Željko Dujić

Aerobic exercise before diving reduces venous gas bubble formation in humans

We have previously shown in a rat model that a single bout of high‐intensity aerobic exercise 20h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280kPa at a rate of 100kPamin−1 breathing air and remaining at pressure for 80min. The ascent rate was 9mmin−1 with a 7min stop at 130kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3min, followed by exercise at 50% of maximum heart rate for 2min; this was repeated eight times for a total exercise period of 40min. Venous gas bubbles were monitored with an ultrasonic scanner every 20min for 80min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm−2(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre‐dive exercise, thereby increasing safety. This is the first report to indicate that pre‐dive exercise may form the basis for a new way of preventing serious decompression sickness.

The effects of acute oral antioxidants on diving-induced alterations in human cardiovascular function

Diving‐induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo‐controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non‐randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow‐mediated dilatation (FMD) and heart function with increased mean PAP. Twenty‐four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P= 0.005), while right ventricle ejection fraction (RV‐EF), left ventricle EF and endocardial fractional shortening were reduced much less (∼2–3%). At the same time RV end‐systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post‐dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre‐dive placebo, whereas for most cardiovascular parameters this occurred earlier (24–48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.

Triggers of acute myocardial infarction regarding its site.

We have studied the incidence of possible triggers of the myocardial infarction regarding its site in 750 patients with anterior and 731 patients with inferior infarction. Infarctions occurred most frequently without recalling any triggering activity, especially in patients with anterior infarction (67 vs. 44%). Physical effort as the possible precipitator was also more frequent in anterior infarctions (22 vs. 16%). However, the onset of inferior infarction was more frequent during meteorological stress (9 vs. 2%), emotional stress (10 vs. 3%), after overeating (13 vs. 3%) and nicotine abuse (6 vs. 1.5%). These triggers were independent and highly significant (P < 0.02 in each case) discriminators of the site of myocardial infarction. Bimodal circadian rhythm, with primary peak between 6 and 9 h a.m. and the secondary peak between 3 and 6 p.m. was observed in patients which did not recall any triggering activity, and this was more pronounced in patients with inferior infarction. These results support the hypothesis that the influence of the vegetative tone is most pronounced in the onset of myocardial infarction of inferior wall.

Spirometric disorders in women with genital descensus

Background. We hypothesized that abnormalities in connective tissue, found in women with genital descensus, could impact their pulmonary function.

A no-decompression air dive and ultrasound lung comets

INTRODUCTION Increased accumulation of extravascular lung water after repetitive deep trimix dives was recently reported. This effect was evident 40 min post-dive, but in subsequent studies most signs of this lung congestion were not evident 2-3 h post-dive, indicating no major negative effects on respiratory gas exchange following deep dives. Whether this response is unique for trimix dives or also occurs in more frequent air dives is presently unknown. METHODS A single no-decompression field dive to 33 m with 20 min bottom time was performed by 12 male divers. Multiple ultrasound lung comets (ULC), bubble grade (BG), and single-breath lung diffusing capacity (DLCO) measurements were made before and up to 120 min after the dive. RESULTS Median BG was rather high with maximal values observed at 40 min post-dive [median 4 (4-4)]. Arterialization of bubbles from the venous side was observed only in one diver lasting up to 60 min post-dive. Despite high BG, no DCS symptoms were noted. DLCO and ULC were unchanged after the dive at any time point (DLCO(corr) was 33.6 +/- 1.9 ml x min(-1) mmHg(-1) pre-dive, 32.7 +/- 3.8 ml x min(-1) x mmHg(-1) at 60 min post-dive, and 33.2 +/- 5.3 ml x min(-1) x mmHg(-1) at 120 min post-dive; ULC count was 4.1 +/- 1.9 pre-dive, 4.9 +/- 3.3 at 20 min post-dive, and 3.3 +/- 1.9 at 60 min post-dive. DISCUSSION These preliminary findings show no evidence of increased accumulation of extravascular lung water in male divers after a single no-decompression air dive at the limits of accepted Norwegian diving tables.

Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale

What is the central question of this study? Does a patent foramen ovale contribute to resting arterial hypoxaemia, defined as arterial oxygen saturation <95%, in subjects with chronic heart failure with or without pulmonary arterial hypertension? What is the main finding and its importance? The presence of a patent foramen ovale contributed to resting arterial hypoxaemia only in subjects with chronic heart failure with pulmonary arterial hypertension. These data suggest that the presence of a patent foramen ovale should be considered in chronic heart failure patients with arterial hypoxaemia and pulmonary hypertension.

Early Changes in Platelet Size and Number in Patients with Acute Coronary Syndrome

Abstract A strong relationship exists between acute coronary syndrome (ACS) and platelets (PLTs) volume. Mean platelet volume (MPV) is a parameter of PLT functions and a marker for increased PLT activation. The aim of this study was to determine early changes in number of total PLT and MPV in different manifestation of ACS and to find out predictive value of MPV in the spectrum of ACS. This was a prospective study. One hundred thirty‐four ACS patients were enrolled, 76 of them finished the study. PLT and MPV in patients with unstable angina, non‐ST elevation, and ST elevation myocardial infarctions were determined on arrival and 1, 3, 72 hours, and 7 days after the admission to hospital. There was decrease in PLT and MPV in all three groups after 3 hours of arrival in hospital in comparison with admission values. In the later time period (72 hours and 7 days), there was an increase in PLT and MPV only in patients with acute myocardial infarction (AMI). We have revealed completely new dynamics in early changes in MPV and PLT count in patients with AMI. Biphasic changes were found in early phase after admission to the hospital. Fast response in these parameters raises new questions about their origin.

The Authors' Reply Pulmonary Artery Pressure and Right-to-Left Shunting Through Foramen Ovale after Diving

Dear Editor, We are aware of the letter submitted to you by Dr. Alain Boussuges regarding our above mentioned manuscript by Valic et al (9). We support the view that a right to left shunting can occur through a patent foramen ovale during certain phases of cardiac cycle (during early diastole and during isovolumetric contraction of the right ventricle of each cardiac cycle) even in normal state (7). Increase in pulmonary artery pressure (PAP), coughing or Valsalva maneuver can make this passage even greater. Moreover, we have recently found by two non-invasive ultrasonic techniques (AcT/RVET and tricuspid jet regurgitation) that mean and systolic PAP are increased for about 30% after field dives to 30 msw for 30 minutes with the mild exercise during the bottom phase of the dive (3). Therefore, real field diving causes different changes in pulmonary hemodynamics after diving when compared with simulated chamber diving. This is caused by added stressors such as reduced water temperature, exercise, resistance of the breathing apparatus, dehydration, centralization of the blood volume, psychological effects, etc. Thus, we think that reversal of the right-to-left pressure gradient is possible after field diving. Unfortunately, we did not measure nor estimate left atrial pressure (LAP) in our study. Recently, a new non-invasive ultrasonic method for measurement of LAP and LA compliance was published (6). Invasive measurement of LAP could not be performed outside hospital environment, and our participants would be very unlikely to give informed consent for such study. We agree that additional studies are needed in order to address this topic. We propose to perform animal studies first which can give us initial data on LAP. Only if such studies show reversal of the right to left pressure gradient, invasive and risky studies on human subjects can be proposed. The other possibility for arterialization of venous gas bubbles is passage through intra-pulmonary vascular shunts. Recently, Eldridge et al (5) have shown that during high intensity post-dive exercise contrast bubbles cross through the intra-pulmonary shunts. This suggested that post-dive exercise should be avoided. However, we have shown with the same level, type and duration of post-dive exercise that no bubbles crossed to the left side though intra-pulmonary shunts (4). We also agree with dr Boussuges about the possibility of unequal pressures in the right and left atrium after diving due not only to reduced venous return (1, 2) and pulmonary vascular vasoreactivity (8), but also to reduced right and left ventricle function after field diving (3). Thus, we think that future studies have to be conducted to assess the risk of righ-to-left shunting after diving due to changes in inter-atrial pressure gradient.