Acute respiratory distress syndrome (ARDS) is severe medicalcondition
occurring in critically ill patients and with mortality of 33-52 % is one of the leading causes of death in critically ill patients. To better understand pathophysiology of ARDS and to verify novel therapeutical approaches a reliable animal model is needed. Therefore we have developed modified
lavage model of ARDS in the pig. After premedication (ketamine and midazolam)35 healthy pigs were anesthetized (propofol, midazolam,
morphin, pipecuronium) and orotracheally intubated and ventilated. Primary
ARDS was induced by repeated cycles of lunglavage with a detergent Triton X100 diluted in saline (0.03 %) heated to 37 °C preceded by pre
-oxygenation with 100 % O2. Single cycle included two subsequent lavages
followed by detergent suction. Eachcyclewas followed by hemodynamic
andventilation stabilization for approx. 15 min, with eventualadministration of vasopressors according to an arterial bloodpressure. The lavage procedure
was repeated until the paO2/FiO2index after stabilization remained below 100 at PEEP 5 cm H2O. In 33 pigs we have achieved the desired degree
of severe ARDS(PaO2/FiO2<100). Typical number of lavages was 2-3 (min. 1,max.5). Hemodynamictolerance and the need for vasopressors
were strongly individual. In remainingtwo animalsan unmanageable hypotension developed. For other subjects theexperimental ARDS stability was good and allowed reliablemeasurement for more than 10 h. The
present model of theARDS is clinically relevant and thus it is suitable for further research of the pathophysiology and management of this serious
medical condition.
Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a method used for the treatment most severe cases of decompensated heart failure. The purpose of this study was to evaluate the risk of the formation of microembolisms during VA-ECMO-based therapy. Heart failure was induced with simultaneous detection of microembolisms and the measurement of blood flow rate in the common carotid artery (CCA) without VA-ECMO (0 l/min) and at the VA-ECMO blood flow rate of 1, 2, 3 and 4 l/min. If embolisms for VA-ECMO 0 l/min and the individual regimes for VA-ECMO 1, 2, 3, 4 l/min are compared, a higher VA-ECMO flow rate is accompanied by a higher number of
microembolisms. The final microembolism value at 16 min was for the VA-ECMO flow rate of 0 l/min 0.0 (0, 1), VA-ECMO l/min 7.5 (4, 19), VA-ECMO 2 l/min 12.5 (4, 26), VA-ECMO 3 l/min, 21.0 (18, 57) and VA-ECMO 4 l/min, 27.5 (21, 64). Such a comparison is statistically significant if VA-ECMO 0 vs. 4 l/min p<0.0001, 0 vs. 3 l/min p<0.01 and 1 vs. 4 l/min p<0.01 are compared. The results confirm that high VA-ECMO flow rates pose a risk with regards to the formation of a significantly higher number of microemboli in the blood circulation and that an increase in blood flow rates in the CCA corresponds to changes in the VA-ECMO flow rates.
Cardiac resynchronization therapy (CRT) has proven efficacious in reducing or even eliminating cardiac dyssynchrony and thus improving heart failure symptoms. However, quantification of mechanical dyssynchrony is still difficult and identification of CRT candidates is currently based just on the morphology and width of the QRS complex. As standard 12-lead ECG brings only limited information about the pattern of ventricular activation, we aimed to study changes produced by different pacing modes on the body surface potential maps (BSPM). Total of 12 CRT recipients with symptomatic heart failure (NYHA II-IV), sinus rhythm and QRS width ≥120 ms and 12 healthy controls were studied. Mapping system Biosemi (123 unipolar electrodes) was used for BSPM acquisition. Maximum QRS duration, longest and shortest activation times (ATmax and ATmin) and dispersion of QT interval (QTd) were measured and/or calculated during spontaneous rhythm, single-site right- and left-ventricular pacing and biventricular pacing with ECHO-optimized AV delay. Moreover we studied the impact of CRT on the locations of the early and late activated regions of the heart. The average values during the spontaneous rhythm in the group of patients with dyssynchrony (QRS 140.5±10.6 ms, ATmax 128.1±10.1 ms, ATmin 31.8±6.7 ms and QTd 104.3±24.7 ms) significantly
differed from those measured in the control group (QRS 93.0±10.0 ms, ATmax 79.1±3.2 ms, ATmin 24.4±1.6 ms and QTd 43.6±10.7 ms). Right ventricular pacing (RVP) improved significantly only ATmax [111.2±10.6 ms (p<0.05)] but no other measured parameters. Left ventricular pacing (LVP) succeeded in improvement of all parameters [QRS 105.1±8.0 ms (p<0.01), ATmax 103.7±7.1 ms (p<0.01), ATmin 20.2±3.7 ms (p<0.01) and QTd 52.0±9.4 ms (p<0.01)]. Biventricular pacing (BVP) showed also a beneficial effect in all parameters [QRS 121.3±8.9 ms (p<0.05), ATmax 114.3±8.2 ms (p<0.05), ATmin 22.0±4.1 ms (p<0.01) and QTd 49.8±10.0 ms (p<0.01)]. Our results proved beneficial outcome of LVP and BVP in evaluated parameters (what seems to be important particularly in the case of activation times) and revealed a complete return of activation
times to normal distribution when using these CRT modalities.
The aim of the study was to detect the changes of QT dispersion (QTd) due to cardiotoxicity of tricyclic antidepressant dosulepin. Electrocardiographic and vectorcardiographic recordings were obtained using Cardiag 112.2 diagnostic system from 28 psychiatric outpatients treated with prophylactic doses of dosulepin and compared to those obtained from 37 healthy volunteers. From these recordings following parameters were evaluated: QTd, spatial QRS-STT angle and amplitude of T-wave. The acquired data were correlated with the dosulepin plasma levels using Spearman´s rank order correlation test. The average QTd (±S.D.) in the dosulepin group was significantly higher (70±21 ms) than that in the control group (34±12 ms) (P<0.001). Moreover, the correlation between QTd and the dosulepin plasma levels was highly significant (r = 0.7871, P<0.001). Similar results were obtained when QTc dispersion was used. On the contrary, the QRS-STT space angle did not correlate with the dosulepin plasma levels. Furthermore, the T-wave amplitude was not significantly correlated to the QT-interval. Thus we can conclude that the QT dispersion could be used as a simple marker of the dosulepin effect on the myocardium.
Venoarterial extracorporeal membrane oxygenation (VA ECMO) is widely used in treatment of decompensated heart failure. Our aim was
to investigate its effects on regional perfusion and tissueoxygenation with respect to extracorporeal blood flow (EBF). In five swine, decompensated low-output chronic heart failure was induced by long-term rapid ventricular pacing. Subsequently, VA ECMO was introduced and left ventricular (LV) volume, aorticblood pressure, regional arterial flow and tissue oxygenation
were continuously recorded at different levels of EBF. With increasing
EBF from minimal to 5 l/min, mean arterial pressureincreased from 47±22 to
84±12 mm Hg (P<0.001) and arterial blood flow increased in carotid artery
from 211±72 to 479±58 ml/min (P<0.01) and in subclavian artery from 103
±49 to 296±54 ml/min (P<0.001). Corresponding brain and brachial tissue oxygenation increased promptly from 57±6 to 74±3 % and from 37±6 to
77±6 %, respectively (both P<0.01).Presented results confirm that
VA ECMO is a capable form of heart support. Regional arterial flow and tissue oxygenationsuggest that partial circulatory support may be sufficient to supply brain and peripheral tissue by oxygen.
Hemodynamics in the distal end-to-side anastomosis is related to early development of intimal hyperplasia and bypass failure. In this study we investigated the effect of diameter ratios between the target artery and the bypass at three different angles of the connection. The pulsatile flow field was visualized using particle image velocimetry in transparent models with three different angles of the connection (25°, 45°, 60°) and the diameter ratio between the bypass and the target artery was 4.6 mm : 6 mm, 6 mm :
6 mm, and 7.5 mm : 6 mm. Six parameters including location and oscillation of the stagnation point, local energy dissipation, wall shear stress (WSS), oscillatory shear index, spatial and temporal gradient of WSS and their distribution in the target artery were calculated from the flow field. In the wider bypass, the stagnation point oscillated in a greater range and was located more proximal to the anastomosis. Energy dissipation was minimal in a wider bypass with a more acute angle. The maximum WSS values were tree times greater in a narrow bypass and concentrated in a smaller circular region at the floor of the anastomosis. The oscillatory shear index increased with wider bypass and more acute angle. The maximum of spatial gradient of WSS concentrated around the floor and toe of the anastomosis and decreased with more acute angle and wider bypass, the temporal gradient of WSS was stretched more towards the side wall. Greater bypass to target vessel ratio and more acute anastomosis angle promote hemodynamics known to reduce formation of intimal hyperplasia.