Tiêu đề 14. SHOCK.pdf ✅

PHARMD GURU Page 1 DEFINITION: Shock is an acute state of inadequate perfusion of critical organs that can lead to death if therapy is not optimal. Shock is defined as systolic blood pressure (SBP) less than 90 mm Hg or reduction of at least 40 mm Hg from baseline with perfusion abnormalities despite adequate fluid resuscitation. (OR) Shock is the final common pathway for several potentially lethal clinical events, including severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis. Shock is characterized by systemic hypotension due either to reduced cardiac output or to reduced effective circulating blood volume. The consequences are impaired tissue perfusion and cellular hypoxia. At the outset the cellular injury is reversible; however, prolonged shock eventually leads to irreversible tissue injury that often proves fatal. TYPES OF SHOCK: Although in a given clinical case, two or more factors may be involved in causation of true shock, a simple etiologic classification of shock syndrome divides it into following 3 major types and a few other variants (Table 5.4): 1. HYPOVOLAEMIC SHOCK: This form of shock results from inadequate circulatory blood volume by various etiologic factors that may be either from the loss of red cell mass and plasma from haemorrhage, or from the loss of plasma volume alone. 2. CARDIOGENIC SHOCK: Acute circulatory failure with sudden fall in cardiac output from acute diseases of the heart without actual reduction of blood volume (normovolaemia) results in cardiogenic shock. SHOCK
PHARMD GURU Page 2 3. SEPTIC (TOXAEMIC) SHOCK: Severe bacterial infections or septicaemia induce septic shock. It may be the result of Gramnegative septicaemia (endotoxic shock) which is more common, or Gram- positive septicaemia (exotoxic shock). 4. OTHER TYPES: These include following types:  Traumatic shock: Shock resulting from trauma is initially due to hypovolaemia, but even after haemorrhage has been controlled, these patients continue to suffer loss of plasma volume into the interstitium of injured tissue and hence is considered separately in some descriptions.  Neurogenic shock: Neurogenic shock results from causes of interruption of sympathetic vasomotor supply.  Hypoadrenal shock: Hypoadrenal shock occurs from unknown adrenal insufficiency in which the patient fails to respond normally to the stress of trauma, surgery or illness. ETIOLOGY: 1. HYPOVOLAEMIC SHOCK IS CAUSED BY:  Acute haemorrhage  Dehydration from vomitings, diarrhoea  Burns  Excessive use of diuretics  Acute pancreatitis 2. CARDIOGENIC SHOCK IS CAUSED BY: i) Deficient emptying. Ex:  Myocardial infarction  Cardiomyopathies  Rupture of the heart, ventricle or papillary muscle  Cardiac arrhythmias ii) Deficient filling. Ex:  Cardiac tamponade from haemopericardium iii)Obstruction to the outflow. Ex:  Pulmonary embolism
PHARMD GURU Page 3  Ball valve thrombus  Tension pneumothorax  Dissecting aortic aneurysm 3. SEPTIC SHOCK IS CAUSED BY:  Gram-negative septicaemia (endotoxic shock) e.g. Infection with E. coli, Proteus, Klebsiella, Pseudomonas and bacteroides  Gram-positive septicaemia (exotoxic shock) e.g. Infection with streptococci, pneumococci 4. OTHER TYPES i) Traumatic shock  Severe injuries  Surgery with marked blood loss  Obstetrical trauma ii) Neurogenic shock  High cervical spinal cord injury  Accidental high spinal anaesthesia  Severe head injury iii)Hypoadrenal shock  Administration of high doses of glucocorticoids  Secondary adrenal insufficiency (e.g. in tuberculosis, metastatic disease, bilateral adrenal haemorrhage, idiopathic adrenal atrophy). PATHOGENESIS/MECHANISMS: In general, all forms of shock involve following 3 derangements: 1) Reduced effective circulating blood volume. 2) Reduced supply of oxygen to the cells and tissues with resultant anoxia. 3) Inflammatory mediators and toxins released from shock induced cellular injury. These derangements initially set in compensatory mechanisms (discussed below) but eventually a vicious cycle of cell injury and severe cellular dysfunction lead to breakdown of organ function (Fig. 5.15).
PHARMD GURU Page 4 1) REDUCED EFFECTIVE CIRCULATING BLOOD VOLUME: It may result by either of the following mechanisms: i) By actual loss of blood volume as occurs in hypovolaemic shock; or ii) By decreased cardiac output without actual loss of blood (normovolaemia) as occurs in cardiogenic shock and septic shock. 2) IMPAIRED TISSUE OXYGENATION. Following reduction in the effective circulating blood volume from either of the above two mechanisms and from any of the etiologic agents, there is decreased venous return to the heart resulting in decreased cardiac output. This consequently causes reduced supply of oxygen to the organs and tissues and hence tissue anoxia, which sets in cellular injury. 3) RELEASE OF INFLAMMATORY MEDIATORS: In response to cellular injury, innate immunity of the body gets activated as a body defense mechanism and release inflammatory mediators but eventually these agents themselves become the cause of cell injury.
PHARMD GURU Page 5 Endotoxins in bacterial wall in septic shock stimulate massive release of pro- inflammatory mediators (cytokines) but a similar process of release of these agents takes place in late stages of shock from other causes. Several pro-inflammatory inflammatory mediators are released from monocytes- macrophages, other leucocytes and other body cells, the most important being the tumour necrosis factor — (TNF)-α and interleukin-1 (IL-1) cytokines (Fig. 5.16).