experience, and imaging[3,7,8].

Complications can be categorized as either patient-related, reflective of baseline cardiopulmonary function, or procedure-related, both with potential to cause hypotension[3,7-10]. Hemodynamic instability may result from arrhythmias, ventricular dysfunction, and the effects of general anesthesia[3,8-12]. Injury to cardiovascular tissues include the access site, the cavae, atrial and ventricular myocardial tissues, the interatrial septum, and the mitral valve, with the latter including worsening of regurgitation[3,8,9,11]. One result of cardiac injury is the development of a pericardial effusion with or without cardiac tamponade[4,8].

In addition to guiding the TEER procedure, intraoperative transesophageal echocardiography (TEE) monitors for complications with frequent surveillance for new or worse cardiac dysfunctions, and for injuries as a result of the delivery apparatus, to allow prompt recognition and management to prevent long-term consequences. For the same reason, point-of-care ultrasound (POCUS) should be immediately available for evaluation of patients with cardiopulmonary dysfunction after structural heart procedures[13]. We present the case of an elderly patient who underwent successful mitral TEER that was complicated by hypotension due to low pressure pericardial tamponade related to an acute hemothorax. Immediate post-procedure POCUS was instrumental in discerning the cause and guiding management.

CASE PRESENTATION

Chief complaints

The patient was a 74-year-old woman with mitral valve bileaflet prolapse, severe MR, and congestive heart failure who presented for mitral TEER.

History of present illness

The patient’s symptoms included increasing dyspnea and declining exercise capacity. The patient was considered a poor surgical candidate and was scheduled for TEER under general anesthesia with TEE guidance.

History of past illness

Additional medical issues included a history of kyphoscoliosis, Parkinson’s disease, hypertension, and depression.

Personal and family history

The patient’s past surgical history included posterior spinal fusion instrumentation of the thoracolumbar (T1-L3) spine. Medications included lisinopril, furosemide, and atenolol.

Physical examination

As noted.

Laboratory examinations

As noted.

Imaging examinations

Pre-procedure echocardiography reported mild-moderately reduced left ventricular function, an estimated left ventricular ejection fraction (LVEF) of 45%, left ventricular and atrial dilation, and normal right ventricular size and contractility. The mitral valve was mildly calcified with moderate annular calcification, bileaflet prolapse, and severe regurgitation. The mitral valve area was between 4-4.4 cm² by three-dimensional planimetry measurements. A small pericardial effusion was reported. Electrocardiogram showed a sinus rhythm rate of 64 beats/min and evidence of left ventricular hypertrophy. Preoperative chest radiography (CXR) revealed an enlarged heart and no pulmonary pathology. Spine instrumentation extending from the cervical spine to below the diaphragm was noted. Prior computed tomography imaging showed a leftward cardiac displacement related to the kyphoscoliosis.

Intraoperative monitors included standard ASA noninvasive monitors and an intra-arterial catheter for continuous blood pressure monitoring and blood sampling as needed. Pre-induction glycopyrrolate and dexmedetomidine were administered. General endotracheal anesthesia was induced with propofol and maintained with sevoflurane and rocuronium. An intravenous norepinephrine infusion was administered to maintain a systolic blood pressure above 100 mmHg. During the procedure, the infusion dose of norepinephrine ranged from 3-8 mcg/min and was titrated off during emergence.

The pre-procedure baseline TEE exam confirmed severe (4+) MR with a flail P2 scallop and torn chordae tendinae, and otherwise myxomatous appearing posterior and anterior leaflets. There was significant leaflet and annular calcification (Video 1). Pulse wave Doppler revealed reversal on pulmonary venous systolic flow. Qualitatively, the left ventricle appeared dilated and the estimated LVEF was 45%-50%. Right ventricular size and function appeared normal. The interatrial septum was aneurysmal and a small-sized hemodynamically insignificant circumferential pericardial effusion was noted.

MULTIDISCIPLINARY EXPERT CONSULTATION

The TEER procedure was performed from a right femoral venous access site. Guidewires were placed from the femoral vein into the superior vena cava (SVC) with some difficulty likely due to the patient’s spine deformity and cardiac rotation. An 8-French Versacross (Boston Scientific, Marlborough, MA, United States) transseptal sheath and dilator were advanced to the SVC over the guidewires and the Versacross sheath was passed along the interatrial septum 4.0 cm posterior to the mitral annulus. The initial mean left atrial (LA) pressure was 40 mmHg with a V-wave of 80 mmHg. Intravenous heparin was administered to achieve an activated clotting time > 250 seconds. The Versacross sheath was exchanged for a 24F guide sheath through which the MitraClip (Abbott, Santa Clara, United States) was passed. Attempts to advance the clip to the mitral valve failed and it was decided that the transseptal puncture was not optimal to allow for proper orientation of the clip perpendicular to the mitral annulus.

After removing the MitraClip, the 24F sheath was pulled back into the right atrium (RA) and the Versacross wire advanced back to the SVC, again with mild difficulty. A second transseptal procedure was performed approximately 4.5 cm posterior to the mitral annulus. At this time, there were no changes to the pericardial space and patient hemodynamics remained stable.

The first MitraClip (XTW) was advanced and deployed across the A2/P2 scallops with a modest reduction in MR (Video 2). A second MitraClip (NTW) was then placed lateral to the first with a reduction in MR to mild/moderate (1-2+) (Video 2). This was associated with hemodynamic improvement, including normalization of pulmonary venous flows, a reduction of the mean LA pressure to 20 mmHg and V-wave to 30 mmHg, and an increase in the left ventricular outflow pulse wave Doppler time velocity integral from 16 cm to 18.5 cm. The peak and mean transmitral pressure gradients were 8 and 4 mmHg respectively. Three-dimensional planimetry estimated the mitral valve area to be > 2.0 cm².

After removing the sheath from the LA to RA, there were two small iatrogenic atrial septal defects with left to right flow. The pericardial effusion remained unchanged in size. Heparin was reversed with 20 mg of protamine. Good hemostasis was reported after removal of the femoral sheaths.

Hemodynamics remained stable throughout the majority of the procedure. The blood pressure trended down toward the conclusion of the procedure and during emergence from general anesthesia but remained within normal ranges. The patient’s airway was extubated uneventfully. She was awake and responsive, and transferred to the recovery area. Within 10 minutes of arrival to the post-procedure care unit, the patient developed hypotension and dyspnea (Table 1).

Table 1 Vital signs, vasoactive medications, fluid totals, and blood gas data prior to induction of general anesthesia, in the operating room, upon extubation, and in the post-procedure care unit.

	Pre-induction	Operating room	Extubation	PCU 0-10 minutes	PCU 20 minutes	PCU post
Heart rate (beats/min)	67	62→70	64	90	95-100	90
Blood pressure (mmHg)	177/83	140-150/75-88	95/55	80/40	80/45	95/60
Norepinephrine (mcg/min)		2-4	0	0-8	8-10	2
Respiratory Rate (breaths/min)	15	12	18	28	30	25
SaO2 (%)	100	100	98	85	95	98
Respiratory mode	Spont	Vent	Vent→Spont	Spont	BiPAP	Vent
Hgb (gm/dL)	11			8.7		11
Fluids (mL)		500 mL LR		500 mL LR; 1050 mL PRBCs
pH					6.99	7.32
PaCO2 (mmHg)					98	37
PaO2 (mmHg)					> 400	252

Hgb: Hemoglobin; SaO₂: Arterial oxygen saturation; BiPAP: Bi-level positive airway pressure; PaCO₂: Partial pressure of carbon dioxide in arterial blood; PaO₂: Partial pressure of oxygen in arterial blood; PCU: Post-procedure care unit; PRBC: Packed red blood cells; LR: Lactated ringers.

The cardiac monitor showed a sinus rhythm with a rate of 90 beats/min. The norepinephrine infusion was restarted at 7 mcg/min and a 500 mL fluid bolus was administered. On exam, the patient was sitting upright and appeared dyspneic. Breath sounds were significantly reduced on the right side. The trachea appeared to be midline. There was a mild systolic murmur. There was no jugular venous distention.

A point-of-care hemoglobin was noted to be 8.7 g/dL which was reduced from 11.0 m/dL preoperatively. Blood component therapy was instituted given the reduced Hgb and hemodynamic instability. The patient was resuscitated with 500 mL intravenous lactated Ringers solution and 3 units (approximately 1050 mL total) packed red blood cells but attempts to wean the norepinephrine infusion were unsuccessful.

A bedside transthoracic echocardiographic (TTE) exam was performed. While the pericardial effusion appeared unchanged, the right heart chambers were small and there was an inward motion of the right atrium during early ventricular systole, or atrial diastole (Figure 1; Video 3). Subcostal imaging revealed an inferior vena cava (IVC) diameter of 0.8 cm with 50% change during spontaneous respiration (Figure 1). A clear space was noted postero-lateral to the right atrium in the apical four-chamber window (Figure 1; Video 3). The transducer was repositioned toward the right chest and revealed a large right-sided pleural fluid collection with lung collapse (Figure 1; Video 3). Lung sliding was present. CXR confirmed a new large right chest fluid collection without changes in mediastinal space (Figure 2).

Figure 1 Point-of-care ultrasound exam. A: Post-procedure cardiac apical four-chamber view showing large fluid collection posterior and lateral (PlEff) to the right atrium (RA) causing RA collapse (white arrow showing inward position of the RA wall) during ventricular systole (i.e., atrial diastole); B: Post-procedure cardiac subcostal view showing four chambers and RA collapse during atrial diastole (white arrows showing inward position of the RA wall) and a small right ventricle (RV); C: Transesophageal echocardiographic view, obtained during the procedure, showing pericardial effusion along the RA and right ventricular chambers (RV) measuring approximately 1.1 to 1.2 cm; D: Post-procedure subcostal view showing inferior cava diameter of 0.8 cm; E: Ultrasound of the right chest demonstrating collapsed lung and a large right chest fluid.

Figure 2 Chest X-ray. A: Pre-procedure chest radiograph obtained the day before the scheduled mitral clip procedure. The lung fields appear hyperinflated with flattened diaphragms. There is extensive hardware (rods) seen along the spine; B: Post-procedure chest radiograph showing new haziness (white arrow) consistent with fluid. At this time, the patient was hypotensive and severely acidotic most due to a respiratory acidosis presumably related to extensive right lung collapse; C: Post-chest-tube-placement chest radiograph showing clearance of right pleural fluid. The lung fields appear smaller perhaps consistent with pulmonary atelectasis. As the prior films also see, there is extensive hardware along the spine.

Hypoxemia improved with the initiation of bi-level positive airway pressure. However, the patient was severely acidotic, and hypercarbic (Table 1). Hemodynamic instability persisted. A tube thoracostomy was requested. Although endotracheal intubation was planned, it was deferred until after the thoracostomy because of suspected tamponade physiology. Upon placement of the chest tube, bloody fluid was forcibly expelled. Over the course of 1-2 minutes, a total of 1.2 L of bloody fluid was drained, which was associated with improved patient hemodynamics and a reduction in the norepinephrine infusion rate. CXR confirmed placement of the tube thoracostomy and improved lung fields (Figure 2).

Although cardiopulmonary function was improved, the patient still appeared dyspneic. Since computed tomographic imaging was planned to evaluate etiology of hemothorax, the patient was sedated, intubated, and placed on mechanical ventilatory support. The norepinephrine infusion was weaned off.

Subsequent computed tomographic imaging did not reveal an active bleeding site; however, imaging artifact was reported due to previous spine instrumentation. It was speculated that a vena caval injury likely due to stiff wires and catheters created a communication from the SVC into the right pleural space. The change from positive pressure ventilation to spontaneous ventilation, a more upright position, and resolution of anticoagulation, reduced caval pressures and helped seal the possible injury.

There was no more drainage from the chest tube.

FINAL DIAGNOSIS

Low-pressure tamponade.

TREATMENT

As described above.

OUTCOME AND FOLLOW-UP

After 24 hours of observation and continued hemodynamic stability, the patient was successfully extubated on postoperative day 1. The patient was eventually discharged on postoperative day 4 and recovered uneventfully.

DISCUSSION

The causes of cardiopulmonary dysfunction associated with TEER are multiple, including the effects of general anesthesia, new ventricular dysfunction, trauma to the mitral apparatus and/or new stenosis, and trauma to cardiovascular tissues[3,8-11]. A new or worsening pericardial effusion during TEER is reported in up to 3% of patients but has declined to a rate of < 0.5%[3,5,7,8-10,12]. Cardiac tamponade is reported between 0% and 2.8% of TEER cases[8]. The risk of pericardial injury and effusion may be highest during the transseptal puncture, with placement of wires, dilators, guides, or sheaths possibly causing injury to cardiac structures, especially the thinner tissues including caval-atrial connections, the right atrium and ventricle, the left atrium, and pulmonary veins[7,8,9,14]. Cases of left ventricular injury are also reported[12]. With improved echocardiographic imaging guiding transseptal puncture and passage and positioning of delivery components, the occurrence or worsening of a pericardial effusion is low[7,9,12,15].

Acute pulmonary complications are uncommon during TEER but can result from general anesthesia, new ventricular dysfunction, and/or acute mitral valve dysfunction[8,9,16,17]. A new pleural effusion is reported in < 1% of cases and pulmonary embolism occurs in 0%-0.2%[8,9,14]. Respiratory failure requiring reintubation occurs in up to 2%[8,9]. Isolated cases reports describe pulmonary hemorrhage due to guidewires passed into the pulmonary vein[18]. In the present case, there was no preoperative pleural effusion noted by chest radiogram (Figure 2). The right hemothorax occurred as a complication of the procedure due to passage of stiff wires in the cava. The pleural fluid was detected by POCUS.

The patient presented was at increased risk for both patient and procedure-related complications[7,10,17-20]. A pre-procedure reduced LVEF and left ventricular dilation are predictors of left ventricular afterload mismatch and dysfunction, which is described in up to 25% of patients[10,17-19]. The risk of tissue injury is increased with a thick or aneurysmal interatrial septum and/or difficult placement of delivery systems in patients with an altered anatomy, such as kyphoscoliosis, which is known to distort the mediastinal space and position of the heart and great vessels and can contribute toward difficulties in passing wires and guides through the cavae and right atrium[20,21]. Additionally, patients with indwelling pacing wires and/or central venous catheters are at greater risk for injury during transeptal procedures[7,12].

This case highlights the importance of procedural monitoring and imaging, the awareness of procedural related complications, and the availability of emergency resources to evaluate and manage cardiopulmonary dysfunction[22-24]. The procedural echocardiographer regularly scans the surrounding tissues for changes in function and structure[24]. Expected findings include a reduction in mitral valve regurgitation, a reduction in mitral valve area, and an iatrogenic atrial septal defect, with or without left ventricular dysfunction[10,17,19,22]. Injury to cardiovascular tissues including the mitral valve leaflets and apparatus, the atrial wall, or pulmonary veins is less common[25-33]. While imaging guidelines have been described to assess cardiac function and anatomy, none describe imaging of the pleural spaces[24-26]. In the case presented, earlier detection of the right pleural fluid would have allowed management while the patient was still under general anesthesia.

Tamponade

Cardiac tamponade is a form of obstructive shock due to a buildup of pressure surrounding the heart causing an inward compressive gradient impairing filling of the cardiac chambers[27,28]. While a pericardial effusion is the most common cause, tamponade can result from other pathologies creating an inward pressure gradient[27,28]. The reduction in stroke volume and cardiac output results in cardiogenic shock. Clinical findings have varying incidences, sensitivities, specificities, and predictive values[28-30]. Dyspnea, tachypnea, and/or tachycardia are each reported in 65%-90% of patients with tamponade[28-30]. Hypotension, defined as either a systolic blood pressure of < 100 or < 90 mmHg, occurs in fewer than 50% with a reported sensitivity and specificity of 24% and 83%, respectively[28-30]. The individual components of the classically described Beck’s triad (hypotension, jugular venous distention, and muffled heart sounds) occur between 14%-88% of cases, each having sensitivities less than 50%, with very few patients presenting with all three findings[28-30]. Since presentations vary, the diagnosis of tamponade relies on suspicion which initiates ultrasound imaging to delineate pathology and guide therapy. Improved hemodynamic function after treatment confirms the diagnosis.

Tachycardia, which has been defined as a heart rate greater than 100 beats/min, has a pooled sensitivity of 77% and a lower specificity for diagnosing tamponade[31]. Although not definitively tachycardic, the patient’s heart rate increased significantly from a baseline of 60-70 bpm to 90-100 bpm in the recovery room. This change is notable, particularly given the patient’s medical regimen which included daily atenolol and a single dose of dexmedetomidine prior to induction of anesthesia. Despite heart rates remaining below 100 bpm, the substantial rise in an unstable patient proved clinically significant[31]. Given the variable sensitivity and specificity of the signs and symptoms of tamponade, perhaps significant changes in vital signs are valuable to consider the next step to assess cardiovascular dysfunction, which, in the case presented, included POCUS.

POCUS

POCUS is a non-invasive bedside ultrasound exam used to assess cardiovascular and pulmonary dysfunctions, thereby improving diagnostic pathways and accuracy, reducing the time to diagnosis, and facilitating care[13,32-36]. Differentiation between the causes of shock helps to direct care[37]. Compared to a focused cardiac ultrasound exam, POCUS include a more comprehensive evaluation including scans of the heart, lungs, and abdomen. Lung ultrasound allows detection of fluid collections, lung masses, lung collapse, and pneumothorax[37]. In the present case, the combination of cardiac and lung ultrasound was critical in evaluating hypotension, suspecting tamponade, and directing therapy.

Right atrial (RA) compression/collapse/inversion during ventricular systole (atrial diastole) is a sensitive marker while right ventricular collapse during ventricular diastole is considered more specific[28]. In a study of 127 patients with moderate to large pericardial effusions, 19 had tamponade[38]. All 19 patients had RA “inversion” (sensitivity 100%) while 19 others with inversion did not have a diagnosis of tamponade (specificity 82%; predictive value of 50%)[38]. The predictive value of RA inversion increased when collapse occurred over > 34% of the atrial diastolic period (sensitivity 94%; specificity 100%; positive predictive value was 100%)[38]. While there are gradations of tamponade, from early to late, RA collapse indicates the onset of hemodynamic dysfunction[39]. The POCUS exam revealed impaired RA filling and a small right ventricle. The small pericardial effusion was not thought to be hemodynamically significant nor easy to drain percutaneously.

Caval size and compressibility/low pressure tamponade

The diagnosis of tamponade was uncertain by the absence of caval congestion. Venous hypertension and congestion, or “plethora”, defined as an IVC diameter > 2.1 cm with a < 50% reduction after deep inspiration or a sniff, typically occurs with tamponade and its absence has a sensitivity and negative predictive value > 95% and a 40% specificity[40,41]. While the presence of IVC plethora is sensitive for tamponade, it is less specific as it can be seen in patients with lung disease, heart failure, and right-sided valvular lesions[28,40]. In the case presented, the IVC was not dilated nor congested despite the suspicion of tamponade, which was based on hemodynamics and RA diastolic collapse and small right heart chambers.

Although vena cava plethora is a very sensitive marker of tamponade, exceptions are noted in patients with localized effusions or in those with hypovolemia[41-43]. Low-pressure tamponade is described mainly in case reports[44-48]. In a review of 279 patients with pericarditis who underwent right heart catheterization and pericardiocentesis, 29 were classified as having ‘low pressure’ described by the absence of jugular venous distention, and the IVC not “plethoric”[44]. Pericardial and RA pressures were low to normal or ≤ 15 mmHg[44]. Nevertheless, an inward pressure gradient and diastolic chamber compression/collapse were present. Despite the absence of more classic hemodynamic tamponade features, these patients experienced hemodynamic benefit from drainage of the pericardial fluid[44]. In the present case, treatment of hypotension with intravenous fluids and vasopressor was not effective, prompting the performance of POCUS. Similar to the study by Sagristà-Sauleda et al[44], with the combination of hemodynamic instability, RA diastolic collapse, and a small right ventricle, it is reasonable to suspect the presence of tamponade, despite the absence of IVC plethora.

Pleural effusion as a cause of tamponade

POCUS permits imaging a “bigger” picture[49]. The initial imaging depth of 20 cm produced a comprehensive image of the heart and surrounding spaces and tissues, which demonstrated a hypolucent space and prompted imaging of the right chest revealing the large fluid collection in the pleural space[50] (Figure 1; Video 3). In the context of hypotension, a small right heart, and RA diastolic collapse, the discovery of a new large right pleural effusion prompts suspicion of a tamponade syndrome. The absence of venous congestion suggests the diagnosis of low-pressure tamponade.

Extracardiac pericardial pressure is most commonly due to a pericardial effusion. However, other pathologies can cause tamponade including pericardial masses, chest wall anomalies, or infection[27,51]. Large pleural effusions with increased intrapleural pressure may create an inward extra-cardiac pressure gradient impairing both right and left heart filling and has been reported both clinically and experimentally[52-57]. In 116 patients with a pleural effusion and no pericardial effusion, diastolic chamber collapse was noted in 21 (18%) patients[58]. The effect of pleural pathologies is increased in patients with small otherwise hemodynamically insignificant pericardial effusions[48,51-56]. Pleural fluid volumes as low as 500-600 mL have been associated with cardiac chamber collapse[51], but volumes > 1000 mL are commonly reported[52-56,59-61]. Drainage of pleural fluid typically restores normal cardiac chamber filling and improves hemodynamics[51-56,59-61]. In studies of patients with unilateral or bilateral pleural effusions, only 17% exhibited RA collapse and 48% showed IVC plethora in one study[62], while the other study reported RV collapse and elevated jugular venous pressure in 55% of cases[55]. However, 85%-100% of patients demonstrated respiratory variation of tricuspid and mitral valve flow velocities, which improved after thoracentesis[55,62]. Experimentally, intrapericardial pressures have been shown to rise linearly with intrapleural fluid infusion due to the proximity of the pleural membrane to the pericardial space[52]. Across multiple studies, large pleural effusions are associated with hemodynamic signs of tamponade, with resolution following drainage of pleural fluid[52-56,59-61].

In the present case, the acute accumulation of blood into the right pleural space exerted pressure on the right heart, causing RA collapse and underfilling of the right heart. While hypotension may have also resulted from hypovolemia or acidosis, the patient exhibited poor hemodynamic response to fluid therapy. The immediate hemodynamic improvement following chest tube insertion and drainage of the pleural fluid was consistent with tamponade. The absence of caval plethora was likely related to a low volume state; however, the diagnosis of low-pressure tamponade was considered and definitively managed with right tube thoracostomy[43-48].

CONCLUSION

Application of POCUS is critically important to detect, diagnose, and properly manage cardiac dysfunctions and procedural complications associated with TEER. While tamponade is classically due to a pericardial effusion associated with vena caval plethora, their absence does not dismiss the suspicion or diagnosis of tamponade. The value of the POCUS exam was demonstrated in the case above. Low-pressure tamponade caused by a large pressurized pleural effusion suspected by the clinical exam and POCUS was confirmed by a thoracentesis and immediate hemodynamic improvement.

Under specific clinical scenarios, hemodynamic instability may point toward its cause, while imaging is needed to suspect a diagnosis. The diagnosis of tamponade is confirmed from the performance of a therapeutic procedure, which, as seen in the case presented, was a thoracentesis. POCUS was critical in diagnosing low-pressure tamponade.