Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
An idea of arteriovenous shunts (AVS) was proposed for explanation of dynamic regulation of oxygenation and venous hyperoxia. A formula enabling calculation of AVS and real CO2 production has recently been derived by comparing data of arterial and venous blood gases. Regarding venous hyperoxia, there is a need to differentiate capillary to tissue transport defect (low oxygen utilisation-LOU) from AVS, which may exist simultaneously. The AVS may be associated with normal or relatively high oxygen utilization from the capillary vessels and increased CO2 production. AVS is proposed to carry protective and 'stealing' properties including renal, cardiac, and pulmonary hemodynamic. Calculations of the AVS may be important for dynamic assessment of vascular and metabolic status and in emergency medicine.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1177/0960327109357216 | DOI Listing |
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