Shock Julye N. Carew, M.D. December 9, 2005. Shock  Definition  Clinical Evaluation  Cardiogenic Shock  Hypovolemia  Sepsis  Management of septic

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Sepsis mortality Dellinger, Crit Care Med, 2003

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<ul><li><p>ShockJulye N. Carew, M.D.December 9, 2005</p></li><li><p>ShockDefinitionClinical Evaluation Cardiogenic ShockHypovolemiaSepsisManagement of septic shock</p></li><li><p>Sepsis mortalityDellinger, Crit Care Med, 2003</p></li><li><p>DefinitionOften misdefined as hypotensionMultisystem end-organ hypoperfusion and hypoxia with lactic acidosis commonly seenHypotensionTachycardiaTachypneaCool skin and extremitiesAltered mental statusOliguria/Anuria</p></li><li><p>Clinical EvaluationPatients are commonly hypotensiveInitial evaluation should begin with identification of adequate cardiac output (CO)DIMINISHEDnarrow pulse pressure, cool extremities and delayed capillary refillINCREASED widened pulse pressure, warm extremities, bounding pulses and rapid capillary refillPulse pressure is a surrogate for SV</p></li><li><p>Clinical EvaluationMAP= CO X SVRCO= SV X HR</p><p>Pulse pressure is a surrogate for stroke volume: Increased in high output states, Reduced in hypovolemia and cardiogenic shock</p></li><li><p>Clinical EvaluationJugular venous pulseCardiac gallopEdemaRalesCXRcardiomegaly, Kerley B lines, pulmonary edema</p></li><li><p>CHFMurray and Nadel, Textbook of Resp. Medicine, 4th ed</p></li><li><p>Clinical EvaluationFeverLeukocytosis/leukopeniaPancreatitis, hepatic failure, burns, anaphylaxis, thyrotoxicosis</p><p>Evidence of GI blood loss, diarrhea, vomiting, polyuria</p></li><li><p>ResuscitationFew minutes to complete history and physical examinationBegin aggressive, early resuscitation to establish perfusion and minimize end-organ damageABCs Ventilatory failure due to increased load on respiratory system LA, pulmonary edema, inadequate perfusion to RR muscles</p></li><li><p>ResuscitationAggressive IVFs in patients with decreased volume status, sepsisCrystalloid is preferred, may be increased mortality with colloidEarly administration of vasoactive drugs in hypovolemic patient is not recommendedTransfusion of PRBCs to hemoglobin of 7 g/dLGOAL IS OXYGEN DELIVERY AND END ORGAN FUNCTION, not BP mental status, UOP</p></li><li><p>ResuscitationIf evidence of hypoperfusion persists, then consider vasoactive drugs and invasive monitoring (PA catheter), echocardiography, etc.</p></li><li><p>Cardiogenic ShockCardiac output is low despite adequate venous return (RAP) 50-80% mortalitySystolic dysfunctionDiastolic dysfunctionValvular diseaseRight heart failureOther</p></li><li><p>Systolic dysfunctionMost common cause is acute coronary ischemiaStarling mechanism of compensationand by fluid retention and increase in sympathetic toneCardiogenic shock reported to complicate 10% of all acute MIInotropes, intra-aortic balloon pumpNo data to suggest that lytics improve mortality (Col, et al, 1994)</p></li><li><p>Cardiogenic ShockImproved mortality with early revascularizationPTCA and CABGHochman, et al. 1999 randomized 152 patients to revascularization (PTCA or CABG) vs. medical therapy aloneSix-month mortality was 50.3 vs. 63.1% (P=0.027). Treatment benefit was only achieved in those younger than 75 years</p></li><li><p>Diastolic dysfunctionVERY common phenomenon, less likely to cause frank shockLV chamber stiffness with impaired LV fillingMay be difficult to treatInotropes may be ineffectiveAggressive management of tachycardia with volume administration and negative chonotropic agents. NSR very important</p></li><li><p>Valvular DiseaseAS decrease HR, NSR, NO afterload reductionAI use of chronotropic agents to decrease regurgitant filling time and afterload reductionMR NSR, afterload reductionMSnegative chronotropic agents to maximize diastolic filling timeARRYTHMIAS</p></li><li><p>Right heart failureMurray and Nadel, Textbook of Resp. Medicine</p></li><li><p>Right Ventricular FailureMost common cause is concominant LV failureElevated JVP with clear lungs, LE edemaPE, ARDS, RV infarctionVolume administration, Dobutamine and NETreat underlying conditioneg., Lytic therapy</p></li><li><p>OthersCardiac tamponade (Kussmauls sign=increased JVP with inspiration, pulsus and RAP=RVP=PCWPPericardial effusion, tension pneumothorax, ascites, pneumopericardium, large pleural effusions</p></li><li><p>Hypovolemia GI blood loss, trauma, coagulopathyAggressive volume resuscitation with large volumes of crystalloid and blood productsWiggers 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</p><p>Wiggers, NY Commonwealth Fund, 1950.</p></li><li><p>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</p></li><li><p>Septic shockInfection with state of hypoperfusion and end-organ damageSIRS, sepsis, severe sepsis, septic shockHigh cardiac output stateWidened pulse pressure, warm extremities, brisk capillary refillSubgroup of patients with depressed cardiac function (myocardial depressant factors)-- ?NE and dobutamine</p></li><li><p>Septic shockSepsis is the leading cause of death in non-CCUs, 750,000 cases/yearUnregulated inflammation and a hypercoagulable state favoring microvascular coagulationARF carries a poorer prognosis&gt;80% of patients will require mechanical ventilation</p></li><li><p>DelliDellinger, Crit Care Med 2004.</p></li><li><p>Septic ShockSociety of CC Medicine wrote consensus opinion on recommendations treatment of septic shock, 2004Graded 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)</p><p>Dellinger,Crit Care Med, 2004</p></li><li><p>Reommendations for treatment of septic shockResuscitation (B): CVP 8-12 mmHg MAP&gt;65 mm Hg UOP &gt; 0.5 ml/kg/hr Mixed venous&gt; 70%Diagnosis (D): Appropriate cultures prior to ABX therapyAntibiotics (E and D): Begun within 1 hour and cover appropriate organisms (eg. Neutropenia)</p><p>Source Control (E): drain abscesses and removed infected devicesFluids (C and E): crystalloid or colloid, 1 L over 30 minutes and repeat if necessary</p><p>Dellinger, Crit Care Med, 2004</p></li><li><p>Treatment of septic shockVasopressors:1. DA or NE (D)2. NO low-dose DA for renal protection(B)3. Vasopressin in refractory patients(E)</p><p>Dellinger, Crit Care Med, 2004</p></li><li><p>Recommendations for treatment of septic shockInotropes (E and A): patients with low COtry dobutamine, a pre-defined CI is not recommended</p><p>Dellinger, Crit Care Med, 2004</p></li><li><p>Treatment of septic shockSteroids:1. Stress-dose hydrocortisone in refractory shock for 7 days 2. ACTH stimulation test (E)3. DO NOT use doses &gt;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)</p><p>Dellinger, Crit Care Med, 2004</p></li><li>Treatment of septic shockrhAPC: for those at high risk of death (APACHE&gt;25, MOFS, shock) without contraindication (B)Blood products: 1.Transfuse PRBCs only when Hgb</li><li><p>Treatment of septic shockSedation: 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)</p><p>Modified Ramsey Sedation Scale.</p><p>1. Anxious, Agitated, Restless</p><p>2. Cooperative, Oriented, TranquilAccepts mechanical ventilation.</p><p>3. Responds to commands only</p><p>4. Brisk response to light glabellar tap or loud noise.</p><p>5. Sluggish response to light glabellar tap or loud noise.</p><p>6. No Response.</p><p>Dellinger, Crit Care Med, 2004</p></li><li><p>Treatment of Septic ShockGlucose Control: Maintain CBG7.15 (C)DVT prophylaxis:YES!!! (A)Ulcer prophylaxis: YES!!! (A)`</p></li><li><p>HydrocortisoneOppert, et al. (German) looked at 41 patients with septic shock18 received hydrocortisone 50 mg bolus followed by 0.18 mg/kg/hr (70 kg would receive 350 mg/24 hours), 23 placeboPrimary endpoints: duration of shock, reduction in pro-inflammatory cytokines</p></li><li><p>HydrocortisoneOppert, Crit Care Med, 2005</p></li><li><p>HydrocortisoneUse of this content is subject to the Terms and Conditions of the MD Consult web site. Critical Care MedicineVolume 33 Number 11 November 2005Copyright 2005 Lippincott Williams &amp; Wilkins </p><p>Bookmark URL: /das/journal/view/53019296-2/N/15873375?ja=504790&amp;PAGE=If0560538x002.fig&amp;ANCHOR=top&amp;source=MI Oppert, Crit Care Med, 2005</p><p> About MD Consult | Contact Us | Tems and Conditions | Privacy Policy | Registered User Agreemen </p></li><li><p>HydrocortisoneOppert, Crit Care Med, 2005</p></li><li><p>HydrocortisoneNot adequate power to determine mortality benefitShowed a trend toward better outcome with ACTH respondersThe jury is still out</p></li><li><p>VasopressorsSharshar, et al. Looked at circulating vasopressin levels in septic shockFound 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 patientsI use vasopressin for patients who do not initially respond to NE (dose .04 units/min)</p></li><li><p>The End!!</p></li></ul>