A New Approach to Barrier Verification

Objectives/Scope Verification and testing of a wellbore barrier, in older assets has proven to be challenging. Even more so when the well has structural issues, indemnities or weak spots in the barrier envelope, that limits the possibility to get a positive pressure verification of the barrier with an applied surface pressure. The paper will air on the operational use of this novel test method and the tools used, to allow an in well verification of any type of barrier to secure the well for a repair or a upcoming P/A operation. A pilot job case history will be included to illustrate use of the principles. Methods, Procedures, Process Find a suitable location with necessary support and strength in the well. If installing a mechanical barrier by means of a bridge plug as the primary barrier, we will monitor the installation forces in the anchoring and sealing sequence. This individual signature will be verified towards a nominal base line signature towards a library of thousands of collected installation profiles. Any abnormality can trigger a release and possible relocating of the barrier. A second verification barrier will then be installed above the primary barrier. When both installation signatures are accounted for, we can pressure test the installed barriers. This is done with a pressure inflow tool, where we introduce a calculated predetermined pressure drop between the installed primary barrier and the verification barrier. By monitoring this pressure alteration vs. the pressure above the verification barrier, we can determine if we have a verified barrier. Results, Observations, Conclusions We now have the Primary Barrier verified in the direction of flow (negative pressure test). And verification barrier as the secondary barrier (verified with a positive pressure test). If a dual barrier is requested, you can leave the verification barrier as secondary barrier. Novel/Additional Information Pressure manipulation is done with existing and proven technology and is re-usable after re-setting at surface. By monitoring this pressure alteration, we can verify the installed primary and verification barrier in one run. This without any time-consuming pressure manipulating from surface.

Heart Rate Variability Analysis During Lower Body Negative Pressure Test Induced Central Hypovolemia

In clinical patient monitoring scenarios, the detection of hemorrhage is still a major problem. Traditional vital signs like heart rate and blood pressure are insensitive to blood loss due to compensatory mechanisms in the body that can sustain these parameters until shortly before cardiovascular collapse. These compensatory mechanisms during blood loss are primarily driven by the autonomic nervous system. Heart rate variability analysis is a viable tool in the quantitative analysis of the autonomic nervous system and shows promising results in the context of hypovolemia detection. In order to investigate if HRV parameters suitably reflect a mild to moderate blood volume reduction, we conducted a lower body negative pressure test study with 30 volunteering participants thereby simulating progressive central hypovolemia. Here, HRV parameters from the time domain (mean HR, SDNN, RMSSD, rSDRM, pNN50), the frequency domain (VLF, LF, HF, LF/HF), non-linear HRV parameters (SD1, SD2, SD1/SD2, SampEn, ApEn) and the respiratory rate (RR) were collected. The changes of the evaluated parameters as a consequence of the reduced blood volume were statistically evaluated. A statistically significant deviation from their baseline values could be found for RMSSD, rSDRM, pNN50, HF, LF/HF, SD1 and SD1/SD2 at a chamber pressures starting at −30 mmHg. Therefore, we support the proposition that heart rate variability analysis can help in detecting otherwise occult hypovolemia.

Orthostatic intolerance during a 13-day bed rest does not result from increased leg compliance

Increased leg compliance (LC) has been proposed as a mechanism for orthostatic intolerance after spaceflight or bed rest. Using venous occlusion plethysmography with mercury-in-Silastic strain gauge, we evaluated LC before, during, and after a 13-day head-down (-6 degrees) bed rest in 10 men. LC was measured by the relationship between the increased calf areas (in cm2) at thigh cuff occlusions of 20, 30, 50, 70, and 80 mmHg. Orthostatic tolerance was evaluated by a presyncopal-limited lower body negative pressure test (PSL-LBNP) before and after bed rest. The 10 subjects were divided into TOL (n = 5) and INT (n = 5) groups for which the orthostatic tolerance was similar and lower after bed rest, respectively. For TOL (INT) before bed rest, calf area increases were 2.2 +/- 0.5 (SE) (1.3 +/- 0.4), 3.5 +/- 0.7 (2.3 +/- 0.5), 5.0 +/- 0.9 (3.5 +/- 0.6), 5.6 +/- 0.9 (4.4 +/- 0.6), and 6.4 +/- 1.1 (4.7 +/- 0.6) cm2 for thigh occlusion pressures of 20, 30, 50, 70, and 80 mmHg, respectively. Neither for INT nor for TOL were these results significantly changed by bed rest. These results suggest that other mechanisms than increased LC have to be taken into account to explain the decreased orthostatic tolerance induced by this 13-day bed rest.