9572195.ppt

1. EM Clerkship: Diagnosis and Treatment of Shock

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

3.  “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?

4. 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

5. 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

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

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

8. 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

9. Hemorrhagic Shock: Epidemiology • 30k deaths annually (U.S.) – 50% in 1st 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

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

11. 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

13. 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

14. 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

15. Neurogenic Shock Clinical Triad • Hypotension • Bradycardia • Hypothermia

16. 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

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

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

20. 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

21. 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 < 4,000 mm3 or > 10% bands

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

23. 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

24. 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

25. 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 ScvO2 ≥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

27. 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?

28. 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

29. 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

31. 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

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

33. 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

34. 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

35. 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

36. 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

38. 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?

39. What are your immediate actions ? • Needle decompression • Chest tube thoracostomy

40. 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

42. 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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