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Modes of induced cardiac arrest: hyperkalemia and hypocalcemia - Literature review
The entry of sodium and calcium play a key effect on myocyte subjected to cardiac arrest by hyperkalemia. They cause cell swelling, acidosis, consumption of adenosine triphosphate and trigger programmed cell death. Cardiac arrest caused by hypocalcemia maintains intracellular adenosine triphosphate...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Sociedade Brasileira de Cirurgia Cardiovascular
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412334/ https://www.ncbi.nlm.nih.gov/pubmed/25372919 http://dx.doi.org/10.5935/1678-9741.20140074 |
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author | de Oliveira, Marcos Aurélio Barboza Brandi, Antônio Carlos dos Santos, Carlos Alberto Botelho, Paulo Henrique Husseini Cortez, José Luis Lasso Braile, Domingo Marcolino |
author_facet | de Oliveira, Marcos Aurélio Barboza Brandi, Antônio Carlos dos Santos, Carlos Alberto Botelho, Paulo Henrique Husseini Cortez, José Luis Lasso Braile, Domingo Marcolino |
author_sort | de Oliveira, Marcos Aurélio Barboza |
collection | PubMed |
description | The entry of sodium and calcium play a key effect on myocyte subjected to cardiac arrest by hyperkalemia. They cause cell swelling, acidosis, consumption of adenosine triphosphate and trigger programmed cell death. Cardiac arrest caused by hypocalcemia maintains intracellular adenosine triphosphate levels, improves diastolic performance and reduces oxygen consumption, which can be translated into better protection to myocyte injury induced by cardiac arrest. |
format | Online Article Text |
id | pubmed-4412334 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Sociedade Brasileira de Cirurgia Cardiovascular |
record_format | MEDLINE/PubMed |
spelling | pubmed-44123342015-04-30 Modes of induced cardiac arrest: hyperkalemia and hypocalcemia - Literature review de Oliveira, Marcos Aurélio Barboza Brandi, Antônio Carlos dos Santos, Carlos Alberto Botelho, Paulo Henrique Husseini Cortez, José Luis Lasso Braile, Domingo Marcolino Rev Bras Cir Cardiovasc Special Articles The entry of sodium and calcium play a key effect on myocyte subjected to cardiac arrest by hyperkalemia. They cause cell swelling, acidosis, consumption of adenosine triphosphate and trigger programmed cell death. Cardiac arrest caused by hypocalcemia maintains intracellular adenosine triphosphate levels, improves diastolic performance and reduces oxygen consumption, which can be translated into better protection to myocyte injury induced by cardiac arrest. Sociedade Brasileira de Cirurgia Cardiovascular 2014 /pmc/articles/PMC4412334/ /pubmed/25372919 http://dx.doi.org/10.5935/1678-9741.20140074 Text en http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Special Articles de Oliveira, Marcos Aurélio Barboza Brandi, Antônio Carlos dos Santos, Carlos Alberto Botelho, Paulo Henrique Husseini Cortez, José Luis Lasso Braile, Domingo Marcolino Modes of induced cardiac arrest: hyperkalemia and hypocalcemia - Literature review |
title | Modes of induced cardiac arrest: hyperkalemia and hypocalcemia -
Literature review |
title_full | Modes of induced cardiac arrest: hyperkalemia and hypocalcemia -
Literature review |
title_fullStr | Modes of induced cardiac arrest: hyperkalemia and hypocalcemia -
Literature review |
title_full_unstemmed | Modes of induced cardiac arrest: hyperkalemia and hypocalcemia -
Literature review |
title_short | Modes of induced cardiac arrest: hyperkalemia and hypocalcemia -
Literature review |
title_sort | modes of induced cardiac arrest: hyperkalemia and hypocalcemia -
literature review |
topic | Special Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4412334/ https://www.ncbi.nlm.nih.gov/pubmed/25372919 http://dx.doi.org/10.5935/1678-9741.20140074 |
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