ASUHAN KEPERAWATAN SYOK KARDIOGENIK PDF

Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. If you continue browsing the site, you agree to the use of cookies on this website. See our User Agreement and Privacy Policy. See our Privacy Policy and User Agreement for details.

Author:Vogar Shakabar
Country:Lithuania
Language:English (Spanish)
Genre:Art
Published (Last):4 April 2018
Pages:18
PDF File Size:4.57 Mb
ePub File Size:9.43 Mb
ISBN:415-3-24089-976-8
Downloads:72853
Price:Free* [*Free Regsitration Required]
Uploader:Tugore



To browse Academia. Skip to main content. By using our site, you agree to our collection of information through the use of cookies. To learn more, view our Privacy Policy.

Log In Sign Up. Sri Asmawati. Hemorrhagic or Hypovolemic Shock The most common cause of shock in the surgical or trauma patient is loss of circulating volume from hemorrhage. Acute blood loss results in reflexive decreased baroreceptor stimulation from stretch receptors in the large arteries, resulting in decreased inhibition of vasoconstrictor centers in the brain stem, increased chemoreceptor stimulation of vasomotor centers, and diminished output from atrial stretch receptors.

These changes increase vasoconstriction and peripheral arterial resistance. Hypovolemia also induces sympathetic stimulation, leading to epinephrine and norepinephrine release, activation of the renin- angiotensin cascade, and increased vasopressin release. Peripheral vasoconstriction is prominent, while lack of sympathetic effects on cerebral and coronary vessels and local autoregulation promote maintenance of cardiac and CNS blood flow.

Penyebab paling umum syok pada pasien bedah atau trauma adalah hilangnya volume sirkulasi dari perdarahan. Hasil kehilangan darah akut di refleksif penurunan stimulasi baroreseptor dari peregangan reseptor di arteri besar, yang mengakibatkan penurunan penghambatan pusat vasokonstriktor di batang otak, meningkatkan stimulasi kemoreseptor pusat vasomotor, dan output berkurang dari atrium stretch reseptor. Perubahan ini meningkatkan vasokonstriksi dan resistensi arteri perifer.

Hipovolemia juga menginduksi stimulasi simpatis, yang menyebabkan epinefrin dan norepinefrin rilis, aktivasi kaskade renin-angiotensin, dan peningkatan pelepasan vasopressin.

Vasokonstriksi perifer adalah menonjol, sementara kurangnya efek simpatik pada pembuluh darah serebral dan koroner dan autoregulasi lokal mempromosikan pemeliharaan aliran darah jantung dan SSP.

Diagnosis Treatment of shock is initially empiric. The airway must be secured and volume infusion for restoration of blood pressure initiated while the search for the cause of the hypotension is pursued.

Shock in a trauma patient and postoperative patient should be presumed to be due to hemorrhage until proven otherwise. The clinical signs of shock may be evident with an agitated patient, including cool clammy extremities, tachycardia, weak or absent peripheral pulses, and hypotension. However, substantial volumes of blood may be lost before the classic clinical manifestations of shock are evident. Thus when a patient is significantly tachycardiac or hypotensive, this represents both significant blood loss and physiologic decompensation.

The clinical and physiologic response to hemorrhage has been classified according to the magnitude of volume loss. Hypotension, marked tachycardia [i. Young healthy patients with vigorous compensatory mechanisms may tolerate larger volumes of blood loss while manifesting fewer clinical signs despite the presence of significant peripheral hypoperfusion.

These patients may maintain a near-normal blood pressure until a precipitous cardiovascular collapse occurs. Elderly patients may be taking medications that either promote bleeding e. Jalan nafas harus diamankan dan volume infus untuk pemulihan tekanan darah dimulai ketika mencari penyebab hipotensi ini dikejar.

Syok pada pasien trauma dan pasien pasca operasi harus dianggap disebabkan oleh perdarahan sampai terbukti sebaliknya. Tanda- tanda klinis syok mungkin jelas dengan pasien gelisah, termasuk ekstremitas dingin berkeringat, takikardia, denyut perifer lemah atau tidak ada, dan hipotensi. Namun, volume besar darah mungkin akan hilang sebelum manifestasi klinis klasik syok yang jelas. Jadi ketika pasien secara signifikan tachycardiac atau hipotensi, ini merupakan kedua kehilangan darah yang signifikan dan dekompensasi fisiologis.

Respon klinis dan fisiologis perdarahan telah diklasifikasikan menurut besarnya penyusutan volume. Pasien sehat muda dengan mekanisme kompensasi yang kuat dapat mentolerir volume yang lebih besar kehilangan darah saat mewujudkan tanda-tanda klinis lebih sedikit meskipun kehadiran hipoperfusi perifer yang signifikan. Pasien-pasien ini mungkin mempertahankan tekanan darah mendekati normal sampai kolaps kardiovaskular terjal terjadi.

Lansia pasien dapat mengambil obat yang baik mempromosikan perdarahan misalnya, warfarin atau aspirin , atau menutupi tanggapan kompensasi untuk perdarahan misalnya, beta blockers. Selain itu, penyakit aterosklerosis vaskular, kepatuhan jantung berkurang dengan usia, ketidakmampuan untuk meningkatkan denyut jantung atau kontraktilitas jantung sebagai respons terhadap perdarahan, dan penurunan keseluruhan dalam cadangan fisiologis menurunkan kemampuan pasien lansia untuk mentolerir perdarahan.

Treatment Control of ongoing hemorrhage is an essential component of the resuscitation of the patient in shock. As mentioned above, treatment of hemorrhagic shock is instituted concurrently with diagnostic evaluation to identify a source.

Patients who fail to respond to initial resuscitative efforts should be assumed to have ongoing active hemorrhage from large vessels and require prompt operative intervention. The appropriate priorities in these patients are 1 secure the airway, 2 control the source of blood loss, and 3 intravenous volume resuscitation. Identifying the body cavity harboring active hemorrhage will help focus operative efforts; however, because time is of the essence, rapid treatment is essential and diagnostic laparotomy or thoracotomy may be indicated.

The actively bleeding patient cannot be resuscitated until control of ongoing hemorrhage is achieved. Patients who respond to initial resuscitative efforts, but then deteriorate hemodynamically, frequently have injuries that require operative intervention.

The magnitude and duration of their response will dictate whether diagnostic maneuvers can be performed to identify the site of bleeding. However, hemodynamic deterioration generally denotes ongoing bleeding for which some form of intervention i. Patients who have lost significant intravascular volume, but hemorrhage is controlled or abated, will often respond to resuscitative efforts if the depth and duration of shock have been limited.

Seperti disebutkan di atas, pengobatan syok hemoragik dilembagakan bersamaan dengan evaluasi diagnostik untuk mengidentifikasi sumber.

Pasien yang gagal untuk merespon paraf upaya resusitasi harus diasumsikan memiliki perdarahan aktif yang sedang berlangsung dari kapal- kapal besar dan memerlukan intervensi operasi prompt. Prioritas yang tepat pada pasien ini adalah 1 mengamankan jalan nafas, 2 mengontrol sumber kehilangan darah, dan 3 intravena resusitasi volume. Mengidentifikasi rongga tubuh menyimpan perdarahan aktif akan membantu memfokuskan upaya operasi; Namun, karena waktu adalah esensi, pengobatan cepat sangat penting dan laparotomi diagnostik atau torakotomi dapat diindikasikan.

Pasien secara aktif perdarahan tidak dapat diresusitasi sampai kontrol perdarahan yang sedang berlangsung dicapai. Pasien yang merespon paraf upaya resusitasi, tapi kemudian memburuk hemodinamik, sering memiliki cedera yang memerlukan intervensi operasi. Besarnya dan durasi respon mereka akan menentukan apakah manuver diagnostik dapat dilakukan untuk mengidentifikasi lokasi perdarahan. Namun, penurunan hemodinamik umumnya menunjukkan perdarahan yang sedang berlangsung yang beberapa bentuk intervensi yaitu, operasi atau radiologi intervensi diperlukan.

Pasien yang telah kehilangan volume intravaskular yang signifikan, namun perdarahan yang dikendalikan atau berkurang, akan sering merespon resusitasi upaya jika kedalaman dan durasi renjatan telah terbatas. Cardiogenic Shock Cardiogenic shock is defined clinically as circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia, in the setting of adequate intravascular volume. Hemodynamic criteria include sustained hypotension i.

Acute, extensive myocardial infarction MI is the most common cause of cardiogenic shock; a smaller infarction in a patient with existing left ventricular dysfunction may also precipitate shock.

Conversely, cardiogenic shock is the most common cause of death in patients hospitalized with acute MI. Although shock may develop early after myocardial infarction, it is typically not found on admission. Seventy-five percent of patients who have cardiogenic shock complicating acute MIs develop signs of cardiogenic shock within 24 hours after onset of infarction average 7 hours.

Recognition of the patient with occult hypoperfusion is critical to prevent progression to obvious cardiogenic shock with its high mortality rate; early initiation of therapy to maintain blood pressure and cardiac output is vital. Prevention of infarct extension is a critical component. Large segments of nonfunctional but viable myocardium contribute to the development of cardiogenic shock after MI.

In the setting of acute MI, expeditious restoration of cardiac output is mandatory to minimize mortality; the extent of myocardial salvage possible decreases exponentially with increased time to restoration of coronary blood flow. The degree of coronary flow after percutaneous transluminal coronary angioplasty PTCA correlates with in-hospital mortality i.

The pathophysiology of cardiogenic shock involves a vicious cycle of myocardial ischemia which causes myocardial dysfunction, which results in more myocardial ischemia. The majority of these patients have multivessel disease, with limited vasodilator reserve and pressure-dependent coronary flow in multiple areas of the heart. Myocardial diastolic function is impaired in cardiogenic shock as well. Decreased compliance results from myocardial ischemia, and compensatory increases in left ventricular filling pressures progressively occur.

Syok kardiogenik Syok kardiogenik didefinisikan secara klinis sebagai kegagalan pompa sirkulasi yang mengarah ke aliran maju berkurang dan hipoksia jaringan berikutnya, dalam pengaturan volume intravaskular yang memadai. Akut, infark miokard luas MI adalah penyebab paling umum syok kardiogenik; infark yang lebih kecil pada pasien dengan disfungsi ventrikel kiri yang ada juga bisa memicu shock. Sebaliknya, syok kardiogenik adalah penyebab paling umum kematian pada pasien rawat inap dengan MI akut.

Meskipun syok dapat berkembang awal setelah infark miokard, itu biasanya tidak ditemukan pada penerimaan. Tujuh puluh lima persen dari pasien yang memiliki syok kardiogenik rumit MI akut mengembangkan tanda-tanda syok kardiogenik dalam waktu 24 jam setelah onset infark rata-rata 7 jam. Pengakuan pasien dengan hipoperfusi okultisme sangat penting untuk mencegah timbulnya syok kardiogenik jelas dengan angka kematian yang tinggi; inisiasi awal terapi untuk mempertahankan tekanan darah dan curah jantung sangat penting.

Kajian cepat, resusitasi yang memadai, dan pembalikan iskemia miokard sangat penting dalam mengoptimalkan hasil pada pasien dengan MI akut. Pencegahan ekstensi infark adalah komponen penting. Segmen besar nonfungsional tapi layak miokardium berkontribusi pada pengembangan syok kardiogenik setelah MI.

Dalam pengaturan MI akut, pemulihan cepat dari curah jantung adalah wajib untuk meminimalkan tingkat kematian; tingkat penyelamatan miokard kemungkinan penurunan secara eksponensial dengan peningkatan waktu untuk pemulihan aliran darah koroner. Patofisiologi syok kardiogenik melibatkan lingkaran setan iskemia miokard yang menyebabkan disfungsi miokard, yang menghasilkan iskemia miokard lebih. Sebagian besar pasien ini memiliki penyakit multi, dengan cadangan vasodilator terbatas dan tekanan-tergantung aliran koroner di beberapa daerah jantung.

Fungsi diastolik miokard terganggu pada syok kardiogenik juga. Penurunan hasil kepatuhan dari iskemia miokard, dan peningkatan kompensasi dalam tekanan pengisian ventrikel kiri progresif terjadi. Diagnosis Rapid identification of the patient with pump failure and institution of corrective action are essential in preventing the ongoing spiral of decreased cardiac output from injury causing increased myocardial oxygen needs that cannot be met, leading to progressive and unremitting cardiac dysfunction.

In evaluation of possible cardiogenic shock, other causes of hypotension must be excluded, including hemorrhage, sepsis, pulmonary embolism, and aortic dissection. Signs of circulatory shock include hypotension, cool and mottled skin, depressed mental status, tachycardia, and diminished pulses.

Cardiac exam may include dysrhythmia, precordial heave, or distal heart tones. Confirmation of a cardiac source for the shock requires electrocardiogram and urgent echocardiography. Other useful diagnostic tests include chest radiograph, arterial blood gases, electrolytes, complete blood count, and cardiac enzymes. Invasive cardiac monitoring, which is generally not necessary, can be useful to exclude right ventricular infarction, hypovolemia, and possible mechanical complications.

Making the diagnosis of cardiogenic shock involves the identification of cardiac dysfunction or acute heart failure in a susceptible patient. Since patients with blunt cardiac injury typically have multisystem injury, hemorrhagic shock from intra-abdominal bleeding, intrathoracic bleeding, and bleeding from fractures must be excluded.

Relatively few patients with blunt cardiac injury will develop cardiac pump dysfunction. Those who do generally exhibit cardiogenic shock early in their evaluation. Therefore, establishing the diagnosis of blunt cardiac injury is secondary to excluding other etiologies for shock and establishing that cardiac dysfunction is present. Invasive hemodynamic monitoring with a pulmonary artery catheter may uncover evidence of diminished cardiac output and elevated pulmonary artery pressure.

Dalam evaluasi kemungkinan syok kardiogenik, penyebab lain dari hipotensi harus dikeluarkan, termasuk perdarahan, sepsis, emboli paru, dan diseksi aorta.

DETTOL HAND SANITIZER PDF

ASUHAN KEPERAWATAN PJK: ANGINA PEKTORIS DAN INFARK MIOKARDIUM

Thank you for interesting in our services. We are a non-profit group that run this website to share documents. We need your help to maintenance this website. Please help us to share our service with your friends.

BC307B DATASHEET PDF

DOWNLOAD ASUHAN KEPERAWATAN SYOK KARDIOGENIK

Pada klien yang dapat berbicara dapat dianggap jalan napas bersih. Dilakukan pula pengkajian adanya suara napas tambahan seperti snoring. Palpasi pengembangan paru, auskultasi suara napas, kaji adanya suara napas tambahan seperti ronchi, wheezing, dan kaji adanya trauma pada dada. Pengkajian juga meliputi status hemodinamik, warna kulit, nadi. Pola nafas tidak efektif berhubungan dengan gangguan pertukaran gas.

FORTUNATELY REMY CHARLIP PDF

Askep Icu Syok Kardiogenik

After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi typically travel more distally, occluding smaller vessels in the lung periphery. These are more likely to produce pleuritic chest pain by initiating an inflammatory response adjacent to the parietal pleura. Most pulmonary emboli are multiple, and the lower lobes are involved more commonly than the upper lobes. Factor V Leiden mutation causing resistance to activated protein C is the most common risk factor. Primary or acquired deficiencies in protein C, protein S, and antithrombin III are other risk factors. The risk of pulmonary embolism increases with prolonged bed rest or immobilization of a limb in a cast.

Related Articles