Myocardial Infarction in a Young Patient After Acute Exposure to Carbon Monoxide
Yazarlar (5)
Ozkan Onal
Derya Çelik
Doç. Dr. Emine Aslanlar Selçuk Üniversitesi, Türkiye
Prof. Dr. Ahmet AVCI Zonguldak Bülent Ecevit Üniversitesi, Türkiye
Prof. Dr. Jale Bengi Çelik Selçuk Üniversitesi, Türkiye
| Makale Türü | Diğer (Teknik, not, yorum, vaka takdimi, editöre mektup, özet, kitap krıtiği, araştırma notu, bilirkişi raporu ve benzeri) (ESCI dergilerinde yayınlanan teknik not, editöre mektup, tartışma, vaka takdimi ve özet türünden makale) | ||
| Dergi Adı | Anesthesiology and Pain Medicine | ||
| Dergi ISSN | 2228-7523 Scopus Dergi | ||
| Dergi Tarandığı Indeksler | Emerging Sources Citation Index | ||
| Makale Dili | İngilizce | Basım Tarihi | 02-2016 |
| Cilt / Sayı / Sayfa | 6 / 3 / – | DOI | 10.5812/aapm.33154 |
| Makale Linki | https://doi.org/10.5812/aapm.33154 | ||
| Özet |
| Carbon monoxide (CO) is an odorless, colorless, clear gas that attaches to the hemoglobin (Hb). Its affinity for Hb is approximately 200 times higher than that of oxygen, and CO blocks the capacity of Hb to carry oxygen (1). One of the most important effects of CO is tissue hypoxia, especially in the parts of tissues with the highest demand for oxygen and the lowest metabolic stores, such as the brain and heart, which are therefore more vulnerable. CO intoxications are usually expressed as neurological events, but cardiological events can also occur (2). Myocardial injury may arise via electrical, functional, and morphological changes in the heart through severe general tissue hypoxia; there may be a direct toxic effect on the myocardial mitochondria promptly after exposure, or this may be delayed for several days (3). CO can induce a tendency toward coronary vasospasm and thrombus formation by slowing the … |
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| Google Scholar | 5 |