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Shock
Classification and external resources
ICD-10 many incl. R57.
ICD-9 785
DiseasesDB 12013
MedlinePlus 000039
eMedicine emerg/531 med/285 emerg/533
MeSH D012769

Circulatory shock, commonly known simply as shock, is a serious, life-threatening medical condition characterized by a decrease in tissue perfusion to a point at which it is inadequate to meet cellular metabolic needs. As the blood carries oxygen and nutrients around the body, reduced flow hinders the delivery of these components to the tissues, and can stop the tissues from functioning properly.[1] The process of blood entering the tissues is called perfusion, so when perfusion is not occurring properly this is called a hypoperfusional (hypo = below) state.

A circulatory shock should not be confused with the emotional state of shock, as the two are not related. Medical 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 arrest (the heart stopping).[2][3][4][5][6][7][8]

The essential signs of shock are seen as tachycardia/tachypnoea (compensatory mechanisms), hypotension, and signs of poor end-organ perfusion (such as low urine output, confusion or loss of consciousness) (failure to compensate). Other signs should be looked for to establish the underlying cause for the shock to guide effective treatment.

Contents

Signs of severity

The severity of shock can be graded 1-4 based on the physical signs. This approximates to the effective loss of blood volume. The blood volume does not have to actually be lost from the circulation as an expansion in the volume of the circulatory system (e.g. in septic shock) will render the patient proportionally hypovolaemic.

Grade 1
Up to about 15% loss of effective blood volume (~750ml in an average adult who is assumed to have a blood volume of 5 liters). This leads to a mild resting tachycardia and can be well tolerated in otherwise healthy individuals. In the elderly or those with underlying conditions such as ischaemic heart disease the additional myocardial oxygen demands may not be tolerated so well.
Grade 2
Between 15-30% loss of blood volume (750-1500ml) will provoke a moderate tachycardia and begin to narrow the pulse pressure. The time taken for the capillaries to refill after 5 seconds of pressure (capillary refill time) will be extended.
Grade 3
At 30 - 40% loss of effective blood volume (1500 - 2000 ml) the compensatory mechanisms begin to fail and hypotension, tachycardia and low urine output (<0.5ml/kg/hr in adults) are seen.
Grade 4
At 40-50% loss of blood volume (2000 -2500 ml) profound hypotension will develop and if prolonged will cause end-organ damage and death.

Signs relating to different causes

Hypovolemic shock
Direct loss of effective circulating blood volume leading to:
  • Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia
  • Hypotension due to decrease in circulatory volume
  • A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia
  • Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction
  • Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis
  • Hypothermia due to decreased perfusion and evaporation of sweat
  • Thirst and dry mouth, due to fluid depletion
  • Fatigue due to inadequate oxygenation
  • Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient perfusion of the skin
  • Distracted look in the eyes or staring into space, often with pupils dilated
Cardiogenic shock
Similar to hypovolemic shock but in addition:
Obstructive shock
Similar to hypovolemic shock but in addition:
Septic shock
Similar to hypovolemic shock except in the first stages:
Neurogenic shock
Anaphylactic shock
  • Skin eruptions and large bumps

Pathophysiology

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.[9]

Initial 
During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate (ATP). Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extra-cellular fluid, and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.
Compensatory (Compensating) 
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 adrenaline and noradrenaline. Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas adrenaline 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. This is known as Cushing reflex and its triad is the subjective identifying characteristic of this stage. Renin-angiotensin axis is activated and arginine vasopressin (Anti-diuretic hormone; ADH) is released to conserve fluid via the kidneys. Also, 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 .
Progressive (Decompensating) 
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[1]. 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[1]. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock[1].
Refractory (Irreversible)
At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.

Types

Hinshaw and Cox classification

In 1972 Hinshaw and Cox suggested the following classification which is still used today.[2] It names four types of shock: hypovolemic, cardiogenic, distributive and obstructive shock:[3][4][5][8][10] In many patients, shock is a combination of two or more of these four types of shock.

Hypovolemic shock

This is the most common type of shock and based on insufficient circulating volume. Its primary cause is loss of fluid from the circulation (most often "hemorrhagic shock"). Causes may include internal bleeding, traumatic bleeding, high output fistulae or severe burns.

Cardiogenic shock

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

Distributive shock

As in hypovolaemic shock there is an insufficient intravascular volume of blood. This form of "relative" hypovolaemia is the result of dilation of blood vessels which diminishes systemic vascular resistance. Examples of this form of shock are:

  • Septic shock
    • Caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negative bacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body, and other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic shock: ". . .sepsis-induced hypotension (systolic blood pressure <90 mm Hg or a reduction of 40 mm Hg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified."
  • Anaphylactic shock
  • Neurogenic shock

Obstructive shock

In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest. Several conditions result in this form of shock.

Other proposed types of shock

Revisions to the Hinshaw and Cox classification have been proposed. Several types of shock have been proposed as a "fifth type of shock", including hypoglycemic shock, cytotoxic shock and endocrine shock. However, each of these is actually a subtype of one of the four types of shock in Hinshaw and Cox's original model.

For example:

Endocrine shock
Based on endocrine disturbances such as:

Treatment

Shock requires immediate interventions to preserve life. Therefore, the early recognition and treatment is essential even before a specific diagnosis is made (As a general rule, you should treat for a sustained wound and shock). Most forms of shock seen in trauma or sepsis respond initially to aggressive intravenous fluids (e.g. 1 liter normal saline bolus over 10 minutes or 20ml/kg in a child). Therefore this treatment is usually instituted as the person is being further evaluated.[11]

Re-establishing perfusion to the organs is the primary goal through restoring and maintaining the blood circulating volume ensuring oxygenation and blood pressure are adequate, achieving and maintaining effective cardiac function, and preventing complications. Patients attending with the symptoms of shock will have, regardless of the type of shock, their airway managed and oxygen therapy initiated. In case of respiratory insufficiency (i.e. diminished levels of consciousness, hyperventilation due to acid-base disturbances or pneumonia) intubation and mechanical ventilation may be necessary. A paramedic may intubate in emergencies outside the hospital, whereas a patient with respiratory insufficiency in-hospital will be intubated usually by a respiratory therapist, paramedic, or physician.

The aim of these acts is to ensure survival during the transportation to the hospital; they do not cure the cause of the shock. Specific treatment depends on the cause.

Hypovolemic shock

In hypovolemic shock, usually hemorrhagic shock caused by traumatic injury, it is necessary to immediately control the bleeding and restore the casualty's blood volume by giving infusions of isotonic crystalloid solutions. Blood transfusions, packed red blood cells (RBCs), Albumin (or other colloid solutions), or fresh-frozen plasma are necessary for loss of large amounts of blood (e.g. greater than 20% of blood volume), but can be avoided in smaller and slower losses. Hypovolemia due to burns, diarrhea, vomiting, etc. is treated with infusions of electrolyte solutions that balance the nature of the fluid lost. Sodium is essential to keep the fluid infused in the extracellular and intravascular space whilst preventing water intoxication and brain swelling. Metabolic acidosis (mainly due to lactic acid) accumulates as a result of poor delivery of oxygen to the tissues, and mirrors the severity of the shock. It is best treated by rapidly restoring intravascular volume and perfusion as above. Inotropic and vasoconstrictive drugs should be avoided, as they may interfere in knowing blood volume has returned to normal.[2][3][4][5]

Regardless of the cause, the restoration of the circulating volume is priority. As soon as the airway is maintained and oxygen administered the next step is to commence replacement of fluids via the intravenous route. A size 14g intravenous in the arm will flow at twice the rate of a 16g central venous catheter.[12]

Opinion varies on the type of fluid used in shock. The most common are:

  • Crystalloids – Such as sodium chloride (0.9%), or Lactated Ringer's solution (Hartmann's solution). Dextrose solutions which contain free water are less effective at re-establishing circulating volume, and promote hyperglycaemia.
  • Colloids – For example, polysaccharide (Dextran), polygeline (Haemaccel), succinylated gelatin (Gelofusine) and hetastarch (Hespan). Colloids are, in general, much more expensive than crystalloid solutions and have not conclusively been shown to be of any benefit in the initial treatment of shock.
  • Combination – Some clinicians argue that individually, colloids and crystalloids can further exacerbate the problem and suggest the combination of crystalloid and colloid solutions.
  • Blood – Essential in severe hemorrhagic shock, often pre-warmed and rapidly infused.

It is to be noted that NO plain water should be given to the patient at any point, as the patient's low electrolyte levels would easily cause water intoxication, leading to premature death. An isotonic or solution high in electrolytes should be administered if intravenous delivery of recommended fluids is unavailable.

Vasoconstrictor agents have no role in the initial treatment of hemorrhagic shock, due to their relative inefficacy in the setting of acidosis, and because the body, in the setting of hemorrhagic shock, is in an endogenously catecholaminergic state. Definitive care and control of the hemorrhage is absolutely necessary, and should not be delayed.

Cardiogenic shock

In cardiogenic shock, depending on the type of myocardial infarction, one can infuse fluids such as or in shock refractory to infusing fluids, normal saline would be an example of said fluids inotropic agents. Inotropic agents, which enhance the heart's pumping capabilities, are used to improve the contractility and correct the hypotension. Should that not suffice, an intra-aortic balloon pump can be considered (which reduces the workload for the heart and improves perfusion of the coronary arteries) or a left ventricular assist device (which augments the pump-function of the heart.)[2][3][4][5]

The main goals of the treatment of cardiogenic shock are the re-establishment of circulation to the myocardium, minimizing heart muscle damage and improving the heart's effectiveness as a pump. This is most often performed by percutaneous coronary intervention and insertion of a stent in the culprit coronary lesion or sometimes by cardiac bypass.

Although this is a protection reaction, the shock itself will induce problems; the circulatory system being less efficient, the body gets "exhausted" and finally, the blood circulation and the breathing slow down and finally stop (cardiac arrest). The main way to avoid this deadly consequence is to make the blood pressure rise again with

  • Fluid replacement with intravenous infusions;
  • Use of vasopressing drugs (e.g. to induce vasoconstriction);
  • Use of Pneumatic anti-shock Garment(PASG) that compress the legs and concentrate the blood in the vital organs (lungs, heart, brain).
  • Use of blankets to keep the patient warm – metallic PET film emergency blankets are used to reflect the patient's body heat back to the patient.

Distributive shock

In distributive shock caused by sepsis the infection is treated with antibiotics and supportive care is given (i.e. inotropica, mechanical ventilation, renal function replacement). Anaphylaxis is treated with epinephrine "adrenaline" to stimulate cardiac performance and corticosteroids to reduce the inflammatory response. In neurogenic shock because of vasodilation in the legs, one of the most suggested treatments is placing the patient in the Trendelenburg position, thereby elevating the legs and shunting blood back from the periphery to the body's core. However, since bloodvessels are highly compliant, and expand as result of the increased volume locally, this technique does not work. More suitable would be the use of vasopressors such as Norepinephrine to decrease vasodilatation.[2][3][4][5]

Obstructive shock

In obstructive shock, the only therapy consists of removing the obstruction. Pneumothorax or hemothorax is treated by inserting a chest tube, pulmonary embolism requires thrombolysis (to reduce the size of the clot), or embolectomy (removal of the thrombus), tamponade is treated by draining fluid from the pericardial space through pericardiocentesis.[2][3][4][5]

Endocrine Shock

Endocrine shock is defined as a significant (and usually life-threatening) disturbance to an animal's endocrine (hormone production) system. Examples of conditions which may cause endocrine shock include hypothyroidism, hyperthyroidism (thyrotoxicosis) and acute adrenal deficiency. The major and generally accepted modalities for treatment of hyperthyroidism in humans involve initial temporary use of suppressive thyrostatics medication, and possibly later use of permanent surgical or radioisotope therapy. All approaches may cause under active thyroid function (hypothyroidism) which is easily managed with levothyroxine supplementation. Adrenal deficiencies are often treated with application of corticosteroids.

Prognosis

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 and with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse. [2]

Shock is said to evolve from reversible to irreversible in experimental hemorrhagic shock involving certain animal species (dogs, rats, mice) that develop intense vasoconstriction of the gut. Death is due to hemorrhagic necrosis of the intestinal lining when shed blood in reinfused. In pigs and humans 1) this is not seen and cessation of bleeding and restoration of blood volume is usually very effective; however 2) prolonged hypovolemia and hypotension does carry a risk of respiratory and then cardiac arrest. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment (cessation of bleeding, rapid restoration of circulating blood volume and ready respiratory support) is essential for a good prognosis in hypovolemic shock.

See also

Notes

  1. ^ a b c d e f g h i j 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
  2. ^ a b c d e f g Irwin, Richard S.; Rippe, James M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-3548-3. 
  3. ^ a b c d e f Marino, Paul L. (September 2006). The ICU Book. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-4802-X. 
  4. ^ a b c d e f "Fundamental Critical Care Support, A standardized curriculum of Critical Care". Society of Critical Care Medicine, Des Plaines, Illinois. http://www.sccm.org/SCCM/FCCS+and+Training+Courses/FCCS/FCCSCourseAdmin.htm. 
  5. ^ a b c d e f Harrison's Principles of Internal Medicine. http://books.mcgraw-hill.com/medical/harrisons/. 
  6. ^ "Cecil Textbook of Medicine". http://www.cecilmedicine.com/buy.cfm?book=goldman. 
  7. ^ The Oxford Textbook of Medicine. http://www.oup.com/us/catalog/general/subject/Medicine/PrimaryCare/?ci=0192629220&view=usa. 
  8. ^ a b Shock: An Overview PDF by Michael L. Cheatham, MD, Ernest F.J. Block, MD, Howard G. Smith, MD, John T. Promes, MD, Surgical Critical Care Service, Department of Surgical Education, Orlando Regional Medical Center Orlando, Florida
  9. ^ 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. 
  10. ^ Joynt, Gavin (April 2003). "Introduction to management of shock for junior ICU trainees and medical students". The Chinese University of Hong Kong. http://www.aic.cuhk.edu.hk/web8/shock.htm. Retrieved 9 October 2006. 
  11. ^ American College of Surgeons (2008). Atls, Advanced Trauma Life Support Program for Doctors. Amer College of Surgeons. pp. 58. ISBN 1-880696-31-6. 
  12. ^ Amal Mattu; Deepi Goyal; Barrett, Jeffrey W.; Joshua Broder; DeAngelis, Michael; Peter Deblieux; Gus M. Garmel; Richard Harrigan; David Karras; Anita L'Italien; David Manthey (2007). Emergency medicine: avoiding the pitfalls and improving the outcomes. Malden, Mass: Blackwell Pub./BMJ Books. pp. 59. ISBN 1-4051-4166-2. 

References

  • 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.
  • Collins, T. (2000) "Understanding Shock". Nursing Standard. Vol. 14(49), pp. 35–41.
  • Cuthbertson, B.H. and Webster, N.R. (1995) "Nitric oxide in critical care medicine". British Journal of Hospital Medicine. Vol. 54(11), pp. 579–582.
  • Emerson, William R.: Shock: A Universal Malady (Prenatal and Perinatal Origins of Suffering), excerpted from Origins of Adversity: the Treatment of Prenatal and Perinatal Shock, Petaluma: Emerson Training Seminars
  • Hand, H. (2001) "Shock". Nursing Standard. Vol. 15(48), pp. 45–55.
  • Hobler, K, Napadono,R, "Tolerance of Swine to Acute Blood Volume Deficits", Journal of Trauma, 1974, August 14 (8):716–8.
  • Irwin, R.S. and Rippe, J.M. (2003) Irwin and Rippe's Intensive Care Medicine (5th edition). Boston: Lippincott, Williams and Wilkins
  • Irwin, R.S., Rippe, J.M., Curley, F.J., Heard, S.O. (1997) Procedures and Techniques in Intensive Care Medicine (3rd edition). Boston: Lippincott, Williams and Wilkins.
  • Ledingham, I.M. and Ramsey, G. (1986) "Shock". British Journal of Anaesthesia Vol. 58, pp. 169–189.
  • Marino, P. (1997) The ICU Book. (2nd edition). Philadelphia: Lippincott, Williams and Wilkins.
  • Porth, C.M. (2005) Pathophysiology: Concepts of Altered Health States. (7th edition). Philadelphia: Lippincott, Williams and Wilkins
  • Sheppard, M. (2005) Principles and practice of high dependency nursing. Edinburgh: Bailliere Tindall.
  • Society of Critical Care Medicine. Fundamental Critical Care Support, A standardized curriculum of critical care. SSCM Illinois, 2001.
  • Tortora, G.J. (2005) Principles of anatomy and physiology New Jersey: John Wiley, Inc

Simple English

A person is in shock when blood is not sufficient to bring oxygen to the brain. The shock is progressive and can be lethal if it is not promptly made well.

The normal first aid action is the Trendelenburg position, the person is laying face upward, with his legs lifted. The blood is forced to flow to the brain.









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