Shock (circulatory)

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Shock is a state of low blood perfusion to the network that results in inadequate cellular injury and network functionality. Typical signs of shock are low blood pressure, rapid heart rate, signs of poor end organ perfusion (eg, low urine output, confusion, or loss of consciousness), and a weak pulse.

Shock is divided into four main types based on underlying causes: hypovolemic, cardiogenic, obstructive, and distributive shock. The shock index (SI), defined as the heart rate divided by systolic blood pressure, is an accurate diagnostic measure that is more useful than hypotension and tachycardia in isolation. Under normal conditions, a number between 0.5 and 0.8 is usually seen. If that number increases, so does the suspicion of underlying shock conditions.

Neural circulation is not associated with emotional shock conditions. Nerve distribution is a life-threatening medical emergency and one of the most common causes of death. Shock can have multiple effects, all with similar results, but all are related to problems with the body's circulatory system. For example, shock may cause lack of oxygen, heart, or respiratory distress.

Video Shock (circulatory)

Signs and symptoms

Presentation of shock varies with some people having only minimal symptoms such as confusion and weakness. While the common signs for all types of shock are low blood pressure, decreased urine output, and confusion, this may not always be there. While fast heartbeat is common, those who are in? -blockers, those who are athletic and in 30% of cases with shock due to abdominal bleeding can have a normal or slow heartbeat. Specific shock subtype may have additional symptoms.

Hypovolaemic

Hypovolemia is a direct loss of an effective volume of blood circulation leading to:

• Rapid, weak, moderate pulse due to decreased blood flow combined with tachycardia
• Cold skin, sweating due to vasoconstriction and vasoconstrictive stimulation
• Rapid and shallow breathing due to stimulation of the sympathetic nervous system and acidosis
• Hypothermia due to decreased perfusion and sweat evaporation
• Thirst and dry mouth, due to thinning of liquids
• Cold and dappled skin (Livedo reticularis), especially the extremities, due to inadequate skin perfusion

The severity of hemorrhagic shock can be assessed on a scale of 1-4 on physical signs. This is close to the effective loss of blood volume. The 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 is not well established in pregnancy-related bleeding.

Cardiogenic

Symptoms of cardiogenic shock include:

• The jugular veins are distended due to increased jugular venous pressure
• Breath is weak or absent
• Abnormal heart rhythms, often fast heartbeats
• Pulsus paradoxus in tamponade case
• Reduce blood pressure

Distributive

Distributive shock includes infections, anaphylactic, endocrine (eg, adrenal insufficiency), salicylate toxicity, and neurogenic causes. SIRS features usually occur in early septic shock.

Septic shock

• Systemic lymphocyte adhesion to endothelial cells
• Reduces cardiac contractility
• Activation of the coagulation pathway, resulting in disseminated intravascular coagulation
• Increase in neutrophil levels

The main manifestations are produced because of the very large release of histamine which causes intense dilation of the blood vessels. People with septic shock will also tend to be positive for SIRS criteria. The most commonly accepted treatments for these patients are early symptom recognition, and the provision of broad-spectrum antibiotics and specific antibiotics at an early stage.

Obstructive

Obstructive shocks include cardiac tamponade, pulmonary embolism and aortic stenosis

Maps Shock (circulatory)

Cause

Shock is the common end point of many medical conditions. It has been divided into four main types based on underlying causes: hypovolemic, distributive, cardiogenic, and obstructive. Some additional classifications sometimes used include: endocrinologic shock.

Hypovolaemic

Hypovolemic shock is the most common type of shock and is caused by inadequate circulation volume. The main cause is bleeding (internal or external), or loss of fluid from the circulation. Vomiting and diarrhea are the most common causes in children. Other causes include burns, environmental exposures, and excessive urine loss due to diabetic ketoacidosis and diabetes insipidus.

Cardiogenic

Cardiogenic shock is caused by heart failure to pump effectively. This can be due to damage to the heart muscle, most often from large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), cordial contusions, or valvular heart disease problems.

Obstructive

Obstructive shock is due to obstruction of blood flow outside the heart. Some conditions can produce this form of shock.

• Heart tamponade in which the fluid in the pericardium prevents blood flow to the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.
• Tension pneumothorax By increasing intrathoracic pressure, blood flow to the heart is prevented (venous return).
• Pulmonary embolism is the result of a thromboembolic incidence in the pulmonary vasculature and prevents the return of blood to the heart.
• Aortic stenosis blocks the circulation by blocking the ventricular outlet
• Hypertrophic sub-aortic stenosis is a very thick ventricular muscle that dynamically closes the ventricular outlet.

Distributive

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

• Septic shock is the most common cause of distributive shock. Caused by an overwhelming systemic infection resulting in vasodilation leads to hypotension. Septic shock may be caused by Gram negative bacteria such as (i) Escherichia coli , Proteus species, Klebsiella pneumoniae that have endotoxin on the surface that results in adverse biochemistry, immunology. and sometimes harmful neurological effects to the body, and other Gram-positive cocci, such as pneumococcus and streptococci, and certain fungi as well as Gram-positive bacterial bacteria. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined the septic shock: ".. Syphilis induced hypothesis (systolic blood pressure & lt; 90 mmHg or 40 mmHg reduction from baseline) despite adequate fluid resuscitation along with perfusion. may include, but is not limited to, lactic acidosis, oliguria, or acute changes in mental status.Patients receiving inotropic agents or vasopressors may have normalized blood pressure when the perfusion disorder is identified. "
• anaphylactic shock is caused by severe anaphylactic reactions to allergens, antigens, drugs or foreign proteins that cause histamine release that causes widespread vasodilatation, leading to hypotension and increased capillary permeability.
• High spinal injury can cause neurogenic shock. Classic symptoms include a slow heartbeat due to loss of sympathetic tone of the heart and warm skin due to dilation of peripheral blood vessels. (This term may be confused with spinal shock which is a loss of recoverable spinal function after injury and does not refer to hemodynamic instability.)

Endocrine

Based on endocrine disorders such as:

• Hypothyroidism (can be considered as a form of cardiogenic shock) in critically ill patients, reduces cardiac output and may cause respiratory hypotension and insufficiency.
• Thyrotoxicosis (cardiogenic shock) may induce reversible cardiomyopathy.
• Acute adrenal insufficiency (distributive shock) is often caused by the cessation of corticosteroid treatment without dose reduction. However, surgery and recurrent disease in patients with corticosteroid therapy without adjusting the dose to accommodate increased requirements may also lead to this condition.
• relative adrenal insufficiency (distributive shock) in critically ill patients where current hormone levels are insufficient to meet higher demands

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Pathophysiology

There are four stages of shock. Since this is a complex and sustainable condition there is no sudden transition from one stage to the next. At the cellular level, shock is the process of requiring oxygen to be greater than the supply of oxygen.

One of the main hazards of shock is that it develops through positive feedback mechanisms. Poor blood supply causes cell damage, which results in an inflammatory response to increase blood flow to the affected area. This is usually very useful for matching blood supply levels with tissue demand for nutrients. However, if enough tissue causes this, it will remove essential nutrients from other parts of the body. In addition, the ability of the circulatory system to meet this increase in demand leads to saturation, and this is the main result, where other body parts begin responding in the same way; thus, exacerbating the problem. Because of this series of events, direct treatment of shock is essential for survival.

Start

During this stage, the state of hypoperfusion leads to hypoxia. Due to lack of oxygen, cells perform lactic acid fermentation. Because oxygen, the terminal electron acceptor in the electron transport chain, is not abundant, it slows the entry of pyruvate into the Krebs cycle, resulting in accumulation. Collecting pyruvate is converted to lactate by lactate dehydrogenase and hence lactate accumulates (causing lactic acidosis).

Compensation

This stage is characterized by the body using 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 rid the body of carbon dioxide (CO ₂ ). CO ₂ indirectly acts to acidify the blood and by removing the body trying to raise blood pH. Baroreceptors in the arteries detect the resulting hypotension, and cause the release of epinephrine and norepinephrine. Norepinephrine causes the dominant vasoconstriction with a mild increase in heart rate, whereas epinephrine is predominantly leading to an increase in heart rate with little effect on blood vessel tone; combined effects result in an increase in blood pressure. The renin-angiotensin axis is activated, and vasopressin arginine (Anti-diuretic hormone; ADH) is released to save fluids through the kidneys. These hormones cause vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. Lack of blood to the kidney system leads to low urine production. But the effects of the renin-angiotensin axis take time and are not essential for homeostatic mediation directly from shock.

Progressive

If the cause of the crisis is unsuccessful, the shock will progress to a progressive stage and the compensation mechanism begins to fail. Due to decreased cell perfusion, sodium ions accumulate inside while potassium ions leak out. When anaerobic metabolism persists, it increases the metabolic acidosis of the body, the arteriolar smooth muscle and the preecapillary sphincter will relax in such a way that the blood remains in the capillaries. Because of this, hydrostatic pressure will increase and, combined with the release of histamine, this will cause leakage of fluids and proteins to surrounding tissues. Because this fluid is lost, blood concentration and viscosity increase, causing sludging microcirculation. Prolonged vasoconstriction will also cause vital organs to be compromised due to reduced perfusion. If the intestines become sufficiently ischemic, bacteria can enter the bloodstream, resulting in increased complications of endotoxic shock.

Refractory

At this stage, vital organs have failed and shock can no longer be reversed. Brain damage and cell death occur, and death will occur in the near future. One of the main reasons that shock can not be changed at this point is that many cellular ATPs have been degraded into adenosine in the absence of oxygen as electron receptors in the mitochondrial matrix. Adenosine easily excretes perfusion from cell membranes to extracellular fluids, promotes capillary vasodilation, and then converts to uric acid. Since the cell can only produce adenosine at a rate of about 2% of the total cell requirement per hour, even recovering oxygen is useless at this point because there is no adenosine to phosphorylate to ATP.

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Diagnosis

The first visible changes in shock are increased cardiac output followed by decreased venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. The central venous oxygen saturation (ScvO2) measured through the center line correlates well with SmvO2 and is easier to obtain. If shock persists anaerobic metabolism will begin to occur with an increase in blood lactic acid as a result. While many laboratory tests are usually performed there are no tests that make or exclude the diagnosis. A chest X-ray or emergency ultrasound examination may be useful for determining the state of the volume.

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Management

The best evidence exists for the treatment of septic shock in adults and as pathophysiology appears to be similar in children and other types of shock therapy that has been extrapolated to this area. Management may include securing the airway through intubation if necessary to reduce respiratory work and to guard against respiratory attacks. Oxygen supplements, intravenous fluids, passive leg lifting (not Trendelenburg positions) should be initiated and blood transfusion added if severe blood loss. It is important to keep the person warm and manage enough pain and anxiety as this can increase oxygen consumption.

Fluid

Aggressive intravenous fluids are recommended in most types of shock (eg normal 1-2-liter saline over 10 minutes or 20 ml/kg in children) that are usually instituted when people are being evaluated further. Higher intravenous fluids, colloids or crystalloids, still have not been determined. Therefore, crystals are cheaper. If the person remains in shock after initial resuscitation packed red blood cells should be administered to keep hemoglobin greater than 100 g/l.

For those with hemorrhagic shock, current evidence supports the limitation of fluid use to penetrate the thoracic and abdominal wounds that allow mild hypotension to persist (known as permissive hypotension). Targets include an average arterial pressure of 60 mmHg, systolic blood pressure 70-90 mmHg, or to adequate mentation and peripheral. Hypertonic fluid can also be an option in this group.

Drugs

Vasopressors can be used if blood pressure does not improve with fluids. There is no evidence of substantial superiority of one vasopressor above the other; However, using dopamine causes an increased risk of arrhythmias when compared with norepinephrine. Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma but may be used in neurogenic shock. Active protein C (Xigris) is temporarily aggressively promoted for the management of septic shock has been found to not improve survival and is associated with a number of complications. Xigris was withdrawn from the market in 2011, and clinical trials were discontinued. The use of sodium bicarbonate is controversial because it has not been shown to improve yield. If used at all, it should only be considered if the pH is less than 7.0.

Mechanical support

• Intra-aortic balloon pump (IABP)
• Ventricular help devices (VAD)
• Artificial heart (TAH)
• Extracorporeal membrane oxygenation (ECMO)

Treatment goals

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

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Epidemiology

Haemorrhagic shock occurs in about 1-2% of trauma cases. Up to one-third of people admitted to the intensive care unit (ICU) are in circulatory shock. Of these, cariogenic shocks account for about 20% of cases, hypovolemic about 20% and then septic shock about 60% of cases.

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Prognosis

The prognosis of shock depends on the underlying cause and the nature and extent of the problem simultaneously. Hypovolemic, anaphylactic, and neurogenic shock can be treated promptly and respond well to medical therapy. However septic shock is a serious condition with mortality rates between 30% and 50%. The prognosis of cardiogenic shock is even worse with mortality rates between 70% and 90%.

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History

In 1972 Hinshaw and Cox suggested a classification system for the surprises that are still in use today.

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See also

• RNCHAMPS (mnemonic for types of shock)

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References

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External links

• SIRS, Sepsis and Septic Shock Criteria

Source of the article : Wikipedia