Shock (circulatory)

"Acute shock" redirects here. For the psychological condition, see Acute stress reaction.

Shock

ICD-10	many incl. R57
ICD-9	785
DiseasesDB	12013
MedlinePlus	000039
eMedicine	emerg/531 med/285 emerg/533

Circulatory shock, commonly known simply as shock, is a life-threatening medical condition that occurs due to inadequate substrate for aerobic cellular respiration.^[1] In the early stages this is generally an inadequate tissue levels of oxygen.^[2]

The typical signs of shock are low blood pressure, a rapid heartbeat and signs of poor end-organ perfusion or "decompensation" (such as low urine output, confusion or loss of consciousness). There are times that a person's blood pressure may remain stable, but may still be in circulatory shock, so it is not always a symptom.^[3]

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).^[4]

One of the key dangers of shock is that it progresses by a positive feedback mechanism. Once shock begins, it tends to make itself worse. This is why immediate treatment of shock is critical.^[3]

Signs and symptoms

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness.^[2] While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion these may not always be present.^[2] While a fast heart rate is common, those on B-blockers, those who are athletic and in 30% of cases those with shock due to intra abdominal bleeding may have a normal or slow heart rate.^[5] Specific subtypes of shock may have additional symptoms.

Hypovolemic

Hemorrhage classes^[6]

Class	Blood loss	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

Direct loss of effective circulating blood volume leading to:

• 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
• Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient perfusion of the skin

The severity of hemorrhagic shock can be graded on a 1-4 scale on the physical signs. This approximates to the effective loss of blood volume.

Cardiogenic

• Distended jugular veins due to increased jugular venous pressure
• Weak or absent pulse
• Arrhythmia, often tachycardic
• Pulsus paradoxus in case of tamponade

Distributive

Systemic inflammatory response syndrome^[7]

Finding	Value
Temperature	<36 °C (97 °F) or >38 °C (100 °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 includes infectious, anaphylactic, and neurogenic causes. The SIRS features typically occur in early septic shock.^[2]

Septic shock

• Fever may occur in sepsis
• Warm and sweaty skin due to vasodilation

Anaphylaxisis

• Hives may present on the skin
• Localised oedema, especially around the face
• Weak and rapid pulse
• Breathlessness and cough due to narrowing of airways and swelling of the throat

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.^[8] At a cellular level shock is oxygen demand greater than oxygen supply.^[2]

Initial

During this stage, the hypoperfusional state causes hypoxia. Due to the lack of oxygen, the cell membranes become damaged^[why?], 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.^{[citation needed]}

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. 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. 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.^{[citation needed]}

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 smooth muscle and precapillary sphincters relax such that blood remains in the capillaries.^[9] 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.^[9] If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.^[9][3]

Refractory

At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cell's total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP.^[3]

Septic shock

• Systemic leukocyte adhesion to endothelial tissue^[9]
• Reduced contractility of the heart^[9]
• Activation of the coagulation pathways, resulting in disseminated intravascular coagulation^[9]
• Increased levels of neutrophils^[9]

Diagnosis

The first changes seen in shock is an increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed there is no test that either makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume state.^[2][5]

Differential diagnosis

Shock is a common end point of many medical conditions.^[1] It has been divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic and obstructive.^[10] A few additional classifications are occasionally used including: endocrinologic shock.^[1]

Hypovolemic

This is the most common type of shock and is caused by insufficient circulating volume.^[2] Its primary cause is hemorrhage or loss of fluid from the circulation. Vomiting and diarrhea are the most common cause in children.^[1] With other causes including burns, environmental exposure and excess urine loss due to diabetic ketoacidosis and diabetes insipidus.^[1]

Cardiogenic

This type of shock is caused by the failure of the heart to pump effectively.^[2] This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), contusio cordis, or cardiac valveproblems.^[1]

Obstructive

Obstructive shock is due to obstruction of blood flow outside of the heart.^[2] Several conditions can result in this form of shock.

• Cardiac tamponade^[1] in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.
• Tension pneumothorax^[1] Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return).
• Pulmonary embolism is the result of a thromboembolic incident in the bloodvessels of the lungs and hinders the return of blood to the heart.
• Aortic stenosis hinders circulation by obstructing the ventricular outflow tract

Distributive

Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell.^[2] Examples of this form of shock are:

• Septic shock is the most common cause of distributive shock.^[1] Caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negativebacteria 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 Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability.
• High spinal injuries may cause neurogenic shock.^[11] The classic symptoms include a slow heartrate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels.^[12] (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the haemodynamic instability per se.)

Endocrine

Based on endocrine disturbances such as:

• Hypothyroidism (Can be considered a form of Cardiogenic shock) in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.
• Thyrotoxicosis (Cardiogenic shock)
  • may induce a reversible cardiomyopathy.
• Acute adrenal insufficiency (Distributive shock) 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 (Distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands

Management

The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas.^[1] Management may include securing the airway via intubation to decrease the work of breathing, oxygen supplementation, intravenous fluids and a passive leg raise (not Trendelenburg position), and blood transfusions.^[2] It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.^[2]

Fluids

Aggressive intravenous fluids are recommended in shock (e.g. 1-2 liter normal saline bolus over 10 minutes or 20ml/kg in a child) which is usually instituted as the person is being further evaluated.^[13] Which intravenous fluid is superior, colloids or crystalloids, remains undetermined.^[2] Thus as crystalloids are less expensive they are recommended.^[14] If the person remains in shock after initial resuscitation packed red blood cells should be administered to keep the hemoglobin greater than 100 gms/l.^[2]

Medications

Vasopressors may be used if blood pressure does not improve with fluids. There is no evidence of superiority of one vasopressor over another.^[15] Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma^[16] but may be of use in neurogenic shock.^[12] Activated protein C (Xigris) while once aggressively promoted for the management of septic shock has not been found to improve survival and is associated with a number of complications, thus is no longer recommended.^[17] The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.^[18] If used at all it should only be considered if the pH is less than 7.0.^[18]

Treatment goals

The goal of treatment is to achieve a urine output of greater than 0.5 cc/kg/hr, a central venous pressure of 8-12 mmHg and a mean arterial pressure of 65-95 mmHg.^[2]

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.^[19]

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 is 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.

History

In 1972 Hinshaw and Cox suggested the classification system for shock which is still used today.^[19]

References

1. ^ ^{a b c d e f g h i j} Silverman, Adam (Oct 2005). "Shock: A Common Pathway For Life-Threatening Pediatric Illnesses And Injuries". Pediatric Emergency Medicine Practice 2 (10). http://www.ebmedicine.net/topics.php?paction=showTopic&topic_id=149. 
2. ^ ^{a b c d e f g h i j k l m n o} Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 165–172. ISBN 0-07-148480-9. 
3. ^ ^{a b c d} Guyton, Arthur; Hall, John (2006). "Chapter 24: Circulatory Shock and Physiology of Its Treatment". In Gruliow, Rebecca. Textbook of Medical Physiology (11th ed.). Philadelphia, Pennsylvania: Elsevier Inc.. pp. 278–288. ISBN 0-7216-0240-1. 
4. ^ Marino, Paul L. (September 2006). The ICU Book. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-4802-X. http://www.lww.com/product/?978-0-7817-4802-5. 
5. ^ ^{a b} Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 174–175. ISBN 0-07-148480-9. 
6. ^ Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. ISBN 0-07-148480-9. 
7. ^ "American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis". Crit. Care Med. 20 (6): 864–74. 1992. doi:10.1097/00003246-199206000-00025. PMID 1597042. http://www.chestjournal.org/content/101/6/1644.full.pdf. 
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. ^ ^{a b c d e f g} 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
10. ^ Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 168. ISBN 0-07-148480-9. 
11. ^ Cite error: Invalid <ref> tag; no text was provided for refs named Trauma; see Help:Cite errors/Cite error references no text
12. ^ ^{a b} Cocchi, MN; Kimlin, E, Walsh, M, Donnino, MW (2007 Aug). "Identification and resuscitation of the trauma patient in shock.". Emergency medicine clinics of North America 25 (3): 623–42, vii. PMID 17826209. 
13. ^ American College of Surgeons (2008). Atls, Advanced Trauma Life Support Program for Doctors. Amer College of Surgeons. pp. 58. ISBN 1-880696-31-6. 
14. ^ Perel, P; Roberts, I (2007 Oct 17). "Colloids versus crystalloids for fluid resuscitation in critically ill patients.". Cochrane database of systematic reviews (Online) (4): CD000567. PMID 17943746. 
15. ^ Havel, C; Arrich, J, Losert, H, Gamper, G, Müllner, M, Herkner, H (2011-05-11). "Vasopressors for hypotensive shock.". Cochrane database of systematic reviews (Online) 5: CD003709. doi:10.1002/14651858.CD003709.pub3. PMID 21563137. 
16. ^ Diez, C; Varon, AJ (2009 Dec). "Airway management and initial resuscitation of the trauma patient.". Current opinion in critical care 15 (6): 542–7. PMID 19713836. 
17. ^ Martí-Carvajal, AJ; Solà, I, Lathyris, D, Cardona, AF (2011 Apr 13). "Human recombinant activated protein C for severe sepsis.". Cochrane database of systematic reviews (Online) (4): CD004388. PMID 21491390. 
18. ^ ^{a b} Boyd, JH; Walley, KR (2008 Aug). "Is there a role for sodium bicarbonate in treating lactic acidosis from shock?". Current opinion in critical care 14 (4): 379–83. PMID 18614899. 
19. ^ ^{a b} Irwin, Richard S.; Rippe, James M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia & London. ISBN 0-7817-3548-3. http://www.lww.com/product/?0-7817-3548-3.