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Experimental and Therapeutic Medicine Sep 2023Negative pressure pulmonary edema (NPPE) is a complication resulting from acute or chronic upper airway obstruction, often posing challenges in recognition and diagnosis... (Review)
Review
Negative pressure pulmonary edema (NPPE) is a complication resulting from acute or chronic upper airway obstruction, often posing challenges in recognition and diagnosis for clinicians. If left untreated, NPPE can lead to hypoxemia, heart failure and even shock. Furthermore, the drug treatment of NPPE remains a subject of controversy. The primary pathophysiological mechanism of NPPE involves the need for high inspiratory pressure to counteract upper airway obstruction, subsequently causing a progressive rise in negative pressure within the pleural cavity. Consequently, this results in increased pulmonary microvascular pressure, leading to the infiltration of pulmonary capillary fluid into the alveoli. NPPE exhibits numerous risk factors and causes, with laryngospasm following anesthesia and extubation being the most prevalent. The diagnosis of NPPE often presents challenges due to confusion with conditions such as gastroesophageal reflux or cardiogenic pulmonary edema, given the similarity in initial factors triggering both diseases. Upper airway patency, positive pressure non-invasive ventilation, supplemental oxygen and re-intubation mechanical ventilation are the foundation of the treatment of NPPE. The present review aims to discuss the etiology, clinical presentation, pathophysiology and management of NPPE.
PubMed: 37614417
DOI: 10.3892/etm.2023.12154 -
Chest Jul 2023We previously showed in patients with poorly controlled eosinophilic asthma that a single dose of benralizumab resulted in significantly improved Asthma Control...
BACKGROUND
We previously showed in patients with poorly controlled eosinophilic asthma that a single dose of benralizumab resulted in significantly improved Asthma Control Questionnaire (ACQ-6) score and Xe MRI ventilation defect percent (VDP) 28 days postinjection, and Xe MRI VDP and CT airway mucus occlusions were shown to independently predict this early ACQ-6 response to benralizumab.
RESEARCH QUESTION
Do early VDP responses at 28 days persist, and do FEV, fractional exhaled nitric oxide, and mucus plug score improve during a 2.5 year treatment period?
STUDY DESIGN AND METHODS
Participants with poorly controlled eosinophilic asthma completed spirometry, ACQ-6, and MRI, 28 days, 1 year, and 2.5 years after initiation of treatment with benralizumab; chest CT was acquired at enrollment and 2.5 years later.
RESULTS
Of 29 participants evaluated at 28 days post-benralizumab, 16 participants returned for follow-up while on therapy at 1 year, and 13 participants were evaluable while on therapy at 2.5 years post-benralizumab initiation. As compared with 28 days post-benralizumab, ACQ-6 score (2.0 ± 1.4) significantly improved after 1 year (0.5 ± 0.6, P = .02; 95% CI, 0.1-1.1) and 2.5 years (0.5 ± 0.5, P = .03; 95% CI, 0.1-1.1). The mean VDP change at 2.5 years (-4% ± 3%) was greater than the minimal clinically important difference, but not significantly different from VDP measured 28 days post-benralizumab. Mucus score (3 ± 4) was significantly improved at 2.5 years (1 ± 1, P = .03; 95% CI, 0.3-5.5). In six of eight participants with previous occlusions, mucus plugs vanished or substantially diminished 2.5 years later. VDP (P < .001) and mucus score (P < .001) measured at baseline, but not fractional exhaled nitric oxide or FEV, independently predicted ACQ-6 score after 2.5 years.
INTERPRETATION
In poorly controlled eosinophilic asthma, early MRI VDP responses at 28 days post-benralizumab persisted 2.5 years later, alongside significantly improved mucus scores and asthma control.
Topics: Humans; Nitric Oxide; Asthma; Pulmonary Eosinophilia; Airway Obstruction; Mucus; Magnetic Resonance Imaging; Tomography, X-Ray Computed; Anti-Asthmatic Agents
PubMed: 36781102
DOI: 10.1016/j.chest.2023.02.009 -
Sleep & Breathing = Schlaf & Atmung Dec 2023The purpose of this study is to examine the pathophysiology underlying sleep apnea (SA). (Review)
Review
OBJECTIVE
The purpose of this study is to examine the pathophysiology underlying sleep apnea (SA).
BACKGROUND
We consider several critical features of SA including the roles played by the ascending reticular activating system (ARAS) that controls vegetative functions and electroencephalographic findings associated with both SA and normal sleep. We evaluate this knowledge together with our current understanding of the anatomy, histology, and physiology of the mesencephalic trigeminal nucleus (MTN) and mechanisms that contribute directly to normal and disordered sleep. MTN neurons express γ-aminobutyric acid (GABA) receptors which activate them (make chlorine come out of the cells) and that can be activated by GABA released from the hypothalamic preoptic area.
METHOD
We reviewed the published literature focused on sleep apnea (SA) reported in Google Scholar, Scopus, and PubMed databases.
RESULTS
The MTN neurons respond to the hypothalamic GABA release by releasing glutamate that activates neurons in the ARAS. Based on these findings, we conclude that a dysfunctional MTN may be incapable of activating neurons in the ARAS, notably those in the parabrachial nucleus, and that this will ultimately lead to SA. Despite its name, obstructive sleep apnea (OSA) is not caused by an airway obstruction that prevents breathing.
CONCLUSIONS
While obstruction may contribute to the overall pathology, the primary factor involved in this scenario is the lack of neurotransmitters.
Topics: Humans; Sleep Apnea Syndromes; Sleep Apnea, Obstructive; Respiration; Sleep; gamma-Aminobutyric Acid
PubMed: 36976413
DOI: 10.1007/s11325-023-02783-7