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 reninangiotensin 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. Such apparent clinical shock results from at least 25 to 30% loss of
the blood volume. 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. 75 Loss of up to 15% of the circulating volume (700 to 750 mL
for a 70-kg patient) may produce little in terms of obvious symptoms, while loss of up to 30%
of the circulating volume (1.5 L) may result in mild tachycardia, tachypnea, and anxiety.
Hypotension, marked tachycardia [i.e., pulse >110 to 120 beats per minute (bpm)], and
confusion may not be evident until more than 30% of the blood volume has been lost; loss of
40% of circulating volume (2 L) is immediately life threatening, and generally requires
operative control of bleeding. 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.g., warfarin or aspirin), or
mask the compensatory responses to bleeding (e.g., beta blockers). In addition,
atherosclerotic vascular disease, diminishing cardiac compliance with age, inability to elevate

heart rate or cardiac contractility in response to hemorrhage, and overall decline in

physiologic reserve decrease the elderly patient's ability to tolerate hemorrhage.
diagnosa

Pengobatan syok awalnya empiris. 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. Tandatanda klinis syok mungkin jelas dengan pasien gelisah, termasuk ekstremitas dingin berkeringat,
takikardia, denyut perifer lemah atau tidak ada, dan hipotensi. Seperti jelas sengatan klinis dari
kehilangan setidaknya 25 sampai 30% dari volume darah. 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. 75 Kehilangan sampai 15% dari volume sirkulasi (700-750 mL untuk
pasien 70 kg) dapat menghasilkan sedikit dalam hal gejala yang jelas, sedangkan kerugian hingga
30% dari volume sirkulasi (1,5 L) dapat mengakibatkan takikardia ringan, takipnea, dan kecemasan.
Hipotensi, takikardia ditandai [yaitu, pulsa> 110 sampai 120 denyut per menit (bpm)], dan
kebingungan mungkin tidak jelas sampai lebih dari 30% dari volume darah telah hilang; kehilangan
40% dari volume sirkulasi (2 L) segera mengancam kehidupan, dan umumnya membutuhkan kontrol
operasi perdarahan. 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.e., operation or interventional radiology) is required.
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.
pengobatan
Pengendalian perdarahan yang sedang berlangsung merupakan komponen penting dari resusitasi
pasien shock. 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 kapalkapal 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.e., SBP <90 mm Hg for at least 30
minutes), reduced cardiac index (<2.2 L/min per square meter), and elevated pulmonary
artery wedge pressure (>15 mm Hg). 78 Mortality rates for cardiogenic shock are 50 to 80%.
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. Cardiogenic shock complicates 5 to 10% of acute MIs. 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. Rapid assessment, adequate resuscitation, and

reversal of the myocardial ischemia are essential in optimizing outcome in patients with acute
MI. 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.e., 33%
mortality with complete reperfusion, 50% mortality with incomplete reperfusion, and 85%
mortality with absent reperfusion). 79 Inadequate cardiac function can be a direct result of
cardiac injury, including profound myocardial contusion, blunt cardiac valvular injury, or
direct myocardial damage 7880 (Table 4-2). The pathophysiology of cardiogenic shock
involves a vicious cycle of myocardial ischemia which causes myocardial dysfunction, which
results in more myocardial ischemia. 78 When sufficient mass of the left ventricular wall is
necrotic or ischemic and fails to pump, the stroke volume decreases. Autopsy series of
patients dying from cardiogenic shock have found damage to 40% of the left ventricle. 81
Ischemia distant from the infarct zone may contribute to the systolic dysfunction in patients
with cardiogenic shock. 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. Kriteria hemodinamik termasuk berkelanjutan hipotensi (yaitu, SBP <90 mm Hg
selama paling sedikit 30 menit), mengurangi indeks jantung (<2.2 L / min per meter persegi), dan
paru tekanan baji arteri tinggi (> 15 mm Hg). 78 Tingkat kematian untuk syok kardiogenik adalah 50
sampai 80%. 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. Syok
kardiogenik mempersulit 5 sampai 10% dari MI akut. 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. Tingkat aliran koroner perkutan setelah angioplasti koroner transluminal (PTCA)
berkorelasi dengan mortalitas di rumah sakit (yaitu, kematian 33% dengan reperfusi lengkap,
mortalitas 50% dengan reperfusi tidak lengkap, dan kematian 85% dengan reperfusi absen). 79
fungsi jantung yang tidak memadai dapat menjadi akibat langsung dari cedera jantung, termasuk

memar mendalam miokard, tumpul cedera katup jantung, atau kerusakan miokard langsung 78-80
(Tabel 4-2). Patofisiologi syok kardiogenik melibatkan lingkaran setan iskemia miokard yang
menyebabkan disfungsi miokard, yang menghasilkan iskemia miokard lebih. 78 Ketika massa yang
cukup dari dinding ventrikel kiri adalah nekrotik atau iskemik dan gagal untuk memompa, stroke
volume menurun. Seri otopsi pasien meninggal akibat syok kardiogenik telah menemukan kerusakan
40% dari ventrikel kiri. 81 Iskemia jauh dari zona infark dapat menyebabkan disfungsi sistolik pada
pasien dengan syok kardiogenik. 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.
diagnosa

Identifikasi cepat pasien dengan kegagalan pompa dan institusi tindakan korektif sangat penting
dalam mencegah spiral berkelanjutan curah jantung menurun dari cedera menyebabkan
peningkatan kebutuhan oksigen miokard yang tidak dapat dipenuhi, menyebabkan disfungsi jantung
progresif dan tak henti-hentinya. Dalam evaluasi kemungkinan syok kardiogenik, penyebab lain dari
hipotensi harus dikeluarkan, termasuk perdarahan, sepsis, emboli paru, dan diseksi aorta. Tandatanda syok sirkulasi meliputi hipotensi, kulit dingin dan berbintik-bintik, status mental tertekan,
takikardia, dan kacang-kacangan berkurang. Pemeriksaan jantung mungkin termasuk disritmia,

Heave prekordial, atau nada jantung distal. Konfirmasi sumber jantung untuk shock memerlukan
elektrokardiogram dan ekokardiografi mendesak. Tes diagnostik lainnya yang berguna termasuk
rontgen dada, gas darah arteri, elektrolit, hitung darah lengkap, dan enzim jantung. Monitoring
jantung invasif, yang umumnya tidak diperlukan, dapat berguna untuk mengecualikan ventrikel
infark kanan, hipovolemia, dan komplikasi mekanik mungkin.
Membuat diagnosis syok kardiogenik melibatkan identifikasi disfungsi jantung atau gagal jantung
akut pada pasien yang rentan. Karena pasien dengan cedera jantung tumpul biasanya memiliki
cedera multisistem, syok hemoragik dari intra-abdomen perdarahan, perdarahan intratoraks, dan
perdarahan dari patah tulang harus dikeluarkan. Relatif sedikit pasien dengan cedera jantung tumpul
akan mengembangkan disfungsi pompa jantung. Mereka yang umumnya menunjukkan syok
kardiogenik awal evaluasi mereka. Oleh karena itu, penegakan diagnosis cedera jantung tumpul
adalah sekunder untuk tidak termasuk etiologi lainnya untuk shock dan menetapkan bahwa
disfungsi jantung hadir. Pemantauan hemodinamik invasif dengan kateter arteri pulmonalis dapat
mengungkap bukti curah jantung berkurang dan tekanan arteri pulmonalis meningkat.

Treatment
After ensuring that an adequate airway is present and ventilation is sufficient, attention
should be focused on support of the circulation. Intubation and mechanical ventilation are
often required, if only to decrease work of breathing and facilitate sedation of the patient.
Rapidly excluding hypovolemia and establishing the presence of cardiac dysfunction is
essential. Treatment of cardiac dysfunction includes maintenance of adequate oxygenation to
ensure adequate myocardial oxygen delivery and judicious fluid administration to avoid fluid
overload and development of cardiogenic pulmonary edema. Electrolyte abnormalities,
commonly hypokalemia and hypomagnesemia, should be corrected. Pain is treated with
intravenous morphine sulfate or fentanyl. Significant dysrhythmias and heart block must be
treated with antiarrhythmic drugs, pacing, or cardioversion if necessary. Early consultation
with cardiology is essential in current management of cardiogenic shock, particularly in the
setting of acute myocardial infarction. 78
When profound cardiac dysfunction exists, inotropic support may be indicated to improve
cardiac contractility and cardiac output. Dobutamine primarily stimulates cardiac
1
receptors to increase cardiac output, but may also vasodilate peripheral vascular beds, lower
total peripheral resistance, and lower systemic blood pressure through effects on
2
receptors. Ensuring adequate preload and intravascular volume is therefore essential prior to
instituting therapy with dobutamine. Dopamine stimulates

receptors (vasoconstriction),

1 receptors (cardiac stimulation), and

2 receptors (vasodilation), with its effects on
receptors predominating at lower doses. Dopamine may be preferable to dobutamine in
treatment of cardiac dysfunction in hypotensive patients. Tachycardia and increased
peripheral resistance from dopamine infusion may worsen myocardial ischemia. Titration of
both dopamine and dobutamine infusions may be required in some patients.

pengobatan

Setelah memastikan bahwa jalan napas yang adekuat hadir dan ventilasi cukup, perhatian
harus difokuskan pada dukungan dari sirkulasi. Intubasi dan ventilasi mekanis sering
diperlukan, jika hanya untuk mengurangi kerja pernapasan dan memfasilitasi sedasi pasien.
Cepat tidak termasuk hipovolemia dan membangun kehadiran disfungsi jantung sangat
penting. Pengobatan disfungsi jantung termasuk pemeliharaan oksigenasi yang memadai
untuk memastikan pengiriman oksigen miokard memadai dan pemberian cairan bijaksana
untuk menghindari kelebihan cairan dan pengembangan edema paru kardiogenik. Kelainan
elektrolit, umumnya hipokalemia dan hipomagnesemia, harus diperbaiki. Nyeri diobati
dengan intravena morfin sulfat atau fentanyl. Disritmia signifikan dan blok jantung harus
diobati dengan obat antiaritmia, mondar-mandir, atau kardioversi jika perlu. Konsultasi awal
dengan kardiologi sangat penting dalam manajemen saat syok kardiogenik, terutama dalam
pengaturan infark miokard akut. 78

Ketika disfungsi jantung yang mendalam ada, dukungan inotropik dapat diindikasikan untuk
meningkatkan kontraktilitas jantung dan curah jantung. Dobutamin terutama merangsang
jantung 1 reseptor untuk meningkatkan curah jantung, tetapi juga dapat vasodilate tempat
tidur vaskular perifer, resistensi perifer total yang lebih rendah, dan tekanan darah sistemik
rendah melalui efek pada 2 reseptor. Memastikan preload memadai dan volume intravaskular
Oleh karena itu penting sebelum melembagakan terapi dengan dobutamin. Dopamin
menstimulasi reseptor (vasokonstriksi), 1 reseptor (stimulasi jantung), dan 2 reseptor
(vasodilatasi), dengan efek pada reseptor mendominasi pada dosis yang lebih rendah.
Dopamin mungkin lebih baik untuk dobutamin dalam pengobatan disfungsi jantung pada
pasien hipotensi. Takikardia dan peningkatan tahanan perifer dari infus dopamin dapat
memperburuk iskemia miokard. Titrasi kedua dopamin dan dobutamin infus mungkin
diperlukan pada beberapa pasien.

Vasodilatory Shock (Septic Shock)

In the peripheral circulation, profound vasoconstriction is the typical physiologic response to
arterial pressure that is insufficient for tissue perfusion, usually causing cardiogenic or
hemorrhagic shock. In vasodilatory shock, hypotension results from failure of the vascular
smooth muscle to constrict appropriately. Vasodilatory shock is characterized by both
peripheral vasodilatation with resultant hypotension, and resistance to treatment with
vasopressors. Despite the hypotension, plasma catecholamine levels are elevated and the
renin-angiotensin system is activated in vasodilatory shock. 84,85 The most frequently
encountered form of vasodilatory shock is septic shock. Other causes of vasodilatory shock
include hypoxic lactic acidosis, carbon monoxide poisoning, decompensated and irreversible
hemorrhagic shock, terminal cardiogenic shock, and postcardiotomy shock (Table 4-3). Thus,
vasodilatory shock seems to represent the final common pathway for profound and prolonged
shock of any etiology. 17

Dalam sirkulasi perifer, vasokonstriksi mendalam adalah respon fisiologis yang khas
untuk tekanan arteri yang cukup untuk perfusi jaringan, biasanya menyebabkan kardiogenik
atau syok hemoragik. Pada syok vasodilatasi, hasil hipotensi dari kegagalan otot polos
pembuluh darah mengerut tepat. Syok vasodilatasi ditandai oleh kedua vasodilatasi perifer
dengan hipotensi yang dihasilkan, dan ketahanan terhadap pengobatan dengan vasopressor.
Meskipun hipotensi, tingkat katekolamin plasma meningkat dan sistem renin-angiotensin
diaktifkan di vasodilator shock. 84,85 Bentuk yang paling sering ditemui dari vasodilatasi
syok syok septik. Penyebab lain vasodilator syok termasuk asidosis laktat hipoksia,
keracunan karbon monoksida, dekompensasi dan tidak dapat diubah syok hemoragik, syok
kardiogenik terminal, dan postcardiotomy syok (Tabel 4-3). Dengan demikian, shock
vasodilatasi tampaknya mewakili jalur akhir yang umum untuk shock mendalam dan
berkepanjangan etiologi apapun. 17
Table 4-3 Causes of Vasodilatory Shock

Sepsis
Prolonged and severe hypotension
Hemorrhagic shock
Cardiogenic shock
Cardiopulmonary bypass
Inadequate tissue oxygenation
Hypoxic lactic acidosis
Carbon monoxide poisoning

Modified with permission from Landry et al. 17

Diagnosis
Attempts to standardize terminology have led to the establishment of criteria for the diagnosis
of sepsis in the hospitalized adult. These criteria include manifestations of the host response
to infection, in addition to identification of an offending organism. The terms sepsis, severe
sepsis, and septic shock are used to quantify the magnitude of the systemic inflammatory
reaction. Patients with sepsis have evidence of an infection, as well as systemic signs of
inflammation (e.g., fever, leukocytosis, and tachycardia). Hypoperfusion with signs of organ
dysfunction is termed severe sepsis.Septic shock requires the presence of the above,
associated with more significant evidence of tissue hypoperfusion and systemic hypotension.
Beyond the hypotension, maldistribution of blood flow and shunting in the microcirculation
further compromise delivery of nutrients to the tissue beds. 90
Recognizing septic shock begins with defining the patient at risk. The clinical manifestations
of septic shock will usually become evident and prompt the initiation of treatment before
bacteriologic confirmation of an organism or the source of an organism is identified. In
addition to fever, tachycardia, and tachypnea, signs of hypoperfusion such as confusion,

malaise, oliguria, or hypotension may be present. These should prompt an aggressive search
for infection including a thorough physical exam, inspection of all wounds, evaluation of
intravascular catheters or other foreign bodies, obtaining appropriate cultures, and adjunctive
imaging studies as needed.
iagnosa

Upaya untuk membakukan terminologi telah menyebabkan pembentukan kriteria untuk

diagnosis sepsis dalam dewasa dirawat di rumah sakit. Kriteria ini termasuk manifestasi dari
respon host terhadap infeksi, selain identifikasi organisme menyinggung. Istilah sepsis, sepsis
berat, dan syok septik yang digunakan untuk mengukur besarnya reaksi inflamasi sistemik.
Pasien dengan sepsis memiliki bukti infeksi, serta tanda-tanda sistemik peradangan
(misalnya, demam, leukositosis, dan takikardia). Hipoperfusi dengan tanda-tanda disfungsi
organ disebut syok sepsis.Septic parah membutuhkan kehadiran di atas, terkait dengan bukti
yang lebih signifikan hipoperfusi jaringan dan hipotensi sistemik. Di luar hipotensi,
maldistribution aliran darah dan shunting dalam mikrosirkulasi pengiriman kompromi lebih
lanjut dari nutrisi ke tempat tidur jaringan. 90
Menyadari syok septik dimulai dengan mendefinisikan pasien pada risiko. Manifestasi klinis
syok septik biasanya akan menjadi jelas dan meminta memulai pengobatan sebelum
konfirmasi bakteriologis dari suatu organisme atau sumber organisme diidentifikasi. Selain
demam, takikardia, dan takipnea, tanda-tanda hipoperfusi seperti kebingungan, malaise,
oliguria, atau hipotensi mungkin ada. Ini harus segera pencarian agresif untuk infeksi
termasuk pemeriksaan menyeluruh fisik, pemeriksaan semua luka, evaluasi kateter
intravaskular atau badan asing lainnya, mendapatkan budaya yang tepat, dan studi pencitraan
ajuvan sesuai kebutuhan.
Treatment
Evaluation of the patient in septic shock begins with an assessment of the adequacy of their
airway and ventilation. Severely obtunded patients and patients whose work of breathing is
excessive require intubation and ventilation to prevent respiratory collapse. Since
vasodilation and decrease in total peripheral resistance may produce hypotension, fluid
resuscitation and restoration of circulatory volume with balanced salt solutions is essential.
Empiric antibiotics must be chosen carefully based on the most likely pathogens (gramnegative rods, gram-positive cocci, and anaerobes), since the portal of entry of the offending
organism and its identity may not be evident until culture data return or imaging studies are
completed. Knowledge of the bacteriologic profile of infections in an individual unit can be
obtained from most hospital infection control departments and will suggest potential
responsible organisms. Antibiotics should be tailored to cover the responsible organisms once
culture data are available, and if appropriate, the spectrum of coverage narrowed. Long-term
empiric broad-spectrum antibiotic use should be minimized to reduce the development of
resistant organisms, and to avoid the potential complications of fungal overgrowth and
antibiotic-associated colitis from overgrowth of Clostridium difficile. Intravenous antibiotics
will be insufficient to adequately treat the infectious episode in the settings of infected fluid
collections, infected foreign bodies, and devitalized tissue. These situations may require
multiple operations to ensure proper wound hygiene and healing.

Evaluasi pasien dalam syok septik dimulai dengan penilaian terhadap kecukupan saluran
napas dan ventilasi mereka. Parah pasien obtunded dan pasien yang kerja pernapasan
berlebihan membutuhkan intubasi dan ventilasi untuk mencegah keruntuhan pernapasan.
Karena vasodilatasi dan penurunan resistensi perifer total dapat menghasilkan hipotensi,
resusitasi cairan dan pemulihan volume sirkulasi dengan larutan garam seimbang sangat
penting. Antibiotik empiris harus dipilih dengan cermat berdasarkan patogen yang paling
mungkin (batang gram negatif, gram-positif cocci, dan anaerob), karena portal masuk dari
organisme menyinggung dan identitasnya mungkin tidak jelas sampai kembali data yang
budaya atau pencitraan studi selesai. Pengetahuan tentang profil bakteriologis infeksi di unit
masing-masing dapat diperoleh dari sebagian departemen pengendalian infeksi di rumah sakit
dan akan menyarankan organisme yang bertanggung jawab potensial. Antibiotik harus
disesuaikan untuk menutupi organisme yang bertanggung jawab setelah data budaya yang
tersedia, dan jika sesuai, spektrum cakupan menyempit. Empiris jangka panjang spektrum
luas penggunaan antibiotik harus diminimalkan untuk mengurangi perkembangan organisme
resisten, dan untuk menghindari potensi komplikasi pertumbuhan berlebih jamur dan
antibiotik colitis dari pertumbuhan berlebih dari Clostridium difficile. Antibiotik intravena
akan cukup untuk mengobati memadai episode menular dalam pengaturan koleksi terinfeksi
cairan, benda asing yang terinfeksi, dan jaringan devitalized. Situasi ini mungkin memerlukan
beberapa operasi untuk memastikan kebersihan luka yang tepat dan penyembuhan.
The majority of septic patients have hyperdynamic physiology with supranormal cardiac
output and low systemic vascular resistance. On occasion, septic patients may have low
cardiac output despite volume resuscitation and even vasopressor support. Mortality in this
group is high. Despite the increasing incidence of septic shock over the past several decades,
the overall mortality rates have changed little. Studies of interventions including
immunotherapy, resuscitation to pulmonary artery endpoints with hemodynamic optimization
(cardiac output and oxygen delivery, even to supranormal values), and optimization of mixed
venous oxygen measurements up to 72 hours after admission to the intensive care unit have
not changed mortality. Negative results from these studies have led to the suggestion that
earlier interventions directed at improving global tissue oxygenation may be of benefit. To
this end, Rivers and colleagues reported that goal-directed therapy of septic shock and severe
sepsis initiated in the emergency department and continued for 6 hours significantly
improved outcome. 91 This approach involved adjustment of cardiac preload, afterload, and
contractility to balance oxygen delivery with oxygen demand. They found that goal-directed
therapy during the first 6 hours of hospital stay (initiated in the emergency department) had
significant effects, such as higher mean venous oxygen saturation, lower lactate levels, lower
base deficit, higher pH, and decreased 28-day mortality (49.2 vs. 33.3%) compared to the
standard therapy group. The frequency of sudden cardiovascular collapse was also
significantly less in the group managed with goal-directed therapy (21.0 vs. 10.3%).
Interestingly, the goal-directed therapy group received more intravenous fluids during the
initial 6 hours, but the standard therapy group required more intravenous fluid by 72 hours.
The authors emphasize that continued cellular and tissue decompensation is subclinical and
often irreversible when obvious clinically. Goal-directed therapy allowed identification and
treatment of these patients with insidious illness (global tissue hypoxia in the setting of
normal vital signs).
After first-line therapy of the septic patient with antibiotics, intravenous fluids, and intubation
if necessary, vasopressors may be necessary to treat patients with septic shock.
Catecholamines are the vasopressors used most often. Occasionally, patients with septic
shock will develop arterial resistance to catecholamines. Arginine vasopressin, a potent

vasoconstrictor, is often efficacious in this setting. 18

Hyperglycemia and insulin resistance are typical in critically-ill and septic patients, including
patients without underlying diabetes mellitus. A recent study reported significant positive
impact of tight glucose management on outcome in critically-ill patients. 92 The two
treatment groups in this randomized, prospective study were assigned to receive intensive
insulin therapy (maintenance of blood glucose between 80 and 110 mg/dL) or conventional
treatment (infusion of insulin only if the blood glucose level exceeded 215 mg/dL, with a
goal between 180 and 200 mg/dL). The mean morning glucose level was significantly higher
in the conventional treatment as compared to the intensive insulin therapy group (153 vs. 103
mg/dL). Mortality in the intensive insulin treatment group (4.6%) was significantly lower
than in the conventional treatment group (8.0%), representing a 42% reduction in mortality.
This reduction in mortality was most notable in the patients requiring longer than 5 days in
the ICU. Furthermore, intensive insulin therapy reduced episodes of septicemia by 46%,
reduced duration of antibiotic therapy, and decreased the need for prolonged ventilatory
support and renal replacement therapy.

fatal. 88 Sepsis accounts for 9.3% of deaths in the United States, as many yearly as
myocardial infarction. Septic shock is a by-product of the body's response to invasive or
severe localized infection, typically from bacterial or fungal pathogens. In the attempt to
eradicate the pathogens, the immune and other cell types (e.g., endothelial cells) elaborate
soluble mediators that enhance macrophage and neutrophil killing effector mechanisms,
increase procoagulant activity and fibroblast activity to localize the invaders, and increase
microvascular blood flow to enhance delivery of killing forces to the area of invasion. When
this response is overly exuberant or becomes systemic rather than localized, manifestations of
sepsis may be evident. These findings include enhanced cardiac output, peripheral
vasodilation, fever, leukocytosis, hyperglycemia, and tachycardia. In septic shock, the
vasodilatory effects are due in part to the upregulation of the inducible isoform of nitric oxide
synthase (iNOS or NOS 2) in the vessel wall. iNOS produces large quantities of nitric oxide
for sustained periods of time. This potent vasodilator suppresses vascular tone and renders the
vasculature resistant to the effects of vasoconstricting agents. 89
Diagnosis
Attempts to standardize terminology have led to the establishment of criteria for the diagnosis
of sepsis in the hospitalized adult. These criteria include manifestations of the host response
to infection, in addition to identification of an offending organism. The terms sepsis, severe
sepsis, and septic shock are used to quantify the magnitude of the systemic inflammatory
reaction. Patients with sepsis have evidence of an infection, as well as systemic signs of
inflammation (e.g., fever, leukocytosis, and tachycardia). Hypoperfusion with signs of organ
dysfunction is termed severe sepsis.Septic shock requires the presence of the above,
associated with more significant evidence of tissue hypoperfusion and systemic hypotension.
Beyond the hypotension, maldistribution of blood flow and shunting in the microcirculation
further compromise delivery of nutrients to the tissue beds. 90
Recognizing septic shock begins with defining the patient at risk. The clinical manifestations
of septic shock will usually become evident and prompt the initiation of treatment before
bacteriologic confirmation of an organism or the source of an organism is identified. In

addition to fever, tachycardia, and tachypnea, signs of hypoperfusion such as confusion,

malaise, oliguria, or hypotension may be present. These should prompt an aggressive search
for infection including a thorough physical exam, inspection of all wounds, evaluation of
intravascular catheters or other foreign bodies, obtaining appropriate cultures, and adjunctive
imaging studies as needed.
Treatment
Evaluation of the patient in septic shock begins with an assessment of the adequacy of their
airway and ventilation. Severely obtunded patients and patients whose work of breathing is
excessive require intubation and ventilation to prevent respiratory collapse. Since
vasodilation and decrease in total peripheral resistance may produce hypotension, fluid
resuscitation and restoration of circulatory volume with balanced salt solutions is essential.
Empiric antibiotics must be chosen carefully based on the most likely pathogens (gramnegative rods, gram-positive cocci, and anaerobes), since the portal of entry of the offending
organism and its identity may not be evident until culture data return or imaging studies are
completed. Knowledge of the bacteriologic profile of infections in an individual unit can be
obtained from most hospital infection control departments and will suggest potential
responsible organisms. Antibiotics should be tailored to cover the responsible organisms once
culture data are available, and if appropriate, the spectrum of coverage narrowed. Long-term
empiric broad-spectrum antibiotic use should be minimized to reduce the development of
resistant organisms, and to avoid the potential complications of fungal overgrowth and
antibiotic-associated colitis from overgrowth of Clostridium difficile. Intravenous antibiotics
will be insufficient to adequately treat the infectious episode in the settings of infected fluid
collections, infected foreign bodies, and devitalized tissue. These situations may require
multiple operations to ensure proper wound hygiene and healing.
The majority of septic patients have hyperdynamic physiology with supranormal cardiac
output and low systemic vascular resistance. On occasion, septic patients may have low
cardiac output despite volume resuscitation and even vasopressor support. Mortality in this
group is high. Despite the increasing incidence of septic shock over the past several decades,
the overall mortality rates have changed little. Studies of interventions including
immunotherapy, resuscitation to pulmonary artery endpoints with hemodynamic optimization
(cardiac output and oxygen delivery, even to supranormal values), and optimization of mixed
venous oxygen measurements up to 72 hours after admission to the intensive care unit have
not changed mortality. Negative results from these studies have led to the suggestion that
earlier interventions directed at improving global tissue oxygenation may be of benefit. To
this end, Rivers and colleagues reported that goal-directed therapy of septic shock and severe
sepsis initiated in the emergency department and continued for 6 hours significantly
improved outcome. 91 This approach involved adjustment of cardiac preload, afterload, and
contractility to balance oxygen delivery with oxygen demand. They found that goal-directed
therapy during the first 6 hours of hospital stay (initiated in the emergency department) had
significant effects, such as higher mean venous oxygen saturation, lower lactate levels, lower
base deficit, higher pH, and decreased 28-day mortality (49.2 vs. 33.3%) compared to the
standard therapy group. The frequency of sudden cardiovascular collapse was also
significantly less in the group managed with goal-directed therapy (21.0 vs. 10.3%).
Interestingly, the goal-directed therapy group received more intravenous fluids during the
initial 6 hours, but the standard therapy group required more intravenous fluid by 72 hours.
The authors emphasize that continued cellular and tissue decompensation is subclinical and
often irreversible when obvious clinically. Goal-directed therapy allowed identification and

treatment of these patients with insidious illness (global tissue hypoxia in the setting of
normal vital signs).
After first-line therapy of the septic patient with antibiotics, intravenous fluids, and intubation
if necessary, vasopressors may be necessary to treat patients with septic shock.
Catecholamines are the vasopressors used most often. Occasionally, patients with septic
shock will develop arterial resistance to catecholamines. Arginine vasopressin, a potent
vasoconstrictor, is often efficacious in this setting
Sebagian besar pasien septik memiliki fisiologi hiperdinamik dengan curah jantung di atas normal
dan resistensi vaskular sistemik yang rendah. Pada kesempatan, pasien sepsis mungkin memiliki
curah jantung rendah meskipun resusitasi volume dan bahkan dukungan vasopressor. Kematian
dalam kelompok ini adalah tinggi. Meskipun meningkatnya insiden syok septik selama beberapa
dekade terakhir, tingkat kematian secara keseluruhan telah berubah sedikit. Studi intervensi
termasuk imunoterapi, resusitasi untuk endpoint arteri pulmonalis dengan optimasi hemodinamik
(curah jantung dan pengiriman oksigen, bahkan di atas normal nilai), dan optimalisasi campuran
pengukuran oksigen vena hingga 72 jam setelah masuk ke unit perawatan intensif tidak berubah
kematian. Hasil negatif dari studi ini telah menyebabkan saran bahwa intervensi sebelumnya
diarahkan untuk meningkatkan oksigenasi jaringan global yang mungkin bermanfaat. Untuk tujuan
ini, Sungai dan rekannya melaporkan bahwa terapi diarahkan pada tujuan dari syok septik dan sepsis
berat dimulai di departemen darurat dan dilanjutkan selama 6 jam secara signifikan meningkatkan
hasil. 91 Pendekatan ini melibatkan penyesuaian preload jantung, afterload, dan kontraktilitas untuk
menyeimbangkan pengiriman oksigen dengan kebutuhan oksigen. Mereka menemukan bahwa
terapi diarahkan pada tujuan selama 6 jam pertama menginap di rumah sakit (dimulai di
departemen darurat) memiliki efek signifikan, seperti saturasi yang lebih tinggi berarti vena oksigen,
kadar laktat yang lebih rendah, defisit basa rendah, pH yang lebih tinggi, dan penurunan 28-hari
mortalitas (49,2 vs 33,3%) dibandingkan dengan kelompok terapi standar. Frekuensi runtuh
kardiovaskular mendadak juga secara signifikan lebih sedikit pada kelompok yang dikelola dengan
terapi diarahkan pada tujuan (21,0 vs 10,3%). Menariknya, kelompok terapi diarahkan pada tujuan
menerima lebih banyak cairan intravena selama awal 6 jam, tetapi kelompok terapi standar yang
diperlukan cairan intravena lebih sebesar 72 jam. Para penulis menekankan bahwa lanjutan
dekompensasi seluler dan jaringan yang subklinis dan sering ireversibel ketika jelas secara klinis.
Terapi memungkinkan identifikasi diarahkan pada tujuan dan pengobatan pasien dengan penyakit
berbahaya (hipoksia jaringan global dalam pengaturan tanda-tanda vital normal).

Setelah terapi lini pertama pasien septik dengan antibiotik, cairan intravena, dan intubasi jika perlu,
vasopressor mungkin diperlukan untuk mengobati pasien dengan syok septik. Katekolamin adalah
vasopressor paling sering digunakan. Kadang-kadang, pasien dengan syok septik akan
mengembangkan resistensi arteri terhadap katekolamin. Vasopressin arginin, suatu vasokonstriktor
kuat, sering manjur dalam pengaturan ini. 18

Hiperglikemia dan resistensi insulin yang khas pada pasien sakit kritis dan septic, termasuk pasien
tanpa mendasari diabetes mellitus. Sebuah studi baru-baru ini melaporkan dampak positif yang
signifikan dari manajemen glukosa ketat pada hasil pada pasien sakit kritis. 92 Kedua kelompok

perlakuan dalam, studi prospektif ini dilakukan secara acak ditugaskan untuk menerima terapi
insulin intensif (pemeliharaan glukosa darah antara 80 dan 110 mg / dL) atau pengobatan
konvensional (infus insulin hanya jika tingkat glukosa darah melebihi 215 mg / dL, dengan tujuan
antara 180 dan 200 mg / dL). Tingkat glukosa pagi rata-rata secara signifikan lebih tinggi dalam
pengobatan konvensional dibandingkan dengan kelompok terapi insulin intensif (153 vs 103 mg /
dL). Kematian pada kelompok terapi insulin intensif (4,6%) secara signifikan lebih rendah dibanding
pada kelompok konvensional pengobatan (8,0%), yaitu penurunan 42% angka kematian. Penurunan
mortalitas adalah yang paling menonjol pada pasien yang membutuhkan lebih dari 5 hari di ICU.
Selanjutnya, terapi insulin intensif mengurangi episode septikemia sebesar 46%, mengurangi durasi
terapi antibiotik, dan penurunan kebutuhan untuk berkepanjangan dukungan ventilasi dan terapi
penggantian ginjal.

Neurogenic Shock
Neurogenic shock refers to diminished tissue perfusion as a result of loss of vasomotor tone
to peripheral arterial beds. Loss of vasoconstrictor impulses results in increased vascular
capacitance, decreased venous return, and decreased cardiac output. Neurogenic shock is
usually secondary to spinal cord injuries from vertebral body fractures of the cervical or high
thoracic region that disrupt sympathetic regulation of peripheral vascular tone. Rarely, a
spinal cord injury without bony fracture, such as an epidural hematoma impinging on the
spinal cord, can produce neurogenic shock. Sympathetic input to the heart, which normally
increases heart rate and cardiac contractility, and input to the adrenal medulla, which
increases catecholamine release, may also be disrupted, preventing the typical reflex
tachycardia that occurs with hypovolemia. Acute spinal cord injury results in activation of
multiple secondary injury mechanisms: (1) vascular compromise to the spinal cord with loss
of autoregulation, vasospasm, and thrombosis, (2) loss of cellular membrane integrity and
impaired energy metabolism, and (3) neurotransmitter accumulation and release of free
radicals. Importantly, hypotension contributes to the worsening of acute spinal cord injury as
the result of further reduction in blood flow to the spinal cord. Management of acute spinal
cord injury with attention to blood pressure control, oxygenation, and hemodynamics,
essentially optimizing perfusion of an already ischemic spinal cord, seems to result in
improved neurologic outcome. Patients with hypotension from spinal cord injury are best
monitored in an intensive care unit, and carefully followed for evidence of cardiac or
respiratory dysfunction.
neurogenik Syok

Syok neurogenik mengacu pada perfusi jaringan berkurang sebagai akibat dari hilangnya tonus
vasomotor ke arteri perifer tidur. Kehilangan hasil impuls vasokonstriktor peningkatan kapasitansi
vaskular, penurunan aliran balik vena, dan penurunan curah jantung. Syok neurogenik biasanya
sekunder untuk cedera tulang belakang dari fraktur tubuh vertebral dari daerah thoraks serviks atau
tinggi yang mengganggu regulasi simpatik tonus pembuluh darah perifer. Jarang, cedera tulang
belakang tanpa fraktur tulang, seperti hematoma epidural menimpa pada saraf tulang belakang,
dapat menghasilkan syok neurogenik. Masukan simpatik terhadap jantung, yang biasanya

meningkatkan denyut jantung dan kontraktilitas jantung, dan masukan ke medula adrenal, yang
meningkatkan pelepasan katekolamin, juga akan terganggu, mencegah refleks takikardia khas yang
terjadi dengan hipovolemia. Akut tulang belakang hasil cedera tulang dalam aktivasi beberapa
mekanisme cedera sekunder: (1) gangguan vaskular ke sumsum tulang belakang dengan hilangnya
autoregulasi, vasospasme, dan trombosis, (2) hilangnya integritas membran sel dan metabolisme
energi terganggu, dan (3) neurotransmitter akumulasi dan pelepasan radikal bebas. Yang penting,
hipotensi berkontribusi terhadap memburuknya cedera tulang belakang akut sebagai akibat dari
pengurangan lebih lanjut dalam aliran darah ke sumsum tulang belakang. Pengelolaan cedera tulang
belakang akut dengan memperhatikan pengendalian tekanan darah, oksigenasi, dan hemodinamik,
pada dasarnya mengoptimalkan perfusi dari sumsum tulang belakang yang sudah iskemik,
tampaknya menghasilkan peningkatan hasil neurologis. Pasien dengan hipotensi dari cedera tulang
belakang yang terbaik dipantau di unit perawatan intensif, dan hati-hati diikuti untuk bukti disfungsi
jantung atau pernapasan.

Diagnosis
Acute spinal cord injury may result in bradycardia, hypotension, cardiac dysrhythmias,
reduced cardiac output, and decreased peripheral vascular resistance. The severity of the
spinal cord injury seems to correlate with the magnitude of cardiovascular dysfunction.
Patients with complete motor injuries are over five times more likely to require vasopressors
for neurogenic shock, as compared to those with incomplete lesions. 96 The classic
description of neurogenic shock consists of decreased blood pressure associated with
bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge), warm
extremities (loss of peripheral vasoconstriction), motor and sensory deficits indicative of a
spinal cord injury, and radiographic evidence of a vertebral column fracture. Patients with
multisystem trauma that includes spinal cord injuries often have head injuries that may make
identification of motor and sensory deficits difficult in the initial evaluation. Furthermore,
associated injuries may occur that result in hypovolemia, further complicating the clinical
presentation. In a subset of patients with spinal cord injuries from penetrating wounds, most
of the patients with hypotension had blood loss as the etiology (74%) rather than neurogenic
causes, and few (7%) had the classic findings of neurogenic shock. 97 In the multiply-injured
patient, other causes of hypotension including hemorrhage, tension pneumothorax, and
cardiogenic shock must be sought and excluded.
diagnosa

Cedera tulang belakang akut dapat menyebabkan bradikardia, hipotensi, disritmia jantung,
penurunan curah jantung, dan penurunan resistensi pembuluh darah perifer. Tingkat keparahan
cedera tulang belakang tampaknya berkorelasi dengan besarnya disfungsi kardiovaskular. Pasien
dengan cedera bermotor yang lengkap lebih dari lima kali lebih mungkin untuk memerlukan
vasopresor untuk shock neurogenik, dibandingkan dengan mereka dengan lesi yang tidak lengkap.
96 Gambaran klasik syok neurogenik terdiri dari penurunan tekanan darah yang berhubungan
dengan bradikardia (tidak adanya takikardia refleksif karena terganggu debit simpatik), ekstremitas
hangat (hilangnya vasokonstriksi perifer), motorik dan defisit sensorik indikasi dari cedera tulang
belakang, dan bukti radiografi dari kolom patah tulang belakang. Pasien dengan trauma multisistem
yang mencakup cedera tulang belakang sering memiliki cedera kepala yang dapat membuat

identifikasi motor dan defisit sensorik sulit dalam evaluasi awal. Selanjutnya, cedera terkait dapat
terjadi akibat bahwa pada hipovolemia, lebih rumit presentasi klinis. Dalam subset dari pasien
dengan cedera tulang belakang dari luka tembus, sebagian besar pasien dengan hipotensi memiliki
kehilangan darah sebagai etiologi (74%) daripada penyebab neurogenik, dan beberapa (7%) memiliki
temuan klasik syok neurogenik. 97 Pada pasien multiply-luka, penyebab lain dari hipotensi termasuk
perdarahan, ketegangan pneumotoraks, dan syok kardiogenik harus dicari dan dikecualikan.

Treatment
After the airway is secured and ventilation is adequate, fluid resuscitation and restoration of
intravascular volume will often improve perfusion in neurogenic shock. Most patients with
neurogenic shock will respond to restoration of intravascular volume alone, with satisfactory
improvement in perfusion and resolution of hypotension. Administration of vasoconstrictors
will improve peripheral vascular tone, decrease vascular capacitance, and increase venous
return, but should only be considered once hypovolemia is excluded as the cause of the
hypotension, and the diagnosis of neurogenic shock established. If the patient's blood
pressure has not responded to what is felt to be adequate volume resuscitation, dopamine may
be utilized first. A pure
-agonist, such as phenylephrine may be used primarily or in
patients unresponsive to dopamine. Specific treatment for the hypotension is often of brief
duration, as the need to administer vasoconstrictors typically lasts 24 to 48 hours. On the
other hand, life-threatening cardiac dysrhythmias and hypotension may occur up to 14 days
after spinal cord injury.
The duration of the need for vasopressor support for neurogenic shock may correlate with the
overall prognosis or chances of improvement in neurologic function. As mentioned,
appropriate rapid restoration of blood pressure and circulatory perfusion may improve
perfusion to the spinal cord, prevent progressive spinal cord ischemia, and minimize
secondary cord injury. Restoration of normal blood pressure and adequate tissue perfusion
should precede any operative attempts to stabilize the vertebral fracture.
pengobatan

Setelah jalan napas dijamin dan ventilasi memadai, resusitasi cairan dan pemulihan volume
intravaskular sering akan meningkatkan perfusi shock neurogenik. Kebanyakan pasien dengan syok
neurogenik akan merespon pemulihan volume intravaskular saja, dengan peningkatan yang
memuaskan dalam perfusi dan resolusi hipotensi. Administrasi vasokonstriktor akan meningkatkan
tonus pembuluh darah perifer, menurunkan kapasitansi vaskular, dan meningkatkan aliran balik
vena, tetapi hanya harus dipertimbangkan setelah hipovolemia dikecualikan sebagai penyebab
hipotensi, dan diagnosis syok neurogenik didirikan. Jika tekanan darah pasien tidak menanggapi apa
yang dirasakan resusitasi volume yang memadai, dopamin dapat digunakan terlebih dahulu. Sebuah
-agonist murni, seperti phenylephrine dapat digunakan terutama atau pada pasien tidak responsif
terhadap dopamin. Pengobatan khusus untuk hipotensi sering durasi singkat, sebagai kebutuhan
untuk mengelola vasokonstriktor biasanya berlangsung 24 sampai 48 jam. Di sisi lain, detak jantung
tak beraturan yang mengancam jiwa dan hipotensi dapat terjadi hingga 14 hari setelah cedera tulang
belakang.

Durasi perlunya dukungan vasopressor untuk shock neurogenik dapat berkorelasi dengan prognosis
keseluruhan atau kemungkinan peningkatan fungsi neurologis. Seperti disebutkan, pemulihan yang
cepat tepat tekanan darah dan perfusi sirkulasi dapat meningkatkan perfusi ke sumsum tulang
belakang, mencegah progresif iskemia saraf tulang belakang, dan meminimalkan cedera tulang
sekunder. Pemulihan tekanan darah normal dan perfusi jaringan yang memadai harus mendahului
setiap upaya operasi untuk menstabilkan patah tulang belakang.