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==Overview==
==Overview==
[[Shock]] is a clinical [[syndrome]] resulting from the [[hypoperfusion]] of the [[tissues]]. Regardless of the underlying cause, this [[hypoperfusion]] leads to the failure to meet tissues' [[nutritional]] and [[oxygen]] needs, causing [[cellular]] dysfunction. The affected [[tissues]] lead to the production and release of [[inflammatory]] mediators that will further jeopardize [[perfusion]] through changes in the [[vasculature]]. The results of these changes are [[organ failure]] and death if treatment in not timely applied. According to the underlying cause, there will be different types of [[shock]], which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. Cardiogenic shock is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|cardiac failure]], in the presence of adequate [[intravascular]] volume, typically followed by [[hypotension]], which leads to insufficient ability to meet [[oxygen]] and [[nutrient]] demands of [[organs]] and other peripheral tissues. It may range from mild to severe [[hypoperfusion]] and may be defined in terms of [[hemodynamic]] parameters, which according to most studies, means a state in which [[systolic blood pressure]] is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right [[ventricular]] filling pressures that does not respond to isolated fluid administration, is secondary to [[heart failure|cardiac failure]] and occurs with signs of [[hypoperfusion]] ([[oliguria]], [[cool extremities]], [[cyanosis]] and [[altered mental status]]) or a [[cardiac index]] of < 2.2 L/min/m² (on [[inotropic]], [[vasopressor]] or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg.
[[Shock]] is a clinical [[syndrome]] resulting from the [[hypoperfusion]] of the [[tissues]]. Regardless of the underlying cause, this [[hypoperfusion]] leads to the failure to meet tissues' [[nutritional]] and [[oxygen]] needs, causing [[cellular]] dysfunction. The affected [[tissues]] lead to the production and release of [[inflammatory]] mediators that will further jeopardize [[perfusion]] through changes in the [[vasculature]]. The results of these changes are [[organ failure]] and death if treatment in not timely applied. According to the underlying cause, there will be different types of [[shock]], which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. [[Cardiogenic shock]] is a clinical condition, defined as a state of systemic [[hypoperfusion]] originated in [[heart failure|cardiac failure]], in the presence of adequate [[intravascular]] volume, typically followed by [[hypotension]], which leads to insufficient ability to meet [[oxygen]] and [[nutrient]] demands of [[organs]] and other peripheral tissues. It may range from mild to severe [[hypoperfusion]] and may be defined in terms of [[hemodynamic]] parameters, which according to most studies, means a state in which [[systolic blood pressure]] is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right [[ventricular]] filling pressures that does not respond to isolated fluid administration, is secondary to [[heart failure|cardiac failure]] and occurs with signs of [[hypoperfusion]] ([[oliguria]], [[cool extremities]], [[cyanosis]] and [[altered mental status]]) or a [[cardiac index]] of < 2.2 L/min/m² (on [[inotropic]], [[vasopressor]] or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and [[pulmonary artery wedge pressure]] > 18 mm Hg.


==Differential Diagnosis==
==Differential Diagnosis==
Depending on the author and the source used there will be different ways of organizing the types of [[shock]]. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of [[shock]] since components of each type may combine in a single patient. The clinical presentation of [[shock]] is usually the result of a complexity of processes, such as the [[sympathetic]] and [[endocrine]] responses to [[hypoperfusion]], along with manifestations of [[organ failure]]. Patients who present with [[signs]] and [[symptoms]] of [[hypoperfusion]] following a diagnosed or suspected [[myocardial infarction]], are commonly suffering a cardiogenic shock as a [[complication]] of the [[MI]]. However, other clinical scenarios, not related to acute [[MI]], may present similarly:<ref>{{Cite book  | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref><ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref>
Depending on the author and the source used there will be different ways of organizing the types of [[shock]]. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of [[shock]] since components of each type may combine in a single patient. The clinical presentation of [[shock]] is usually the result of a complexity of processes, such as the [[sympathetic]] and [[endocrine]] responses to [[hypoperfusion]], along with manifestations of [[organ failure]]. Patients who present with [[signs]] and [[symptoms]] of [[hypoperfusion]] following a diagnosed or suspected [[myocardial infarction]], are commonly suffering a [[cardiogenic shock]] as a [[complication]] of the [[MI]]. However, other clinical scenarios, not related to acute [[MI]], may present similarly:<ref>{{Cite book  | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages =  }}</ref><ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref>
:*'''[[Hypovolemic shock]]'''
:*'''[[Hypovolemic shock]]'''
::*More than a simple loss of [[intravascular]] volume, [[hypovolemic shock]] is a dynamic process in which the responses to the initial insult, and the period of time during which they are in practice, will dictate the response to treatment and therefore the [[outcome]]. Several causes may be in the origin of this type of [[shock]], including: [[hemorrhage]], [[dehydration]], [[GI]] or [[urinary]] losses and severe [[vasodilation|venodilation]] (in the setting of other conditions). There is a relationship between the clinical status of the patient and the amount of circulating [[blood]] volume, the [[signs]] may include  [[pallor]], [[cool extremities]], [[tachycardia]] and [[tachypnea]], [[oliguria]] and decreased [[consciousness]]. Compensatory mechanisms are responsible for tolerating initial [[blood loss]], however they begin to fail after about 20-25% of [[blood]] has been lost. This tolerance will be dictated mostly by the previous [[cardiac]] reserve of the patient, along with the velocity of loss of [[intravascular]] volume<ref name="pmid29404656">{{cite journal |vauthors=Lier H, Bernhard M, Hossfeld B |title=[Hypovolemic and hemorrhagic shock] |language=German |journal=Anaesthesist |volume=67 |issue=3 |pages=225–244 |date=March 2018 |pmid=29404656 |doi=10.1007/s00101-018-0411-z |url=}}</ref><ref name="pmid23153876">{{cite journal |vauthors=Kobayashi L, Costantini TW, Coimbra R |title=Hypovolemic shock resuscitation |journal=Surg. Clin. North Am. |volume=92 |issue=6 |pages=1403–23 |date=December 2012 |pmid=23153876 |doi=10.1016/j.suc.2012.08.006 |url=}}</ref>.
::*More than a simple loss of [[intravascular]] volume, [[hypovolemic shock]] is a dynamic process in which the responses to the initial insult, and the period of time during which they are in practice, will dictate the response to treatment and therefore the [[outcome]]. Several causes may be in the origin of this type of [[shock]], including: [[hemorrhage]], [[dehydration]], [[GI]] or [[urinary]] losses and severe [[vasodilation|venodilation]] (in the setting of other conditions). There is a relationship between the clinical status of the patient and the amount of circulating [[blood]] volume, the [[signs]] may include  [[pallor]], [[cool extremities]], [[tachycardia]] and [[tachypnea]], [[oliguria]] and decreased [[consciousness]]. Compensatory mechanisms are responsible for tolerating initial [[blood loss]], however they begin to fail after about 20-25% of [[blood]] has been lost. This tolerance will be dictated mostly by the previous [[cardiac]] reserve of the patient, along with the velocity of loss of [[intravascular]] volume<ref name="pmid29404656">{{cite journal |vauthors=Lier H, Bernhard M, Hossfeld B |title=[Hypovolemic and hemorrhagic shock] |language=German |journal=Anaesthesist |volume=67 |issue=3 |pages=225–244 |date=March 2018 |pmid=29404656 |doi=10.1007/s00101-018-0411-z |url=}}</ref><ref name="pmid23153876">{{cite journal |vauthors=Kobayashi L, Costantini TW, Coimbra R |title=Hypovolemic shock resuscitation |journal=Surg. Clin. North Am. |volume=92 |issue=6 |pages=1403–23 |date=December 2012 |pmid=23153876 |doi=10.1016/j.suc.2012.08.006 |url=}}</ref>.

Revision as of 17:12, 16 January 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]

Overview

Shock is a clinical syndrome resulting from the hypoperfusion of the tissues. Regardless of the underlying cause, this hypoperfusion leads to the failure to meet tissues' nutritional and oxygen needs, causing cellular dysfunction. The affected tissues lead to the production and release of inflammatory mediators that will further jeopardize perfusion through changes in the vasculature. The results of these changes are organ failure and death if treatment in not timely applied. According to the underlying cause, there will be different types of shock, which will have similar presentations. It is mandatory to determine the underlying cause of the condition so that proper treatment may be started. Cardiogenic shock is a clinical condition, defined as a state of systemic hypoperfusion originated in cardiac failure, in the presence of adequate intravascular volume, typically followed by hypotension, which leads to insufficient ability to meet oxygen and nutrient demands of organs and other peripheral tissues. It may range from mild to severe hypoperfusion and may be defined in terms of hemodynamic parameters, which according to most studies, means a state in which systolic blood pressure is persistently < 90 mm Hg or < 80 mm Hg, for longer than 1 hour, with adequate or elevated left and right ventricular filling pressures that does not respond to isolated fluid administration, is secondary to cardiac failure and occurs with signs of hypoperfusion (oliguria, cool extremities, cyanosis and altered mental status) or a cardiac index of < 2.2 L/min/m² (on inotropic, vasopressor or circulatory device support) or < 1.8-2.2 L/min/m² (off support) and pulmonary artery wedge pressure > 18 mm Hg.

Differential Diagnosis

Depending on the author and the source used there will be different ways of organizing the types of shock. Sometimes it might be difficult to differentiate, from the clinical standpoint, two types of shock since components of each type may combine in a single patient. The clinical presentation of shock is usually the result of a complexity of processes, such as the sympathetic and endocrine responses to hypoperfusion, along with manifestations of organ failure. Patients who present with signs and symptoms of hypoperfusion following a diagnosed or suspected myocardial infarction, are commonly suffering a cardiogenic shock as a complication of the MI. However, other clinical scenarios, not related to acute MI, may present similarly:[1][2]

Classification of shock based on hemodynamic parameters. (CO, cardiac output; CVP; central venous pressure; PAD, pulmonary artery diastolic pressure; PAS, pulmonary artery systolic pressure; RVD, right ventricular diastolic pressure; RVS, right ventricular systolic pressure; SVO2, systemic venous oxygen saturation; SVR, systemic vascular resistance.)[10][11]
Type of Shock Etiology CO SVR PCWP CVP SVO2 RVS RVD PAS PAD
Cardiogenic Acute Ventricular Septal Defect ↓↓ N — ↑ ↑↑ ↑ — ↑↑ N — ↑ N — ↑ N — ↑
Acute Mitral Regurgitation ↓↓ ↑↑ ↑ — ↑↑ N — ↑
Myocardial Dysfunction ↓↓ ↑↑ ↑↑ N — ↑ N — ↑ N — ↑
Right Ventricular Infarction ↓↓ N — ↓ ↑↑ ↓ — ↑ ↓ — ↑ ↓ — ↑
Obstructive Pulmonary Embolism ↓↓ N — ↓ ↑↑ ↓ — ↑ ↓ — ↑ ↓ — ↑
Cardiac Tamponade ↓ — ↓↓ ↑↑ ↑↑ N — ↑ N — ↑ N — ↑
Distributive Septic Shock N — ↑↑ ↓ — ↓↓ N — ↓ N — ↓ ↑ — ↑↑ N — ↓ N — ↓
Anaphylactic Shock N — ↑↑ ↓ — ↓↓ N — ↓ N — ↓ ↑ — ↑↑ N — ↓ N — ↓
Hypovolemic Volume Depletion ↓↓ ↓↓ ↓↓ N — ↓ N — ↓

References

  1. Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
  2. Parrillo, Joseph (2013). Critical care medicine principles of diagnosis and management in the adult. Philadelphia, PA: Elsevier/Saunders. ISBN 0323089291.
  3. Lier H, Bernhard M, Hossfeld B (March 2018). "[Hypovolemic and hemorrhagic shock]". Anaesthesist (in German). 67 (3): 225–244. doi:10.1007/s00101-018-0411-z. PMID 29404656.
  4. Kobayashi L, Costantini TW, Coimbra R (December 2012). "Hypovolemic shock resuscitation". Surg. Clin. North Am. 92 (6): 1403–23. doi:10.1016/j.suc.2012.08.006. PMID 23153876.
  5. "Shock: Shock and Fluid Resuscitation: Merck Manual Professional".
  6. Pich H, Heller AR (May 2015). "[Obstructive shock]". Anaesthesist (in German). 64 (5): 403–19. doi:10.1007/s00101-015-0031-9. PMID 25994928.
  7. Dababneh E, Siddique MS. PMID 28613734. Missing or empty |title= (help)
  8. Smith N, Lopez RA, Silberman M. PMID 29261964. Missing or empty |title= (help)
  9. Alyeşil C, Doğan NÖ, Özturan İU, Güney S (June 2017). "Distributive Shock in the Emergency Department: Sepsis, Anaphylaxis, or Capillary Leak Syndrome?". J Emerg Med. 52 (6): e229–e231. doi:10.1016/j.jemermed.2017.01.012. PMID 28238385.
  10. Parrillo, Joseph E.; Ayres, Stephen M. (1984). Major issues in critical care medicine. Baltimore: William Wilkins. ISBN 0-683-06754-0.
  11. Judith S. Hochman, E. Magnus Ohman (2009). Cardiogenic Shock. Wiley-Blackwell. ISBN 9781405179263.


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