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Troponin dan Manajemen Iskemia Miokardium Perioperatif Leksana, Ery; Purnomo, Ika Cahyo
Majalah Anestesia dan Critical Care Vol 32 No 1 (2014): Februari
Publisher : Perdatin Pusat

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Abstract

Penyakit jantung iskemik sering memberikan gambaran dan perkembangan yang membahayakan. Kejadian dari tahun ke tahun terus meningkat dan menyumbang angka mortalitas yang tinggi. Angina pectoris, gambaran iskemia pada EKG, dan peningkatan petanda jantung menunjukkan terjadinya infark miokard akut. Pasien dalam kondisi demikian sangat berisiko untuk menjalani proses pembiusan. Pemeriksaan troponin bersenstivitas tinggi telah diperkenalkan, namun hal ini memberikan tantangan yang baru dalam hal sensitivitas vs spesivisitas. Berbagai panduan telah diterbitkan untuk memandu dokter ahli anestesi melewati rintangan risiko pada penderita dengan iskemia miokard. Kata kunci: Anestesi, iskemia miokardium, troponin Troponin and Perioperative Management in Iskemia Myokard Troponin Ischemic heart disease often develop harmful conditions. Incidence from year to year continues to increase and accounted for high mortality rate. Angina pectoris, marked ECG changes and elevation of cardiac markers, especially troponins indicate the presence of acute myocardial infarct. Patients in this condition is very risky to undergo anesthesia process. High sensitivity troponin test were introduced, but it gave new challenge of sensitivity vs specificity. Guidelines have been published to guide the anesthesiologist through the obstacles of risks in patients with myocardial ischemia. Key words: Anesthesia, myocardial ischemia, troponin Reference Wu AH, Apple FS, Gibler WB, Jesse RL, Warshaw MM, Valdes R Jr. National Academy of Clinical Biochemistry Standards of laboratory practice: recommendations for the use of cardiac markers in coronary artery diseases. Clin Chem. Jul 1999;45(7):1104–21. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined--a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol. Sep 2000;36(3):959–69. Antman EM. Decision making with cardiac troponin tests. N Engl J Med. Jun 27 2002;346(26):2079–82. Morrow DA, Cannon CP, Jesse RL, Newby LK, Ravkilde J, Storrow AB, dkk. National academy of clinical biochemistry laboratory medicine practice guidelines: clinical characteristics and utilization of biochemical markers in acute coronary syndromes. Clin Chem. Apr 2007;53(4):552–74. Hamm CW, Giannitsis E, Katus HA. Cardiac troponin elevations in patients without acute coronary syndrome. Circulation. Dec 3 2002;106(23):2871–2. Ammann P, Fehr T, Minder EI, Günter C, Bertel O. Elevation of troponin I in sepsis and septic shock.Intensive Care Med. Jun 2001;27(6):965–9. Bakshi TK, Choo MK, Edwards CC, Scott AG, Hart HH, Armstrong GP. Causes of elevated troponin I with a normal coronary angiogram. Intern Med J. Nov 2002;32(11):520–5. Nunes JP, Mota Garcia JM, Farinha RM, dkkl. Cardiac troponin I in aortic valve disease. Int J Cardiol. Jun 2003;89(2–3):281–5. Hamwi SM, Sharma AK, Weissman NJ, Goldstein SA, Apple S, Caños DA. Troponin-I elevation in patients with increased left ventricular mass. Am J Cardiol. Jul 1 2003;92(1):88–90. Velmahos GC, Karaiskakis M, Salim A, Toutouzas KG, Murray J, Asensio J. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma. Jan 2003;54(1):45–50; discussion 50–1. Smith SC, Ladenson JH, Mason JW, Jaffe AS. Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. Circulation. Jan 7 1997;95(1):163–8. Brandt RR, Filzmaier K, Hanrath P. Circulating cardiac troponin I in acute pericarditis. Am J Cardiol. Jun 1 2001;87(11):1326–8.
Dehidrasi dan Syok Leksana, Ery
Cermin Dunia Kedokteran Vol 42, No 5 (2015): Kardiologi
Publisher : PT. Kalbe Farma Tbk.

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (140.897 KB) | DOI: 10.55175/cdk.v42i5.1016

Abstract

Dehidrasi didefinisikan sebagai suatu kondisi kehilangan cairan dan elektrolit tubuh. Kondisi dehidrasi berat dapat berdampak pada kejadian syok. Syok merupakan suatu kegagalan sirkulasi dan perfusi jaringan, umumnya disebabkan oleh kehilangan volume cairan intravaskuler, yang ditandai gejala klinis seperti takikardi dan hipotensi. Tujuan penanganan syok tahap awal adalah mengembalikan perfusi dan oksigenasi jaringan dengan mengembalikan volume sirkulasi intravaskuler. Terapi cairan merupakan terapi yang paling penting pada syok distributif dan syok hipovolemik. Penanganan syok dini dapat berdampak sangat bermakna pada perbaikan outcome klinis. Keberhasilan resusitasi syok dapat dinilai berdasarkan perbaikan hemodinamik, seperti MAP, CVP, urine output, mixed venous oxygen saturation , dan status mental.Dehydration is defined as a condition of losing of body fluid and electrolyte. Severe dehydration could lead into shock. Shock is a condition caused by failure of circulatory and tissue oxygenation system due to excessive loss of intravascular fluid which is often marked by tachycardia and hypotension. The early goal of shock therapy is to recover adequate tissue perfusion and oxygenation by recovering intravascular circulatory volume. Fluid therapy is the most crucial step in distributive and hypovolemic shock. The early goal-directed therapy has been shown to significantly improve clinical outcomes. Adequacy of resuscitation is monitored by the improvement of hemodynamic stability, such as MAP, CVP, urine output, mixed venous oxygen saturation, and mental status.