Bachelor of Chinese Medicine Shock

Transcription

1 BCM Year 2 Dr. Irene Ng Jan 28, :30 am 1:00 pm Rm 004 UPB Bachelor of Chinese Medicine Shock Learning objectives Be able to: know the definition of shock know the classification and causes of shock know the development of shock and its mechanism know the pathological changes resulting from shock know the principles to treat shock Shock 1. Definition A state of generalized hypoperfusion of all cells and tissues due to reduction in blood volume or cardiac output or to redistribution of blood resulting in an inadequate effective circulatory volume. It is at first reversible but if protracted leads to irreversible injury and patient death. 2. Clinical Presentation Hypotension (low blood pressure) Weak and rapid pulse Cold clammy extremities Peripheral cyanosis Pallor Hyperventilation Oliguria Variable mental changes Presentation of the precipitating disease (e.g. gastrointestinal bleeding, sepsis) 3. Classification and causes of shock Basic factor : inadequate cardiac output fi hypotension a. Hypovolemia (reduction of blood volume) Haemorrhage (e.g. GI bleeding, ruptured ectopic pregnancy) Excess fluid loss e.g Severe vomiting or diarrhea (cholera) Burn (excessive fluid loss from burned skin) b. Cardiogenic (Hypotension due to failure of myocardial pump) Myocardial infarction Arrhythmias 1

2 cardiac rupture cardiac tamponade dissecting aneurysm massive pulmonary embolism (outflow obstruction) The cardiac filling pressure is raised due to intrinsic myocardial damage, extrinsic pressure (cardiac tamponade) or obstruction to outflow. c. Septic (Septicemia) d. Anaphylactic e. Neurogenic shock Anesthesia, spinal cord injury Vasovagal attack is a simple faint caused by bradycardia as a result of increased vagal drive. It is transient and will not lead to impaired tissue perfusion and, strictly speaking, should not be included as a kind of shock. 4. Development of shock and its mechanism: using hypovolemic shock as an example a. Causes Hemorrhage External (e.g. trauma, GI bleeding) Internal (e.g. fractured femur, ruptured ectopic pregnancy) Fluid loss (e.g. severe diarrhea) Burns (fluid loss + sepsis) b. Stages Asymtomatic (<10% loss) Early Stage (15-25% loss) : compensated hypotension Hypotension as a result of reduced effective circulatory volume and cardiac output Sympathico-adrenal stimulation Release of vasopressors (catecholamines) to maintain blood pressure by peripheral vasoconstriction Activation of renin-angiotensin-aldosterone system + increased ADH release Fluid retention by kidneys, further vasoconstriction Renal perfusion: impaired Brain and heart perfusion: maintained by autoregulation 2

3 Progressive / Advanced Stage (tissue hypoperfusion; decompensation) If no therapeutic intervention is given, compensatory mechanisms become harmful and autoregulation of cerebral and coronary circulation break down resulting in inadequate tissue perfusion. Stasis in the circulation: reduction of arteriolar constriction and results in pooling of blood in capillary beds increased transudation into interstitial space aggravates hypovolemia Hypoxic damage to cells : metabolic acidosis (lactic acidosis) as a result of anaerobic respiration sick cell syndrome release of lysosomal enzymes endothelial cell injury predisposed to DIC Irreversible shock Irreversible hypoxic injury to vital organs 5. Pathology of shock Tissue hypoperfusion Basic pathological changes in shock: hemorrhages, cell/tissue necrosis, fibrin thrombi in capillaries and small veins. Heart Lung Kidney myocardial ischemia focal myocardial necrosis subendocardial infarction adult respiratory distress syndrome (diffuse alveolar damage) damage to type I pneumocytes & endothelial cells patchy intra-alveolar and intraseptal oedema with hyaline membrane formation, atelectasis and vascular thrombosis organization by fibrosis or resolution complication: secondary infection acute tubular necrosis (pre-renal failure) Brain hypoxic and ischemic damage to the boundary zones and other areas - hippocampus, basal ganglion and cerebellum Other organs Gastrointestinal tract Liver Adrenals mucosal ischemia, hemorrhage, necrosis, erosion and ulcers Ischemic bowel disease (small and large bowels) centrilobular necrosis and fatty change focal necrosis diffuse hemorrhagic destruction 3

4 Pancreas hemorrhagic pancreatitis necrosis 6. Other types of shock: Septic shock Commonly due to gram-negative endotoxin-producing bacteria e.g. E.coli, Klebsiella, Proteus and pseudomonas. Endotoxin is a lipopolysaccharide present in the outer part of the cell wall of most Gran-negative bacteria. May accompany gram-positive (streptococcal, pneumococcal) septicemia. Other organisms which can give rise to septic shock include fungi (candida) and spirochetes. Pathogenesis Microbial and host factors that lead to establishment of infection Tissue injury and/toxin production Generation of inflammatory/injurious mediators Hemodynamic consequences Predisposing factors: debilitating illness complication of instrumentation and treatment burns Direct toxic injury causing arteriolar vasodilatation and pooling of blood in microcirculation (initially warm, flushed skin) with consequent leakage of fluid into interstitial space reduction in systemic vascular resistance (Note: patients in early septic shock often have a normal or increased cardiac output and a warm, dry skin) Generation of inflammatory/injurious mediators: Inflammatory reaction: vasodilatation mediated by histamine and complements Disseminated intravascular coagulation: activation of clotting factors and platelets Endothelial cell damage: increased transudation and exudation of fluid out of vascular compartment Release of interleukin-1 and tumour necrosis factor-α from macrophages 7. Other types of shock: Anaphylactic shock Exposure to specific antigens with history of previous sensitization 4

5 Foreign antigen combines with cell-bound IgE and triggers the release of vaso-active mediators from mast cells. The mediators concerned include histamine, complements and prostaglandins and these lead to vasodilatation and fluid extravasation. Associated with urticarial skin rash, angioneurotic edema and bronchospasm 8. Principles to treat shock Treatment and monitoring in intensive care unit (continuous electrocardiographic monitoring, cardiac output, arterial blood gases, serum electrolytes and coagulation parameters) Maintain blood pressure and ensure adequate perfusion For hypovolemic shock infusion of fluid (volume expansion and vasopressor) For cardiogenic shock reducing myocardial ischemia (oxygen and drugs to dilate coronary arteries) For septic shock eliminate focus of infection, maintain adequate organ perfusion (volume and oxygen), and interrupt the pathogenic sequence leading to septic shock (inhibition of toxic mediators) 5