1. Shock SEVRANCE EM R1 손재돈 ATLS

2. Objectives Define shock and apply this definition to clinical practice. Define shock and apply this definition to clinical practice. Recognize the clinical shock syndrome correlate acute clinical signs with the degree of volume deficit. Recognize the clinical shock syndrome correlate acute clinical signs with the degree of volume deficit. The importance of early identification and control of the source of hemorrhage The importance of early identification and control of the source of hemorrhage Clinical presentation of patients with the various etiologies of the shock state Clinical presentation of patients with the various etiologies of the shock state

3. I. Introduction Initial Step : recognize its presence Initial Step : recognize its presence No laboratory test diagnosis shock No laboratory test diagnosis shock Based on inadequate tissue perfusion Based on inadequate tissue perfusion 2nd Step : identify the probable cause 2nd Step : identify the probable cause Related mechanism of injury Related mechanism of injury Hemorrhage is most common cause Hemorrhage is most common cause

4. A. Basic cardiac physiology - Preload : volume status - Volume contributes venous pressure  venous drive venous pressure  venous drive B. Blood loss physiology –Progressive vasoconstriction –Tachycardia : earliest measurable sign –Shifting anaerobic metabolism  Lactic acidosis & Metabolic acidosis

5. II. Initial patient assessment A. Recognition of shock Vasoconstriction & tachycardia > early sign Systolic BP preserve till 30% loss Respiratory rate, skin circulation, pulse pressure Tachycardia : >160 in infant, >120 in school age >100 in adult >100 in adult Narrow pulse pressure -> significant blood loss Hb & Hct : unreliable factor on acute blood loss

6. Clinical differentiation of etiology of shock Clinical differentiation of etiology of shock –In trauma patient, classified hemorrhagic or nonhemorrhagic shock. –Blunt myocardial injury, tamponade, & tension pneumothorax. –Initial determination etiology of shock  Appropriate Hx. & Careful P/Ex.  CVP, chest/pelvic X-rays, U/S

7. 1. Hemorrhagic shock -Most common cause after injury -but, most nonhemorrhagic shock respond to fluid resuscitation. 2. Nonhemorrhagic shock a.Cardiogenic shock Blunt thoracic injury patient need EKG monitoring Blunt thoracic injury patient need EKG monitoring Cardiac enzyme & echo are not practical Cardiac enzyme & echo are not practical FAST -> pericardial effusion & tamponade

8. b. Tension pneumothorax True surgical emergency ->Thoracostomy without CXR ->Thoracostomy without CXR Intrapleural pressure ↑ -> total lung collapse & shift of mediastinum to opposite & impairment venous return Subcutaneous emphysema/breath sound absent/ hyperreasonance/trachea shift C. Neurogenic shock Spinal cord injury -> loss of sympathetic tone Hypotention without tachycardia, vasoconstriction & narrow pulse pressure & narrow pulse pressure

9. III. Hemorrhagic shock in the injured patient A. Definition of hemorrhage -Acute loss of circulation volume B. Direct effects of Hemorrhage -Potential for hemorrhagic shock Age, severity injury, time laps injury time & treat time, chronic medication -Fluid resuscitation must be initiated without classification without classification

10. 1.Class I hemorrhage No measurable changes in BP, PR, RR 2. Class II hemorrhage Tachycardia, tachypnea, decrease pulse pressure Urinary output mildly affected 20~30ml/hr Eventually Transfusion 가능.

11. 3. Class III hemorrhage -> BP down Present classic signs tachycardia, tachypnea, mental change, Hypotention tachycardia, tachypnea, mental change, Hypotention Always require transfusion But, priority is to stop the hemorrhage The decision of transfusion is based on response of initial fluid resuscitation 4. Class IV hemorrhage Markedly classic sign, U/O negligible Rapid Transfusion & surgical intervention

13. C. Fluid changes to soft tissue injuries –Major soft tissue injuries & fractures compromises hemodynamic status 1 st > blood loss Tibia or humerus > 750ml, femur > 1500ml Pelvic Fx. With retroperitoneal hematoma > several liters 2 nd > tissue edema

14. @ 3-for-1 rules 1470ml loss(Class III) -> 4410ml fluid replacement 1470ml loss(Class III) -> 4410ml fluid replacement @ Nonresponse indicates 1) persistent blood loss 1) persistent blood loss 2)unrecognized fluid loss 2)unrecognized fluid loss 3)nonhemorrhagic shock 3)nonhemorrhagic shock

15. IV. Initial manage of hemorrhagic shock Basic management is to stop bleeding & replace volume loss Basic management is to stop bleeding & replace volume loss A. Physical examination 1.Airway & breathing 2.Circulation & hemorrhagic control 3.Disability-Neurologic examination 4.Exposure-Complete examination 5.Gastric dilatation-Decompression 6.Urinary catheter insertion

16. B. Vascular access lines Promptly 2 short, large peripheral lines Full Blood sampling C. Initial fluid therapy - Warm isotonic solutions : initial - Ringer’s solution is choice, N/S is second - N/S -> cause hyperchloremic acidosis -Rapidly, 1~2L for adult & 20ml/kg for pediatric by pumping devices by pumping devices -Evidence of adequate end-organ perfusion eg, U/O, consciousness & peripheral perfusion eg, U/O, consciousness & peripheral perfusion

17. v. Evaluation of fluid resuscitation and organ perfusion A. General -Positive sign : Return of normal BP, pulse pressure & PR -UO : sensitive indicator of renal perfusion. -Changes in CVP is useful information B. Urinary output -0.5ml/kg/hr in adult, 1ml/kg/hr in pediatric, 2ml/kg/hr in infant -Increasing specific gravity -> inadequate perfusion -> inadequate perfusion

18. C. Acid/base balance -In early hypovolemic shock > Resp. Alkalosis due to tachypnea, followed metabolic acidodis > Resp. Alkalosis due to tachypnea, followed metabolic acidodis > not require treatment > not require treatment -Severe shock > severe metabolic acidosis > caused inadequate tissue perfusion, ongoing > caused inadequate tissue perfusion, ongoing blood loss, lactic acidosis blood loss, lactic acidosis -Base deficit : useful in severity of perfusion deficit. -Bivon should not be used routinely to meta. Acidosis in Hypovolemic status

19. VI. Therapeutic decisions based on response to initial fluid resusciation The patient response is the key to detemining subsequent therapy The patient response is the key to detemining subsequent therapy > Blood loss was greater than estimated > Blood loss was greater than estimated  ongoing bleeding who require OP.  ongoing bleeding who require OP. Hemodynamic stable VS normal Hemodynamic stable VS normal -Stable : tachycardic, tachypneic, and oliguric > clearly still in shock > clearly still in shock -Normal : no signs of inadequate perfusion.

21. VII. Blood replacement A. Crosmatched, Type-specific, and Type O blood -Purpose : restore the oxygen-carrying capacity -Purpose : restore the oxygen-carrying capacity 1. Fully crossmatched blood is preferable. But require 1 hour, So rapid response group But require 1 hour, So rapid response group 2. Type-specific blood -> within 10 mins Transient response group Transient response group 3. Type O indicated no response group

22. B. Warming fluids-plasma and crystalloid -Hypothermia prevented and reversed -Most efficient way : to heat fluid to 39’ -Blood products by through IV fluid warmers C. Coagulopathy -Rare problem in the first hour -By massive transfusion, hypothermia -History of coagulopathy & medication -PT, PTT, PLT count is base line study

23. VIII. Special considerations in the diagnosis and treatment of shock A. Equating blood pressure with cardiac output -Increased BP should not be equated with concomitant increased in cardiac output. Ex, increased peripheral resistance by vasopressor Ex, increased peripheral resistance by vasopressor  no change CO & Increased BP  no change CO & Increased BP  no improvement tissue perfusion  no improvement tissue perfusion

24. B. Age -Deficit in the receptor response to catecholamine  decreased symphathetic activity  decreased symphathetic activity - Cardiac compliance decreased, atherosclerosis, chronic malnutrition, medication - Reduction in Pul/Kidney Capacity - Mortality and morbidity increased with age - Treatment begins with prompt, aggressive resuscitation -> returned to preinjury status -> returned to preinjury status

25. C. Athletes -Ability to compensate for blood loss > truly remarkable > truly remarkable D. Pregnancy -Physiologic hypervolemia -> greater blood loss ->manifest inadequate perfusion ->manifest inadequate perfusion E. Medication -β-blocker, CCB -> masking hemodynamic status -Insulin, Diuretics, NSAID, Anticoagulant

26. F. Hypothermia -Often develop coagulopathy -Trauma victim under alcohol/cold temp. -> rapid warming by warm fluid, warming devices -> rapid warming by warm fluid, warming devices -Best treatment is prevention. G. Pacemaker -Unable to respond to blood loss -CVP monitoring is invaluable

27. IX. Reassessing patient response and avoiding complications A. Continue hemorrhage -Obscure hemorrhage is most common complication -Generally transient response group -Surgical intervention recommend B. Fluid overload and CVP monitoring -Minimized by close monitoring -CVP is standard guide for fluid load

28. @ CVP monitoring Ideal position is SVC, just proximal to RA Ideal position is SVC, just proximal to RA 1.CVP is indirect, so avoid overdependence 2.Initial CVP is not related actual blood vol. 3.Minimal rise & Low CVP in the initial resuscitation  need for further volume expansion  need for further volume expansion 4.Declining CVP suggests ongoing bleeding 5.Abrupt or persistent elevation in CVP  inadequate replacement, too rapid, cardiac compromise  inadequate replacement, too rapid, cardiac compromise 6.High CVP in hypovolemia  Overtransfusion, cardiac dysfunction, tamponade,  Overtransfusion, cardiac dysfunction, tamponade, tension pneumothorax, catheter malposition tension pneumothorax, catheter malposition

29. X. Summary Immediately hemorrhagic control and fluid or blood replacement Immediately hemorrhagic control and fluid or blood replacement If fail to response, operative intervention If fail to response, operative intervention In transient or non responders In transient or non responders considered other cause of shock considered other cause of shock The goal is restoration of perfusion The goal is restoration of perfusion Vasopressor is Contraindication Vasopressor is Contraindication at hypovolemic shock at hypovolemic shock CVP is valuable tool for volume status CVP is valuable tool for volume status