Shock (circulatory)

"Acute shock" redirects here. For the psychological condition, see Acute stress reaction.
Classification and external resources
Specialty Cardiology, critical care medicine
ICD-10 R57
ICD-9-CM 785.50
DiseasesDB 12013
MedlinePlus 000039
eMedicine emerg/531 med/285 emerg/533
MeSH D012769

Circulatory shock, commonly known as shock, is a life-threatening medical condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function.[1][2] The typical signs of shock are low blood pressure, rapid heart rate, signs of poor end-organ perfusion (i.e.: low urine output, confusion, or loss of consciousness), and weak pulses.

The shock index (SI), defined as heart rate divided by systolic blood pressure, is an accurate diagnostic measure that is more useful than hypotension and tachycardia in isolation.[3] Under normal conditions, a number between 0.5 and 0.8 is typically seen. Should that number increase, so does suspicion of an underlying state of shock. Blood pressure alone may not be a reliable sign for shock, as there are times when a person is in circulatory shock but has a stable blood pressure.[4]

Circulatory shock is not related to the emotional state of shock. Circulatory shock is a life-threatening medical emergency and one of the most common causes of death for critically ill people. Shock can have a variety of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. For example, shock may lead to hypoxemia (a lack of oxygen in arterial blood) or cardiac and/or respiratory arrest.[5]

One of the key dangers of shock is that it progresses by a positive feedback mechanism. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. This is normally very useful to match up supply with tissue demand for nutrients. However, if enough tissue causes this, it will deprive vital nutrients from other parts of the body. Additionally, the ability of the circulatory system to meet this increase in demand causes saturation. A major result of which is that other parts of the body begin to respond in a similar way, thus exacerbating the problem. Due to these chain of events, immediate treatment of shock is critical to survival.[4]

Signs and symptoms

Video explanation of shock

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness.[2] While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present.[2] While a fast heart rate is common, those on β-blockers, those who are athletic and in 30% of cases those with shock due to intra abdominal bleeding may have a normal or slow heart rate.[6] Specific subtypes of shock may have additional symptoms.


Hemorrhage classes[7]
Class Blood loss Response Treatment
I <15 %(0.75 l) min. fast heart rate, normal blood pressure minimal
II 15-30 %(0.75-1.5 l) fast heart rate, min. low blood pressure intravenous fluids
III 30-40 %(1.5-2 l) very fast heart rate, low blood pressure, confusion fluids and packed RBCs
IV >40 %(>2 l) critical blood pressure and heart rate aggressive interventions

Hypovolemia is a direct loss of effective circulating blood volume leading to:

The severity of hemorrhagic shock can be graded on a 1-4 scale on the physical signs. This approximates to the effective loss of blood volume. The shock index (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone.[3] This relationship has not been well established in pregnancy-related bleeding.[8]


Symptoms of cardiogenic shock include:


Systemic inflammatory response syndrome[9]
Finding Value
Temperature <36 °C (96.8 °F) or >38 °C (100.4 °F)
Heart rate >90/min
Respiratory rate >20/min or PaCO2<32 mmHg (4.3 kPa)
WBC <4x109/L (<4000/mm³), >12x109/L (>12,000/mm³), or 10% bands

Distributive shock includes infectious, anaphylactic, endocrine and neurogenic causes. The SIRS features typically occur in early septic shock.[2]


Obstructive shock includes cardiac tamponade, pulmonary embolism and aortic stenosis

Septic shock

Main manifestations are produced due to massive release of histamine which causes intense vasodilation. Patients with septic shock will also likely be positive for the SIRS Criteria. The most generally accepted treatment for these patients is early recognition of symptoms, and early administration of broad spectrum and organism specific antibiotics.[11]


Effects of inadequate perfusion on cell function.

There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.[12] At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply.[2]


During this stage, the state of hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor in the electron transport chain, is not abundant, this slows down entry of pyruvate into the Krebs cycle, resulting in its accumulation. Accumulating pyruvate is converted to lactate by lactate dehydrogenase and hence lactate accumulates (causing lactic acidosis).


This stage 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 acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of epinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. The renin–angiotensin axis is activated, and arginine vasopressin (Anti-diuretic hormone; ADH) is released to conserve fluid via the kidneys. These hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the renin–angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.


Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries.[10] Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.[10] If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.[4][10]


At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage 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 cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. 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 phosphorylate into ATP.[4]


The first changes seen in shock is an increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed there is no test that either makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume state.[2][6]

Differential diagnosis

Shock is a common end point of many medical conditions.[1] It has been divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic and obstructive.[13] A few additional classifications are occasionally used including: endocrinologic shock.[1]


Hypovolemic shock is the most common type of shock and is caused by insufficient circulating volume.[2] Its primary cause is haemorrhage (internal and/or external), or loss of fluid from the circulation. Vomiting and diarrhea are the most common cause in children.[1] With other causes including burns, environmental exposure and excess urine loss due to diabetic ketoacidosis and diabetes insipidus.[1]


Cardiogenic shock is caused by the failure of the heart to pump effectively.[2] This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), contusio cordis, or cardiac valve problems.[1]


Obstructive shock is due to obstruction of blood flow outside of the heart.[2] Several conditions can result in this form of shock.


Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell.[2] Examples of this form of shock are:


Based on endocrine disturbances such as:


The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas.[1] Management may include securing the airway via intubation if necessary to decrease the work of breathing and for guarding against respiratory arrest. Oxygen supplementation, intravenous fluids, passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe.[2] It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.[2]


Aggressive intravenous fluids are recommended in most types of shock (e.g. 1-2 liter normal saline bolus over 10 minutes or 20 ml/kg in a child) which is usually instituted as the person is being further evaluated.[15] Which intravenous fluid is superior, colloids or crystalloids, remains undetermined.[2] Thus as crystalloids are less expensive they are recommended.[16] If the person remains in shock after initial resuscitation packed red blood cells should be administered to keep the hemoglobin greater than 100 g/l.[2]

For those with haemorrhagic shock the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension).[17] Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70-90 mmHg,[2][18] or until their adequate mentation and peripheral pulses.[18]


Vasopressors may be used if blood pressure does not improve with fluids. There is no evidence of superiority of one vasopressor over another.[19] Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma[20] but may be of use in neurogenic shock.[14] Activated protein C (Xigris) while once aggressively promoted for the management of septic shock has been found not to improve survival and is associated with a number of complications.[21] The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.[22] If used at all it should only be considered if the pH is less than 7.0.[22]

Mechanical support

Treatment goals

The goal of treatment is to achieve a urine output of greater than 0.5 ml/kg/h, a central venous pressure of 8-12 mmHg and a mean arterial pressure of 65-95 mmHg. In trauma the goal is to stop the bleeding which in many cases requires surgical interventions.


Haemorrhagic shock occurs in about 1-2% of trauma cases.[18] Up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock.[23]


The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse with a mortality rate between 70% and 90%.[24]


In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today.[24]

See also


  1. 1 2 3 4 5 6 7 8 9 10 Silverman, Adam (Oct 2005). "Shock: A Common Pathway For Life-Threatening Pediatric Illnesses And Injuries". Pediatric Emergency Medicine Practice. 2 (10).
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 165–172. ISBN 0-07-148480-9.
  3. 1 2 Olaussen A, Blackburn T, Mitra B, Fitzgerald M (2014). "Review article: shock index for prediction of critical bleeding post-trauma: a systematic review". Emergency medicine Australasia. 26 (3): 223–8. doi:10.1111/1742-6723.12232. PMID 24712642.
  4. 1 2 3 4 Guyton, Arthur; Hall, John (2006). "Chapter 24: Circulatory Shock and Physiology of Its Treatment". In Gruliow, Rebecca. Textbook of Medical Physiology (11th ed.). Philadelphia, Pennsylvania: Elsevier Inc. pp. 278–288. ISBN 0-7216-0240-1.
  5. Marino, Paul L. (September 2006). The ICU Book. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-4802-X.
  6. 1 2 Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 174–175. ISBN 0-07-148480-9.
  7. Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. ISBN 0-07-148480-9.
  8. Pacagnella RC, Souza JP, Durocher J, Perel P, Blum J, Winikoff B, Gülmezoglu AM (2013). "A systematic review of the relationship between blood loss and clinical signs". PLoS ONE. 8 (3): e57594. doi:10.1371/journal.pone.0057594. PMC 3590203Freely accessible. PMID 23483915.
  9. "American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis" (PDF). Critical Care Medicine. 20 (6): 864–74. 1992. doi:10.1097/00003246-199206000-00025. PMID 1597042.
  10. 1 2 3 4 5 6 7 Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 102-103 ISBN 978-1-4160-2973-1
  11. "Surviving Sepsis Campaign Responds to ProCESS Trial" (PDF). Surviving Sepsis Campaign. Retrieved 2015-03-25.
  12. Armstrong, D.J. (2004). Shock. In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. Nursing Practice. Hospital and Home. The Adult.(2nd edition): Edinburgh: Churchill Livingstone.
  13. Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. p. 168. ISBN 0-07-148480-9.
  14. 1 2 3 Cocchi, MN; Kimlin, E; Walsh, M; Donnino, MW (August 2007). "Identification and resuscitation of the trauma patient in shock". Emergency medicine clinics of North America. 25 (3): 623–42, vii. doi:10.1016/j.emc.2007.06.001. PMID 17826209.
  15. American College of Surgeons (2008). Atls, Advanced Trauma Life Support Program for Doctors. Amer College of Surgeons. p. 58. ISBN 1-880696-31-2.
  16. Perel, P; Roberts, I (Oct 17, 2007). Perel, Pablo, ed. "Colloids versus crystalloids for fluid resuscitation in critically ill patients". Cochrane database of systematic reviews (Online) (4): CD000567. doi:10.1002/14651858.CD000567.pub3. PMID 17943746.
  17. Marx, J (2010). Rosen's emergency medicine: concepts and clinical practice 7th edition. Philadelphia, PA: Mosby/Elsevier. p. 2467. ISBN 978-0-323-05472-0.
  18. 1 2 3 Cherkas, David (Nov 2011). "Traumatic Hemorrhagic Shock: Advances In Fluid Management". Emergency Medicine Practice. 13 (11).
  19. Havel, C; Arrich, J; Losert, H; Gamper, G; Müllner, M; Herkner, H (2011-05-11). Herkner, Harald, ed. "Vasopressors for hypotensive shock". Cochrane database of systematic reviews (Online). 5 (5): CD003709. doi:10.1002/14651858.CD003709.pub3. PMID 21563137.
  20. Diez, C; Varon, AJ (December 2009). "Airway management and initial resuscitation of the trauma patient". Current opinion in critical care. 15 (6): 542–7. doi:10.1097/MCC.0b013e328331a8a7. PMID 19713836.
  21. Martí-Carvajal, AJ; Solà, I; Lathyris, D; Cardona, AF (Apr 13, 2011). Martí-Carvajal, Arturo J, ed. "Human recombinant activated protein C for severe sepsis". Cochrane database of systematic reviews (Online) (4): CD004388. doi:10.1002/14651858.CD004388.pub4. PMID 21491390.
  22. 1 2 Boyd, JH; Walley, KR (August 2008). "Is there a role for sodium bicarbonate in treating lactic acidosis from shock?". Current opinion in critical care. 14 (4): 379–83. doi:10.1097/MCC.0b013e3283069d5c. PMID 18614899.
  23. Finfer, Simon R.; Vincent, Jean-Louis; Vincent, Jean-Louis; De Backer, Daniel (31 October 2013). "Circulatory Shock". New England Journal of Medicine. 369 (18): 1726–1734. doi:10.1056/NEJMra1208943.
  24. 1 2 Irwin, Richard S.; Rippe, James M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-3548-3.
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