Browsing by Subject "diving"

Now showing 1 - 5 of 5
  • Thumbnail Image
    ItemOpen Access
    Can my patient dive after a first episode of primary spontaneous pneumothorax? A systematic review of the literature.
    (Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc, 2018-03) Villela, M Alvarez; Dunworth, S; Harlan, NP; Moon, RE
    Patients with prior primary spontaneous pneumothorax (PSP) frequently seek clearance to dive. Despite wide consensus in precluding compressed-air diving in this population, there is a paucity of data to support this decision. We reviewed the literature reporting the risk of PSP recurrence.A literature search was performed in PubMed and Web of Science using predefined terms. Studies published in English reporting the recurrence rate after a first PSP were included.Forty studies (n=3,904) were included. Risk of PSP recurrence ranged 0-67% (22 ± 15.5%; mean ± SD). Mean follow-up was 36 months, and 63 ± 39% of recurrences occurred during the first year of follow-up. Elevated height/weight ratio and emphysema-like changes (ELCs) are associated with PSP recurrence. ELCs are present in 59%-89% (vs. 0-15%) of patients with recurrence and can be detected effectively with high-resolution CT scan (sensitivity of 84-88%). Surgical pleurodesis reduces the risk of recurrence substantially (4.0 ± 4% vs. 22 ± 15.5%).Risk of PSP recurrence seems to decline over time and is associated to certain radiological and clinical risk factors. This could be incremented by the stresses of compressed-air diving. A basis for informed patient-physician discussions regarding future diving is provided in this review.
  • Thumbnail Image
    ItemOpen Access
    Diagnosis of Swimming Induced Pulmonary Edema-A Review.
    (Frontiers in physiology, 2017-01) Grünig, Hannes; Nikolaidis, Pantelis T; Moon, Richard E; Knechtle, Beat
    Swimming induced pulmonary edema (SIPE) is a complication that can occur during exercise with the possibility of misdiagnosis and can quickly become life threatening; however, medical literature infrequently describes SIPE. Therefore, the aim of this review was to analyse all individual cases diagnosed with SIPE as reported in scientific sources, with an emphasis on the diagnostic pathways and the key facts resulting in its diagnosis. Due to a multifactorial and complicated pathophysiology, the diagnosis could be difficult. Based on the actual literature, we try to point out important findings regarding history, conditions, clinical findings, and diagnostic testing helping to confirm the diagnosis of SIPE. Thirty-eight cases from seventeen articles reporting the diagnosis of SIPE were selected. We found remarkable differences in the individual described diagnostic pathways. A total of 100% of the cases suffered from an acute onset of breathing problems, occasionally accompanied by hemoptysis. A total of 73% showed initial hypoxemia. In most of the cases (89%), an initial chest X-Ray or chest CT was available, of which one-third (71%) showed radiological signs of pulmonary edema. The majority of the cases (82%) experienced a rapid resolution of symptoms within 48 h, the diagnostic hallmark of SIPE. Due to a foreseeable increase in participation in swimming competitions and endurance competitions with a swimming component, diagnosis of SIPE will be important, especially for medical teams caring for these athletes.
  • Thumbnail Image
    ItemOpen Access
    Environmental Physiology and Diving Medicine.
    (Frontiers in psychology, 2018-01) Bosco, Gerardo; Rizzato, Alex; Moon, Richard E; Camporesi, Enrico M
    Man's experience and exploration of the underwater environment has been recorded from ancient times and today encompasses large sections of the population for sport enjoyment, recreational and commercial purpose, as well as military strategic goals. Knowledge, respect and maintenance of the underwater world is an essential development for our future and the knowledge acquired over the last few dozen years will change rapidly in the near future with plans to establish secure habitats with specific long-term goals of exploration, maintenance and survival. This summary will illustrate briefly the physiological changes induced by immersion, swimming, breath-hold diving and exploring while using special equipment in the water. Cardiac, circulatory and pulmonary vascular adaptation and the pathophysiology of novel syndromes have been demonstrated, which will allow selection of individual characteristics in order to succeed in various environments. Training and treatment for these new microenvironments will be suggested with description of successful pioneers in this field. This is a summary of the physiology and the present status of pathology and therapy for the field.
  • Thumbnail Image
    ItemOpen Access
    Hypercapnia in diving: a review of CO₂ retention in submersed exercise at depth.
    (Undersea Hyperb Med, 2017-05) Dunworth, Sophia A; Natoli, Michael J; Cooter, Mary; Cherry, Anne D; Peacher, Dionne F; Potter, Jennifer F; Wester, Tracy E; Freiberger, John J; Moon, Richard E
    Carbon dioxide (CO₂) retention, or hypercapnia, is a known risk of diving that can cause mental and physical impairments leading to life-threatening accidents. Often, such accidents occur due to elevated inspired carbon dioxide. For instance, in cases of CO₂ elimination system failures during rebreather dives, elevated inspired partial pressure of carbon dioxide (PCO₂) can rapidly lead to dangerous levels of hypercapnia. Elevations in PaCO₂ (arterial pressure of PCO₂) can also occur in divers without a change in inspired PCO₂. In such cases, hypercapnia occurs due to alveolar hypoventilation. Several factors of the dive environment contribute to this effect through changes in minute ventilation and dead space. Predominantly, minute ventilation is reduced in diving due to changes in respiratory load and associated changes in respiratory control. Minute ventilation is further reduced by hyperoxic attenuation of chemosensitivity. Physiologic dead space is also increased due to elevated breathing gas density and to hyperoxia. The Haldane effect, a reduction in CO₂ solubility in blood due to hyperoxia, may contribute indirectly to hypercapnia through an increase in mixed venous PCO₂. In some individuals, low ventilatory response to hypercapnia may also contribute to carbon dioxide retention. This review outlines what is currently known about hypercapnia in diving, including its measurement, cause, mental and physical effects, and areas for future study.
  • Thumbnail Image
    ItemOpen Access
    Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil.
    (Circulation, 2016-03-08) Moon, RE; Peacher, DF; Potter, JF; Wester, TE; Cherry, AD; Natoli, M; Otteni, CE; Kernagis, DN; White, WD; Freiberger, J
    BACKGROUND: Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise than in the general population and are reduced by sildenafil. METHODS AND RESULTS: Ten study subjects with a history of SIPE (mean age, 41.6 years) and 20 control subjects (mean age, 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6 to 7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptible subjects. Average o2 and cardiac output in controls and SIPE-susceptible subjects were: o2 2.42 L·min(-1) versus 1.95 L·min(-1), P=0.2; and cardiac output 17.9 L·min(-1) versus 13.8 L·min(-1), P=0.01. Accounting for differences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L·min(-1) was 22.5 mm Hg in controls versus 34.0 mm Hg in SIPE-susceptible subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18.8 mm Hg (P=0.028). After sildenafil, there were no statistically significant differences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible subjects and controls. CONCLUSIONS: These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00815646.