Tonči Batinić

Cardiac magnetic resonance imaging during pulmonary hyperinflation in apnea divers.

PURPOSE Apnea divers hyperinflate the lung by taking a deep breath followed by glossopharyngeal insufflation. The maneuver can lead to symptomatic arterial hypotension. We tested the hypotheses that glossopharyngeal insufflation interferes with cardiac function further reducing cardiac output (CO) using cardiac magnetic resonance imaging (MRI) to fully sample both cardiac chambers. METHODS Eleven dive athletes (10 men, 1 woman; age = 26 ± 5 yr, body mass index = 23.5 ± 1.7 kg·m(-2)) underwent cardiac MRI during breath holding at functional residual capacity (baseline), at total lung capacity (apnea), and with submaximal glossopharyngeal insufflation. Lung volumes were estimated from anatomic images. Short-axis cine MR images were acquired to study biventricular function. Dynamic changes were followed by long-axis cine MRI. RESULTS Left and right ventricular end-diastolic volumes (LVEDV, RVEDV) decreased during apnea with and without glossopharyngeal insufflation (baseline: LVEDV = 198 ± 19 mL, RVEDV = 225 ± 30 mL; apnea: LVEDV = 125 ± 38 mL, RVEDV = 148 ± 37 mL, P < 0.001; glossopharyngeal insufflation: LVEDV = 108 ± 26 mL, RVEDV = 136 ± 29 mL, P < 0.001 vs baseline). CO decreased during apnea (left = -29 ± 4 %, right = -29 ± 4 %) decreasing further with glossopharyngeal insufflation (left = -38% ± 4%, right = -39% ± 4%, P < 0.05). HR increased 16 ± 4 bpm with apnea and 17 ± 5 bpm with glossopharyngeal insufflation (P < 0.01). Ejection fraction moderately decreased (apnea: left = -5% ± 2%, right = -7% ± 2%, glossopharyngeal insufflation: left = -6% ± 2%, right = -10% ± 2%, P < 0.01). With continued apnea with and without glossopharyngeal insufflation, LVEDV and CO increased over time by a similar but small amount (P < 0.01). CONCLUSIONS The major finding of our study was that submaximal glossopharyngeal insufflation decreased CO further albeit by a small amount compared to maximal inspiratory apnea. The response was not associated with severe biventricular dysfunction.

Influence of lung volume on the interaction between cardiac output and cerebrovascular regulation during extreme apnoea

What is the central question of this study? Does the reduction in cardiac output observed during extreme voluntary apnoea, secondary to high lung volume, result in a reduction in cerebral blood flow, perfusion pressure and oxygen delivery in a group of elite free divers? What is the main finding and its importance? High lung volumes reduce cardiac output and ventricular filling during extreme apnoea, but changes in cerebral blood flow are observed only transiently during the early stages of apnoea. This reveals that whilst cardiac output is important in regulating cerebral haemodynamics, the role of mean arterial pressure in restoring cerebral perfusion pressure is of greater significance to the regulation of cerebral blood flow.

Dynamic diaphragmatic MRI during apnea struggle phase in breath-hold divers

The purpose of the study was to provide insight in diaphragmatic involuntary breathing movements (IBM) during struggle phase of apnea at total lung capacity (TLC) and functional residual capacity (FRC) using magnetic resonance imaging along with measurements of hemodynamics and arterial oxygenation. The study was performed in eight elite breath-hold divers. There was a similar increase in diaphragmatic cranio-caudal excursions towards the end of TLC and FRC apnea. The greatest diaphragmatic excursion in both apneas and during tidal breathing was in the middle and posterior part of the diaphragm. Diaphragm thickness in elite BHD was within the reference range of normal values suggesting no diaphragmatic hypertrophy in this population. We found that the range of diaphragmatic excursions increases toward the end of apneas. Additionally, our data suggest that the diaphragm participates in IBM occurrence and that various segments of the diaphragm behave nonhomogenously both in tidal breathing and IBMs.

CASTLEMAN'S DISEASE PRESENTING AS A TUMOROUS PARACARDIAC FORMATION.

Castlemans disease (in the literature also known as angiofollicular hyperplasia) is a rare benign lymphoproliferative disease. Clinically, it can manifest as unicentric or multicentric disease. Unicentric disease is most often diagnosed by accident or by symptomatology resulting from compression upon the adjoining anatomical structures. Considering its lymphatic origin, tumor mass can theoretically occur in any body region. We present a case of paracardiac localization of unicentric Castlemans disease in a previously healthy 24-year-old woman. In such clinical cases, the specific localization of the tumor and its radiological properties can pose a differential diagnostic dilemma. Correct diagnosis is only possible after complete surgical excision and histopathologic analysis, which is the optimal therapeutic approach in this disease.

Castelman’s disease presenting as tumorous paracardial formation

pRIKAz sLUČAJA: Prikazujemo slučaj od ranije zdrave 24-godišnje žene koja se javila na Hitni kirurški prijam Kliničkog bolničkog centra Split zbog protrahiranih bolova u leđima koji su nastali dva dana ranije kada je doživjela prometnu nezgodu. U sklopu dijagnostičke obrade urađena je rendgenska snimka torakalnih organa kojom se postavi sumnja na tumorsku tvorbu prednjeg medijastinuma. Žurna obrada se nadopuni MSCT-om prsišta i transtorakalnom ehokardiografijom koje su ukazale na postojanje moguće pseudoaneurizme lijeve klijetke (slika 1). Daljnjim dijagnostičkim postupcima (MSCT angiografija) odbaci se INTROdUCTION: Castelman’s disease is a rare benign lymphoprolipherative disease. Clinically it can manifest as unicentric or multicentric.