Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand, But Not a Surrogate for Outcome?
Background Spontaneous blood pressure increase is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). These episodes of spontaneous blood pressure alterations are usually tolerated under the assumption of an endogenous response to maintain cerebral perfusion. The relevance of blood...
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| Veröffentlicht in: | Neurocritical care 2018-10, Vol.29 (2), p.214-224 |
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| creator | Teping, F. Albanna, W. Clusmann, H. Schulze-Steinen, H. Mueller, M. Hoellig, A. Schubert, G. A. |
| description | Background
Spontaneous blood pressure increase is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). These episodes of spontaneous blood pressure alterations are usually tolerated under the assumption of an endogenous response to maintain cerebral perfusion. The relevance of blood pressure variability and its relationship to disease severity and outcome, however, remain obscure.
Methods
A total of 115 consecutive patients with aSAH were included for this retrospective analysis of a continuously collected data pool. Demographics, initial clinical severity of aSAH (HH°, mFS), treatment modality, clinical course, and outcome (development of DCI, cerebral infarction, and GOS after 3 months) were recorded. Hemodynamic information—recorded automatically with a frequency of 1/15 min—was analyzed for spontaneous blood pressure increase (SBI) and endogenous persistent hypertension (EPH) after exclusion of iatrogenic factors and relevant co-medication. Subgroup analysis included stratification for day 0–3, 4–14, and 14–21.
Results
SBI and EPH incidence varied from 17 to 84% depending on detection threshold (15–35 mmHg) and time period under scrutiny. Incidence of blood pressure increase correlated with disease severity upon admission (
p
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| doi_str_mv | 10.1007/s12028-018-0528-6 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2022127510</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2022127510</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-30b1c1e86621a663b7a5835c5253a25d2758b305559087d738cac867ad24155e3</originalsourceid><addsrcrecordid>eNp1kU1P3DAQhi3UCijtD-BSjdQLh6b1x9qOuaAFllIJlUpbzpY3mUBQEgfbQeLeH15vA61UqYfRjDTPvGPPS8gho58YpfpzZJzysqAsh8yF2iH7TEpVUKPYq229YIUyQuyRNzHeU8q10XKX7PHcN0qaffJzPfohuQH9FGHV4aNLrR_AN3DaeV_D94AxTgFh2SQMsF5eHsNygNXYjnc4-D7Hb_q8jegiwhofMbTpCdxQwzn2OX2E0ynBN5_AwXoKwd-6hND4ANdTqrLEyVvyunFdxHfP-YDcXKx-nF0WV9dfvp4tr4pKaJ4KQTesYlgqxZlTSmy0k6WQleRSOC5rrmW5EVRKaWipay3KylWl0q7mi3wWFAfkaNYdg3-YMCbbt7HCrpv_b_M1OcsqjGb0wz_ovZ_CkF9nuWFmoY2hKlNspqrgYwzY2DG0vQtPllG7tcjOFtlskd1aZLcz75-Vp02P9Z-JF08ywGcg5tZwi-Hv6v-r_gIJv5nZ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2919479906</pqid></control><display><type>article</type><title>Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand, But Not a Surrogate for Outcome?</title><source>Springer Nature - Complete Springer Journals</source><source>ProQuest Central</source><creator>Teping, F. ; Albanna, W. ; Clusmann, H. ; Schulze-Steinen, H. ; Mueller, M. ; Hoellig, A. ; Schubert, G. A.</creator><creatorcontrib>Teping, F. ; Albanna, W. ; Clusmann, H. ; Schulze-Steinen, H. ; Mueller, M. ; Hoellig, A. ; Schubert, G. A.</creatorcontrib><description>Background
Spontaneous blood pressure increase is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). These episodes of spontaneous blood pressure alterations are usually tolerated under the assumption of an endogenous response to maintain cerebral perfusion. The relevance of blood pressure variability and its relationship to disease severity and outcome, however, remain obscure.
Methods
A total of 115 consecutive patients with aSAH were included for this retrospective analysis of a continuously collected data pool. Demographics, initial clinical severity of aSAH (HH°, mFS), treatment modality, clinical course, and outcome (development of DCI, cerebral infarction, and GOS after 3 months) were recorded. Hemodynamic information—recorded automatically with a frequency of 1/15 min—was analyzed for spontaneous blood pressure increase (SBI) and endogenous persistent hypertension (EPH) after exclusion of iatrogenic factors and relevant co-medication. Subgroup analysis included stratification for day 0–3, 4–14, and 14–21.
Results
SBI and EPH incidence varied from 17 to 84% depending on detection threshold (15–35 mmHg) and time period under scrutiny. Incidence of blood pressure increase correlated with disease severity upon admission (
p
< 0.05), but the anticipated association with outcome was not observed. SBI and EPH were more likely to occur between day 4 and 14 (
p
< 0.001), but only early occurrence (day 0–3) was associated with higher incidence of DCI (
p
< 0.05). Persistent blood pressure elevation between day 4 and 21 was associated with fewer DCI. However, no influence of spontaneous upregulation on clinical outcome after three months was observed.
Conclusions
Spontaneous hemodynamic upregulation is a frequent phenomenon after aSAH. Our data support the hypothesis that spontaneous blood pressure alterations reflect an endogenous, demand-driven response correlating with disease severity. Early alterations may indicate an aggravated clinical course, while later upregulation in particular—if permitted—does not translate into a higher risk of unfavorable outcome.</description><identifier>ISSN: 1541-6933</identifier><identifier>EISSN: 1556-0961</identifier><identifier>DOI: 10.1007/s12028-018-0528-6</identifier><identifier>PMID: 29619659</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Aneurysms ; Antihypertensives ; Blood pressure ; Clinical outcomes ; Critical Care Medicine ; Datasets ; Documentation ; Hemodynamics ; Hypertension ; Intensive ; Internal Medicine ; Intervention ; Ischemia ; Medicine ; Medicine & Public Health ; Neurology ; Original Article ; Patients ; Stroke ; Tomography ; Ultrasonic imaging</subject><ispartof>Neurocritical care, 2018-10, Vol.29 (2), p.214-224</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society 2018</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society 2018.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-30b1c1e86621a663b7a5835c5253a25d2758b305559087d738cac867ad24155e3</citedby><cites>FETCH-LOGICAL-c372t-30b1c1e86621a663b7a5835c5253a25d2758b305559087d738cac867ad24155e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12028-018-0528-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2919479906?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,776,780,21367,27901,27902,33721,33722,41464,42533,43781,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29619659$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Teping, F.</creatorcontrib><creatorcontrib>Albanna, W.</creatorcontrib><creatorcontrib>Clusmann, H.</creatorcontrib><creatorcontrib>Schulze-Steinen, H.</creatorcontrib><creatorcontrib>Mueller, M.</creatorcontrib><creatorcontrib>Hoellig, A.</creatorcontrib><creatorcontrib>Schubert, G. A.</creatorcontrib><title>Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand, But Not a Surrogate for Outcome?</title><title>Neurocritical care</title><addtitle>Neurocrit Care</addtitle><addtitle>Neurocrit Care</addtitle><description>Background
Spontaneous blood pressure increase is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). These episodes of spontaneous blood pressure alterations are usually tolerated under the assumption of an endogenous response to maintain cerebral perfusion. The relevance of blood pressure variability and its relationship to disease severity and outcome, however, remain obscure.
Methods
A total of 115 consecutive patients with aSAH were included for this retrospective analysis of a continuously collected data pool. Demographics, initial clinical severity of aSAH (HH°, mFS), treatment modality, clinical course, and outcome (development of DCI, cerebral infarction, and GOS after 3 months) were recorded. Hemodynamic information—recorded automatically with a frequency of 1/15 min—was analyzed for spontaneous blood pressure increase (SBI) and endogenous persistent hypertension (EPH) after exclusion of iatrogenic factors and relevant co-medication. Subgroup analysis included stratification for day 0–3, 4–14, and 14–21.
Results
SBI and EPH incidence varied from 17 to 84% depending on detection threshold (15–35 mmHg) and time period under scrutiny. Incidence of blood pressure increase correlated with disease severity upon admission (
p
< 0.05), but the anticipated association with outcome was not observed. SBI and EPH were more likely to occur between day 4 and 14 (
p
< 0.001), but only early occurrence (day 0–3) was associated with higher incidence of DCI (
p
< 0.05). Persistent blood pressure elevation between day 4 and 21 was associated with fewer DCI. However, no influence of spontaneous upregulation on clinical outcome after three months was observed.
Conclusions
Spontaneous hemodynamic upregulation is a frequent phenomenon after aSAH. Our data support the hypothesis that spontaneous blood pressure alterations reflect an endogenous, demand-driven response correlating with disease severity. Early alterations may indicate an aggravated clinical course, while later upregulation in particular—if permitted—does not translate into a higher risk of unfavorable outcome.</description><subject>Aneurysms</subject><subject>Antihypertensives</subject><subject>Blood pressure</subject><subject>Clinical outcomes</subject><subject>Critical Care Medicine</subject><subject>Datasets</subject><subject>Documentation</subject><subject>Hemodynamics</subject><subject>Hypertension</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Intervention</subject><subject>Ischemia</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Original Article</subject><subject>Patients</subject><subject>Stroke</subject><subject>Tomography</subject><subject>Ultrasonic imaging</subject><issn>1541-6933</issn><issn>1556-0961</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp1kU1P3DAQhi3UCijtD-BSjdQLh6b1x9qOuaAFllIJlUpbzpY3mUBQEgfbQeLeH15vA61UqYfRjDTPvGPPS8gho58YpfpzZJzysqAsh8yF2iH7TEpVUKPYq229YIUyQuyRNzHeU8q10XKX7PHcN0qaffJzPfohuQH9FGHV4aNLrR_AN3DaeV_D94AxTgFh2SQMsF5eHsNygNXYjnc4-D7Hb_q8jegiwhofMbTpCdxQwzn2OX2E0ynBN5_AwXoKwd-6hND4ANdTqrLEyVvyunFdxHfP-YDcXKx-nF0WV9dfvp4tr4pKaJ4KQTesYlgqxZlTSmy0k6WQleRSOC5rrmW5EVRKaWipay3KylWl0q7mi3wWFAfkaNYdg3-YMCbbt7HCrpv_b_M1OcsqjGb0wz_ovZ_CkF9nuWFmoY2hKlNspqrgYwzY2DG0vQtPllG7tcjOFtlskd1aZLcz75-Vp02P9Z-JF08ywGcg5tZwi-Hv6v-r_gIJv5nZ</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Teping, F.</creator><creator>Albanna, W.</creator><creator>Clusmann, H.</creator><creator>Schulze-Steinen, H.</creator><creator>Mueller, M.</creator><creator>Hoellig, A.</creator><creator>Schubert, G. A.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20181001</creationdate><title>Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand, But Not a Surrogate for Outcome?</title><author>Teping, F. ; Albanna, W. ; Clusmann, H. ; Schulze-Steinen, H. ; Mueller, M. ; Hoellig, A. ; Schubert, G. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-30b1c1e86621a663b7a5835c5253a25d2758b305559087d738cac867ad24155e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Aneurysms</topic><topic>Antihypertensives</topic><topic>Blood pressure</topic><topic>Clinical outcomes</topic><topic>Critical Care Medicine</topic><topic>Datasets</topic><topic>Documentation</topic><topic>Hemodynamics</topic><topic>Hypertension</topic><topic>Intensive</topic><topic>Internal Medicine</topic><topic>Intervention</topic><topic>Ischemia</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurology</topic><topic>Original Article</topic><topic>Patients</topic><topic>Stroke</topic><topic>Tomography</topic><topic>Ultrasonic imaging</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Teping, F.</creatorcontrib><creatorcontrib>Albanna, W.</creatorcontrib><creatorcontrib>Clusmann, H.</creatorcontrib><creatorcontrib>Schulze-Steinen, H.</creatorcontrib><creatorcontrib>Mueller, M.</creatorcontrib><creatorcontrib>Hoellig, A.</creatorcontrib><creatorcontrib>Schubert, G. A.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Neurocritical care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Teping, F.</au><au>Albanna, W.</au><au>Clusmann, H.</au><au>Schulze-Steinen, H.</au><au>Mueller, M.</au><au>Hoellig, A.</au><au>Schubert, G. A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand, But Not a Surrogate for Outcome?</atitle><jtitle>Neurocritical care</jtitle><stitle>Neurocrit Care</stitle><addtitle>Neurocrit Care</addtitle><date>2018-10-01</date><risdate>2018</risdate><volume>29</volume><issue>2</issue><spage>214</spage><epage>224</epage><pages>214-224</pages><issn>1541-6933</issn><eissn>1556-0961</eissn><abstract>Background
Spontaneous blood pressure increase is frequently observed after aneurysmal subarachnoid hemorrhage (aSAH). These episodes of spontaneous blood pressure alterations are usually tolerated under the assumption of an endogenous response to maintain cerebral perfusion. The relevance of blood pressure variability and its relationship to disease severity and outcome, however, remain obscure.
Methods
A total of 115 consecutive patients with aSAH were included for this retrospective analysis of a continuously collected data pool. Demographics, initial clinical severity of aSAH (HH°, mFS), treatment modality, clinical course, and outcome (development of DCI, cerebral infarction, and GOS after 3 months) were recorded. Hemodynamic information—recorded automatically with a frequency of 1/15 min—was analyzed for spontaneous blood pressure increase (SBI) and endogenous persistent hypertension (EPH) after exclusion of iatrogenic factors and relevant co-medication. Subgroup analysis included stratification for day 0–3, 4–14, and 14–21.
Results
SBI and EPH incidence varied from 17 to 84% depending on detection threshold (15–35 mmHg) and time period under scrutiny. Incidence of blood pressure increase correlated with disease severity upon admission (
p
< 0.05), but the anticipated association with outcome was not observed. SBI and EPH were more likely to occur between day 4 and 14 (
p
< 0.001), but only early occurrence (day 0–3) was associated with higher incidence of DCI (
p
< 0.05). Persistent blood pressure elevation between day 4 and 21 was associated with fewer DCI. However, no influence of spontaneous upregulation on clinical outcome after three months was observed.
Conclusions
Spontaneous hemodynamic upregulation is a frequent phenomenon after aSAH. Our data support the hypothesis that spontaneous blood pressure alterations reflect an endogenous, demand-driven response correlating with disease severity. Early alterations may indicate an aggravated clinical course, while later upregulation in particular—if permitted—does not translate into a higher risk of unfavorable outcome.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29619659</pmid><doi>10.1007/s12028-018-0528-6</doi><tpages>11</tpages></addata></record> |
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| source | Springer Nature - Complete Springer Journals; ProQuest Central |
| subjects | Aneurysms Antihypertensives Blood pressure Clinical outcomes Critical Care Medicine Datasets Documentation Hemodynamics Hypertension Intensive Internal Medicine Intervention Ischemia Medicine Medicine & Public Health Neurology Original Article Patients Stroke Tomography Ultrasonic imaging |
| title | Spontaneous Elevation of Blood Pressure After SAH: An Epiphenomenon of Disease Severity and Demand, But Not a Surrogate for Outcome? |
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