Browsing by Autor "Zubieta-DeUrioste, Natalia"

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Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema: A view from the High Andes.
(2021) Zubieta-Calleja, Gustavo; Zubieta-DeUrioste, Natalia
BACKGROUND: Travelling to high altitude for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlanders' point of view was mostly based on mountain climbing. Nowadays, descent is not mandatory in populated highland cities. METHODS: We present how to diagnose and treat acute high altitude pathologies (hypobaric hypoxic diseases) based on 50 years of experience in both: high altitude physiology research and medical practice as clinicians, in La Paz, Bolivia (3,600 m; 11,811 ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI - IPPA). RESULTS: Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are medical conditions faced by some travelers. These can occasionally present after flights to high altitude cities, both in lowlanders or in high altitude residents during re-entry, having spent more than 20 days at sea level. CONCLUSIONS: Traveling to high altitude should not be feared as it has many benefits; Acute high altitude ascent diseases can be adequately diagnosed and treated without descent.
COVID-19 and Pneumolysis Simulating Extreme High-altitude Exposure with Altered Oxygen Transport Physiology; Multiple Diseases, and Scarce Need of Ventilators: Andean Condor's-eye-view.
(2020) Zubieta-Calleja, Gustavo; Zubieta-DeUrioste, Natalia; Venkatesh, Thuppil; Das, Kusal K; Soliz, Jorge
BACKGROUND: Critical hypoxia in this COVID-19 pandemic results in high mortality and economic loss worldwide. Initially, this disease' pathophysiology was poorly understood and interpreted as a SARS (Severe Acute Respiratory Syndrome) pneumonia. The severe atypical lung CAT scan images alerted all countries, including the poorest, to purchase lacking sophisticated ventilators. However, up to 88% of the patients on ventilators lost their lives. It was suggested that COVID-19 could be similar to a High-Altitude Pulmonary Edema (HAPE). New observations and pathological findings are gradually clarifying the disease. METHODS: As high-altitude medicine and hypoxia physiology specialists working and living in the highlands for over 50 years, we perform a perspective analysis of hypoxic diseases treated at high altitudes and compare them to Covid-19. Oxygen transport physiology, SARS-Cov-2 characteristics, and its transmission, lung imaging in COVID-19, and HAPE, as well as the causes of clinical signs and symptoms, are discussed. RESULTS: High-altitude oxygen transport physiology has been systematically ignored. COVID-19 signs and symptoms indicate a progressive and irreversible failure in the oxygen transport system, secondary to pneumolysis produced by SARS-Cov-2's alveolar-capillary membrane "attack". HAPE's pulmonary compromise is treatable and reversible. COVID-19 is associated with several diseases, with different individual outcomes, in different countries, and at different altitudes. CONCLUSIONS: The pathophysiology of High-altitude illnesses can help explain COVID-19 pathophysiology, severity, and management. Early diagnosis and use of EPO, acetylsalicylic-acid, and other anti-inflammatories, oxygen therapy, antitussives, antibiotics, and the use of Earth open-circuit- astronaut-resembling suits to return to daily activities, should all be considered. Ventilator use can be counterproductive. Immunity development is the only feasible long-term survival tool.
Erythropoietin Produces a Dual Effect on Carotid Body Chemoreception in Male Rats.
(2021) Arias-Reyes, Christian; Laouafa, Sofien; Zubieta-DeUrioste, Natalia; Joseph, Vincent; Bairam, Aida; Schneider Gasser, Edith M; Soliz, Jorge
Erythropoietin (EPO) regulates respiration under conditions of normoxia and hypoxia through interaction with the respiratory centers of the brainstem. Here we investigate the dose-dependent impact of EPO in the CB response to hypoxia and hypercapnia. We show, in isolated "en bloc" carotid body (CB) preparations containing the carotid sinus nerve (CSN) from adult male Sprague Dawley rats, that EPO acts as a stimulator of CSN activity in response to hypoxia at concentrations below 0.5 IU/ml. Under hypercapnic conditions, EPO did not influence the CSN response. EPO concentrations above 0.5 IU/ml decreased the response of the CSN to both hypoxia and hypercapnia, reaching complete inhibition at 2 IU/ml. The inhibitory action of high-dose EPO on the CSN activity might result from an increase in nitric oxide (NO) production. Accordingly, CB preparations were incubated with 2 IU/ml EPO and the unspecific NO synthase inhibitor (L-NAME), or the neuronal-specific NO synthase inhibitor (7NI). Both NO inhibitors fully restored the CSN activity in response to hypoxia and hypercapnia in presence of EPO. Our results show that EPO activates the CB response to hypoxia when its concentration does not exceed the threshold at which NO inhibitors masks EPO's action.
High Altitude Pulmonary Edema, High Altitude Cerebral Edema, and Acute Mountain Sickness: an enhanced opinion from the High Andes - La Paz, Bolivia 3,500 m.
(2023) Zubieta-Calleja, Gustavo R; Zubieta-DeUrioste, Natalia
Traveling to high altitudes for entertainment or work is sometimes associated with acute high altitude pathologies. In the past, scientific literature from the lowlander point of view was primarily based on mountain climbing. Sea level scientists developed all guidelines, but they need modifications for medical care in high altitude cities. Acute Mountain Sickness, High Altitude Pulmonary Edema, and High Altitude Cerebral Edema are medical conditions that some travelers can face. We present how to diagnose and treat acute high altitude pathologies, based on 51 years of high altitude physiology research and medical practice in hypobaric hypoxic diseases in La Paz, Bolivia (3,600 m; 11,811 ft), at the High Altitude Pulmonary and Pathology Institute (HAPPI - IPPA). These can occasionally present after flights to high altitude cities, both in lowlanders or high-altitude residents during re-entry. Acute high altitude ascent diseases can be adequately diagnosed and treated in high altitude cities following the presented guidelines. Treating these high-altitude illnesses, we had no loss of life. Traveling to a high altitude with sound medical advice should not be feared as it has many benefits. Nowadays, altitude descent and evacuation are not mandatory in populated highland cities, with adequate medical resources.
Letter to the Editor re: "Bicarbonate Values for Healthy Residents Living in Cities Above 1500 Meters of Altitude: A Theoretical Model and Systematic Review" by Ramirez-Sandoval et al. (High Alt Med Biol 2016;17:85-92).
(2016) Zubieta-Calleja, Gustavo; Zubieta-DeUrioste, Natalia; Paulev, Poul-Erik
Morphological and functional findings in COVID-19 lung disease as compared to Pneumonia, ARDS, and High-Altitude Pulmonary Edema.
(2023) Zubieta-Calleja, Gustavo R; Zubieta-DeUrioste, Natalia; de Jesús Montelongo, Felipe; Sanchez, Manuel Gabriel Romo; Campoverdi, Aurio Fajardo; Rocco, Patricia Rieken Macedo; Battaglini, Denise; Ball, Lorenzo; Pelosi, Paolo
Coronavirus disease-2019 (COVID-19) may severely affect respiratory function and evolve to life-threatening hypoxia. The clinical experience led to the implementation of standardized protocols assuming similarity to severe acute respiratory syndrome (SARS-CoV-2). Understanding the histopathological and functional patterns is essential to better understand the pathophysiology of COVID-19 and then develop new therapeutic strategies. Epithelial and endothelial cell damage can result from the virus attack, thus leading to immune-mediated response. Pulmonary histopathological findings show the presence of Mallory bodies, alveolar coating cells with nuclear atypia, reactive pneumocytes, reparative fibrosis, intra-alveolar hemorrhage, moderate inflammatory infiltrates, micro-abscesses, microthrombus, hyaline membrane fragments, and emphysema-like lung areas. COVID-19 patients may present different respiratory stages from silent to critical hypoxemia, are associated with the degree of pulmonary parenchymal involvement, thus yielding alteration of ventilation and perfusion relationships. This review aims to: discuss the morphological (histopathological and radiological) and functional findings of COVID-19 compared to acute interstitial pneumonia, acute respiratory distress syndrome (ARDS), and high-altitude pulmonary edema (HAPE), four entities that share common clinical traits, but have peculiar pathophysiological features with potential implications to their clinical management.
Pneumolysis and "Silent Hypoxemia" in COVID-19.
(2021) Zubieta-Calleja, Gustavo; Zubieta-DeUrioste, Natalia
COVID-19 can evolve to a severe lung compromise with life-threatening hypoxemia. The mechanisms involved are not fully understood. Their understanding is crucial to improve the outcomes. Initially, past-experience lead to the implementation of standardized protocols assuming this disease would be the same as SARS-CoV. Impulsive use of ventilators in extreme cases ended up in up to 88% fatality. We compare medical and physiological high altitude acute and chronic hypoxia experience with COVID-19 hypoxemia. A pathophysiological analysis is performed based on literature review and histopathological findings. Application of the Tolerance to Hypoxia formula = Hemoglobin/PaCO2 + 3.01 to COVID-19, enlightens its critical hypoxemia. Pneumolysis is defined as progressive alveolar-capillary destruction resulting from the CoV-2 attack to pneumocytes. The adequate interpretation of the histopathological lung biopsy photomicrographs reveals these alterations. The three theoretical pathophysiological stages of progressive hypoxemia (silent hypoxemia, gasping, and death zone) are described. At high altitude, normal low oxygen saturation (SpO2) levels (with intact lung tissue and adequate acid-base status) could be considered silent hypoxemia. At sea level, in COVID-19, the silent hypoxemia starting at SpO2 ≤ 90% (comparable to a normal SPO2 {88-92%} at 3500 m) suddenly evolves to critical hypoxemia. This, as a consequence of progressive pneumolysis + inflammation + overexpressed immunity + HAPE-type edema resulting in pulmonary shunting. The proposed treatment is based on the improvement of the Tolerance to Hypoxia (Hemoglobin factor), oxygen therapy, inflammation reduction, antibiotics, antitussives, rehydration & anticoagulation if required. Understanding the pathophysiology of COVID-19 may assist in this disease's management.
Re: "Mortality Attributed to COVID-19 in High-Altitude Populations" by Woolcott and Bergman.
(2021) Zubieta-Calleja, Gustavo; Merino-Luna, Alfredo; Zubieta-DeUrioste, Natalia; Armijo-Subieta, N Freddy; Soliz, Jorge; Arias-Reyes, Christian; Escalante-Kanashiro, Raffo; Carmona-Suazo, Jose Antonio; López-Bascope, Alberto; Calle-Aracena, Jose Manuel; Epstein, Murray; Maravi, Enrique
The Oxygen Transport Triad in High-Altitude Pulmonary Edema: A Perspective from the High Andes.
(2021) Zubieta-Calleja, Gustavo; Zubieta-DeUrioste, Natalia
Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article "Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude Cerebral Edema, a View from the High Andes" was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any "loss of adaptation". A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.