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The article presents a case study of a 50-year-old man with pulmonary hypertension. Topics include developing tachycardia and hypoxemia prompting transfer to the intensive care unit (ICU); computed tomography (CT) pulmonary angiogram showing bilateral lower lobe opacities and the ratio of right ventricle and left ventricle; and echocardiogram demonstrating mild tricuspid regurgitation.

During the ongoing coronavirus disease (COVID-19) pandemic, reports in social media and the lay press indicate that a subset of patients are presenting with severe hypoxemia in the absence of dyspnea, a problem unofficially referred to as "silent hypoxemia." To decrease the risk of complications in such patients, one proposed solution has been to have those diagnosed with COVID-19 but not sick enough to warrant admission monitor their arterial oxygenation by pulse oximetry at home and present for care when they show evidence of hypoxemia. Though the ease of use and low cost of pulse oximetry makes this an attractive option for identifying problems at an early stage, there are important considerations with pulse oximetry about which patients and providers may not be aware that can interfere with successful implementation of such monitoring programs. Only a few independent studies have examined the performance of pocket oximeters and smart phone-based systems, but the limited available data raise questions about their accuracy, particularly as saturation falls below 90%. There are also multiple sources of error in pulse oximetry that must be accounted for, including rapid fluctuations in measurements when the arterial oxygen pressure/tension falls on the steep portion of the dissociation curve, data acquisition problems when pulsatile blood flow is diminished, accuracy in the setting of severe hypoxemia, dyshemoglobinemias, and other problems. Recognition of these issues and careful counseling of patients about the proper means for measuring their oxygen saturation and when to seek assistance can help ensure successful implementation of needed monitoring programs. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? Do the pulmonary vascular responses to hypoxia change during progressive exposure to high altitude and can alterations in these responses be related to changes in concentrations of circulating biomarkers that affect the pulmonary circulation?, What is the main finding and its importance? In our field study with healthy volunteers, we demonstrate changes in pulmonary artery pressure suggestive of remodelling in the pulmonary circulation, but find no changes in the acute responsiveness of the pulmonary circulation to changes in oxygenation during 2 weeks of exposure to progressive hypoxia. Pulmonary artery pressure changes were associated with changes in erythropoietin, 8-isoprostane, nitrite and guanosine 3′,5′-cyclic monophosphate., We sought to determine whether changes in pulmonary artery pressure responses to hypoxia suggestive of vascular remodelling occur during progressive exposure to high altitude and whether such alterations are related to changes in concentrations of circulating biomarkers with known or suspected actions on the pulmonary vasculature during ascent. We measured tricuspid valve transvalvular pressure gradients (TVPG) in healthy volunteers breathing air at sea level (London, UK) and in hypoxic conditions simulating the inspired O2 partial pressures at two locations in Nepal, Namche Bazaar (NB, elevation 3500 m) and Everest Base Camp (EBC, elevation 5300 m). During a subsequent 13 day trek, TVPG was measured at NB and EBC while volunteers breathed air and hyperoxic or hypoxic mixtures simulating the inspired O2 partial pressures at the other locations. For each location, we determined the slope of the relationship between TVPG and arterial oxygen saturation ( [ABSTRACT FROM AUTHOR]

Luks, Andrew M., and Erik R. Swenson. Clinician's Corner: Evaluating the risks of high altitude travel in chronic liver disease patients. High Alt Med Biol 16:80-88, 2015.-With improvements in the quality of health care, people with chronic medical conditions are experiencing better quality of life and increasingly participating in a wider array of activities, including travel to high altitude. Whenever people with chronic diseases travel to this environment, it is important to consider whether the physiologic responses to hypobaric hypoxia will interact with the underlying medical condition such that the risk of acute altitude illness is increased or the medical condition itself may worsen. This review considers these questions as they pertain to patients with chronic liver disease. While the limited available evidence suggests there is no evidence of liver injury or dysfunction in normal individuals traveling as high as 5000 m, there is reason to suspect that two groups of cirrhosis patients are at increased risk for problems, hepatopulmonary syndrome patients, who are at risk for severe hypoxemia following ascent, and portopulmonary hypertension patients who may be at risk for high altitude pulmonary edema and acute right ventricular dysfunction. While liver transplant patients may tolerate high altitude exposure without difficulty, no information is available regarding the risks of long-term residence at altitude with chronic liver disease. All travelers with cirrhosis require careful pre-travel evaluation to identify conditions that might predispose to problems at altitude and develop risk mitigation strategies for these issues. Patients also require detailed counseling about recognition, prevention, and treatment of acute altitude illness and may require different medication regimens to prevent or treat altitude illness than used in healthy individuals. [ABSTRACT FROM AUTHOR]

With the growing interest in adventure travel and the increasing ease and affordability of air, rail, and road-based transportation, increasing numbers of individuals are traveling to high altitude. The decline in barometric pressure and ambient oxygen tensions in this environment trigger a series of physiologic responses across organ systems and over a varying time frame that help the individual acclimatize to the low oxygen conditions but occasionally lead to maladaptive responses and one or several forms of acute altitude illness. The goal of this Physiology in Medicine article is to provide information that providers can use when counseling patients who present to primary care or travel medicine clinics seeking advice about how to prevent these problems. After discussing the primary physiologic responses to acute hypoxia from the organ to the molecular level in normal individuals, the review describes the main forms of acute altitude illness--acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema--and the basic approaches to their prevention and treatment of these problems, with an emphasis throughout on the physiologic basis for the development of these illnesses and their management. [ABSTRACT FROM AUTHOR]

While antiviral therapy is an important component of care in patients with the acute respiratory distress syndrome ( ARDS) following influenza infection, it is not sufficient to ensure good outcomes, and additional measures are usually necessary. Patients usually receive high levels of supplemental oxygen to counteract the hypoxemia resulting from severe gas exchange abnormalities. Many patients also receive invasive mechanical ventilation for support for oxygenation, while in resource-poor settings, supplemental oxygen via face mask may be the only available intervention. Patients with ARDS receiving mechanical ventilation should receive lung-protective ventilation, whereby tidal volume is decreased to 6 ml/kg of their predicted weight and distending pressures are maintained ≤30 cm H2O, as well as increased inspired oxygen concentrations and positive end-expiratory pressure ( PEEP) to prevent atelectasis and support oxygenation. While these measures are sufficient in most patients, a minority develop refractory hypoxemia and may receive additional therapies, including prone positioning, inhaled vasodilators, extracorporeal membrane oxygenation, recruitment maneuvers followed by high PEEP, and neuromuscular blockade, although recent data suggest that this last option may be warranted earlier in the clinical course before development of refractory hypoxemia. Application of these 'rescue strategies' is complicated by the lack of guidance in the literature regarding implementation. While much attention is devoted to these strategies, clinicians must not lose sight of simple interventions that affect patient outcomes including head of bed elevation, prophylaxis against venous thromboembolism and gastrointestinal bleeding, judicious use of fluids in the post-resuscitative phase, and a protocol-based approach to sedation and spontaneous breathing trials. [ABSTRACT FROM AUTHOR]

Keywords: ARDS; high altitude pulmonary edema; hypoxemia; nifedipine EN ARDS high altitude pulmonary edema hypoxemia nifedipine 192 193 2 06/22/20 20200601 NES 200601 As medical providers around the world struggle to care for patients with acute respiratory failure secondary to corona virus disease 2019 (COVID-19), extensive efforts have been made to compare this entity to other forms of acute respiratory failure observed prior to the current pandemic. Among the variety of theories put forth, one argument that has been made and amplified via social media is that COVID-19 lung injury is not like typical acute respiratory distress syndrome (ARDS) and instead is similar to high altitude pulmonary edema (HAPE) (Solaimanzadeh, [1]). COVID-19 mediated lung injury has proven to be a heterogeneous disease in which patients present with varying degrees of hypoxemia, alterations in lung compliance and other physiologic derangements. [Extracted from the article]

For often unclear reasons, the survival times of critically buried avalanche victims vary widely from minutes to hours. Individuals can survive and sustain organ function if they can breathe under the snow and maintain sufficient delivery of oxygen and efflux of carbon dioxide. We review the physiological responses of humans to critical avalanche burial, a model which shares similarities and differences with apnoea and accidental hypothermia. Within a few minutes of burial, an avalanche victim is exposed to hypoxaemia and hypercapnia, which have important effects on the respiratory and cardiovascular systems and pose a major threat to the central nervous system. As burial time increases, an avalanche victim also develops hypothermia. Despite progressively reduced metabolism, reduced oxygen and increased carbon dioxide tensions may exacerbate the pathophysiological consequences of hypothermia. Hypercapnia seems to be the main cause of cardiovascular instability, which, in turn, is the major reason for reduced cerebral oxygenation despite reductions in cerebral metabolic activity caused by hypothermia. ‘Triple H syndrome’ refers to the interaction of hypoxia, hypercapnia and hypothermia in a buried avalanche victim. Future studies should investigate how the respiratory gases entrapped in the porous snow structure influence the physiological responses of buried individuals and how haemoconcentration, blood viscosity and cell deformability affect blood flow and oxygen delivery. Attention should also be devoted to identifying strategies to prolong avalanche survival by either mitigating hypoxia and hypercapnia or reducing core temperature so that neuroprotection occurs before the onset of cerebral hypoxia. [ABSTRACT FROM AUTHOR]