Shock (circulatory)

Source: Wikipedia, the free encyclopedia.
For other uses, see Shock (disambiguation).
Shock
vasopressors[2]
PrognosisRisk of death 20 to 50%[3]
Frequency1.2 million per year (US)[3]

Shock is the state of insufficient

sweating, anxiety, and increased thirst.[1] This may be followed by confusion, unconsciousness, or cardiac arrest, as complications worsen.[1]

Shock is divided into four main types based on the underlying cause:

overdoses.[1][4]

The diagnosis is generally based on a combination of symptoms,

fast heart rate in isolation.[5][6]

Treatment of shock is based on the likely underlying cause.

Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] 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%.[3]

Signs and symptoms

The presentation of shock is variable, with some people having only minimal symptoms such as confusion and weakness.

urine output, and confusion, these may not always be present.[7] While a fast heart rate is common, those on β-blockers, 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.[8]
Specific subtypes of shock may have additional symptoms.

Dry

capillary refill time, weak peripheral pulses, and cold extremities can be early signs of shock.[9]

Low volume

Main articles:
hemorrhage (internal or external); however, vomiting and diarrhea are more common causes in children.[10] Other causes include burns, as well as excess urine loss due to diabetic ketoacidosis and diabetes insipidus.[10]

Hemorrhage classes[11]
Class Blood loss (liters) 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

Signs and symptoms of hypovolemic shock include:

The severity of hemorrhagic shock can be graded on a 1–4 scale on the physical signs. 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.[5] This relationship has not been well established in pregnancy-related bleeding.[12]

Cardiogenic

Main article: Cardiogenic shock

myocardial contusion, or valvular heart disease problems.[10]

Symptoms of cardiogenic shock include:

Obstructive

Main article: Obstructive shock

Obstructive shock is a form of shock associated with physical obstruction of the great vessels of the systemic or pulmonary circulation.[13] Several conditions can result in this form of shock.

Many of the signs of obstructive shock are similar to cardiogenic shock, however treatments differ. Symptoms of obstructive shock include:

Distributive

Main article: Distributive shock
Systemic inflammatory response syndrome[16]
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 is low blood pressure due to a dilation of blood vessels within the body.[7][17] This can be caused by systemic infection (septic shock), a severe allergic reaction (anaphylaxis), or spinal cord injury (neurogenic shock).

Main article: Septic shock

Endocrine

Although not officially classified as a subcategory of shock, many endocrinology disturbances in their severe form can result in shock.[citation needed]

Cause

Type Cause
Low volume Fluid loss such as bleeding or diarrhea
Cardiogenic Ineffective pumping due to heart damage
Obstructive Blood flow to or from the heart is blocked
Distributive Abnormal flow within the small blood vessels[21]

Shock is a common end point of many medical conditions.

blood loss is known as hypovolemic shock, shock caused by sepsis is known as septic shock, etc. Shock itself is a life-threatening condition as a result of compromised body circulation.[22] It can be divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive.[23] A few additional classifications are occasionally used, such as endocrinologic shock.[10]

Pathophysiology

Effects of inadequate perfusion on cell function

There are four stages of shock. Shock is a complex and continuous condition, and there is no sudden transition from one stage to the next.[24] At a cellular level, shock is the process of oxygen demand becoming greater than oxygen supply.[7]

One of the key dangers of shock is that it progresses by a positive feedback 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.

As such, shock is a runaway condition of homeostatic 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.[6]

Initial

During the Initial stage (Stage 1), the state of

pyruvate into the Krebs cycle, resulting in its accumulation. The accumulating pyruvate is converted to lactate (lactic acid) by lactate dehydrogenase. The accumulating lactate causes lactic acidosis
.

Compensatory

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

homeostatic mediation of shock.[citation needed
]

Progressive/decompensated

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,

ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.[6][18]

Refractory

At Refractory stage (stage 4), the vital

phosphorylate into ATP.[6]

Diagnosis

The diagnosis of shock is commonly based on a combination of symptoms, physical examination, 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.[25] A high degree of suspicion is necessary for the proper diagnosis of shock.

The first change seen in shock is increased

chest X-ray or emergency department ultrasound may be useful to determine volume status.[7][8]

Management

The best evidence exists for the treatment of

passive leg raising (not Trendelenburg position) should be started and blood transfusions added if blood loss is severe.[7] In select cases, compression devices like non-pneumatic anti-shock garments (or the deprecated military anti-shock trousers) can be used to prevent further blood loss and concentrate fluid in the body's head and core.[27] It is important to keep the person warm to avoid hypothermia[28] as well as adequately manage pain and anxiety as these can increase oxygen consumption.[7] Negative impact by shock is reversible if it's recognized and treated early in time.[22]

Fluids

Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter

crystalloids appear to be equally effective with respect to outcomes.,[30] Balanced crystalloids and normal saline also appear to be equally effective in critically ill patients.[31] 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.[7]

For those with hemorrhagic shock, the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild

mentation and peripheral pulses.[33] Hypertonic fluid may also be an option in this group.[34]

Medications

Epinephrine auto-injector

Vasopressors may be used if blood pressure does not improve with fluids. Common vasopressors used in shock include: norepinephrine, phenylephrine, dopamine, and dobutamine
.

There is no evidence of substantial benefit of one vasopressor over another;

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.[38] Activated protein C was withdrawn from the market in 2011, and clinical trials were discontinued.[38] The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.[39] If used at all it should only be considered if the blood pH is less than 7.0.[39]

People with anaphylactic shock are commonly treated with

Albuterol
, normal saline, and steroids are also commonly given.

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. A good urine output indicates that the kidneys are getting enough blood flow.

Epidemiology

Septic shock (a form of distributive shock), is the most common form of shock. Shock from blood loss occurs in about 1–2% of trauma cases.[33] Overall, up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock.[41] Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20%, and septic shock about 60% of cases.[42]

Prognosis

Sepsis mortality

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. Septic shock, 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.[43]

History

There is no evidence of the word shock being used in its modern-day form prior to 1743. However, there is evidence that Hippocrates used the word exemia to signify a state of being "drained of blood".[44] Shock or "choc" was first described in a trauma victim in the English translation of Henri-François LeDran'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 gun-shot wounds.)[45] 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.

Prior to

George W. Crile who suggested in his 1899 monograph, "An Experimental Research into Surgical Shock", that shock was quintessentially defined as a state of circulatory collapse (vasodilation) due to excessive nervous stimulation.[46] 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.[47] 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.[48][49] In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today.[50][43]

References

  1. ^
    ISBN 978-1292-17084-8
    .
  2. ^
    ISBN 978-78-0-9968267
    .
  3. ^
    ISBN 978-1455700257
    .
  4. PMID 29261964
    .
  5. ^
    S2CID 19881753
    .
  6. ^
    ISBN 978-0-7216-0240-0
    .
  7. ^
    ISBN 978-0-07-148480-0
    .
  8. ^
    ISBN 978-0-07-148480-0
    .
  9. ^ Assessing dehydration and shock. National Collaborating Centre for Women's and Children's Health (UK). April 2009. Retrieved 2019-05-09. {{cite book}}: |website= ignored (help)
  10. ^ a b c d e f g h i Silverman, Adam (Oct 2005). "Shock: A Common Pathway For Life-Threatening Pediatric Illnesses And Injuries". Pediatric Emergency Medicine Practice. 2 (10).
  11. ISBN 978-0-07-148480-0
    .
  12. PMID 23483915
    .
  13. S2CID 39461027
    .
  14. S2CID 42407737
    .
  15. S2CID 10770608
    .
  16. PMID 1303622
    .
  17. OCLC 785442005
    .
  18. ^
    OCLC 69672074.{{cite book}}: CS1 maint: date and year (link
    )
  19. ^ "Surviving Sepsis Campaign Responds to ProCESS Trial" (PDF). Surviving Sepsis Campaign. Survivingsepsis.org. Archived from the original (PDF) on 2015-09-24. Retrieved 2015-03-25.
  20. ^
    PMID 17826209
    .
  21. PMID 16879732
    .
  22. ^ a b "Definition, classification, etiology, and pathophysiology of shock in adults". UpToDate. Retrieved 2019-02-22.
  23. ISBN 978-0-07-148480-0
    .
  24. ^ Armstrong, D.J. (2004). Shock (2nd ed.). In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. Nursing Practice. Hospital and Home. The Adult.: Edinburgh: Churchill Livingstone.
  25. ISSN 0012-3692
    .
  26. PMID 8774804
    .
  27. PMID 30340602
    .
  28. S2CID 45691590
    .
  29. ISBN 978-1-880696-31-6
    .
  30. PMID 30073665
    .
  31. PMID 30852043
    .
  32. ISBN 978-0-323-05472-0
    .
  33. ^
    PMID 22164397. Archived from the original
    on 2012-01-18.
  34. S2CID 39310937
    .
  35. PMID 26878401
    .
  36. PMID 26878401
    .
  37. S2CID 19918811
    .
  38. ^
    PMID 23235609
    .
  39. ^
    S2CID 22613993
    .
  40. S2CID 6900105
    .
  41. S2CID 6900105
    .
  42. PMID 25392034
    .
  43. ^
    ISBN 978-0-7817-3548-3. Archived from the original
    on 2005-11-07.
  44. ^ Cannon, Walter Bradford (1918). The Nature and Treatment of Wound Shock and Allied Conditions. American Medical Association.
  45. PMID 5328405
    .
  46. LCCN 99000784. Alt URL
  47. doi:10.1016/S0140-6736(00)69075-X
    .
  48. doi:10.1001/jama.1919.02610290016008
    .
  49. ^ Cannon, W. B.; Bayliss, W. M. (1919). "Note on Muscle Injury in Relation to Shock". Special Report Series, Medical Research Council, London. 26 (8). Medical Research Committee, Special Investigation Committee on Surgical Shock and Allied Conditions: 19.
  50. OCLC 549969
    .

External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=Shock_(circulatory)&oldid=1219903363"