Mats H. Linér

Pulmonary edema after competitive breath-hold diving

During an international breath-hold diving competition, 19 of the participating divers volunteered for the present study, aimed at elucidating possible symptoms and signs of pulmonary edema after deep dives. Measurements included dynamic spirometry and pulse oximetry, and chest auscultation was performed on those with the most severe symptoms. After deep dives (25-75 m), 12 of the divers had signs of pulmonary edema. None had any symptoms or signs after shallow pool dives. For the whole group of 19 divers, average reductions in forced vital capacity (FVC) and forced expiratory volume in the first second (FEV(1)) were -9 and -12%, respectively, after deep dives compared with after pool dives. In addition, the average reduction in arterial oxygen saturation (Sa(O(2))) was -4% after the deep dives. In six divers, respiratory symptoms (including dyspnea, cough, fatigue, substernal chest pain or discomfort, and hemoptysis) were associated with aggravated deteriorations in the physiological variables (FVC: -16%; FEV(1): -27%; Sa(O(2)): -11%). This is the first study showing reduced spirometric performance and arterial hypoxemia as consequences of deep breath-hold diving, and we suggest that the observed changes are caused by diving-induced pulmonary edema. From the results of the present study, it must be concluded that the great depths reached by these elite apnea divers are associated with a risk of pulmonary edema.

Asystole and increased serum myoglobin levels associated with 'packing blackout' in a competitive breath-hold diver.

Many competitive breath‐hold divers use ‘glossopharyngeal insufflation’, also called ‘lung packing’, to overfill their lungs above normal total lung capacity. This increases intrathoracic pressure, decreases venous return, compromises cardiac pumping, and reduces arterial blood pressure, possibly resulting in a syncope breath‐hold divers call ‘packing blackout’. We report a case with a breath‐hold diver who inadvertently experienced a packing blackout. During the incident, an electrocardiogram (ECG) and blood pressure were recorded, and blood samples for determinations of biomarkers of cardiac muscle perturbation (creatine kinase‐MB isoenzyme (CK‐MB), cardiac troponin‐T (TnT), and myoglobin) were collected. The ECG revealed short periods of asystole during the period of ‘packing blackout’, simultaneous with pronounced reductions in systolic, diastolic, and pulse pressures. Serum myoglobin concentration was elevated 40 and 150 min after the incident, whereas there were no changes in CK‐MB or TnT. The ultimate cause of syncope in this diver probably was a decrease in cerebral perfusion following glossopharyngeal insufflation. The asystolic periods recorded in this diver could possibly indicate that susceptible individuals may be put at risk of a serious cardiac incident if the lungs are excessively overinflated by glossopharyngeal insufflation. This concern is further substantiated by the observed increase in serum myoglobin concentration after the event.

Suspected arterial gas embolism after glossopharyngeal insufflation in a breath-hold diver.

INTRODUCTION Many competitive breath-hold divers employ the technique of glossopharyngeal insufflation in order to increase their lung gas volume for a dive. After a maximal inspiration, using the oral and pharyngeal muscles repeatedly, air in the mouth is compressed and forced into the lungs. Such overexpansion of the lungs is associated with a high transpulmonary pressure, which could possibly cause pulmonary barotrauma. CASE REPORT We report a case of transient neurological signs and symptoms occurring within 1 min after glossopharyngeal insufflation in a breath-hold diver. He complained of paresthesia of the right shoulder and a neurological exam revealed decreased sense of touch on the right side of the neck as compared to the left side. Motor function was normal. The course of events in this case is suggestive of arterial gas embolism. DISCUSSION Although the diver recovered completely within a few minutes, the perspective of a more serious insult raises concerns in using the glossopharyngeal insufflation technique. In addition to a neurological insult, damage to other organs of the body has to be considered. Both acute and long-term negative health effects are conceivable.