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.

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.

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.

[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.