Shock (medical)

Shock
Classification & external resources
ICD-10many incl. R57.
ICD-9785
DiseasesDB12013
MedlinePlus000039
eMedicineemerg/531  med/285 emerg/533
MeSHD012769


For other uses, see Shock.
Shock is a serious, often life-threatening medical condition where insufficient blood flow reaches the body tissues. As blood is the body's carrier of oxygen and nutrients, this leads to a deficiency of these essential inputs to life. The process affected, where blood enters the tissues, is called perfusion and this process not occurring properly causes a hypoperfusional (hypo = below) state.

Medical shock must not be confused with the emotional state, and the two are not related. Medical shock is a life-threatening medical emergency and one of the leading causes of death for critically ill people. This primary cause may lead to many other medical emergencies, such as hypoxia (a lack of oxygen in the body tissues) or cardiac arrest (the heart stopping).[1][2][3][4][5][6][7]

Shock can have a number of effects, all with similar outcomes, but all relate to a problem with the body's circulatory system. Key types of shock are:
  • Hypovolemic shock - A lack of blood in the normally closed circulatory system, usually caused by bleeding. (Hypo=low, volemic=volume of blood)
  • Cardiogenic shock - Inefficient pumping of the blood around the body (Cardio=heart)
  • Distributive shock - A range of conditions which prevent the efficient distribution of blood, by dilating blood vessels, leading to a critical drop in blood pressure.
  • Obstructive shock - Another range of conditions where a physical object (such as a blood clot) stops blood from flowing around the body.

Stages of shock

Enlarge picture
Effects of inadequate perfusion on cell function.


There are four stages of shock.[8]
Initial
During this stage, the hypoperfusional state causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate. 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
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. Renin-angiotensin axis is activated and arginine vasopressin 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
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 and precapillary sphincters constrict such that blood remains in the capillaries. 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.
Refractory
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.


Shock is a complex and continuous condition and there is no sudden transition from one stage to the next.

Types of shock

In 1972 Hinshaw and Cox suggested the following classification which is still used today.[1] It uses four types of shock: hypovolaemic, cardiogenic, distributive and obstructive shock:[2][3][4][7][9] Recently a fifth form of shock has been introduced:[1]
  • Endocrine shock based on endocrine disturbances.
  • Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.
  • Thyrotoxycosis may induce a reversible cardiomyopathy.
  • Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid 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.
  • Relative adrenal insufficiency in critically ill patients where present hormone levels are insufficient to meet the higher demands

Signs and symptoms

  • Hypovolaemic shock
  • 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.
  • Cardiogenic shock, similar to hypovolaemic shock but in addition:
  • Distended jugular veins due to increased jugular venous pressure.
  • Absent pulse due to tachyarrhythmia.
  • Obstructive shock, similar to hypovolaemic shock but in addition:
  • Distended jugular veins due to increased jugular venous pressure.
  • Pulsus paradoxus in case of tamponade
  • Septic shock, similar to hypovolaemic shock except in the first stages:
  • Pyrexia and fever, or hyperthermia, due to overwhelming bacterial infection.
  • Vasodilation and increased cardiac output due to sepsis.
  • Neurogenic shock, similar to hypovolaemic shock except in the skin's characteristics. In neurogenic shock, the skin is warm and dry.
  • Anaphylactic shock
  • Skin eruptions and large welts.
  • Localised edema, especially around the face.
  • Weak and rapid pulse.
  • Breathlessness and cough due to narrowing of airways and swelling of the throat.

Treatment

Enlarge picture
Modified and adapted from Alexander M.F., Fawcett J.N. and Runciman, P.N. (2004) Nursing Practice. The Hospital and Home. The Adult. (2nd edition) Edinburgh: Churchill Livingstone
In the early stages, shock requires immediate intervention to preserve life. Therefore, the early recognition and treatment depends on the transfer to a hospital.

The management of shock requires immediate intervention, even before a diagnosis is made. 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 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.

A compromise must be found between:
  • raising the blood pressure to be able to transport "safely" (when the blood pressure is too low, any motion can lower the heart and brain perfusion, and thus cause death);
  • respecting the golden hour. If surgery is required, it should be performed within the first hour to maximise the patient's chance of survival.
This is the stay and play versus the load and go debate.

Hypovolaemic shock

In hypovolaemic shock, caused by bleeding, it is necessary to immediately control the bleeding and restore the victim's blood volume by giving infusions of balanced salt solutions. Blood transfusions 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. Hypovolaemia due to burns, diarrhoea, 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.[1][2][3][4]

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.

Opinion varies on the type of fluid used in shock. The most common are:
  • Crystalloids - Such as sodium chloride (0.9%), or Hartmann's solution (Ringer's lactate). Dextrose solutions which contain free water are less effective at re-establishing circulating volume, and promote hyperglycaemia.
  • Colloids - For example, synthetic albumin (Dextran™), polygeline (Haemaccel™), succunylated gelatin (Gelofusine™) and hetastarch (Hepsan™). 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 haemorrhagic shock, often pre-warmed and rapidly infused.
Vasoconstrictor agents have no role in the initial treatment of hemorrhagic shock, due to their relative inefficacy in the setting of acidosis, and due to the fact that 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 myocardal infarction one can infuse fluids or in shock refractory to infusing 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 -which reduces workload for the heart, and improves perfusion of the coronary arteries- can be considered or a left ventricular assist device -which augments the pump-function of the heart.[1][2][3][4]

The main goals of the treatment of cardiogenic shock are the re-establishment of circulation to the myocardium, minimising 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 anti-shock trousers 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 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.[1][2][3][4]

Obstructive shock

In obstructive shock, the only therapy consists of removing the obstruction. Pneumothorax or haemothorax 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.[1][2][3][4]

Endocrine shock

In endocrine shock the hormone disturbances are corrected. Hypothyroidism requires supplementation by means of levothyroxine, in hyperthyroidism the production of hormone by the thyroid is inhibited through thyreostatica, i.e. methimazole (Tapazole®) or PTU (propylthiouracil). Adrenal insufficiency is treated by supplementing corticosteroids. [1]

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. [1]

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.

Notes

1. ^ Irwin, Richard S.; Rippe, James M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-3548-3. 
2. ^ Marino, Paul L. (September 2006). The ICU Book. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-4802-X. 
3. ^ Fundamental Critical Care Support, A standardized curriculum of Critical Care. Society of Critical Care Medicine, Des Plaines, Illinois.
4. ^ Harrison's Principles of Internal Medicine. 
5. ^ Cecil Textbook of Medicine.
6. ^ The Oxford Textbook of Medicine. 
7. ^ 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
8. ^ 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. 
9. ^ Joynt, Gavin (April 2003). Introduction to management of shock for junior ICU trainees and medical students. The Chinese University of Hong Kong. Retrieved on 9 October, 2006.

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.
  • 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

See also



The International Statistical Classification of Diseases and Related Health Problems (most commonly known by the abbreviation ICD
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List of ICD-10 codes. The version for 2007 is available online at [1]

Chapter Blocks Title
I Certain infectious and parasitic diseases
II Neoplasms
III Diseases of the blood and blood-forming organs and certain disorders involving the immune mechanism
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The International Statistical Classification of Diseases and Related Health Problems (most commonly known by the abbreviation ICD
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The following is a list of codes for International Statistical Classification of Diseases and Related Health Problems. These codes are in the public domain.

See also


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The Diseases Database is a free website that provides information about the relationships between medical conditions, symptoms, and medications.

It directly integrates the Unified Medical Language System.

External links

  • Diseases Database

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MedlinePlus is a website containing health information from the world's largest medical library, the United States National Library of Medicine. The site is intended to be used by health care providers and patients, and designed to provide up-to-date, authoritative information.
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eMedicine is an online clinical medical knowledge base that was founded in 1996 by Scott Plantz and Richard Lavely, two medical doctors. It was sold to WebMD in January 2006.
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Medical Subject Headings (MeSH) is a huge controlled vocabulary (or metadata system) for the purpose of indexing journal articles and books in the life sciences. Created and updated by the United States National Library of Medicine (NLM), it is used by the MEDLINE/PubMed
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Medicine is the science and "" of maintaining and/or restoring human health through the study, diagnosis, and treatment of patients. The term is derived from the Latin ars medicina meaning the art of healing.
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Biological tissue is a collection of interconnected cells that perform a similar function within an organism.

The study of tissue is known as histology, or, in connection with disease, histopathology.
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2, −1
(neutral oxide)
Electronegativity 3.44 (Pauling scale)
Ionization energies
(more) 1st: 1313.9 kJmol−1
2nd: 3388.3 kJmol−1
3rd: 5300.5 kJmol−1

Atomic radius 60 pm
Atomic radius (calc.
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macronutrients and those needed in relatively small quantities are called micronutrients.

See healthy diet for information on the role of nutrients in human nutrition.

Types of human nutrients

Macronutrients are defined in several different ways.
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In physiology, perfusion is the process of nutritive delivery of arterial blood to a capillary bed in the biological tissue.

Tests of adequate perfusion are a part of patient triage performed by medical or emergency personnel in a mass casualty incident.
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Acute stress reaction (also called acute stress disorder or simply shock) is a psychological condition arising in response to a terrifying event.

"Acute Stress Response", was first described by Walter Cannon in the 1920s as a theory that animals react to threats with a
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Medical Emergency is an Australian reality television series screened on the Seven Network. Medical Emergency is narrated by actor Chris Gabardi who also appears in drama series All Saints.
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For other uses of the term "hypoxia", see hypoxia.


Hypoxia is a pathological condition in which the body as a whole (generalised hypoxia) or region of the body (tissue hypoxia) is deprived of adequate oxygen supply.
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Cardiac arrest
Classification & external resources

ICD-10 I 46.
ICD-9 427.5

A cardiac arrest, also known as cardiorespiratory arrest, cardiopulmonary arrest or circulatory arrest
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Bleeding, technically known as hemorrhage (American English) or haemorrhage (British English) is the loss of blood from the circulatory system.[1] Bleeding can occur internally, where blood leaks from blood vessels inside the body or externally, either
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For other uses of the term "hypoxia", see hypoxia.


Hypoxia is a pathological condition in which the body as a whole (generalised hypoxia) or region of the body (tissue hypoxia) is deprived of adequate oxygen supply.
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Adenosine 5'-triphosphate (ATP) is a multifunctional nucleotide that is most important as a "molecular currency" of intracellular energy transfer. In this role, ATP transports chemical energy within cells for metabolism.
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The factual accuracy of part of this article is disputed.
The dispute is about Lactic acid fermentation.
Please see the relevant discussion on the talk page .
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Lactic acid (IUPAC systematic name: 2-hydroxypropanoic acid), also known as milk acid, is a chemical compound that plays a role in several biochemical processes.
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Pyruvic acid (CH3COCO2H) is an alpha-keto acid which plays an important role in biochemical processes. The carboxylate anion of pyruvic acid is known as pyruvate.

Chemistry

Pyruvic acid is a colorless liquid with a smell similar to acetic acid.
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Metabolic acidosis
Classification & external resources

Davenport diagram
ICD-10 E 87.2
ICD-9 276.2

DiseasesDB 92
MedlinePlus 000335
eMedicine emerg/312   med/1458 ped/15

In medicine, metabolic acidosis
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liver is an organ present in vertebrates and some other animals. It plays a major role in metabolism and has a number of functions in the body, including glycogen storage, decomposition of red blood cells, plasma protein synthesis, and detoxification.
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MeSH D000138
For acidosis referring to acidity of the urine, see renal tubular acidosis.
Acidosis is an increased acidity (i.e. an increased hydrogen ion concentration). If not further qualified, it refers to acidity of the blood plasma.
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Hyperventilation
Classifications and external resources

ICD-10 R 06.4
ICD-9 786.01

In medicine, hyperventilation (or overbreathing
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Baroreceptors (or baroceptors) in the human body detect the pressure of blood flowing through them, and can send messages to the central nervous system to increase or decrease total peripheral resistance and cardiac output.
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