Respironics Inc.

Respironics has recalled its PLV Continuum Ventilator after finding a defect in an internal flow valve. The home-based portable ventilator can suddenly stop providing mechanical ventilation and can potentially cause serious injury or death. 269 ventilators representing all models and serial numbers of the PLV® Continuum(TM) Ventilator have been recalled.

Posted by
Aubergine
on April 6, 2018

Acute earaches began 3rd day of use. After i quit using the cpap machine, I am left w/terrible earaches, hard to hear because it sounds like I am under water. I haven't used the machine in months and find that I am an invalid a couple days a week due to earaches that require heavy pain medication.

Posted by
Roy Ijams
on January 22, 2016

6/8/12 I, sleep walked out of semi while on cpap and my wife was about 50 -60 at the time. On 1/10/12 trying to get back to work I sleep 8 hours on cpap and felt disoriented that morning. A few minutes after I took off cpap I had a grand mall seizure. My wife and I each had 2 million safe driving awards before using cpap. Had never sleep walked before. We have been married 33yrs.

Oxygen toxicity occurs when the partial pressure of alveolar O2 (PAO2) exceeds that which is breathed under normal conditions. With continuous exposure to supraphysiologic concentrations of O2, a state of hyperoxia develops. Under hyperoxic pathological conditions, a large influx of reactive O2 species (ROS) are produced. In intracellular and extracellular biological systems, the mass effect of ROS elevation, caused by O2 overexposure, disrupts the balance between oxidants and antioxidants, and this disruption of homeostasis can result in damage to cells and tissues [8–11]. Exposure time, atmospheric pressure, and fraction of inspired O2 (FIO2) determine the cumulative O2 dose leading to toxicity. Oxygen is toxic to the lungs when high FIO2 (>0.60) is administered over extended exposure time (?24 hours) at normal barometric pressure (1 atmospheres absolute (ATA)). This type of exposure is referred to as low pressure O2 poisoning, pulmonary toxicity, or the Lorraine Smith effect. Oxygen exposure after approximately 12 hours leads to lung passageway congestion, pulmonary edema, and atelectasis caused by damage to the linings of the bronchi and alveoli. The formation of fluid in the lungs causes a feeling of shortness of breath combined with a burning of the throat and chest, and breathing becomes very painful [12]. The reason for this effect in the lungs but not in other tissues is that the air spaces of the lungs are directly exposed to the high O2 pressure. Oxygen is delivered to the other body tissues at almost normal partial pressure of O2 (PO2) because of the hemoglobin-O2 buffer system [13–15]. Toxicity also occurs when the ATA is high (1.6–4) and the high FIO2 exposure time is short. This type of exposure is referred to as high pressure O2 poisoning or the Paul Bert effect and is toxic to the central nervous system (CNS). Central nervous system toxicity results in seizures followed by coma in most people within 30 to 60 minutes. Seizures often occur without warning and are likely to be lethal. Other symptoms include nausea, muscle twitching, dizziness, disturbances of vision, irritability, and disorientation [13, 16–20]. Oceanic divers are more likely to experience CNS toxicity [17].Pulmonary capillary endothelial and alveolar epithelial cells are targets for ROS resulting in injury-induced lung edema, alveolar flooding, hemorrhage, and collagen, elastin, and hyaline membrane deposits [11, 21, 22]. Above a critical PAO2, the hemoglobin-O2 buffering mechanism fails and the tissue PO2 can rise to hundreds or thousands of mm?Hg. At high levels of O2, protective endogenous antioxidant enzyme systems become consumed by ROS leading to cell death [16, 23]. Oxygen toxicity caused by ROS progresses in overlapping phases based on degree of severity and reversibility of injury. The phases are initiation, inflammation, proliferation, and fibrosis. Initially, there are increased ROS and depleted antioxidant levels, and the lung fails to clear itself of mucous. The inflammation phase or exudative phase is characterized by the destruction of the pulmonary lining and migration of leukocyte derived inflammatory mediators to the sites of injury. The proliferative phase is subacute and there are cellular hypertrophy, increased secretions from surfactant secreting alveolar type II cells, and increased monocytes. The final terminal phase is the fibrotic phase in which the changes to the lung are irreversible and permanent. There is collagen deposition and thickening of the pulmonary interstitial space and the lung becomes fibrotic [24–27].Clinically, progressive hypoxemia, or high O2 tension in the blood, requires increased FIO2 and assisted ventilation, which further aggravate the pathophysiological changes associated with O2 toxicity. Chest X-rays may show an alveolar interstitial pattern in an irregular distribution with evidence of a moderate loss of volume from atelectasis, however there is no clinical way of diagnosing O2 toxicity. Lung biopsy specimens may show changes consistent with O2 toxicity but the primary value of the biopsy is to exclude other causes of lung injury. Air pressure changes within the enclosed lung cavity and ventilator-induced injury may accompany and be indistinguishable from O2 toxicity. Oxygen toxicity can be minimized by keeping the PAO2 less than 80?mm Hg or the FIO2 below 0.40 to 0.50 [12]. The pulmonary cellular response to hyperoxic exposure and increased ROS is well described. Anatomically, the pulmonary epithelial surface is vulnerable to a destructive inflammatory response. This inflammation damages the alveolar capillary barrier leading to impaired gas exchange and pulmonary edema. Reactive O2 species induces pulmonary cell secretion of chemoattractants, and cytokines stimulate macrophage and monocyte mobilization and accumulation into the lungs, leading to additional ROS. The ROS leukocyte interaction further exacerbates injury. Research has shown that as these highly reduced cell layers become increasingly oxidized and levels of antioxidants fall, ROS-induced activation of multiple upstream signal transduction pathways regulates the cellular response: adaptation, repair, or cell death by apoptosis, oncosis, or necrosis [28, 29]. Mitogen-activated protein kinase (MAPK), toll-like receptor 4 (TLR4), signal transducers and activators of transcription (STAT), and nuclear factor kappa beta (NF k?) are a few well-researched protein pathways that communicate the receptor signal to the deoxyribonucleic acid (DNA) of the cell thereby determining the cellular response. The MAPK pathway is a regulator of cell death genes, stress, and transformation and growth regulation. Mitogen-activated protein kinase activation precedes extracellular signal regulated kinase (ERK1/2), a promoter of cell proliferation. C-Jun-terminal protein kinase (JNK1/2) and p38 kinase both induce cell death and inflammation [30]. The TLR4, STAT, and nuclear regulatory factor 2 (Nrf2) pathways are associated with survival gene expression such as caspase-3 proteins and antioxidant response element (ARE) [31, 32]. The NF k? pathway is an up-stream signal for inflammation and survival genes: anti-oxidant enzymes (AOE), Bcl-2, AKT, heme oxygenase (HO-1), and heat shock proteins (HSPs). The AKT1-4 family of signals plays an important role in glucose metabolism, cell proliferation, apoptosis, transcription, and cell migration. The Bcl-2 proteins are antiapoptotic while HO-1 and HSPs are ubiquitous stress-response proteins [33]. These signaling pathways are regulators of the pulmonary epithelial cell response to increases in ROS and hyperoxia [18, 34]. Cytokine and chemokine overexpression in response to hyperoxic stress can be protective. Tumor necrosis factor alpha (TNF?), interleukin 1 beta (IL-1?), interleukin 6 (IL-6), chemokine receptor 2 (CXCR2), interleukin 11 (IL-11), insulin and keratinocyte growth factor expression, and the beta subunit of Na, K-ATPase have been shown to attenuate death signals [35–37].3. The Formation of Free RadicalsOxygen is a requirement for cellular respiration in the metabolism of glucose and the majority of O2 consumed by the mitochondria is utilized for adenosine triphosphate (ATP) generation [38, 39]. The mitochondrial electron transport chain reduces the elemental molecular O2 to ionic O2 by the relay of electrons making O2 usable for ATP generation, during this process, oxidizing free radicals are generated [40, 41]. Toxic levels of O2 lead to the formation of additional ROS, which can impose damage to lipid membranes, proteins, and nucleic acids. Reactive O2 species mediate physiological and pathophysiological roles within the body [42]. Free radicals are a type of unstable, reactive, short-lived chemical species that have one or more unpaired electrons and may possess a net charge or be neutral. The species is termed free because the unpaired electron in the outer orbit is free to interact with surrounding molecules [42, 43].

Posted by
Sheila Smith
on December 4, 2015

Can someone call me?