Definitions

circulatory

toxic shock syndrome

Bacterial disease caused by a toxin produced by the bacterium Staphylococcus aureus. It was first recognized in 1978 in women using superabsorbent tampons. High fever, diarrhea, vomiting, and rash may progress to abdominal tenderness, drop in blood pressure, shock, respiratory distress, and kidney failure. The syndrome also has other causes, including postsurgical infection. Antibiotics are not effective. With intensive supportive therapy, most patients recover in 7–10 days, but 10–15percnt die. Many patients have a milder recurrence within eight months.

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Device for controlling unwanted motion of a spring-mounted vehicle. On an automobile, the springs act as a cushion between the axles and the body and reduce the shocks produced by a rough road surface. Since some combinations of road surface and car speed may result in excessive up-and-down motion of the car body, shock absorbers—which today are hydraulic devices that oppose both compression and stretching of the springs—slow down and reduce the magnitude of these vibratory motions. Seealso damping.

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State in which the circulatory system fails to supply enough blood to peripheral tissues to meet basic requirements. Symptoms—weak, rapid pulse; low blood pressure; and cold, sweaty skin—are not all present in every case. Causes include low blood volume, caused by bleeding or fluid loss from burns or dehydration; inability of the heart to pump enough blood, due to heart attack, pulmonary embolism, or cardiac tamponade (compression of the heart by fluid in the membrane around it); and blood-vessel dilation as a result of septicemia, allergy (including anaphylaxis), or drugs. All result in reduced capillary blood flow; reflexes increase heart rate and constrict small blood vessels to protect the blood supply to essential organs. Without treatment of the underlying cause, these mechanisms fail; since the cause is not always clear, cases tend to require different and occasionally contradictory treatment (e.g., intravenous fluids can save the life of a patient with massive blood loss but can overload a weakened heart).

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Physical effect of an electric current that enters the body, ranging from a minor static-electricity discharge to a power-line accident or lightning strike but most often resulting from house current. The effects depend on the current (not the voltage), and the worst damage occurs along its path from the entry to the exit point. Causes of immediate death are ventricular fibrillation and paralysis of the brain's breathing centre or of the heart. Cardiopulmonary resuscitation is the best first aid. Though most survivors recover completely, aftereffects may include cataract, angina pectoris, or nervous-system disorders.

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Circulatory shock, commonly known as just shock, is a serious, life-threatening medical condition where insufficient blood flow reaches the body tissues. 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. 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.

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).

Stages of shock

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. 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. 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 (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. 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. If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting the increased complication of endotoxic shock. 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 of shock

In 1972 Hinshaw and Cox suggested the following classification which is still used today. It uses four types of shock: hypovolemic, cardiogenic, distributive and obstructive shock:

Recently a fifth form of shock has been introduced:

  • Endocrine shock based on endocrine disturbances.
    • Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.
    • Thyrotoxicosis 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

  • Hypovolemic 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.
    • Distracted look in the eyes or staring into space, often with pupils dilated.
  • Cardiogenic shock, similar to hypovolaemic shock but in addition:
  • Obstructive shock, similar to hypovolaemic shock but in addition:
  • Septic shock, similar to hypovolaemic shock except in the first stages:
  • Neurogenic shock, similar to hypovolemic shock except in the skin's characteristics. In neurogenic shock, the skin is warm and dry.
  • Anaphylactic shock

Treatment

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 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.

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.

Hypovolemic shock

In hypovolemic shock, caused by bleeding, 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.

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 Lactated Ringer's. Dextrose solutions which contain free water are less effective at re-establishing circulating volume, and promote hyperglycaemia.
  • Colloids - For example, polysaccharide (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 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 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 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.)

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.

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.

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.

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.

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

References

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  • 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
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  • 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.
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  • Tortora, G.J. (2005) Principles of anatomy and physiology New Jersey: John Wiley, Inc

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