Circulatory сollapse, Shock, Coma
Emergency states are the general grave conditions of an organism. They develop under action of extreme factors of the external or internal environment and are characterized by significant frustration of ability to live of the organism and may result in death.
Emergency states manifest by limiting activation and the subsequent exhaustion of mechanisms of adaptation, frustration of functions of organs and physiological systems.
Extreme conditions demand emergency therapy.
A circulatory collapse, a shock, a coma and poisonings are most frequent and clinically significant urgent conditions.
Circulatory Collapse is acute vessel insufficiency and it is characterized
low arterial pressure;
decrease of volume of сirculating blood
Types of circulatory collapses
Cardiogenic collapse develops if output of blood from ventricles of heart decreases
Hypovolemic collapse develops at reduction of volume of circulating blood
Vasodilatory collapse develops at decrease in the general peripheral vascular resistance
The causes of a circulatory collapse
Сardiogenic collapse is observed at:
- acute cardiac insufficiency (result from ischemia and a myocardial infarction, arrhythmia of a heart);
- the conditions complicating inflow of blood to heart (at stenosis of valval apertures, emboly or a stenosis of vessels of system of a pulmonary artery);
Hypovolemic collapse. It results from:
- Acute massive bleeding;
- Fast and significant dehydration of the organism (at a profuse diarrhea, poisonings, increased sweating, pernicious vomiting);
- Loss of the big volume of blood plasma (for example, at extensive burns);
- Redistribution of blood with deposition of its in venous vessels, blood sine and capillaries (for example, at a shock, gravitational overloads, some intoxications).
- Heavy infections, intoxications, hyperthermia, endocrinopathies (at hypothyrosis, acute and chronic adrenal insufficiency),
- Injection of some medical products (for example, sympatholytic, narcotics, antagonists of calcium), hypocapnia, surplus in blood of adenosine, histamine, hypoxia etc.)
Conditions. (Risk factors)
Development of the circulatory collapse depends from of some conditions:
- Physical characteristics of environment (low or a heat, a level of barometric pressure, humidity);
- Conditions of the organism (presence or absence of any illness and pathological processes, psychoemotional status, etc.).
Collapse results from disturbance between the lumen of vessels and the volume of blood in them.
It is conditionally possible to signify two basic mechanisms of development of a circulatory collapse which are often combined.
Action on vassels. Direct action on the vasomotor center, vascular receptors (the sinocarotid zone, the arch of an aorta, etc.) and a vascular wall of the causal factor lead to widespread arterial and venous vasodilation, peripheral resistance decreases. Venous return is reduced as blood pools in the venous system, leading to a drop in cardiac output and hypotension. When arterial pressure and tissue perfusion are reduced, compensatory mechanisms are activated to maintain perfusion to the heart and brain. Compensatory mechanisms increase heart rate. Reduced blood flow to the kidney activates the renin-angiotensin-aldosterone system, causing sodium and water retention, leading to increased blood volume and venous return.
Decrease of volume of circulating blood. The left ventricle cannot maintain an adequate cardiac output or fluid is lost from the intravascular space. The volume of circulating blood decreases. A variety of neurohumoral mechanisms help maintain cardiac output and blood pressure. These include baroreceptor reflexes, release of catecholamines, activation of the renin-angiotensin axis, antidiuretic hormone release, and generalized sympathetic stimulation. The net effect is tachycardia, peripheral vasoconstriction, and renal conservation of fluid.
However, these mechanisms can be insufficient. Eventually, with a severe fall in blood pressure, blood flow does not adequately meet the energy demands of tissues and organs.
The main changes of hemodynamic indices in circulatory collapse developing according to cardiogenic, hypovolemic and vasodilator types are presented in table 24.
Table 24 The main changes of hemodynamic
CO- cardiac output; LVEDV- left-ventricular end-diastolic volume; PVR - peripheral vascular resistance.
Definition of shock
Shock is the state of organism arising under action of extreme factors and leading to reduced perfusion of tissues and organs and, eventually, organ dysfunction and failure.
Shock proper can be considered neither a symptom, nor a disease, nor a syndrome, it can’t be considered separately from nosological notions. Shock is a continuous pathologic systemic process, which arises at the moment, when the power and the time of action of primary lesions exceed the ‘shock threshold’ and a generalized reaction appears. Shock has been a major cause of morbidity and mortality in intensive care units and despite endeavors to suppress portions of the immune response, the outcome of shock has been unchanged in the past 50 years.
Shocks of any aetiology have a number of pathogenic characteristics in common.
Decreased volume of circulating blood volume (VCB) in combination with increased vessel resistance owing to catecholamines.
Cell hypoxia, deficient energy genesis which is followed by accumulation of waste materials and acidosis.
Emergence of necrosis loci.
Damage of a cell nucleus, impairment of DNA-chains and irreversible disorganization of cells.
Tapes of Shock
Shock is classified according to pathogenic mechanisms: hypovolemic, cardiogenic, extracardiac obstructive, distributive.
Hypovolemic shock is the most common type of shock seen clinically. It is due to a reduction in circulating blood volume, which leads to inadequate ventricular filling and inadequate cardiac output.
Cardiogenic shock results from severe depression of cardiac performance.
Extracardiac obstructive shock is caused by pericardial tamponade and massive pulmonary embolism.
Distributive shock Distributive shock is caused by profound peripheral vasodilation with inadequate tissue perfusion, although cardiac output may be normal or high. Distributive shock includes septic, anaphylaxis and neurogenic shock as well as shock in adrenal insufficiency.
Obstructive shock Blood cannot be ejected from the left into systemic circulation because the heart is displaced or compressed. If the blood cannot physically get out of the heart to the rest of the body, the vascular space will be depleted. Therefore, the body thinks it is in shock, even though the blood is still in the body.
Causes of hypovolemic shock may include: blood loss (most common cause), gastrointestinal fluid loss, burns, trauma, renal loss (diabetic ketoacidosis, diabetes insipidus, adrenal insufficiency), fluid shifts: ascites, peritonitis, hemothorax.
Causes of cardiogenic shock may include: myocardial infarction (most common cause), heart failure, cardiomyopathy, arrhythmias,
Causes of extracardiac obstructive shock pericardial tamponade, tension pneumothorax, pulmonary embolism. Increased pericardial pressure or obstruction of more than 50 to 60% of the pulmonary vascular bed by thrombus impair ventricular diastolic filling, stroke volume, and cardiac output.
Causes of septic shock may include: gram-negative bacteria (most common cause), gram-positive bacteria, viruses, fungi, Rickettsiae, parasites, yeast, protozoa, or mycobacteria.
Causes of anaphylactic shock may include: medications, vaccines, venom, foods, contrast media, ABO-incompatible blood.
Causes of neurogenic shock may include: spinal cord injury, spinal anesthesia, vasomotor center depression, severe pain, medications, hypoglycemia.
Causes of obstructive shock: Cardiac tamponade, cardiac myxoma (heart ventricle tumor), mediastinal shift, diaphragmatic hernia or diaphragmatic rupture, pneumothorax.
The condition of reactivity determines the shock threshold and its course.
There may be specific (biological) and group reactivity. The role of the specific reactivity may be examplified with an anaphylactic shock. Only higher animals may have it, while lower animals may not. The following factors underlie specific reactivity: sex, age, constitution, condition of the body systems (immune, endocrine, nervous systems). No doubt, special reactivity depends on the sex. Thus, men are more tolerant to pain; the female organism is more tolerant to hypoxia and blood loss that leads to the development of shock at different levels of damage. It is necessary to mention that the female reactivity changes depend on menstrual cycle, pregnancy.
The role of age in shock development is undoubted. An early child age is characterized by low reactivity due to incomplete development of the nervous, endocrine and immune systems, imperfect external and internal barriers. The highest reactivity is registered at a middle age, gradually decreasing by an old age. The factors determining the low tolerance of a child’s organism to blood and other losses are as follows: high level of liquid – up to 70% of all volume per 24 h, higher heart rate, less efficient regulation of vessel tone due to the prevalence of sympathetic influences, the lability of thermoregulation. In case of shock reactivity changes being depressed in relation to infections and other morbific influences. Phagocytosis is depressed, sensitivity to drugs changes.
The role of constitution in shock development can be proved statistically. For example, cardiogenic and repale shocks often occur in hypersthenic people. Hyposthenic people are very sensitive to blood loss, that’s why they are more subject to shock in case of blood loss unlike hyperstenic people.
The role of the nervous system can be proved by the fact, that the differences in its functioning determine the character of shock phases. For example, a choleric person has a more noticeably marked erectile phase of shock, while in a melancholiac person an erectile phase is more smooth and less marked.
Stress may play a different role in shock development. Depending on the phase of stress, when a stimulus acts, (an alarm phase or an emaciation phase), the severity, course and the terms of shock development may change. Previous diseases (radiation sickness, anemia, starvation) decrease the organism’s tolerance to shock.
Stages of shock
Shock is phasic process. There are three basic stages common to each type of shock:
the compensatory, which perfusion to vital organs is maintained
the progressive decrease in tissue perfusion
the irreversible or refractory stages.
Clinical stages of shock
1. Early reversible (inicial, non progressive) shock. Patients exhibit tachypnea and tachycardia, but their blood pressure is normal.
2. Late reversible shock. Patients are in cardiopulmonary distress. Their renal output is decreased and they are hypotensive. Acidosis is noted.
3. Irreversible shock is signaled by multiple organ failure.
There is another сlinical classification of stages of shock:
the erectile stage
the torpent stage
death – an agony stage
According to its power, length and affected topographic area, shock passes two almost simultaneous stages – an intracellular stage and an extracellular one.
General pathogenesis of shock
Compensatory stage. Shock is triggered by excessive afferent impulses. Moreover, it can be either painful (trauma) or painless (due to the stimulation of organ and tissue receptors as a result of blood circulation impaired by hypoxia, metabolism disturbances).
Excessive information, especially painful one, passes through different afferent tracts and reaches different parts of the brain (the reticular formation, hypothalamus, cortex). It stimulates their defense reactions, whose power becomes excessive. Compensatory mechanisms sustain the patient. This entails emergency mobilization of skeletal muscles, a manifold increase in the activity of non-specific adaptation systems such as sympathoadrenal and hypophysial-corticoadrenal systems involving the relevant peripheral effects. It also involves secretion of neurohypophysial hormones and enzymatic substances (glucose and fatty acids) in the blood.
On the other hand, the bodily functions, which don’t contribute to the survival of the organism are urgently inhibited in these conditions (alimentary, reproductive, proliferative, excretive systems, etc.).
The listed phenomena result from the vasoconstriction of peripheral vessels. A spasm arises due to the activation of -adrenal vascular receptors including those in precapillary sphincters. A part of the organism is deprived of the blood. Arterial vasoconstriction directs the reduced cardiac output away from the skin (pallor), the abdominal organs, and the kidneys to vital organs (coronary arteries, the brain), bringing about centralization of the circulation. The skin and kidneys, splanchnic circulation and later skeletal muscles, in which -adrenal receptors prevail, become ‘sacrificed’. The spasm of vessels doesn’t affect the circulation of the coronary, cerebral, hypophysial, thyroid areas as well as the adrenal cortex and diaphragm.
Fig 4. The pathogenesis of shock
Reduced blood flow to the kidney activates the renin-angiotensin-aldosterone system, causing vasoconstriction and sodium and water retention, leading to increased blood volume and venous return. As a result of these compensatory mechanisms, cardiac output and tissue perfusion are maintained. When tissue perfusion are reduced, compensatory mechanisms are activated to maintain perfusion to the heart and brain.
The first consequence of spasm is mobilization of blood in the central vessels and shunting of some organs and tissues. The vasoconstrictive reaction at the level of microcirculatory channel is a real ‘autotransfusion’ and it is the cause of blood circulation centralization, when blood from arterioles passes to the venous section through arteriolovenular anastomoses, avoiding the capillaries of ‘sacrificed’ organs. The heart, the brain and the liver are better supplied with blood because of the circulation centralization. This period of shock is another called an erectile phase or an early reversible shock
Progressive stage. It is the torpent or late reversible shock. This stage of shock begins as compensatory mechanisms fail to maintain cardiac output. Both resistive (arterial) and capacitive (venous) vessels, in which normally about 80% of blood is concentrated, simultaneously undergo spasms. This results in fluid being filled with lymph whose volume reaches 2 – 4 litres.
Acidosis develops due to hypoxia and results in the relaxation of the precapillary sphincters. Therefore, the gole, remaining closed by the venules, opens. The quantity of the fluid accumulating in it is 3 – 4 times as much as compared to the norm. This phenomenon is called “pooling” or “sequestration” of blood.
Volum circulating blood decreases and cardiac output falls. Tissues become hypoxic because of poor perfusion. As cells switch to anaerobic metabolism, lactic acid builds up, producing metabolic acidosis. This acidotic state depresses myocardial function.
Depressed regulating function of the CNS is one of the causes of a decrease in systemic arterial pressure. For example, at this stage early weakened or perverse sinocarotid pressor reflexes or even their disapperance are registered.
Tissue hypoxia also promotes the release of endothelial mediators, which produce vasodilation and endothelial abnormalities, leading to venous pooling and increased capillary permeability. Sluggish blood flow increases the risk of disseminated intravascular coagulation.
Irreversible (refractory) stage. As the shock syndrome progresses, permanent organ damage occurs as compensatory mechanisms can no longer maintain cardiac output. Reduced perfusion damages cell membranes, lysosomal enzymes are released, and energy stores are depleted, possibly leading to cell death. As cells use anaerobic metabolism, lactic acid accumulates, increasing capillary permeability and the movement of fluid out of the vascular space. This loss of intravascular fluid further contributes to hypotension. Perfusion to the coronary arteries is reduced, causing myocardial depression and a further reduction in cardiac output. Eventually, circulatory and respiratory failure occur. Death is inevitable.
Features of pathogenesis of various types of the shock.
When fluid is lost from the intravascular space through external losses or the shift of fluid from the vessels to the interstitial or intracellular spaces, venous return to the heart is reduced. This reduction in preload decreases ventricular filling, leading to a drop in stroke volume. Then, cardiac output falls, causing reduced perfusion of the tissues and organs.
In cardiogenic shock, the left ventricle can't maintain an adequate cardiac output. Compensatory mechanisms increase heart rate, strengthen myocardial contractions, promote sodium and water retention, and cause selective vasoconstriction. However, these mechanisms increase myocardial workload and oxygen consumption, which reduces the heart's ability to pump blood, especially if the patient has myocardial ischemia. Consequently, blood backs up, resulting in pulmonary edema. Eventually, cardiac output falls and multisystem organ failure develops as the compensatory mechanisms fail to maintain perfusion. The differences between hypovolemic and cardiogenic shock are conditioned by the pressure of the filled left ventricle in the diastole: in case of a cardiogenic shock it increases, and in case of a hypovolemic shock it decreases
In case of the shock caused by vasodilation a fall of arterial pressure is conditioned by a primary decrease in the peripheral resistance. In this type of shock, vasodilation causes a state of hypovolemia.
Neurogenic shock. A loss of sympathetic vasoconstrictor tone in the vascular smooth muscle and reduced autonomic function lead to widespread arterial and venous vasodilation. Venous return is reduced as blood pools in the venous system, leading to a drop in cardiac output and hypotension.
Septic shock. An immune response is triggered when bacteria release endotoxins. In response, macrophages secrete tumor necrosis factor (TNF) and interleukins. These mediators, in turn, are responsible for increase release of platelet-activating factor (PAF), prostaglandins, leukotrienes, thromboxane A2, kinins, and complement. The consequences are vasodilation and vasoconstriction, increased capillary permeability, reduced systemic vascular resistance, microemboli, and an elevated cardiac output. Endotoxins also stimulate the release of histamine, further increasing capillary permeability.
The organism reacts by increasing the cardiac output which involves higher heart rate and stroke volume. It is a hyperdynamic reaction. It can be interpreted in the following way: the organism tries to send to the periphery as much blood as it can to compensate the damage. Moreover, myocardial depressant factor, TNF, PAF, and other factors depress myocardial function. At later stages сardiac output and arterial pressure falls the resulting in multisystem organ failure.
Anaphylactic shock. Triggered by an allergic reaction, anaphylactic shock occurs when a person is exposed to an antigen to which he has already been sensitized. Exposure results in the production of specific immunoglobulin E (IgE) antibodies by plasma cells that bind to membrane receptors on mast cells and basophils. On reexposure, the antigen binds to IgE antibodies or cross-linked IgE receptors, triggering the release of powerful chemical mediators from mast cells. IgG or IgM enters into the reaction and activates the release of complement factors. At the same time, the chemical mediators bradykinin and leukotrienes induce vascular collapse by stimulating contraction of certain groups of smooth muscles and by increasing vascular permeability. Both peripheral and volume vessels lose their tone. The accumulation of blood in capillaries and veins and plasma leakage into the extravascular tissues leads to a relative deficiency of circulating blood volume and decreased stroke volume. A sympatho-adrenal reaction doesn’t develop here, as it is impaired in response to sympathetic irritation, thus, causing the dramatic development of an anaphylactic shock. Bronchospasm and laryngeal edema also occur.
Signs and symptoms
In the compensatory stage of shock signs and symptoms may include: tachycardia and bounding pulse due to sympathetic stimulation; restlessness and irritability related to cerebral hypoxia; tachypnea to compensate for hypoxia; reduced urinary output secondary to vasoconstriction; cool, pale skin associated with vasoconstriction; warm, dry skin in septic shock due to vasodilation.
In the progressive stage of shock, signs and symptoms may include: hypotension as compensatory mechanisms begin to fail; narrowed pulse pressure associated with reduced stroke volume; weak, rapid, thready pulse caused by decreased cardiac output; shallow respirations as the patient weakens; reduced urinary output as poor renal perfusion continues; cold, clammy skin caused by vasoconstriction; cyanosis related to hypoxia.
Shock is not synonymous with circulatory collapse, although hypotension is often part of the shock. Collapse occurs in case of a sudden decrease of the content of vessels (haematogenic collapse) or in case of sudden dilation of vessels (vasomotoric collapse). Collapse is a sign of a haemodynamic disturbance between the lumen of vessels and the volume of blood in them.
In cause of shock hypotension is actually a late sign in shock and indicates a failure of compensation. In the course of uncompensated shock, a rapid fall of blood circultion leads to impaired cellular metabolism and death. The distinction between shock and collapse is important clinically because rapid restoration of systemic blood flow is the primary goal in treating shock. In case of shock circulation becomes centralized, it can be treated with vasodilators When blood pressure alone is raised with vasopressive drugs, systemic blood flow may actually be diminished. While collapse is treated with vasoconstrictors.
Disorders in the Extracellular space and Cell
An extracellular stage involves all changes of the neuroendocrine regulation as well as those of circulation of systemic fluids (microcirculation, lymphatic circulation and interstitial circulation).
An intracellular stage quickly joins the previous stage owing to the information delivered by nervous impulses, which pass through cell membrane and reach the terminal points inside the polinucleotide chain of the genetic code. This stage involves all changes of intracellular regulation of enzymatic processes.
The extracellular stage The continuous afferent impulsation from the point of a trauma is coupled with the stimulation of the receptors of internal organs, which results from developing hypoxia and the formation of products of disturbed metabolism, the so-called stimulators of the secondnd order. They can cause serious disturbances of the functions of organs and tissues, development of polyorgan insufficiency and death of an organism.
The accumulation of the biologically active substances (BAS) in blood – histamine, kinins, prostaglandins, acetylcholine, etc. – directly induces a decrease of excitability of different cerebral structures. The inhibition processes develop. The biological implication of this inhibition consists in maintaining energy homeostasis of the CNS for prolongation vital activity of the brain.
The BAS are of special importance in disturbing systemic hemodynamics and microcirculation. Damage of cells leads to the activation of the proteolytic systems – kallikrein-kinin system, complement system, blood coagulation system, fibrinolysis. The activation of the complement cascade is accompanied by the formation of anaphylatoxins (C3a, C4a, C5a), which activate leucocytes and result in the formation of aggregates and microemboli and disorder of microcirculation; The BAS cause an increase of vascular permeability and therefore, a decrease of CBV.
Stagnation and acidosis pave the way for a start of intravascular coagulation (IC). The aggregation of the formed elements, a sludge-syndrome, formation of thrombi and emboli are observed, which impairs microcirculation and aggravates hypoxia.
A decrease of the vascular tone, massive outflow of the fluid from the vessels into the interstitial tissue, more serious rheological disorders of blood result in decreased reverse backward venous bloodflow.
Cellular stage of shock development
Hypoxia solely cannot account for a change in a shock cell as hypoxia can be avoided for a while owing to enzymatic rearrangement of a cell.
The following changes occur in shock states:
1) Deficiency of ATP develops.
2) activation and after then emaciation of glycolysis and glycogenolysis, ATP is used completely, metabolites are stored.
3) Acidosis. If endocellular pH amounts to 5.5, corrosion of the lysosomal sacs begins. This result in the opening of the lysosomal cisterns and the catalases are released into the blood.
4) During shock the cellular membrane potential decrease that is conducive to transmineralization, K+ escape and Na+ entry, the arrest of H+ transfer through the membrane. These phenomena cause edema.
Till recently a cell was thought to be affected only at the late stages of shock, and the therapeutic efforts were targeted only hemodynamics. However, the experimental and clinical research has established that even before such signs of the disturbed perfusion as hypotonia or decreased urination arise, lactate acidosis, which is the evidence of early disturbances of cellular metabolism occurs. The membrane potential decreases and, therefore, the elective pumpes stop immediately (!) after action of the shock-causing factor. In 6 (!) minutes after shock begins, the antibodies of anti-DNA were generated and their concentration correlates with the gravity of shock. Their presence is the evidence of a rapid autoimmune attack on the genetic matrix of protein synthesis and on the system of cellular coordination by means of perversion of nucleic acids.
In case of oxygen deficit tissue metabolism changes from aerobic to anaerobic one. Increased lactate in blood is an indirect sign of inadequate oxygen supply of tissues.
In case of shock the concentration of glucose in blood increases due to gluconeogenesis from substrates of anaerobic metabolism (lactate) and proteolysis (alanine and other amino acids). Gluconeogenesis is stimulated by increased amount of stress hormones – catecholamines, hydrocortisone, somatotropine, glucagon in blood.
Protein metabolism is balanced by proteolysis and synthesis of new proteins. Protein metabolism changes significantly in case of shock: proteolysis in muscles increases abruptly, amino acids get from muscles to the liver and intestines. They act as substrates of gluconeogenesis and synthesis of acute phase proteins.
The acute phase proteins are fibrinogen (which is necessary for haemostasis), α2-macroglobulin, α1-antitrypsin (the inhibitors of the systemic proteases), hepatocuprein (it removes the free radicals), C-reactive protein (it participates in opsonisation of bacteria, activation of the complement system and phagocytosis). Cytokines play an important role in changing protein metabolism. The synthesis of the acute phase proteins is stimulated in the liver; its main activators are interleukin 1, interleukine 6, tumour necrosis factor, hydrocortisone and glucagons. Interleukin-1 and tumour necrosis factor suppress albumin synthesis in the liver. It is important because albumin synthesis requires most of amino acids as energy substrates to form acute phase proteins in the state of shock.
In critical conditions lipolysis in adipose tissue intensifies, being stimulated by hydrocortisone, catecholamins and glucagon.
Consequences and complications of shock
If the organism goes safely through the phase of early reversible shock, it may survive.
Shock is associated with changes in a number of organs, including acute renal tubular necrosis, acute respiratory distress syndrome, liver failure, depression of host defense mechanisms, and heart failure.
The disturbed perfusion of the heart disturbes its functioning which is accompanied by decreased cardiac output. That, in its turn, decreases the perfusion of all organs, including the blood supply of the heart.
The heart shows petechial hemorrhages of the epicardium and endocardium. Haemorrhages in the subendocardium arise in the heart after serious shock (the mechanism is not clear). The so-called “zonal lesions” are registered at hemorrhagic shock. The sarcomeres are excessively contracted; there are loci of microthromboses and micronecroses in these zones. As a rule, such changes arise after the periods of heart overstrain with increased heart rate and force. They are caused by high concentrations of catecholamins known as “adrenal myocarditis”.
The poor perfusion of the kidneys disturbs their function and the excretion of acidic metabolites stops. That induces systemic acidosis. Decreased perfusion can result in tubular necrosis and accumulation of toxic metabolites.
Acute tubular necrosis (acute renal failure), a major complication of shock, has been divided into three phases: (1) initiation, from the onset of injury to the beginning of renal failure; (2) maintenance, from the onset of renal failure to a stable, reduced renal function; and (3) recovery. In those who survive an episode of shock, the recovery phase begins about 10 days after its onset and may last up to 8 weeks.
Renal blood flow is restricted to one-third of normal following the acute ischemic phase. This effect is even more severe in the outer cortex. The constriction of arterioles reduces the filtration pressure, thereby reducing the amount of filtrate and contributing to oliguria. Interstitial edema occurs, possibly through a process termed backflow. Excessive vasoconstriction is also related to stimulation of the renin-angiotensin system.
During acute renal failure, the kidney is large, swollen, and congested, although the cortex may be pale. A cross-section reveals blood pooling in the outer stripe of the medulla. Microscopically, fully developed acute tubular necrosis is evidenced by dilation of the proximal tubules and focal necrosis of cells.
After the onset of severe and prolonged shock, injury to alveolar walls can result in shock lung, which is a cause of acute respiratory distress syndrome (ARDS). The sequence of changes is mediated by polymorphonuclear leukocytes and includes interstitial edema, necrosis of endothelial and alveolar epithelial cells, and formation of intravascular microthrombi and hyaline membranes lining the alveolar surface.
Macroscopically, the lung is firm and congested and a frothy fluid often exudes from the cut surface.
Shock-induced lung injury leads to alveolar hyaline membranes, which also frequently line alveolar ducts and terminal bronchioles. These lung changes may heal entirely, but in half of patients, the repair processes cause a thickening of the alveolar wall. These chronic changes may result in persistent respiratory distress and even death.
Shock often results in diffuse gastrointestinal hemorrhage. Erosions of the gastric mucosa and superficial ischemic necrosis in the intestines are the usual sources of this bleeding.
The decreased perfusion of the intestine results in the disturbance of the mucosal barrier (the intestine is very sensitive to ischemia), bacteria can pass into the bloodstream and cause septic shock in addition. Besides, the disturbance of the mucous membranes causes additional fluid loss from an organism.
As a rule, the intestine, filled with gram-negative bacteria, is considered as the initiator of nosocomial pneumonias in the post-resuscitation period as well as of septic state and polyorgan insufficiency. The functions of other organs – the heart, kidneys, lungs, liver, system of the mononuclear phagocytes, immune system – can be paralysed, and, finally, the brain function can be disturbed, a coma may occur.
The hypoperfusion of the liver stimulates anaerobic metabolism and considerable lactification which is conducive to the development of metabolic acidosis, which, in its turn, disturbs the function of the cardiovascular system. In these conditions the liver becomes unable to inactivate active mediators and toxins circulating in the bloodstream. Shock whose duration is less than 10 hours is seldom accompanied by the necrosis of hepatocytes, but in 24 hours of shock necroses of the liver are probable. The serious complications that may set in are coagulopathy, DIC-syndrome and massive bleedings. They are conditioned by decreased synthesis of the coagulative factors in the liver, consumption of the plasma factors and thrombocytes
In patients who die in shock, the liver is enlarged and has a mottled cut surface that reflects marked centrilobular pooling of blood. The most prominent histologic lesion is centrilobular congestion and necrosis. Pancreas
The splanchnic vascular bed, which supplies the pancreas, is particularly affected by impaired circulation during shock. Resulting ischemic damage to the exocrine pancreas unleashes activated catalytic enzymes and causes acute pancreatitis, a complication that further promotes shock.
Disturbance of the pancreas perfusion results in the formation of peptides, which suppress the heart function. The example of suppression of the contractility of the cardiac muscle by the circulating myocardium-suppressing factor (MSF).
The lesion of the brain may be generalized, resulting in a coma, but it may also be local. The main problem is hypoxia and ischemia of the brain, which result in the swelling of cells (i.e. to intracellular edema), as a result, intracranial pressure increases, which additionally decreases the blood supply of the brain and thus, the pathological circle closes.
Brain lesions are rare in shock. Microscopic hemorrhages may be seen, but patients who recover do not ordinarily have neurologic deficits. In severe cases, particularly in persons with cerebral atherosclerosis, hemorrhage and necrosis may appear in the overlapping region between the terminal distributions of major arteries.
In severe shock, adrenal glands exhibit conspicuous hemorrhage in the inner cortex. The hemorrhage is often focal. However, it can be massive and accompanied by hemorrhagic necrosis of the entire gland (as seen in the Waterhouse-Friderichsen syndrome) wish loss of function of adrenal glands and catostrofic fall of arterial presser.
The patient’s condition gets worse again as kidneys, lungs, liver and other organs become affected after the serious, especially continuous, stages of shock and subsequent stabilization of the respiration and circulation; pathological dependences arise
Polyorgan insufficiency is a dangerous complication, which may often cause death. There are few patients who can survive if they have insufficiency of three organs. Insufficiency of any system often makes traditional methods of treatment inefficient; in this case there is no standard way of treatment.
Possible complications of shock include: acute respiratory distress syndrome, acute tubular necrosis, disseminated intravascular coagulation (DIC), cerebral hypoxia.
Outcome of Shock and its criteria
There are 3 possibilities, depending on several shock factors:
Recovery after convalescence, which may be long
Suvival with permanent damage of various organs
The factors, which order to recovery or to progression of shock summarized in table 25.
Table 25. The factors ordered to recovery or to progression of shock
Factors favouring recovery
Factors favouring progression to shock
Availability of early treatment of
the initiating cause
Good general health
Dealay in treatment
Poor general health
Pre-existing Cardiovascula and lung disease
Onset of Complication
The attempts to define shock resulted in singling out a number of repeated elements, the so-called shock criteria:
A time interval necessary for a bodily general reaction and, for general mobilization of energetic and genetic mechanisms of the organism to start.
Anatomic and functional integrity of the central neuroendocrine system, i.e. as a ‘manager’ able to transmit a reaction conveying the power of shock throughout the whole organism.
Decreased efficient volume of the circulating blood.
Onset of cell metabolism disturbance.
Potentially lethal character of lesions and their tendency to be self-supportive and irreversible.
The most important parameters for predicting the survival rate are hemodynamic parameters, the second important parameters are parameters of gases of blood (oxygen transport to tissues and oxygen consumption by tissues).
The resulting (blood) volume deficit can be estimated by means of the shock index (heart rate per minute/systolic blood pressure in mm Hg):
• 0.5 = normal or blood deficit < 10%;
• 1.0 = blood deficit < 20–30% (compensated shock);
• 1.5 = blood deficit > 30– 50% (decompensated shock).
Hemodynamic monitoring provides information on intracardiac pressures and cardiac output. Cardiac output is the amount of blood ejected by the heart each minute. Normal: 4 to 8 liters; varies with a patient's weight, height, and body surface area. Adjusting the cardiac output to the patient's size yields a measurement called the cardiac index. The cardiac index is 2.4 -3.5 l/min, slightly higher in males and considerably higher in children.
General principles of treatment
Elimination of a shock-causing factor. Primary management of the wound using anaesthetics.
Tranquillizers – to decrease the involvement of the vasomotor and cardiac centres in the shock reaction.
The restoration of CBV (the plasma, blood substitutes) makes it possible to increase the venous return that increases stroke volume (SV) and cardiac output (CO).
The restoration of systemic arterial pressure (SAP).
To improve microcirculation
Levelling of endocrine metabolic disturbances. Glucocorticoids stabilise the membranes; glucagon increases CO, AP; the inhibitors of the proteolytic enzymes decrease the quantity of vasoactive substances.
Alkaline balance is normalised by the introduction of sodium bicarbonate and antihypoxants.
Normalization of the coagulative balance
Antibacterial treatment and prevention of sepsis.
Coma is an unconscious state from which the patient cannot be aroused by any external stimulus. Cardiovascular, thermoregulatory and neuroendocrine control is not preserved.
Coma may result from widespread damage in both hemispheres, suppression of cerebral function and brainstem lesions. Destructive lesions affecting the brainstem and adjacent structures of the upper pons, midbrain, and diencephalon may produce coma. One of the major signs of coma is compression of the third cranial nerve with pupillary dilation.
Lesions confined to the cerebral hemispheres do not immediately affect the brainstem reticular activating system (RAS). Secondary dysfunction of the brainstem and diencephalic RAS results from compression by a mass in a cerebral hemisphere induced by brain edema or intracranial hemorrhage. Compression of midbrain, than the pons, and finally the medulla leads to sequential appearance of neurologic signs and to progressively diminished alertness.
Causes of coma include direct and indirect trauma (compression of the brain by subdural or epidural hematoma), intoxication by endogenous and exogenous toxins including drugs (with or/and without damage of the blood brain barrier), hypoxia/ischemia, hypo- and hyperosmia, disturbances of electrolyte and acid base balance, brain edema.
Principal mechanisms underling coma include disturbances of cellular metabolism, membrane and neurotransmitter abnormalities. Hypoxia, ischemia and hypoglycemia cause inadequate energy production.
The pathogenesis of coma see fig 5
Fig 5 The main stages of coma pathogenesis
Clinical classification of coma is based on its origin, for example renal coma, hepatic coma, hypoglycemic coma, alcohol coma, coma of unclear etiology and so on.
Hepatic coma is associated with accumulation of ammonia in the brain. This substance interferes with energy metabolism and the Na+,K+-ATPase pump, and results in the production of “false” neurotransmitters. Certain metabolites produced during hepatic insufficiency may bind to benzodiazepine-gamma-aminobutyric receptors to cause central nervous system depression.
Encephalopathy in renal coma is associated with increased permeability of the blood brain barrier to toxic substances and accumulation of intracellular calcium.
Abnormalities of osmolality are involved in the pathogenesis of varying types of coma. Sodium levels below 115 mM/L may initiate coma and convulsions. Serum osmolality that is above 350 mosmol/L leads to hyperosmolar coma. Hypercapnia produces a diminished level of consciousness proportional to the PaCO2 tension in the blood. An association has been noted between acidosis in cerebral spinal fluid and the severity of symptoms of coma.
Coma following seizures, termed the postictal state, may be due to exhaustion of energy metabolites or be secondary to locally toxic effects of excitatory amino acids such as glutamate and aspartate.
The differential diagnosis
In conclusion, we shall give a short description of differential diagnostics of several shock conditions:
Syncope which is a temporary loss of consciousness as a result of insufficient blood flow to the brain (cardiac rate disturbance, stimulation of the carotid sinus, pulmonary embolism). The action of the vagus nerve prevails (in case of shock sympathetic innervation prevails).
Fainting is considered as a symptom and consists in incomplete transient loss of consciousness accompanied by decreased tone of muscular vessels of low extremities and bradycardia. In case of shock a person may have tachycardia, cool sweat, loss of consciousness or may go pale.
Coma is a partial or complete loss of consciousness when vegetative functions are normal and the correlating functions are depressed in case of primary brain lesions such as hypoxia, acidosis; it can occur at the final stage of shock.
Collapse occurs either in case of a sudden decrease of the content of vessels (haematogenic collapse) or in case of sudden dilation of vessels (vasomotoric collapse). In case of shock circulation becomes centralized, it can be treated with vasodilators while collapse is treated with vasoconstrictors.