Shock (medicine)

from Wikipedia, the free encyclopedia

Classification according to ICD-10
R57 shock
R57.0 Cardiogenic shock
R57.1 Hypovolemic shock
R57.8 Other forms of shock
R57.9 Shock, unspecified
O75.1 Shock during or after labor and delivery; Birth shock
T78.2 Anaphylactic shock
ICD-10 online (WHO version 2019)

In medicine, the term shock describes a life-threatening condition. A severe circulatory disorder develops, in which the blood circulation in the capillaries is usually reduced. As a result, the tissues are under-supplied with oxygen and, ultimately, metabolic failure occurs.

The cause is usually a significant decrease in circulating blood . Loss of blood or fluid, a failure of the circulatory regulation in the body periphery, for example in the case of blood poisoning or allergic reactions of the immediate type ( anaphylaxis ), can cause shock. Shock can also occur when the heart fails and is no longer able to pump enough blood to the periphery.

In contrast to everyday language, the consequences of extreme psychological stress are not referred to as shock in medical terminology, but rather as an acute stress reaction .


Largely independent of the cause, all forms of shock result in a physiological reaction by the body that tries to stabilize its blood pressure . The release of alarm hormones such as adrenaline and noradrenaline is increased. In addition to an increase in the heart rate, these also cause the hair vessels ( arterioles and venules ) to constrict, i.e. reactions that lead to an increase in blood pressure. Therefore, in the initial stages of shock, blood pressure can still be normal. The starting points of the catecholamines in the body are the α and β adrenoceptors . They are distributed differently in the body, so that through the redistribution of the circulating blood (centralization), the blood flow to the heart and brain is maintained for as long as possible. Initially, this stabilization of blood pressure is additionally supported by the reactive influx of interstitial fluid into the bloodstream.

The constriction of the hair vessels and the associated throttling of the blood flow leads to an inadequate supply of the tissues, so that hypoxia occurs there. As a result, the acidic end products of the anaerobic carbohydrate metabolism ( lactate ) accumulate . This in turn leads to a measurable acidification of the body (metabolic acidosis ) as well as to the leakage of fluid from the hair vessels into the tissue (transcapillary loss of intravascular fluid) , i.e. a loss of blood volume .

The over-acidification also causes the small arterial vessels that carry the blood to the hair vessels to relax; The small veins that drain the blood from the hair vessels do not slacken, however, which can lead to a congestion of red blood cells (sludge) in the hair vessels and lead to microthrombi . In extreme cases this can lead to consumption coagulopathy .

Shock can begin for a variety of reasons, but if left untreated, it will progress monomorphically regardless of the cause.

  • Cause - blood loss : The blood loss leads to reduced blood volume (hypovolemia) , which reactively reduces the pumping capacity of the heart. This in turn leads to hypoxia and accompanying acidosis, the consequence of which is the atony of the arterioles with damage to the capillaries. The resulting loss of fluid from the vessels in turn increases the hypovolemia.
  • Cause - heart failure : Here the heart's pumping capacity is primarily reduced, which in turn leads to hypoxia and accompanying acidosis in the tissue, as a result of which the capillaries are damaged. The resulting loss of fluid from the vessels in turn increases the hypovolemia.
  • Cause - sepsis / anaphylaxis : Damage to the capillaries leads to fluid loss from the vessels, i.e. hypovolemia. This reactively decreases the heart's pumping capacity, which in turn leads to hypoxia and acidosis in the tissue, which in turn lead to damage to the capillaries.

Ultimately, it does not matter where the life-threatening event begins, the process is always the same. It is ultimately a vicious circle , which is also known as a "shock spiral".

(→ For the effects on the kidneys, see also the main article shock kidney .)

Classification, clinic and basics

Graphic illustration of different types of shock: no shock (left), distributive shock with widening of the blood vessels (middle), volume deficiency shock due to blood loss (right)

A distinction is made between hypovolemic, distributive and obstructive shock among the types of shock. These three main groups differ mainly in the organ system affected. The volume deficiency shock refers to the volume of blood and fluid, the distributive shock to the vascular system and the obstructive shock to the circulatory system.

Simple examinations such as measuring blood pressure and heart rate provide crucial diagnostic information.

The diagnosis consists of recognizing the cause and the clinical picture of the shock. As a rule, the clinical picture of the shock shows a decreased systolic blood pressure (<90 mmHg - exception: previously existing high blood pressure ) or a decreased blood pressure amplitude and an increased heart rate (> 100 beats per minute in humans - exception: existing therapy with beta blockers ) and thus the image of a pulsus celer et parvus . In addition, patients often have pale, pale gray and damp skin (as a sign of "centralization" - exception: septic shock in the hyperdynamic phase), a changed state of consciousness (restlessness, fear, apathy) and disturbed vigilance (somnolence, coma) to find. However, these criteria may also be missing, especially in the early stages. Under stationary conditions, more detailed (and thus significantly more (time) consuming) scoring systems such as B. the Acute Physiology And Chronic Health Evaluation, APACHE for short , more reliable and more accurate forecasts. Various laboratory tests ( blood gas analysis , in which the hemoglobin , hematocrit , erythrocyte , lactate and pH values ​​are measured) and, if required, an apparatus-based diagnosis (e.g. sonography , echocardiography , magnetic resonance tomography, etc.) provide more accurate diagnoses and additional information on causes.

In rescue medicine , the fingernail test (or Rekap test ) is a method for determining the peripheral blood flow situation , which allows a rough conclusion to be drawn about the circulatory situation, especially if there is little time to examine each injured person, for example in the event of disasters and accidents. The nail is briefly pressed into the nail bed so that it turns white due to the displacement of blood from the capillaries. If the time until re- coloring ( recapillarization ) is longer than one second, there is insufficient blood flow. However, previous nail injuries can falsify the result.

Volume depletion shock

Volume depletion shock , also known as hypovolemic shock , is caused by excessive fluid loss, which reduces the amount of blood circulating in the vessels.

The cause can be a large blood loss (hemorrhagic shock) , which can occur after an accident. Typical cases for this are on the one hand a fracture of the pelvis or large tubular bones and on the other hand the tear ( rupture ) of internal organs. Without an accident, the bursting of large vessels (especially aortic aneurysm rupture ), blood loss during or after surgery or childbirth, and spontaneous bleeding in the case of coagulation disorders (e.g. hemophilia , drug abuse ) can have the same effect.

The loss of water and electrolytes e.g. B. intestinal obstruction ( ileus ) , ascites ( ascites ) , severe diarrhea (diarrhea) and vomiting as well as withdrawal or insufficient supply of water ( dehydration ) can lead to hypovolemic shock. A blood loss of 20% (about 1 liter in humans) is still well compensated - the arterial blood pressure remains normal - while a loss above that increases the risk of developing a shock. The central venous pressure decreases measurably with losses of 10%.

As an (unreliable) rule of thumb for estimating the severity of a volume deficiency shock , the “ shock index ” had established itself in everyday clinical practice. The pulse rate is divided by the level of the systolic blood pressure (the units are ignored; the correct unit of the shock index (usually around 0.5) would be 1 / minmmHg). Values ​​above 1 suggest the existence of a manifest shock.

Three degrees of severity of a volume deficiency shock can be derived from this. In the early stages (not yet sure signs of decompensation), blood pressure is normal and the skin is often damp, cool and pale. In stage 2 (first signs of decompensation) the pulse is accelerated ( tachycardia ) and usually weak, the systolic blood pressure is less than 100 mmHg, while lying down, the neck veins have collapsed (collapsed), the patients complain of severe thirst, and urinary excretion is continuous decreased kidney function ( oliguria ) . In stage 3 (massive signs of decompensation) the systolic blood pressure drops below 60 mmHg, the pulse is barely palpable, breathing is shallow and fast, impaired consciousness and failure of kidney function ( anuria ) occur.

Cardiogenic shock

The cardiogenic shock is triggered by a massive reduction in cardiac output . The heart does not pump enough blood into the circulation.

Cardiogenic shock can be caused by diseases of the heart itself, such as myocardial infarction , myocarditis , endocarditis , cardiomyopathy , heart failure or even severe cardiac arrhythmias , acute mitral or aortic valve insufficiency . However, they can also lie outside the heart (e.g. cardiac tamponade , pericarditis , pulmonary embolism or tension pneumothorax ).

Typical are a systolic blood pressure of less than 90 mmHg (millimeters of mercury), a heart index of less than 1.8 l / min / m² (liters / minute / square meter of body surface; correct (l / min) / m² = mm / min) and a left ventricular end-diastolic pressure greater than 20 mmHg.

Clinically, there are breathing difficulties with moist rattling noises over the basal sections of the lungs and signs of pulmonary congestion in the chest x-ray . The cause and extent of the reduced cardiac output (e.g. pericardial tamponade, valve function, ventricular function) can be identified in the echocardiogram . Invasive diagnostics using a right heart catheter examination is also generally indicated. The other clinical symptoms correspond to those of the cause (e.g. heart attack) and require further diagnosis.

Distributive shock

Strictly speaking, the distributive shock is a relative volume deficiency shock, which can result from an uncontrolled widening of the vessels or from increased diffusion of fluid into the intercellular space.

Septic shock

In septic shock, the organism reacts to a generalized or locally limited infection by microorganisms with the effect of toxins . The presence of antigens (e.g. bacteria or their products) in the bloodstream is required here. Inflammation of the peritoneum ( peritonitis ) , the pancreas ( pancreatitis ) , the gall bladder ( cholecystitis ) or the bile ducts ( cholangitis ) , inflammation of the kidneys ( pyelonephritis ) or pneumonia ( pneumonia ) as well as infections caused by foreign matter (e.g. urine ) introduced into the body - or venous catheter ) or in the case of immunosuppression and the burn disease can set the chain reactions of the immune and blood coagulation cascade in motion and thus lead to the full clinical picture of sepsis .

One speaks of septic shock if the symptoms of the systemic inflammatory response syndrome (SIRS) are present, an infectious cause has been proven and the systolic blood pressure is below 90 mmHg for at least one hour despite sufficient volume administration. In the early phase (hyperdynamic form) the peripheral resistance and the difference in oxygen content between venous and arterial blood are significantly reduced, blood pressure and central venous pressure (CVP) are normal or only slightly reduced, and the skin is warm, dry and rosy. In the next phase (hypodynamic form) the skin becomes pale, moist and cool, blood pressure, CVP and urine volume decrease and the peripheral resistance and the difference in oxygen content between venous and arterial blood are increased.

Septic shock can take a particularly fulminant course in meningococcal sepsis , Waterhouse-Friderichsen syndrome , after splenectomy or in " toxic shock syndrome ".

Anaphylactic shock

Main article: anaphylaxis

The anaphylactic shock , the most severe form of allergic reaction . The enormous release of histamine causes the vessels dilation with relative dehydration and low blood pressure. The cardiac output decreases and the bronchi can narrow. Medicines such as analgesics , anesthetics or penicillin or other so-called allergens , e.g. B. Insect venom ( insect venom allergy ). Patients with an increased susceptibility to allergies ( atopy ) are particularly at risk ( neurodermatitis , hay fever , etc.).

The course of an anaphylactic reaction can basically be divided into five stages, whereby a locally limited skin reaction, without accompanying general symptoms, is rated as grade 0 , i.e. not an anaphylactic shock in the actual sense. The leichtesten degree (grade 1) provide generalized skin symptoms such as hives ( urticaria ), itching , or flushing ( Flush is) that of general symptoms such as dizziness accompanied, headache or anxiety. In grade 2 there is also a drop in blood pressure and a racing heart ( tachycardia ), often accompanied by nausea and vomiting, as well as slight shortness of breath. Severe shortness of breath (bronchospasm that clinically looks like an asthma attack or, rarely, laryngeal edema ), accompanied by a massive drop in blood pressure (to <90 mmHg) and a rapid heart rate, characterize the third degree . If there is a circulatory or respiratory arrest, it is referred to as grade 4 .

Neurogenic shock

In neurogenic shock, a nervous failure of the regulation of circulatory and / or vascular tone results in circulatory failure. Common causes of neurogenic shock are lesions of the spinal cord , spinal anesthesia and injuries or intoxication of the central nervous system (e.g. traumatic brain injury in a traffic accident). Even cancer , meningitis ( meningitis ) and brain inflammation ( encephalitis ) are one of the causes of neurogenic shock. Functional neurogenic shock is less common, for example in the case of very strong pain stimuli.

As a result of the interruption of the nerve supply to the blood vessels, paralysis of the smooth muscles of the veins occurs. They are set as wide as possible and there can be no counter-regulation of the sympathetic nervous system. The result is a relative lack of volume through literal "sinking" of the blood in the leg veins. In the case of a neurogenic shock, symptoms such as anhydrosis or hypohidrosis as well as a limitation of the thermoregulation of the affected body area can appear.

Obstructive shock

Obstructive shock is caused by a blockage of large blood vessels or the heart itself. The symptoms are the same as those of cardiogenic shock, but its treatment is fundamentally different and focuses primarily on removing the blockage. Causes can be, for example:

Special forms

In the case of particularly characteristic constellations, other terms for forms of shock have become commonplace in everyday clinical language. These are also based on the physiological mechanisms described above. The following examples are mentioned here:

Classification according to ICD-10
G95.8 Other specified diseases of the spinal cord
ICD-10 online (WHO version 2019)

Spinal shock

A fundamental distinction is made between neurogenic shock and spinal shock, which denotes a failure of all spinal cord functions after injuries and does not necessarily result in a relative lack of volume. The clinical picture can be reversible and then express itself as flaccid paralysis or turn into spastic paresis.

Endocrine shock

Endocrine shock is caused by over- or under-functioning of hormones (e.g. in hyperthyroidism , Addison's disease , Waterhouse-Friderichsen syndrome or hypothyroidism ). (→ see their respective main article)

Other forms

In the specialist literature , the following attributes are also mentioned in connection with the term "shock":

  • apoplectic and paralytic - use in the sense of neurogenic shock, i.e. failure of circulatory and / or vascular regulation,
  • decompensated, irreversible and refractory - use in the sense of an untreated, infinitely progressive shock,
  • electrical - use in the sense of the consequences of an electrical accident with consecutive restriction of the cardiac output and accompanying disturbance of the circulatory and / or vascular regulation,
  • febrile - use in the sense of anaphylactic, but also volume deficiency shock (dehydration as a direct consequence of fever ),
  • hypoglycemic or insulin shock - use in the sense of disorders of consciousness and central respiratory and circulatory regulation that occur as a result of reduced blood sugar levels ,
  • compensated and latent - use in the sense of the initial stage of a shock event,
  • orthostatic - ultimately used in the sense of spinal shock, i.e. disturbance of circulatory and / or vascular regulation with an upright body position ("sinking of the blood") , and
  • psychological - use in the sense of a psychotrauma , respectively
  • iatrogenic - use in the sense of a consequence of shock treatment in psychiatric diseases; in extreme cases progression through disruption of circulatory and / or vascular regulation.


Correct positioning and protection against hypothermia are important acute measures in case of shock (picture of an exercise).

If there is a shock, action must be taken as soon as possible. This is possible to a different extent depending on the area of ​​the rescue chain where the patient is located. In the run-up to the therapy, however, it is always necessary to differentiate the present form of shock according to the classification described above. Prompt recognition of cardiogenic shock is of particular importance. Anamnesis , clinical picture (heart rate, blood pressure and other abnormalities) and, if possible, additional examinations such as EKG , CVP , laboratory parameters and the determination of the oxygen content of the blood by means of blood gas analysis or pulse oximetry are used for diagnosis .

The basic measures are to keep the airways free, protect the patient from hypothermia and give oxygen through a nasogastric tube . The measures of "shock positioning" (also "passive leg raising" or "PLR"; raising the patient's legs with the intention of redistributing the blood in the body towards the heart) or the Trendelenburg positioning are widespread and will continue to be informed, but the study situation comes to partially contradicting results regarding the effectiveness. Some authors even suggest possible negative effects, especially in the Trendelenburg position. Both positions are still recommended in standard works on the subject of emergency medicine and in the current recommendations of the DIVI commission in the context of shock control in the case of absolute volume deficiency shock as well as in anaphylactic and septic-toxic shock. A patient in cardiogenic shock should be placed in a sitting position to relieve the heart. Consistent monitoring of pulse rate, blood pressure, EKG (monitoring). CVP, diuresis and arterial oxygen saturation of the blood, supplemented by laboratory parameters such as small blood counts , coagulation analysis , urea , creatinine and electrolyte status, as well as pulmonary pressure and cardiac output, especially in cardiogenic shock , are not only necessary for follow-up, but also to detect complications as early as possible and be able to treat them in a targeted manner

Hypovolemic shock

The focus here is on normalizing blood volume in order to break the shock spiral. Basically, this is done by administering isotonic crystalline and colloidal infusion solutions (ratio 2: 1 to 3: 1) using large peripheral accesses . For some years now, hyperosmolar infusion solutions have also been available for initial therapy, which increase the intravascular volume particularly quickly and effectively, as they combine the effect of hyperosmolar crystalline (increase in the osmotic gradient and thus fluid displacement from the intracellular space and interstitium into the blood vessels) with that of colloidal volume expanders . The volume replacement should compensate for the hypovolemia, but not lead to any notable hypervolemia (CVP not exceeding 14 cmH 2 O).

The most frequently used preparation in Germany, hydroxyethyl starch, has a special position among volume substitutes . It is particularly well tolerated (anaphylactic reaction in 1: 1 million cases) , has an anti-aggregation effect and thus prevents the capillary damage that typically occurs in the course of a shock. However, itching, deterioration in kidney function and a possible increase in the risk of bleeding should be weighed as adverse effects before use. In principle, synthetic colloids such as dextrans or gelatine as well as pasteurized plasma protein solutions, thawed frozen fresh plasma and red cell concentrates can also be used as volume substitutes.

The primary treatment for blood loss is hemostasis; further symptomatic therapy consists of balancing out the metabolic acidosis with bicarbonate buffer solution , preventing the occurrence of a shock kidney or stress ulcer and, if necessary, treating shock-related lung damage and blood clotting failure .

Cardiogenic shock

In cardiogenic shock, the patient's upper body should be elevated.

As symptomatic therapy, if at all possible, the patient's upper body is elevated, adequate pain reduction and calming are initiated, the cardiac strength is increased by means of suitable measures (e.g. the administration of dobutamine ) and an adequate oxygen supply to the body (if necessary also by means of artificial Ventilation with the administration of 100 percent oxygen).

The causal treatment of the triggering heart disease (e.g. myocardial infarction , cardiac arrhythmia , myocarditis and pericarditis ) is, however, in the foreground.

Septic shock

The causal therapy of septic shock ( lethality up to 70%) is based on infection control and effective antibiotic therapy . Treatment of the cardiovascular parameters is symptomatic (target values: CVP = 8–12 cmH 2 O, MAP = 65–90 mmHg, hematocrit ≥ 30%, central venous blood oxygen saturation ≥ 70%). This may require the administration of colloidal and crystalline infusion solutions as well as the transfusion of blood products and the administration of circulatory-supporting medication (e.g. norepinephrine) as well as a high level of oxygen administration, possibly with artificial respiration. In addition, care should be taken to ensure that blood sugar levels are as normal as possible, as well as adrenal insufficiency (then substitution of hydrocortisone ) and prevent complications such as consumption coagulopathy through administration of heparin . As a preventive measure , in addition to checking the antithrombin level , artificial ventilation is recommended to avoid shock-related damage to the lungs.

Anaphylactic shock

Shock positioning is suitable for symptoms and, if possible, further antigen administration should be stopped as quickly as possible. In addition, the administration of prednisolone , histamine antagonists (fenistil and ranitidine) (H1 and H2 blockers) , volume expanders and adrenaline is indicated. In bronchospasm, β2-mimetics as aerosol and theophylline may also be necessary. If the condition persists over a longer period of time, the positive inotropic dopamine is helpful. Ensure that the blood is adequately oxygenated.

Special forms

Particularly in unclear states of shock, special forms should be considered as a supplementary differential diagnosis in emergency medicine and, as far as possible with the available equipment, clarified. Hypoglycemia, which is particularly important in this context, can already be successfully treated preclinically (i.e. before the start of hospital treatment) by simply administering a highly concentrated glucose solution.


In 1731, the French surgeon Henry François Le Dran described a fatal collapse of the life functions of an injured person. In 1743 he published an article on injuries on the battlefield (Traité ou réflexions tirées de la pratique sur les playes d'armes à feu) . In the English translation, the term "shock" was used for the first time in medical literature. The term was quickly used in English and German speaking countries in connection with injuries. In his attempt to explain, Le Dran resorted to the humoral pathology of ancient Greek medicine .

The term shock as it is today goes back to a monograph by Morris from 1867 and has been used widely since then. At the end of the 19th century, clinical observations made the symptoms of shock increasingly more specific. The surgeon Timothée Piechaud described it in 1880 in his treatise Que faut-il entendre par l'expression de choc traumatique as a consequence of an accident, which is characterized by a weakening of the heart's actions, drop in blood pressure, general pallor and muscle weakness. With this he came very close to the description that is still valid today, but ultimately the interpretation of the shock from the symptoms never succeeded.

Alfred Blalock achieved initial success in shock treatment with his research, according to which volume substitution, for example with blood plasma, could reduce the effects of shock. This knowledge was already used in World War II, but the death rate was still very high. As a result, it was possible to define a reversible and an irreversible phase in the course of the shock, which later, supplemented by a third, preceding phase, became known as the Wiggers model .

The trigger for modern shock research was then the Vietnam War , in the course of which the shock lung was described for the first time and attributed to a "clumping" of blood cells in the hair vessels. An analysis of the blood gases and the ZVD was also carried out promptly for scientific reasons, while still on the battlefield.


Individual evidence

  1. a b c d e f g h Herold: Internal medicine. 2007, pp. 286-290.
  2. ^ Deutscher Ärzteverlag GmbH, editorial office of the Deutsches Ärzteblatt: nomenclature, definition and differentiation of forms of shock. November 9, 2018, accessed March 2, 2019 .
  3. S3 guideline for infarct-related cardiogenic shock - diagnosis, monitoring and therapy . In: AWMF online
  4. ^ S2 guideline diagnosis and therapy of sepsis . In: AWMF online
  5. Alphabetical directory for the ICD-10-WHO version 2019, volume 3. German Institute for Medical Documentation and Information (DIMDI), Cologne, 2019, p. 786
  6. ^ Spinal shock, Orthopädie Lexikon
  7. ^ Roche Lexicon Medicine. 5th edition. Urban & Fischer, 2003; (on-line)
  8. The use of the shock position in the preclinical setting for acute hypotension. November 20, 2012. Retrieved November 21, 2012 .
  9. Sonia Johnson, Sean O. Henderson: Myth: the Trendelenburg position improves circulation in cases of shock. ( Memento of March 8, 2013 in the Internet Archive )
  10. ^ HA Adams et al.: Statement by the DIVI "Shock" section on the shock situation. In: emergency doctor. 28, 2012, pp. 12-16.
  11. Kersten Enke, Andreas Flemming, Hans-Peter Hündorf, Peer G. Knacke, Roland Lipp, Peter Rupp: LPN 1 textbook for preclinical emergency medicine: Volume 1 - Basics and techniques. 4th edition. Stump & Kossendey Verlag, Edewecht 2009, ISBN 978-3-938179-68-0 , pp. 302-204.
  12. ^ D. Kühn, J. Luxem, K. Runggaldier: Rescue Service. 3. Edition. Urban & Fischer Verlag, Munich 2004, ISBN 3-437-46191-5 .
  13. M. Welte: Volume replacement and shock control in emergency patients . Lecture notes of the Darmstadt Clinic, 2004.
  14. K. Werdan et al.: Heart attack-related cardiogenic shock - diagnosis, monitoring and therapy . In: Deutsches Ärzteblatt International . No. 109 (19) , 2012, pp. 343–351 ( Clinical Guideline ).
  15. ^ S2 guideline for acute treatment of anaphylactic reactions . In: AWMF online
  16. HF Le Dran: Observation de Chirurgie. Paris 1731; 2, pp. 253-254. In: RM Hardaway: Wound Shock: A History of Its Study and Treatment by Military Surgeons. In: Military Medicine. Spring, 2004. (online)
  17. HM Baillie: Understanding shock: a brief history. In: Can J Gen Intern Med. 3 (1), 2008, pp. 22-25.
  18. a b F. Povacz: history of trauma . Springer Verlag, 2007, ISBN 978-3-540-74844-1 , p. 384. (online)
  19. ^ A. Blalock: Experimental Shock: The cause of low blood pressure produced by muscle injury. In: Arch Surg . 20, 1930, pp. 959-969.
  20. ^ LH Hess, M. Warner, E. Okabe: Hemorrhagic Shock. In: Handbook of Shock and Trauma. Raven Press, New York 1983, pp. 393-412.
  21. ^ H. Frank, A. Seligman, J. Fine: Traumatic Shock. X .: "The treatment of hemorrhagic shock irreversible to replacement of blood volume deficiency". In: J Clin Invest. 24, 1945, pp. 435-444.
  22. RM Hardaway, JM James, RW Anderson et al .: Intensive study and treatment of shock in man. In: J Am Med Assoc. 199, 1967, pp. 779-790.
  23. RM Hardaway, CH Williams, M. Marvasti et al: Prevention of adult respiratory distress syndrome with plasminogen activator in pigs. In: Crit Care Med. 18, 1990, pp. 1413-1418.
  24. ^ RM Hardaway, CH Williams: Prevention of multiple organ failure with plasminogen activator. In: Curr Ther Res. 59, 1991, pp. 721-722.
  25. RM Hardaway: Traumatic and septic shock alias post-trauma critical illness. In: Br J Surg . 85, 1998, pp. 1473-1479.
  26. ^ RM Hardaway, CH Williams, Y. Vasquez: DIC in sepsis. In: Semin Thromb Hemost. 27, 2001, pp. 577-583.
  27. RM Hardaway, H. Harke, AH Tyroch et al .: Treatment of severe acute respiratory distress syndrome: a final report on a Phase I study. In: At the Surgeon. 67, 2001, pp. 377-382.
  28. ^ Robert M. Hardaway: Wound Shock: A History of Its Study and Treatment by Military Surgeons . In: Military Medicine . tape 169 , no. 4 , April 1, 2004, ISSN  0026-4075 , p. 265–269 , doi : 10.7205 / MILMED.169.4.265 ( [accessed January 12, 2019]).


  • Werner Böcker, Helmut Denk, Philipp U. Heitz (Hrsg.): Pathology. 3., completely redesigned. Edition. Urban & Fischer, Elsevier, Munich / Jena 2004, ISBN 3-437-42381-9 .
  • Gerd Herold : Internal Medicine . Self-published, Cologne 2007.
  • Rolando Rossi, Günter Dobler (ed.): Emergency pocket book. Stumpf and Kossendey, Vienna 1998, ISBN 3-932750-01-2 .
  • Michael Bauer, Frank M. Brunkhorst, Tobias Welte, H. Gerlach, K. Reinhart: Sepsis - Current Aspects of Pathophysiology. Diagnostics and therapy. In: The anesthesiologist. Volume 55. No. 8, 2006, pp. 835-845.
  • Jörg Braun: Resuscitation and circulatory stabilization. In: Jörg Braun, Roland Preuss (Ed.): Clinic Guide Intensive Care Medicine. 9th edition. Elsevier, Munich 2016, ISBN 978-3-437-23763-8 , pp. 151–183, here: pp. 159–164 ( shock ).
This version was added to the list of articles worth reading on September 14, 2008 .