SHOCK idol/shock-to-the- system/USCA idol/shock-to-the- system/USCA

Definition  A complex clinical syndrome of decreased blood flow to body tissues resulting in cellular  Dysfunction and eventual organ death  =9a7N9AU1GiQ&feature=related =9a7N9AU1GiQ&feature=related =9a7N9AU1GiQ&feature=related

Basic Pathogenesis c3MTIw.html c3MTIw.html 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

Progression of Shock  Initial stage  Compensatory stage  Progressive stage  Refractory stage

Initial Stage  Tissue perfusion is decreased  Decreased oxygen to cells/tissues  Anaerobic metabolism increases  Excess lactic acid produced  No clinical signs

Compensatory Stage  Goal: restore cardiac output and tissue perfusion to vital organs  Interrelated mechanisms:  Neural compensation  Hormonal compensation  Chemical compensation

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

Progressive Phase  Third Stage  Severe hypoperfusion leads to multiple organ dysfunction and failure

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

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

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

Progressive: Renal  ATN r/t prolonged hypoperfusion  Acute renal failure develops  Creatinine & BUN retained in blood  Develop metabolic acidosis

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”

Progressive: Hematologic  Hyperdynamic = hyperglycemic  Clotting cascade  Altered due to mediator release and inflammatory process  Develop DIC (Disseminated Intravascular Coagulation)

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

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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Hypovolemic Shock

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.

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

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

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

Fluids & Resuscitation (Crystalloids)  Isotonic  Osmolarity = to serum: expands intravascular volume  Example: LR, NS  Hypotonic  Osmolarity less than serum  Hypertonic  Osmolarity greater than serum

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

Cardiogenic Shock

Etiology  “Pump failure”= decreased cardiac output  Mainly “systolic” dysfunction  Etiology:  MI  Open heart surgery  Cardiomyopathies  Severe systemic or pulmonary hypertension

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

Treatment – Cardiogenic  Cardiac monitor  ABGs w/serum lactate  Multiple labs  Swan catheter  Meds  Vasopressors  Diuretics  Nitrates  IABP

Obstructive Shock

 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

Treatment of Obstructive Shock  Address cause  Pericardiocentesis  Pericardial window (chronic)  Chest tube  Oxygen therapy  Fluid resuscitation  Ongoing monitoring (cardiac, renal, resp)

Distributive Shock Neurogenic, Anaphylactic, Septic

Neurogenic Shock

 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

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)

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

Anaphylactic Shock ?v=QM_cRFvkzl4 ?v=QM_cRFvkzl4

Anaphylactic Shock  Massive vasodilation, decreased peripheral resistance, and increased capillary permeability  Etiology:  Allergic reaction  Drugs  Food  Bee stings  Latex

Pathophysiology: Anaphylaxis  Clinical Manifestations: Anaphylaxis  Generalized erythema  Urticaria  Pruritus  Angioedema  Decreased respiratory status: stridor, bronchoconstriction  Hypotension  Decreased LOC

Anaphylaxis Treatment  Avoidance #1  Epinephrine #1  Fluid resuscitation  Benadryl (liquid vs. pill???)  H2 Blockers  Bronchodilators  Magnesium Sulfate

Sepsis

Sepsis - Septic Shock  Severe, overwhelming infection & massive inflammatory response  Continuum development  Risk:  Multiple  Etiology  Any microorganism