Patofisiologi dan Penanganan Kardiomiopati Peripartum
Abstract
Kardiomiopati peripartum adalah salah satu penyebab dari kardiomiopati dilatasi yang timbul pada waktu akhir trimester tiga kehamilan sampai 5 bulan kelahiran. Tanda karakteristik kardiomiopati peripatum adalah berkurangnya fraksi ejeksi ventrikel kiri dan berhubungan dengan gagal jantung kongesti, yang dapat meningkatkan resiko aritmia, tromboemboli dan henti jantung mendadak. Pengertian mendalam tentang fisiologi selama kehamilan dan patofisiologi penyakit jantung pada ibu sangat penting untuk dokter anestesi, dokter kandungan dan dokter jantung yang terlibat pada penanganan pasien PPCM selama periode kehamilan dan persalinan (perawatan peripartum). Penatalaksanaan kardiomiopati peripartum sebagian besar bersifat suportif. Tujuan terapi pada pasien dengan kardiomiopati peripartum adalah optimalisasi hemodinamik, mengoptimalkan preload, menurunkan afterload dan meningkatkan kontraktilitas. Keputusan jenis persalinan pasien dengan kardiomiopati peripartum harus dibuat berdasarkan indikasi obstetri. Pilihan tehnik anestesi yang akan digunakan disesuaikan dengan kondisi klinis ibu pada saat itu dengan memperhatikan efek obat terhadap ibu maupun janin. Baik tehnik anestesi umum maupun tehnik anestesi regional dapat digunakan untuk parturien dengan kardiomiopati peripartum.
Pathophysiology and Management of Peripartum Cardiomyopathy
Abstract
Peripartum cardiomyopathy (PPCM) is a number of cause of dilated cardiomyopathy which occured during the end third trimester of pregnancy until the fifth months of birth. The characteristic sign of peripartum cardiomyopathy is reduced the ejection fraction of left ventricle and associated to congestive heart failure, increased risk of arrhythmia, thromboemboli and sudden cardiac arrest. A comprehensive understanding of the physiology of pregnancy and pathophysiology of maternal cardiac disease is importance for anesthesiologist, gynecologists and cardiologists involved in peripartum care in patients with peripartum cardiomyopathy during the pregnancy and childbirth periods. Management of peripartum cardiomyopathy is mostly supportive therapy. The goal of therapy in patients with peripartum cardiomyopathy is hemodynamic optimization, such as maintaining preload, reducing afterload and improving contractility. Decision of the mode of delivery of patient with peripartum cardiomyopathy hould be based on obstetric indication. The choice of anesthesia technique should consider the current clinical condition of parturient and the effect of the drug for the mother and fetus. Both general anesthesia and regional anesthesia techniques can be an option for parturients with peripartum cardiomyopathy.
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References
Maron BJ. Cardiomyopathies. In: Fuster V, editor. The AHA Guidelines and Scientific Statements Handbook. New York:Willey‐Blackwell; 2009;236‐43.
Lilly LS, Lee TC, Dec GW. The Cardiomyopathies. In: Pathophysiology of heart disease, 5th edition. Lippincott William & Wilkins, 2011; 244–60.
Oakley CM. Peripartum cardiomyopathy. In: Women & Heart Disease, 2nd edition. Taylor & Francis, 2005;341–48.
Foster O, Ansari AA, Sliwa K. Current issues in the diagnosis and management of peripartum cardiomyopathy. Women’s Health, 2006;2(4): 587–96.
Shaikh N. An obstetric emergency called peripartum cardiomyopathy. Journal of Emergency Trauma and Shock 2010;3:39–42.
Foley MR, Rokey R, Belfort MA. Cardiac Disease. In: Critical care obstetrics, 5th edition. Blackwell Publishing Ltd, 2010; 256–77.
Richards NA, Yentis SM. Anaesthesia, analgesia and peripartum management in women with pre-existing cardiac and respiratory disease. Fetal and maternal medicine review, 2006;17(4):327–47.
Chestnut DH, Polley LS, Tsen LC, Wong CA. Chestnut’s obstetric anesthesia principles and practice, 4th edition. Mosby elsevier, 2009;15–36.
Hilfi ker-Kleiner D, Kaminski K, Podewski E, Bonda T, Schaefer A, Sliwa K, et al. A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy. Cell 2007;128:589–600.
Watkins H, Ashrafian H, Redwood C. Inherited cardiomyopathies. New England Journal Medicine 2011;17:1643–56.
Lata I, Gupta R, Sahu S, Singh H. Emergency management of decompensated peripartum cardiomyopathy. Journal of emergency, trauma and shock, 2009;12:124–8.
McHugh AMG. Recognizing and treating peripartum cardiomyopathy. Nursing, 1999;29(3):32C8.
Fragneto RY. The high-risk obstetric patient. In: Obtsteric and gynecologic anesthesia: the requisites in anesthesiology. Elsevier mosby, 2006:79–113.
Carvalho B, Jackson E. Structural heart disease in pregnant women. In: Obstetric anesthesia and uncommon disorders, 2nd edition. Cambridge university press, 2008;1–27.
Maitra G, Sengupta S, Rudra A, Debnath S. Pregnancy and non-valvular heart disease-anesthetic considerations. Annals of cardiac anaesthesia, 2010;132:102–9.
Morales A, Painter T, Li R, Siegfried JD, Li DX, Norton N. Mutations in 6 Genes Identified in Patients With Peripartum Cardiomyopathy. JACC March 9 2010;55;10A:1029–168.
Sliwa K1, Hilfiker-Kleiner D, Petrie MC, Mebazaa A, Pieske B, Buchmann E, et al. Position statement on current state of kowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Working Group on Peripartum Cardiomyopathy. European Journal Heart Failure 2012;12:767–78. http://eurjhf.oxfordjournals.org/content/12/8/767.full.pdf+html
Jurnal Anestesi Obstetri Indonesia
