Bedside ultrasonographic assessment of the lung and pleura provides rapid, noninvasive, and essential information in diagnosis and management of various pulmonary conditions. Ultrasonography helps in diagnosing common conditions, including consolidation, interstitial syndrome, pleural effusions and masses, pneumothorax, and diaphragmatic dysfunction. It provides procedural guidance for various pulmonary procedures, including thoracentesis, chest tube insertion, transthoracic aspiration, and biopsies. This article describes major applications of ultrasonography for the pulmonary consultant along with illustrative figures and videos.
Chronic obstructive pulmonary disease (COPD) and heart failure with reduced ejection fraction (HFrEF) commonly coexist in clinical practice. The prevalence of COPD among HFrEF patients ranges from 20 to 32 %. On the other hand; HFrEF is prevalent in more than 20 % of COPD patients. With an aging population, the number of patients with coexisting COPD and HFrEF is on rise. Coexisting COPD and HFrEF presents a unique diagnostic and therapeutic clinical conundrum. Common symptoms shared by both conditions mask the early referral and detection of the other. Beta blockers (BB), angiotensin-converting enzyme inhibitors, and aldosterone antagonists have been shown to reduce hospitalizations, morbidity, and mortality in HFrEF while long-acting inhaled bronchodilators (beta-2-agonists and anticholinergics) and corticosteroids have been endorsed for COPD treatment. The opposing pharmacotherapy of BBs and beta-2-agonists highlight the conflict in prescribing BBs in COPD and beta-2-agonists in HFrEF. This has resulted in underutilization of evidence-based therapy for HFrEF in COPD patients owing to fear of adverse effects. This review aims to provide an update and current perspective on diagnostic and therapeutic management of patients with coexisting COPD and HFrEF.
Neuro-hormonal activation may lead to or be associated with pulmonary arterial hypertension (PAH) and right ventricular dysfunction. Notwithstanding whether it is the cause or the consequence of PAH-related right ventricle (RV) dysfunction neurohormonal activation contributes to significant morbidity and mortality in patients with PAH and the progression of RV dysfunction. Experimental data regarding the use of beta adrenergic blockade and renin-angiotensin aldosterone system modulation are encouraging. However, clinical studies have largely been negative or neutral; and, neuro-hormonal modulation is discouraged in patients with PAH related RV dysfunction for fear of systemic hypotension. Herein, we summarize the pathophysiological background that supports the potential role of neuro-hormonal modulation in the management of PAH related RV dysfunction; also present current clinical experience; and, discuss the need for controlled studies to move forward. Lastly, we review potential non- pharmacological modalities for neuro-hormonal modulations in PAH patients with RV dysfunction.
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