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Abstract från föredrag hållet vid yrkesmedicinsk konferens I Bergen 2002.


Hans Örnhagen, Director of Research, Swedish Defence Research Agency, Defence Medicine, Karolinska Institutet, Stockholm, Sweden

Oxygen is a component of air and is necessary for life. Thanks to hemoglobin and enzymes we can operate over a wide range of partial pressures. In the metabolism the most common end product is CO2, which is leaving the body in an opposite way to oxygen coming in.

In diving both hypoxic an hyperoxic conditions are seen. Inspiratory  PO2 lower than 18 kPa are normally seen as hypoxic while the hyperoxic limit is more floating. For an unlimited exposure, a PO2 of 50 kPa is generally accepted as the maximum and for therapy up to 300 kPa are used, but only for limited time and under careful observation.

Since oxygen is consumed in the tissues it does not build up in dissolved form in the tissues, as inert gas does, even at high partial pressures. The higher the fraction of oxygen is in the lungs the lower the inert gas fraction. These two facts can be used to reduce loading of inert gas during diving. That is; by addition of oxygen to the breathing mix, less inert gas is loaded in the body, and longer time can be spent at depth for the same decompression time. The technique is normally called nitrox- or “oxygen enriched air”- diving. The trade off is the risk for oxygen toxicity of lungs and CNS. These side effects maximize the PO2  in diving to 150 - 180 kPa for short exposures (h) and to 50 kPa for long exposures (days). The highest gain is in the depth interval 10 – 25 m.

Oxygen breathing can be used after a standard dive on air to increase the off-gassing of nitrogen or other inert gas both during the stay at surface pressure after a dive and during the decompression in water or in a pressure chamber. For the same reasons as for reduced nitrogen loading during nitrox diving the capillary blood contains less inert gas when breathing pure oxygen or an oxygen enriched air, which promotes acceptance of inert gas from the tissues to the blood without formation of bubbles. Freedom from bubbles in venous blood is usually considered to be advantageous as it reduces the risk to sustain decompression illness.

Oxygen at different partial pressures is used for therapy in certain medical conditions. Most well known is maybe the 100% oxygen given to near drowning victims. In the treatment of decompression illness pure oxygen can be administrated both at surface pressure and at elevated pressure in a recompression chamber. The most commonly used regime is the US Navy table 6, which require a compression to 280 kPa or 18 m during breathing of pure oxygen. The combination of pressure and inert gas free blood is considered the optimum treatment for decompression illness today. The pre-capillary vaso-constriction that follows the elevated oxygen partial pressure is an advantage since it promotes resorption of edema in tissues that have been hypoxic due to decompression illness. On the other hand the same vaso-constriction reduces the blood flow, which lowers the wash out of inert gas. The balance between these factors is not known.

Oxygen at high pressure or HBO (Hyperbaric oxygen treatment) is also used for some conditions not related to diving such as infection with anaerobic bacteria, CO-intoxication and air embolism related to heart lung surgery.

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Minipaper från EUBS konferens sommaren 2002 I Brugge.

Magnus Johansson, Per Arnell, Christian Bardin, and Hans Örnhagen

Foramen ovale is a connection between the atria that permits oxygenated blood to reach the arterial circulation during foetal life. When the child starts breathing the pressure in the left atrium rises and becomes higher than in the right, which forces the septum primum towards the rim of the foramen. In most cases the foramen will be anatomically sealed. However, in a quarter of the population this does not happen [1]. A patent foramen ovale (PFO) opens when the pressure in the right atrium exceeds the pressure in the left atrium, which can happen temporarily when jumping into water, after a forceful Valsalva, during coughing, or when laying down from erect to supine position. Blood can then pass directly to the arterial circulation without passing the filter function of the lung. PFO has been shown to be associated with cryptogenic stroke [2]. Studies have also shown an association between PFO and neurological decompressions illness in divers [3]. In this study an unselected population of divers recompressed because of neurological symptoms after diving were later examined with echocardiography.

Material and methods
A total of 59 divers were treated with recompression at Sahlgrenska University hospital on the Swedish west coast during a 4 year period (1998 - 2001). All 36 patients with neurological symptoms were offered a follow up examination. Six did not participate. The remaining thirty were studied with contrast echocardiography. Two of them went through transthoracic contrast echocardiography and 28 a  transesophageal contrast echocardiography (TEE). One of the authors (Johansson) performed 18 of them. After pharyngeal anaesthesia and mild sedation a TEE was performed. Two ml echo contrast in the form of aerated bovine gelatine solution (Haemaccel, Aventis Pharma) was injected as a bolus into the antecubital vein during Valsalva manoeuvre. The patient was instructed to release strain when the contrast filled the right atrium. PFO was defined as presence of gas in the left atrium within three heart beats. A minimum of three injections were given. The DCI was classified as mild or severe depending on the signs and symptoms. It was considered mild in patients with only sensory losses and severe in patients with symptoms of motor weakness, vertigo or confusion. Risk factors for DCI were looked for and the dive was considered safe when no risk factors were identified. Factors sought for were missed decompression stops, uncontrolled rapid ascent, decompression illness in a companion exposed to the same pressure profile, frequent diving (more than three dives/day to more than 10 meters),[4]

Table 1: Number of patients with neurological DCI examined with echocardiography

Patients examined (n)
Examined with TTE (n)
Examined with TEE (n)
Patients with mild DCI (n) 
Patients with severe DCI (n)

Six, or 20%, of the divers with DCI examined with TEE had a PFO. All of them in the TEE- examined group. No other source of emboli that could have explained the clinical findings was found on the TEE such as an intra cardiac thrombus, aortic atherosclerosis or systolic left ventricular dysfunction. The signs and symptoms of DCI in the treated divers were considered mild in 22 cases, and serious in 8 cases. All cases of serious DCI had a début within 60 min of ascent.  No patient showed life-threatening symptoms.

Table 2: Prevalence of PFO in patients with mild and serious neurological DCI

PFO ( %)
  No PFO (%)
Serious DCI n (%)
3 (40)
5 (60)
Mild DCI n (%)
3 (13)
19 (87)
6 (20)
24 (80)

Of the 8 cases of serious DCI, 5 were the results of what has been called “safe diving” while only 3 cases of DCI were encountered as results of “high risk dives”.

The prevalence of PFO in this mixed population was in the same range as expected for a healthy population. Fisher found a PFO in 9 % with contrast TEE. Autopsy has however shown an overall prevalence of 27 % [1, 5]. This indicates that contrast TEE, even though considered to be golden standard for detection of PFO, frequently can be false negative for PFO. Opening of a PFO is only temporarily and happens when the pressure in the right atrium exceeds that of the left and the interatrial septum bulges over to the left side. To avoid false negative results, no examinations should be called negative unless there has been no passage of contrast despite a bulging septum and a contrast rich right atrium.  In this study we used aerated gelatine solution as contrast medium, which, according to our experience, gives more intense contrast than just aerated saline. The flow dynamics of the right atrium directs the blood from vena cava inferior towards the foramen ovale and the flow from cava superior towards the tricuspid valve, especially if there is a prominent Eustachian valve. That this phenomenon has importance for the diagnosis of PFO using TEE is shown in a study by Hamann[6] in which the prevalence of PFO in a young population with cryptogenic stroke was only18% with antecubital injection  while it increased to 50% with femoral injection.
The results presented here do not give any support to the hypothesis that a PFO should be more common in a population of patients treated for neurological DCI. However, if patients with severe symptoms are treated as a group an increase in the prevalence of PFO to 40 % is found compared to 13 % among patients with mild DCI. These results are in agreement with earlier publications [7,8,9]. A closer analysis of the data showed that all 8 cases of serious DCI had had signs and symptoms that started within 60 min after the dive, while 15 of 22 cases of mild DCI started later than 60 min after the dive. This speaks in favour of the hypothesis that embolizing events are behind serious DCI since it coincides in time with the presence of venous gas bubbles as observed with ultrasound Doppler after dives following  accepted depth-time exposures [10]. The information that most of the cases of serious DCI among our patients were the outcome of “safe” dives just reflects the fact that the vast majority of the dives are performed according to the rules, and venous bubbles are seen also after dives that follow decompression procedures that are regarded as “safe” from a DCI perspective.
In routine TEE PFO screenings there could be a high number of false negatives mainly related to insufficient positive pressure in the right atrium during the presence of contrast in the atrium. This, in combination with uncertainty how the information regarding the presence of a PFO shall be handled, together with the inconvenience to the examined, makes us believe that TEE is not a technique for the routine examinations regarding fitness to dive . The TTE on the other hand, being less inconvenient, does often not give a good enough signal to allow interpretation of a possible gas passage and presence of a PFO.

However, PFO should probably be sought for in divers who have had severe DCI, because in these cases knowledge about a PFO can lead to advice that increase the safety in future diving. In those selected patients the preferred technique should be TEE with femoral injection of bovine gelatine contrast during Valsalva. Upon arrival of the contrast to the right atrium the examined is asked to release the Valsalva   and the septum is inspected so it bulges into the left atrium. This being the indicator of a higher pressure in the right than in the left atrium. The gelatine contrast has the advantage over the new generation of echo contrast such as Optison because the gelatine contrast disappears when it passes the lungs and new contrast injections can be made readily.

The population in this study was consecutive cases with neurological symptoms of DCI treated with recompression. They represent divers from a geographic region that came to the hospital because of symptoms of neurological DCI. Our finding is in accordance with other studies [7, 8]. The increased risk for DCI with PFO has been limited to a population with severe neurological symptoms, especially within 60 minutes of ascent. Because of a risk with false negative results, screening with TEE for PFO should be limited to only a few specialised clinics and to cases after severe DCI in which the knowledge about a PFO could be used for advice regarding future diving.

1.    Hagen, p., Incidence and size of patent foramen ovale during the first 10 decades of life. An autopy study of 965 normal hearts. Mayo clin proc, 1984. 59: p. 17-20.
2.    Di Tullio, M., et al., Patent foramen ovale as a risk factor for cryptogenic stroke. Ann Intern Med, 1992. 117(6): p. 461-5.
3.    Wilmshurst, P.T., J.C. Byrne, and M.M. Webb-Peploe, Neurological decompression sickness. Lancet, 1989. 1(8640): p. 731.
4.    Wilmshurst, P.T., J.C. Byrne, and M.M. Webb-Peploe, Relation between interatrial shunts and decompression sickness in divers. Lancet, 1989. 2(8675): p. 1302-6.
5.    Fisher, D.C., et al., The incidence of patent foramen ovale in 1,000 consecutive patients. A contrast transesophageal echocardiography study. Chest, 1995. 107(6): p. 1504-9.
6.    Hamann, G.F., et al., Femoral injection of echo contrast medium may increase the sensitivity of testing for a patent foramen ovale. Neurology, 1998. 50(5): p. 1423-1428.
7.    Bove, A.A., Risk of decompression sickness with patent foramen ovale. Undersea Hyperb Med, 1998. 25(3): p. 175-8.
8.    Moon, R.E., E.M. Camporesi, and J.A. Kisslo, Patent foramen ovale and decompression sickness in divers. Lancet, 1989. 1(8637): p. 513-4.
9.    Hencke, J., and M. McCabe. Patent foramen ovale (PFO) in unexplainable scuba diving accidents – a pilot study. EUBS 1998 Proceedings. Ed. M Gennser FOA Report: FOA-B--98-00342--721--SE.  Stockholm. 1998
10.    Marroni,A., R Cali Corleo, C.Balestra, P. Longobardi, E. Voellm, M. Pieri, R. Pepoli. Effects of the variation of ascent speed and profile on the production of circulating venous gas emboli and the incidence of DCI in compressed air diving. Phase 1. Introduction of extra deep stops in the ascent profile without changing the original ascent rates. DSL special project 01/2000. EUBS 2000 Proceedings ed R Cali-Corleo. Malta. 2000.

Magnus Johansson, Clinical Physiology, SU/ÖSTRA, 416 85 Gothenburg, Sweden.
Per Arnell, Anaesthesiology, SU/ÖSTRA, 416 85 Gothenburg, Sweden.
Christian Bardin, Anaesthesiology, SU/ÖSTRA, 416 85 Gothenburg, Sweden.
Hans Örnhagen, FOI, Defence Medicine, Karolinska Institutet, Solna, Sweden.

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Abstract från föredrag hållet vid årlig idrottsmedicinsk konferens i Köln 2001.

Hans Örnhagen
Swedish Defence Research Institute, Man Machine Interaction, Defence Medicine,
Karolinska Institutet, SE-171 77 Stockholm, Sweden
and Consulting doctor at the Swedish Sports diving Federation.

     Fatalities in recreational diving usually create sensations in the tabloid press. Often a statement that fatalities are increasing is included without any reference to proper statistics. In the Nordic countries, Sweden, Norway, Finland and Denmark the total number of sports diving fatalities each year varies within a broad range. In 1988, 17 persons died in diving related accidents, while the number two years later, 1990, was only 6. Another three years later, 1993 the number was again high with 20 dead divers. This makes statistics difficult, but calculation of a 10 year average gives a fatality rate of 13 in 1987 and ten years later, 1997, 17 dead in a total population of 20 million persons. This is an increase in absolute numbers, but in relation to the number of active sports divers, that has more than doubled over the 10-year period, we can see that the fatality rate actually has gone down.

The lack of adequate statistics makes a deeper analysis of the fatalities difficult and most often different causes behind the accidents are just listed because without a reliable denominator further analysis of trend or closer causality is impossible. We know that a great proportion (approximately 70 – 80%) of the fatalities have a “human factor” or mistake component but there is a wish to know more.

What parameter shall be used as denominator to express diving accident rate?
Comparing fatality statistics by years in the same region or different regions the same year is not easy because there is no good common denominator to use. Some of the more commonly used parameters are:
•    Population in the region (country, costal area etc)
•    Number of divers with license
•    Number of active divers
•    Number of dives per year

Of the above parameters the population in the region and the number of issued licenses are the easiest to find and they are also often used. The number of licenses issued is in no way the same as number of active divers, and even if “active divers” is used, this does not reflect how many dives are made. The fact is that it is only during diving that you are exposed to the risk to be involved in a diving accident. In traffic accident statistics, accidents are often expressed per million passenger kilometers, which gives a good expression of the number of accidents in relation to the exposure. A similar dimension in diving should be hours under water multiplied by the diving depth or “meter hours”. It is obvious to everyone that it is difficult to get hold of this dimension without a very rigorous control and an enormous amount of work, which makes it impossible to use for anything but small samples of diver populations.

There is, however, a parameter that is well related to the “exposure” and that is not too difficult to collect: the amount of air consumed by the divers. Firstly the deeper the diver goes the more air is consumed per unit time, secondly the harder the diver works or swims the more air he/she consumes per unit time. Both depth and physical activity increase the over all risk for an accident, which makes air consumption an ideal parameter for use in accident statistics.

Furthermore, the air used in diving is compressed and sold at a limited number of dive shops, clubs, and tour organizers and there are rules and regulations how to run the compressors (filter change etc) that makes it simple to document and report the total amount of air compressed. The relatively low number of privately owned compressors will cause only a minor uncertainty in the over all statistics.

This means that the dive organizations like PADI, NAUI, CMAS etc, within which almost all air used for recreational diving is compressed, have a possibility to contribute to future diving safety by providing a good denominator for accident statistics “The annual consumption of divers air” to those who analyze diving accidents.
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Pressrelease Riksstämma 981124, Örnhagen

Grodandning eller “Buccal pumping”, en ny riskfaktor inom sportdykning?

Hans Örnhagen, forskningschef, Försvarets forskningsanstalt, FOA, Navalmedicin, 130 61 Hårsfjärden (och förbundsläkare, Svenska Sportdykarförbundet)
Studierna berdivs i samarbete med Dr Erika Schagatay, Inst för Zoofysiologi,  Lunds Universitet och Dr Per Gustafsson, Barnkliniken Kärnsjukhuset Skövde.

Grodandning dvs aktiv nedpumpning av luft till lungorna med hjälp av svalgets muskulatur praktiseras av personer med partiell andningsmuskelförlamning (exempelvis efter polio) för att blåsa upp lungorna när ett extra stort andetag kan behövas. Tekniken har också använts sedan länge av en liten grupp andhållningsdykare ffa i Medelhavsländerna för att öka lungvolymen och på detta sätt kunna nå större dykdjup.
Det stigande intresset för äventyrsidrott i Sverige innebär att grodandningstekniken nu riskerar att spridas i större grupper där man inte känner riskerna med tekniken.

Poliopatienten börjar sin grodandning från en reducerad lungvolym medan andhållningsdykaren börjar grodandningen efter en maximal inandning, vilket påtagligt ökar riskerna för skada. När lungorna övertänjs sker två saker:
- Lungvävnaden riskerar att brista.
- Brösthåletrycket blir så stort att blodet inte kan återvända till hjärtat.

Vi har visat att upp till 150 ml extra luft kan tillföras per grodandetag. Efter 10 s grodandning kan trycket i lungorna ha dubblats från 3 till 6 kPa (30 till 60 cm vattenpelare) och den tidigare maximala lungvolymen ökat med mer än 20 %. När trycket i brösthålan blir högre än ventrycket tillförs inget blod till hjärtat och blodtrycket sjunket. På grund av det sjunkande blodtrycket upplever utövaren i allmänhet obehag, slutar grodandas och släpper ut luften, vilket återställer cirkulationen och förhindrar svimning.
Om grodandningen inte upphör i tid kan man svimma av eller lungvävnaden brista och luft läcka ut i bröstskiljeväggen eller in i lungkärlen. Luft som kommer in i lungvenerna kan sedan passera vänsterhjärtat och embolisera hjärnan med allvarliga följder. Denna olycksmekanism tros vara den samma som vid lungbristning och arteriell luftemboli i samband med fri uppstigning som tränas av bl a ubåtspersonal. (Detta är en av orsakerna till FOA Navalmedicin intresse rörande grodandning)

Det finns anledning att påpeka att riskerna är störst vid tävling eftersom dykaren då tenderar att bortse från varningssignaler och gärna pressar sig till det yttersta.

Örnhagen, Schagatay, Andersson, Bergsten, Gustafsson and Sandström. Mechanisms of “Buccal pumping”(Lung packing) and its pulmonary effects. EUBS collection of manuscripts 1998. FOA report B 98-00342--721--SE. ISSN 1104-9162.

Andersson, Schagatay, Gustafsson and Örnhagen. Cardiovascular effects of “Buccal pumping” in breath-hold divers. EUBS collection of manuscripts 1998. FOA report B 98-00342--721--SE. ISSN 1104-9162.
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Skador inom sportdykning.
Abstract från föredrag hållet vid 6:e skadeförebyggande konferensen i Borås, Oktober 1998

Forskningschef Hans Örnhagen, FOA, Navalmedicin 130 61 Hårsfjärden.
(Förbundsläkare Svenska sportdykarförbundet)

Amatördykning betraktades från början som sport och kom att bli en gren av Idrottsrörelsen. Det militära dykeriet stod som förebild och det var allmänt accepterat att dykning var för ett fåtal starka och djärva individer. Därav namnet sportdykning. Under senare decenier har termen rekreationsdykning börjat användas och man talar om dykning som en aktivitet som de flesta kan deltaga i. Samtidigt har under de sista åren termer som äventyrsidrott kommit att användas för aktiviteter där mod och fysisk kapacitet måste finnas. Dykning är inte lämplig som äventyrsidrott i och med att säkerhetstänkandet då ofta går förlorat.

Dödsfall inom sportdykning tilldrar sig stor publicitet och inte sällan läser vi om hur antalet döda ökar dramatiskt. I själva verket har antalet döda per år i norden (Danmark, Finland, Norge och Sverige) under de senaste 10 åren gått upp från ca 14 döda/år till ca 17 döda/år medan antalet aktiva dykare mångdubblats och det skattade antalet dykningar per år ökat från ca 300 000 till nära 1 miljon. Detta betyder inte att sportdykarorganisationerna inte betraktar dödsfallen som ett stort problem. Det stora problemet med dödsfallen är att de orsakas av mänsklig faktor sk beteendefel och därför är svåra att finna motmedel mot. Den som har god hälsa, godkänd och välskött utrustning samt dyker enligt gällande regler omkommer inte.

Den vanligaste typen av skada inom sportdykning är orsakad av luftens kompression och expansion. Trumhinneskador, bihåleblödningar, yrsel och nedsatt hörsel hör till denna kategori. Endast ett fåtal får bestående skador.

Dykarsjuka och lungbristning med cerebral luftemboli är specifika dykarskador. Mellan 30 och 50 dykare med dessa diagnoser, nästan undantagslöst sportdykare, behandlas varje år i svenska tryckkammare.  Förutom de som omkommer i dessa sjukdomar får ytterst få bestående men.

Den bästa skadeprevention är att vara bra utbildad och förstå att konsekvensen av  felfunktion och egna felgrepp kan innebära döden och att en välutbildad parkamrat kan vara faktorn som skiljer tillbud från olycksfall.

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