EM Clerkship: Diagnosis and Treatment of Shock

Goals and objectives Definition of shock Understand the basic physiology of shock Understand the different types of shock Understand acute management of shock

“A momentary pause in the act of death” JC Warren – 1895 “A rude unhinging of the machinery of life” SG Gross WHAT IS SHOCK?

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

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

Classification Hypovolemic Distributive Cardiogenic Obstructive Non-hemorrhagic Hemorraghic Neurogenic Septic shock Anaphylaxis

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

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

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

Hemorrhagic Shock: how would they present ? Tachycardia Tachypnea Weak / thready pulse Hypotension Cool & Clammy Anxiety ↓↓ Urine output

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

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

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

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

Neurogenic Shock Clinical Triad Hypotension Bradycardia Hypothermia

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

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

Case 3 77 y/o female c/o increased lethargy, confusion. Vitals: BP 90/40 HR 110, Temp:38.9

Immediate actions at this time? ABCs IV fluids Critical labs :Lactate Give BROAD Spectrum antibiotics Assess fluid status/hemodynamic monitoring (CVP,US,Art line)

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

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

Interrelation between SIRS, Sepsis and Infection Bone et al Chest 1992

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

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

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

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

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?

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

Anaphylaxis: Immediate Management Epinephrine Dose – 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

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

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

Cardiogenic shock Most common etiology is acute myocardial infarction >40% of myocardium effected 6-8% of all AMI Mortality of 80%

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

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

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

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

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

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?

What are your immediate actions ? Needle decompression Chest tube thoracostomy

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

Shock Physiology CVPSVRCO/CI Hypovolemic Cardiogenic Distributive Obstructive CVP: Central Venous Pressure, SVR: Systemic Vascular Resistance CO/CI: Cardiac Output/Index

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