• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content







Total Views
Views on SlideShare
Embed Views



6 Embeds 34

http://blackboard.butte.edu 11
https://blackboard.butte.edu 9
http://www.slideshare.net 7
http://www.uab.edu 5
http://elearning.kctcs.edu 1
http://elearning.alvernia.edu 1



Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

S S Presentation Transcript

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