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Shock (circulatory)
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<h2 id="signs-and-symptoms">Signs and symptoms</h2> <p>The presentation of shock is variable, with some people having only minimal symptoms such as confusion and weakness.<a class="footnote-ref" id="fnref:12" href="#fn:12"><sup>12</sup></a> While the general signs for all types of shock are <a href="/facts/Hypotension/BhrdVVRS">low blood pressure</a>, decreased <a href="/facts/Urine_output/H4qYz02K">urine output</a>, and confusion, these may not always be present.<a class="footnote-ref" id="fnref:13" href="#fn:13"><sup>13</sup></a> While a fast heart rate is common, in those on <a href="/facts/Beta_blocker/PRsWgpLV">β-blockers</a>, those who are athletic, and in 30% of cases of those with shock due to intra abdominal bleeding, heart rate may be normal or slow.<a class="footnote-ref" id="fnref:14" href="#fn:14"><sup>14</sup></a> Specific subtypes of shock may have additional symptoms. </p><p>Dry <a href="/facts/Mucous_membranes/oIw0vyel">mucous membrane</a>, reduced <a href="/facts/Skin_turgor/2RXJ8GGI">skin turgor</a>, prolonged <a href="/facts/Capillary_refill_time/cMVGB55I">capillary refill time</a>, weak peripheral pulses, and cold extremities can be early signs of shock.<a class="footnote-ref" id="fnref:15" href="#fn:15"><sup>15</sup></a> </p> <h3>Low volume</h3> <p class="note">Main articles: <a href="/facts/Hypovolemia/MmP8TsPw">Hypovolemia</a> and <a href="/facts/Hypovolemic_shock/f0hWLC8R">Hypovolemic shock</a></p><p><a href="/facts/Hypovolemic_shock/f0hWLC8R">Hypovolemic shock</a> is the most common type of shock and is caused by insufficient circulating <a href="/facts/Blood_volume/6UcBgKGs">volume</a>.<a class="footnote-ref" id="fnref:16" href="#fn:16"><sup>16</sup></a> The most common cause of hypovolemic shock is <a href="/facts/Haemorrhage/CGyFMU0F">hemorrhage</a> (internal or external); however, <a href="/facts/Vomiting/R2vQkHqV">vomiting</a> and <a href="/facts/Diarrhea/6TBHaRdA">diarrhea</a> are more common causes in children.<a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a> Other causes include burns, as well as excess urine loss due to <a href="/facts/Diabetic_ketoacidosis/QhhbSbeM">diabetic ketoacidosis</a> and <a href="/facts/Diabetes_insipidus/mtAXABCU">diabetes insipidus</a>.<a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a> </p>Hemorrhage classes<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a><table><tbody><tr><th>Class</th><th>Blood loss (liters)</th><th>Response</th><th>Treatment</th></tr><tr><td>I</td><td><15% (0.75 L)</td><td>min. fast heart rate, normal blood pressure</td><td>minimal</td></tr><tr><td>II</td><td>15–30% (0.75–1.5 L)</td><td>fast heart rate, min. low blood pressure</td><td>intravenous fluids</td></tr><tr><td>III</td><td>30–40% (1.5–2 L)</td><td>very fast heart rate, low blood pressure, confusion</td><td>fluids and packed RBCs</td></tr><tr><td>IV</td><td>>40% (>2 L)</td><td>critical blood pressure and heart rate</td><td>aggressive interventions</td></tr></tbody></table> <p>Signs and symptoms of hypovolemic shock include: </p> <ul><li>A rapid, weak, thready pulse due to decreased blood flow combined with <a href="/facts/Tachycardia/ycmyzP7q">tachycardia</a></li> <li>Cool skin due to <a href="/facts/Vasoconstriction/9hdY0aR2">vasoconstriction</a> and stimulation of vasoconstriction</li> <li>Rapid and <a href="/facts/Shallow_breathing/nDBG3vNn">shallow breathing</a> due to <a href="/facts/Sympathetic_nervous_system/hs8psNRd">sympathetic nervous system</a> stimulation and <a href="/facts/Acidosis/hmfAo1uR">acidosis</a></li> <li><a href="/facts/Hypothermia/lIYDCIAv">Hypothermia</a> due to decreased <a href="/facts/Perfusion/EFVLNUTg">perfusion</a> and evaporation of sweat</li> <li>Thirst and dry mouth, due to fluid depletion</li> <li>Cold and mottled skin (<a href="/facts/Livedo_reticularis/jJ9WBGlh">livedo reticularis</a>), especially extremities, due to insufficient perfusion of the skin</li></ul> <p>The severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. The <a href="/facts/Shock_index/f0hWLC8R">shock index</a> (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone.<a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> This relationship has not been well established in pregnancy-related bleeding.<a class="footnote-ref" id="fnref:21" href="#fn:21"><sup>21</sup></a> </p> <h3>Cardiogenic</h3> <p class="note">Main article: <a href="/facts/Cardiogenic_shock/d6YCjHXm">Cardiogenic shock</a></p> <p><a href="/facts/Cardiogenic_shock/d6YCjHXm">Cardiogenic shock</a> is caused by the failure of the heart to pump effectively.<a class="footnote-ref" id="fnref:22" href="#fn:22"><sup>22</sup></a> This can be due to damage to the heart muscle, most often from a large <a href="/facts/Myocardial_infarction/xoGw0qcG">myocardial infarction</a>. Other causes of cardiogenic shock include <a href="/facts/Cardiac_dysrhythmia/ooEpr46Q">dysrhythmias</a>, <a href="/facts/Cardiomyopathy/rhXF3Vcj">cardiomyopathy</a>/<a href="/facts/Myocarditis/ypoBJ4Pp">myocarditis</a>, <a href="/facts/Congestive_heart_failure/7fckX3Jm">congestive heart failure</a> (CHF), <a href="/facts/Myocardial_contusion/G7p6Ck9W">myocardial contusion</a>, or <a href="/facts/Valvular_heart_disease/jbURjwR9">valvular heart disease</a> problems.<a class="footnote-ref" id="fnref:23" href="#fn:23"><sup>23</sup></a> </p><p>Symptoms of <a href="/facts/Cardiogenic_shock/d6YCjHXm">cardiogenic shock</a> include: </p> <ul><li>Distended <a href="/facts/Jugular_vein/FPQY4pWm">jugular veins</a> due to increased <a href="/facts/Jugular_venous_pressure/wcKkeCU2">jugular venous pressure</a></li> <li>Weak or absent pulse</li> <li><a href="/facts/Heart_arrhythmia/ooEpr46Q">Abnormal heart rhythms</a>, often a <a href="/facts/Tachycardia/ycmyzP7q">fast heart rate</a></li> <li><a href="/facts/Pulsus_paradoxus/Brw8Tx2k">Pulsus paradoxus</a> in case of <a href="/facts/Cardiac_tamponade/kfzbVAw7">tamponade</a></li> <li><a href="/facts/Hypotension/BhrdVVRS">Reduced blood pressure</a></li> <li><a href="/facts/Shortness_of_breath/1jBfFzxU">Shortness of breath</a>, due to <a href="/facts/Pulmonary_congestion/sVS5UDxl">pulmonary congestion</a></li></ul> <h3>Obstructive</h3> <p class="note">Main article: <a href="/facts/Obstructive_shock/t17mh00C">Obstructive shock</a></p> <p><a href="/facts/Obstructive_shock/t17mh00C">Obstructive shock</a> is a form of shock associated with physical obstruction of the <a href="/facts/Great_vessels/21fgmf3a">great vessels</a> of the systemic or pulmonary circulation.<a class="footnote-ref" id="fnref:24" href="#fn:24"><sup>24</sup></a> Several conditions can result in this form of shock. </p> <ul><li><a href="/facts/Cardiac_tamponade/kfzbVAw7">Cardiac tamponade</a>, in which fluid in the <a href="/facts/Pericardium/ePd4gkeT">pericardium</a> prevents inflow of blood into the heart (<a href="/facts/Venous_return/DYRAPkS3">venous return</a>).<a class="footnote-ref" id="fnref:25" href="#fn:25"><sup>25</sup></a></li> <li><a href="/facts/Constrictive_pericarditis/0a1T0Gnj">Constrictive pericarditis</a>, in which the <a href="/facts/Pericardium/ePd4gkeT">pericardium</a> shrinks and hardens, is similar in presentation.</li> <li><a href="/facts/Tension_pneumothorax/oaCPSynh">Tension pneumothorax</a>; Through increased intrathoracic pressure, venous return is impeded.<a class="footnote-ref" id="fnref:26" href="#fn:26"><sup>26</sup></a></li> <li><a href="/facts/Pulmonary_embolism/LPjKCPba">Pulmonary embolism</a> is thromboembolism of the <a href="/facts/Lung/gTWXI6Fj">lungs</a>, hindering oxygenation and return of blood to the heart.</li> <li><a href="/facts/Aortic_stenosis/JGeoGPw2">Aortic stenosis</a> hinders circulation by obstructing the <a href="/facts/Cardiac_output/7JCDn6Ht">cardiac output</a>.</li> <li><a href="/facts/Hypertrophic_sub-aortic_stenosis/NmPkh1rh">Hypertrophic sub-aortic stenosis</a> is overly thick ventricular muscle that dynamically occludes the <a href="/facts/Ventricular_outflow_tract/5dpafByD">ventricular outflow tract</a>.</li> <li><a href="/facts/Abdominal_compartment_syndrome/fexrwPse">Abdominal compartment syndrome</a> defined as an increase in intra-abdominal pressure to > 20 mmHg with organ dysfunction.<a class="footnote-ref" id="fnref:27" href="#fn:27"><sup>27</sup></a> Increased intra-abdominal pressure can result from <a href="/facts/Sepsis/n52bkffJ">sepsis</a> and severe abdominal trauma. This increased pressure reduces venous return, thereby reducing lung-heart function, resulting in signs and symptoms of shock.<a class="footnote-ref" id="fnref:28" href="#fn:28"><sup>28</sup></a></li></ul> <p>Many of the signs of obstructive shock are similar to cardiogenic shock, although treatments differ. Symptoms of obstructive shock include: </p> <ul><li><a href="/facts/Heart_arrhythmia/ooEpr46Q">Abnormal heart rhythms</a>, often a <a href="/facts/Tachycardia/ycmyzP7q">fast heart rate</a>.</li> <li>Reduced blood pressure.</li> <li>Cool, clammy, mottled skin, often due to low blood pressure and vasoconstriction.</li> <li><a href="/facts/Oliguria/T7t2onvx">Decreased urine output</a>.</li></ul> <h3>Distributive</h3> <p class="note">Main article: <a href="/facts/Distributive_shock/cuJ0WVgs">Distributive shock</a></p> <a href="/facts/Systemic_inflammatory_response_syndrome/yBfYlqoA">Systemic inflammatory response syndrome</a><a class="footnote-ref" id="fnref:29" href="#fn:29"><sup>29</sup></a><table><tbody><tr><th>Finding</th><th>Value</th></tr><tr><td><a href="/facts/Normal_human_body_temperature/zbWKsEhF">Temperature</a></td><td><36 °C (96.8 °F) or >38 °C (100.4 °F)</td></tr><tr><td><a href="/facts/Heart_rate/YngB0bzg">Heart rate</a></td><td>>90/min</td></tr><tr><td><a href="/facts/Respiratory_rate/Ja9lsl6E">Respiratory rate</a></td><td>>20/min or <a href="/facts/Arterial_blood_gas/LGJ1peJh">PaCO2</a><32 mmHg (4.3 kPa)</td></tr><tr><td><a href="/facts/White_blood_cell_count/NF9lNJL3">WBC</a></td><td><4x109/L (<4000/mm3), >12x109/L (>12,000/mm3), or ≥10% <a href="/facts/Immature_neutrophil/nLpqbgAx">bands</a></td></tr></tbody></table> <p><a href="/facts/Distributive_shock/cuJ0WVgs">Distributive shock</a> is low blood pressure due to a <a href="/facts/Vasodilation/cjzrU8Ro">dilation of blood vessels</a> within the body.<a class="footnote-ref" id="fnref:30" href="#fn:30"><sup>30</sup></a><a class="footnote-ref" id="fnref:31" href="#fn:31"><sup>31</sup></a> This can be caused by systemic infection (<a href="/facts/Sepsis/n52bkffJ">septic shock</a>), a severe allergic reaction (<a href="/facts/Anaphylaxis/F9IDQxeL">anaphylaxis</a>), or spinal cord injury (<a href="/facts/Neurogenic_shock/roP6TUd4">neurogenic shock</a>). </p><p class="note">Main article: <a href="/facts/Septic_shock/yc9mgmrz">Septic shock</a></p> <ul><li><a href="/facts/Septic_shock/yc9mgmrz">Septic shock</a> is the most common cause of distributive shock.<a class="footnote-ref" id="fnref:32" href="#fn:32"><sup>32</sup></a> It is caused by an overwhelming systemic infection resulting in <a href="/facts/Vasodilation/cjzrU8Ro">vasodilation</a> leading to hypotension. Septic shock can be caused by <a href="/facts/Gram_negative/S1PbVtp4">Gram negative</a> bacteria such as (among others) <i><a href="/facts/Escherichia_coli/nR4Gvl56">Escherichia coli</a></i>, <a href="/facts/Proteus_(bacterium)/pedFoHmr">Proteus</a> species, <i><a href="/facts/Klebsiella_pneumoniae/edtyTP4E">Klebsiella pneumoniae</a></i> (which have an <a href="/facts/Endotoxin/Ch967TXw">endotoxin</a> on their surface that produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body), other <a href="/facts/Gram-positive/H6WYQ17e">Gram-positive</a> cocci, such as <a href="/facts/Pneumococci/B5XxK27j">pneumococci</a> and <a href="/facts/Streptococci/Fx8lJ0nz">streptococci</a>, and certain fungi as well as Gram-positive <a href="/facts/Microbial_toxin/AXmhkDDE">bacterial toxins</a>. Septic shock also includes some elements of cardiogenic shock. In 1992, the <a href="/facts/American_College_of_Chest_Physicians/N4pdb3lk">ACCP</a>/<a href="/facts/Society_of_Critical_Care_Medicine/Ru4c49sU">SCCM</a> Consensus Conference Committee defined septic shock: " ... sepsis-induced hypotension (systolic blood pressure < 90 mmHg or a reduction of 40 mmHg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to: <a href="/facts/Lactic_acidosis/PSDwP9lP">lactic acidosis</a>, oliguria, or an acute alteration in mental status. Patients who are receiving <a href="/facts/Inotrope/A58XE1pa">inotropic</a> or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified. The pathophysiology behind septic shock is as follows: 1) Systemic <a href="/facts/Leukocyte/vsDunUK0">leukocyte</a> adhesion to endothelial cells<a class="footnote-ref" id="fnref:33" href="#fn:33"><sup>33</sup></a> 2) Reduced <a href="/facts/Myocardial_contractility/0BdQPIsv">contractility of the heart</a><a class="footnote-ref" id="fnref:34" href="#fn:34"><sup>34</sup></a> 3) Activation of the <a href="/facts/Coagulation_pathway/vnfEevM0">coagulation pathways</a>, resulting in <a href="/facts/Disseminated_intravascular_coagulation/CuWaSKQW">disseminated intravascular coagulation</a><a class="footnote-ref" id="fnref:35" href="#fn:35"><sup>35</sup></a> 4). Increased levels of <a href="/facts/Neutrophils/KL6oTt8b">neutrophils</a><a class="footnote-ref" id="fnref:36" href="#fn:36"><sup>36</sup></a> <ul><li>The main manifestations of septic shock are due to the massive release of <a href="/facts/Histamine/Vfjda665">histamine</a> which causes intense dilation of the blood vessels. People with septic shock will also likely be positive for <a href="/facts/Systemic_inflammatory_response_syndrome/yBfYlqoA">SIRS</a> criteria. The most generally accepted treatment for these patients is early recognition of symptoms, and early administration of broad spectrum and organism specific antibiotics.<a class="footnote-ref" id="fnref:37" href="#fn:37"><sup>37</sup></a></li> <li>Signs of septic shock include: <ul><li><a href="/facts/Heart_arrhythmia/ooEpr46Q">Abnormal heart rhythms</a>, often a <a href="/facts/Tachycardia/ycmyzP7q">fast heart rate</a></li> <li>Reduced blood pressure</li> <li><a href="/facts/Oliguria/T7t2onvx">Decreased urine output</a></li> <li><a href="/facts/Altered_level_of_consciousness/bzGqcsUV">Altered mental status</a></li></ul></li></ul></li> <li><a href="/facts/Anaphylactic_shock/F9IDQxeL">Anaphylactic shock</a> is caused by a severe <a href="/facts/Anaphylaxis/F9IDQxeL">anaphylactic reaction</a> to an <a href="/facts/Allergen/bnM4cttq">allergen</a>, <a href="/facts/Antigen/9JlAernG">antigen</a>, <a href="/facts/Drug/FFFUI9n4">drug</a>, or foreign protein causing the release of <a href="/facts/Histamine/Vfjda665">histamine</a> which causes widespread vasodilation, leading to hypotension and increased <a href="/facts/Capillary_permeability/AnyAKbX2">capillary permeability</a>. Signs typically occur after exposure to an allergen and may include: <ul><li>Skin changes, such as <a href="/facts/Hives/zMkVo9qL">hives</a>, itching, flushing, and swelling.</li> <li>Wheezing and <a href="/facts/Shortness_of_breath/1jBfFzxU">shortness of breath</a>.</li> <li><a href="/facts/Abdominal_pain/aF6gPB0G">Abdominal pain</a>, <a href="/facts/Diarrhea/6TBHaRdA">diarrhea</a>, and <a href="/facts/Vomiting/R2vQkHqV">vomiting</a>.</li> <li>Lightheadedness, <a href="/facts/Altered_state_of_consciousness/97vjsHXF">confusion</a>, <a href="/facts/Headache/mdmmC9DP">headaches</a>, <a href="/facts/Loss_of_consciousness/SS240v32">loss of consciousness</a>.</li></ul></li> <li>High spinal injuries may cause <a href="/facts/Neurogenic_shock/roP6TUd4">neurogenic shock</a>, which is commonly classified as a subset of distributive shock.<a class="footnote-ref" id="fnref:38" href="#fn:38"><sup>38</sup></a> The classic symptoms include <a href="/facts/Bradycardia/70msP5HD">a slow heart rate</a> due to loss of cardiac <a href="/facts/Sympathetic_nervous_system/hs8psNRd">sympathetic tone</a> and warm skin due to dilation of the peripheral blood vessels.<a class="footnote-ref" id="fnref:39" href="#fn:39"><sup>39</sup></a> (This term can be confused with <a href="/facts/Spinal_shock/Sc33Hblg">spinal shock</a> which is a recoverable loss of function of the <a href="/facts/Spinal_cord/XbWLr917">spinal cord</a> after injury and does not refer to the hemodynamic instability.)</li></ul> <h4>Endocrine</h4> <p>Although not officially classified as a subcategory of shock, many <a href="/facts/Endocrinological/PDvN5cpj">endocrinological</a> disturbances in their severe form can result in shock. </p> <ul><li><a href="/facts/Hypothyroidism/oqtQDu2F">Hypothyroidism</a> (can be considered a form of <a href="/facts/Cardiogenic_shock/d6YCjHXm">cardiogenic shock</a>) in people who are critically ill patients reduces <a href="/facts/Cardiac_output/7JCDn6Ht">cardiac output</a> and can lead to <a href="/facts/Hypotension/BhrdVVRS">hypotension</a> and respiratory insufficiency.</li> <li><a href="/facts/Hyperthyroidism/H9Eqmbgk">Thyrotoxicosis</a> (<a href="/facts/Cardiogenic_shock/d6YCjHXm">cardiogenic shock</a>) may induce a reversible <a href="/facts/Cardiomyopathy/rhXF3Vcj">cardiomyopathy</a>.</li> <li>Acute <a href="/facts/Adrenal_insufficiency/7oxdJtF4">adrenal insufficiency</a> (<a href="/facts/Distributive_shock/cuJ0WVgs">distributive shock</a>) is frequently the result of discontinuing <a href="/facts/Corticosteroid/jeL2QeIL">corticosteroid</a> treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.</li> <li>Relative <a href="/facts/Adrenal_insufficiency/7oxdJtF4">adrenal insufficiency</a> (<a href="/facts/Distributive_shock/cuJ0WVgs">distributive shock</a>) in critically ill patients where present <a href="/facts/Cortisol/5IvRV0cm">hormone levels</a> are insufficient to meet the higher demands.</li></ul> <h2 id="cause">Cause</h2> <table><tbody><tr><th>Type</th><th>Cause</th></tr><tr><td>Low volume</td><td>Fluid loss such as bleeding or diarrhea</td></tr><tr><td>Cardiogenic</td><td>Ineffective pumping due to heart damage</td></tr><tr><td>Obstructive</td><td>Blood flow to or from the heart is blocked</td></tr><tr><td>Distributive</td><td>Abnormal flow within the small blood vessels<a class="footnote-ref" id="fnref:40" href="#fn:40"><sup>40</sup></a></td></tr></tbody></table> <p>Shock is a common end point of many medical conditions.<a class="footnote-ref" id="fnref:41" href="#fn:41"><sup>41</sup></a> Shock triggered by a serious <a href="/facts/Allergic_reaction/dYAVosh8">allergic reaction</a> is known as <a href="/facts/Anaphylactic_shock/F9IDQxeL">anaphylactic shock</a>, shock triggered by severe <a href="/facts/Dehydration/2RXJ8GGI">dehydration</a> or <a href="/facts/Blood_loss/CGyFMU0F">blood loss</a> is known as <a href="/facts/Hypovolemic_shock/f0hWLC8R">hypovolemic shock</a>, shock caused by sepsis is known as <a href="/facts/Septic_shock/yc9mgmrz">septic shock</a>, etc. Shock itself is a life-threatening condition as a result of compromised <a href="/facts/Circulatory_system/WXwudzzc">body circulation</a>.<a class="footnote-ref" id="fnref:42" href="#fn:42"><sup>42</sup></a> It can be divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive.<a class="footnote-ref" id="fnref:43" href="#fn:43"><sup>43</sup></a> A few additional classifications are occasionally used, such as endocrinologic shock.<a class="footnote-ref" id="fnref:44" href="#fn:44"><sup>44</sup></a> </p> <h2 id="pathophysiology">Pathophysiology</h2> <p>Shock is a complex and continuous condition, and there is no sudden transition from one stage to the next.<a class="footnote-ref" id="fnref:45" href="#fn:45"><sup>45</sup></a> At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply.<a class="footnote-ref" id="fnref:46" href="#fn:46"><sup>46</sup></a> </p><p>One of the key dangers of shock is that it progresses by a <a href="/facts/Positive_feedback/eFGatCpF">positive feedback</a> loop. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. Normally, this causes the blood supply level to match with tissue demand for nutrients. However, if there is enough increased demand in some areas, it can deprive other areas of sufficient supply, which then start demanding more. This then leads to an ever escalating cascade. </p><p>As such, shock is a <a href="/facts/Chain_reaction/5UwHTKXS">runaway</a> condition of <a href="/facts/Homeostasis/rloTGAHa">homeostatic</a> failure, where the usual corrective mechanisms relating to oxygenation of the body no longer function in a stable way. When it occurs, immediate treatment is critical in order to return an individual's metabolism into a stable, self-correcting trajectory. Otherwise the condition can become increasingly difficult to correct, surprisingly quickly, and then progress to a fatal outcome. In the particular case of anaphylactic shock, progression to death might take just a few minutes.<a class="footnote-ref" id="fnref:47" href="#fn:47"><sup>47</sup></a> </p> <h3>Initial</h3> <p>During the Initial stage (Stage 1), the state of <a href="/facts/Hypoperfusion/EFVLNUTg">hypoperfusion</a> causes <a href="/facts/Hypoxia_(medical)/JWV04G89">hypoxia</a>. Due to the lack of oxygen, the cells perform <a href="/facts/Lactic_acid_fermentation/8eQ5uBDq">lactic acid fermentation</a>. Since oxygen, the terminal electron acceptor in the <a href="/facts/Electron_transport_chain/QjcIkgeR">electron transport chain</a>, is not abundant, this slows down entry of <a href="/facts/Pyruvate/qJTgl4J9">pyruvate</a> into the <a href="/facts/Citric_acid_cycle/EGJL9NXP">Krebs cycle</a>, resulting in its accumulation. The accumulating pyruvate is converted to <a href="/facts/Lactic_acid/BsVRFx7s">lactate (lactic acid)</a> by <a href="/facts/Lactate_dehydrogenase/FGuLGcXe">lactate dehydrogenase</a>. The accumulating lactate causes <a href="/facts/Lactic_acidosis/PSDwP9lP">lactic acidosis</a>. </p> <h3>Compensatory</h3> <p>The Compensatory stage (Stage 2) is characterised by the body employing physiological mechanisms, including neural, hormonal, and bio-chemical mechanisms, in an attempt to reverse the condition. As a result of the <a href="/facts/Acidosis/hmfAo1uR">acidosis</a>, the person will begin to <a href="/facts/Hyperventilation/ElocGGlI">hyperventilate</a> in order to rid the body of carbon dioxide (CO2) since it indirectly acts to acidify the blood; the body attempts to return to <a href="/facts/Acid%E2%80%93base_homeostasis/y4U6UENE">acid–base homeostasis</a> by removing that acidifying agent. The <a href="/facts/Baroreceptors/WDLRp2vB">baroreceptors</a> in the <a href="/facts/Artery/Y1Yj0jat">arteries</a> detect the <a href="/facts/Hypotension/BhrdVVRS">hypotension</a> resulting from large amounts of blood being redirected to distant tissues, and cause the release of <a href="/facts/Epinephrine/k7vvMI7E">epinephrine</a> and <a href="/facts/Norepinephrine/AjTIC9ox">norepinephrine</a>. Norepinephrine causes predominately <a href="/facts/Vasoconstriction/9hdY0aR2">vasoconstriction</a> with a mild increase in <a href="/facts/Heart_rate/YngB0bzg">heart rate</a>, whereas <a href="/facts/Epinephrine/k7vvMI7E">epinephrine</a> predominately causes an increase in <a href="/facts/Heart_rate/YngB0bzg">heart rate</a> with a small effect on the <a href="/facts/Blood_vessel/FG3GjPNW">vascular</a> tone; the combined effect results in an increase in <a href="/facts/Blood_pressure/VtqqSM2J">blood pressure</a>. The <a href="/facts/Renin%E2%80%93angiotensin_system/9XLt8PQL">renin–angiotensin axis</a> is activated, and <a href="/facts/Arginine_vasopressin/B1EksWWY">arginine vasopressin</a> (anti-diuretic hormone) is released to conserve fluid by reducing its excretion via the <a href="/facts/Renal/HBspPrv9">renal</a> system. These hormones cause the vasoconstriction of the <a href="/facts/Kidney/HBspPrv9">kidneys</a>, <a href="/facts/Gastrointestinal_tract/nK2zwqBS">gastrointestinal tract</a>, and other organs to divert blood to the heart, <a href="/facts/Lungs/gTWXI6Fj">lungs</a> and <a href="/facts/Brain/EKla9NkJ">brain</a>. The lack of blood to the renal system causes the characteristic low <a href="/facts/Urine/oNUYVtvX">urine</a> production. However, the effects of the renin–angiotensin axis take time and are of little importance to the immediate <a href="/facts/Homeostatic/rloTGAHa">homeostatic</a> mediation of shock. </p> <h3>Progressive/decompensated</h3> <p>The Progressive stage (stage 3) results if the underlying cause of the shock is not successfully treated. During this stage, compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells in the body, <a href="/facts/Sodium/eYuSPu2V">sodium</a> ions build up within the intracellular space while <a href="/facts/Potassium/FWPwS7Rj">potassium</a> ions leak out. Due to lack of oxygen, <a href="/facts/Cellular_respiration/kb6gpsvL">cellular respiration</a> diminishes and <a href="/facts/Anaerobic_respiration/IMSY03HG">anaerobic metabolism</a> predominates. As anaerobic metabolism continues, the arteriolar smooth muscle and precapillary <a href="/facts/Sphincters/tNRad48q">sphincters</a> relax such that blood remains in the <a href="/facts/Capillaries/4BIzKJAe">capillaries</a>.<a class="footnote-ref" id="fnref:48" href="#fn:48"><sup>48</sup></a> Due to this, the <a href="/facts/Hydrostatics/GYu6ljQ0">hydrostatic pressure</a> will increase and, combined with <a href="/facts/Histamine/Vfjda665">histamine</a> release, will lead to <a href="/facts/Extravasation/ht89d2LM">leakage of fluid</a> and <a href="/facts/Protein/Jxmagu3E">protein</a> into the surrounding tissues. As this fluid is lost, the blood concentration and <a href="/facts/Viscosity/QLVfrdCz">viscosity</a> increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to <a href="/facts/Ischemia/ySL9xbCl">reduced perfusion</a>.<a class="footnote-ref" id="fnref:49" href="#fn:49"><sup>49</sup></a> If the bowel becomes sufficiently <a href="/facts/Ischemic/ySL9xbCl">ischemic</a>, bacteria may enter the blood stream, resulting in the increased complication of <a href="/facts/Septic_shock/yc9mgmrz">endotoxic shock</a>.<a class="footnote-ref" id="fnref:50" href="#fn:50"><sup>50</sup></a><a class="footnote-ref" id="fnref:51" href="#fn:51"><sup>51</sup></a> </p> <h3>Refractory</h3> <p>At Refractory stage (stage 4), the vital <a href="/facts/Organ_failure/h5YCohyQ">organs have failed</a> and the shock can no longer be reversed. <a href="/facts/Brain_damage/70hWCEhs">Brain damage</a> and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much of the cellular <a href="/facts/Adenosine_triphosphate/nB9bwgcU">ATP</a> (the basic energy source for cells) has been degraded into <a href="/facts/Adenosine/MwyTJ2wR">adenosine</a> in the absence of oxygen as an electron receptor in the <a href="/facts/Mitochondrial_matrix/tgC0ENLv">mitochondrial matrix</a>. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary <a href="/facts/Vasodilation/cjzrU8Ro">vasodilation</a>, and then is transformed into <a href="/facts/Uric_acid/gPMSfLcT">uric acid</a>. Because cells can only produce adenosine at a rate of about 2% of the cell's total need per hour, even restoring oxygen is futile at this point because there is no adenosine to <a href="/facts/Phosphorylate/LXUEEeIL">phosphorylate</a> into ATP.<a class="footnote-ref" id="fnref:52" href="#fn:52"><sup>52</sup></a> </p> <h2 id="diagnosis">Diagnosis</h2> <p>The diagnosis of shock is commonly based on a combination of symptoms, <a href="/facts/Physical_examination/qzI0BK5P">physical examination</a>, and laboratory tests. Many signs and symptoms are not sensitive or specific for shock, thus many clinical decision-making tools have been developed to identify shock at an early stage.<a class="footnote-ref" id="fnref:53" href="#fn:53"><sup>53</sup></a> A high degree of suspicion is necessary for the proper diagnosis of shock. </p><p>Shock is, <a href="/facts/Hemodynamic/HzubzJpn">hemodynamically</a> speaking, inadequate blood flow or <a href="/facts/Cardiac_output/7JCDn6Ht">cardiac output</a>, Unfortunately, the measurement of cardiac output requires an invasive catheter, such as a pulmonary artery catheter. <a href="/facts/Mixed_venous_oxygen_saturation/UVhwuc26">Mixed venous oxygen saturation</a> (SmvO2) is one of the methods of calculating cardiac output with a pulmonary artery catheter. <a href="/facts/Central_venous_oxygen_saturation/UVhwuc26">Central venous oxygen saturation</a> (ScvO2) as measured via a central line correlates well with SmvO2 and is easier to acquire. Tissue oxygenation is critically dependent on blood flow. When the oxygenation of tissues is compromised <a href="/facts/Anaerobic_metabolism/IMSY03HG">anaerobic metabolism</a> will begin and lactic acid will be produced. <a class="footnote-ref" id="fnref:54" href="#fn:54"><sup>54</sup></a> </p> <h2 id="management">Management</h2> <p>Treatment of shock is based on the likely underlying cause.<a class="footnote-ref" id="fnref:55" href="#fn:55"><sup>55</sup></a> An open <a href="/facts/Airway/nnG9UEmr">airway</a> and sufficient <a href="/facts/Breathing/92Wov2gk">breathing</a> should be established.<a class="footnote-ref" id="fnref:56" href="#fn:56"><sup>56</sup></a> Any ongoing bleeding should be stopped, which may require surgery or <a href="/facts/Embolization/zPNry9cY">embolization</a>.<a class="footnote-ref" id="fnref:57" href="#fn:57"><sup>57</sup></a> <a href="/facts/Intravenous_fluid/AwwuD3Nu">Intravenous fluid</a>, such as <a href="/facts/Ringer%27s_lactate/Aae1Y9VR">Ringer's lactate</a> or <a href="/facts/Packed_red_blood_cells/PlmjsB1A">packed red blood cells</a>, is often given.<a class="footnote-ref" id="fnref:58" href="#fn:58"><sup>58</sup></a> Efforts to maintain a normal <a href="/facts/Body_temperature/V692hIjw">body temperature</a> are also important.<a class="footnote-ref" id="fnref:59" href="#fn:59"><sup>59</sup></a> <a href="/facts/Vasopressors/GPCuG4aT">Vasopressors</a> may be useful in certain cases.<a class="footnote-ref" id="fnref:60" href="#fn:60"><sup>60</sup></a> Shock is both common and has a high risk of death.<a class="footnote-ref" id="fnref:61" href="#fn:61"><sup>61</sup></a> In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%.<a class="footnote-ref" id="fnref:62" href="#fn:62"><sup>62</sup></a> </p><p>The best evidence exists for the treatment of <a href="/facts/Septic_shock/yc9mgmrz">septic shock</a> in adults. However, the pathophysiology of shock in children appears to be similar so treatment methodologies have been extrapolated to children.<a class="footnote-ref" id="fnref:63" href="#fn:63"><sup>63</sup></a> Management may include securing the airway via <a href="/facts/Intubation/R8ltvGLT">intubation</a> if necessary to decrease the work of breathing and for guarding against respiratory arrest. <a href="/facts/Oxygen_therapy/38BdReab">Oxygen supplementation</a>, <a href="/facts/Intravenous_therapy/AwwuD3Nu">intravenous fluids</a>, <a href="/facts/Passive_leg_raising_test/FUSmgSru">passive leg raising</a> (not <a href="/facts/Trendelenburg_position/PhW5waxa">Trendelenburg position</a>) should be started and <a href="/facts/Blood_transfusion/fb0Mk6Dx">blood transfusions</a> added if blood loss is severe.<a class="footnote-ref" id="fnref:64" href="#fn:64"><sup>64</sup></a> In select cases, compression devices like <a href="/facts/Non-pneumatic_anti-shock_garment/Agjm1Agh">non-pneumatic anti-shock garments</a> (or the deprecated <a href="/facts/Military_anti-shock_trousers/KextAsb6">military anti-shock trousers</a>) can be used to prevent further blood loss and concentrate fluid in the body's head and core.<a class="footnote-ref" id="fnref:65" href="#fn:65"><sup>65</sup></a> It is important to keep the person warm to avoid <a href="/facts/Hypothermia/lIYDCIAv">hypothermia</a><a class="footnote-ref" id="fnref:66" href="#fn:66"><sup>66</sup></a> as well as adequately manage pain and anxiety as these can increase oxygen consumption.<a class="footnote-ref" id="fnref:67" href="#fn:67"><sup>67</sup></a> Negative impact by shock is reversible if it's recognized and treated early in time.<a class="footnote-ref" id="fnref:68" href="#fn:68"><sup>68</sup></a> </p> <h3>Fluids</h3> <p>Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter <a href="/facts/Normal_saline/wNMLPtho">normal saline</a> bolus over 10 minutes or 20 mL/kg in a child) which is usually instituted as the person is being further evaluated.<a class="footnote-ref" id="fnref:69" href="#fn:69"><sup>69</sup></a> <a href="/facts/Colloids/9EVucqND">Colloids</a> and <a href="/facts/Crystalloid_fluid/aV90zqjo">crystalloids</a> appear to be equally effective with respect to outcomes.,<a class="footnote-ref" id="fnref:70" href="#fn:70"><sup>70</sup></a> Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients.<a class="footnote-ref" id="fnref:71" href="#fn:71"><sup>71</sup></a> If the person remains in shock after initial resuscitation, <a href="/facts/Packed_red_blood_cells/PlmjsB1A">packed red blood cells</a> should be administered to keep the <a href="/facts/Hemoglobin/RsD1MzYA">hemoglobin</a> greater than 100 g/L.<a class="footnote-ref" id="fnref:72" href="#fn:72"><sup>72</sup></a> </p><p>For those with hemorrhagic shock, the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild <a href="/facts/Hypotension/BhrdVVRS">hypotension</a> to persist (known as <a href="/facts/Permissive_hypotension/15XhVbkc">permissive hypotension</a>).<a class="footnote-ref" id="fnref:73" href="#fn:73"><sup>73</sup></a> Targets include a <a href="/facts/Mean_arterial_pressure/5q1fu4x9">mean arterial pressure</a> of 60 mmHg, a <a href="/facts/Systolic_blood_pressure/VtqqSM2J">systolic blood pressure</a> of 70–90 mmHg,<a class="footnote-ref" id="fnref:74" href="#fn:74"><sup>74</sup></a><a class="footnote-ref" id="fnref:75" href="#fn:75"><sup>75</sup></a> or until the patient has adequate <a href="/facts/Mentation/3MwTL0G5">mentation</a> and peripheral pulses.<a class="footnote-ref" id="fnref:76" href="#fn:76"><sup>76</sup></a> <a href="/facts/Tonicity/ev5qcKQh">Hypertonic fluid</a> may also be an option in this group.<a class="footnote-ref" id="fnref:77" href="#fn:77"><sup>77</sup></a> </p> <h3>Medications</h3> <p><a href="/facts/Vasopressors/GPCuG4aT">Vasopressors</a> may be used if blood pressure does not improve with fluids. Common vasopressors used in shock include: <a href="/facts/Norepinephrine_(medication)/faPlPMnD">norepinephrine</a>, <a href="/facts/Phenylephrine/sf4DxQws">phenylephrine</a>, <a href="/facts/Dopamine/5gNy8Xkd">dopamine</a>, and <a href="/facts/Dobutamine/EmoMfuvL">dobutamine</a>. </p><p>There is no evidence of substantial benefit of one vasopressor over another;<a class="footnote-ref" id="fnref:78" href="#fn:78"><sup>78</sup></a> however, using dopamine leads to an increased risk of arrhythmia when compared with norepinephrine.<a class="footnote-ref" id="fnref:79" href="#fn:79"><sup>79</sup></a> Vasopressors have not been found to improve outcomes when used for <a href="/facts/Hemorrhagic_shock/MmP8TsPw">hemorrhagic shock</a> from <a href="/facts/Trauma_(medical)/vAIyyy22">trauma</a><a class="footnote-ref" id="fnref:80" href="#fn:80"><sup>80</sup></a> but may be of use in <a href="/facts/Neurogenic_shock/roP6TUd4">neurogenic shock</a>.<a class="footnote-ref" id="fnref:81" href="#fn:81"><sup>81</sup></a> <a href="/facts/Activated_protein_C/sHW1LwrJ">Activated protein C</a> (Xigris), while once aggressively promoted for the management of <a href="/facts/Septic_shock/yc9mgmrz">septic shock</a>, has been found not to improve survival and is associated with a number of complications.<a class="footnote-ref" id="fnref:82" href="#fn:82"><sup>82</sup></a> Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued.<a class="footnote-ref" id="fnref:83" href="#fn:83"><sup>83</sup></a> The use of <a href="/facts/Sodium_bicarbonate/S9oSol0R">sodium bicarbonate</a> is controversial as it has not been shown to improve outcomes.<a class="footnote-ref" id="fnref:84" href="#fn:84"><sup>84</sup></a> If used at all it should only be considered if the blood pH is less than 7.0.<a class="footnote-ref" id="fnref:85" href="#fn:85"><sup>85</sup></a> </p><p>People with anaphylactic shock are commonly treated with <a href="/facts/Epinephrine_autoinjector/BEE2FaUv">epinephrine</a>. <a href="/facts/Antihistamine/HuMC25lt">Antihistamines</a>, such as <a href="/facts/Benadryl/WAWopCS7">Benadryl</a> (<a href="/facts/Diphenhydramine/XbbIg1Nv">diphenhydramine</a>) or <a href="/facts/Ranitidine/rddBabbF">ranitidine</a> are also commonly administered. <a href="/facts/Albuterol/s5KYCt8j">Albuterol</a>, normal saline, and steroids are also commonly given. </p> <h3>Mechanical support</h3> <ul><li><a href="/facts/Intra-aortic_balloon_pump/kjFJafqa">Intra-aortic balloon pump</a> (IABP) – a device inserted into the aorta that mechanically raises the blood pressure. Use of Intra-aortic balloon pumps is not recommended in cardiogenic shock.<a class="footnote-ref" id="fnref:86" href="#fn:86"><sup>86</sup></a></li> <li><a href="/facts/Ventricular_assist_device/kzwCcA9r">Ventricular assist device</a> (VAD) – A mechanical pump that helps pump blood throughout the body. Commonly used in short term cases of refractory primary cardiogenic shock.</li> <li><a href="/facts/Artificial_heart/BeLtuRoE">Artificial heart</a> (TAH)<a class="footnote-ref" id="fnref:87" href="#fn:87"><sup>87</sup></a></li> <li><a href="/facts/Extracorporeal_membrane_oxygenation/RxxmXV8h">Extracorporeal membrane oxygenation</a> (ECMO) – an external device that completely replaces the work of the heart.</li></ul> <h3>Treatment goals</h3> <p>The goal of treatment is to achieve a urine output of greater than 0.5 mL/kg/h, a <a href="/facts/Central_venous_pressure/hnIlJr3k">central venous pressure</a> of 8–12 mmHg and a <a href="/facts/Mean_arterial_pressure/5q1fu4x9">mean arterial pressure</a> of 65–95 mmHg. In trauma the goal is to stop the bleeding which in many cases requires surgical interventions. A good urine output indicates that the kidneys are getting enough blood flow. </p> <h2 id="epidemiology">Epidemiology</h2> <p><a href="/facts/Septic_shock/yc9mgmrz">Septic shock</a> (a form of distributive shock) is the most common form of shock. Shock from blood loss occurs in about 1–2% of trauma cases.<a class="footnote-ref" id="fnref:88" href="#fn:88"><sup>88</sup></a> Overall, up to one-third of people admitted to the <a href="/facts/Intensive_care_unit/j77VBgtt">intensive care unit</a> (ICU) are in circulatory shock.<a class="footnote-ref" id="fnref:89" href="#fn:89"><sup>89</sup></a> Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20%, and septic shock about 60% of cases.<a class="footnote-ref" id="fnref:90" href="#fn:90"><sup>90</sup></a> </p> <h2 id="prognosis">Prognosis</h2> <p>The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Low volume, anaphylactic, and neurogenic shock are readily treatable and respond well to medical therapy. <a href="/facts/Septic_shock/yc9mgmrz">Septic shock</a>, especially septic shock where treatment is delayed or the antimicrobial drugs are ineffective, however has a mortality rate between 30% and 80%; cardiogenic shock has a mortality rate of up to 70% to 90%, though quick treatment with vasopressors and inotropic drugs, cardiac surgery, and the use of assistive devices can lower the mortality.<a class="footnote-ref" id="fnref:91" href="#fn:91"><sup>91</sup></a> </p> <h2 id="history">History</h2> <p>There is no evidence of the word shock being used in its modern-day form prior to 1743. However, there is evidence that <a href="/facts/Hippocrates/lXUElFQD">Hippocrates</a> used the word <i>exemia</i> to signify a state of being "drained of blood".<a class="footnote-ref" id="fnref:92" href="#fn:92"><sup>92</sup></a> Shock or "choc" was first described in a trauma victim in the English translation of <a href="/facts/Henri_Fran%C3%A7ois_Le_Dran/eJW7BGTQ">Henri-François LeDran</a>'s 1740 text, Traité ou Reflexions Tire'es de la Pratique sur les Playes d'armes à feu (A treatise, or reflections, drawn from practice on <a href="/facts/Gunshot_wound/NXTnoXJm">gun-shot wounds</a>.)<a class="footnote-ref" id="fnref:93" href="#fn:93"><sup>93</sup></a> In this text he describes "choc" as a reaction to the sudden impact of a missile. However, the first English writer to use the word shock in its modern-day connotation was James Latta, in 1795. </p><p>Prior to <a href="/facts/World_War_I/vITTUanQ">World War I</a>, there were several competing hypotheses behind the <a href="/facts/Pathophysiology/Tp3Dny0c">pathophysiology</a> of shock. Of the various theories, the most well regarded was a theory penned by <a href="/facts/George_W._Crile/CAymRntu">George W. Crile</a> who suggested in his 1899 monograph, "<i>An Experimental Research into Surgical Shock"</i>, that shock was quintessentially defined as a state of circulatory collapse (<a href="/facts/Vasodilation/cjzrU8Ro">vasodilation</a>) due to excessive nervous stimulation.<a class="footnote-ref" id="fnref:94" href="#fn:94"><sup>94</sup></a> Other competing theories around the turn of the century included one penned by Malcom in 1907, in which the assertion was that prolonged vasoconstriction led to the pathophysiological signs and symptoms of shock.<a class="footnote-ref" id="fnref:95" href="#fn:95"><sup>95</sup></a> In the following World War I, research concerning shock resulted in experiments by Walter B. Cannon of Harvard and William M. Bayliss of London in 1919 that showed that an increase in permeability of the capillaries in response to trauma or toxins was responsible for many clinical manifestations of shock.<a class="footnote-ref" id="fnref:96" href="#fn:96"><sup>96</sup></a><a class="footnote-ref" id="fnref:97" href="#fn:97"><sup>97</sup></a> In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today.<a class="footnote-ref" id="fnref:98" href="#fn:98"><sup>98</sup></a><a class="footnote-ref" id="fnref:99" href="#fn:99"><sup>99</sup></a> </p> <h2 id="external-links">External links</h2> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN 978-1292-17084-8. <a href="978-1292-17084-8" target="_blank">978-1292-17084-8</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN 978-1292-17084-8. <a href="978-1292-17084-8" target="_blank">978-1292-17084-8</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>ATLS – Advanced Trauma Life Support – Student Course Manual (10 ed.). American College of Surgeons. 2018. pp. 43–52, 135. ISBN 978-78-0-9968267. <a href="978-78-0-9968267" target="_blank">978-78-0-9968267</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN 978-1292-17084-8. <a href="978-1292-17084-8" target="_blank">978-1292-17084-8</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN 978-1292-17084-8. <a href="978-1292-17084-8" target="_blank">978-1292-17084-8</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN 978-1292-17084-8. <a href="978-1292-17084-8" target="_blank">978-1292-17084-8</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. ISBN 978-1292-17084-8. <a href="978-1292-17084-8" target="_blank">978-1292-17084-8</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></p></li> <li id="fn:8"><p>Smith, N; Lopez, RA; Silberman, M (January 2019). "Distributive Shock". StatPearls (Internet). PMID 29261964. <a href="/wiki/PMID_(identifier)" target="_blank">/wiki/PMID_(identifier)</a> <a href="#fnref:8" class="footnote-back-ref">↩</a></p></li> <li id="fn:9"><p>ATLS – Advanced Trauma Life Support – Student Course Manual (10 ed.). American College of Surgeons. 2018. pp. 43–52, 135. ISBN 978-78-0-9968267. <a href="978-78-0-9968267" target="_blank">978-78-0-9968267</a> <a href="#fnref:9" class="footnote-back-ref">↩</a></p></li> <li id="fn:10"><p>International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–73. 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