Hemoglobin concentration and blood shift during dry static apnea in elite breath hold divers.

Introduction: Elite breath-hold divers (BHD) enduring apneas of more than 5 min are characterized by tolerance to arterial blood oxygen levels of 4.3 kPa and low oxygen-consumption in their hearts and skeletal muscles, similar to adult seals. Adult seals possess an adaptive higher hemoglobin-concentration and Bohr effect than pups, and when sedated, adult seals demonstrate a blood shift from the spleen towards the brain, lungs, and heart during apnea. We hypothesized these observations to be similar in human BHD. Therefore, we measured hemoglobin- and 2,3-biphosphoglycerate-concentrations in BHD (n = 11) and matched controls (n = 11) at rest, while myocardial mass, spleen and lower extremity volumes were assessed at rest and during apnea in BHD. Methods and results: After 4 min of apnea, left ventricular myocardial mass (LVMM) determined by 15O-H2O-PET/CT (n = 6) and cardiac MRI (n = 6), was unaltered compared to rest. During maximum apnea (∼6 min), lower extremity volume assessed by DXA-scan revealed a ∼268 mL decrease, and spleen volume, assessed by ultrasonography, decreased ∼102 mL. Compared to age, BMI and VO2max matched controls (n = 11), BHD had similar spleen sizes and 2,3- biphosphoglycerate-concentrations, but higher total hemoglobin-concentrations. Conclusion: Our results indicate: 1) Apnea training in BHD may increase hemoglobin concentration as an oxygen conserving adaptation similar to adult diving mammals. 2) The blood shift during dry apnea in BHD is 162% more from the lower extremities than from the spleen. 3) In contrast to the previous theory of the blood shift demonstrated in sedated adult seals, blood shift is not towards the heart during dry apnea in humans.

Extreme Hypoxia Causing Brady-Arrythmias During Apnea in Elite Breath-Hold Divers.

Introduction: The cardiac electrical conduction system is very sensitive to hypoglycemia and hypoxia, and the consequence may be brady-arrythmias. Weddell seals endure brady-arrythmias during their dives when desaturating to 3.2 kPa and elite breath-hold-divers (BHD), who share metabolic and cardiovascular adaptions including bradycardia with diving mammals, endure similar desaturation during maximum apnea. We hypothesized that hypoxia causes brady-arrythmias during maximum apnea in elite BHD. Hence, this study aimed to define the arterial blood glucose (Glu), peripheral saturation (SAT), heart rhythm (HR), and mean arterial blood pressure (MAP) of elite BHD during maximum apneas. Methods: HR was monitored with Direct-Current-Pads/ECG-lead-II and MAP and Glu from a radial arterial-catheter in nine BHD performing an immersed and head-down maximal static pool apnea after three warm-up apneas. SAT was monitored with a sensor on the neck of the subjects. On a separate day, a 12-lead-ECG-monitored maximum static apnea was repeated dry (n = 6). Results: During pool apnea of maximum duration (385 ± 70 s), SAT decreased from 99.6 ± 0.5 to 58.5 ± 5.5% (∼PaO2 4.8 ± 1.5 kPa, P < 0.001), while Glu increased from 5.8 ± 0.2 to 6.2 ± 0.2 mmol/l (P = 0.009). MAP increased from 103 ± 4 to 155 ± 6 mm Hg (P < 0.005). HR decreased to 46 ± 10 from 86 ± 14 beats/minute (P < 0.001). HR and MAP were unchanged after 3-4 min of apnea. During dry apnea (378 ± 31 s), HR decreased from 55 ± 4 to 40 ± 3 beats/minute (P = 0.031). Atrioventricular dissociation and junctional rhythm were observed both during pool and dry apneas. Conclusion: Our findings contrast with previous studies concluding that Glu decreases during apnea diving. We conclude during maximum apnea in elite BHD that (1) the diving reflex is maximized after 3-4 min, (2) increasing Glu may indicate lactate metabolism in accordance with our previous results, and (3) extreme hypoxia rather than hypoglycemia causes brady-arrythmias in elite BHD similar to diving mammals.

Cardiac hypoxic resistance and decreasing lactate during maximum apnea in elite breath hold divers.

Breath-hold divers (BHD) enduring apnea for more than 4 min are characterized by resistance to release of reactive oxygen species, reduced sensitivity to hypoxia, and low mitochondrial oxygen consumption in their skeletal muscles similar to northern elephant seals. The muscles and myocardium of harbor seals also exhibit metabolic adaptations including increased cardiac lactate-dehydrogenase-activity, exceeding their hypoxic limit. We hypothesized that the myocardium of BHD possesses similar adaptive mechanisms. During maximum apnea 15O-H2O-PET/CT (n = 6) revealed no myocardial perfusion deficits but increased myocardial blood flow (MBF). Cardiac MRI determined blood oxygen level dependence oxygenation (n = 8) after 4 min of apnea was unaltered compared to rest, whereas cine-MRI demonstrated increased left ventricular wall thickness (LVWT). Arterial blood gases were collected after warm-up and maximum apnea in a pool. At the end of the maximum pool apnea (5 min), arterial saturation decreased to 52%, and lactate decreased 20%. Our findings contrast with previous MR studies of BHD, that reported elevated cardiac troponins and decreased myocardial perfusion after 4 min of apnea. In conclusion, we demonstrated for the first time with 15O-H2O-PET/CT and MRI in elite BHD during maximum apnea, that MBF and LVWT increases while lactate decreases, indicating anaerobic/fat-based cardiac-metabolism similar to diving mammals.

Oxygen conserving mitochondrial adaptations in the skeletal muscles of breath hold divers.

BACKGROUND: The performance of elite breath hold divers (BHD) includes static breath hold for more than 11 minutes, swimming as far as 300 m, or going below 250 m in depth, all on a single breath of air. Diving mammals are adapted to sustain oxidative metabolism in hypoxic conditions through several metabolic adaptations, including improved capacity for oxygen transport and mitochondrial oxidative phosphorylation in skeletal muscle. It was hypothesized that similar adaptations characterized human BHD. Hence, the purpose of this study was to examine the capacity for oxidative metabolism in skeletal muscle of BHD compared to matched controls. METHODS: Biopsies were obtained from the lateral vastus of the femoral muscle from 8 Danish BHD and 8 non-diving controls (Judo athletes) matched for morphometry and whole body VO2max. High resolution respirometry was used to determine mitochondrial respiratory capacity and leak respiration with simultaneous measurement of mitochondrial H2O2 emission. Maximal citrate synthase (CS) and 3-hydroxyacyl CoA dehydrogenase (HAD) activity were measured in muscle tissue homogenates. Western Blotting was used to determine protein contents of respiratory complex I-V subunits and myoglobin in muscle tissue lysates. RESULTS: Muscle biopsies of BHD revealed lower mitochondrial leak respiration and electron transfer system (ETS) capacity and higher H2O2 emission during leak respiration than controls, with no differences in enzyme activities (CS and HAD) or protein content of mitochondrial complex subunits myoglobin, myosin heavy chain isoforms, markers of glucose metabolism and antioxidant enzymes. CONCLUSION: We demonstrated for the first time in humans, that the skeletal muscles of BHD are characterized by lower mitochondrial oxygen consumption both during low leak and high (ETS) respiration than matched controls. This supports previous observations of diving mammals demonstrating a lower aerobic mitochondrial capacity of the skeletal muscles as an oxygen conserving adaptation during prolonged dives.

Patent foramen ovale and atrial fibrillation as causes of cryptogenic stroke: is treatment with surgery superior to device closure and anticoagulation? A review of the literature.

Closure of persistent foramen ovale (PFO) to avoid cryptogenic strokes is performed globally with enthusiasm but lacks prove of efficacy. We present a 79-year-old man who had had a PFO device introduced nine years previously because of cryptogenic strokes presenting as syncopes. The patient was referred from his general practitioner with two new syncopes. Transthoracic echocardiography revealed no cardiac causes of embolism. Transesophageal echocardiography (TEE) revealed a misplaced device like an umbrella in a storm, but no septum defects. Holter revealed seconds-long episodes of atrial fibrillation (AF). The patient was successfully treated with anticoagulation. A literature review showed that: (i) the efficacy of PFO closure devices has not been proven in any trial, but was demonstrated in a meta-analysis comparing three different devices; (ii) PFO devices are rarely controlled by TEE during or after insertion; (iii) residual shunts are detected in up to 45% of cases; (iv) there is an increased rate of post-arrhythmic complications; (v) the risk of AF in congenital heart disease increases with increasing age, with a 13% risk of transient ischemic attacks and stroke; and (vi) surgical treatment of PFO was found to have a 4.1% risk of complications including stroke. The question to be asked is whether device closure of PFO should be avoided, considering that PFO is a congenital heart defect with risks of AF and (cryptogenic) stroke? Heart surgery should be a treatment option for symptomatic PFO.

Ischemic preconditioning of one forearm enhances static and dynamic apnea.

INTRODUCTION: Ischemic preconditioning enhances ergometer cycling and swimming performance. We evaluated whether ischemic preconditioning of one forearm (four times for 5 min) also affects static breath hold and underwater swimming, whereas the effect of similar preconditioning on ergometer rowing served as control because the warm-up for rowing regularly encompasses intense exercise and therefore reduced muscle oxygenation. METHODS: Six divers performed a dry static breath hold, 11 divers swam underwater in an indoor pool, and 14 oarsmen rowed "1000 m" on an ergometer. RESULTS: Ischemic preconditioning reduced the forearm oxygen saturation from 65% ± 7% to 19% ± 7% (mean ± SD; P < 0.001), determined using spatially resolved near-infrared spectroscopy. During the breath hold (315 s, range = 280-375 s), forearm oxygenation decreased to 29% ± 10%; and in preparation for rowing, right thigh oxygenation decreased from 66% ± 7% to 33% ± 14% (P < 0.05). Ischemic preconditioning prolonged the breath hold from 279 ± 72 to 327 ± 39 s, and the underwater swimming distance from 110 ± 16 to 119 ± 14 m (P < 0.05) and also the rowing time was reduced (from 186.5 ± 3.6 to 185.7 ± 3.6 s; P < 0.05). CONCLUSIONS: We conclude that while the effect of ischemic preconditioning (of one forearm) on ergometer rowing was minimal, probably because of reduced muscle oxygenation during the warm-up, ischemic preconditioning does enhance both static and dynamic apnea, supporting that muscle ischemia is an important preparation for physical activity.

Resuscitation by hyperbaric exposure from a venous gas emboli following laparoscopic surgery.

Venous gas embolism is common after laparoscopic surgery but is only rarely of clinical relevance. We present a 52 year old woman undergoing laparoscopic treatment for liver cysts, who also underwent cholecystectomy. She was successfully extubated. However, after a few minutes she developed cardiac arrest due to a venous carbon dioxide (CO2) embolism as identified by transthoracic echocardiography and aspiration of approximately 7 ml of gas from a central venous catheter. She was resuscitated and subsequently treated with hyperbaric oxygen to reduce the size of remaining gas bubbles. Subsequently the patient developed one more episode of cardiac arrest but still made a full recovery. The courses of events indicate that bubbles had persisted in the circulation for a prolonged period. We speculate whether insufficient CO2 flushing of the laparoscopic tubing, causing air to enter the peritoneal cavity, could have contributed to the formation of the intravascular gas emboli. We conclude that persistent resuscitation followed by hyperbaric oxygen treatment after venous gas emboli contributed to the elimination of intravascular bubbles and the favourable outcome for the patient.

[Rupture of free left ventricle wall, septum and papillary muscle in acute myocardial infarction]. / Ruptur af fri venstre ventrikelvaeg, septum og papillaermuskler ved akut myokardieinfarkt.

The risk of complications to acute myocardial infarction (AMI), such as cardiogenic shock, is 5-10%. The cause is often left heart failure and sometimes right heart failure, but it can be mechanical AMI complications (MCA) in the form of rupture of the left ventricle and papillary muscle rupture. This risk of MCA can be reduced by sufficient revascularisation, but these rare differential diagnoses to cardiogenic shock remain important. Echocardiography is the diagnostic gold standard. First line treatment is medical and often mechanical stabilization, but this should not delay quick surgical intervention.

Facial immersion in cold water enhances cerebral blood velocity during breath-hold exercise in humans.

The diving response is initiated by apnea and facial immersion in cold water and includes, besides bradycardia, peripheral vasoconstriction, while cerebral perfusion may be enhanced. This study evaluated whether facial immersion in 10 degrees C water has an independent influence on cerebral perfusion evaluated as the middle cerebral artery mean flow velocity (MCA V(mean)) during exercise in nine male subjects. At rest, a breath hold of maximum duration increased the arterial carbon dioxide tension (Pa(CO(2))) from 4.2 to 6.7 kPa and MCA V(mean) from 37 to 103 cm/s (mean; approximately 178%; P < 0.001). Similarly, during 100-W exercise, a breath hold increased Pa(CO(2)) from 5.9 to 8.2 kPa (P < 0.001) and MCA V(mean) from 55 to 113 cm/s ( approximately 105%), and facial immersion further increased MCA V(mean) to 122 cm/s ( approximately 88%; both P < 0.001). MCA V(mean) also increased during 180-W exercise (from 47 to 53 cm/s), and this increment became larger with facial immersion (76 cm/s, approximately 62%; P < 0.001), although Pa(CO(2)) did not significantly change. These results indicate that a breath hold diverts blood toward the brain with a >100% increase in MCA V(mean), largely because Pa(CO(2)) increases, but the increase in MCA V(mean) becomes larger when combined with facial immersion in cold water independent of Pa(CO(2)).

[Recurrence after surgery of varices in the region of the long saphenous vein]. / Recidiv efter operation for varicer i vena saphena magna-området.

The article documents that among patients with saphenofemoral reflux inadequate surgery on the saphenofemoral junction was the cause of recurrence in 40% and 43% respectively of patients treated at hospitals and in out-clinics, but in only 14% when operation was performed by a specialized vascular surgeon. The causes of recurrence are described in the literature as follows: inadequate ligation, recanalisation, neovascularisation, non-saphenofemoral reflux, long saphenous vein duplication, incompetent perforator veins and inadequate stripping of the long saphenous vein. Our examination of the past ten years of literature in this area leads to the conclusion that patients with varicose veins caused by saphenofemoral reflux should be examined clinically as well as with colour-Doppler-ultrasonography. The main cause of recurrence is insufficient surgery. The surgeon may reduce recurrence rates by combining stripping of the long saphenous vein to the knee including duplications with thorough ligation of the saphenofemoral junction and ligation of adjacent side-branches. Stab avulsions are obligatory.