Effect of hypothermia on transthoracic defibrillation in a swine model
Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented. In 39 swine (21.4 ± 1.3(S.E.) kg) hypothermia was induced by surrou...
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| Veröffentlicht in: | Resuscitation 2005-04, Vol.65 (1), p.79-85 |
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| creator | Rhee, Benjamin J Zhang, Yi Boddicker, Kimberly A. Davies, Loyd R. Kerber, Richard E. |
| description | Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented.
In 39 swine (21.4
±
1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30
°C) (
n
=
10), (2) severe H followed by N (
n
=
10), (3) N followed by moderate H (33
°C) (
n
=
10) and (4) moderate H followed by N (
n
=
9). After 30
s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20
J, 30
J, 50
J and 100
J in random order in both N and H conditions.
For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58;
p
<
0.0001), despite the fact that impedance rose from 39
±
3
Ω (N) to 42
±
3
Ω (H) (
p
<
0.001) and current fell from 22
±
8 (N) to 21
±
7
A (H) (
p
<
0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (
p
=
0.0002).
Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation. |
| doi_str_mv | 10.1016/j.resuscitation.2004.10.013 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67571800</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0300957204004344</els_id><sourcerecordid>67571800</sourcerecordid><originalsourceid>FETCH-LOGICAL-c411t-bb1381506f853114e2534e354ca961bffcc56b44b182eed3fd8b0ddc47b835bb3</originalsourceid><addsrcrecordid>eNqNkE1LAzEURYMoWqt_QQKiu6nJZDKZwZVI_QDBja5DPl5oysykJlPFf29qC8WdqyzuebnvHYQuKZlRQuub5SxCWifjRzX6MMxKQqqczAhlB2hCG8EKygU5RBPCCClaLsoTdJrSkhDCeCuO0UnOW1GKdoIe5s6BGXFwePG9CuMCYu8VDgMeoxrSuAhRGW-wBed19F3324n9gBVOX34A3AcL3Rk6cqpLcL57p-j9Yf52_1S8vD4-39-9FKaidCy0pqyhnNSu4YzSCkrOKmC8MqqtqXbOGF7rqtK0KQEsc7bRxFpTCd0wrjWbouvtv6sYPtaQRtn7ZCCvNUBYJ1kLLmiT75yi2y1oYkgpgpOr6HsVvyUlcqNRLuUfjXKjcRNmjXn6Ylez1j3Y_ezOWwaudoBKRnUuuzI-7bm6zly54eZbDrKUTw9R5kIYDFgfs3Zpg__XQj_cTZmF</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67571800</pqid></control><display><type>article</type><title>Effect of hypothermia on transthoracic defibrillation in a swine model</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Rhee, Benjamin J ; Zhang, Yi ; Boddicker, Kimberly A. ; Davies, Loyd R. ; Kerber, Richard E.</creator><creatorcontrib>Rhee, Benjamin J ; Zhang, Yi ; Boddicker, Kimberly A. ; Davies, Loyd R. ; Kerber, Richard E.</creatorcontrib><description>Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented.
In 39 swine (21.4
±
1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30
°C) (
n
=
10), (2) severe H followed by N (
n
=
10), (3) N followed by moderate H (33
°C) (
n
=
10) and (4) moderate H followed by N (
n
=
9). After 30
s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20
J, 30
J, 50
J and 100
J in random order in both N and H conditions.
For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58;
p
<
0.0001), despite the fact that impedance rose from 39
±
3
Ω (N) to 42
±
3
Ω (H) (
p
<
0.001) and current fell from 22
±
8 (N) to 21
±
7
A (H) (
p
<
0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (
p
=
0.0002).
Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.</description><identifier>ISSN: 0300-9572</identifier><identifier>EISSN: 1873-1570</identifier><identifier>DOI: 10.1016/j.resuscitation.2004.10.013</identifier><identifier>PMID: 15797279</identifier><identifier>CODEN: RSUSBS</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Disease Models, Animal ; Electric Countershock ; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care ; Heart Arrest - complications ; Heart Arrest - physiopathology ; Heart Arrest - therapy ; Hemodynamics ; Hypothermia ; Hypothermia, Induced ; Intensive care medicine ; Medical sciences ; Pharmacology. Drug treatments ; Reference Values ; Shock - etiology ; Swine ; Transthoracic defibrillation ; Ventricular fibrillation</subject><ispartof>Resuscitation, 2005-04, Vol.65 (1), p.79-85</ispartof><rights>2004 Elsevier Ireland Ltd</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-bb1381506f853114e2534e354ca961bffcc56b44b182eed3fd8b0ddc47b835bb3</citedby><cites>FETCH-LOGICAL-c411t-bb1381506f853114e2534e354ca961bffcc56b44b182eed3fd8b0ddc47b835bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.resuscitation.2004.10.013$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27928,27929,45999</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16697229$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15797279$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rhee, Benjamin J</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Boddicker, Kimberly A.</creatorcontrib><creatorcontrib>Davies, Loyd R.</creatorcontrib><creatorcontrib>Kerber, Richard E.</creatorcontrib><title>Effect of hypothermia on transthoracic defibrillation in a swine model</title><title>Resuscitation</title><addtitle>Resuscitation</addtitle><description>Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented.
In 39 swine (21.4
±
1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30
°C) (
n
=
10), (2) severe H followed by N (
n
=
10), (3) N followed by moderate H (33
°C) (
n
=
10) and (4) moderate H followed by N (
n
=
9). After 30
s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20
J, 30
J, 50
J and 100
J in random order in both N and H conditions.
For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58;
p
<
0.0001), despite the fact that impedance rose from 39
±
3
Ω (N) to 42
±
3
Ω (H) (
p
<
0.001) and current fell from 22
±
8 (N) to 21
±
7
A (H) (
p
<
0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (
p
=
0.0002).
Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Disease Models, Animal</subject><subject>Electric Countershock</subject><subject>Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care</subject><subject>Heart Arrest - complications</subject><subject>Heart Arrest - physiopathology</subject><subject>Heart Arrest - therapy</subject><subject>Hemodynamics</subject><subject>Hypothermia</subject><subject>Hypothermia, Induced</subject><subject>Intensive care medicine</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Reference Values</subject><subject>Shock - etiology</subject><subject>Swine</subject><subject>Transthoracic defibrillation</subject><subject>Ventricular fibrillation</subject><issn>0300-9572</issn><issn>1873-1570</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1LAzEURYMoWqt_QQKiu6nJZDKZwZVI_QDBja5DPl5oysykJlPFf29qC8WdqyzuebnvHYQuKZlRQuub5SxCWifjRzX6MMxKQqqczAhlB2hCG8EKygU5RBPCCClaLsoTdJrSkhDCeCuO0UnOW1GKdoIe5s6BGXFwePG9CuMCYu8VDgMeoxrSuAhRGW-wBed19F3324n9gBVOX34A3AcL3Rk6cqpLcL57p-j9Yf52_1S8vD4-39-9FKaidCy0pqyhnNSu4YzSCkrOKmC8MqqtqXbOGF7rqtK0KQEsc7bRxFpTCd0wrjWbouvtv6sYPtaQRtn7ZCCvNUBYJ1kLLmiT75yi2y1oYkgpgpOr6HsVvyUlcqNRLuUfjXKjcRNmjXn6Ylez1j3Y_ezOWwaudoBKRnUuuzI-7bm6zly54eZbDrKUTw9R5kIYDFgfs3Zpg__XQj_cTZmF</recordid><startdate>20050401</startdate><enddate>20050401</enddate><creator>Rhee, Benjamin J</creator><creator>Zhang, Yi</creator><creator>Boddicker, Kimberly A.</creator><creator>Davies, Loyd R.</creator><creator>Kerber, Richard E.</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20050401</creationdate><title>Effect of hypothermia on transthoracic defibrillation in a swine model</title><author>Rhee, Benjamin J ; Zhang, Yi ; Boddicker, Kimberly A. ; Davies, Loyd R. ; Kerber, Richard E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-bb1381506f853114e2534e354ca961bffcc56b44b182eed3fd8b0ddc47b835bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Disease Models, Animal</topic><topic>Electric Countershock</topic><topic>Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care</topic><topic>Heart Arrest - complications</topic><topic>Heart Arrest - physiopathology</topic><topic>Heart Arrest - therapy</topic><topic>Hemodynamics</topic><topic>Hypothermia</topic><topic>Hypothermia, Induced</topic><topic>Intensive care medicine</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Reference Values</topic><topic>Shock - etiology</topic><topic>Swine</topic><topic>Transthoracic defibrillation</topic><topic>Ventricular fibrillation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rhee, Benjamin J</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Boddicker, Kimberly A.</creatorcontrib><creatorcontrib>Davies, Loyd R.</creatorcontrib><creatorcontrib>Kerber, Richard E.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Resuscitation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rhee, Benjamin J</au><au>Zhang, Yi</au><au>Boddicker, Kimberly A.</au><au>Davies, Loyd R.</au><au>Kerber, Richard E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of hypothermia on transthoracic defibrillation in a swine model</atitle><jtitle>Resuscitation</jtitle><addtitle>Resuscitation</addtitle><date>2005-04-01</date><risdate>2005</risdate><volume>65</volume><issue>1</issue><spage>79</spage><epage>85</epage><pages>79-85</pages><issn>0300-9572</issn><eissn>1873-1570</eissn><coden>RSUSBS</coden><abstract>Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented.
In 39 swine (21.4
±
1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30
°C) (
n
=
10), (2) severe H followed by N (
n
=
10), (3) N followed by moderate H (33
°C) (
n
=
10) and (4) moderate H followed by N (
n
=
9). After 30
s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20
J, 30
J, 50
J and 100
J in random order in both N and H conditions.
For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58;
p
<
0.0001), despite the fact that impedance rose from 39
±
3
Ω (N) to 42
±
3
Ω (H) (
p
<
0.001) and current fell from 22
±
8 (N) to 21
±
7
A (H) (
p
<
0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (
p
=
0.0002).
Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>15797279</pmid><doi>10.1016/j.resuscitation.2004.10.013</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Resuscitation, 2005-04, Vol.65 (1), p.79-85 |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Disease Models, Animal Electric Countershock Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care Heart Arrest - complications Heart Arrest - physiopathology Heart Arrest - therapy Hemodynamics Hypothermia Hypothermia, Induced Intensive care medicine Medical sciences Pharmacology. Drug treatments Reference Values Shock - etiology Swine Transthoracic defibrillation Ventricular fibrillation |
| title | Effect of hypothermia on transthoracic defibrillation in a swine model |
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