Mechanical, extracardiac compression by large pleural effusions can impair cardiac filling and cause hemodynamic changes consistent with cardiac tamponade. In this case, a 68-year-old woman presented with fatigue and mild dyspnea on exertion one month following bioprosthetic mitral valve replacement for severe mitral regurgitation. Initial examination revealed hypotension, tachycardia, and pulsus paradoxus. Imaging demonstrated a large right pleural effusion, a small anterior pericardial effusion, and echocardiographic tamponade. After bedside thoracentesis, echocardiographic findings of tamponade resolved, and the patient's symptoms improved. In this patient, a large pleural effusion caused tamponade physiology rather than a pericardial effusion. Increased intrathoracic pressure can impair cardiac filling and result in tamponade physiology, and thoracentesis can resolve tamponade physiology even without pericardiocentesis. This case highlights the importance of recognizing extracardiac factors that may cause cardiac tamponade and warrant a tailored diagnostic and therapeutic approach.

Effusive-constrictive pericarditis (ECP) is a condition where acute pericarditis causes a pericardial effusion and stiffening of the pericardium, which can result in haemodynamic instability due to compression of right-sided cardiac chambers. Here, we present a patient with cardiac tamponade followed by ECP complicating treatment of acute myocardial infarction/cardiogenic shock supported with a percutaneous left ventricular assist device (PVAD).

Cardiac tamponade is a life-threatening condition resulting from fluid accumulation within the pericardial sac, leading to impaired cardiac filling and output. Signs described in the literature, such as Beck's triad (hypotension, jugular venous distension (JVD), muffled heart sounds) or pulsus paradoxus can be absent especially in the early stages, particularly in non-trauma patients, making early diagnosis challenging. In this case series, we present three patients who developed tamponade with subtle symptoms, including shortness of breath and tachycardia, but without hypotension or other hallmark signs. Cardiac point-of-care ultrasound (POCUS) played a critical role in early detection, revealing pericardial effusion and right ventricular (RV) diastolic collapse. Rapid diagnosis facilitated timely pericardiocentesis, which resolved symptoms and prevented further decompensation. This series underscores the value of POCUS in detecting early-stage tamponade, where traditional clinical markers of hypotension, JVD, muffled heart sounds, and pulsus paradoxus may not be present. The main purpose of this article is to showcase how early use of cardiac POCUS can prompt cardiology consultation and appropriate management, improving patient outcomes.

This article describes the prompt diagnosis and life-saving intervention facilitated by point-of-care ultrasound (POCUS) in a patient presenting with tamponade secondary to a rare case of purulent pericarditis. Within a remarkable timeframe of only 40 minutes from emergency department (ED) presentation to pericardial drainage, POCUS not only confirmed the diagnosis but also expedited critical treatment measures. The etiology of the underlying purulent pericardial effusion was traced to a Streptococcus pneumoniae infection. Ultimately, the patient had untreated X-linked agammaglobulinemia (XLA), a rare immunodeficiency disorder, adding layers of complexity to the clinical scenario. Notably, only three other documented cases exist in the literature detailing adult XLA patients afflicted with purulent pericarditis, rendering this case both exceptional and informative.

Pulsus paradoxus refers to an exaggerated fall in a patient’s blood pressure during inspiration by greater than 10 mm Hg. Pulsus paradoxus results from alterations in the mechanical forces imposed on the chambers of the heart and pulmonary vasculature often due to pericardial disease, particularly cardiac tamponade and to a lesser degree constrictive pericarditis. However, it is important to understand that pulsus paradoxus may be seen in non-pericardial cardiac diseases such as right ventricular myocardial infarction and restrictive cardiomyopathy. Additionally, non-cardiac disease states can occasionally lead to pulsus paradoxus including pulmonary disease (severe chronic obstructive pulmonary disease [COPD], asthma, tension pneumothorax, large bilateral pleural effusions, pulmonary embolism), as well as any cause of cardiac compression (iatrogenic during surgery, marked obesity, pectus excavatum). Finally, pulsus paradoxus may also manifest secondary to severe hypovolemic shock.[1][2][3][4]

A male patient in his 20s with a medical history of common variable immunodeficiency disorder, non-compliant with therapy, presented to the emergency department with respiratory distress and severe hypoxaemia. Chest radiography demonstrated extensive bilateral infiltrates and an increased cardiothoracic ratio. Streptococcus pneumoniae urine antigen test was positive. ECG demonstrated diffuse ST-segment elevation. An arterial line was placed and demonstrated pulsus paradoxus. Transthoracic echocardiography revealed an extensive pericardial effusion, with echocardiographic signs of cardiac tamponade. Emergency subxiphoid pericardiocentesis was performed with an initial drainage of 750 mL of purulent fluid consistent with pyopericardium. Immediate haemodynamic improvement was observed. The patient required a second pericardiocentesis for drainage of a relapsing pericardial effusion. The course was complicated by effusive-constrictive pericarditis requiring anterior interphrenic pericardiectomy. Treatment with intravenous immunoglobulin and antibiotics led to a complete recovery.

Asthma encompasses of respiratory symptoms that occur intermittently and with varying intensity accompanied by reversible expiratory airflow limitation. In acute exacerbations, it can be life-threatening due to its impact on ventilatory mechanics. Moreover, asthma has significant effects on the cardiovascular system, primarily through heart-lung interaction-based mechanisms. Dynamic hyperinflation and increased work of breathing caused by a sharp drop in pleural pressure, can affect cardiac function and cardiac output through different mechanisms. These mechanisms include an abrupt increase in venous return, elevated right ventricular afterload and interdependence between the left and right ventricle. Additionally, Pulsus paradoxus, which reflects the maximum consequences of this heart lung interaction when intrathoracic pressure swings are exaggerated, may serve as a convenient bedside tool to assess the severity of acute asthma acute exacerbation and its response to therapy.

Pulsus alternans, not to be confused with pulsus paradoxus or electrical alternans, is an arterial pulse with alternating strong and weak beats. Systolic pressures will vary from beat-to-beat as identified on physical exam and echocardiogram. Pulsus alternans is found in the setting of severe ventricular dysfunction and other forms of cardiac pathology. Variations of pulsus alternans include left ventricular alternans, right ventricular alternans, and biventricular alternans. The treatment and clinical outcomes for pulsus alternans vary depending upon the underlying causative etiology, though its presence generally suggests a poor prognostic outlook.[1]