Middlesex Hospital was a teaching hospital located in the Fitzrovia area of London, England. First opened as the Middlesex Infirmary in 1745 on Windmill Street, it was moved in 1757 to Mortimer Street where it remained until it was finally closed in 2005. Its staff and services were transferred to various sites within the University College London Hospitals NHS Trust. The Middlesex Hospital Medical School, with a history dating back to 1746, merged with the medical school of University College London in 1987.
Abstract Introduction Cardiac tamponade is difficult to recognize in advanced lung disease. In pulmonary hypertension or marked hyperinflation, elevated right-sided and intrathoracic pressures can blunt right-atrial and right-ventricular diastolic collapse despite hemodynamic compromise [1,2]. Dyspnea, elevated JVP, and abnormal lung sounds are also easily attributed to COPD or heart failure, reinforcing bias and encouraging dismissal of a significant pericardial effusion as incidental [1-3]. Case Report A 78-year-old man with severe COPD on home oxygen and ischemic cardiomyopathy presented with two days of progressive dyspnea and nonproductive cough. Three weeks earlier he had complete heart block with cardiogenic shock requiring permanent pacemaker placement. On arrival he was tachypneic (30-40/min), saturating 92-93% on baseline oxygen with borderline blood pressure. Examination showed increased work of breathing, basal crackles, elevated JVP, distant heart sounds, and bilateral edema—initially attributed to COPD and acute decompensated heart failure. Chest radiograph demonstrated pulmonary venous congestion and small pleural effusions. Bedside POCUS described a large circumferential pericardial effusion with a dilated IVC and right-ventricular extrinsic compression, but the working diagnosis remained COPD/heart failure, and he was treated with IV furosemide, bronchodilators, and BiPAP. He developed worsening respiratory failure and hypotension, prompting MICU admission for undifferentiated shock. An arterial line revealed pulsus paradoxus and repeat focused echocardiography now showed right-atrial systolic and right-ventricular diastolic collapse. After 2.5 L crystalloid for preload optimization, emergent pericardiocentesis drained 300 mL of hemorrhagic fluid under pressure (intrapericardial pressure 37 mm Hg) with rapid improvement in perfusion, consistent with pacemaker-related tamponade. Discussion In COPD or pulmonary hypertension, chronically elevated pleural and right-sided pressures narrow the transmural gradient across the right atrium and ventricle; diastolic chamber collapse may therefore be subtle or absent on transthoracic echocardiography, even when intrapericardial pressure is markedly elevated [2,3]. In this setting, right-atrial diastolic collapse has reduced sensitivity and a “negative” study cannot reliably exclude tamponade when hemodynamics suggest obstructive physiology [1,2]. Diagnostic reasoning is further complicated by bias: in patients with advanced COPD or heart failure, dyspnea, elevated JVP, abnormal lung examination, and radiographic congestion are easily ascribed to familiar pulmonary or volume-overload syndromes, down-ranking tamponade despite a large effusion. For patients with COPD or pulmonary hypertension—particularly after recent cardiac instrumentation—new or progressive dyspnea with elevated JVP, muffled heart sounds, or otherwise unexplained hypotension should trigger a structured tamponade assessment with focused echocardiography and arterial waveform analysis for pulsus paradoxus, with tamponade kept high on the differential until definitively excluded. This abstract is funded by: None
Background:Hypoglossal nerve stimulation (HGNS) is an established surgical therapy for obstructive sleep apnea (OSA), yet treatment response is variable and appears to be influenced by both body mass index (BMI) and pattern of upper airway collapse. Whether excess body weight differentially affects HGNS efficacy across pharyngeal collapse patterns remains unclear. Methods:We combined data from two independent HGNS cohorts (n=760) to examine whether the association between BMI and HGNS efficacy depends on pharyngeal collapse pattern identified by drug-induced sleep endoscopy. Collapse was categorized as predominantly laterally directed or anteroposterior (AP). Multivariable regression models assessed HGNS efficacy-quantified primarily as percent reduction in apnea-hypopnea index (AHI) on titration polysomnography and secondarily as treatment success (≥50% AHI reduction to <15 events/h)-while testing for effect modification by collapse pattern and adjusting for baseline AHI, partial collapse, surgical center, follow-up sleep study type, and prior or concomitant pharyngeal surgery. Results:Increasing BMI was associated with substantially lower HGNS efficacy among patients with laterally directed collapse, whereas the relationship between BMI and efficacy was attenuated in those with AP collapse. Specifically, each 5 kg/m2 increase in BMI was associated with a -19.7% (95% CI: -33.2 to -6.2) greater reduction in efficacy in lateral collapse compared with -3.8% (-8.0 to 0.36) in AP collapse (interaction p=0.027). Higher BMI also corresponded to reduced odds of treatment success in lateral collapse (odds ratio 4.4 [95% CI: 1.4-14.3] per 5 kg/m2), with no significant association observed in AP collapse (1.1 [0.75-1.5]; interaction p=0.023). Conclusions:The influence of BMI on HGNS treatment response differs meaningfully by pharyngeal collapse phenotype. Incorporating collapse pattern into BMI-based eligibility criteria may improve patient selection and optimize HGNS outcomes.
