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SHOCK http://www.vevo.com/watch/billy- idol/shock-to-the- system/USCA30800056 http://www.vevo.com/watch/billy- idol/shock-to-the- system/USCA30800056
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Definition A complex clinical syndrome of decreased blood flow to body tissues resulting in cellular Dysfunction and eventual organ death http://www.youtube.com/watch?v =9a7N9AU1GiQ&feature=related http://www.youtube.com/watch?v =9a7N9AU1GiQ&feature=related http://www.youtube.com/watch?v =9a7N9AU1GiQ&feature=related
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Basic Pathogenesis http://v.youku.com/v_show/id_XMTU2NT c3MTIw.html http://v.youku.com/v_show/id_XMTU2NT c3MTIw.html http://v.youku.com/v_show/id_XMTU2NT c3MTIw.html Tissue perfusion decreases Compensatory mechanisms triggered Blood goes to primary organs only Vascular system fails (refractory hypotension) Hypoxia at cellular level with massive acidosis Increased capillary permeability with leakage Coagulation cascade activated Blood pools in periphery Organ death
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Progression of Shock Initial stage Compensatory stage Progressive stage Refractory stage
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Initial Stage Tissue perfusion is decreased Decreased oxygen to cells/tissues Anaerobic metabolism increases Excess lactic acid produced No clinical signs
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Compensatory Stage Goal: restore cardiac output and tissue perfusion to vital organs Interrelated mechanisms: Neural compensation Hormonal compensation Chemical compensation
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Clinical Manifestations during Compensatory Phase Blood pressure normal Tachycardia Cool, pale, moist skin Thirst Urine output <30 cc/hour Restless, confused, agitated Able to respond to verbal commands Tachypnea
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Progressive Phase Third Stage Severe hypoperfusion leads to multiple organ dysfunction and failure
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Progressive: Cardiovascular Decreased preload r/t loss of autoregulation & increased capillary permeability Fluid leaves capillaries Blood flow sluggish Imbalance of supply & demand to heart muscle Arrhythmias Hypotension appears
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Progressive: Pulmonary Pulmonary arterioles constrict r/t hypoxia, edema, mediator release Develop pulmonary hypertension Decreased pulmonary blood flow, increased physiologic dead space Impaired gas exchange - decreased PaO2, increased PCO2 Alveoli collapse/edema r/t decreased surfactant production & increased capillary permeability Further decreased oxygen diffusion Respiratory failure with ARDS development
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Progressive: Neurologic Decreased cerebral perfusion with decreased cardiac output & blood pressure Deteriorating LOC Responds only to painful stimuli becoming totally flaccid and nonresponsive to pain
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Progressive: Renal ATN r/t prolonged hypoperfusion Acute renal failure develops Creatinine & BUN retained in blood Develop metabolic acidosis
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Progressive: GI Develop ischemic gut syndrome r/t prolonged hypoperfusion and vasoconstriction Develop paralytic ileus Mucosa erodes: Increased chance of GI bleed Release of bacteria into gut – “translocation”
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Progressive: Hematologic Hyperdynamic = hyperglycemic Clotting cascade Altered due to mediator release and inflammatory process Develop DIC (Disseminated Intravascular Coagulation)
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Progressive: Clinical Manifestations Cardiovascular: Weak peripheral pulses, extremities cyanotic & cold, B/P falling, decreased urine output, decreased LOC, increased HR Pulmonary: respiratory failure with ARDS, increased RR Neuro: decreased LOC without response to pain at end Renal: acute renal failure with increased creatinine/BUN GI: s/s sepsis and/or GI bleed Hematologic: DIC & hyperglycemia
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Refractory Stage of Shock Cell destruction severe Condition refractory to treatment Multiple organ failure Refractory hypotension Refractory hypoxemia Renal shutdown GI failure (no absorption of nutrients) Neurological failure (no response)
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http://www.youtube.com/watch?v=PrkNmVPI9sc http://www.youtube.com/watch?v=CbM4Ui hE1TQ
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Hypovolemic Shock
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Definition Decreased intravascular volume Inadequate fluid volume in the intravascular compartment results in decreased blood flow and reduced tissue perfusion Can result from loss of either blood, plasma, or extracellular fluid.
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Etiology: Hypovolemia Internal fluid shifts Internal hemorrhage Increased capillary permeability r/t thermal injuries, sepsis, anaphylaxis Third spacing - ascites External fluid losses Trauma – GSW GI upset Large exudative lesions
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Pathophysiology: Hypovolemia Clinical Manifestations: Hypovolemic Shock S/S of compensatory changes Altered mentation Cool, clammy skin Tachypnea U/O decreased and dark Poor peripheral pulses
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Treatment of Hypovolemic Shock Treat the cause RESUSCITATE with fluids Fluid challenge of 500 cc or greater Crystalloids, Colloids or Blood products Monitor response – WHAT TO ASSESS???? Administer vasoactives Oxygen support Cardiac monitor, hemodynamic lines
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Fluids & Resuscitation (Crystalloids) Isotonic Osmolarity = to serum: expands intravascular volume Example: LR, NS Hypotonic Osmolarity less than serum Hypertonic Osmolarity greater than serum
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Colloids or Blood Products Colloids Do not diffuse through capillary walls Increases osmotic pressure = fluid stays in vascular compartment Examples Albumin, dextran Blood/blood products
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Cardiogenic Shock
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Etiology “Pump failure”= decreased cardiac output Mainly “systolic” dysfunction Etiology: MI Open heart surgery Cardiomyopathies Severe systemic or pulmonary hypertension
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Pathophysiology: Cardiogenic Narrow pulse pressure JVD & pulmonary congestion Arrhythmias Chest pain Cool, pale, moist skin Oliguria Decreased LOC Increased HR, Increased RR, SBP <85, decreased CO
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Treatment – Cardiogenic Cardiac monitor ABGs w/serum lactate Multiple labs Swan catheter Meds Vasopressors Diuretics Nitrates IABP
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Obstructive Shock
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Heart compression with obstruction to atrial filling and/or outflow from the heart Etiology: Cardiac tamponade Tension Pneumothorax or massive PE Dissecting aneurysm Clinical manifestations: Muffled heart sounds, s/s decreased perfusion
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Treatment of Obstructive Shock Address cause Pericardiocentesis Pericardial window (chronic) Chest tube Oxygen therapy Fluid resuscitation Ongoing monitoring (cardiac, renal, resp)
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Distributive Shock Neurogenic, Anaphylactic, Septic
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Neurogenic Shock
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An abnormality in the vasculature that changes the normal distribution of vascular volume Massive vasodilation due to loss of sympathetic tone/vasomotor control Etiology: Spinal cord injury (spinal shock) Spinal anesthesia Adrenergic blocking drugs Barbituate overdose Severe emotional distress
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Pathophysiology: Neurogenic Clinical Manifestations: Neurogenic Hypotension Bradycardia Loss of temperature control Loss of or diminished sensation, motor movement, and reflexes Skin dry (warmth dependent on temperature of environment)
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Treatment of Neurogenic Shock Supportive care Solumedrol therapy Oxygen therapy Judicial fluid resuscitation May require vasoactive drips Monitor closely V/S, u/o, LOC, skin, hemodynamics
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Anaphylactic Shock http://www.youtube.com/watch ?v=QM_cRFvkzl4 http://www.youtube.com/watch ?v=QM_cRFvkzl4
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Anaphylactic Shock Massive vasodilation, decreased peripheral resistance, and increased capillary permeability Etiology: Allergic reaction Drugs Food Bee stings Latex
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Pathophysiology: Anaphylaxis Clinical Manifestations: Anaphylaxis Generalized erythema Urticaria Pruritus Angioedema Decreased respiratory status: stridor, bronchoconstriction Hypotension Decreased LOC
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Anaphylaxis Treatment Avoidance #1 Epinephrine #1 Fluid resuscitation Benadryl (liquid vs. pill???) H2 Blockers Bronchodilators Magnesium Sulfate
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Sepsis
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Sepsis - Septic Shock Severe, overwhelming infection & massive inflammatory response Continuum development Risk: Multiple Etiology Any microorganism
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