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Shock -Carew (1).ppt

  1. Shock Julye N. Carew, M.D. December 9, 2005
  2. Shock  Definition  Clinical Evaluation  Cardiogenic Shock  Hypovolemia  Sepsis  Management of septic shock
  3. Sepsis mortality Dellinger, Crit Care Med, 2003
  4. Definition  Often misdefined as “hypotension”  Multisystem end-organ hypoperfusion and hypoxia with lactic acidosis commonly seen  Hypotension  Tachycardia  Tachypnea  Cool skin and extremities  Altered mental status  Oliguria/Anuria
  5. Clinical Evaluation  Patients are commonly hypotensive  Initial evaluation should begin with identification of adequate cardiac output (CO)  DIMINISHED—narrow pulse pressure, cool extremities and delayed capillary refill  INCREASED– widened pulse pressure, warm extremities, bounding pulses and rapid capillary refill  Pulse pressure is a surrogate for SV
  6. Clinical Evaluation  MAP= CO X SVR  CO= SV X HR  Pulse pressure is a surrogate for stroke volume: Increased in high output states, Reduced in hypovolemia and cardiogenic shock
  7. Clinical Evaluation  Jugular venous pulse  Cardiac gallop  Edema  Rales  CXR—cardiomegaly, Kerley B lines, pulmonary edema
  8. CHF Murray and Nadel, Textbook of Resp. Medicine, 4th ed
  9. Clinical Evaluation  Fever  Leukocytosis/leukopenia  Pancreatitis, hepatic failure, burns, anaphylaxis, thyrotoxicosis  Evidence of GI blood loss, diarrhea, vomiting, polyuria
  10. Resuscitation  Few minutes to complete history and physical examination  Begin aggressive, early resuscitation to establish perfusion and minimize end- organ damage  ABCs Ventilatory failure due to increased load on respiratory system– LA, pulmonary edema, inadequate perfusion to RR muscles
  11. Resuscitation  Aggressive IVFs in patients with decreased volume status, sepsis  Crystalloid is preferred, may be increased mortality with colloid  Early administration of vasoactive drugs in hypovolemic patient is not recommended  Transfusion of PRBCs to hemoglobin of 7 g/dL  GOAL IS OXYGEN DELIVERY AND END ORGAN FUNCTION, not BP– mental status, UOP
  12. Resuscitation  If evidence of hypoperfusion persists, then consider vasoactive drugs and invasive monitoring (PA catheter), echocardiography, etc.
  13. Cardiogenic Shock  Cardiac output is low despite adequate venous return (RAP) 50-80% mortality  Systolic dysfunction  Diastolic dysfunction  Valvular disease  Right heart failure  “Other”
  14. Systolic dysfunction  Most common cause is acute coronary ischemia  Starling mechanism of compensation—and by fluid retention and increase in sympathetic tone  Cardiogenic shock reported to complicate 10% of all acute MI  Inotropes, intra-aortic balloon pump  No data to suggest that lytics improve mortality (Col, et al, 1994)
  15. Cardiogenic Shock  Improved mortality with early revascularization—PTCA and CABG  Hochman, et al. 1999 randomized 152 patients to revascularization (PTCA or CABG) vs. medical therapy alone  Six-month mortality was 50.3 vs. 63.1% (P=0.027). Treatment benefit was only achieved in those younger than 75 years
  16. Diastolic dysfunction  VERY common phenomenon, less likely to cause frank shock  LV chamber stiffness with impaired LV filling  May be difficult to treat  Inotropes may be ineffective  Aggressive management of tachycardia with volume administration and negative chonotropic agents. NSR very important
  17. Valvular Disease  AS– decrease HR, NSR, NO afterload reduction  AI– use of chronotropic agents to decrease regurgitant filling time and afterload reduction  MR– NSR, afterload reduction  MS—negative chronotropic agents to maximize diastolic filling time  ARRYTHMIAS
  18. Right heart failure Murray and Nadel, Textbook of Resp. Medicine
  19. Right Ventricular Failure  Most common cause is concominant LV failure  Elevated JVP with clear lungs, LE edema  PE, ARDS, RV infarction  Volume administration, Dobutamine and NE  Treat underlying condition—eg., Lytic therapy
  20. “Others”  Cardiac tamponade (Kussmaul’s sign=increased JVP with inspiration, pulsus and RAP=RVP=PCWP  Pericardial effusion, tension pneumothorax, ascites, pneumopericardium, large pleural effusions
  21. Hypovolemia  GI blood loss, trauma, coagulopathy  Aggressive volume resuscitation with large volumes of crystalloid and blood products  “Wigger’s preparation”  1. several hours of severe hypotension produced “irreversible shock”  2. ECF deficit could be corrected with administration of crystalloid in volumes 2-3X blood loss “3:1 rule” Wiggers, NY Commonwealth Fund, 1950.
  22. Hypovolemia  More recent studies suggest that more moderate volume repletion with crystalloid is preferable (Kaweski,1990. Bickell, 1994)  Mechanism? Interference of effective thrombus and continued secondary hemorrhage  Bottom line: Volume resuscitate, correct coagulopathy, fix the underlying problem
  23. Septic shock  Infection with state of hypoperfusion and end- organ damage  SIRS, sepsis, severe sepsis, septic shock  High cardiac output state  Widened pulse pressure, warm extremities, brisk capillary refill  Subgroup of patients with depressed cardiac function (myocardial depressant factors)-- ?NE and dobutamine
  24. Septic shock  Sepsis is the leading cause of death in non-CCUs, 750,000 cases/year  Unregulated inflammation and a hypercoagulable state favoring microvascular coagulation  ARF carries a poorer prognosis  >80% of patients will require mechanical ventilation
  25. D e l Dellinger, Crit Care Med 2004.
  26. Septic Shock  Society of CC Medicine wrote consensus opinion on recommendations treatment of septic shock, 2004  Graded recommendations based upon available data  Grade A- at least two level I studies (large, randomized with clear results)  Grade B- one level I study  Grade C- level II investigations (small, randomized with uncertain results)  Grade D- at least one level III (nonrandomized)  Grade E- level IV and V support (historical controls, expert opinion; case series) Dellinger,Crit Care Med, 2004
  27. Reommendations for treatment of septic shock  Resuscitation (B): CVP 8- 12 mmHg MAP>65 mm Hg UOP > 0.5 ml/kg/hr Mixed venous> 70%  Diagnosis (D): Appropriate cultures prior to ABX therapy  Antibiotics (E and D): Begun within 1 hour and cover appropriate organisms (eg. Neutropenia)  Source Control (E): drain abscesses and removed infected devices  Fluids (C and E): crystalloid or colloid, 1 L over 30 minutes and repeat if necessary Dellinger, Crit Care Med, 2004
  28. Treatment of septic shock  Vasopressors:  1. DA or NE (D)  2. NO low-dose DA for “renal protection”(B)  3. Vasopressin in refractory patients(E) Dellinger, Crit Care Med, 2004
  29. Recommendations for treatment of septic shock  Inotropes (E and A): patients with low CO—try dobutamine, a pre-defined CI is not recommended Dellinger, Crit Care Med, 2004
  30. Treatment of septic shock  Steroids:  1. Stress-dose hydrocortisone in refractory shock for 7 days  2. ACTH stimulation test (E)  3. DO NOT use doses >300 mg/day (A)  4. In the absence of shock steroids should not be used, except for usual dose or if adrenal insufficiency is suspected (E) Dellinger, Crit Care Med, 2004
  31. Treatment of septic shock  rhAPC: for those at high risk of death (APACHE>25, MOFS, shock) without contraindication (B)  Blood products: 1.Transfuse PRBCs only when Hgb<7 (B) 2. No routine EPO (B) 3. No FFP (E) or AT3 (B) 4. PLT for PLT<5000 (E)  Mechanical ventilation: 1. Low tidal volume (6 cc/kg), plateau pressures<30 (B) 2. Hypercarbia is acceptable to reduce plateau pressure (C) 3. PEEP to lower FiO2(E) 4. Keep patients at 45 degrees to prevent VAP (C) 5. Weaning protocol and spontaneous breathing trials (A) Dellinger, Crit Care Med, 2004
  32. Treatment of septic shock  Sedation:  1. Sedation protocols and scales should be used (B)  2. Bolus vs. continuous with daily interruptions (B)  3. NM blockers should be avoided, but if necessary train of four should be followed (E)  Modified Ramsey Sedation Scale. 1. Anxious, Agitated, Restless 2. Cooperative, Oriented, Tranquil Accepts mechanical ventilation. 3. Responds to commands only 4. Brisk response to light glabellar tap or loud noise. 5. Sluggish response to light glabellar tap or loud noise. 6. No Response. Dellinger, Crit Care Med, 2004
  33. Treatment of Septic Shock  Glucose Control: Maintain CBG<150 (D), enteral feeding preferable (E)  Renal Replacement: CVVH and intermittent HD are equivalent in hemodynamically stable patients (B)  Bicarbonate: NOT recommended for pH>7.15 (C)  DVT prophylaxis:YES!!! (A)  Ulcer prophylaxis: YES!!! (A)`
  34. Hydrocortisone  Oppert, et al. (German) looked at 41 patients with septic shock  18 received hydrocortisone 50 mg bolus followed by 0.18 mg/kg/hr (70 kg would receive 350 mg/24 hours), 23 placebo  Primary endpoints: duration of shock, reduction in pro-inflammatory cytokines
  35. Hydrocortisone Oppert, Crit Care Med, 2005
  36. Hydrocortisone Oppert, Crit Care Med, 2005
  37. Hydrocortisone Oppert, Crit Care Med, 2005
  38. Hydrocortisone  Not adequate power to determine mortality benefit  Showed a trend toward better outcome with ACTH responders  The jury is still out
  39. Vasopressors  Sharshar, et al. Looked at circulating vasopressin levels in septic shock  Found that plasma vasopressin levels were almost always increased at the initial phase of septic shock and decrease afterward. Vasopressin deficiency was seen in 1/3 of late septic shock patients  I use vasopressin for patients who do not initially respond to NE (dose .04 units/min)
  40. The End!!