Your SlideShare is downloading. ×
0
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
S
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

S

9,764

Published on

Published in: Health & Medicine
0 Comments
11 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
9,764
On Slideshare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
1,222
Comments
0
Likes
11
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide
  • Transcript

    • 1. Shock Loring W. Rue, III, MD, FACS Professor and Vice Chairman Department of Surgery University of Alabama at Birmingham
    • 2. Shock <ul><li>What is it? </li></ul><ul><li>How to deal with it </li></ul>
    • 3. Shock- Surgical Legacy <ul><li>G.J. Guthrie was the first to use the term shock in the context of physiologic instability </li></ul><ul><li>Surgeon for Duke of Wellington in Peninsula campaign against Napoleon </li></ul>
    • 4. Shock- Surgical Legacy <ul><li>George Crile </li></ul><ul><ul><li>Developed experimental models of hemorrhagic shock </li></ul></ul><ul><ul><li>First to describe the decrease in CVP and cardiac output associated with hemorrhage </li></ul></ul><ul><ul><ul><li>An Experimental Research into Surgical Shock (1899) </li></ul></ul></ul>
    • 5. Shock- Surgical Legacy <ul><li>Alfred Blalock </li></ul><ul><ul><li>Demonstrated the hypovolemia associated with hemorrhage resulted in: </li></ul></ul><ul><ul><ul><li>HYPOTENSION </li></ul></ul></ul><ul><ul><ul><li>METABOLIC ACIDOSIS </li></ul></ul></ul><ul><ul><ul><li>IMPAIRED OXYGEN DELIVERY TO TISSUES </li></ul></ul></ul><ul><ul><li>Physiologic derangements corrected by volume resuscitation </li></ul></ul>
    • 6. What is Shock? <ul><li>Inadequate provision of oxygen to peripheral tissues resulting from either insufficient perfusion or abnormal extraction of oxygen </li></ul><ul><li>Results in anaerobic metabolic pathways </li></ul>
    • 7. Shock- Pathophysiology <ul><li>In the setting of adequate oxygen: </li></ul><ul><ul><li>Glucose metabolized via citric acid cycle yielding a net of 36 ATP </li></ul></ul><ul><li>In the setting of inadequate oxygen: </li></ul><ul><ul><li>No citric acid cycle-lactate generated yielding 2 ATP </li></ul></ul>
    • 8. Shock- Anaerobic Metabolism <ul><li>Results in significant intracellular energy deficits: </li></ul><ul><ul><li>Cell membrane repair mechanisms altered </li></ul></ul><ul><ul><li>Electrolyte disturbances occur </li></ul></ul><ul><ul><li>Rupture of endoplasmic reticulum </li></ul></ul><ul><ul><li>Mitochondrial dysfunction occurs </li></ul></ul><ul><ul><li>Rupture of lysosomes </li></ul></ul>
    • 9. Shock and Reperfusion Injury <ul><li>Resuscitation and tissue reperfusion in this setting results in free radical generation </li></ul><ul><li>Can lead to cell death and organ dysfunction </li></ul>
    • 10. Shock and Metabolic Acidosis: Not A Good Thing <ul><li>Cardiac Effects: </li></ul><ul><ul><li>Blood flow is redistributed from endocardium to epicardium with potential myocardial dysfunction </li></ul></ul><ul><ul><li>Poor response to systemic catecholamines </li></ul></ul>
    • 11. Shock and Metabolic Acidosis: Not A Good Thing <ul><li>Pulmonary Effects </li></ul><ul><ul><li>Impairment of central respiratory drive </li></ul></ul><ul><li>CNS Effects </li></ul><ul><ul><li>Autoregulatory mechanisms of cerebral blood flow overridden with MAP &lt; 60 </li></ul></ul>
    • 12. Shock and Metabolic Acidosis: Not A Good Thing <ul><li>Renal Effects </li></ul><ul><ul><li>Afferent arteriolar vasoconstriction with RBF redistributed from cortex to medulla </li></ul></ul><ul><ul><li>GFR decreases: oliguria / anuria </li></ul></ul><ul><li>Gastrointestinal Effects </li></ul><ul><ul><li>Gut ischemia &gt; mucosal necrosis &gt; bacterial translocation </li></ul></ul>
    • 13. Shock- Systemic Compensatory Mechanisms <ul><li>Intravascular volume </li></ul><ul><li>Baroreceptor activity </li></ul><ul><li>Mechanoreceptor activity </li></ul>CNS Response Pituitary releases -ADH -ACTH Na/Water retention Cortisol released Sympathetic nervous stimulation <ul><li>Epinepherine </li></ul><ul><li>Norepinepherine </li></ul><ul><li>Renin/Angio/Aldo </li></ul>Enhanced cardiac function Peripheral vasoconstriction Na/Water retention Peripheral vasoconstriction
    • 14. Shock- Clinical Features <ul><li>Hypotension </li></ul><ul><li>Tachypnea </li></ul><ul><li>Oliguria / Anuria </li></ul><ul><li>Impaired Mental Status </li></ul><ul><ul><li>Depending upon cause, may also demonstrate </li></ul></ul><ul><li>Narrowing of pulse pressure </li></ul><ul><li>Tachycardia </li></ul>
    • 15. Shock- Management Priorities <ul><li>Airway adequacy </li></ul><ul><li>Breathing restoration </li></ul><ul><li>Circulatory support- method dependent upon cause of shock </li></ul>
    • 16. Shock - Resuscitation Endpoints <ul><li>Classic </li></ul><ul><ul><li>Restoration of blood pressure </li></ul></ul><ul><ul><li>Normalization of heart rate and urine output </li></ul></ul><ul><ul><li>Appropriate mental status </li></ul></ul><ul><li>Improved </li></ul><ul><ul><li>All of the above plus </li></ul></ul><ul><ul><li>Normalization of serum lactate levels </li></ul></ul><ul><ul><li>Resolution of base deficit </li></ul></ul>
    • 17. Shock- Judging the Adequacy of Resuscitation <ul><li>Monitor resuscitation with serial ABGs (attention to base deficit) and serum lactate levels. </li></ul>
    • 18. Shock Causality <ul><li>Hypovolemic </li></ul><ul><li>Cardiac Tamponade </li></ul><ul><li>Tension Pneumothorax </li></ul><ul><li>Cardiogenic </li></ul><ul><li>Neurogenic </li></ul><ul><li>Septic </li></ul>
    • 19. Approach to the Trauma Patient - Appropriate for Any Patient in Shock <ul><li>Triage </li></ul><ul><li>Primary Survey </li></ul><ul><li>Resuscitation </li></ul><ul><li>Secondary Survey </li></ul><ul><li>Monitoring and Re-evaluation </li></ul><ul><li>Definitive Care </li></ul>
    • 20. Initial Assessment of the Trauma Patient– Primary Survey <ul><li>A – AIRWAY with C-SPINE CONTROL </li></ul><ul><li>B – BREATHING </li></ul><ul><li>C – CIRCULATION with BLEEDING CONTROL </li></ul><ul><li>D – DISABILITY, NEUROLOGIC STATUS </li></ul><ul><li>E – EXPOSURE and ENVIRONMENT </li></ul><ul><li>Life threatening problems identified and managed simultaneously </li></ul>
    • 21. Hypovolemic Shock <ul><li>Must treat the source of hypovolemia and arrest ongoing fluid losses </li></ul><ul><li>The usual suspects: </li></ul><ul><ul><li>Thorax (CXR or CT) </li></ul></ul><ul><ul><li>Abdomen (CT or Ultrasound) </li></ul></ul><ul><ul><li>Pelvis (CT or plain film) </li></ul></ul><ul><ul><li>Retroperitoneal (CT) </li></ul></ul><ul><ul><li>Extremities – fractures or open wounds (plain films) </li></ul></ul><ul><li>All can be evaluated by operative intervention </li></ul>
    • 22. Initial Assessment – Radiographs <ul><li>Cervical spine </li></ul><ul><li>Chest </li></ul><ul><li>Pelvis </li></ul>
    • 23. Hypovolemic Shock <ul><li>Categorized by severity as Class I-IV </li></ul>
    • 24. Hypovolemic Shock <ul><li>Mainstay of therapy- Volume restoration </li></ul><ul><ul><li>Crystalloids </li></ul></ul><ul><ul><li>Colloids </li></ul></ul><ul><ul><ul><li>Blood </li></ul></ul></ul><ul><ul><ul><li>Plasma </li></ul></ul></ul><ul><ul><ul><li>Blood Substitutes </li></ul></ul></ul>
    • 25. Hypovolemic Shock – Basic Management Principles-1 <ul><li>Immediate and rapid administration of 2 liters warm Lactated Ringers through large bore peripheral IVs </li></ul><ul><li>Check for response to therapy </li></ul><ul><li>If no response, either: </li></ul><ul><ul><li>Not enough “treatment given” </li></ul></ul><ul><ul><li>Incorrect treatment </li></ul></ul>
    • 26. Hypovolemic Shock – Basic Management Principles-2 <ul><li>Consequently, repeat fluid bolus </li></ul><ul><li>Re-assess </li></ul><ul><li>If no response, either: </li></ul><ul><ul><li>Massive exsanguinating hemorrhage </li></ul></ul><ul><ul><li>Other causes: think Cardiogenic or Neurogenic in the trauma patient </li></ul></ul>
    • 27. Tension Pneumothorax
    • 28. Tension Pneumothorax <ul><li>Progressive entry of air into pleural space </li></ul><ul><li>Collapse of ipsilateral lung </li></ul><ul><li>Mediastinal shift </li></ul><ul><li>Compromised venous return to heart </li></ul><ul><li>Hypotension / decreased cardiac output </li></ul><ul><li>Cardiovascular collapse </li></ul><ul><li>Needle decompression / chest tube </li></ul>
    • 29. Tension Pneumothorax <ul><li>Hypotension </li></ul><ul><li>Absent breath sounds </li></ul><ul><li>Neck vein distension </li></ul><ul><li>Hyperresonant thoracic percussion note </li></ul><ul><li>Contralateral tracheal shift </li></ul><ul><li>Subcutaneous emphysema </li></ul><ul><li>Mechanism of injury </li></ul><ul><li>Clinical diagnosis </li></ul>
    • 30. Cardiogenic Shock <ul><li>The heart fails to deliver an adequate amount of blood to the body resulting in hypoperfusion of peripheral tissues </li></ul><ul><li>The heart cannot generate a sufficient stroke volume and cardiac output </li></ul><ul><li>Can be the result of impaired diastolic or systolic function or a combination of the two </li></ul>
    • 31. Cardiogenic Shock <ul><li>Most often due to myocardial ischemia or infarction or resultant complications of papillary muscle rupture or ventricular septal rupture </li></ul><ul><li>In trauma setting, think cardiac contusion in blunt force trauma and cardiac tamponade in penetrating trauma. </li></ul>
    • 32. Cardiogenic Shock- Basic Management Principles <ul><li>For pure “pump” failure, options include: </li></ul><ul><ul><li>Pharmacologic agents </li></ul></ul><ul><ul><li>Re-perfusion strategies </li></ul></ul><ul><ul><ul><li>Lytic agents </li></ul></ul></ul><ul><ul><ul><li>Stents </li></ul></ul></ul><ul><ul><ul><li>Coronary bypass </li></ul></ul></ul><ul><ul><li>Mechanical assists (Intra-aortic balloon) </li></ul></ul><ul><li>For tamponade physiology- surgery </li></ul>
    • 33. Cardiac Tamponade
    • 34. Penetrating Cardiac Injury
    • 35. Penetrating Cardiac Injuries <ul><li>Etiology usually knives or bullets on the streets, but </li></ul><ul><li>In the hospital lines, catheters </li></ul>
    • 36. Penetrating Cardiac Injuries <ul><li>Relative role of tamponade vs. severe hemorrhage determined by : </li></ul><ul><ul><li>Size of pericardial rent </li></ul></ul><ul><ul><li>Rate of bleeding from cardiac wound </li></ul></ul><ul><ul><li>Chamber of heart involved </li></ul></ul><ul><ul><li>STAB WOUNDS – TAMPONADE </li></ul></ul><ul><ul><li>GSW - BLEED </li></ul></ul>
    • 37. Penetrating Cardiac Injuries <ul><li>Tamponade Physiology: </li></ul><ul><ul><li>Blood accumulates in pericardium </li></ul></ul><ul><ul><li>Stroke volume decreases </li></ul></ul><ul><ul><li>Right atrial pressure increases </li></ul></ul><ul><ul><li>Right ventricle distends </li></ul></ul><ul><ul><li>Ventricular septum shifts to left </li></ul></ul><ul><ul><li>Left ventricle filling compromised </li></ul></ul><ul><ul><li>Cardiac output decreases, hypotension ensues </li></ul></ul>
    • 38. Penetrating Cardiac Injuries <ul><li>Pre-hospital : </li></ul><ul><ul><li>Get patient to hospital ASAP </li></ul></ul><ul><ul><li>Mattox / Feliciano study of 100 consecutive patients – if external CPR &gt; 3 minutes- 100% mortality </li></ul></ul><ul><li>Emergency department : </li></ul><ul><ul><li>Hemodynamics stable- ECHO +/- subxyphoid window </li></ul></ul><ul><ul><li>Hemodynamics unstable – ED thoracotomy / OR * </li></ul></ul>
    • 39. Neurogenic Shock <ul><li>A form of distributive shock caused by the sudden loss of CNS signals to vascular smooth muscle following spinal cord injury </li></ul><ul><li>Results in an immediate decrease in peripheral vascular resistance and hypotension </li></ul><ul><li>May be associated with normal heart rate or even bradycardia </li></ul>
    • 40. Neurogenic Shock Basic Management Principles <ul><li>Adequate oxygenation </li></ul><ul><li>Spine immobilization </li></ul><ul><li>Restore vasomotor tone after insuring adequate volume status </li></ul><ul><ul><li>Alpha agonist pharmacologic agents </li></ul></ul><ul><li>Often a role for early use of flow directed pulmonary artery catheter </li></ul>
    • 41. Septic Shock <ul><li>A type of distributive shock related to loss of vasomotor tone in response to severe systemic infection or inflammatory response </li></ul><ul><li>Results from release of multiple cellular mediators which stimulate a neurohormonal systemic response and influence vascular resistance </li></ul>
    • 42. Septic Shock <ul><li>Inadequate treatment can lead to ARDS and multiple organ failure </li></ul><ul><li>Mortality approaches 50% </li></ul>
    • 43. Septic Shock Basic Management Principles <ul><li>Remove the source of infection or nidus for unlimited inflammatory response </li></ul><ul><li>Antimicrobial therapy directed against offending organisms </li></ul><ul><li>Support organ function </li></ul><ul><li>Alpha agonists to maintain vasomotor tone </li></ul><ul><li>Aggressive use of flow directed pulmonary artery catheters </li></ul>
    • 44. Shock A Guide to Resuscitation Flow Directed Pulmonary Artery Catheter <ul><li>AKA the Swan- Ganz catheter, introduced into clinical practice in 1970 </li></ul><ul><li>Integrates cardiopulmonary physiologic data of the patient </li></ul><ul><li>Aides in determining appropriate theraputic interventions when cause of shock unknown </li></ul><ul><li>Allows resuscitation to physiologic endpoints </li></ul>
    • 45. Shock Flow Directed PA Catheters
    • 46. Shock The Role of the PA Catheter <ul><li>Most often used in conjunction with standard intravascular monitoring devices (central venous line, arterial line) , EKG and pulse oximetry </li></ul><ul><li>Provide both measured and calculated physiologic indices </li></ul>
    • 47. Shock The Role of the PA Catheter, etc <ul><li>Measured physiologic indices: </li></ul><ul><ul><li>Mean arterial pressure (a-line) </li></ul></ul><ul><ul><li>Heart rate (EKG, a-line) </li></ul></ul><ul><ul><li>Central venous pressure (CVL, PA catheter) </li></ul></ul><ul><ul><li>Pulmonary artery occlusion pressure, AKA the “wedge pressure” (PA catheter) </li></ul></ul><ul><ul><li>Oxygen saturation (pulse oximetry, ABG) </li></ul></ul>
    • 48. Shock The Role of the PA Catheter, etc <ul><li>The measured indices enable calculation of other parameters: </li></ul><ul><ul><li>Systemic Vascular Resistance </li></ul></ul><ul><ul><ul><li>[(MAP-CVP) x 80] / CO </li></ul></ul></ul><ul><ul><li>Stroke Volume </li></ul></ul><ul><ul><ul><li>CO / HR </li></ul></ul></ul><ul><ul><ul><li>Usually “indexed” by patient BSA (SV / BSA) </li></ul></ul></ul>
    • 49. Shock The Role of the PA Catheter, etc <ul><li>Invasive hemodynamic monitoring can provide insight into the principal determinants of CO and hence tissue perfusion: </li></ul><ul><ul><li>Preload : (CVP, better yet PAOP) </li></ul></ul><ul><ul><li>Afterload : (SVR and MAP) </li></ul></ul><ul><ul><li>Contractility : (SI) </li></ul></ul>
    • 50. Shock- How Can the PA catheter help? <ul><li>Hypovolemic shock- </li></ul><ul><ul><li>Low CO, low PAOP and CVP, high SVR </li></ul></ul><ul><li>Cardiogenic shock- </li></ul><ul><ul><li>Low CO, high PAOP and CVP, low SI </li></ul></ul><ul><li>Septic shock- </li></ul><ul><ul><li>High CO, low PAOP and CVP, low SVR </li></ul></ul>
    • 51. Shock The Role of the PA Catheter, etc <ul><li>Therapy can be directed where intervention needed: </li></ul><ul><ul><li>Inadequate Preload = Hypovolemia </li></ul></ul><ul><ul><ul><li>Volume- either crystalloids or colloids depending upon patient Hb and coagulation parameters </li></ul></ul></ul><ul><ul><li>Excess Preload = Congestive Heart Failure </li></ul></ul><ul><ul><ul><li>Diuretics +/- Inotropes </li></ul></ul></ul>
    • 52. Shock The Role of the PA Catheter, etc <ul><li>Therapy can be directed where intervention needed: </li></ul><ul><ul><li>Inadequate afterload = neurogenic or septic shock </li></ul></ul><ul><ul><ul><li>Alpha agonists AKA Pressors (Norepinephrine or Neosynephreine) </li></ul></ul></ul><ul><ul><li>Excessive afterload = Hypertensive CVD </li></ul></ul><ul><ul><ul><li>Vasodilators ( Sodium Nitroprusside, Nitroglycerine) </li></ul></ul></ul>
    • 53. Shock The Role of the PA Catheter, etc <ul><li>Therapy can be directed where intervention needed: </li></ul><ul><ul><li>Inadequate contractility = cardiogenic shock </li></ul></ul><ul><ul><ul><li>Beta agonists AKA Inotropes </li></ul></ul></ul><ul><ul><ul><ul><li>Epinepherine </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Dobutamine (good if increased afterload as well) </li></ul></ul></ul></ul>
    • 54. Shock- Pitfalls in Management <ul><li>Assuming blood pressure equates to cardiac output </li></ul><ul><li>Extremes of age </li></ul><ul><li>Hypothermia </li></ul><ul><li>Athletes </li></ul><ul><li>Pregnancy </li></ul><ul><li>Medications / Pacemakers </li></ul>
    • 55. Points for the Student <ul><li>Understand the rationale for the pitfalls in shock management as listed on slide </li></ul><ul><li>What is the optimal and most efficient diagnostic modalities for the patient with presumed hypovolemic shock? </li></ul><ul><li>Understand the clinical features of the 6 major causes of shock. </li></ul><ul><li>Trivia question: Who is depicted on the slide “Penetrating Cardiac Injury” ? </li></ul>
    • 56. Patient Scenario - 1 <ul><li>42 yo woman ejected from car following collision with a tree. Pre-hospital data: </li></ul><ul><ul><li>HR 110 BP 88/46 RR 26 </li></ul></ul><ul><ul><li>Confused, skin cold and clammy </li></ul></ul><ul><li>Is she in shock? If so what are potential etiologies? How do we assess and treat? </li></ul>
    • 57. Patient Scenario - 2 <ul><li>42 yo woman involved in MVC arrives in ED with full spine protection and supplement oxygen </li></ul><ul><ul><li>HR 120 BP 80 /46 RR 32 </li></ul></ul><ul><li>Is she in shock? If so what are potential etiologies? How do we assess and treat? </li></ul>
    • 58. Patient Scenario - 2 <ul><li>After 2000cc warm lactated Ringers: </li></ul><ul><ul><li>HR 90 BP 110 / 80 RR 22 </li></ul></ul><ul><li>How has the patient responded? What are the diagnostic implications? </li></ul>
    • 59. Patient Scenario - 2 <ul><li>What if the same patient, after 2000cc warm lactated Ringers: </li></ul><ul><ul><li>HR 130 BP 80 / 60 RR 40 </li></ul></ul><ul><li>Clinical interpretation? </li></ul>
    • 60. Patient Scenario - 3 <ul><li>18 yo man stabbed in the left chest with large kitchen knife </li></ul><ul><ul><li>BP 80 / 60 HR 130 RR 30 </li></ul></ul><ul><li>Is he in shock ? Diagnostic possibilities ? How do you quickly evaluate and treat ? </li></ul>
    • 61. Patient Scenario - 4 <ul><li>56 yo man now 6 days after undergoing a left hemicolectomy for cancer. Develops oliguria and altered sensorium. Transferred to the ICU- PA catheter placed </li></ul><ul><li>Several hours later, patient is hypotensive BP 80 / 60 HR 140 </li></ul><ul><li>What are the diagnostic possibilities ? What would the PA catheter data look like for the various diagnostic possibilities? </li></ul>

    ×