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 the treatment of patients with heart failure and
dyssynchronous activation. Currently, we select suitable CRT
candidates based on the QRS complex duration (QRSd) and
morphology with left bundle branch block being the optimal
substrate for resynchronization. To improve CRT response rates,
recommendations emphasize attention to electrical parameters
both before implant and after it. Therefore, we decided to study
activation times before and after CRT on the body surface
potential maps (BSPM) and to compare thus obtained results with
data from electroanatomical mapping using the CARTO system.
Total of 21 CRT recipients with symptomatic heart failure (NYHA
II-IV), sinus rhythm, and QRSd ≥150 ms and 7 healthy controls
were studied. The maximum QRSd and the longest and shortest
activation times (ATmax and ATmin) were set in the BSPM maps
and their locations on the chest were compared with CARTO
derived time interval and site of the latest (LATmax) and earliest
(LATmin) ventricular activation. In CRT patients, all these
parameters were measured during both spontaneous rhythm and
biventricular pacing (BVP) and compared with the findings during
the spontaneous sinus rhythm in the healthy controls. QRSd was
169.7±12.1 ms during spontaneous rhythm in the CRT group and
104.3±10.2 ms after CRT (p<0.01). In the control group the
QRSd was significantly shorter: 95.1±5.6 ms (p<0.01). There
was a good correlation between LATmin(CARTO) and
ATmin(BSPM). Both LATmin and ATmin were shorter in the
control group (LATmin(CARTO) 24.8±7.1 ms and ATmin(BSPM)
29.6±11.3 ms, NS) than in CRT group (LATmin(CARTO) was
48.1±6.8 ms and ATmin(BSPM) 51.6±10.1 ms, NS). BVP
produced shortening compared to the spontaneous rhythm of
CRT recipients (LATmin(CARTO) 31.6±5.3 ms and ATmin(BSPM)
35.2±12.6 ms; p<0.01 spontaneous rhythm versus BVP). ATmax
exhibited greater differences between both methods with higher
values in BSPM: in the control group LATmax(CARTO) was
72.0±4.1 ms and ATmax (BSPM) 92.5±9.4 ms (p<0.01), in the
CRT candidates LATmax(CARTO) reached only 106.1±6.8 ms
whereas ATmax(BSPM) 146.0±12.1 ms (p<0.05), and BVP paced
rhythm in CRT group produced improvement with
LATmax(CARTO) 92.2±7.1 ms and ATmax(BSPM) 130.9±11.0 ms
(p<0.01 before and during BVP). With regard to the propagation
of ATmin and ATmax on the body surface, earliest activation
projected most often frontally in all 3 groups, whereas projection
of ATmax on the body surface was more variable. Our results
suggest that compared to invasive electroanatomical mapping
BSPM reflects well time of the earliest activation, however
provides longer time-intervals for sites of late activation.
Projection of both early and late activated regions of the heart on
the body surface is more variable than expected, very likely due
to changed LV geometry and interposed tissues between the
heart and superficial ECG electrode.
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.
The growth in the experimental research of facilities to support extracorporeal circulation requires the further development of models of acute heart failure that can be well controlled and reproduced. Two types of acute heart failure were examined in domestic pigs (Sus scrofa domestica ): a hypoxic model (n=5) with continuous perfusion of the left coronary artery by hypoxic deoxygenated blood and ischemic model (n=9) with proximal closure of the left coronary artery and controlled hypoperfusion behind the closure. The aim was a severe, stable heart pump failure defined by hemodynamic parameters changes: a) decrease in cardiac output by at least 50 %; b) decrease in mixed venous blood saturation to under 60 %; c) left ventricular ejection fraction below 25 %; and d) decrease in flow via the carotid arteries at least 50 %. Acute heart failure developed in the first group in one animal with no acute mortality and in the second group in 8 animals with no acute mortality. In the case of ischemic model the cardiac output fell from 6.70±0.89 l/min to 2.89±0.75 l/min. The saturation of the mixed venous blood decreased from 83±2 % to 58±8 %. The left ventricular ejection fraction decreased from 50±8 % to 19±2 %. The flow via the carotid arteries decreased from 337±78 ml/min to 136±59 ml/min (P≤0.001 for all comparisons). The proposed ischemic model is not burdened with acute mortality in the development of heart failure and is suitable for further use in experimental research into extracorporeal circulatory support., S. Lacko, M. Mlček, P. Hála, M. Popková, D. Janák, M. Hrachovina, J. Kudlička, V. Hrachovina, P. Ošťádal, O. Kittnar., and Obsahuje bibliografii