Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Shock Definition Failure of circulation, that leads to inadequate tissue perfusion. Despite the compensatory mechanisms tissue hypoxia is developed. Tissue hypoxia leads to functional and morfological changes in organs. The result of untreated shock is irreversible organ failure and death. Pathomechanisms different mechanisms leading to: Decrease in return of blood to the heart (!) Decrease in cardiac output Hypotension Hypoperfusion of peripheral tissues General activation of different neural, humoral response at systemic, organ, tissue and cellular level Stages of shock 1. stage – reversible, compensated Response of compensatory mechanisms activation of SAS – peripheral vasoconstriction (skin, kidneys), vasodilatation in „central“ organs (brain, heart) RAAS activation increased ADH secretion And pro- and antiinflammatory cytokines as procalcitonin and many others Stages of shock 2. stage – developed, decompensated Failure of compensatory mechanisms Microcirculation failure – increased blood viscosity, higher platelets agregation, thrombosis – higher concentration of vasoactive mediators (histamine, bradykinin...) – higher permeability, the cytokines as a double-edged sword Metabolic (lactate) acidosis Stages of shock 3. stage - irreversible Cell damage, necrosis or apoptosis MODS (multiple organ dysfunction syndrome) – – – – – – – ARDS – „shock“ lungs acute kidney failure acute liver failure loss of consciousness, coma, DIC ulcers, bleeding in GIT ... Types of shock hypovolemic shock – haemorrhagic - bleeding – nonhaemorrhagic – GIT – diarhea, vomiting; kidneys – treatment with diuretics, DM; skin - burns cardiogenic shock – inadequate contractility – acute MI, myocarditis, cardiomyopathies – arrhythmias – mechanical obstruction – acute valves dysfunction, rupture of ventricular septum, cardiac tamponade (obstructive shock) distributive shock – septic – toxic – anaphylactic – neurogenic – CNS, spinal cord damage Clinical signs low minute cardiac output – hypotension SAS activation – – – – tachycardia sweating piloerection cold, pale skin inadequate peripheral perfusion – cyanosis – oliguria – unconsciousness – muscle weakness Hypovolemic shock Deficiency in volume of extracelular fluid Most frequent form – haemorrhagic shock – bleeding – traumatic shock – bleeding + pain other – nonhaemorhagic shock – GIT – diarhea, vomiting – kidneys – treatment with diuretics, patient with diabetes mellitus – burns (burn shock) Cardiogenic shock heart failure reduced cardiac output – inadequate contractility – acute MI, myocarditis, cardiomyopathies – arrhythmias – ventricular tachycardia, supraventricular tachycardia, atrial fibrilation, AV block - bradycardia, WPW syndrome – mechanical obstruction – acute valves dysfunction, acute rupture of ventricular septum in MI, cardiac tamponade... Anaphylactic shock accelerated allergic reaction increase of vasoactive mediators – histamine – marked vasodilatation 8 – 10% - lethal signs – itching, nausea, erythema, dyspnoe – larynx oedema, bronchospasm – circulation failure, unconsciousness, cramps Septic shock bacterial, viral infection release of vasoactive mediators – permeability, vasodilatation platelets adhesion and agregation Neurogenic shock acute damage of brain or spinal cord inflammation, trauma, bleeding, anaesthesia loss of vasomotoric regulation marked vasodilatation irritation of n. vagus bradycardia, damage of respiratory centre hypoventilation