Increased intra-abdominal pressure affects respiratory variations in arterial pressure in normovolaemic and hypovolaemic mechanically ventilated healthy pigs
To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model. Experimental study in a research laboratory. Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hy...
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| Vydané v: | Intensive care medicine Ročník 33; číslo 1; s. 163 - 171 |
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| Hlavní autori: | , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Heidelberg
Springer
01.01.2007
Berlin Springer Nature B.V |
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| ISSN: | 0342-4642, 1432-1238 |
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| Abstract | To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model.
Experimental study in a research laboratory.
Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal.
Abdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg.
Variations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP.
In this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed. |
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| AbstractList | To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model.
Experimental study in a research laboratory.
Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal.
Abdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg.
Variations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP.
In this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed. To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model. Experimental study in a research laboratory. Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal. Abdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg. Variations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP. In this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed. To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model.OBJECTIVETo evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model.Experimental study in a research laboratory.DESIGN AND SETTINGExperimental study in a research laboratory.Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal.SUBJECTSSeven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal.Abdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg.INTERVENTIONAbdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg.Variations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP.MEASUREMENTS AND MAIN RESULTSVariations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP.In this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed.CONCLUSIONSIn this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed. |
| Author | Lhuillier, Franck Duperret, Serge Metton, Olivier Bendjelid, Karim Vivier, Emmanuel Branche, Patricia Piriou, Vincent Annat, Guy Viale, Jean Paul |
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| Keywords | Hypertension Systolic pressure Intensive care Echocardiography Cardiovascular disease Pig Intra-abdominal hypertension Vertebrata Mammalia Arterial pressure Artiodactyla Hemodynamics Systolic pressure variations Ungulata Resuscitation |
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| References_xml | – start-page: 183 volume-title: Respiratory–circulation interactions in health and disease. Edited by year: 1998 ident: 412_CR1 – volume: 119 start-page: 867 year: 2001 ident: 412_CR8 publication-title: Chest doi: 10.1378/chest.119.3.867 – volume: 116 start-page: 176 year: 1999 ident: 412_CR21 publication-title: Chest doi: 10.1378/chest.116.1.176 – volume: 169 start-page: 151 year: 2004 ident: 412_CR13 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.200211-1360CC – volume: 30 start-page: 1740 year: 2004 ident: 412_CR16 publication-title: Intensive Care Med doi: 10.1007/s00134-004-2259-8 – volume: 29 start-page: 1613 year: 2003 ident: 412_CR19 publication-title: Intensive Care Med doi: 10.1007/s00134-003-1886-9 – volume: 69 start-page: 1961 year: 1990 ident: 412_CR14 publication-title: J Appl Physiol doi: 10.1152/jappl.1990.69.6.1961 – volume: 78 start-page: 46 year: 1994 ident: 412_CR6 publication-title: Anesth Analg doi: 10.1213/00000539-199401000-00009 – volume: 31 start-page: 517 year: 2005 ident: 412_CR20 publication-title: Intensive Care Med doi: 10.1007/s00134-005-2586-4 – volume: 68 start-page: 266 year: 1983 ident: 412_CR3 publication-title: Circulation doi: 10.1161/01.CIR.68.2.266 – volume: 67 start-page: 498 year: 1987 ident: 412_CR4 publication-title: Anesthesiology doi: 10.1097/00000542-198710000-00009 – volume: 89 start-page: 1313 year: 1998 ident: 412_CR5 publication-title: Anesthesiology doi: 10.1097/00000542-199812000-00007 – volume-title: Biostatistics: a methodology for the health sciences year: 1993 ident: 412_CR11 – volume: 30 start-page: 822 year: 2004 ident: 412_CR9 publication-title: Intensive Care Med doi: 10.1007/s00134-004-2169-9 – volume: 162 start-page: 134 year: 2000 ident: 412_CR7 publication-title: Am J Respir Crit Care Med doi: 10.1164/ajrccm.162.1.9903035 – volume: 29 start-page: 476 year: 2003 ident: 412_CR18 publication-title: Intensive Care Med doi: 10.1007/s00134-003-1649-7 – volume: 169 start-page: 534 year: 2004 ident: 412_CR17 publication-title: Am J Respir Crit Care Med doi: 10.1164/rccm.200209-1060OC – volume: 27 start-page: 584 year: 1966 ident: 412_CR2 publication-title: Anesthesiology doi: 10.1097/00000542-196609000-00009 – volume: 96 start-page: 701 year: 2006 ident: 412_CR10 publication-title: Br J Anaesth doi: 10.1093/bja/ael071 – volume: 89 start-page: 1309 year: 1998 ident: 412_CR12 publication-title: Anesthesiology doi: 10.1097/00000542-199812000-00005 – volume: 27 start-page: 953 year: 1999 ident: 412_CR15 publication-title: Crit Care Med doi: 10.1097/00003246-199905000-00033 – reference: 2076989 - J Appl Physiol (1985). 1990 Dec;69(6):1961-72 – reference: 11243970 - Chest. 2001 Mar;119(3):867-73 – reference: 9856702 - Anesthesiology. 1998 Dec;89(6):1309-10 – reference: 8267179 - Anesth Analg. 1994 Jan;78(1):46-53 – reference: 15754196 - Intensive Care Med. 2005 Apr;31(4):517-23 – reference: 9856704 - Anesthesiology. 1998 Dec;89(6):1313-21 – reference: 12579420 - Intensive Care Med. 2003 Mar;29(3):476-80 – reference: 14718237 - Am J Respir Crit Care Med. 2004 Jan 15;169(2):151-5 – reference: 12904854 - Intensive Care Med. 2003 Sep;29(9):1613 – reference: 6861305 - Circulation. 1983 Aug;68(2):266-74 – reference: 5331459 - Anesthesiology. 1966 Sep-Oct;27(5):584-90 – reference: 14758472 - Intensive Care Med. 2004 May;30(5):822-9 – reference: 10424523 - Chest. 1999 Jul;116(1):176-86 – reference: 17102963 - Intensive Care Med. 2007 Jan;33(1):6-8 – reference: 3310740 - Anesthesiology. 1987 Oct;67(4):498-502 – reference: 14670801 - Am J Respir Crit Care Med. 2004 Feb 15;169(4):534-41 – reference: 10362419 - Crit Care Med. 1999 May;27(5):953-8 – reference: 10903232 - Am J Respir Crit Care Med. 2000 Jul;162(1):134-8 – reference: 16595615 - Br J Anaesth. 2006 Jun;96(6):701-7 – reference: 15034650 - Intensive Care Med. 2004 Sep;30(9):1740-6 |
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| SubjectTerms | Abdomen Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Anesthesiology Animals Biological and medical sciences Blood Pressure Catheters Emergency and intensive respiratory care Hogs Hypovolemia - physiopathology Injuries of the thorax. Foreign bodies. Diseases due to physical agents Intensive care Intensive care medicine Medical sciences Positive-Pressure Respiration Pressure Respiration Swine Traumas. Diseases due to physical agents Ultrasonic imaging Ventilators |
| Title | Increased intra-abdominal pressure affects respiratory variations in arterial pressure in normovolaemic and hypovolaemic mechanically ventilated healthy pigs |
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