Sabtu, 29 Oktober 2011
Rabu, 26 Oktober 2011
I.2. Pemahaman & Pengertian EKG
1. Pemahaman yang di maksud disini adalah :
Banyak sekali rekan-rekan perawat yang belum memahami akan peranan dan pentingnya EKG (elektrokardiografi).
Yang kedua adalah persepsi dan pemahaman yang salah tentang EKG (elektrokardiografi), dimana menurut sebagian rekan-rekan perawat EKG hanya bisa dikonsumsi untuk dokter jantung (cardiologist), dokter atau perawat yang bekerja di ruangan jantung saja seperti ICCU, ICU, telemetry dll.
Yang ketiga adalah sistematika pengajaran EKG (elektrokardiografi) yang kurang pas penyajiannya, dimana rekan-rekan yang sudah mempunyai motivasi bagus untuk belajar EKG masih mengalami kesulitan dalam memahami dan mencerna ilmu EKG dengan baik dan benar, sehingga apa yang didapatkan dalam akhir pembelajaran atau pelatihan mereka rasakan sia-sia.
Di blog ini, saya ingin mengajak rekan-rekan perawat untuk sama-sama membuka mata dan pikiran dalam memahami ilmu EKG (elektrokardiografi). Sebelumnya saya ingin bertanya, ada berapa jumlah rumah sakit pemerintah dan swasta di Indonesia?Masih adakah rumah sakit yang tidak menggunakan fasilitas EKG? Kalau saya tebak jawaban anda adalah puluhan bahkan ratusan jumlah rumah sakit di Indonesia dan tak satupun yang tidak menggunakan fasilitas EKG. Ini menunjukkan bahwa begitu pentingnya peranan EKG dalam dunia medis.
Di era global seperti sekarang ini, dimana setiap rumah sakit baik di dalam maupun di luar negeri saling berpacu dalam meningkatkan pelayanannya dengan menyediakan fasilitas-fasilitas yang memuaskan bagi pengunjungnya. Salah satunya adalah perekaman EKG yang mana mesin-mesin EKG ini mulai dari unit gawat darurat, bangsal umum/vip, klinik, ruang operasi, ICU/ICCU,telemetry dan tempat-tempat lainnya dengan mudah anda temukan. Jadi tidaklah benar kalau EKG dikonsumsi untuk dokter dan sebagian para perawat yang bekerja diruang jantung.
Apakah anda tidak menyadari kalau sebenarnya kita (profesi keperawatan) masih pantas menyandang gelar "ROBOT" atau "PEMBANTU DOKTER", kenapa demikian? Kalau seorang perawat hanya bisa menjalankan order dokter saja tanpa bisa memberikan klarifikasi atau pendapat yang perlu demi kebaikan pasien, sama saja kita sebagai robot atau pembantu dokter. Seperti halnya dengan EKG(elektrokardiografi), anda cuma bisa melakukan perekaman EKG setelah itu menyerahkan ke dokter dan menjalankan apa yang diinstruksikan oleh dokter, padahal intruksi yang diberikan oleh dokter tidak selamanya tepat. Jadi kita sebagai partner (bukan pembantu dokter) harus bisa mengklarifikasi instruksi dokter tersebut. Bagaimana bila anda tidak menguasai basic EKG, sementara dokter tidak memberikan terapi untuk MI (miokardiac Infark) padahal jelas sekali gambaran EKG menunjukan adanya MI. Ingat! anda sudah mendeklarasikan diri sebagai tenaga perawat yang profesional. Buktikan dong.......
Melalui blog ini,Insya allah saya akan memberikan pembelajaran EKG secara sederhana dan sistematis, dengan bahasa yang sederhana serta mudah dicerna oleh rekan-rekan perawat sehingga bisa mengarahkan anda untuk menjadi interpreter EKG yang handal.
2. Pengertian EKG (elektrokardiografi)
Anda boleh menyebutkan kepanjangan EKG tersebut dengan "elektrokardiografi" atau "elekrokardiogram" karena grafik yang tercatat atau terekam oleh mesin EKG dinamakan Elektrokardiogram, sedangkan ilmu yang mempelajari EKG dinamakan Elektrokardiografi. Kalau saya uraikan arti dari kata elektrokardiografi/elektrokardiogram adalah elektro=listrik, kardio = jantung, grafi/gram = grafik. Jadi pengertian EKG secara lengkap adalah rekaman aktivitas listrik jantung atau bioelektrikal pada jantung yang digambarkan dengan sebuah grafik EKG atau dengan kata lain grafik EKG menggambarkan rekaman aktifitas listrik jantung.
Bagaimana cara merekam aktivitas listrik jantung? Yaitu dengan menempatkan sandapan-sandapan berupa elektroda yang di tempatkan dipermukaan tubuh, dimana elektroda-elektroda tersebut merekam aktivitas listrik jantung dari sudut yang berbeda, sehingga gambaran EKG yang terekam ditiap lead akan berbeda karena tergantung dari arah aksis jantung si pasien. (baca aksis jantung)
EKG (elektrokardiografi) merupakan salah satu bentuk pemeriksaan laboratorium yang membantu dalam menegakkan suatu diagnosa, khususnya penyakit jantung. Ingat! Gambaran klinis pasien adalah nomor satu yang harus dipikirkan dalam menegakkan diagnosa penyakit jantung. Karena dilapangan seringkali ditemukan pasien dengan gambaran EKG abnormal tapi secara klinis jantung pasien normal. Begitu sebaliknya, gambaran EKG normal tapi secara klinis pasien mengalami gangguan pada jantung. Jadi obati pasien, bukan EKGnya !
EKG sangat bermanfaat sekali dalam mengidentifikasi :
1. Gangguan Aritmia or dysritmia (aritmia = dysritmia)
2. Jantung ischemia
3. Myocardiac Infarction
4. Hypertrophy Otot jantung ( untuk otot ventrikel), Dilatasi otot jantung (untuk otot atrium)
5. Gangguan keseimbangan elektrolit
6. Efek obat-obatan
7. Fungsi pacu jantung
8. Dan lain-lain
Banyak sekali rekan-rekan perawat yang belum memahami akan peranan dan pentingnya EKG (elektrokardiografi).
Yang kedua adalah persepsi dan pemahaman yang salah tentang EKG (elektrokardiografi), dimana menurut sebagian rekan-rekan perawat EKG hanya bisa dikonsumsi untuk dokter jantung (cardiologist), dokter atau perawat yang bekerja di ruangan jantung saja seperti ICCU, ICU, telemetry dll.
Yang ketiga adalah sistematika pengajaran EKG (elektrokardiografi) yang kurang pas penyajiannya, dimana rekan-rekan yang sudah mempunyai motivasi bagus untuk belajar EKG masih mengalami kesulitan dalam memahami dan mencerna ilmu EKG dengan baik dan benar, sehingga apa yang didapatkan dalam akhir pembelajaran atau pelatihan mereka rasakan sia-sia.
Di blog ini, saya ingin mengajak rekan-rekan perawat untuk sama-sama membuka mata dan pikiran dalam memahami ilmu EKG (elektrokardiografi). Sebelumnya saya ingin bertanya, ada berapa jumlah rumah sakit pemerintah dan swasta di Indonesia?Masih adakah rumah sakit yang tidak menggunakan fasilitas EKG? Kalau saya tebak jawaban anda adalah puluhan bahkan ratusan jumlah rumah sakit di Indonesia dan tak satupun yang tidak menggunakan fasilitas EKG. Ini menunjukkan bahwa begitu pentingnya peranan EKG dalam dunia medis.
Di era global seperti sekarang ini, dimana setiap rumah sakit baik di dalam maupun di luar negeri saling berpacu dalam meningkatkan pelayanannya dengan menyediakan fasilitas-fasilitas yang memuaskan bagi pengunjungnya. Salah satunya adalah perekaman EKG yang mana mesin-mesin EKG ini mulai dari unit gawat darurat, bangsal umum/vip, klinik, ruang operasi, ICU/ICCU,telemetry dan tempat-tempat lainnya dengan mudah anda temukan. Jadi tidaklah benar kalau EKG dikonsumsi untuk dokter dan sebagian para perawat yang bekerja diruang jantung.
Apakah anda tidak menyadari kalau sebenarnya kita (profesi keperawatan) masih pantas menyandang gelar "ROBOT" atau "PEMBANTU DOKTER", kenapa demikian? Kalau seorang perawat hanya bisa menjalankan order dokter saja tanpa bisa memberikan klarifikasi atau pendapat yang perlu demi kebaikan pasien, sama saja kita sebagai robot atau pembantu dokter. Seperti halnya dengan EKG(elektrokardiografi), anda cuma bisa melakukan perekaman EKG setelah itu menyerahkan ke dokter dan menjalankan apa yang diinstruksikan oleh dokter, padahal intruksi yang diberikan oleh dokter tidak selamanya tepat. Jadi kita sebagai partner (bukan pembantu dokter) harus bisa mengklarifikasi instruksi dokter tersebut. Bagaimana bila anda tidak menguasai basic EKG, sementara dokter tidak memberikan terapi untuk MI (miokardiac Infark) padahal jelas sekali gambaran EKG menunjukan adanya MI. Ingat! anda sudah mendeklarasikan diri sebagai tenaga perawat yang profesional. Buktikan dong.......
Melalui blog ini,Insya allah saya akan memberikan pembelajaran EKG secara sederhana dan sistematis, dengan bahasa yang sederhana serta mudah dicerna oleh rekan-rekan perawat sehingga bisa mengarahkan anda untuk menjadi interpreter EKG yang handal.
2. Pengertian EKG (elektrokardiografi)
Anda boleh menyebutkan kepanjangan EKG tersebut dengan "elektrokardiografi" atau "elekrokardiogram" karena grafik yang tercatat atau terekam oleh mesin EKG dinamakan Elektrokardiogram, sedangkan ilmu yang mempelajari EKG dinamakan Elektrokardiografi. Kalau saya uraikan arti dari kata elektrokardiografi/elektrokardiogram adalah elektro=listrik, kardio = jantung, grafi/gram = grafik. Jadi pengertian EKG secara lengkap adalah rekaman aktivitas listrik jantung atau bioelektrikal pada jantung yang digambarkan dengan sebuah grafik EKG atau dengan kata lain grafik EKG menggambarkan rekaman aktifitas listrik jantung.
Bagaimana cara merekam aktivitas listrik jantung? Yaitu dengan menempatkan sandapan-sandapan berupa elektroda yang di tempatkan dipermukaan tubuh, dimana elektroda-elektroda tersebut merekam aktivitas listrik jantung dari sudut yang berbeda, sehingga gambaran EKG yang terekam ditiap lead akan berbeda karena tergantung dari arah aksis jantung si pasien. (baca aksis jantung)
EKG (elektrokardiografi) merupakan salah satu bentuk pemeriksaan laboratorium yang membantu dalam menegakkan suatu diagnosa, khususnya penyakit jantung. Ingat! Gambaran klinis pasien adalah nomor satu yang harus dipikirkan dalam menegakkan diagnosa penyakit jantung. Karena dilapangan seringkali ditemukan pasien dengan gambaran EKG abnormal tapi secara klinis jantung pasien normal. Begitu sebaliknya, gambaran EKG normal tapi secara klinis pasien mengalami gangguan pada jantung. Jadi obati pasien, bukan EKGnya !
EKG sangat bermanfaat sekali dalam mengidentifikasi :
1. Gangguan Aritmia or dysritmia (aritmia = dysritmia)
2. Jantung ischemia
3. Myocardiac Infarction
4. Hypertrophy Otot jantung ( untuk otot ventrikel), Dilatasi otot jantung (untuk otot atrium)
5. Gangguan keseimbangan elektrolit
6. Efek obat-obatan
7. Fungsi pacu jantung
8. Dan lain-lain
I. EKG
Elektrokardiografi
by Abu Nazmah
Untuk menjadi seorang interpreter EKG yang handal, anda harus membaca topik yang telah saya susun secara sistematis mulai dari pengetahuan dasar yang terkait dengan EKG sampai dengan topik yang nantinya akan mengarahkan anda untuk menjadi seorang interpreter yang handal. Sebenarnya kursus ini memerlukan tatap muka agar perlu pejelasan yang gamblang. Akan tetapi saya akan berusaha semaksimal mungkin untuk menyajikannya tanpa harus bertatap muka. Anda juga boleh mengajukan pertanyaan lewat email atau langsung lewat chating via yahoo messenger. Add saja abu_nazmah@yahoo.com.
Adapun topik yang telah saya susun adalah dibawah ini :
Bagian I
1. Pemahaman dan Pengertian Elektrokardiografi
2. Anatomi dan Fisiologi Jantung
3. Elektrofisiologi Jantung
Bagian II
4. Kertas EKG (elektrokardiografi)
5. Konfigurasi Gelombang EKG (elektrokardiografi)
6. Axis Jantung
Bagian III
7. Cara menghitung frekfensi detak jantung (heart rate)
8. Normal Ekg dan Variant Normal EKG
9. Arrythmia atau Dysrythmia
Bagian IV
10. Myocardiac Infarction dan Ischemia
11. Pembesaran Otot Jantung (Hypertropy dan Enlargment)
12. Pengaruh Obat-obatan dan Gangguan Keseimbangan Elektrolit
Bagian V
13. Interpretasi EKG (elektrokardiografi)
Ingat 4 K !!! Kemauan, Kesungguhan, Kosentrasi dan Kesabaran adalah faktor yang menentukan anda untuk menjadi seorang interpreter ekg (elektrokardiografi) yang handal.
Bagian I
1. Pemahaman dan Pengertian Elektrokardiografi
2. Anatomi dan Fisiologi Jantung
3. Elektrofisiologi Jantung
Bagian II
4. Kertas EKG (elektrokardiografi)
5. Konfigurasi Gelombang EKG (elektrokardiografi)
6. Axis Jantung
Bagian III
7. Cara menghitung frekfensi detak jantung (heart rate)
8. Normal Ekg dan Variant Normal EKG
9. Arrythmia atau Dysrythmia
Bagian IV
10. Myocardiac Infarction dan Ischemia
11. Pembesaran Otot Jantung (Hypertropy dan Enlargment)
12. Pengaruh Obat-obatan dan Gangguan Keseimbangan Elektrolit
Bagian V
13. Interpretasi EKG (elektrokardiografi)
Ingat 4 K !!! Kemauan, Kesungguhan, Kosentrasi dan Kesabaran adalah faktor yang menentukan anda untuk menjadi seorang interpreter ekg (elektrokardiografi) yang handal.
Pemahaman & Pengertian EKG
1. Pemahaman yang di maksud disini adalah :
Banyak sekali rekan-rekan perawat yang belum memahami akan peranan dan pentingnya EKG (elektrokardiografi).
Yang kedua adalah persepsi dan pemahaman yang salah tentang EKG (elektrokardiografi), dimana menurut sebagian rekan-rekan perawat EKG hanya bisa dikonsumsi untuk dokter jantung (cardiologist), dokter atau perawat yang bekerja di ruangan jantung saja seperti ICCU, ICU, telemetry dll.
Yang ketiga adalah sistematika pengajaran EKG (elektrokardiografi) yang kurang pas penyajiannya, dimana rekan-rekan yang sudah mempunyai motivasi bagus untuk belajar EKG masih mengalami kesulitan dalam memahami dan mencerna ilmu EKG dengan baik dan benar, sehingga apa yang didapatkan dalam akhir pembelajaran atau pelatihan mereka rasakan sia-sia.
Di blog ini, saya ingin mengajak rekan-rekan perawat untuk sama-sama membuka mata dan pikiran dalam memahami ilmu EKG (elektrokardiografi). Sebelumnya saya ingin bertanya, ada berapa jumlah rumah sakit pemerintah dan swasta di Indonesia?Masih adakah rumah sakit yang tidak menggunakan fasilitas EKG? Kalau saya tebak jawaban anda adalah puluhan bahkan ratusan jumlah rumah sakit di Indonesia dan tak satupun yang tidak menggunakan fasilitas EKG. Ini menunjukkan bahwa begitu pentingnya peranan EKG dalam dunia medis.
Di era global seperti sekarang ini, dimana setiap rumah sakit baik di dalam maupun di luar negeri saling berpacu dalam meningkatkan pelayanannya dengan menyediakan fasilitas-fasilitas yang memuaskan bagi pengunjungnya. Salah satunya adalah perekaman EKG yang mana mesin-mesin EKG ini mulai dari unit gawat darurat, bangsal umum/vip, klinik, ruang operasi, ICU/ICCU,telemetry dan tempat-tempat lainnya dengan mudah anda temukan. Jadi tidaklah benar kalau EKG dikonsumsi untuk dokter dan sebagian para perawat yang bekerja diruang jantung.
Apakah anda tidak menyadari kalau sebenarnya kita (profesi keperawatan) masih pantas menyandang gelar "ROBOT" atau "PEMBANTU DOKTER", kenapa demikian? Kalau seorang perawat hanya bisa menjalankan order dokter saja tanpa bisa memberikan klarifikasi atau pendapat yang perlu demi kebaikan pasien, sama saja kita sebagai robot atau pembantu dokter. Seperti halnya dengan EKG(elektrokardiografi), anda cuma bisa melakukan perekaman EKG setelah itu menyerahkan ke dokter dan menjalankan apa yang diinstruksikan oleh dokter, padahal intruksi yang diberikan oleh dokter tidak selamanya tepat. Jadi kita sebagai partner (bukan pembantu dokter) harus bisa mengklarifikasi instruksi dokter tersebut. Bagaimana bila anda tidak menguasai basic EKG, sementara dokter tidak memberikan terapi untuk MI (miokardiac Infark) padahal jelas sekali gambaran EKG menunjukan adanya MI. Ingat! anda sudah mendeklarasikan diri sebagai tenaga perawat yang profesional. Buktikan dong.......
Melalui blog ini,Insya allah saya akan memberikan pembelajaran EKG secara sederhana dan sistematis, dengan bahasa yang sederhana serta mudah dicerna oleh rekan-rekan perawat sehingga bisa mengarahkan anda untuk menjadi interpreter EKG yang handal.
2. Pengertian EKG (elektrokardiografi)
Anda boleh menyebutkan kepanjangan EKG tersebut dengan "elektrokardiografi" atau "elekrokardiogram" karena grafik yang tercatat atau terekam oleh mesin EKG dinamakan Elektrokardiogram, sedangkan ilmu yang mempelajari EKG dinamakan Elektrokardiografi. Kalau saya uraikan arti dari kata elektrokardiografi/elektrokardiogram adalah elektro=listrik, kardio = jantung, grafi/gram = grafik. Jadi pengertian EKG secara lengkap adalah rekaman aktivitas listrik jantung atau bioelektrikal pada jantung yang digambarkan dengan sebuah grafik EKG atau dengan kata lain grafik EKG menggambarkan rekaman aktifitas listrik jantung.
Bagaimana cara merekam aktivitas listrik jantung? Yaitu dengan menempatkan sandapan-sandapan berupa elektroda yang di tempatkan dipermukaan tubuh, dimana elektroda-elektroda tersebut merekam aktivitas listrik jantung dari sudut yang berbeda, sehingga gambaran EKG yang terekam ditiap lead akan berbeda karena tergantung dari arah aksis jantung si pasien. (baca aksis jantung)
EKG (elektrokardiografi) merupakan salah satu bentuk pemeriksaan laboratorium yang membantu dalam menegakkan suatu diagnosa, khususnya penyakit jantung. Ingat! Gambaran klinis pasien adalah nomor satu yang harus dipikirkan dalam menegakkan diagnosa penyakit jantung. Karena dilapangan seringkali ditemukan pasien dengan gambaran EKG abnormal tapi secara klinis jantung pasien normal. Begitu sebaliknya, gambaran EKG normal tapi secara klinis pasien mengalami gangguan pada jantung. Jadi obati pasien, bukan EKGnya !
EKG sangat bermanfaat sekali dalam mengidentifikasi :
1. Gangguan Aritmia or dysritmia (aritmia = dysritmia)
2. Jantung ischemia
3. Myocardiac Infarction
4. Hypertrophy Otot jantung ( untuk otot ventrikel), Dilatasi otot jantung (untuk otot atrium)
5. Gangguan keseimbangan elektrolit
6. Efek obat-obatan
7. Fungsi pacu jantung
8. Dan lain-lain
Banyak sekali rekan-rekan perawat yang belum memahami akan peranan dan pentingnya EKG (elektrokardiografi).
Yang kedua adalah persepsi dan pemahaman yang salah tentang EKG (elektrokardiografi), dimana menurut sebagian rekan-rekan perawat EKG hanya bisa dikonsumsi untuk dokter jantung (cardiologist), dokter atau perawat yang bekerja di ruangan jantung saja seperti ICCU, ICU, telemetry dll.
Yang ketiga adalah sistematika pengajaran EKG (elektrokardiografi) yang kurang pas penyajiannya, dimana rekan-rekan yang sudah mempunyai motivasi bagus untuk belajar EKG masih mengalami kesulitan dalam memahami dan mencerna ilmu EKG dengan baik dan benar, sehingga apa yang didapatkan dalam akhir pembelajaran atau pelatihan mereka rasakan sia-sia.
Di blog ini, saya ingin mengajak rekan-rekan perawat untuk sama-sama membuka mata dan pikiran dalam memahami ilmu EKG (elektrokardiografi). Sebelumnya saya ingin bertanya, ada berapa jumlah rumah sakit pemerintah dan swasta di Indonesia?Masih adakah rumah sakit yang tidak menggunakan fasilitas EKG? Kalau saya tebak jawaban anda adalah puluhan bahkan ratusan jumlah rumah sakit di Indonesia dan tak satupun yang tidak menggunakan fasilitas EKG. Ini menunjukkan bahwa begitu pentingnya peranan EKG dalam dunia medis.
Di era global seperti sekarang ini, dimana setiap rumah sakit baik di dalam maupun di luar negeri saling berpacu dalam meningkatkan pelayanannya dengan menyediakan fasilitas-fasilitas yang memuaskan bagi pengunjungnya. Salah satunya adalah perekaman EKG yang mana mesin-mesin EKG ini mulai dari unit gawat darurat, bangsal umum/vip, klinik, ruang operasi, ICU/ICCU,telemetry dan tempat-tempat lainnya dengan mudah anda temukan. Jadi tidaklah benar kalau EKG dikonsumsi untuk dokter dan sebagian para perawat yang bekerja diruang jantung.
Apakah anda tidak menyadari kalau sebenarnya kita (profesi keperawatan) masih pantas menyandang gelar "ROBOT" atau "PEMBANTU DOKTER", kenapa demikian? Kalau seorang perawat hanya bisa menjalankan order dokter saja tanpa bisa memberikan klarifikasi atau pendapat yang perlu demi kebaikan pasien, sama saja kita sebagai robot atau pembantu dokter. Seperti halnya dengan EKG(elektrokardiografi), anda cuma bisa melakukan perekaman EKG setelah itu menyerahkan ke dokter dan menjalankan apa yang diinstruksikan oleh dokter, padahal intruksi yang diberikan oleh dokter tidak selamanya tepat. Jadi kita sebagai partner (bukan pembantu dokter) harus bisa mengklarifikasi instruksi dokter tersebut. Bagaimana bila anda tidak menguasai basic EKG, sementara dokter tidak memberikan terapi untuk MI (miokardiac Infark) padahal jelas sekali gambaran EKG menunjukan adanya MI. Ingat! anda sudah mendeklarasikan diri sebagai tenaga perawat yang profesional. Buktikan dong.......
Melalui blog ini,Insya allah saya akan memberikan pembelajaran EKG secara sederhana dan sistematis, dengan bahasa yang sederhana serta mudah dicerna oleh rekan-rekan perawat sehingga bisa mengarahkan anda untuk menjadi interpreter EKG yang handal.
2. Pengertian EKG (elektrokardiografi)
Anda boleh menyebutkan kepanjangan EKG tersebut dengan "elektrokardiografi" atau "elekrokardiogram" karena grafik yang tercatat atau terekam oleh mesin EKG dinamakan Elektrokardiogram, sedangkan ilmu yang mempelajari EKG dinamakan Elektrokardiografi. Kalau saya uraikan arti dari kata elektrokardiografi/elektrokardiogram adalah elektro=listrik, kardio = jantung, grafi/gram = grafik. Jadi pengertian EKG secara lengkap adalah rekaman aktivitas listrik jantung atau bioelektrikal pada jantung yang digambarkan dengan sebuah grafik EKG atau dengan kata lain grafik EKG menggambarkan rekaman aktifitas listrik jantung.
Bagaimana cara merekam aktivitas listrik jantung? Yaitu dengan menempatkan sandapan-sandapan berupa elektroda yang di tempatkan dipermukaan tubuh, dimana elektroda-elektroda tersebut merekam aktivitas listrik jantung dari sudut yang berbeda, sehingga gambaran EKG yang terekam ditiap lead akan berbeda karena tergantung dari arah aksis jantung si pasien. (baca aksis jantung)
EKG (elektrokardiografi) merupakan salah satu bentuk pemeriksaan laboratorium yang membantu dalam menegakkan suatu diagnosa, khususnya penyakit jantung. Ingat! Gambaran klinis pasien adalah nomor satu yang harus dipikirkan dalam menegakkan diagnosa penyakit jantung. Karena dilapangan seringkali ditemukan pasien dengan gambaran EKG abnormal tapi secara klinis jantung pasien normal. Begitu sebaliknya, gambaran EKG normal tapi secara klinis pasien mengalami gangguan pada jantung. Jadi obati pasien, bukan EKGnya !
EKG sangat bermanfaat sekali dalam mengidentifikasi :
1. Gangguan Aritmia or dysritmia (aritmia = dysritmia)
2. Jantung ischemia
3. Myocardiac Infarction
4. Hypertrophy Otot jantung ( untuk otot ventrikel), Dilatasi otot jantung (untuk otot atrium)
5. Gangguan keseimbangan elektrolit
6. Efek obat-obatan
7. Fungsi pacu jantung
8. Dan lain-lain
Cardiomyopathy
Definition
The disease that coming from heart muscle and effect cardiac fungtion is known Cardiomyopathy.
The most common cardiomyopathy are DCM (Dilated Cardiomyopathy), HCM
(Hypertrophic Cardiomyopathy), RCM (Restrictive Cardiomyopathy). In all
3 types of Cardiomyopathy, patients may exprience heart failure.
A. Restrictive Cardiomyopathy
There is change in the composition of the heart muscle, that is the muscle become stiff and noncompliant,sistolic function in Restrictive Cardiomyopathy may remain near normal but ventricles are not able to relax properly, diastolic filling reducing leading to systemic and pulmonary venous congestion.
Signs and Symptoms
Signs and symptoms of cardiac failure like: Bradycardia,neck vein distention, peripheral edema, liver congestion, abdominal ascites.
Fatigue, weaknes
Late signs include nocturnal dyspnea, Heart sound S3, pink proty sputum, cough, crackles, orthopnea, tachycardia and restlessness
It is important to try to differentiate between restrictive and constrictive pericarditis, the most effective diagnostic tool for making this distinction are magnetic resonance imaging (MRI).
Test Diagnostic
EKG--> detect abnormalities in heart`s electrical activity
Echocardiography (Echo)--> to show enlarge heart muscle
MRI --> to detect abnormal texture in heart muscle
Cardiac Catheterization --> meassure pressure in heart chambers
Biopsy --> identifies infiltrating substance
Treatment
Around 70% of patients die within 5 years of symptom development, medications not helpful. remove of blood at regular interval to reduce amount of stored iron in clients with iron overload, heart transplant need it.
B. Hypertrophic Cardiomyopathy
The main causes for hypertrophic cardiomyopathy is some higher presser in the systemic vascular like any blood obtruction to pass out from left ventricle.
Uncontrolled hypertension causes ventricle and septum muscle to become hypertrophic. The actual chambers of the heart to become very small and little volume ejects out of the heart, decreasing CO so less forward flow leads to backward flow. (See pic 1)
(Pic : 1 A= Normal heart B= Hypertrophic Cardiomyopathy)
Inherited gene ---> The inherited gene effect the cells of the myocardium so that there is hypertrophy and asymmetry of the left ventricle.
Acromegaly ---> Excessive growth of the heart muscle due to overproduction of growth hormone.
Valvular heary diseases, increased volume or increased resistance to out flow in the chamber of the heart over time distends the chambers and the muscle become stretched, thinned and weakened.
Signs and Symptoms
Many patients with HCM (hypertrophic cardiomyopathy) remain asymptomatic for a long periode of time.
If symptomatic is reported manifestations of HCM are shortness of breath, orthopnea, dyspnea on exertion, nocturnal dyspnea, fatigue, generalize weaknes, dry cough at night.
Peripheral edema, hepatomegaly, jugular vein distension, weight gain.
Test Diagnostic
Chest X-ray --> will show mild to moderate increase in heart size
Thalium scan --> to reveal myocardial perfusion defects
ECHO -> will show left ventricular hypertrophy and thick interventricular septum
Cardiac catheterization --> to meassure pressure in the heart chambers
EKG --> will show left ventricilar hypertrophy, ventricular and atrium arrhytmias.
Treatment
Beta-adrenergis blockers --> to slow heart rate, to reduce myocardial O2 demand, increase ventricular filling by relaxing obstructing muscle.
Calcuim channal blockers--> to increase ventricular filling by relaxing obstructing muscle.
Antiarrhymic drugs --> to control arrhytmias
Anti coagulants --> to reduce risk of systemic embolism with atrial fibrilation
Heart transplant --> to replace the damage heart
C. Dilated Cardiomyopathy
In patient with dilated cardiomyopathy the left ventricle become dilated, resulting in impaired contraction. Those are possible caused :
Chemotheraphy ---> Toxic effect of the drugs on the myocardial cell dilate the ventricles and they can not contract properly.
Alcohol and drugs ---> Direct toxic effect of alcohol on the myocytes( cardiac cells)
Coronary heart diseaes---> Decrease O2 delivery to the heart muscle leads to pump failure.
Valvular heary diseases ---> increased volume or increased resistance to out flow in the chamber of the heart over time distends the chambers and the muscle become stretched, thinned and weakened. ( See pic 2)
( pic:2 A=Normal heart B= Dilated Cardiomyopathy)
Signs and Symptoms
Clients will increasingly display signs and symptoms of heart failure
Peripheral edema , hepatomegaly, jugular vein distension, and weight gain.
Peripheral cyanosis, tachycardia, murmur, arrhythmia, chest pain, palpitation, syncope.
Test Diagnostic
Angiography --> to rule out ischemic heart disease
Chest X-ray --> will show moderate to marked cardiomegaly and pulmonary edema
Echocardiography --> to confirm degree of left ventricular dilation and dysfunction
EKG --> to rule out ischemic heart disease
Cardiac catheterization
Endomyocardial biopsy.
Treatment
O2 therapy
ACE Inhibitors --> to reduce afterload through vasodilation
Diuretic --> to reduce fluid retention
Beta-adrenergic blockers --> to reduce demand
Antiarrhymic drugs --> to control arrhytmias
Valvular repair or replacement --> to manage dilated cardimyopathy fro valve dysfunction
Heart transplant --> to replace the damage heart
Lifestyle modifications
A. Restrictive Cardiomyopathy
There is change in the composition of the heart muscle, that is the muscle become stiff and noncompliant,sistolic function in Restrictive Cardiomyopathy may remain near normal but ventricles are not able to relax properly, diastolic filling reducing leading to systemic and pulmonary venous congestion.
Signs and Symptoms
Signs and symptoms of cardiac failure like: Bradycardia,neck vein distention, peripheral edema, liver congestion, abdominal ascites.
Fatigue, weaknes
Late signs include nocturnal dyspnea, Heart sound S3, pink proty sputum, cough, crackles, orthopnea, tachycardia and restlessness
It is important to try to differentiate between restrictive and constrictive pericarditis, the most effective diagnostic tool for making this distinction are magnetic resonance imaging (MRI).
Test Diagnostic
EKG--> detect abnormalities in heart`s electrical activity
Echocardiography (Echo)--> to show enlarge heart muscle
MRI --> to detect abnormal texture in heart muscle
Cardiac Catheterization --> meassure pressure in heart chambers
Biopsy --> identifies infiltrating substance
Treatment
Around 70% of patients die within 5 years of symptom development, medications not helpful. remove of blood at regular interval to reduce amount of stored iron in clients with iron overload, heart transplant need it.
B. Hypertrophic Cardiomyopathy
The main causes for hypertrophic cardiomyopathy is some higher presser in the systemic vascular like any blood obtruction to pass out from left ventricle.
Uncontrolled hypertension causes ventricle and septum muscle to become hypertrophic. The actual chambers of the heart to become very small and little volume ejects out of the heart, decreasing CO so less forward flow leads to backward flow. (See pic 1)
(Pic : 1 A= Normal heart B= Hypertrophic Cardiomyopathy)
Inherited gene ---> The inherited gene effect the cells of the myocardium so that there is hypertrophy and asymmetry of the left ventricle.
Acromegaly ---> Excessive growth of the heart muscle due to overproduction of growth hormone.
Valvular heary diseases, increased volume or increased resistance to out flow in the chamber of the heart over time distends the chambers and the muscle become stretched, thinned and weakened.
Signs and Symptoms
Many patients with HCM (hypertrophic cardiomyopathy) remain asymptomatic for a long periode of time.
If symptomatic is reported manifestations of HCM are shortness of breath, orthopnea, dyspnea on exertion, nocturnal dyspnea, fatigue, generalize weaknes, dry cough at night.
Peripheral edema, hepatomegaly, jugular vein distension, weight gain.
Test Diagnostic
Chest X-ray --> will show mild to moderate increase in heart size
Thalium scan --> to reveal myocardial perfusion defects
ECHO -> will show left ventricular hypertrophy and thick interventricular septum
Cardiac catheterization --> to meassure pressure in the heart chambers
EKG --> will show left ventricilar hypertrophy, ventricular and atrium arrhytmias.
Treatment
Beta-adrenergis blockers --> to slow heart rate, to reduce myocardial O2 demand, increase ventricular filling by relaxing obstructing muscle.
Calcuim channal blockers--> to increase ventricular filling by relaxing obstructing muscle.
Antiarrhymic drugs --> to control arrhytmias
Anti coagulants --> to reduce risk of systemic embolism with atrial fibrilation
Heart transplant --> to replace the damage heart
C. Dilated Cardiomyopathy
In patient with dilated cardiomyopathy the left ventricle become dilated, resulting in impaired contraction. Those are possible caused :
Chemotheraphy ---> Toxic effect of the drugs on the myocardial cell dilate the ventricles and they can not contract properly.
Alcohol and drugs ---> Direct toxic effect of alcohol on the myocytes( cardiac cells)
Coronary heart diseaes---> Decrease O2 delivery to the heart muscle leads to pump failure.
Valvular heary diseases ---> increased volume or increased resistance to out flow in the chamber of the heart over time distends the chambers and the muscle become stretched, thinned and weakened. ( See pic 2)
( pic:2 A=Normal heart B= Dilated Cardiomyopathy)
Signs and Symptoms
Clients will increasingly display signs and symptoms of heart failure
Peripheral edema , hepatomegaly, jugular vein distension, and weight gain.
Peripheral cyanosis, tachycardia, murmur, arrhythmia, chest pain, palpitation, syncope.
Test Diagnostic
Angiography --> to rule out ischemic heart disease
Chest X-ray --> will show moderate to marked cardiomegaly and pulmonary edema
Echocardiography --> to confirm degree of left ventricular dilation and dysfunction
EKG --> to rule out ischemic heart disease
Cardiac catheterization
Endomyocardial biopsy.
Treatment
O2 therapy
ACE Inhibitors --> to reduce afterload through vasodilation
Diuretic --> to reduce fluid retention
Beta-adrenergic blockers --> to reduce demand
Antiarrhymic drugs --> to control arrhytmias
Valvular repair or replacement --> to manage dilated cardimyopathy fro valve dysfunction
Heart transplant --> to replace the damage heart
Lifestyle modifications
Infectious cardiac disease
Infectious cardiac disease is a general term used to describe an infectious
disease process of the endocardium or lining of the heart. The most common is in the mitral valve site that is affected by the infection.Microorganisms, such as bacteria
or fungi. They entered through the blood and colonize on heart valves. This colonization
makes the site extremely resistant to antibiotic treatment. The presence of the thrombus on the valve, though, increases the likelihood of infection developing.
Thera are 2 type of infectious cardiac diseases :
1. Infective endocarditis
2. Pericarditis.
A. . Infective endocarditis
An infection of the endocardium, heart valves or any cardiac prosthosis is called infective endocarditis.
Bacteria is the common causing of infective endocarditis.
Once the microorganism begin to proliferate on the valve, it will form what we called vegetation or purulent stuff attached to the heart valve. The bacteria than can attached or attack the heart are streptococci, staphylococci also fungi. Others causes of infective cendocarditis are prosthetic valve, long term indwelling catheters,recent cardiac surgery, rheumatic heart diseases, congenital heart defect, valvular dysfunction, IV druigs abuse.
Signs and symtomps :
Fever, splenomegaly, petechia, hematuria, cardiac murmur,pleuritic pain, fatigue and weakness. In the late symptoms is found signs left heart failure
B Pericarditis
If there is any inflamation in the sac surrounding the heart and this area becoming roughened and scarred. This condition is called acut pericarditis. Pericarditis will guide to perform exudate and pericardial effusion are possible.
See picture
Causes :
Myocardiac infarction --> The inflammatory response will activate the mediators migrate to the injury area as caused by myocardiac infarction. The chemical mediator such as histamine, prostaglandins, bradykinins, serotonin are cause vasodilation and increase capillary permeability. Increasing in the capillary permeability will alow some substance such as protein, RBCs leak to the tissue.
So it will make the inner and outermost linings become roughened and scarred.
Radiation--> If any damage from radiation causes activation of the imflammatory response.
Bacterial, fungal or viral infection, autoimmune disorders, previous trauma or cardiac surgery.
Signs and Symptomps
Pericardial friction rub --> the scraping together of the inner and outermost layers produce a sound called friction rub.
Dyspagia --> the pressure on the nerve ending suppling the esophagus
Chest pain --> any inflammation process will stimulate the pain receptors in the heart.
Chronic Pericarditis
Chronic pericarditis is the result of continued irritation to the pericardial lining. The lining becomes thickened and stiff and the client may develop restrictive pericarditis.
Signs and symptoms :
Weakness also with signs of right side heart failure
disease process of the endocardium or lining of the heart. The most common is in the mitral valve site that is affected by the infection.Microorganisms, such as bacteria
or fungi. They entered through the blood and colonize on heart valves. This colonization
makes the site extremely resistant to antibiotic treatment. The presence of the thrombus on the valve, though, increases the likelihood of infection developing.
Thera are 2 type of infectious cardiac diseases :
1. Infective endocarditis
2. Pericarditis.
A. . Infective endocarditis
An infection of the endocardium, heart valves or any cardiac prosthosis is called infective endocarditis.
Bacteria is the common causing of infective endocarditis.
Once the microorganism begin to proliferate on the valve, it will form what we called vegetation or purulent stuff attached to the heart valve. The bacteria than can attached or attack the heart are streptococci, staphylococci also fungi. Others causes of infective cendocarditis are prosthetic valve, long term indwelling catheters,recent cardiac surgery, rheumatic heart diseases, congenital heart defect, valvular dysfunction, IV druigs abuse.
Signs and symtomps :
Fever, splenomegaly, petechia, hematuria, cardiac murmur,pleuritic pain, fatigue and weakness. In the late symptoms is found signs left heart failure
B Pericarditis
If there is any inflamation in the sac surrounding the heart and this area becoming roughened and scarred. This condition is called acut pericarditis. Pericarditis will guide to perform exudate and pericardial effusion are possible.
See picture
Causes :
Myocardiac infarction --> The inflammatory response will activate the mediators migrate to the injury area as caused by myocardiac infarction. The chemical mediator such as histamine, prostaglandins, bradykinins, serotonin are cause vasodilation and increase capillary permeability. Increasing in the capillary permeability will alow some substance such as protein, RBCs leak to the tissue.
So it will make the inner and outermost linings become roughened and scarred.
Radiation--> If any damage from radiation causes activation of the imflammatory response.
Bacterial, fungal or viral infection, autoimmune disorders, previous trauma or cardiac surgery.
Signs and Symptomps
Pericardial friction rub --> the scraping together of the inner and outermost layers produce a sound called friction rub.
Dyspagia --> the pressure on the nerve ending suppling the esophagus
Chest pain --> any inflammation process will stimulate the pain receptors in the heart.
Chronic Pericarditis
Chronic pericarditis is the result of continued irritation to the pericardial lining. The lining becomes thickened and stiff and the client may develop restrictive pericarditis.
Signs and symptoms :
Weakness also with signs of right side heart failure
Cardiac Tamponade
Cardiac tamponade
is caused by collection or accumulation of fluid or blood between the
two layers of the pericardium. It is the most serious complication of
pericarditis.
What causes it :
Trauma to the chest --> Cardiac contusion may occur. (Bruising of the heart muscle.) Blood and fluid leak into the pericardial sac.
Myocardial infarction --> Inflammation at the site of the infarction leads to increased capillary permeability. Fluid can leak into the pericardial sac resulting in a tamponade.
Cardiac bypass surgery --> Normally blood and fluid accumulate around the heart after heart surgery. Sometimes, though, one of the sutures to a graft may burst. This may cause sudden accumulation of blood in the mediastinum, resulting in a cardiac tamponade
Signs and symptoms :
Jugular vein distension (JVD) --> Heart is “squeezed” so blood cannot fill heart. Instead blood backs up into venous system, causing distension of jugular vein.
Drop in blood pressure The heart squeezes -->CO drops --> decreased forward flow of volume. Remember: less volume, less pressure.
Muffled heart sounds --> Fluid accumulates around the heart muffling heart sounds.
Pulsus paradoxus --> Blood pressure drops more than 10 mm Hg with inspiration. This is because with inspiration there is even more pressure “squeezing” down on heart.
Change in level of consciousness --> Decreased head perfusion due to drop (LOC) in CO.
Increased HR --> Compensation for drop in CO
Edema --> Blood backing up into the venous system
Tests Diagnostic :
Chest x-ray: widened mediastinum due to blood accumulation.
Echocardiography: detects compression of the heart, variation in blood flow in heart that occurs with breathing; shows fluid accumulation.
Electrocardiography: fast, slow, or normal HR with no pulse.
Treatments:
Echocardiography: monitors fluid removal.
Pericardiocentesis: removes fluid from the pericardium.
Percutaneous balloon pericardiotomy: drains fluid using a balloon-tipped
catheter inserted through the skin.
Subxiphoid limited pericardiotomy: drains fluid using a balloon-tipped
catheter inserted through a small incision in the chest.
Pericardiectomy: removal of the pericardium.
Sclerotheraphy: obliterates the pericardium by causing scar tissue
to form.
Oxygen therapy: increases oxygenation and tissue perfusion.
Intravascular volume expansion: increases blood volume and
oxygenation.
Inotropic agents: controls heart rate and decreases atrial fibrillation.
What can harm my client?
A sudden accumulation of fluid in the pericardial sac or mediastinum is a medical emergency.
Cardiogenic shock.
Death.
What to do?
Assessment for cardiac output.
Clients at risk for cardiac tamponade.
Causes and why.
Signs and symptoms and why.
Pre- and postop care.
IV administration and complications.
Patient teaching regarding bed rest, when to notify the doctor, and
postop infection prevention.
What causes it :
Trauma to the chest --> Cardiac contusion may occur. (Bruising of the heart muscle.) Blood and fluid leak into the pericardial sac.
Myocardial infarction --> Inflammation at the site of the infarction leads to increased capillary permeability. Fluid can leak into the pericardial sac resulting in a tamponade.
Cardiac bypass surgery --> Normally blood and fluid accumulate around the heart after heart surgery. Sometimes, though, one of the sutures to a graft may burst. This may cause sudden accumulation of blood in the mediastinum, resulting in a cardiac tamponade
Signs and symptoms :
Jugular vein distension (JVD) --> Heart is “squeezed” so blood cannot fill heart. Instead blood backs up into venous system, causing distension of jugular vein.
Drop in blood pressure The heart squeezes -->CO drops --> decreased forward flow of volume. Remember: less volume, less pressure.
Muffled heart sounds --> Fluid accumulates around the heart muffling heart sounds.
Pulsus paradoxus --> Blood pressure drops more than 10 mm Hg with inspiration. This is because with inspiration there is even more pressure “squeezing” down on heart.
Change in level of consciousness --> Decreased head perfusion due to drop (LOC) in CO.
Increased HR --> Compensation for drop in CO
Edema --> Blood backing up into the venous system
Tests Diagnostic :
Chest x-ray: widened mediastinum due to blood accumulation.
Echocardiography: detects compression of the heart, variation in blood flow in heart that occurs with breathing; shows fluid accumulation.
Electrocardiography: fast, slow, or normal HR with no pulse.
Treatments:
Echocardiography: monitors fluid removal.
Pericardiocentesis: removes fluid from the pericardium.
Percutaneous balloon pericardiotomy: drains fluid using a balloon-tipped
catheter inserted through the skin.
Subxiphoid limited pericardiotomy: drains fluid using a balloon-tipped
catheter inserted through a small incision in the chest.
Pericardiectomy: removal of the pericardium.
Sclerotheraphy: obliterates the pericardium by causing scar tissue
to form.
Oxygen therapy: increases oxygenation and tissue perfusion.
Intravascular volume expansion: increases blood volume and
oxygenation.
Inotropic agents: controls heart rate and decreases atrial fibrillation.
What can harm my client?
A sudden accumulation of fluid in the pericardial sac or mediastinum is a medical emergency.
Cardiogenic shock.
Death.
What to do?
Assessment for cardiac output.
Clients at risk for cardiac tamponade.
Causes and why.
Signs and symptoms and why.
Pre- and postop care.
IV administration and complications.
Patient teaching regarding bed rest, when to notify the doctor, and
postop infection prevention.
ARTERIOSCLEROSIS
Arteriosclerosis means “hardening of the arteries” and is a general term describing three diseases:
1. Atherosclerosis, in which there is a proliferation of smooth muscle cells and accumulation of lipids in the intima of the large and middle-sized muscular arteries.
2. Medical calcific sclerosis, or Mönckeberg's sclerosis, in which there is an accumulation of calcium in the media of medium-sized arteries.
3. Arteriolar sclerosis, in which there is thickening of the walls and narrowing of the lumen of the small arteries and arterioles, leading to reduced or blocked blood flow and which is often associated with hypertension.
Caused & Why
Repeated injury to the artery wall --> Immune system involvement or direct
toxicity allows materials to deposit on the artery’s inner lining.
High cholesterol High --> levels of cholesterol in the blood injure the artery’s lining, causing an
inflammatory response, allowing cholesterol and other fatty materials to deposit.
Infection due to bacteria or virus --> Damages the lining of the artery’s wall,
encouraging deposits to form.
Atheromas (patchy deposits of fatty material) --> Form where the arteries branch because
of fatty material) the artery’s wall is injured from constant turbulent blood flow.
There are many risk factors associated with atherosclerosis including:
Smoking --> It will decrease high-density lipoprotein (HDL), the good stuff,
and increases the bad stuff, low-density lipoprotein (LDL).
High cholesterol --> risk of heart attack increases when the HDL and
LDL are out of whack.
High blood pressure --> uncontrolled high blood pressure can lead to
heart attack or stroke.
Diabetes mellitus --> the risk for developing atherosclerosis is 2 to 6 times
higher in diabetics because sugar deposits just like fat.
Obesity --> abdominal (truncal) obesity increases the risk for diabetes,
hypertension, and coronary artery disease (CAD).
Physical inactivity --> leads to obesity, high blood pressure, and CAD.
High blood levels of homocysteine --> homocysteine (an amino acid)
may directly injure the lining of the arteries, making the formation of
atheromas more likely.
Signs & symptoms
High blood pressure --> Atheromas grow, causing narrowing of the arteries and calcium accumulation in the arteries.
Decreased peripheral pulses --> Decreased elasticity of the arteries and the narrowed lumen contribute to decreased peripheral circulation.
Angina --> Arteries that supply the heart are narrowed.
Leg cramps (intermittent claudication) --> Narrowing of arteries in the legs.
Stroke --> Blockage of the arteries supplying the brain.
Heart attack --> Arteries supplying the heart are blocked.
Kidney failure --> Arteries supplying one or both kidneys become narrowed or blocked.
Malignant hypertension --> Dangerously high blood pressure caused by narrowing of the arteries.
Tests:
Blood pressure --> monitors hypertension.
Lipid profile --> cholesterol below 200 mg/dL is desired.
Coronary angiography --> shows location and degree of coronary artery stenosis or obstruction, circulation, and condition of the artery beyond the narrowing.
Electrocardiography --> evaluates damaged heart muscle and if there is adequate blood supply.
Cardiac catheterization --> confirms presence of hardening of arteries.
Intravascular ultrasound --> views the inside walls of the arteries.
Nuclear imaging --> dye shows area of blockage.
Exercise stress test --> determines if angiography or coronary artery bypass surgery (CABS) is needed.
Holter monitor --> detects silent ischemia and angina.
Treatements:
Lifestyle modifications: low-fat, low-sodium, high-fiber diet; decreased
alcohol intake; smoking cessation; weight loss program; exercise program.
Nitrates: decrease cardiac pain caused by angina by vasodilating the
coronary arteries, therefore supplying more blood to actual heart muscle.
Antihypertensives: lower blood pressure.
Anticoagulants: prevent blood clots.
Percutaneous transluminal coronary angioplasty (PTCA): balloon compresses fatty plaque or blockage against vessel wall to widen diameter of blood vessel and increase blood flow.
Balloon angioplasty with stenting: stent expands to the size of the artery and holds it open.
Calcium-channel blockers: lower blood pressure.
Angiotensin-converting enzyme (ACE) inhibitors: widen bloods vessels, lower blood pressure.
Beta blocker: reduce blood pressure and improve circulation.
Antiplatelets: prevent platetelets from sticking together and blocking vessels.
What can harm my client?
Stroke.
Heart attack.
Kidney failure.
Malignant hypertension.
Peripheral artery disease.
1. Atherosclerosis, in which there is a proliferation of smooth muscle cells and accumulation of lipids in the intima of the large and middle-sized muscular arteries.
2. Medical calcific sclerosis, or Mönckeberg's sclerosis, in which there is an accumulation of calcium in the media of medium-sized arteries.
3. Arteriolar sclerosis, in which there is thickening of the walls and narrowing of the lumen of the small arteries and arterioles, leading to reduced or blocked blood flow and which is often associated with hypertension.
Caused & Why
Repeated injury to the artery wall --> Immune system involvement or direct
toxicity allows materials to deposit on the artery’s inner lining.
High cholesterol High --> levels of cholesterol in the blood injure the artery’s lining, causing an
inflammatory response, allowing cholesterol and other fatty materials to deposit.
Infection due to bacteria or virus --> Damages the lining of the artery’s wall,
encouraging deposits to form.
Atheromas (patchy deposits of fatty material) --> Form where the arteries branch because
of fatty material) the artery’s wall is injured from constant turbulent blood flow.
There are many risk factors associated with atherosclerosis including:
Smoking --> It will decrease high-density lipoprotein (HDL), the good stuff,
and increases the bad stuff, low-density lipoprotein (LDL).
High cholesterol --> risk of heart attack increases when the HDL and
LDL are out of whack.
High blood pressure --> uncontrolled high blood pressure can lead to
heart attack or stroke.
Diabetes mellitus --> the risk for developing atherosclerosis is 2 to 6 times
higher in diabetics because sugar deposits just like fat.
Obesity --> abdominal (truncal) obesity increases the risk for diabetes,
hypertension, and coronary artery disease (CAD).
Physical inactivity --> leads to obesity, high blood pressure, and CAD.
High blood levels of homocysteine --> homocysteine (an amino acid)
may directly injure the lining of the arteries, making the formation of
atheromas more likely.
Signs & symptoms
High blood pressure --> Atheromas grow, causing narrowing of the arteries and calcium accumulation in the arteries.
Decreased peripheral pulses --> Decreased elasticity of the arteries and the narrowed lumen contribute to decreased peripheral circulation.
Angina --> Arteries that supply the heart are narrowed.
Leg cramps (intermittent claudication) --> Narrowing of arteries in the legs.
Stroke --> Blockage of the arteries supplying the brain.
Heart attack --> Arteries supplying the heart are blocked.
Kidney failure --> Arteries supplying one or both kidneys become narrowed or blocked.
Malignant hypertension --> Dangerously high blood pressure caused by narrowing of the arteries.
Tests:
Blood pressure --> monitors hypertension.
Lipid profile --> cholesterol below 200 mg/dL is desired.
Coronary angiography --> shows location and degree of coronary artery stenosis or obstruction, circulation, and condition of the artery beyond the narrowing.
Electrocardiography --> evaluates damaged heart muscle and if there is adequate blood supply.
Cardiac catheterization --> confirms presence of hardening of arteries.
Intravascular ultrasound --> views the inside walls of the arteries.
Nuclear imaging --> dye shows area of blockage.
Exercise stress test --> determines if angiography or coronary artery bypass surgery (CABS) is needed.
Holter monitor --> detects silent ischemia and angina.
Treatements:
Lifestyle modifications: low-fat, low-sodium, high-fiber diet; decreased
alcohol intake; smoking cessation; weight loss program; exercise program.
Nitrates: decrease cardiac pain caused by angina by vasodilating the
coronary arteries, therefore supplying more blood to actual heart muscle.
Antihypertensives: lower blood pressure.
Anticoagulants: prevent blood clots.
Percutaneous transluminal coronary angioplasty (PTCA): balloon compresses fatty plaque or blockage against vessel wall to widen diameter of blood vessel and increase blood flow.
Balloon angioplasty with stenting: stent expands to the size of the artery and holds it open.
Calcium-channel blockers: lower blood pressure.
Angiotensin-converting enzyme (ACE) inhibitors: widen bloods vessels, lower blood pressure.
Beta blocker: reduce blood pressure and improve circulation.
Antiplatelets: prevent platetelets from sticking together and blocking vessels.
What can harm my client?
Stroke.
Heart attack.
Kidney failure.
Malignant hypertension.
Peripheral artery disease.
Anatomy Fisiology Of The Heart
A. The Heart
In the embryo,the heart begin to beat at 4 weeks of age, even before its nerve supply has been estabilished. If a person lives to be 80 years old, your heart continues to beat an average of 100,000 time a day, every day for each of those 80 years. Imagine trying to squeeze a tennis ball 70 times a minute. After few minutes your arm muscles would begin to tire, then imagine increasing your squeezing rate to 120 times a minute. Most of us could not keep that up very long, but that is what the heart does during exercise. So, A healthy human heart can increase its rate and force of contraction to meet the body`s need for more oxygen.
The primary function of the heart is as single pump for pumping the blood through the arteries, capillaries,and veins. As you known the blood transport oxygen,nutrients and has other important function as well, also the heart is the pump that keeps blood circulation properly.
Your heart is positioned obliquely between the lungs in the space of mediastinum. About twothirds of its bulk lies to the left side of the midline of the body. It is shaped like a blunt cone. It Is about the size of a closed fist. It is approximately 5 inches long (12 cm), 3.5 inches wide at its broadest point (9 cm), and 2.5 inches thick (6 cm).
B. Structure Of The Heart
The heart is composed of 3 layers of tissue (see picture 1) :
• Pericardium
• Myocardium
• Endocardium.
(pic : 1)
Pericardium
The pericardium is made up of two sacs. The outer sac consists of fibrous tissue and the inner of a continuous double layer of serous membrane. The outer fibrous sac is continuous with the tunica adventitia of the great blood vessels above and is adherent to the diaphragm below. Its inelastic, fibrous nature prevents overdistension of the heart.
The outer layer of the serous membrane is the parietal pericardium or lines the fibrous sac. The inner layer is the visceral pericardium, or epicardium, which is continuous with the parietal pericardium, is adherent to the heart muscle. A similar arrangement of a double membrane
forming a closed space is seen also with the pleura, the membrane enclosing the lungs.
The serous membrane consists of flattened epithelialcells. It is the secretes serous fluid into the space between the visceral and parietal layers which allows smooth movement between them when the heart beats. The space between the parietal and visceral pericardium is only a potential space. In health the two layers are in close association, with only the thin film of serous fluid between them. It is named pericardium serous (abaut 20-50 ml).
Myocardium
The myocardium is composed of specialised cardiac muscle found only in the heart. It is notunder voluntary control but, like skeletal muscle, cross-stripes are seen on microscopic examination. Each fibre (cell) has a nucleus and one or more branches. The ends of the cells and their branches are in very close contact with the ends and branches of adjacent cells.
Microscopically these 'joints', or intercalated discs, can be seen as thicker and darker lines than the ordinary cross-stripes. This arrangement will give heart muscle the appearance of being a sheet of muscle rather than a very large number of individual cells. Because of the end-to-end continuity of the fibres, each one does not need to have a separate nerve supply.When an impulse is initiated it spreads from cell to cell via the branches and intercalated discs over the whole 'sheet' of muscle that causing heart muscle contraction. So the 'sheet' arrangement of the myocardium enables the atria and ventricles to contract in a coordinated and efficient manner.
The myocardium is thickest at the apex and thins out towards the base. This reflects the amount of work each chamber contributes for pumping of the blood. The left ventricle is thickest than left ventricle. The atria and the ventricles are separated by a ring of fibrous tissue that does not conduct electrical impulses. Consequently, when a wave of electrical activity passes over the atrial muscle, it can only spread to the ventricles through the conducting system which bridges the fibrous ring from atria to ventricles.
Endocardium
This forms the lining of the myocardium and the heart valves. It is a thin, smooth and glistening membrane which permits smooth flow of blood inside the heart. It consists of flattened epithelial cells and connected with the endothelium that lines the blood vessels.
C. The Chambers of the Heart
The four chambers of the heart are made of cardiac muscle called the myocardium. The chambers are lined with endocardium, simple squamous epithelium that also covers the valves of the heart and continues into the vessels as their lining (endothelium). The important physical characteristic of the endocardium is not thinness, but rather its smoothness.
This very smooth tissue prevents abnormal blood clotting, because clotting would be initiated by
contact of blood with a rough surface.
The upper chambers of the heart are the right and left atria (or atrium), which have relatively thin walls and are separated by a common wall of myocardium called the interatrial septum. The lower chambers are the right and left ventricles, which have more thicker walls than atrial wall and separated by the interventricular septum. Look at the picture below, the atria receive blood, either from the body or the lungs, and the ventricles pump blood to either the lungs or the
body.(see picture 2)
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Right Atrium
The two large caval veins return blood from the body to the right atrium. The superior vena cava carries blood from the upper body, and the inferior vena cava carries blood from the lower body and sinus coronary from the heart itself. From the right atrium, blood will flow through the right atrioventricular (AV) valve, or tricuspid valve, into the right ventricle. The tricuspid valve is made of three flaps (or cusps) of endocardium reinforced with connective tissue. The general purpose of all valves in the circulatory system is to prevent backflow of blood during or abaut to systolic occur.
The specific purpose of the tricuspid valve is to prevent backflow of blood from the right ventricle to the right atrium when the right ventricle contracts. As the ventricle contracts, blood is forced behind the three valve flaps, forcing them upward and together to close the valve.
Left Atrium
The left atrium receives blood from the lungs, by way of four pulmonary veins. This blood will then flow into the left ventricle through the left atrioventricular (AV) valve, also called the mitral valve or bicuspid (two flaps) valve. The mitral valve prevents backflow of blood from the left ventricle to the left atrium when the left ventricle contracts.
Another function of the atria is the production of a hormone involved in blood pressure maintenance. When the walls of the atria are stretched by increased blood volume or blood pressure, the cells produce atrial natriuretic peptide (ANP), also called atrial natriuretic hormone (ANH). (The ventricles of the heart produce a similar hormone called B-type natriuretic peptide, or BNP, but we will use ANP as the representative cardiac hormone.) ANP decreases the reabsorption of sodium ions by the kidneys, so that more sodium ions are excreted in urine and retained some potassium.
Right Ventricle
When the right ventricle contracts, automaticlly the tricuspid valve will closes and the blood is pumped to the lungs through the pulmonary artery (or trunk). At the junction of this large artery and the right ventricle is the pulmonary semilunar valve (or more simply, pulmonary valve). Its three flaps are forced open when the right ventricle contracts and pumps blood into the pulmonary artery. When the right ventricle relaxes, blood tends to come back, but this fills the valve flaps and closes the pulmonary valve to prevent backflow of blood into the right ventricle. Projecting into the lower part of the right ventricle are columns of myocardium called papillary muscles. Strands of fibrous connective tissue, the chordae tendineae, extend from the papillary muscles to the flaps of the tricuspid valve. When the right ventricle contracts, the papillary muscles also contract and pull on the chordae tendineae to prevent inversion of the tricuspid valve. So If you have ever had your umbrella blown inside out by a strong wind, you will see what would happen if the flaps of the tricuspid valve were not anchored by the chordae tendineae and papillary muscles.
Left Ventricle
The walls of the left ventricle are thicker than those of the right ventricle, which enables the left ventricle to contract more forcefully. The left ventricle pumps blood to the body through the aorta, the largest artery of the body. At the junction of the aorta and the left
ventricle is the aortic semilunar valve (or aortic valve). This valve is opened by the force of contraction of the left ventricle, which also closes the mitral valve.
The aortic valve closes when the left ventricle relaxes, to prevent backflow of blood from the aorta to the left ventricle. When the mitral (left AV) valve closes, it prevents backflow of blood to the left atrium; the flaps of the mitral valve are also anchored by chordae tendineae and papillary muscles. All of the valves are connected to the fibrous skeleton of the heart. This is fibrous connective tissue that anchors the outer edgesof the valve flaps and keeps the valve openings from stretching. It also separates the myocardium of the atria and ventricles and prevents the contraction of the atria from reaching the ventricles except by way of the normal conduction pathway.
D. Artery Coronary
The right and left coronary arteries are the first branches of the ascending aorta, just on the aortic semilunar valve. The two arteries branch into smaller arteries and arterioles, then to capillaries. The coronary capillaries merge to form coronary veins, which empty blood into a large coronary sinus that returns blood to the right atrium. (see picture 3)
The purpose of the coronary vessels is to supply blood to the myocardium itself, because oxygen is essential for normal myocardial contraction. If a coronary artery becomes obstructed, by a blood clot for example, part of the myocardium becomes ischemic, that is the deprived of its blood supply.
Prolonged ischemia will create an infarct, an area of necrotic (dead) tissue. This is a myocardial infarction, commonly called a heart attack.
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D. Cardiac Cycle
The function of the heart is to maintain a constant circulation of blood throughout the body which needed for metabolism. The heart acts as a pump and its action consists of a series of events known as the cardiac cycle. During each heartbeat, or cardiac cycle, the heart contracts and then relaxes. The period of contraction is called systole and that of relaxation, diastole.
Stages of the cardiac cycle
The normal number of cardiac cycles per minute ranges from 60 to 80. Taking 74 as an example each cycle lasts about 0.8 of a second and consists of:
• atrial systole — contraction of the atria
• ventricular systole — contraction of the ventricles
• complete cardiac diastole — relaxation of the atria and ventricles.
It does not matter at which stage of the cardiac cycle a description starts. For convenience the period when the atria are filling has been chosen. The superior vena cava and the inferior vena cava transport deoxygenated blood into the right atrium at the same time as the four pulmonary veins conveyoxygenated blood into the left atrium. The atrioventricular valves are open and blood flows through to the ventricles.
The SA node triggers a wave of contraction that spreads over the myocardium of both atria, emptying the atria and completing ventricular filling (atrial systole 0.1 s). When the wave of contraction reaches the AV node it is stimulated to make an impulse which fastly or very fast spreading to the ventricular muscle via the AV bundle, the bundle branches and Purkinje fibres. This results in a wave of contraction which sweeps upwards from the apex of the heart and across the walls of both ventricles pumping the blood into the pulmonary artery and the aorta (ventricular
systole 0.3 s). The high pressure generated during ventricular contraction is greater than that in the aorta and forces the atrioventricular valves to close, preventing backflow of blood into the atria
After contraction of the ventricles there is complete cardiac diastole, a period of 0.4 seconds, when atria and ventricles are relaxed. During this time the myocardium
recovers until it is able to contract again, and the atria refill in preparation for the next cycle.
The valves of the heart and of the great vessels open and close according to the pressure within the chambers of the heart.
The AV valves are opened while the ventricular muscle is relaxed during atrial filling and systole. When the ventricles contract there is a gradual increase in the pressure in these chambers, and when it rises above atrial pressure the atrioventricular valves close. When the ventricular
pressure rises above that in the pulmonary artery and in the aorta, the pulmonary and aortic valves open and blood flows into these vessels. When the ventricles relax and the pressure within them falls, the reverse process occurs. First the pulmonary and aortic valvesclose, then the atrioventricular valves open and the cycle begins again. This sequence of opening and closing valves ensures that the blood flows in only one direction.
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