Shock Evaluation and Management J. Carew

Shock Julye N. Carew, M.D. December 9, 2005 Shock  Definition  Clinical Evaluation  Cardiogenic Shock  Hypovolemia  Sepsis  Management of septic shock Sepsis mortality Dellinger, Crit Care Med, 2003 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 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 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 Clinical Evaluation  Jugular venous pulse  Cardiac gallop  Edema  Rales  CXR—cardiomegaly, Kerley B lines, pulmonary edema CHF Murray and Nadel, Textbook of Resp. Medicine, 4th ed Clinical Evaluation  Fever  Leukocytosis/leukopenia  Pancreatitis, hepatic failure, burns, anaphylaxis, thyrotoxicosis  Evidence of GI blood loss, diarrhea, vomiting, polyuria Resuscitation  Few minutes to complete history and physical examination  Begin aggressive, early resuscitation to establish perfusion and minimize endorgan damage  ABCs Ventilatory failure due to increased load on respiratory system– LA, pulmonary edema, inadequate perfusion to RR muscles 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 Resuscitation  If evidence of hypoperfusion persists, then consider vasoactive drugs and invasive monitoring (PA catheter), echocardiography, etc. Cardiogenic Shock  Cardiac output is low despite adequate venous return (RAP) 50-80% mortality  Systolic dysfunction  Diastolic dysfunction  Valvular disease  Right heart failure  ―Other‖ 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) 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 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 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 Right heart failure Murray and Nadel, Textbook of Resp. Medicine 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 ―Others‖  Cardiac tamponade (Kussmaul’s sign=increased JVP with inspiration, pulsus and RAP=RVP=PCWP  Pericardial effusion, tension pneumothorax, ascites, pneumopericardium, large pleural effusions 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. 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 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 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 D Dellinger, Crit Care Med 2004. e l 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 Reommendations for treatment of septic shock  Resuscitation (B): CVP 8 Source Control (E): drain 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) 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 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 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 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 Treatment of septic shock  rhAPC: for those at high  Mechanical ventilation: 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) 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 Treatment of septic shock  Sedation:  1. Sedation protocols and  Modified Ramsey Sedation Scale. 1. Anxious, Agitated, Restless 2. Cooperative, Oriented, Tranquil Accepts mechanical ventilation. 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) 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 Treatment of Septic Shock  Glucose Control:  Bicarbonate: NOT Maintain CBG<150 (D), enteral feeding preferable (E)  Renal Replacement: CVVH and intermittent HD are equivalent in hemodynamically stable patients (B) recommended for pH>7.15 (C)  DVT prophylaxis:YES!!! (A)  Ulcer prophylaxis: YES!!! (A)` 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 Hydrocortisone Oppert, Crit Care Med, 2005 Hydrocortisone Oppert, Crit Care Med, 2005 Hydrocortisone Oppert, Crit Care Med, 2005 Hydrocortisone  Not adequate power to determine mortality benefit  Showed a trend toward better outcome with ACTH responders  The jury is still out 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) The End!!