State of Shock: What is it? Types, Symptoms, Causes, Diagnosis, Treatment and Prognosis

It is a life-threatening condition of circulatory failure.

The effects of shock (shock) are initially reversible but quickly become irreversible, resulting in multiple organ failure (MOF) and death.

When a patient experiences undifferentiated shock, it is important that the physician immediately initiate treatment while quickly identifying the etiology so that definitive therapy can be administered to reverse the shock and prevent multiple organ failure and death.

Shock is defined as a state of cellular and tissue hypoxia due to reduced oxygen supply and / or increased oxygen consumption or inadequate oxygen utilization.

This occurs most often when there is circulatory failure manifesting as hypotension (ie, reduced tissue perfusion).

Shock is initially reversible, but must be recognized and treated immediately to prevent progression to irreversible organ dysfunction . “Undifferentiated shock” refers to the situation in which a shock is recognized but the cause is unclear.


Shock is divided into four main types based on the underlying cause: hypovolemic, cardiogenic, obstructive, and distributive shock. It can be classified as:


This typically occurs in heart failure and could be caused by “pump failure” such as a heart attack or ostial occlusion caused by valve disease in endocarditis.

septic shock

The sepsis is a clinical syndrome resulting from overwhelming infection and the subsequent development of a generalized tissue injury. The shock that occurs during sepsis can be the result of intravascular volume depletion, poor volume distribution, cardiac dysfunction, or metabolic disorders at the cellular level.


This type of shock usually follows massive bleeding or some other form of fluid loss. By far the most common type of shock in children, it occurs when a decrease in intravascular volume leads to decreased venous return and subsequently less preload.

The decrease in preload results in a decrease in stroke volume. An increase in heart rate often maintains cardiac output initially, but when this compensatory response is inadequate, cardiac output decreases. The formula that defines this relationship is the following:

Heart rate = heart rate × systolic volume.


Also known as hypotensive shock, this results from peripheral vasodilation as in massive sepsis or anaphylactic shock. Distributive shock is caused by a decrease in systemic vascular resistance.


It is a form of shock associated with physical obstruction of the great vessels or of the heart itself. Pulmonary embolism and cardiac tamponade are considered forms of obstructive shock.

Obstructive shock has much in common with cardiogenic shock, and the two are frequently grouped together. Some sources do not recognize obstructive shock as a separate category, classifying pulmonary embolism and cardiac tamponade as cardiogenic shock.

Common to all of these conditions is a circulatory collapse that results from a disproportion between the volume of circulating blood and the vascular space it is supposed to fill. The resulting tissue hypoxia or anoxia leads to multiple organ failure.

The shock index (SI), defined as heart rate divided by systolic blood pressure, is an accurate diagnostic measure that is more helpful than hypotension and tachycardia in isolation.

Under normal conditions, you typically see a number between 0.5 and 0.8. If that number increases, so does the suspicion of an underlying shock state.

Circulatory shock is not related to the emotional state of shock. Circulatory shock is a life-threatening medical emergency and one of the most common causes of death. For example, shock can lead to a lack of oxygen, cardiac or respiratory arrest.

Signs and symptoms

The presentation of shock is variable, and some people have only minimal symptoms, such as confusion and weakness. While the general signs of all types of shock are low blood pressure, decreased urine output, and confusion, these may not always be present.

While a rapid heart rate is common, those on beta blockers, those who are athletic, and in 30% of cases with shock due to intra-abdominal bleeding may have a normal or slow heart rate. Specific subtypes of shock may have additional symptoms.


Symptoms of cardiogenic shock include:

Jugular veins dilated due to increased jugular venous pressure. Weak or absent pulse. Abnormal heart rhythms, often a fast heart rate. Pulsus paradoxus in case of tamponade. Reduction of blood pressure. Distributive.

Distributive shock includes infectious, anaphylactic, endocrine (eg, adrenal insufficiency), salicylate, and neurogenic toxicity. The features of the systemic inflammatory response syndrome generally occur in early septic shock.

septic shock

Systemic leukocyte adherence to endothelial cells. Reduction of the contractility of the heart. Activation of the coagulation pathways, resulting in disseminated intravascular coagulation. Increased levels of neutrophils.

The main manifestations occur due to the massive release of histamine that causes intense dilation of the blood vessels. People with septic shock will also likely be positive for the criteria for systemic inflammatory response syndrome.

The most accepted treatment for these patients is early recognition of symptoms and early administration of broad-spectrum, body-specific antibiotics.


Direct loss of effective circulating blood volume leading to:

  • A fast, weak, threadlike pulse due to decreased blood flow combined with tachycardia.
  • Rapid and shallow breathing due to stimulation and acidosis of the sympathetic nervous system. Hypothermia due to decreased perfusion and evaporation of sweat. Thirst and dry mouth, due to fluid depletion.
  • Cold mottled skin (Livedo reticularis), especially extremities, due to insufficient perfusion of the skin.

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

Shock index (heart rate divided by systolic blood pressure) is a stronger predictor of the impact of blood loss than heart rate and blood pressure alone. This relationship has not been well established in pregnancy-related bleeding.


Vasomotor tone abnormalities cause peripheral blood pooling, leading to decreased effective preload, decreased cardiac output, and inadequate tissue perfusion.

Some drugs can cause severe vasodilation, resulting in shock; These medications include those that cause anaphylaxis and those that cause severe hypotension (eg, beta blockers and calcium channel blockers).


Obstructive shock includes cardiac tamponade, pulmonary embolism, and aortic stenosis.


Shock is a common end point for many medical conditions. It has been divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic, and obstructive. Some additional classifications are sometimes used, including: endocrine shock.


Cardiogenic shock is caused by the failure of the heart to pump effectively. This may be due to damage to the heart muscle, most often from a large heart attack.

septic shock

It is important to consider early septic shock, because an apparently stable patient with minimal findings of infection can rapidly progress to sepsis.


Hypovolemic shock is caused by insufficient circulating volume. Its main cause is bleeding (internal or external) or loss of fluid from the circulation.

Vomiting and diarrhea are the most common cause in children. Other causes include burns, environmental exposure, and excess urine loss due to diabetic ketoacidosis and diabetes insipidus.


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

Septic shock is the most common cause of distributive shock. Caused by an overwhelming systemic infection that produces vasodilation leading to hypotension.

It produces adverse biochemical, immunological and occasionally neurological effects that are harmful to the body, and other gram-positive bacteria, 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 Consensus Conference Committee defined septic shock:

«… Sepsis-induced hypotension (systolic blood pressure <90 mmHg or a reduction of 40 mmHg from baseline) despite adequate fluid resuscitation in conjunction with the presence of perfusion abnormalities may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental state ‘.

“Patients receiving inotropic or vasopressor agents may have normalized blood pressure at the time perfusion abnormalities are identified.”

Anaphylactic shock is caused by a severe anaphylactic reaction to an allergen , antigen, drug, or foreign protein that causes the release of histamine that causes generalized vasodilation, resulting in hypotension and increased capillary permeability.

High spinal injuries can cause neurogenic shock. Classic symptoms include a slow heart rate due to loss of cardiac sympathetic tone and warm skin due to dilation of peripheral blood vessels.


Obstructive shock is due to impaired blood flow outside the heart. Several conditions can result in this form of shock.

Aortic stenosis hinders circulation by obstructing the ventricular outflow tract. Hypertrophic subaortic stenosis is an excessively thick ventricular muscle that dynamically occludes the ventricular outflow tract.


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 failure. Thyrotoxicosis (cardiogenic shock) can induce reversible cardiomyopathy.

Surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dose to accommodate higher requirements can also result in this condition.


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. At the cellular level, shock is the process in which the demand for oxygen becomes greater than the supply of oxygen.

One of the main dangers of shock is that it progresses through a positive feedback mechanism. Poor blood supply leads to cell damage, resulting in an inflammatory response to increase blood flow to the affected area.

This is normally very helpful in matching the level of blood supply with the nutrient demand in the tissues. However, if enough tissue causes this, it will deprive other parts of the body of vital nutrients.

In addition, the ability of the circulatory system to meet this increased demand causes saturation, and this is an important result, from which other parts of the body begin to respond in a similar way; thus, exacerbating the problem.

Due to this chain of events, immediate treatment for shock is critical for survival.


During this stage, the hypoperfused state causes hypoxia. Due to the lack of oxygen, the cells carry out the fermentation of lactic acid.


This stage is characterized by the body employing physiological mechanisms, including neuronal, hormonal, and biochemical mechanisms in an attempt to reverse the condition.

As a result of acidosis, the person will begin to hyperventilate to remove carbon dioxide (CO2) from the body. Carbon dioxide acts indirectly to acidify the blood, and by removing it, the body attempts to raise the pH of the blood.

Baroreceptors in the arteries detect the resulting hypotension and cause the release of epinephrine and norepinephrine.

Norepinephrine predominantly causes vasoconstriction with a slight increase in heart rate, whereas epinephrine predominantly increases heart rate with little effect on vascular tone; the combined effect produces an increase in blood pressure.

The renin-angiotensin axis is activated and arginine vasopressin (antidiuretic hormone) is released to conserve fluid through the kidneys. These hormones cause vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs, and brain.

The lack of blood in the renal system causes the characteristic low urine output. However, the effects of the renin-angiotensin axis take time and are of little importance for the immediate homeostatic mediation of shock.


If the cause of the crisis is not successfully treated, the shock will progress to the progressive stage and the compensatory mechanisms will begin to fail. Due to decreased perfusion of cells, sodium ions accumulate while potassium ions leak out.

As anaerobic metabolism continues, increasing the body’s metabolic acidosis, arteriolar smooth muscle and precapillary sphincters relax so that blood remains in the capillaries.

Due to this, the hydrostatic pressure will increase and, combined with the release of histamine, will cause a leakage of fluid and protein into the surrounding tissues.

As this fluid is lost, the blood concentration and viscosity increase, causing sediment in the microcirculation. Prolonged vasoconstriction will also compromise vital organs due to reduced perfusion.

If the intestine becomes ischemic enough, bacteria can enter the bloodstream, resulting in a further complication of endotoxic shock.


At this stage, the vital organs have failed and the discharge can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently.

One of the main reasons why shock is irreversible at this time is that a large amount of cellular adenosine triphosphate has been degraded to adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix.

Adenosine is easily perfused from cell membranes into the extracellular fluid, promoting capillary vasodilation, and is then 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 useless at this point because there is no adenosine to phosphorylate into adenosine triphosphate.


The first change observed in shock is an increase in cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) measured in the pulmonary artery through a pulmonary artery catheter.

Central venous oxygen saturation (ScvO2) measured through a central line correlates well with mixed venous oxygen saturation and is easier to acquire. If the shock progresses, anaerobic metabolism will begin to occur with an increase in lactic acid in the blood as a result.

While many laboratory tests are generally performed, there is no one test that makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be helpful in determining volume status.


The best evidence exists for the treatment of septic shock in adults, and as the pathophysiology appears to be similar in children and other types of shock treatment, this has been extrapolated to these areas.

Treatment may include securing the airway by intubation, if necessary, to decrease work of breathing and to prevent respiratory arrest.

Oxygen supplementation, IV fluids, passive leg elevation (not Trendelenburg position) should be started, and blood transfusions should be added if blood loss is severe.

It is important to keep the person warm and adequately manage pain and anxiety, as they can increase oxygen consumption.


Aggressive intravenous fluids are recommended in most types of shock (for example, 1-2 liter normal saline bolus over 10 minutes or 20 ml / kg in a child) which is generally instituted as the person is evaluated more.

Which intravenous fluid is superior, colloids or crystalloids, remains undetermined. Therefore, since crystalloids are less expensive, they are recommended.

If the person remains in shock after initial resuscitation, red blood cell concentrates should be given to maintain the hemoglobin concentration above 100 g / L.

For those with hemorrhagic shock, current evidence supports limiting the use of fluids to penetrate injuries to the chest and abdomen, allowing mild hypotension (known as permissive hypotension) to persist.

Goals include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70-90 mmHg, or until adequate implantation and peripheral pulses. Hypertonic fluid may also be an option in this group.


Vasopressors can be used if blood pressure does not improve with fluids. There is no evidence of substantial superiority of one vasopressor over another; however, the use of dopamine leads to an increased risk of arrhythmia compared to norepinephrine.

Vasopressors have not been found to improve outcomes when used for hemorrhagic traumatic shock, but they may be helpful in neurogenic shock.

Activated protein C (Xigris), although aggressively promoted for the control of septic shock, was found not to improve survival and is associated with a number of complications.

Activated protein C (Xigris) was withdrawn from the market in 2011, and clinical trials were suspended. The use of baking soda is controversial as it has not been shown to improve results. If used, it should only be considered if the pH is less than 7.0.

Treatment objectives

The goal of treatment is to achieve a urine output of more than 0.5 ml / kg / h, a central venous pressure of 8-12 mmHg, and a mean arterial pressure of 65-95 mmHg. In trauma, the goal is to stop the bleeding, which in many cases requires surgical interventions.

Shock force

The shock force must be adequate for defibrillation. Subthreshold force strikes are insufficiently powerful to defibrillate. Shock force in considerable excess of this threshold causes damage to the myocardium.

Studies by Gettes and associates showed that over a wide range of body size, the smaller the animal, the less energy is needed for defibrillation.

The larger the animal, the greater the impact force required. It takes less energy to defibrillate young children than it does to defibrillate large adults.

Recurrent ventricular fibrillation can occur after a successful defibrillation. In such circumstances, it is reasonable to use energy levels similar to those that were previously effective.

Particularly in cases where ventricular fibrillation reoccurs frequently, shock resistance should be kept as low as is effective to minimize myocardial damage.

The myocardial injury associated with defibrillation corresponds not only to the total joules used (energy), but also to the time interval between defibrillation shocks.


Hemorrhagic shock occurs in about 1-2% of trauma cases. Up to a third of people admitted to the intensive care unit (ICU) are in circulatory shock.

Of these, cariogenic shock accounts for approximately 20% of cases, hypovolemic for about 20%, and then septic shock for about 60% of cases.


The prognosis of shock depends on the underlying cause and the nature and extent of the concurrent problems. Hypovolemic, anaphylactic, and neurogenic shock are easily treatable and respond well to medical therapy.

However, septic shock is a serious condition with a mortality rate between 30% and 50%. The prognosis for cardiogenic shock is even worse with a mortality rate between 70% and 90%.