Shock - symptoms, causes & pathophysiology

Shock is defined as a clinical state of cardiovascular collapse characterized by (1) an acute reduction of effective circulating blood volume and (2) an inadequate perfusion of cells and tissues

The final result is hypotension and cellular hypoxia and, if uncompensated, may lead to impaired cellular metabolism and death.

Primary or initial shok. It is transient and usually a benign vasovagal attack resulting from sudden reduction of venous return to the heart caused by peripheral pooling of blood. It can occur immediately following trauma, severe pain or emotional over-reaction such as due to fear, sorrow or surprise. The attack usually lasts for a few seconds or minutes

Secondary of true shok. This is the form of shock, which occurs due to hemodynamic derangements with hypoperfusion of the cells. This type of shock is the true shock, which is commonly referred to as “shock” if not specified, and is the type described below.

According to etiology and pathogenesis shock is classified as:

1. Hypovolemic. Reduction in blood volume induces hypovolemic shock. The causes of hypovolemia include: a) Severe hemorrhage (external or internal) e. g. in trauma, surgery, b) Fluid loss e. g. in severe burns, crush injury to a limb, persistent vomitings and severe diarrhea causing dehydration. 

2. Cardiogenic. Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart without actual reduction of blood volume (normovolemia) results in cardiogenic shock. The causes include:

• Deficient emptying (myocardial infarction, rupture of the heart, cardiac arrhythmias).

• Deficient filling (cardiac tamponade from hemopericardium).

• Obstruction to the outflow (pulmonary embolism, ball valve thrombus).

3. Septic. Severe bacterial infections or septicemia induce septic shock:

• Gram-negative septicemia (endotoxic shock,) e.g. infection with E. coli, Proteus Klebsiella, Pseudomonas and bacteroides. 

Endotoxins of gram-negative bacilli have been implicated as the most important mediator of septic shock

• Gram-positive septicemia (exotoxic shock) is less common e.g. infection with streptococci, pneumococci caused by endotoxins).

4. Anaphylactic (immediate reaction of hypersensitivity).

5. Neurogenic (in intoxication with hypnotic preparations, ganglioblockers, narcotics).

6. Shock developing in hormonal insufficiency (thyrotoxic shock, myxedema, adrenal insufficiency).

Pathogenesis

Stages of Shock. Deterioration of the circulation in shock is a progressive phenomenon and can be divided arbitrarily into 3 stages:

1. Non-progressive (initial compensated reversible) shock. In the early stage of shock, an attempt is made to maintain adequate cerebral and coronary blood supply by redistribution of blood. This is achieved by activation of various neurohormonal mechanisms causing widespread vasoconstriction and by fluid conservation by the kidney.

2. Progressive decompensated shock. This is a stage when the patient suffers from some other stress or risk factors besides persistence of the shock so that there is progressive deterioration.

3. Decompensated (irreversible) shock. When the shock is so severe that in spite of compensatory mechanisms and despite therapy and control of etiologic agent, which caused the shock, no recovery takes place it is called decompensated or irreversible shock.

Shock morphology

Three main pathological processes are observed in shock:

• DIC (disseminated intravascular coagulation) syndrome.

• Hemorrhagic diathesis.

• Liquid cadaver blood.

Microscopically, it is characterized by generalized spasms of the vessels, microthrombosis, signs of increased vascular permeability in microcirculatory system, hemorrhages, degenerations, necroses connected with hypoxia and damaging effect of endotoxins.

Morphologic features of complications in Shock

• Shock kidney: degeneration and necrosis in proximal canals with development of necrotic nephrosis (or symmetrical cortical necroses are possible), which results in acute renal insufficiency.

• Shock liver: glycogen amount in the hepatocytes decreases, hydropic degeneration and centrolobular necroses resulting in acute hepatic insufficiency develop. Combination of renal and hepatic insufficiency is called hepatorenal syndrome.

• Shock lung: atelectasis foci, serous-hemorrhagic edema, stases and thromboses in the microcirculatory bed resulting in acute respiratory insufficiency.

• Shock heart: degeneration and necrosis in cardiomyocytes, reduction in glycogen amount, fat degeneration, and necrotic foci.

• Shock gastrointestinal: the hypoperfusion of alimentary tract may result in mucosal and mural infarction called hemorrhagic gastroenteropathy.

• Shock brain: Hypoxic changes in the brain. Ischemic neurons appear shrunken and have eosinophilic cytoplasm. The pericellular spaces are dilated because of edema. Rarification of brain tissue presents.

• Similar changes occur in nervous, endocrine systems, and immune organs.

Shock morphology depends not only on the cause of the shock but also on its stage. At the early stage, disturbances of hemodynamic and DIC syndrome are noted. At the last stages degenerative and necrotic process occurs.

Intensive transfusion therapy of shock masks clinicomorphological picture. But the constant features are liquid cadaver blood irrespective of the composition of transfused fluids. Blood clots in the cardiac cavities and vessels are characteristic for terminal states of nonshock origin. So blood composition is a criterion for differential diagnosis.

Clinical Features

The classical features of decompensated shock are characterized by depression of 4 vital processes:

• Very low blood pressure.

• Subnormal temperature.

• Feeble and irregular pulse.

• Shallow and sighing respiration.

Renal dysfunction in shock is clinically characterized by a phase of oliguria due to ATN and a later phase of diuresis due to regeneration of tubular epithelium. With progression of the condition the patient may develop stupor, coma and death.

Side Lesson from university Moodle Website

Shock - severe pathological condition characterized by circulatory collapse (acute heart failure) after a super impact on hemostasis . There are hypovolemic, cardiogenic, septic shock and vascular types.

Hypovolemic shock  caused by rapid decrease of 20% or more blood volume that is observed in acute blood loss, dehydration. The loss of fluids and electrolytes is possible with extensive burns (due to the release of plasma damaged microcirculatory blood vessels), severe vomiting, profuse diarrhea.

Cardiogenic shock  occurs in response to a decrease in stroke volume of the heart is damaged, there is a myocardial infarction, severe myocarditis, acute mitral or aortic insufficiency, thrombosis valve prosthesis, interventricular septum rupture, cardiac hemotamponadi shirt. The marked drop in blood pressure leads to a significant reduction in blood supply tissue similar to hypovolemic changes.

Septic (toxic - infectious) shock  occurs when the infection is caused by gram - negative ( E . Coli , Proteus , Klebsiella ) less gram - positive (stafilo-, streto-, pneumococci) microflora. Toxins released (mainly endotoxins) activate the complement system, coagulation, fibrinolysis and platelets and neutrophils. As a result, stimulated the formation of nitric oxide (powerful vasodilator), tumor necrosis factor α, interleukin that cause acute circulatory failure.

Vascular shock  may be neurogenic (traumatic, pain at the spinal cord injury as a complication of anesthesia) or anaphylactic that caused generalized hypersensitivity reactions. Due to severe vasodilation, increased permeability of capillaries and arteriovenous reset redistribution of intravascular blood volume, accompanied by a significant decrease in total peripheral vascular resistance.

Shock goes through three stages:
Non- progressive (early) stage of shock is characterized by a decrease in blood pressure and cardiac output volume while maintaining relatively normal blood supply to vital organs. This is due to compensatory vasoconstriction of blood vessels, especially the skin and intestines. After depletion of adaptive mechanisms of shock moves to the next stage.
Progressive stage of shock expressed by different clinical symptoms, deep collapse, which is caused by reduced blood supply of all organs and tissues (tissue hypoperfusion due to arterial dilatation), the development of metabolic and circulatory disorders.
During the irreversible stage of shock, there is a pronounced lack of blood flow at the microcirculation in violation of the integrity of the vascular wall, multiple organ failure, a rapidly growing, ends in death of the patient.

When morphological study noted generalized degenerative and necrotic changes, the phenomenon of DIC (petechial haemorrhages, stasis, blood clots in the microvasculature). In addition, due to the peculiarities of the structure and functioning of various organs, there are typical changes - the shock bodies . Thus, for shock kidney characterized by the development of necrotic nephrosis (necrosis convoluted tubule epithelium). Shock lung appears foci atelectasis, sero-hemorrhagic edema, sometimes with deposition of fibrin strands ( hyaline membrane ). In the brain there is ischemic encephalopathy , manifested by edema, hemorrhage point and focal necrosis. In the heart of the small watch, mainly subendokardialni foci of hemorrhage and necrosis infarction, fatty cardiomyocytes. In cortical layer of the adrenal gland decreases until the complete disappearance of lipid used for the synthesis of steroid hormones. In the gastrointestinal tract are hemorrhage, severe erosion and ulcers in the lining. ShockLiver different fatty hepatocytes, and in some cases even their tsentrolobulyarnym necrosis.

Forecast shock depends on the type, severity, stage at which treatment was started, presence of complications . Currently, in severe cardiogenic or septic shock mortality is 50% higher.