Edward P. Sharpey-Schafer was right: evidence for systemic vasodilatation as a mechanism of hypotension in cough syncope | EP Europace

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Sharpey-Schafer was right: evidence for systemic vasodilatation as a mechanism of hypotension in cough syncope <i class='icon-availability_free' title='Free' ></i> </h1> </div> <div class="wi-authors at-ArticleAuthors"> <div class="al-authors-list"> <span class="al-author-name-more js-flyout-wrap"> <button type="button" class="linked-name js-linked-name-trigger btn-as-link">C. T. Paul Krediet</button><span class='delimiter'>, </span> <span class="al-author-info-wrap arrow-up"> <div class="info-card-author authorInfo_OUP_ArticleTop_Info_Widget"> <div class="name-role-wrap"> <div class="info-card-name"> C. T. Paul Krediet <span class="info-card-footnote"><span class="xrefLink" id="jumplink-cor1"></span><a href="javascript:;" reveal-id="cor1" data-open="cor1" class="link link-ref link-reveal xref-default">*</a></span> </div> </div> <div class="info-card-affilitation"> <div class="aff"><div class="addr-line">Department of Internal Medicine</div> , <div class="institution">Academic Medical Center at the University of Amsterdam</div> , <div class="addr-line">Meibergdreef 9, F4-222, 1105 AZ, Amsterdam</div> , <div class="country">The Netherlands</div></div> </div> <div class="info-author-correspondence"> <div content-id="cor1"><span class="label title-label">*</span> Corresponding author. Tel: +31 20 5669111 ; fax: <div class="fax">+31 20 6919658</div> . <em>E-mail address</em> : <a href="mailto:c.t.krediet@amc.uva.nl" target="_blank">c.t.krediet@amc.uva.nl</a></div> </div> <div class="info-card-search-label"> Search for other works by this author on: </div> <div class="info-card-search info-card-search-internal"> <a href="/europace/search-results?f_Authors=C.+T.+Paul+Krediet" rel="nofollow">Oxford Academic</a> </div> <div class="info-card-search info-card-search-pubmed"> <a href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Krediet C">PubMed</a> </div> <div class="info-card-search info-card-search-google"> <a href="http://scholar.google.com/scholar?q=author:%22Krediet C. T. Paul%22">Google Scholar</a> </div> </div> </span> </span> <span class="al-author-name-more js-flyout-wrap"> <button type="button" class="linked-name js-linked-name-trigger btn-as-link">Wouter Wieling</button><span class='delimiter'></span> <span class="al-author-info-wrap arrow-up"> <div class="info-card-author authorInfo_OUP_ArticleTop_Info_Widget"> <div class="name-role-wrap"> <div class="info-card-name"> Wouter Wieling </div> </div> <div class="info-card-affilitation"> <div class="aff"><div class="addr-line">Department of Internal Medicine</div> , <div class="institution">Academic Medical Center at the University of Amsterdam</div> , <div class="addr-line">Meibergdreef 9, F4-222, 1105 AZ, Amsterdam</div> , <div class="country">The Netherlands</div></div> </div> <div class="info-card-search-label"> Search for other works by this author on: </div> <div class="info-card-search info-card-search-internal"> <a href="/europace/search-results?f_Authors=Wouter+Wieling" rel="nofollow">Oxford Academic</a> </div> <div class="info-card-search info-card-search-pubmed"> <a href="http://www.ncbi.nlm.nih.gov/pubmed?cmd=search&term=Wieling W">PubMed</a> </div> <div class="info-card-search info-card-search-google"> <a href="http://scholar.google.com/scholar?q=author:%22Wieling Wouter%22">Google Scholar</a> </div> </div> </span> </span> </div> </div> <div class="pub-history-wrap clearfix js-history-dropdown-wrap"> <div class="pub-history-row clearfix"> <div class="ww-citation-primary"><em>EP Europace</em>, Volume 10, Issue 4, April 2008, Pages 486–488, <a href='https://doi.org/10.1093/europace/eun022'>https://doi.org/10.1093/europace/eun022</a></div> </div> <div class="pub-history-row clearfix"> <div class="ww-citation-date-wrap"> <div class="citation-label">Published:</div> <div class="citation-date">29 February 2008</div> </div> <a href="javascript:;" class="history-label js-history-dropdown-trigger st-article-history at-ArticleHistory"> <span>Article history</span><i class="icon-general-arrow-filled-down arrow-icon"></i> </a> </div> <div class="ww-history js-history-entries-wrap at-history-entries-wrap"> <div class="history-entry at-history-entry"> <div class="wi-state">Received:</div> <div class="wi-date">27 June 2007</div> </div> <div class="history-entry at-history-entry"> <div class="wi-state">Accepted:</div> <div class="wi-date">12 January 2008</div> </div> <div class="history-entry at-history-entry"> <div class="wi-state">Published:</div> <div class="wi-date">29 February 2008</div> </div> </div> </div> </div> </div> <script> $(document).ready(function () { $('.article-top-widget').on('click', '.ati-toggle-trigger', function () { $(this).find('.icon-general-add, .icon-minus').toggleClass('icon-minus icon-general-add'); 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data-widgetname="ArticleFulltext"> <h2 scrollto-destination=39961475 id="39961475" class="abstract-title js-splitscreen-abstract-title" >Abstract</h2> <section class="abstract"><p class="chapter-para">Cough syncope typically occurs in middle aged and senior, muscularly built males with a history of chronic obstructive lung disease. Originally, cough syncope was thought to be a form of epilepsy and only in the 1940s it was recognized to be of syncopal nature. The circulatory pathophysiology is, however, still not fully understood. We present data on two cough syncope patients in whom we documented the beat-to-beat changes in cardiac output and total peripheral resistance during cough syncope using pulse wave analysis. Our results give support to Edward P. Sharpey-Schafer's hypothesis that a decrease of total peripheral resistance plays a pivotal role in the pathophysiology of cough syncope. Systematic studies are needed to confirm this mechanism in larger series of patients.</p></section> <div class="article-metadata-panel clearfix at-ArticleMetadata"></div> <div class="kwd-group"><a class="kwd-part kwd-main" href="javascript:;" data-keyword=""Situational syncope"">Situational syncope</a>, <a class="kwd-part kwd-main" href="javascript:;" data-keyword=""Cardiac output"">Cardiac output</a>, <a class="kwd-part kwd-main" href="javascript:;" data-keyword=""Total peripheral resistance"">Total peripheral resistance</a>, <a class="kwd-part kwd-main" href="javascript:;" data-keyword="Sneezing">Sneezing</a>, <a class="kwd-part kwd-main" href="javascript:;" data-keyword="Modelflow">Modelflow</a>, <a class="kwd-part kwd-main" href="javascript:;" data-keyword="Smoking">Smoking</a>, <a class="kwd-part kwd-main" href="javascript:;" data-keyword="COPD">COPD</a></div> <h2 scrollto-destination=39961477 id="39961477" class="section-title js-splitscreen-section-title" data-legacy-id=s1>Introduction</h2> <p class="chapter-para"> Cough syncope typically occurs in middle aged and senior, muscularly built males with a history of chronic obstructive lung disease. <sup><span class="xrefLink" id="jumplink-EUN022C1"></span><a href="javascript:;" reveal-id="EUN022C1" data-open="EUN022C1" class="link link-ref link-reveal xref-bibr">1</a> , <span class="xrefLink" id="jumplink-EUN022C2"></span><a href="javascript:;" reveal-id="EUN022C2" data-open="EUN022C2" class="link link-ref link-reveal xref-bibr">2</a></sup> The syndrome was first described by J.-M. Charcot (1825–1893) in 1879. <sup><span class="xrefLink" id="jumplink-EUN022C3"></span><a href="javascript:;" reveal-id="EUN022C3" data-open="EUN022C3" class="link link-ref link-reveal xref-bibr">3</a></sup> Originally, cough syncope was thought to be a form of epilepsy, <sup><span class="xrefLink" id="jumplink-EUN022C3"></span><a href="javascript:;" reveal-id="EUN022C3" data-open="EUN022C3" class="link link-ref link-reveal xref-bibr">3</a></sup> and only in 1940s, it was recognized to be of syncopal nature. <sup><span class="xrefLink" id="jumplink-EUN022C4"></span><a href="javascript:;" reveal-id="EUN022C4" data-open="EUN022C4" class="link link-ref link-reveal xref-bibr">4</a> , <span class="xrefLink" id="jumplink-EUN022C5"></span><a href="javascript:;" reveal-id="EUN022C5" data-open="EUN022C5" class="link link-ref link-reveal xref-bibr">5</a></sup> Typically, syncope occurs immediately after coughing, but rarely it has also been reported interrupting a cough. <sup><span class="xrefLink" id="jumplink-EUN022C2"></span><a href="javascript:;" reveal-id="EUN022C2" data-open="EUN022C2" class="link link-ref link-reveal xref-bibr">2</a> , <span class="xrefLink" id="jumplink-EUN022C6"></span><a href="javascript:;" reveal-id="EUN022C6" data-open="EUN022C6" class="link link-ref link-reveal xref-bibr">6</a></sup> Cough syncope usually occurs while sitting or standing, but may also occur supine. <sup><span class="xrefLink" id="jumplink-EUN022C7"></span><a href="javascript:;" reveal-id="EUN022C7" data-open="EUN022C7" class="link link-ref link-reveal xref-bibr">7</a></sup> Consciousness rapidly recovers (i.e. within seconds), typically with few vasomotor or other sequelae. <sup><span class="xrefLink" id="jumplink-EUN022C7"></span><a href="javascript:;" reveal-id="EUN022C7" data-open="EUN022C7" class="link link-ref link-reveal xref-bibr">7</a></sup> The diagnosis of cough syncope may be confirmed by having the patient cough while sitting up-right, and continuously measuring blood pressure and heart rate. This may also provide an opportunity to show the patient that avoiding violent coughing may prevent syncope. <sup><span class="xrefLink" id="jumplink-EUN022C2"></span><a href="javascript:;" reveal-id="EUN022C2" data-open="EUN022C2" class="link link-ref link-reveal xref-bibr">2</a></sup></p><p class="chapter-para"> Three main mechanisms have been postulated to be involved in cough syncope. First, the increased intra-thoracic pressure during a cough is transmitted to the cerebrospinal fluid, <sup><span class="xrefLink" id="jumplink-EUN022C7"></span><a href="javascript:;" reveal-id="EUN022C7" data-open="EUN022C7" class="link link-ref link-reveal xref-bibr">7</a></sup> causing an acute pressure increase in the skull, compromising cerebral perfusion. <sup><span class="xrefLink" id="jumplink-EUN022C6"></span><a href="javascript:;" reveal-id="EUN022C6" data-open="EUN022C6" class="link link-ref link-reveal xref-bibr">6</a> , <span class="xrefLink" id="jumplink-EUN022C7"></span><a href="javascript:;" reveal-id="EUN022C7" data-open="EUN022C7" class="link link-ref link-reveal xref-bibr">7</a></sup> In addition, the combination of increased venous pressure in the skull (by the increased intra-thoracic pressure <sup><span class="xrefLink" id="jumplink-EUN022C8"></span><a href="javascript:;" reveal-id="EUN022C8" data-open="EUN022C8" class="link link-ref link-reveal xref-bibr">8</a></sup> ) and the lowered arterial pressure results in perfusion stand-still or even back-flow in the brain. <sup><span class="xrefLink" id="jumplink-EUN022C6"></span><a href="javascript:;" reveal-id="EUN022C6" data-open="EUN022C6" class="link link-ref link-reveal xref-bibr">6</a></sup> Secondly, ‘cough concussion’ has been suggested as a potential mechanism which holds that during coughing the combination of acute increases of arterial, venous, and cerebrospinal fluid pressures in the skull, directly compromise cerebral functions. <sup><span class="xrefLink" id="jumplink-EUN022C9"></span><a href="javascript:;" reveal-id="EUN022C9" data-open="EUN022C9" class="link link-ref link-reveal xref-bibr">9</a></sup> The importance of ‘cough concussion’ is unclear. </p><p class="chapter-para"> Thirdly, muscularly built persons with obstructive lung disease are capable of building up the high intra-thoracic pressures that trigger cough syncope (300–450 mmHg compared with <100 mmHg in healthy young subjects <sup><span class="xrefLink" id="jumplink-EUN022C8"></span><a href="javascript:;" reveal-id="EUN022C8" data-open="EUN022C8" class="link link-ref link-reveal xref-bibr">8</a> , <span class="xrefLink" id="jumplink-EUN022C10"></span><a href="javascript:;" reveal-id="EUN022C10" data-open="EUN022C10" class="link link-ref link-reveal xref-bibr">10</a> , <span class="xrefLink" id="jumplink-EUN022C11"></span><a href="javascript:;" reveal-id="EUN022C11" data-open="EUN022C11" class="link link-ref link-reveal xref-bibr">11</a></sup> ). These abrupt very high intra-thoracic pressures diminish venous return and cardiac filling and thereby cardiac output (CO). <sup><span class="xrefLink" id="jumplink-EUN022C2"></span><a href="javascript:;" reveal-id="EUN022C2" data-open="EUN022C2" class="link link-ref link-reveal xref-bibr">2</a></sup> On the arterial side, the abruptly increased intra-thoracic pressure is transferred to the systemic circulation, causing arterial baroreflex-mediated vasodilatation. <sup><span class="xrefLink" id="jumplink-EUN022C2"></span><a href="javascript:;" reveal-id="EUN022C2" data-open="EUN022C2" class="link link-ref link-reveal xref-bibr">2</a> , <span class="xrefLink" id="jumplink-EUN022C8"></span><a href="javascript:;" reveal-id="EUN022C8" data-open="EUN022C8" class="link link-ref link-reveal xref-bibr">8</a></sup> In 1950s, E.P. Sharpey-Schafer (1908–1963) <sup><span class="xrefLink" id="jumplink-EUN022C12"></span><a href="javascript:;" reveal-id="EUN022C12" data-open="EUN022C12" class="link link-ref link-reveal xref-bibr">12</a></sup> documented a decreased fore-arm vascular resistance after coughing in a series of 27 cough syncope patients by venous occlusion plethysmography. <sup><span class="xrefLink" id="jumplink-EUN022C8"></span><a href="javascript:;" reveal-id="EUN022C8" data-open="EUN022C8" class="link link-ref link-reveal xref-bibr">8</a></sup> (He also demonstrated that this decrease occurs only during a bout of coughing—i.e. a repetitive increase of intra-thoracic pressure—in contrast to what happens during a Valsalva's manoeuvre when there is a baroreflex-mediated increase in resistance during a prolonged and steady increased intra-thoracic pressure.) Whether these local changes would have a systemic significance remained to be elucidated. </p><p class="chapter-para">We present data on two cough syncope patients in whom we documented the beat-to-beat changes in CO and total peripheral resistance during cough syncope using pulse wave analysis. Our results give support to Sharpey-Schafer's hypothesis that a decrease in total peripheral resistance plays a pivotal role in the pathophysiology of cough syncope.</p> <h2 scrollto-destination=39961482 id="39961482" class="section-title js-splitscreen-section-title" data-legacy-id=s2>Report</h2> <p class="chapter-para"> Patient A was an obese 59-year-old male with a history of smoking who had experienced eight episodes of transient loss of consciousness (TLOC) following coughing for 3 years. Physical examination revealed obesity [body mass index (BMI), 30 kg/m <sup>2</sup> ], a symmetrically low standing, hypokinetic diaphragm, and generally decreased respiratory sounds. There was no orthostatic hypotension, and there were also no clinical symptoms or signs of cardiovascular disease. An ECG did not reveal any abnormalities related to TLOC. During cardiovascular reflex assessment with continuous non-invasive blood pressure monitoring (BP, by Finapres, Finapres Medical Systems, Amsterdam, The Netherlands), coughing was followed by a decrease of systemic blood pressure and pre-syncopal complaints ( <em> Figure <span class="xrefLink" id="jumplink-EUN022F1"></span><a href="javascript:;" data-modal-source-id="EUN022F1" class="link xref-fig">1</a></em> , left panel). </p> <a id="39961484" scrollto-destination="39961484"></a> <div data-id="eun022f1" data-content-id="eun022f1" class="fig fig-section js-fig-section" swap-content-for-modal="true"><div class="graphic-wrap"><img class="content-image" src="https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/europace/10/4/10.1093_europace_eun022/2/m_eun02201.jpeg?Expires=1734963390&Signature=IOg0imQeKANf9SZj7SzRGJaLoJGDXKf0N9IP7V12VlBA8Hxcdv5V1Y6YiSEYlwo0BzN0b12r07CCdkaI4rwGAz7Re1So5OE8vZHuVgj9zVy6R9Zt8LELdBcS3SFrQctB0P9Tovh6EHQKbaE8fujOwO7e6OOZFKSSD9YhBuWr1LDTpiwXE5~stg0eV4DeztP364OLUSm06EU7lPCeX59ZGuXJQZ8rbetTL4Ezra6eqiZP8SCGSglwngmpp3EDbUnta6gmmYePXcPab3gtdkzyXMvhNabCXaqWABZsUdH0lIVZCiVUf1Wq14-9rSlpowZX030REnzyQUtol11C9h~jnQ__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA" alt=" Cardiovascular reflex assessment. BP, blood pressure; HR, heart rate; CO, cardiac output (arbitrary units); TPR, total peripheral resistance (arbitrary units). Left panel: patient A ; right panel: patient B . " data-path-from-xml="eun02201.jpeg" /><div class="graphic-bottom"><div class="label fig-label" id="label-39961484">Figure 1</div><div class="caption fig-caption"><p class="chapter-para"> Cardiovascular reflex assessment. BP, blood pressure; HR, heart rate; CO, cardiac output (arbitrary units); TPR, total peripheral resistance (arbitrary units). Left panel: patient <em>A</em> ; right panel: patient <em>B</em> . </p></div><div class="ajax-articleAbstract-exclude-regex fig-orig original-slide figure-button-wrap"><a class="fig-view-orig js-view-large at-figureViewLarge openInAnotherWindow" role="button" aria-describedby="label-39961484" href="/view-large/figure/39961484/eun02201.jpeg" data-path-from-xml="eun02201.jpeg" target="_blank">Open in new tab</a><a class="download-slide" role="button" aria-describedby="label-39961484" data-section="39961484" href="/DownloadFile/DownloadImage.aspx?image=https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/europace/10/4/10.1093_europace_eun022/2/eun02201.jpeg?Expires=1734963390&Signature=nZ8NXisDOF0UCxIzIWJsVOYKUS8YMNd5Joc02IWwpt8n5XeqlPxzw4czkp6UfhTbfkSxCpwkDd8hoB64PC0fTQ4uH5q~Jm71r~2FvoPM7hWagp5gZoVqZauqomoh3WqTzJv3lY3hmNSIS7hnWIluJxHpW8lhFo~rTh7ksFAxzZ5wCZdnpRAl2j1j3wSnb4k-N-yC6ZCR13ouHJcZW8GxUBHaI~F1Y6mU1GffUmCKQXVpL4A1iHYZS3WTysyc48v3ZjQttLvxc-O~0ZFFioCtJ3w02ZqfIFvZD0C8p-6R08mHhDJdVFEdpCfKA0lmJ5-91WuPYHGA45uEEv40M5nHMA__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA&sec=39961484&ar=2398535&xsltPath=~/UI/app/XSLT&imagename=&siteId=5374" data-path-from-xml="eun02201.jpeg">Download slide</a></div></div></div></div><p class="chapter-para"> Patient B was a 58-year-old male with TLOC following bouts of coughing and sneezing. Apart from obesity (BMI, 28 kg/m <sup>2</sup> ), physical examination was unremarkable. An ECG was normal. During cardiovascular reflex assessment, a bout of spontaneous sneezing induced pre-syncopal complaints, associated with a decreased systemic blood pressure ( <em> Figure <span class="xrefLink" id="jumplink-EUN022F1"></span><a href="javascript:;" data-modal-source-id="EUN022F1" class="link xref-fig">1</a></em> , right panel). </p><p class="chapter-para"> We performed a pulse wave analysis by Modelflow of the continuous blood pressure records in patients A and B. Modelflow is a model-based algorithm that computes the aortic flow waveform from the arterial blood pressure pulsation by simulating a non-linear, self-adaptive, three-element Windkessel model of the aortic input impedance. <sup><span class="xrefLink" id="jumplink-EUN022C13"></span><a href="javascript:;" reveal-id="EUN022C13" data-open="EUN022C13" class="link link-ref link-reveal xref-bibr">13</a></sup> Modelflow computes stroke volume (SV) by calculating the time-integral of the flow pulse in systole. Subsequently, cardic output is calculated as SV × HR. This approach provides reliable indexes (i.e. tracks the relative changes) of CO and total peripheral resistance (TPR) on a beat-to-beat basis. <sup><span class="xrefLink" id="jumplink-EUN022C13"></span><a href="javascript:;" reveal-id="EUN022C13" data-open="EUN022C13" class="link link-ref link-reveal xref-bibr">13</a> , <span class="xrefLink" id="jumplink-EUN022C14"></span><a href="javascript:;" reveal-id="EUN022C14" data-open="EUN022C14" class="link link-ref link-reveal xref-bibr">14</a></sup></p><p class="chapter-para">The results of the pulse wave analysis are also shown in the figure. From these results it seems that after coughing CO is unchanged (or even increased), whereas total peripheral resistance is markedly decreased.</p> <h2 scrollto-destination=39961488 id="39961488" class="section-title js-splitscreen-section-title" data-legacy-id=s3>Conclusion</h2> <p class="chapter-para">On the basis of these findings in two patients, we conclude that cough syncope could indeed (in part) be facilitated by a baroreflex-mediated fall in total peripheral resistance. Unfortunately, the clinical setting in which our results were obtained did not allow a baroreflex modulating intervention to investigate further this mechanism. However, our data do demonstrate that the findings of Dr Sharpey-Shafer on fore-arm vasodilatation triggered by a bout of coughing have indeed systemic consequences in cough syncope patients. Systematic studies are needed to confirm this mechanism in larger series of patients and to further test the baroreflex involvement.</p> <h2 scrollto-destination=39961490 id="39961490" class="section-title js-splitscreen-section-title" data-legacy-id=s4>Funding</h2> <p class="chapter-para">CTPK is a recipient of Netherlands Heart Foundation grant 2004/T007; this support is gratefully acknowledged.</p> <h2 scrollto-destination=39961492 id="39961492" class="backreferences-title js-splitscreen-backreferences-title" >References</h2> <div class="ref-list js-splitview-ref-list"><div content-id="EUN022C1" class="js-splitview-ref-item" data-legacy-id="EUN022C1"><div class="refLink-parent"><span class="refLink"><a name="jumplink-EUN022C1" href="javascript:;" aria-label="jumplink-EUN022C1" data-id=""></a></span></div><div class="ref false"><div id="ref-auto-EUN022C1" class="ref-content " data-id="EUN022C1"><span class="label title-label">1</span><div class="citation element-citation"><span 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Edward P. Sharpey-Schafer was right: evidence for systemic vasodilatation as a mechanism of hypotension in cough syncope | EP Europace | Oxford Academic