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EM Clerkship: Diagnosis and Treatment of Shock
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Goals and objectives Definition of shock Understand the basic physiology of shock Understand the different types of shock Understand acute management of shock
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“A momentary pause in the act of death” JC Warren – 1895 “A rude unhinging of the machinery of life” SG Gross - 1872 WHAT IS SHOCK?
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What is Shock? A physiologic state characterized by Decrease in tissue perfusion Inadequate oxygen delivery to meet metabolic needs BP is in classic definition suboptimal
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Oxygen Transport 5 L/min CO Venous Oxygen Delivery SvO2 = 75% Oxygen Consumption (V02) 250 mL/min 1000 mL/min Arterial Oxygen Delivery (DO2) 200 mL/L (20% Vol) SaO2 = 100% Arterial Oxygen Content Oxygen Extraction 25% 750 mL/min Venous Oxygen Content
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Classification Hypovolemic Distributive Cardiogenic Obstructive Non-hemorrhagic Hemorraghic Neurogenic Septic shock Anaphylaxis
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Case 1 27 y/o male crashed his motorcycle at a high rate of speed VS: BP 80/ palp HR 122 Physical Exam: pt. is diaphoretic, agitated, abdomen is tense and distended
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Hemorrhagic Shock: Epidemiology 30k deaths annually (U.S.) –50% in 1 st few minutes –Remaining deaths die < 12hr –>12 hr, generally not due to hemorrhage Leading cause of death age 1-44 In the next 30 min. (U.S.) –6 people will die –1000 people will have a disabling injury –$24 million will be spent on these patients
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Hemorrhagic Shock: how would they present ? Tachycardia Tachypnea Weak / thready pulse Hypotension Cool & Clammy Anxiety ↓↓ Urine output
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Hemorrhagic Shock: immediate actions? ABCs STOP THE BLEEDING!!!!!! 2 large bore IV’s (14 or 16 gauge) Fluid resuscitation until SBP > 100mmHg –2L initial infusion Consider blood products
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Case 2 18 y/o male diving into lake Friends say he dove into shallow area Was initially unresponsive but now complaining of inability to feel his legs BP 70/40 HR 40’s What kind of shock does this patient have
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Neurogenic Shock Functional hypovolemia w/o compensation Paralysis of sympathetic chain controlling vascular tone Distributive shock Occurs in pts w/SCI above T6 ↓SVR & bradycardia from unopposed parasympathetic input to SA node
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Neurogenic Shock Clinical Triad Hypotension Bradycardia Hypothermia
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Immediate management? Volume Resuscitation (1-2 L) Vasopressors –Norepinephrine –Phenylephrine Avoid vagal stimulation Atropine 0.5mg IV Rule out other forms of shock before considering neurogenic shock as a diagnosis
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Case 3 77 y/o female c/o increased lethargy, confusion. Vitals: BP 90/40 HR 110, Temp:38.9
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Immediate actions at this time? ABCs IV fluids Critical labs :Lactate Give BROAD Spectrum antibiotics Assess fluid status/hemodynamic monitoring (CVP,US,Art line)
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Sepsis 750,000 cases/yr of severe sepsis in US 215,000 deaths/yr directly related to sepsis Tenth leading cause of death in USA Rate of sepsis cases is increasing faster than the population 37% of severe sepsis patients come through the ED
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SIRS S ystemic I nflammtory R esponse S yndrome Systemic response to insult resulting in ≥2 of the following -Temp > 38 C or < 35 C -HR ≥ 90 bpm -RR > 20 breaths per minute or paC02 < 32 mm Hg -WBC > 12,000 or 10% bands
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Interrelation between SIRS, Sepsis and Infection Bone et al Chest 1992
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INSULT SIRS Sepsis Severe Sepsis Septic Shock ED to ICU: a continuum…. SIRS w/ presumed or confirmed infection Sepsis with ≥1 sign of organ failure Sepsis w/ Refractory hypotension despite fluid rescucitation Bone et al Chest 1992
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Early Goal Directed Therapy ( in a nutshell…) Early aggressive management of severe sepsis/septic shock Early aggressive fluid resuscitation coupled with early initiation of broad spectrum antibiotics Intensive hemodynamic monitoring and optimization
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Severe sepsis confirmed Supplemental oxygen ± endotracheal intubation and mechanical ventilation Central venous and arterial catheterization CVP Crystalloid Colloid <8 mm Hg MAP 8-12 mm Hg Vasopressor <65 mm Hg >90 mm Hg ScvO 2 ≥65 and ≤90 mm Hg Goals achieve d ≥70% Hospital admission Yes No Sedation and/or paralysis (if intubated) Transfusion of red cells to hematocrit ≥30% <70% Dobutamine <70% ≥70% Edwards Lifesciences Rivers et al NEJM 2001 In hospital mortality/ 30 day mortality and 60 day mortality show %16 benefit in EGDT treatment group
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Case 4 26 y/o female Presents to ED in acute respiratory distress from cafeteria HEENT-swollen lips Lungs-diminshed bilateral CV-tachycardic Abd-soft Ext- diffuse erythematous rash HR 118 BP 80/40 What would you immediately do now?
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Anaphylaxis Generally IgE- mediated reactions w/release of mast cell products Chemical mediators vaso-active –smooth muscle spasm –bronchospasm –mucosal edema –inflammation –increased capillary permeability Incidence of anaphylaxis w/shock- 8:100,000 –10% food –18% drugs –59% invenomations/insect Yocurn et al J Clin Imm 1999
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Anaphylaxis: Immediate Management Epinephrine Dose –0.2-0.5 ml of 1:1000 dilution IM –0.1mg (1:10,000 dilution) IV in severe cases Antihistamines –H1 (Diphenhydramine 50mg IV) –H2 (Ranitadine 300mg IV) Intubate early if needed Corticosteroids (Decadron 10mg IV) –20% of patients will have recurrent sxs w/in 8hrs
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Case #5 56 y/o male Presents cool clammy diaphoretic after clutching his chest and dropping to the floor BP 60/palp HR 100 Lungs: diffuse crackles throughout HEENT- prominent JVD Cardiac exam- holosystolic murmur at apex Ext: cool
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Cardiogenic shock Most common etiology is acute myocardial infarction >40% of myocardium effected 6-8% of all AMI Mortality of 80%
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Cardiogenic Shock: how would this patient present? Cyanotic, ashen Cool extremities Diaphoretic Feeble pulses +/- confusion JVD Pulmonary rales Murmurs –S3 (ventricular gallop) –S4 (atrial gallop) Systolic murmur –MR –Ventricular rupture –Both may occur w/o murmur
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Cardiogenic Shock: Other Etiologies Complications of MI: –Papillary Mm Rupture –Ventricular aneurysm –Ventricular septal rupture Other causes: –Cardiomyopathies –Tamponade –Tension pneumothorax –Arrhythmias –Valve disease –Aortic dissection
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Cardiogenic shock management? Airway managment (intubate if necessary) If due to AMI -ASA -Heparin -NTG *Fluid bolus challenge Inotropes -dobutamine –if SBP >70mmhg -dopamine- if SBP < 70 mmhg
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Management of Cardiogenic Shock: AHA/ACC Recommendation Early revascularization is a Class I recommendation for ST elevation/Q wave or new LBBB acute MI. If due to mechanical complications VSD/ruptured valve- Intraoartic balloon pump and early surgical repair
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Case #6 50 y/o male with a 40 pack year of smoking presents with acute onset shortness of breath while taking a drag off a cigarette. VS HR 120, BP 80/40, sat 99% EXAM: right lung breath sounds absent What is the most likely diagnosis?
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What are your immediate actions ? Needle decompression Chest tube thoracostomy
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Obstructive shock Mechanical obstruction causing impaired filling or emptying of the heart or great vessels what are other mechanisms to develop obstructive shock? cardiac tamponade massive pulmonary embolism
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Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index
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Summary Common factor in ALL forms of shock is global tissue hypoperfusion Early recognition of shock is vital Aggressive correction and monitoring of patients in shock can improve outcomes
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