Jakarta, 28 Feb 2011

Manajemen Syok Hemoragik

Pendahuluan Syok adalah keadaan dimana terjadi kegagalan sistem kardiovaskuler yang menyebabkan gangguan perfusi jaringan, keadaan ini menyebabkan hipoksia, gangguan metabolisme seluler, kerusakan jaringan, gagal organ dan kematian. Patofisiologi syok perdarahan adalah terjadi kekurangan volume intravaskuler menyebabkan penurunan venous return sehingga terjadi penurunan pengisian ventrikel, menyebabkan penurunan stroke volume dan cardiac output, sehingga menyebabkan gangguan perfusi jaringan . Resusitasi pada syok perdarahan akan mengurangi angka kematian. Pengelolaan syok perdarahan ditujukan untuk mengembalikan volume sirkulasi, perfusi jaringan dengan mengoreks hemodinamik, kontrol perdarahan, stabilisasi volume sirkulasi, optimalisasi transpor oksigen dan bila perlu pemberian vasokonstriktor bila tekanan darah tetap rendah setelah pemberian loading cairan. Pemberian cairan merupakan hal penting pada pengelolaan syok perdarahan dimulai dengan pemberian kristaloid/koloid dilanjutkan dengan transfusi darah komponen. Koagulopati yang berhubungan dengan transfusi masif masih merupakan masalah klinis yang penting. Strategis terapi termasuk mempertahankan perfusi jaringan, koreksi hipotermi dan anemia, dan penggunaan produk hemostatik untuk mengoreksi microvascular bleeding. STADIUM-STADIUM SYOK Syok memiliki beberapa stadium sebelum kondisi menjadi dekompensasi atau irreversible sebagaimana dilukiskan dalam gambar berikut: Stadium 1 ANTICIPATION STAGE

Gangguan sudah ada tetapi bersifat lokal. Parameter-paramater masih dalam batas normal. Biasanya masih cukup waktu untuk mendiagnosis dan mengatasi kondisi dasar. Stadium 2. PRE-SHOCK SLIDE

Gangguan sudah bersifat sistemik. Parameter mulai bergerak dan mendekati batas atas atau batas bawah kisaran normal. Sadium 3 COMPENSATED SHOCK

Compensated shock bisa berangkat dengan tekanan darah yang normal rendah, suatu kondisi yang disebut "normotensive, cryptic shock" Banyak klinisi gagal mengenali bagian dini dari stadium syok ini. Compensated shock memiliki arti khusus pada pasien DBD dan perlu dikenali dari tanda-tanda berikut: Capillary refill time > 2 detik; penyempitan tekanan nadi, takikardia, takipnea, akral dingin. Stadium 4 DECOMPENSATED SHOCK, REVERSIBLE

Di sini sudah terjadi hipotensi. Normotensi hanya bisa dipulihkan dengan cairan intravena dan/atau vasopresor Stadium 5 DECOMPENSATED IRREVERSIBLE SHOCK

Kerusakan mikrovaskular dan organ sekarang menjadi menetap dan tak bisa diatasi. Klasifikasi Syok Hemoragik Derajat syok hemoragik bisa secara kasar ditaksir menurut beberapa parameter klinis, namun banyak ditentukan oleh respon terhadap resusitasi cairan 1.

Tatalaksana syok hemoragik Terapi awal pada perdarahan akut harus melibatkan tatalaksana jalan napas, mengusahakan ventilasi dan oksigenasi adekuat, mengendalikan perdarahan eksternal (jika ada), dan melindungi medula spinalis (jika berpotensi cedera). Resusitasi Cairan harus memenuhi objektif: (1) memulihkan volume intravaskular yang cukup untuk mengatasi hipoperfusi sistemik dan membatasi hipoperfusi regional; (2) mempertahankan kapasitas pengangkut oksigen yang adekuat sehingga penyampaian oksigen ke jaringan memenuhi kebutuhan oksigen yang kritis; dan (3) membatasi kehilangan eritrosit sirkulasi. Sayang, tidak ada parameter tepat yang tersedia dan memungkinkan klinisi mencapai tiga sasaran ini ditengahtengah perubahan fisiologis yang dinamis pada perdarahan akut dan resusitasi. Namun demikian, pasien mungkin sekali memperoleh manfaat dari upaya klinis untuk mempertahankan imbang ini sebelum perdarahan yang berlangsung bisa dikendalikan dengan operasi. Resusitasi Cairan Penggantian volume intravaskular untuk mengatasi perdarahan merupakan dogma yang telah diterima selama puluhan tahun. Pemulihan volume intravaskular dan tekanan arteri normal umumnya selalu diterima. Yang menjadi silang pendapat adalah cairan resusitasi yang optimal itu apa. Namun, dalam beberapa puluh tahun terakhir, praktek resusitasi pasien ke tekanan darah normal telah dipertanyakan. Kajian-kajian dini mendukung penggantian volume agresif yang dilakukan pada model perdarahan pada hewan. Pada keadaan ini, normovolemia yang cepat dicapai akan menghasilkan prognosis yang baik tanpa efek samping nyata.2 Namun, model laboratorium tidak mencerminkan situasi klinis dengan tepat. Kebanyakan pasien syok hemoragik belum terkontrol perdarahannya sebelum resusitasi cairan dimulai. Fakta ini menimbulkan kekhawatiran apakah tekanan darah normal justru bisa merugikan dengan memperhebat perdarahan yang sedang berlangsung dan akhirnya memperburuk prognosis. Pembentukan bekuan pada daerah daerah kerusakan pembuluh darah difasilitasi dengan tekanan darah yang lebih rendah selama perdarahan. Tekanan darah yang bertambah bisa melepas sumbatan yang baru terbentuk dan rapuh. Karena larutan kristaloid tidak memiliki kapasitas membawa oksigen, setiap eksaserbasi perdarahan yang diakibatkan dari pemberian kristaloid akan mengurangi kapasitas darah sirkulasi dalam membawa oksigen. Model laboratorium dari cedera vaskular akut dengan perdarahan tak terkendali menjelaskan bahwa peningkatan tekanan darah arteri ke kisaran normal meningkatkan laju perdarahan yang sedang berlangsung. Berangkat dari ini muncullah konsep volume terbatas ini atau resusitasi hipotensif.3 Tujuan dari pendekatan terbatas ini adalah menyediakan resusitasi cairan yang cukup untuk memelihara perfusi organ vital dan menghindari kolaps kardiovaskular sementara menjaga tekanan darah arteri relatif rendah (misal, mean arterial pressure 60 mm Hg) dengan harapan membatasi kehilangan sel darah merah lebih lanjut sebelum pengendalian perdarahan dengan operasi dicapai. Efek buruk yang mungkin terjadi dari pendekatan ini adalah ada daerah yang dikorbankan dengan hipoperfusi regional. Efek ini bergantung pada keparahan dan lama hipoperfusi. Sirkulasi splanchnic yag paling dikhawatirkan karena ini merupakan kontributor utama dari perkembangan disfungsi organ ganda. 2 Sayangnya, penilaian klinis yang akurat terhadap hipoperfusi regional belum ada saat ini. Jadi endpoint resusitasi yang optimal tidak jelas dan cenderung bervariasi dari satu pasien ke pasien lain. Suatu uji klinis acak yang bertujuan mengevaluasi resusitasi hipotensif sampai tekanan darah sistolik 70 mm Hg tidak memperlihatkan manfaat pendekatan ini dalam menurunkan

mortalitas.4 Tekanan sasaran sebesar 70 mm Hg susah dipertahankan, dengan TD sistolik pada kelompok hipotensif mencapai rata-rata 100 mm Hg. Ini menunjukkan kesulitan dalam mencapai tekanan darah hipotensif yang spesifik dalam setting resusitasi syok hemoragik yang bersifat dinamis. Dewasa ini, resusitasi volume-kecil masih sebagai konsep dan belum jelas diperlihatkan memperbaiki survival. Namun demikian, logis juga untuk mengingat konsep ini dan menghindari resusitasi cairan berlebihan.

Transfusi Darah Tidak ada patokan jelas kapan mengganti resusitasi kristaloid dengan darah, Tetapi umumnya diterima jika pasien menunjukkan perbaikan hemodinamik minimal atau sedang setelah infus cepat 2 sampai 3 L kristaloid, maka pasien tersebut membutuhkan transfusi darah. Namun demikian, bisa diterima untuk memberi darah segera jika jelas pasien telah mengalami kehilangan banyak darah dan mendekati kolaps sirkulasi. Sebagian pasien mungkin memberikan respon hemodinamik yang adekuat terhadap terapi awal dengan kristaloid yang bersifat sementara. Pada kasus-kasus demikian, infus kristaloid dilanjutkan dari 2 sampai 3 L pertama bisa digunakan untuk mendukung hemodinamik, selama perhatian ditujukan terhadap hemodilusi progresif dan efeknya terhadap hantaran oksigen.2 Hemodilusi ini juga merendahkan konsentrasi faktor-faktor pembekuan dan trombosit yang dibutuhkan untuk hemostasis intrinsik di titik perdarahan. Penilaian serial terhadap kadar hemoglobin berguna pada situasi demikian. An American Society of Anesthesiologists task force review mendapatkan bahwa kadar hemoglobin daeah >10 g/dL (hematokrit >30 %) jarang memerlukan transfusi darah, sedangkan kadar <6 g/dL (hematokrit <18 %) hampir selalu memerlukan transfusi darah. Ini menyisakan kisaran hemoglobin yang cukup lebarantara 6 dan 10 g/dLketika keputusan untuk memberikan darah sangat dipengaruhi oleh banyak faktor, misal keberadaan proses penyakit dasar yang peka terhadap penurunan hantaran oksigen dan laju kehilangan darah yang terus berlanjut. Bisa dipahami, saat kadar hemoglobin menurun, apalagi menjadi 8 g/dL atau kurang, kecenderungan membutuhkan darah meningkat secara mencolok. Bila mungkin, lebih disukai darah dari golongan sama yang telah diuji-silang. Namun pada setting akut dimana tidak ada waktu untuk uji silang lengkap, darah golongan sama adalah opsi terbaik kedua disusul oleh darah golongan O. Darah bisa diberikan sebagai whole blood atau packed RBC. Di AS, tidak ada persediaan whole blood dan hanya ada packed RBC. Pada perdarahan masif dengan resusitasi kristaloid dan darah yang cukup banyak, transfusi fresh-frozen plasma dan trombosit mungkin diperlukan untuk memulihkan koagulopati dilusional. Transfusi eritrosit jelas memulihkan hemoglobin yang hilang, namun komponen darah yang disimpan bisa saja tidak berfungsi penuh dan memiliki efek samping, yang tampaknya lebih besar jika disimpan lebih lama. Dengan pengawet yang digunakan dewasa ini, eritrosit bisa disimpan sampai 42 hari dan telah dilaporkan bahwa usia rata-rata unit darah yang diberikan di AS kira-kira berusia 21 hari. Eritrosit yang disimpan bisa kehilangan deformabilitas. Ini membatasi kemampuannya melewati jaringan kapiler atau bisa menyumbat kapiler. Kurve disosiasi oksigen berubah karena hilangnya 2,3-difosfogliserat dalam eritrosit, yang mempengaruhi pelepasan oksigen ke jaringan. Beberapa uji klinis melaporkan

perburukan iskemia splansnik dan meingkatnya kekerapan disfungsi organ ganda yang berhubungan dengan transfusi eritrosit yang disimpan lebih dari 2 minggu. Oleh karena itu, transfusi eritrosit walaupun sangat penting dalam syok hemoragik berat, memiliki keterbatasan-keterbatasan dan efek samping potensial yang harus selalu diingat. Transfusi PRC (packed red blood cell) dan produk darah lain bersifat esensial dalam tatalaksana syok hemoragik 5. Rekomendasi teranyar untuk pasien ICU yang stabil adalah target hemoglobin 7 sampai 9 g/dL; namun, tidak ada uji acak prospektif yang membatasi regimen transfusi restriktif dan liberal pada pasien trauma dengan syok hemoragik. Fresh frozen plasma (FFP) juga harus ditransfusi ke pasien dengan perdarahan masif atau perdarahan dengan peningkatan waktu protrombin atau APTT 1.5 lebih besar dari kontrol. Data trauma memperlihatkan keparahan koagulopati pada pasien yang baru masuk ICU memiliki nilai prediktif terhadap mortalitas. Ada data yang memberi kesan perlunya transfusi liberal dari FFP pada pasen perdarahan, namun efektivitas klinis butuh penelitian lanjut. Data baru yang dikumpulkan dari Rumah Sakit Angkatan Darat AS pada pasien yang mendapat transfusi masif packed red blood cells (>10 unit dalam 24 jam) memberi kesan bahwa rasio tinggi dari plasma : RBC (1:1.4 units) diikuti dengan survival lebih baik. Trombosit harus ditransfusi pada pasien perdarahan untuk mempertahankan kadar di atas 50 x 109/L. Ada indikasi potensial dari produk darah lain seperti konsentrat fibrinogen, jika kadar menurun < 1 g/L. Obat-obat seperti recombinant activated coagulation factor 7, dan antifibrinolitik seperti -aminocaproic acid, tranexamic acid , dan aprotinin (protease inhibitor) semuanya memiliki manfaat potensial pada perdarahan hebat namun membutuhkan penelitian lanjut. Resusitasi dengan Koloid Beberapa cairan koloid telah dipelajari secara eksperimen dan digunakan di klinis untuk tatalaksana syok hemoragik. Koloid memiliki partikel dengan berat molekul besar dengan tekanan onkotik plasma serupa dengan protein plasma. Oleh karena itu, koloid diharapkan bertahan di rongga intravaskular, menggantikan protein plasma yang hilang sebagai akibat perdarahan, dan lebih efektif mengembalikan volume darah sirkulasi daripada kristaloid. Dukungan terhadap kegunaan koloid adalah kekhawatiran akan berpindahnya cairan kristaloid ke interstisial, termasuk edema interstisial paru dengan gangguan difusi oksigen dan edema intra-abdomen dengan berkurangnya perfusi usus. Akan tetapi, kondisi-kondisi patologis, seperti syok hemoragik dan sepsis, mengakibatkan meningkatnya permeabilitas pembuluh darah yang bisa memungkinkan bocornya molekul koloid ke ekstravaskular. Kontroversi koloid vs kristaloid: Beberapa informasi tambahan Pemilihan koloid vs kristaloid untuk resusitasi volume telah lama menjadi bahan perdebatan di kalangan praktisi rawat kritis, disebabkan kedua bentuk terapi memiliki data-data pendukung. Pada tahun 1998, British Medical Journal mempublikasi suatu meta-analisis pemakaian albumin pada pasien-pasien sakit kritis; 30 uji klinik acak dg kontrol (RCT) yang melibatkan 1419 pasien dianalisis. Kesimpulannya adalah sebenarnya albumin meningkatkan mortalitas (Timothy Evans,MD) Tinjauan ini berdampak terhadap praktik kedokteran, mempengaruhi klinisi mengurangi penggunaan albumin, tetapi kemudian dikritik karena tinjauan-tinjauan berikutnya tidak bisa menjelaskan kesimpulan para penulis 6. Belum lama berselang, kajian SAFE (Saline versus Albumin Evaluation) telah membuka wacana baru tentang isu ini. Dengan tersedianya berbagai koloid dengan sifat fisikokimia yang berbeda, kontroversi koloid vs koloid menjadi isu tambahan.7 Berikut adalah ringkasan keunggulan dan kekurangan koloid maupun kristaloid

Koloid
Keunggulan Kekurangan

1. 2. 3. 4. 5.

Ekspansi volume Plasma tanpa disertai ekspansi volume interstisial Ekspansi volume lebih besar dibandingkan volume sama kristaloid Masa kerja lebih panjang Oksigenasi jaringan lebih baik Gradien alveolar-arterial O2 lebih kecil

1. 2. 3. 4.

Anafilaksis Mahal Albumin bisa memperburuk depresi miokard pada pasien syok, karena berikatan dengan Ca++, yang pada gilirannya menurunkan ion kalsium Kemungkinan koagulopati dan mengganggu uji silang golongan darah

Kristaloid
Keunggulan Kekurangan

1. 2. 3. 4. 5.

tersedia di mana-mana komposisi menyerupai plasma (acetated ringer, lactated ringer) mudah disimpan pada suhu kamar Bebas reaksi anafilaksis ekonomis

1. 2.

efek volume lebih lemah dan singkat dibandingkan koloid oksigenasi jaringan tidak sebaik koloid karena jarang antara pembuluh darah dan jaringan lebih besar

Walaupun edema interstisial merupakan komplikasi yang lebih potensial setelah resusitasi dengan kristaloid, SAMPAI SEKARANG tidak ada bukti fisiologis, klinis dan radiologis bahwa koloid lebih baik daripada kristaloid dalam penyulit edema paru. Kajian SAFE Dalam suatu meta-analisis baru-baru ini, terlihat peningkatan mortalitas 6% pada pasien yang diberi albumin. Temuan ini menimbulkan perdebatan hebat yang akhirnya menuntun ke pembuatan desain dan implementasi SAFE study, yang disajikan oleh Simon Finfer,MD.7 Uji acak tersamar ganda ini merekrut 7000 pasien dari 16 ICU di Australia dan Selandia Baru selama kurun waktu 18 bulan. Pasien diacak mendapat albumin 4% atau normal saline sejak saat masuk ICU sampai meninggal atau pulang. Dalam 4 hari pertama, rasio albumin: saline adalah 1:1,4 yang berarti bahwa volume (koloid vs kristaloid) tidak berbeda bermakna. Tidak ada perbedaan antara kedua kelompok dalam mortalitas 28 hari oleh semua sebab. MAP, tekanan vena sentral, denyut jantung dan insiden gagal organ baru juga serupa pada kedua kelompok. Pada analisis sub-kelompok diamati perbedaan antara pasien trauma dan sepsis. RR (relative risk) kematian pada pasien dengan sepsis berat yang menerima albumin vs saline adalah 0,87. RR kematian pada pasien yang mendapat albumin tanpa sepsis berat adalah 1,05 (P=.059). Hasil ini ber-lawanan pada pasien trauma. Angka kematian pada pasien trauma lebih tinggi bila albumin vs saline digunakan untuk resusitasi volume (13,5% vs 10%, P =.055) Bila pasien dengan Traumatic brain injury (TBI) dikaji secara terpisah, angka kematian adalah 24,6% pada pasien yang mendapat albumin, dibandingkan 15% pada pasien saline (RR 1,62, 95% confidence interval, -1,12 sampai 2,34, P=0,009). Lebih dari itu, bila pasien TBI dikeluarkan, tidak ada perbedaan angka kematian pada pasien-pasien trauma. Berdasarkan hasil-hasil ini, pemberian albumin tampaknya aman selama 28 hari pada populasi pasien sakit kritis yang heterogen dan mungkin bermanfaat pada pasien sepsis berat. Akan tetapi, keamanan pemberian albumin belum jelas pada pasien trauma, termasuk traumatic brain injury(TBI). Walaupun diamati perbedaan mortalitas pada trauma dan TBI pada analisis sub-kelompok, dan dianggap memiliki validitas terbatas, ini merupakan signal kuat khususnya pada pasien TBI. Suatu kajian baru SAFE Brains sudah dirancang untuk memeriksa perbedaan-perbedaan ini. Apa saja yang menjadi sasaran dari terapi cairan resusitasi (resuscitation endpoints)? Keberhasilan manajemen syok hemoragik atau lebih khusus lagi resusitasi cairan bisa dinilai dari parameter-parameter berikut:

Capilary refill time < 2 detik MAP 65-70 mmHg O2 sat >95% Urine output >0.5 ml/kg/jam (dewasa) ; > 1 ml/kg/jam (anak) Shock index = HR/SBP (normal 0.5-0.7) CVP 8 to12 mm Hg ScvO2 > 70%

KESIMPULAN Terapi cairan resusitasi pada pasien syok hemoragik perlu mendapat perhatian lebih serius untuk menurunkan angka mortalitas dan morbiditas. Hal-hal yang menjadi bahan pertimbangan: 1. 2. 3. 4. 5. Mengetahui stadium syok hipvolemik dan perubahan patofisiologi terkait Deteksi dini compensated shock agar cairan bisa diberikan adekuat Mengetahui berapa banyak cairan kristaloid/koloid diberikan Indikasi transfusi darah Bagaimana mengetahui keberhasilan resusitasi.

Referensi: 1. 2. 3. Demling RH, Wilson RF.: Decision Making in Surgical Critical Care.B.C. Decker Inc, 1988. p 64. Tintinalli JE. Tintinallss Emergency Medicine: A comprehensive Study Guide, 6th e4dition Stern SA: Low-volume fluid resuscitation for presumed hemorrhagic shock: Helpful or harmful? Curr Opin Crit Care 7:422, 2001.

4. 5. 6. 7.

Dutton RP, Mackenzie CF, Scalea TM: Hypotensive resuscitation during active hemorrhage: Impact on in-hospital mortality. J Trauma 52:1141, 2002. Brunicardi, FC. Et al. Schwartz's Principles of Surgery, 9e Liolios A. Volume Resuscitation: The Crystalloid vs Colloid Debate Revisited. Medscape 2004 SAFE Study Investigators: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004, 350:2247-2256

Dr. Iyan Darmawan Medical Director iyan@ho.otsuka.co.id

http://www.otsuka.co.id/?content=article_detail&id=219&lang=id

Hypovolemic shock is an emergency condition in which severe blood and fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working.
NEWS & FEATURES

Stalking a Deadly Virus, Battling a Town's Fears New Bandage Could Avert Thousands of Deaths IV Fluids Found Harmful in Trauma Cases THE DOCTOR'S WORLD; BLOOD: A THREATENED RESOURCE EMERGES AS CORNERSTONE OF MEDICINE
REFERENCE FROM A.D.A.M.
Back to TopAlternative

Names

Shock - hypovolemic
Back to TopCauses

Losing about 1/5 or more of the normal amount of blood in your body causes hypovolemic shock. Blood loss can be due to:

Bleeding from cuts Bleeding from other injuries Internal bleeding, such as in the gastrointestinal tract The amount of circulating blood in your body may drop when you lose too many other body fluids, which can happen with:

Burns Diarrhea Excessive perspiration Vomiting

Back to TopSymptoms

Anxiety or agitation Cool, clammy skin

Confusion Decreased or no urine output General weakness Pale skin color (pallor) Rapid breathing Sweating, moist skin Unconsciousness The greater and more rapid the blood loss, the more severe the symptoms of shock.
Back to TopExams

and Tests

An examination shows signs of shock, including:

Low blood pressure Low body temperature Rapid pulse, often weak and thready Tests that may be done include:

Blood chemistry, including kidney function tests Complete blood count (CBC) CT scan, ultrasound, or x-ray of suspected areas Echocardiogram Endoscopy Right heart (Swan-Ganz) catheterization Urinary catheterization (tube placed into the bladder to measure urine output)
Back to TopTreatment

Get immediate medical help. In the meantime, follow these steps:

Keep the person comfortable and warm (to avoid hypothermia). Have the person lie flat with the feet lifted about 12 inches to increase circulation. However, if the person has a head, neck, back, or leg injury, do not change the person's position unless he or she is in immediate danger. Do not give fluids by mouth. If person is having an allergic reaction, treat the allergic reaction, if you know how. If the person must be carried, try to keep him or her flat, with the head down and feet lifted. Stabilize the head and neck before moving a person with a suspected spinal injury. The goal of hospital treatment is to replace blood and fluids. An intravenous (IV) line will be put into the person's arm to allow blood or blood products to be given. Medicines such as dopamine, dobutamine, epinephrine, andnorepinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart (cardiac output). Other methods that may be used to manage shock and monitor the response to treatment include:

Heart monitoring, including Swan-Ganz catheterization

Urinary catheter to collect and monitor how much urine is produced

Back to TopOutlook

(Prognosis)

Hypovolemic shock is always a medical emergency. However, symptoms and outcomes can vary depending on:

Amount of blood volume lost Rate of blood loss Ilness or injury causing the loss Underlying chronic medication conditions, such as diabetes and heart, lung, and kidney disease In general, patients with milder degrees of shock tend to do better than those with more severe shock. In cases of severe hypovolemic shock, death is possible even with immediate medical attention. The elderly are more likely to have poor outcomes from shock.
Back to TopPossible

Complications

Kidney damage Brain damage Gangrene of arms or legs, sometimes leading to amputation Heart attack
Back to TopWhen

to Contact a Medical Professional

Hypovolemic shock is a medical emergency! Call the local emergency number (such as 911) or take the person to the emergency room.
Back to TopPrevention

Preventing shock is easier than trying to treat it once it happens. Quickly treating the cause will reduce the risk of developing severe shock. Early first aid can help control shock.

http://health.nytimes.com/health/guides/disease/hypovolemic-shock/overview.html

Cardiogenic shock is a state in which the heart has been damaged so much that it is unable to supply enough blood to the organs of the body.
NEWS & FEATURES

Evaluations: Are Report Cards for Doctors a Good or Bad Idea? LESSONS OF THE HEART; Three Who've Learned The Hardest Way Brazil Surgeon Develops a Bold, Promising Operation for Patients With Heart Failure
REFERENCE FROM A.D.A.M.
Back to TopAlternative

Names

Shock - cardiogenic
Back to TopCauses

Shock occurs whenever the heart is unable to pump as much blood as the body needs.

The most common causes are serious heart complications. Many of these occur during or after a heart attack (myocardial infarction). These complications include:

A large section of heart muscle that no longer moves well or does not move at all Breaking open (rupture) of the heart muscle due to damage from the heart attack Dangerous heart rhythms, such as ventricular tachycardia,ventricular fibrillation, or supraventricular tachycardia Tear or rupture of the muscles or tendons that support the heart valves, especially the mitral valve Tear or rupture of the wall (septum) between the left and right ventricles (lower heart chambers) Very slow heart rhythm (bradycardia) or problem with the electrical system of the heart (heart block)
Back to TopSymptoms

o o

Chest pain or pressure Fast breathing Fast pulse Heavy sweating, moist skin Restlessness, agitation, confusion Shortness of breath Skin that feels cool to the touch Pale skin color or blotchy skin Weak (thready) pulse Decreased mental ability Loss of ability to concentrate Loss of alertness Coma (loss of consciousness)
Back to TopExams

and Tests

An examination will show:

Low blood pressure (usually less than 90 systolic) Blood pressure drop of more than 10 points when you stand up after lying down (orthostatic hypotension) Weak (thready) pulse To diagnose cardiogenic shock, a catheter (tube) may be placed in the lung artery (right heart catheterization). Tests may show that blood is backing up into the lungs and the heart is not pumping properly. Tests include:

Cardiac catheterization Chest x-ray Coronary angiography Echocardiogram Electrocardiogram Nuclear scans

Other studies may be done to find out why the heart is not working properly. Lab tests include:

Arterial blood gas Blood chemistry (chem-7, chem-20, electrolytes) Cardiac enzymes (troponin, CKMB) Complete blood count (CBC)
Back to TopTreatment

Cardiogenic shock is a medical emergency. You will need to stay in the hospital, usually in the Intensive Care Unit. The goal of treatment is to find and treat the cause of shock to save your life. You may need medicines to increase blood pressure and improve heart function, including:

Dobutamine Dopamine Epinephrine Norepinephrine These medicines may help in the short-term, but they should not be used over the long-term. When a heart rhythm disturbance (dysrhythmia) is serious, urgent treatment may be needed to restore a normal heart rhythm. This may include:

Electrical "shock" therapy (defibrillation or cardioversion) Implanting a temporary pacemaker Medications given through a vein (intravenous) You may receive pain medicine if needed. Bed rest is recommended to reduce demands on the heart. Getting oxygen by a nasal tube or mask worn over the mouth lowers the workload of the heart helping the tissue of the body need less blood. You may receive intravenous fluids, including blood and blood products, if needed. Other treatments for shock may include:

Cardiac catheterization with coronary angioplasty and stenting Heart monitoring to guide treatment Heart surgery (coronary artery bypass surgery, heart valve replacement, left ventricular assist device) Intra-aortic balloon counterpulsation (IABP) to improve heart and blood vessel function Pacemaker
Back to TopOutlook

(Prognosis)

In the past, the death rate from cardiogenic shock ranged from 80 - 90%. In more recent studies, this rate has decreased to 50 - 75%. When cardiogenic shock is not treated, the outlook is poor.

Back to TopPossible

Complications

Brain damage Kidney damage Liver damage

Back to TopWhen

to Contact a Medical Professional

Go to the emergency room or call the local emergency number (such as 911) if you have symptoms of cardiogenic shock. Cardiogenic shock is a medical emergency.
Back to TopPrevention

You may reduce the risk of developing cardiogenic shock by:

Quickly treating its cause (such as heart attack or heart valve problem) Preventing and treating the risk factors for heart disease, such as diabetes, high blood pressure, high cholesterol and triglycerides, or tobacco use

Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion. Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock). Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes of hemorrhagic shock. Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities. Two common causes of rapid internal blood loss are solid organ injury and rupture of an abdominal aortic aneurysm. Hypovolemic shock can result from significant fluid (other than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory gastroenteritis and extensive burns. The remainder of this article concentrates mainly on hypovolemic shock secondary to blood loss and the controversies surrounding the treatment of this condition. The reader is referred to other articles for discussions of the pathophysiology and treatment for hypovolemic shock resulting from losses of fluid other than blood. The many life-threatening injuries experienced during the wars of the 1900s have significantly affected the development of the principles of hemorrhagic shock resuscitation. During World War I, W.B. Cannon recommended delaying fluid resuscitation until the cause of the hemorrhagic shock was repaired surgically. Crystalloids and blood were used extensively during World War II for the treatment of patients in unstable conditions. Experience from the Korean and Vietnam wars revealed that volume resuscitation and early surgical intervention were paramount for surviving traumatic injuries resulting in hemorrhagic shock. These and other principles helped in the development of present guidelines for the treatment of traumatic hemorrhagic shock. However, recent investigators have questioned these guidelines, and today, controversies exist concerning the optimal treatment of hemorrhagic shock. The human body responds to acute hemorrhage by activating the following major physiologic systems: the hematologic, cardiovascular, renal, and neuroendocrine systems. The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release). In addition, platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source. The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot. Approximately 24 hours are needed for complete clot fibrination and mature formation. The cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, increasing myocardial contractility, and constricting peripheral blood vessels. This response occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels). The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract. The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus. Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver. Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex. Aldosterone is responsible for active sodium reabsorption and subsequent water conservation. The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH). ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors). ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle. The pathophysiology of hypovolemic shock is much more involved than what was just listed. To explore the pathophysiology in more detail, references for further reading are provided in the bibliography. These

intricate mechanisms list above are effective in maintaining vital organ perfusion in severe blood loss. Without fluid and blood resuscitation and/or correction of the underlying pathology causing the hemorrhage, cardiac perfusion eventually diminishes, and multiple organ failure soon follows. n a patient with possible shock secondary to hypovolemia, the history is vital in determining the possible causes and in directing the workup. Hypovolemic shock secondary to external blood loss typically is obvious and easily diagnosed. Internal bleeding may not be as obvious as patients may complain only of weakness, lethargy, or a change in mental status. Symptoms of shock, such as weakness, lightheadedness, and confusion, should be assessed in all patients. In the patient with trauma, determine the mechanism of injury and any information that may heighten suspicion of certain injuries (eg, steering wheel damage or extensive passenger compartment intrusion in a motor vehicle accident). If conscious, the patient may be able to indicate the location of pain. Vital signs, prior to arrival in the ED, should also be noted. Chest, abdominal, or back pain may indicate a vascular disorder. The classic sign of a thoracic aneurysm is a tearing pain radiating to the back. Abdominal aortic aneurysms usually result in abdominal, back pain, or flank pain. In patients with GI bleeding, inquiry about hematemesis, melena, alcohol drinking history, excessive nonsteroidal anti-inflammatory drug use, and coagulopathies (iatrogenic or otherwise) is very important. The chronology of vomiting and hematemesis should be determined. The patient who presents with hematemesis after multiple episodes of forceful vomiting is more likely to have Boerhaave syndrome or a Mallory-Weiss tear, whereas a patient with a history of hematemesis from the start is more likely to have peptic ulcer disease or esophageal varices. If a gynecologic cause is being considered, gather information about the following: last menstrual period, risk factors for ectopic pregnancy, vaginal bleeding (including amount and duration), vaginal passage of products of conception, and pain. All women of childbearing age should undergo a pregnancy test, regardless of whether they believe that they are pregnant. A negative pregnancy test typically excludes ectopic pregnancy as a diagnosis. The physical examination should always begin with an assessment of the airway, breathing, and circulation. Once these have been evaluated and stabilized, the circulatory system should be evaluated for signs and symptoms of shock. Do not rely on systolic BP as the main indicator of shock; this practice results in delayed diagnosis. Compensatory mechanisms prevent a significant decrease in systolic BP until the patient has lost 30% of the blood volume. More attention should be paid to the pulse, respiratory rate, and skin perfusion. Also, patients taking beta-blockers may not present with tachycardia, regardless of the degree of shock. Classes of hemorrhage have been defined, based on the percentage of blood volume loss. However, the distinction between these classes in the hypovolemic patient often is less apparent. Treatment should be aggressive and directed more by response to therapy than by initial classification. o o o o o o o Class I hemorrhage (loss of 0-15%) In the absence of complications, only minimal tachycardia is seen. Usually, no changes in BP, pulse pressure, or respiratory rate occur. A delay in capillary refill of longer than 3 seconds corresponds to a volume loss of approximately 10%. Class II hemorrhage (loss of 15-30%) Clinical symptoms include tachycardia (rate >100 beats per minute), tachypnea, decrease in pulse pressure, cool clammy skin, delayed capillary refill, and slight anxiety. The decrease in pulse pressure is a result of increased catecholamine levels, which causes an increase in peripheral vascular resistance and a subsequent increase in the diastolic BP. Class III hemorrhage (loss of 30-40%) By this point, patients usually have marked tachypnea and tachycardia, decreased systolic BP, oliguria, and significant changes in mental status, such as confusion or agitation. In patients without other injuries or fluid losses, 30-40% is the smallest amount of blood loss that consistently causes a decrease in systolic BP.

Most of these patients require blood transfusions, but the decision to administer blood should be based on the initial response to fluids. Class IV hemorrhage (loss of >40%) o Symptoms include the following: marked tachycardia, decreased systolic BP, narrowed pulse pressure (or immeasurable diastolic pressure), markedly decreased (or no) urinary output, depressed mental status (or loss of consciousness), and cold and pale skin. o This amount of hemorrhage is immediately life threatening. In the patient with trauma, hemorrhage usually is the presumed cause of shock. However, it must be distinguished from other causes of shock. These include cardiac tamponade (muffled heart tones, distended neck veins), tension pneumothorax (deviated trachea, unilaterally decreased breath sounds), and spinal cord injury (warm skin, lack of expected tachycardia, neurological deficits). The 4 areas in which life-threatening hemorrhage can occur are as follows: chest, abdomen, thighs, and outside the body. o The chest should be auscultated for decreased breath sounds, because life-threatening hemorrhage can occur from myocardial, vessel, or lung laceration. o The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury. o The thighs should be checked for deformities or enlargement (signs of femoral fracture and bleeding into the thigh). o The patient's entire body should then be checked for other external bleeding. In the patient without trauma, the majority of the hemorrhage is in the abdomen. The abdomen should be examined for tenderness, distension, or bruits. Look for evidence of an aortic aneurysm, peptic ulcer disease, or liver congestion. Also check for other signs of bruising or bleeding. In the pregnant patient, perform a sterile speculum examination. However, with third-trimester bleeding, the examination should be performed as a "double set-up" in the operating room. Check for abdominal, uterine, or adnexal tenderness. The causes of hemorrhagic shock are traumatic, vascular, GI, or pregnancy related. Traumatic causes can result from penetrating and blunt trauma. Common traumatic injuries that can result in hemorrhagic shock include the following: myocardial laceration and rupture, major vessel laceration, solid abdominal organ injury, pelvic and femoral fractures, and scalp lacerations. Vascular disorders that can result in significant blood loss include aneurysms, dissections, and arteriovenous malformations. GI disorders that can result in hemorrhagic shock include the following: bleeding esophageal varices, bleeding peptic ulcers, Mallory-Weiss tears, and aortointestinal fistulas. Pregnancy-related disorders include ruptured ectopic pregnancy,placenta previa, and abruption of the placenta. Hypovolemic shock secondary to an ectopic pregnancy is common. Hypovolemic shock secondary to an ectopic pregnancy in a patient with a negative urine pregnancy test is rare but has been reported.

Prehospital Care
The treatment of patients with hypovolemic shock often begins at an accident scene or at home. The prehospital care team should work to prevent further injury, transport the patient to the hospital as rapidly as possible, and initiate appropriate treatment in the field. Direct pressure should be applied to external bleeding vessels to prevent further blood loss. Prevention of further injury applies mostly to the patient with trauma. The cervical spine must be immobilized, and the patient must be extricated, if applicable, and moved to a stretcher. Splinting of fractures can minimize further neurovascular injury and blood loss. Although in selected cases stabilization may be beneficial, rapid transport of sick patients to the hospital remains the most important aspect of prehospital care. Definitive care of the hypovolemic patient usually requires hospital, and sometimes surgical, intervention. Any delay in definitive care, eg, such as delayed transport, is potentially harmful. Most prehospital interventions involve immobilizing the patient (if trauma is involved), securing an adequate airway, ensuring ventilation, and maximizing circulation.

In the setting of hypovolemic shock, positive-pressure ventilation may diminish venous return, diminish cardiac outcome, and worsen the shock state. While oxygenation and ventilation are necessary, excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock. o Appropriate treatment usually can be initiated without delaying transport. Some procedures, such as starting intravenous (IV) lines or splinting of extremities, can be performed while a patient is being extricated. However, procedures in the field that prolong transportation should be delayed. Benefits to giving IV fluids prior to departure from the scene are not clear; however, IV lines and fluid resuscitation should be started and continued once the patient is en route to definitive care. In recent years, there has been considerable debate regarding the use of military antishock trousers (MAST). MAST were introduced in the 1960s and, based mostly on anecdotal reports of success, their use became standard therapy in the prehospital treatment of hypovolemic shock in the late 1970s. By the 1980s, the American College of Surgeons Committee on Trauma included their use in the standard of care for all patients with trauma and signs or symptoms of shock. Since that time, studies have failed to show improved outcome with the use of MAST. The American College of Surgeons Committee on Trauma no longer recommends the use of MAST.

Emergency Department Care

Three goals exist in the emergency department treatment of the patient with hypovolemic shock as follows: (1) maximize oxygen delivery - completed by ensuring adequacy of ventilation, increasing oxygen saturation of the blood, and restoring blood flow, (2) control further blood loss, and (3) fluid resuscitation. Also, the patient's disposition should be rapidly and appropriately determined. o Maximizing oxygen delivery The patient's airway should be assessed immediately upon arrival and stabilized if necessary. The depth and rate of respirations, as well as breath sounds, should be assessed. If pathology (eg, pneumothorax, hemothorax, flail chest) that interferes with breathing is found, it should be addressed immediately. High-flow supplemental oxygen should be administered to all patients, and ventilatory support should be given, if needed. Excessive positive-pressure ventilation can be detrimental for a patient suffering hypovolemic shock and should be avoided. Two large-bore IV lines should be started. The Poiseuille law states that flow is inversely related to the length of the IV catheter and directly related to its radius to the fourth power. Thus, a short largecaliber IV catheter is ideal; the caliber is much more significant than the length. IV access may be obtained by means of percutaneous access in the antecubital veins, cutdown of saphenous or arm veins, or access in the central veins by using the Seldinger technique. If central lines are obtained, a large-bore single-lumen catheter should be used. Intraosseous access has and continues to be used for hypotensive children younger than 6 years. Intraosseous access has also been used in hypotensive adults.[1] The most important factor in determining the route of access is the practitioner's skill and experience. Placement of an arterial line should be considered for patients with severe hemorrhage. For these patients, the arterial line will provide continuous blood pressure monitoring and also easearterial blood gas testing. Once IV access is obtained, initial fluid resuscitation is performed with an isotonic crystalloid, such as lactated Ringer solution or normal saline. An initial bolus of 1-2 L is given in an adult (20 mL/kg in a pediatric patient), and the patient's response is assessed. If vital signs return to normal, the patient may be monitored to ensure stability, and blood should be sent for typed and cross-matched. If vital signs transiently improve, crystalloid infusion should continue and type-specific blood obtained. If little or no improvement is seen, crystalloid infusion should continue, and type O blood should be given (type O Rh-negative blood should be given to female patients of childbearing age to prevent sensitization and future complications). If a patient is moribund and markedly hypotensive (class IV shock), both crystalloid and type O blood should be started initially. These guidelines for crystalloid and blood infusion are not rules; therapy should be based on the condition of the patient. The position of the patient can be used to improve circulation; one example is raising the hypotensive patient's legs while fluid is being given. Another example of useful positioning is rolling a hypotensive gravid patient with trauma onto her left side, which displaces the fetus from the inferior vena cava and increases circulation. The Trendelenburg position is no longer recommended for hypotensive patients,

o o o

o o

o o

o o

o o

o o o

o o

as the patient is predisposed to aspiration. In addition, the Trendelenburg position does not improve cardiopulmonary performance and may worsen gas exchange. Autotransfusion may be a possibility in some patients with trauma. Several devices that allow for the sterile collection, anticoagulation, filtration, and retransfusion of blood are available. In the trauma setting, this blood almost always is from a hemothorax collected by means of tube thoracostomy. Controlling further blood loss Control of further hemorrhage depends on the source of bleeding and often requires surgical intervention. In the patient with trauma, external bleeding should be controlled with direct pressure; internal bleeding requires surgical intervention. Long-bone fractures should be treated with traction to decrease blood loss. In the patient whose pulse is lost in the ED or just prior to arrival, an emergency thoracotomy with cross-clamping of the aorta may be indicated to preserve blood flow to the brain. This procedure is palliative at best and requires immediate transfer to the operating room. In the patient with GI bleeding, intravenous vasopressin and H2blockers have been used. Vasopressin commonly is associated with adverse reactions, such as hypertension, arrhythmias, gangrene, and myocardial or splanchnic ischemia. Therefore, it should be considered secondary to more definitive measures. H2blockers are relatively safe but have no proven benefit. Somatostatin and octreotide infusions have been shown to reduce gastrointestinal bleeding from varices and peptic ulcer disease. These agents possess the advantages of vasopressin without the significant side effects. In patients with variceal bleeding, use of a Sengstaken-Blakemore tube can be considered. These devices have a gastric balloon and an esophageal balloon. The gastric one is inflated first, and then the esophageal one is inflated if bleeding continues. The use of this tube has been associated with severe adverse reactions, such as esophageal rupture, asphyxiation, aspiration and mucosal ulceration. For this reason, its use should be considered only as a temporary measure in extreme circumstances. Virtually all causes of acute gynecological bleeding that cause hypovolemia (eg, ectopic pregnancy, placenta previa, abruptio placenta, ruptured cyst, miscarriage) require surgical intervention. Early consultation and definitive care are the keys. The goal in the ED is to stabilize the hypovolemic patient, determine the cause of bleeding, and provide definitive care as quickly as possible. If transfer to another hospital is necessary, resources should be mobilized early. In patients with trauma, if the emergency medical services personnel indicate potential serious injury, the surgeon (or trauma team) should be notified prior to the patient's arrival. In a 55-year-old patient with abdominal pain, for example, emergency ultrasonography of the abdomen may be necessary to identify an abdominal aortic aneurysm before the vascular surgeon is notified. Every patient should be individually evaluated, because delaying definitive care can increase morbidity and mortality. Whether crystalloids or colloids are best for resuscitation continues to be a matter for discussion and research. Many fluids have been studied for use in resuscitation; these include isotonic sodium chloride solution, lactated Ringer solution,[2] hypertonic saline, albumin, purified protein fraction, fresh frozen plasma, hetastarch, pentastarch, and dextran 70. Proponents of colloid resuscitation argue that the increased oncotic pressure produced with these substances decreases pulmonary edema. However, the pulmonary vasculature allows considerable flow of material, including proteins, between the intravascular space and interstitium. Maintenance of the pulmonary hydrostatic pressure at less than 15 mm Hg appears to be a more important factor in preventing pulmonary edema. Another argument is that less colloid is needed to increase the intravascular volume. Studies have shown this to be true. However, they still have not demonstrated any difference in outcome with colloids compared with crystalloids. Synthetic colloid solutions, such as hetastarch, pentastarch, and dextran 70, have some advantages compared with natural colloids such as purified protein fraction, fresh frozen plasma, and albumin. They have the same volume-expanding properties, but because of their structures and high molecular weights, they remain mostly in the intravascular space, reducing the occurrence of interstitial edema. Although theoretic advantages exist, studies have failed to show a difference in ventilatory parameters, pulmonary function test results, days using a ventilator, total hospital days, or survival. The combination of hypertonic saline and dextran also has been studied because of previous evidence that it may improve cardiac contractility and circulation. Studies in the US and Japan have

o o o o

o o o

failed to show any difference when this combination was compared with isotonic sodium chloride solution or lactated Ringer solution. Thus, despite the many available resuscitation fluids, current recommendations still advocate the use of normal saline or lactated Ringer solution. In the US, one reason for the predominant use of crystalloids over the other resuscitative fluids is cost. Recent literature suggests that the early administration of FFP and platelets improves survival and decreases overall PRBC need in patients undergoing a massive transfusion. [3] Another area of interest regarding resuscitation is whether the goal should be to restore normal circulating volume and BP prior to definitive control of bleeding. During World War I, Cannon observed and characterized patients in clinical shock. He later suggested a model of permissive hypotension in the treatment of torso wounds, with the intent of minimizing further bleeding. Findings from early studies showed that animals that were bled had increased survival if they received fluid resuscitation. However, in these studies, bleeding was well controlled with ligation after the animals were bled. During the Korean and Vietnam wars, much more aggressive fluid resuscitation, as well as rapid access to definitive care, was emphasized. It was noted that patients who were aggressively resuscitated tended to have better outcomes, and in the 1970s, these principles were widely adopted in civilian patients. Since then, many studies have been conducted to determine if these principles are valid in patients with uncontrolled hemorrhage. Most of these studies revealed increased survival in the permissive hypotension or delayed treatment arms. The theory is that increased pressure causes more bleeding and disrupts initial clots, whereas extreme hypotension may increase the risk of cerebral perfusion. The questions that have not been answered adequately are as follows: Which mechanisms and injury patterns are more amenable to the restoration of circulating blood volume? What BP is adequate but not excessive? Although some data indicate that a systolic BP of 80-90 mm Hg may be adequate in penetrating truncal trauma without head injury, further studies are needed. Current recommendations are for aggressive fluid resuscitation with lactated Ringer solution or normal saline in all patients with signs and symptoms of shock, regardless of underlying cause.

Hypovolemic shock

Hypovolemic shock is an emergency condition in which severe blood and fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working. Causes Losing about 1/5 or more of the normal amount of blood in your body causes hypovolemic shock. Blood loss can be due to: Bleeding from cuts Bleeding from other injuries Internal bleeding, such as in the gastrointestinal tract

The amount of circulating blood in your body may drop when you lose too many other body fluids, which can happen with:

Burns Diarrhea Excessive perspiration Vomiting

Symptoms Anxiety or agitation Cool, clammy skin Confusion Decreased or no urine output General weakness Pale skin color (pallor) Rapid breathing Sweating, moist skin Unconsciousness

The greater and more rapid the blood loss, the more severe the symptoms of shock. Exams and Tests An examination shows signs of shock, including: Low blood pressure Low body temperature Rapid pulse, often weak and thready

Tests that may be done include: Blood chemistry, including kidney function tests Complete blood count (CBC) CT scan, ultrasound, or x-ray of suspected areas Echocardiogram Endoscopy Right heart (Swan-Ganz) catheterization Urinary catheterization (tube placed into the bladder to measure urine output)

Treatment Get immediate medical help. In the meantime, follow these steps: Keep the person comfortable and warm (to avoid hypothermia). Have the person lie flat with the feet lifted about 12 inches to increase circulation. However, if the person has a head, neck, back, or leg injury, do not change the person's position unless he or she is in immediate danger. Do not give fluids by mouth. If person is having an allergic reaction, treat the allergic reaction, if you know how.

If the person must be carried, try to keep him or her flat, with the head down and feet lifted. Stabilize the head and neck before moving a person with a suspected spinal injury.

The goal of hospital treatment is to replace blood and fluids. An intravenous (IV) line will be put into the person's arm to allow blood or blood products to be given. Medicines such as dopamine, dobutamine, epinephrine, and norepinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart (cardiac output). Other methods that may be used to manage shock and monitor the response to treatment include: Heart monitoring, including Swan-Ganz catheterization Urinary catheter to collect and monitor how much urine is produced

Outlook (Prognosis) Hypovolemic shock is always a medical emergency. However, symptoms and outcomes can vary depending on: Amount of blood volume lost Rate of blood loss Ilness or injury causing the loss Underlying chronic medication conditions, such as diabetes and heart, lung, and kidney disease

In general, patients with milder degrees of shock tend to do better than those with more severe shock. In cases of severe hypovolemic shock, death is possible even with immediate medical attention. The elderly are more likely to have poor outcomes from shock. Possible Complications Kidney damage Brain damage Gangrene of arms or legs, sometimes leading to amputation Heart attack

When to Contact a Medical Professional Hypovolemic shock is a medical emergency! Call the local emergency number (such as 911) or take the person to the emergency room. Prevention Preventing shock is easier than trying to treat it once it happens. Quickly treating the cause will reduce the risk of developing severe shock. Early first aid can help control shock. Alternative Names Shock - hypovolemic

http://www.nlm.nih.gov/medlineplus/ency/article/000167.htm