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      • Record: found
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      Extended resuscitative endovascular balloon occlusion of the aorta (REBOA)-induced type 2 myocardial ischemia: a time-dependent penalty

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          Abstract

          Background

          Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) increases cardiac-afterload and is used for patients in hemorrhagic shock. The cardiac tolerance of prolonged afterload augmentation in this context is unknown. The aim of this study is to quantify cardiac injury, if any, following 2, 3 and 4 hours of REBOA.

          Methods

          Anesthetized swine (70–90 kg) underwent a 40% controlled hemorrhage, followed by supraceliac resuscitative endovascular balloon occlusion of the aorta (REBOA) for 2 (n=5), 3 (n=5), and 4 hours (n=5). High-fidelity arterial wave form data were collected, and signal processing techniques were used to extract key inflection points. The adjusted augmentation index (AIx@75; augmentation pressure/pulse pressure, normalized for heart rate) was derived for use as a measure of aortic compliance (higher ratio = less compliance). Endpoints consisted of electrocardiographic, biochemical, and histologic markers of myocardial injury/ischemia. Regression modeling was used to assess the trend against time.

          Results

          All animals tolerated instrumentation, hemorrhage, and REBOA. The mean (±SD) systolic blood pressure (mm Hg) increased from 65±11 to 212±39 (p<0.001) during REBOA. The AIx@75 was significantly higher during REBOA than baseline, hemorrhage, and resuscitation phases (p<0.05). A time-dependent rise in troponin (R 2=0.95; p<0.001) and T-wave deflection (R 2=0.64; p<0.001) was observed. The maximum mean troponin (ng/mL) occurred at 4 hours (14.6±15.4) and maximum T-wave deflection (mm) at 65 minutes (3.0±1.8). All animals demonstrated histologic evidence of acute injury with increasing degrees of cellular myocardial injury.

          Discussion

          Prolonged REBOA may result in type 2 myocardial ischemia, which is time-dependent. This has important implications for patients where prolonged REBOA may be considered beneficial, and strategies to mitigate this effect require further investigation.

          Level of evidence

          II.

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          Most cited references30

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          The influence of heart rate on augmentation index and central arterial pressure in humans.

          I Wilkinson, H MacCallum, L. Flint … (2000)
          Arterial stiffness is an important determinant of cardiovascular risk. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. The aim of the present study was to assess the effect of heart rate on AIx. We elected to use cardiac pacing rather than chronotropic drugs to minimize confounding effects on the systemic circulation and myocardial contractility. Twenty-two subjects (13 male) with a mean age of 63 years and permanent cardiac pacemakers in situ were studied. Pulse wave analysis was used to determine central arterial pressure waveforms, non-invasively, during incremental pacing (from 60 to 110 beats min-1), from which AIx and central blood pressure were calculated. Peripheral blood pressure was recorded non-invasively from the brachial artery. There was a significant, inverse, linear relationship between AIx and heart rate (r = -0.76; P < 0.001). For a 10 beats min-1 increment, AIx fell by around 4 %. Ejection duration and heart rate were also inversely related (r = -0. 51; P < 0.001). Peripheral systolic, diastolic and mean arterial pressure increased significantly during incremental pacing. Although central diastolic pressure increased significantly with pacing, central systolic pressure did not. There was a significant increase in the ratio of peripheral to central pulse pressure (P < 0.001), which was accounted for by the observed change in central pressure augmentation. These results demonstrate an inverse, linear relationship between AIx and heart rate. This is likely to be due to alterations in the timing of the reflected pressure wave, produced by changes in the absolute duration of systole. Consideration of wave reflection and aortic pressure augmentation may explain the lack of rise in central systolic pressure during incremental pacing despite an increase in peripheral pressure.
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            Aortic stiffness is an independent predictor of fatal stroke in essential hypertension.

            Stephane Laurent, Sandrine Katsahian, Céline Fassot … (2003)
            Pulse pressure is a stronger predictor of cardiovascular events than systolic or diastolic blood pressure in large cohorts of French and North American patients. However, its influence on stroke is controversial. Large-artery stiffness is the main determinant of pulse pressure. The influence of arterial stiffness on the occurrence of stroke has never been demonstrated. Our aim was to establish the relationship between aortic stiffness and stroke death in hypertensive patients. We included, in a longitudinal study, 1715 essential hypertensive patients who had a measurement of arterial stiffness at entry (ie, between 1980 and 2001) and no overt cardiovascular disease or symptoms. Mean follow-up was 7.9 years. At entry, aortic stiffness was assessed from the carotid-femoral pulse wave velocity. A Cox proportional hazard regression model was used to estimate the relative risk (RR) of stroke and coronary deaths. Mean+/-SD age at entry was 51+/-13 years. Twenty-five fatal strokes and 35 fatal coronary events occurred. Pulse wave velocity significantly predicted the occurrence of stroke death in the whole population. There was a RR increase of 1.72 (95% CI, 1.48 to 1.96; P<0.0001) for each SD increase in pulse wave velocity (4 m/s). The predictive value of pulse wave velocity remained significant (RR=1.39 [95% CI, 1.08 to 1.72]; P=0.02) after full adjustment for classic cardiovascular risk factors, including age, cholesterol, diabetes, smoking, mean blood pressure, and pulse pressure. In this population, pulse pressure significantly predicted stroke in univariate analysis, with a RR increase of 1.33 (95% CI, 1.16 to 1.51) for each 10 mm Hg of pulse pressure (P<0.0001) but not after adjustment for age (RR=1.19 [95% CI, 0.96 to 1.47]; P=0.10). This study provides the first evidence, in a longitudinal study, that aortic stiffness is an independent predictor of fatal stroke in patients with essential hypertension.
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              Regional wave travel and reflections along the human aorta: a study with six simultaneous micromanometric pressures.

              R D Latham, N Westerhof, P Sipkema … (1985)
              The human aorta and its terminal branches were investigated in normal subjects during elective cardiac catheterization to evaluate regional wave travel and arterial wave reflections. A specially designed catheter with six micromanometers equally spaced at 10 cm intervals was positioned with the tip sensor in the distal external iliac artery and the proximal sensor in the aortic arch. Simultaneous pressures were obtained and analyzed for foot-to-foot wave velocity, and Fourier analysis was used to derive apparent phase velocity. These quantities were assessed during control (n = 9), during Valsalva (n = 8) and Müller (n = 4) maneuvers, and during femoral artery occlusion by bilateral manual compression (n = 8). During control, regional cross-sectional areas, determined from aortography, and regional foot-to-foot pulse wave velocities were used to calculate the local reflection coefficient in the proximal descending aorta (gamma = 0.05), at the junction of the renal arteries (gamma = 0.43), and at the terminal aortic bifurcation (gamma = 0.13). To test the hypothesis that significant reflections originate in the aorta, at the level of the renal arteries, aortograms were used to design a latex tube model with geometric properties similar to the descending aorta. Velocities and reflection characteristics in the model and in vivo were compared. Inspection of thoracic aortic pressures under control conditions revealed a reflected wave originating from the region of the aorta at the level of the renal arterial branches while abdominal pressures exhibited reflection from a site peripheral to the terminal aortic bifurcation. In the low frequency range, apparent phase velocity was found to be higher proximal to the renal arteries as compared with at the distal sites. In addition, the minimum value occurred at a higher frequency in the lower thoracic aorta than at more distal sites. The effects of reflection on apparent wave velocity in the tube model were consistent with data obtained in vivo. The Valsalva maneuver diminished the reflection from the aortic region of the renal arteries, thus allowing the distal reflected wave to become more evident on the thoracic pressure waveforms. Bilateral femoral artery occlusion usually enhanced the distal reflection and the Müller maneuver usually resulted in small increases in reflections. In conclusion, the geometric and elastic nonuniformity of the aorta results in two major sites of arterial wave reflection that influence the aortic pressure waveforms in man.(ABSTRACT TRUNCATED AT 400 WORDS)
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                Author and article information

                Journal
                Journal ID (nlm-ta): Trauma Surg Acute Care Open
                Journal ID (iso-abbrev): Trauma Surg Acute Care Open
                Journal ID (hwp): tsaco
                Journal ID (publisher-id): tsaco
                Title: Trauma Surgery & Acute Care Open
                Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                ISSN (Electronic): 2397-5776
                Publication date Collection: 2019
                Publication date (Electronic): 31 January 2019
                Volume: 4
                Issue: 1
                Electronic Location Identifier: e000194
                Affiliations
                [1 ]R Adams Cowley Shock Trauma Center , Baltimore, Maryland, USA
                [2 ]Shock, Trauma, and Anesthesiology Research Center , Baltimore, Maryland, USA
                [3 ]departmentDivision of Cardiovascular Medicine , University of Maryland School of Medicine , Baltimore, Maryland, USA
                Author notes
                [Correspondence to ] Dr Jonathan J Morrison; jonathan.morrison@ 123456umm.edu
                Author information
                http://orcid.org/0000-0001-7462-8456
                Article
                Publisher ID: tsaco-2018-000194
                DOI: 10.1136/tsaco-2018-000194
                PMC ID: 6361364
                PubMed ID: 30815536
                SO-VID: 5d23569b-3b97-401d-a322-8ea7a7710f1f
                Copyright © © Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
                License:

                This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

                History
                Date received : 04 June 2018
                Date revision received : 21 November 2018
                Date accepted : 27 December 2018
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100000005, U.S. Department of Defense;
                Award ID: W81XWH-16-1-0116
                Categories
                Subject: Original Article
                Subject: 1506
                Custom metadata
                special-feature unlocked

                Keywords: aortic occlusion,resuscitative endovascular balloon occlusion of the aorta,reboa,hemorrhage,cardiac,cardiac injury,ischemia,arterial waveform
                Data availability:
                Keywords: aortic occlusion, resuscitative endovascular balloon occlusion of the aorta, reboa, hemorrhage, cardiac, cardiac injury, ischemia, arterial waveform

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