Hemodynamic optimization in intra-abdominal hypertension
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Hemodynamic optimization in intra-abdominal hypertension
- 1. Hemodynamic optimization in intra- abdominal hypertension Jan J. De Waele MD PhD Surgical ICU Ghent University Hospital Ghent, Belgium.
- 2. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Introduction Hemodynamics? Blood pressure Cardiac function Macro-circulation Micro-circulation and end-organ function may still be affected despite “normal hemodynamics”
- 3. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele IAH affects the cardiovascular system
- 4. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Cardiac output IAP Vascular compression Thoracic pressure Organ compression Preload Contractility Afterload Renin Aldosteron Cardiac compressionVenous return
- 5. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH is different
- 6. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele How does IAH affect preload Cheatham ML et al., Acta Clin Belg Suppl 2007, 98-112.
- 7. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele IAH and preload monitoring 1. Intrathoracic pressure increase • Diaphragm elevation Affected: • Central venous pressure • PAOP • Pleural pressure • SVV, PPV IAP ↑ ITP ↑
- 8. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele IAH and preload monitoring 2. Inferior vena cava flow decrease • Direct pressure on IVC Affected: • Passive leg raising (PLR)
- 9. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele IAH and preload monitoring 3. Cardiac volumes decrease • Diaphragm elevation – cardiac compression Affected: • GEDV, ITBV • LVEDA
- 10. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH CVP/PAOP After Malbrain et al. Current Opinion Crit Care 2004; 10(2): 132-145 0 5 10 15 20 25 Malbrain Hering Schachtrupp * Renner * CVP Baseline IAH 0 5 10 15 20 25 30 Malbrain Hering Renner * PAOP Baseline IAH
- 11. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH SVV and PPV Duperret S, Intensive Care Med 2007 33: 163-171. Normovolemia Hypovolemia
- 12. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH SVV and PPV Jacques D, Crit Care 2011 15: R33. Normovolemia Hypovolemia
- 13. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH GEDV 0 200 400 600 800 1000 1200 Malbrain Hering Schachtrupp Hachenberg Baseline IAH
- 14. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Prediction of fluid responsiveness
- 15. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele
- 16. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH Passive leg raising Malbrain ML, Crit Care Med 2010 38: 1912-5.
- 17. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH Passive leg raising • 31 fluid responsive patients • 48% false negative • IAP >16mmHg ideal cutoff Mahjoub Y, Crit Care Med 2010 38: 1824-9.
- 18. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload evaluation in IAH LVEDA Vivier E et al. Br J Anaesth 2006; 96: 701–7
- 19. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload and IAH: conclusion Application of IAH → Volumetric parameters decrease → Barometric parameters increase → Dynamic indices suggest fluid responsiveness but may be false negative (PLR)
- 20. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Optimizing preload in IAH
- 21. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Preload optimization in IAH Fluid responsiveness = fluid depletion? • Signs of hypoperfusion? • Avoid treating numbers
- 22. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Practical implications for IAH patients IAH mimicks • Fluid overload • Fluid requirement • Fluid responsiveness → SVV and PPV • Accept higher tresholds • Avoid fluid overload – vicious cycle!
- 23. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Practical implications for IAH patients IAH mimicks • Fluid overload • Fluid requirement • Fluid responsiveness → CVP/PAOP • Use transmural pressure?
- 24. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Practical implications for IAH patients → Use transmural filling pressures! CVPTM = CVP - IAP/2 PAOPTM = PAOP - IAP/2 ITP CVP PAOP
- 25. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Practical implications for IAH patients IAH mimicks • Fluid overload • Fluid requirement • Fluid responsiveness → Passive leg raising • Beware of false negative results • Not to be used at all?
- 26. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele The most effective method for hemodynamic optimization is reducing the intra-abdominal pressure
- 27. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Targets for medical management Improve abdominal wall compliance Evacuate intraluminal contents Evacuate intra- abdominal fluid collections Correct positive fluid balance Optimize systemic and regional perfusion
- 28. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele www.wsacs.org
- 29. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele PCD as an alternative for laparotomy Cheatham ML, Chest 2011 140: 1428-35. • 31 patients • 54y, 65% male • APACHE II 24 • SOFA 8 • Indication for PCD • ACS 71% • IAH 23% • Hemoperitoneum 6% • Matched to open decompression patients
- 30. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele PCD as an alternative for laparotomy Cheatham ML, Chest 2011 140: 1428-35. 0 10 20 30 40 50 60 70 80 90 MAP IAP APP UOP PIP Cdyn Lactate Before PCD After PCD
- 31. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Laparotomy remains effective Chiara O, Minerva Anestesiol 2011 77: 457-62. 0 50 100 150 200 250 300 MAP HR P/F ratio Urinary output APP 0 5 10 15 20 25 30 CVP Lactate IAP APACHE2 Before 24h after
- 32. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Before I came here I was confused about this subject. Having listened to your lecture I am still confused. But on a higher level. Enrico Fermi
- 33. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Take home messages • IAH affects the cardiovascular system • All methods of preload evaluation are influenced by IAH • Fluid administration not to used lightly • Lowering IAP is the best method for hemodynamic optimization
- 34. 3rd IFAD – Hemodynamic optimization in IAH – Jan J. De Waele Thank you for your attention Email: Jan.DeWaele@UGent.be Twitter: @CriticCareDoc
Editor's Notes
- 40min
- OBJECTIVES: The passive leg-raising maneuver is a reversible fluid-loading procedure used to predict fluid responsiveness in mechanically ventilated patients. The aim of the present study was to determine whether intra-abdominal hypertension (which impairs venous return) reduces the ability of passive leg raising to detect fluid responsiveness in critically ill ventilated patients. DESIGN: A prospective study. SETTING: The medical and surgical intensive care unit of a university medical center. PATIENTS: Forty-one mechanically ventilated patients with a pulse pressure variation of >12%. INTERVENTIONS: Stroke volume was continuously monitored by esophageal Doppler. Intra-abdominal pressure was measured via bladder pressure. After a passive leg-raising maneuver and a return to baseline, fluid loading with 500 mL of saline was performed. Hemodynamic parameters were recorded at each step. Nonresponders to volume loading were not analyzed (10 patients). Thirty-one patients were classified into two groups according to their response to passive leg raising: responders to passive leg raising (at least a 12% increase in stroke volume) and nonresponders to passive leg raising. MEASUREMENTS AND MAIN RESULTS: Sixteen patients (52%) were responders to passive leg raising, and 15 (48%) were nonresponders to passive leg raising (i.e., false negatives). At baseline, the median intra-abdominal pressure was significantly higher in the nonresponders to passive leg raising than in the responders to passive leg raising (20 [6.5] vs. 11.5 [5.5], respectively; p < .0001). The area under the receiver-operating characteristic curve was 0.969 +/- 0.033. An intra-abdominal pressure cutoff value of 16 mm Hg discriminated between responders to passive leg raising and nonresponders to passive leg raising with a sensitivity of 100% (confidence interval, 78-100) and a specificity of 87.5% (confidence interval, 61.6-98.1). An intra-abdominal pressure of > or =16 mm Hg was the only independent predictor of nonresponse to passive leg raising in a multivariate analysis (odds ratio, 2.6 [confidence interval, 1.1-6.6]; p = .04). CONCLUSIONS: An intra-abdominal pressure of > or =16 mm Hg seems to be responsible for false negatives to passive leg raising. Hence, the intra-abdominal pressure should be measured in critically ill ventilated patients, especially before performing passive leg raising.
- BACKGROUND: In an experimental model we investigated the effects of a gradual increase in intra-abdominal pressure (IAP) on the central circulation. METHODS: Seven pigs were anaesthetized, mechanically ventilated and instrumented. IAP was gradually increased by 5 mm Hg up to 30 mm Hg by abdominal banding in normovolaemic animals, and then they were made hypovolaemic after blood withdrawal. Right atrial pressure (RAP) and left ventricular end-diastolic pressure (LVEDP) at each step and aortic, femoral and inferior vena cava blood flows were measured. Left ventricular end-diastolic area (LVEDA) was determined using epicardial echocardiography. RESULTS: Cardiac output maintained at mild IAP was reduced to 76 (24)% of the initial value at 30 mm Hg IAP [mean (sd)] in normovolaemic animals, and 72 (22)% (P<0.001) in hypovolaemic animals. In normovolaemic animals the LVEDA and LVEDP were significantly increased at an IAP of 10 and 15 mm Hg by 26 (24)% and 38 (23)%, respectively. At these IAP values, the difference between the RAP and IAP was positive. When this gradient became negative, that is beyond 15 mm Hg in normovolaemia and for all IAP values in hypovolaemic animals, the LVEDA declined, reaching 78 (16)% and 62 (22)% (P<0.05) of the initial values in normovolaemic and hypovolaemic groups at the highest IAP value. CONCLUSIONS: These results showed that a gradual increase in IAP led to a redistribution of abdominal blood volume towards the thoracic compartment, at IAP lower than 15 mm Hg in normovolaemia, and at its expense at higher values of IAP. In hypovolaemia there was no thoracic compartment gain. Whereas the absolute or transmural RAPs were not informative of the direction of this blood shift, an RAP greater than IAP was associated with an intrathoracic compartment gain.
- Abstract BACKGROUND:Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) have traditionally been treated surgically through emergent laparotomy. Intensivist-performed bedside drainage of free intra-peritoneal fluid or blood [percutaneous catheter decompression (PCD)] has been advocated as a less-invasive alternative to open abdominal decompression (OAD) METHODS:A single-center disease and severity of illness matched case-control comparison of 62 IAH / ACS patients treated using PCD versus traditional OAD was performed. The relative efficacy of each treatment in reducing elevated intra-abdominal pressure (IAP) and improving organ dysfunction was assessed. Physiologic and demographic predictors of successful PCD therapy were determined. RESULTS:PCD and OAD were both effective in significantly decreasing IAP and peak inspiratory pressure as well as increasing abdominal perfusion pressure. PCD potentially avoided the need for subsequent OAD in 25 of 31 patients treated (81%). Successful PCD therapy was associated with fluid drainage of greater than 1000 mL or a decrease in IAP of greater than 9 mmHg in the first four hours post-decompression. CONCLUSIONS:Intensivist-performed PCD is an effective and less-invasive technique for treating patients with IAH / ACS where free intraperitoneal fluid or blood are present by bedside ultrasound. Failure to drain at least 1000 mL of fluid and/or decrease IAP by at least 9 mmHg in the first four hours post-decompression is associated with PCD failure and should prompt urgent OAD.
- Abstract BACKGROUND:Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) have traditionally been treated surgically through emergent laparotomy. Intensivist-performed bedside drainage of free intra-peritoneal fluid or blood [percutaneous catheter decompression (PCD)] has been advocated as a less-invasive alternative to open abdominal decompression (OAD) METHODS:A single-center disease and severity of illness matched case-control comparison of 62 IAH / ACS patients treated using PCD versus traditional OAD was performed. The relative efficacy of each treatment in reducing elevated intra-abdominal pressure (IAP) and improving organ dysfunction was assessed. Physiologic and demographic predictors of successful PCD therapy were determined. RESULTS:PCD and OAD were both effective in significantly decreasing IAP and peak inspiratory pressure as well as increasing abdominal perfusion pressure. PCD potentially avoided the need for subsequent OAD in 25 of 31 patients treated (81%). Successful PCD therapy was associated with fluid drainage of greater than 1000 mL or a decrease in IAP of greater than 9 mmHg in the first four hours post-decompression. CONCLUSIONS:Intensivist-performed PCD is an effective and less-invasive technique for treating patients with IAH / ACS where free intraperitoneal fluid or blood are present by bedside ultrasound. Failure to drain at least 1000 mL of fluid and/or decrease IAP by at least 9 mmHg in the first four hours post-decompression is associated with PCD failure and should prompt urgent OAD.
- Values 24 after DL in 29 trauma patients with primary ACS