Shock - Classification & Pathophysiology PDF

# Chapter 10: Shock ## 10.1 The Etiology and Classification of Shock ### 10.1.1 Classification of Shock According to Etiology - Hypovolemic shock due to blood loss: - Minor tissue trauma (gunshot/knife wounds), - Gastrointestinal bleeding, - Bleeding disorders. - Traumatic shock:...

# Chapter 10: Shock ## 10.1 The Etiology and Classification of Shock ### 10.1.1 Classification of Shock According to Etiology - Hypovolemic shock due to blood loss: - Minor tissue trauma (gunshot/knife wounds), - Gastrointestinal bleeding, - Bleeding disorders. - Traumatic shock: - Blood loss and major tissue injury (severe damage to muscle or bone) due to battle casualties and car accidents - Myoglobin leakage into circulation causes renal injury. - Burn shock: - Plasma loss from burn wound exudate; hemoconcentration occurs, and increased hematocrit may be seen. - Cardiogenic shock: - Cardiac pump failure, potentially caused by myocardial infarction, cardiac tamponade, and pulmonary embolism. Inadequate cardiac output in the setting of normal blood volume cannot maintain proper tissue perfusion. - Septic shock: - Massive vasodilation caused by gram-negative bacterial endotoxin. - Anaphylactic shock: - Severe allergic, antigen-antibody reactions releasing histamine, causing increased capillary permeability and widespread arteriolar and capillary dilation. - Neurogenic shock: - Loss of sympathetic control of resistance vessels, resulting in dilation of arterioles and venules, increasing vascular space and minimizing current circulatory blood volume (causing hypotension caused by spinal anesthesia, for example). ### 10.1.2 Classification of Shock According to Initial Insult - Hypovolemic shock: - Most common type of circulatory shock. - Profound hemorrhage is the usual precipitating factor, severe dehydration can also be the cause. - Because hemorrhage is closely associated with trauma, hypovolemic shock is more prevalent in younger, active age groups. Volume loss may also be the result of plasma loss from burns. - Cardiogenic shock: - Occurs when the heart is unable to pump sufficient blood to meet the oxygen demand. - Massive myocardial infarction is the most common precipitating factor of cardiogenic shock, which may also develop from severe congestive heart failure (due to coronary artery disease, valvular problems, or myocardial disease). - Vasogenic shock: - Caused by widespread vasodilation from decreased vasomotor tone. - Blood volume remains within normal limits, but vascular capacity is increased. - Increased vessel capacity without corresponding increase in blood volume leads to decreased venous return and further diminished cardiac output. - Two common types of vasogenic shock are septic shock and anaphylactic shock. ## 10.2 The Development Process and Underlying Mechanisms of Shock - Arterial pressure falls as a result of diminished cardiac output. Hypotension is the most immediate antecedent of hypovolemic, cardiogenic, and neurogenic shock. In response to generalized arterial hypotension, various feedback control mechanisms engage to return arterial pressure and tissue perfusion to normal limits. ### Stages of Microcirculatory Alterations: | Stage | Description | |--------------------------------------|---------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------| | Ischemic Hypoxia Stage | Diminished cardiac output results in decreased arterial pressure. This hypotension is the most immediate antecedent of various forms of shock. The following are various feedback mechanisms that attempt to compensate and improve tissue perfusion. Auto blood infusion, auto fluid infusion, redistributed blood perfusion. | | Progressive Stage of Shock (Congestive Hypoxia Stage) | The response of the body to poor tissue perfusion becomes one of positive feedback, establishing a vicious cycle in which cardiac output and tissue perfusion will continually decrease to a point when death becomes inevitable. At this point, shock becomes irreversible, or "decompensated". Microcirculatory characteristics of this stage include vasoconstriction of the arterioles and venules results in decreased blood flow to and through the microcirculation. Surrounding tissues experience ischemic hypoxia. Tissue fluid becomes acidic as the products of metabolism accumulate. Acidity and hypoxia cause arteriolar dilation, but the venules remain constricted. Blood can therefore enter the microcirculation but becomes trapped when the venule constricts. Pressure in the capillary bed is altered so that the net movement of fluid is out of the intravascular compartment and into the interstitial space. At this point, fluid replacement must exceed the amount of blood or fluid lost because of expansion of the vascular space. Once compensatory responses to shock are exhausted, the arterial blood pressure will fall. This stage is reversible if adequate fluid resuscitation is administered. The primary mechanism of microcirculation stasis includes acidosis, locally produced vasodilator substances increase, changes of hemorrheology. | | Late Shock (Failure of Microcirculation) | Late shock is also termed the refractory stage of shock. Because of serious microcirculatory stasis cell, tissue, and organ function are impaired and damaged. Even after blood is transfused, and other anti-shock measures are adopted, reversal and correction of shock is difficult. Microcirculatory features of this stage include microvascular reactivity to vasoactive substances decreases significantly. Blood concentrates and is in a highly viscous state. Disseminated intravascular coagulation (DIC) can easily occur which is why this is also termed the DIC period. Mechanisms of DIC onset include due to severe hypoxia, there is massive accumulation of acidic metabolites that can facilitate DIC onset by damaging vascular endothelial cells and exposing subendothelial collagen. | ## 10.3 Cell Injury and Metabolic Changes in Shock - Cell injury: - Can be injured via secondary damage by compromised circulation. - Primary cellular damage by endotoxin may also occur, altering cellular metabolism. ### 10.3.1 Cellular Damage - Cellular damage occurs first in the biomembranes (cell membrane, mitochondrial membrane, and lysosomal film). Dysfunction and structural damage follow within the organelles, leading up to cellular necrosis or apoptosis, the basis ultimately leading to organ failure. Changes in cell membrane, changes in mitochondria, changes in lysosomes, apoptosis. ### 10.3.2 Cell Metabolism Disorder - Glucose metabolism, protein and fat metabolism, electrolyte and fluid shifts, acidosis. ## 10.4 Organ Dysfunction during Shock - If the ischemia accompanying shock is not corrected, metabolic and structural degeneration will ultimately culminate in cellular death and necrosis. - Clinical symptoms will increasingly reflect cardiac, pulmonary, renal, and cerebral dysfunction related to cellular level changes caused by metabolic derangements. - Multiple organ dysfunctions may lead to death. Pulmonary dysfunction, renal dysfunction, cardiac dysfunction, cerebral dysfunction, gastrointestinal and liver dysfunction, immune dysfunction. ## 10.4.7 Multi-system Organ Dysfunction and Failure - After trauma, infection, shock, or post-shock recovery, multi-system organ dysfunction (MODS), the development of potentially reversible physiologic derangement involving two or more organ systems not involved in the primary disorder resulting in ICU admission, may occur. - When the dysfunction is severe, systemic failure may result in multiple system organ failure (MSOF). - MSOF often appears in late shock, with greater mortality. - Three or more organ systems that fail increase mortality rate to 80% and is a major cause of death in shock patients. - Of the various types of shock, septic shock carries the highest incidence of MSOF. Systemic inflammatory response syndrome (SIRS), compensatory anti-inflammatory response syndrome, mixed antagonistic response syndrome, other factors leading to MODS. ## 10.5 Treatment of Shock and Its Rationale - The goals of treatment include: - Correction of the underlying cause, - Pathogenesis treatment. ### 10.5.2.1 Correction of acid-base imbalance - Acid-base correction should be completed according to the degree of acidosis. ### 10.5.2.2 Improvement of tissue perfusion - Correcting the underlying cause of shock syndrome will improve perfusion. - Immediate pharmacologic intervention is often necessary as such correction of underlying problems require time. ### 10.5.2.3 To improve cell metabolism and prevent cell damage - Micro-circulation must be improved to prevent further cell damage. ### 10.5.2.4 Prevention of complication of shock - Disseminated intravascular coagulation, gastric ulceration, renal insufficiency leading to acute tubular necrosis, and adult respiratory distress syndrome (ARDS, or shock lung) are all shock complications. Once MODS has occurred, in addition to general treatment measures, corresponding treatment measures must be initiated for each different organ type failure. ### 10.5.2.5 Blocking the harmful effects of inflammatory mediators - Inhibitor and antagonists of inflammatory mediators can block the latter's harmful effects, preventing MODS occurrence effectively. **Summary:** Shock is an acute systemic pathological process. When attacked by various factors evoking damage, the effective circulating blood volume decreases. Circulatory blood flow drastically reduces, leading to cell damage, major organ dysfunction, metabolic disorders, and structural injury. Shock tends to evolve through three general stages. During the ischemic hypoxic stage, compensatory mechanisms are activated and perfusion of vital organs is maintained. The stagnant hypoxic stage is characterized by tissue hypoperfusion, worsening circulatory and metabolic imbalances including acidosis. During the microcirculation failure stage, cellular and tissue injuries are severe and it is difficult to correct hemodynamic defects. As a result, DIC and multiple organ dysfunction may occur.