Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta

Stokland, Olav; Miller, M. M.; Ilebekk, Arnfinn; Kiil, Fredrik

doi:10.1152/ajpheart.1980.238.4.h423

Cited by 49 publications

(46 citation statements)

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“…There were no changes in any of the venous circulation parameters including resistance to venous return. Our data are consistent with the classical studies of Herndon and Sagawa (1) and Stokland et al (19,20). These investigators showed that cardiac output was independent ofafterload up to a mean aortic pressure of 180 mmHg (1).…”

Section: Discussionsupporting

confidence: 93%

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Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs.

Lee

Standaert²,

Lancaster³

et al. 1988

J. Clin. Invest.

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To determine the cardiac and peripheral circulatory responses to changes in afterload with angiotension and vasopressin, we increased mean aortic pressure 25% and 50% above control in splenectomized and ganglion-blocked dogs. We compared these responses to similar mechanical increases in aortic pressure produced by partial balloon occlusion of the descending aorta. With 25% or 50% increases in aortic pressure, angiotensin, vasopressin, and balloon inflation produced no changes in heart rate, right atrial, and mean pulmonary artery pressures. At 25% increase in aortic pressure, cardiac output was maintained with angiotensin and balloon occlusion but decreased with vasopressin. At 50% increase in aortic pressure, cardiac output was maintained with only bailloon occlusion and decreased with both angiotensin and vasopressin. Whenever cardiac output fell, central blood volume did not increase as afterload increased. These changes in preload can be explained by alterations in the venous circulation. Vasopressin did not alter venous compliance or unstressed vascular volume but increased resistance to venous return. Angiotensin also increased resistance to venous return but decreased venous compliance and did not change unstressed vascular volume. Balloon occlusion had no effects on these parameters. We conclude that: (a) angiotensin caused significant venoconstriction resulting in maintenance of cardiac output at 25% but not 50% increase in aortic pressure; (b) vasopressin increased the resistance to venous return without venoconstriction; this resulted in a fall in cardiac output even with a 25% increase in aortic pressure; and (c) the effects of the agents on the venous circulation were independent of the mechanical effects of a pressure increase in the arterial circulation. IntroductionIt has been well established that forward flow, within physiologic limits, in the normal heart is not afterload dependent. Cardiac output is maintained with mechanical increases in mean aortic pressures up to 180 mmHg (1). This information has to be reconciled with recent reports which show that humoral mediated increases in aortic pressure with angiotensin

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Section: Discussionsupporting

confidence: 93%

“…These investigators showed that cardiac output was independent ofafterload up to a mean aortic pressure of 180 mmHg (1). As afterload increases there is a redistribution of cardiac output and left ventricular filling is maintained (19). Left (22).…”

Section: Discussionmentioning

confidence: 99%

Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs.

Lee

Standaert²,

Lancaster³

et al. 1988

J. Clin. Invest.

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“…11 Intra-aortic balloon counterpulsation has been demonstrated to improve cerebral blood flow in both animals 12 and humans, 13 but the complex algorithms required to achieve increases in cerebral blood flow have limited clinical adoption in patients with acute stroke. Complete aortic occlusion of either the descending thoracic aorta or the abdominal aorta above the renal arteries results in a prompt increase in blood volume above the occlusion 14,15 and has been shown to specifically increase cerebral blood volume. 14 Interestingly, the increase in blood flow persisted when the balloons were withdrawn.…”

mentioning

confidence: 99%

Partial Aortic Occlusion for Cerebral Perfusion Augmentation

Shuaib

Bornstein

Diener

et al. 2011

Stroke

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“…Data from animal models and from human research demonstrate that aortic occlusion, which is commonly performed by crossclamping the descending aorta for vascular control during aortic surgery, results in net flow diversion to the cerebral from the lower-extremity circulatory beds, thereby increasing cerebral blood flow. [707][708][709][710][711][712][713][714][715] This evidence generated the development of a catheter-based device with 2 balloons near its distal tip placed in the infrarenal and suprarenal positions in the descending aorta (NeuroFlo device; CoAxia, Maple Grove, MN). After insertion via the femoral artery, the balloons are inflated sequentially up to ≈70% of the diameter of the aortic lumen over a period of 45 minutes to an hour, followed by removal.…”

Section: Mechanical Flow Augmentationmentioning

confidence: 99%

Guidelines for the Early Management of Patients With Acute Ischemic Stroke

Jauch¹,

Saver²,

Adams³

et al. 2013

Stroke

5,338

1,801

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Background and Purpose-The authors present an overview of the current evidence and management recommendations for evaluation and treatment of adults with acute ischemic stroke. The intended audiences are prehospital care providers, physicians, allied health professionals, and hospital administrators responsible for the care of acute ischemic stroke patients within the first 48 hours from stroke onset. These guidelines supersede the prior 2007 guidelines and 2009 updates. Methods-Members of the writing committee were appointed by the American Stroke Association Stroke Council's Scientific Statement Oversight Committee, representing various areas of medical expertise. Strict adherence to the American Heart Association conflict of interest policy was maintained throughout the consensus process. Panel members were assigned topics relevant to their areas of expertise, reviewed the stroke literature with emphasis on publications since the prior guidelines, and drafted recommendations in accordance with the American Heart Association Stroke Council's Level of Evidence grading algorithm. Results-The goal of these guidelines is to limit the morbidity and mortality associated with stroke. The guidelines support the overarching concept of stroke systems of care and detail aspects of stroke care from patient recognition; emergency medical services activation, transport, and triage; through the initial hours in the emergency department and stroke unit. The guideline discusses early stroke evaluation and general medical care, as well as ischemic stroke, specific interventions such as reperfusion strategies, and general physiological optimization for cerebral resuscitation. The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest. Guidelines for the Early Management of PatientsThis statement was approved by the American Heart Association Science Advisory and Coordinating Committee on December 12, 2012. A copy of the document is available at http://my.americanheart.org/statements by selecting either the "By Topic" link or the "By Publication Date" link. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.The Executive Summary is available as an online-only Data Supplement with this article at http://stroke.ahajournals.org/lookup/suppl/ doi:10.1161/STR.0b013e318284056a/-/DC1.The American Heart Association requests that this document be cited as follows: Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk BM, Khatri P, McMullan PW Jr, Qureshi AI, Rosenfield K, Scott PA, Summers DR, Wang DZ, Wintermark M, Yonas H; on behalf of the American Heart Association Stroke Council, Council on Cardio...

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Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta

Cited by 49 publications

References 0 publications

Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs.

Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs.

Partial Aortic Occlusion for Cerebral Perfusion Augmentation

Guidelines for the Early Management of Patients With Acute Ischemic Stroke

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