Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Increasing venoarterial extracorporeal membrane oxygenation flow puts higher demands on left ventricular work in a porcine model of chronic heart failure

P. Hála, M. Mlček, P. Ošťádal, M. Popková, D. Janák, T. Bouček, S. Lacko, J. Kudlička, P. Neužil, O. Kittnar

. 2020 ; 18 (1) : 75. [pub] 20200213

Jazyk angličtina Země Velká Británie

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc21020743

BACKGROUND: Venoarterial extracorporeal membrane oxygenation (VA ECMO) is widely used in the treatment of circulatory failure, but repeatedly, its negative effects on the left ventricle (LV) have been observed. The purpose of this study is to assess the influence of increasing extracorporeal blood flow (EBF) on LV performance during VA ECMO therapy of decompensated chronic heart failure. METHODS: A porcine model of low-output chronic heart failure was developed by long-term fast cardiac pacing. Subsequently, under total anesthesia and artificial ventilation, VA ECMO was introduced to a total of five swine with profound signs of chronic cardiac decompensation. LV performance and organ specific parameters were recorded at different levels of EBF using a pulmonary artery catheter, a pressure-volume loop catheter positioned in the LV, and arterial flow probes on systemic arteries. RESULTS: Tachycardia-induced cardiomyopathy led to decompensated chronic heart failure with mean cardiac output of 2.9 ± 0.4 L/min, severe LV dilation, and systemic hypoperfusion. By increasing the EBF from minimal flow to 5 L/min, we observed a gradual increase of LV peak pressure from 49 ± 15 to 73 ± 11 mmHg (P = 0.001) and an improvement in organ perfusion. On the other hand, cardiac performance parameters revealed higher demands put on LV function: LV end-diastolic pressure increased from 7 ± 2 to 15 ± 3 mmHg, end-diastolic volume increased from 189 ± 26 to 218 ± 30 mL, end-systolic volume increased from 139 ± 17 to 167 ± 15 mL (all P < 0.001), and stroke work increased from 1434 ± 941 to 1892 ± 1036 mmHg*mL (P < 0.05). LV ejection fraction and isovolumetric contractility index did not change significantly. CONCLUSIONS: In decompensated chronic heart failure, excessive VA ECMO flow increases demands and has negative effects on the workload of LV. To protect the myocardium from harm, VA ECMO flow should be adjusted with respect to not only systemic perfusion, but also to LV parameters.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc21020743
003      
CZ-PrNML
005      
20210830102407.0
007      
ta
008      
210728s2020 xxk f 000 0|eng||
009      
AR
024    7_
$a 10.1186/s12967-020-02250-x $2 doi
035    __
$a (PubMed)32054495
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxk
100    1_
$a Hála, Pavel $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic. pavel.hala@hotmail.com $u Department of Cardiology, Na Homolce Hospital, Prague, Czech Republic. pavel.hala@hotmail.com
245    10
$a Increasing venoarterial extracorporeal membrane oxygenation flow puts higher demands on left ventricular work in a porcine model of chronic heart failure / $c P. Hála, M. Mlček, P. Ošťádal, M. Popková, D. Janák, T. Bouček, S. Lacko, J. Kudlička, P. Neužil, O. Kittnar
520    9_
$a BACKGROUND: Venoarterial extracorporeal membrane oxygenation (VA ECMO) is widely used in the treatment of circulatory failure, but repeatedly, its negative effects on the left ventricle (LV) have been observed. The purpose of this study is to assess the influence of increasing extracorporeal blood flow (EBF) on LV performance during VA ECMO therapy of decompensated chronic heart failure. METHODS: A porcine model of low-output chronic heart failure was developed by long-term fast cardiac pacing. Subsequently, under total anesthesia and artificial ventilation, VA ECMO was introduced to a total of five swine with profound signs of chronic cardiac decompensation. LV performance and organ specific parameters were recorded at different levels of EBF using a pulmonary artery catheter, a pressure-volume loop catheter positioned in the LV, and arterial flow probes on systemic arteries. RESULTS: Tachycardia-induced cardiomyopathy led to decompensated chronic heart failure with mean cardiac output of 2.9 ± 0.4 L/min, severe LV dilation, and systemic hypoperfusion. By increasing the EBF from minimal flow to 5 L/min, we observed a gradual increase of LV peak pressure from 49 ± 15 to 73 ± 11 mmHg (P = 0.001) and an improvement in organ perfusion. On the other hand, cardiac performance parameters revealed higher demands put on LV function: LV end-diastolic pressure increased from 7 ± 2 to 15 ± 3 mmHg, end-diastolic volume increased from 189 ± 26 to 218 ± 30 mL, end-systolic volume increased from 139 ± 17 to 167 ± 15 mL (all P < 0.001), and stroke work increased from 1434 ± 941 to 1892 ± 1036 mmHg*mL (P < 0.05). LV ejection fraction and isovolumetric contractility index did not change significantly. CONCLUSIONS: In decompensated chronic heart failure, excessive VA ECMO flow increases demands and has negative effects on the workload of LV. To protect the myocardium from harm, VA ECMO flow should be adjusted with respect to not only systemic perfusion, but also to LV parameters.
650    _2
$a zvířata $7 D000818
650    12
$a mimotělní membránová oxygenace $7 D015199
650    12
$a srdeční selhání $x terapie $7 D006333
650    _2
$a hemodynamika $7 D006439
650    _2
$a myokard $7 D009206
650    _2
$a prasata $7 D013552
650    _2
$a funkce levé komory srdeční $7 D016277
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Mlček, Mikuláš $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic
700    1_
$a Ošťádal, Petr $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic $u Department of Cardiology, Na Homolce Hospital, Prague, Czech Republic
700    1_
$a Popková, Michaela $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic
700    1_
$a Janák, David $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic $u Department of Cardiovascular Surgery, Second Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Bouček, Tomáš $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic $u Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University, Prague, Czech Republic
700    1_
$a Lacko, Stanislav $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic
700    1_
$a Kudlička, Jaroslav $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic
700    1_
$a Neužil, Petr $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic $u Department of Cardiology, Na Homolce Hospital, Prague, Czech Republic
700    1_
$a Kittnar, Otomar $u Department of Physiology, First Faculty of Medicine, Charles University, Albertov 5, 128 00, Prague, Czech Republic
773    0_
$w MED00008239 $t Journal of translational medicine $x 1479-5876 $g Roč. 18, č. 1 (2020), s. 75
856    41
$u https://pubmed.ncbi.nlm.nih.gov/32054495 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y p $z 0
990    __
$a 20210728 $b ABA008
991    __
$a 20210830102407 $b ABA008
999    __
$a ok $b bmc $g 1691340 $s 1141189
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2020 $b 18 $c 1 $d 75 $e 20200213 $i 1479-5876 $m Journal of translational medicine $n J Transl Med $x MED00008239
LZP    __
$a Pubmed-20210728

Najít záznam

Citační ukazatele

Nahrávání dat ...

Možnosti archivace

Nahrávání dat ...