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A comprehensive overview of shock, a critical medical condition characterized by inadequate tissue perfusion. Learn about the different types of shock, screening criteria, hemodynamics, and the importance of early recognition and treatment to prevent fatal outcomes.
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Kritikus Foundation Presents S H O C K
ALOC Tachypnea Cool or mottled extremities Decrease urine output Metabolic acidosis Hypothermia SHOCK Shock is a syndrome of inadequate tissue perfusion, with or without hypotension, resulting in one or more of the following:
Inclusion Criteria: high probability of presence of shock } Hypotension SBP < 90, MAP < 60 withoneor more…. or withthreeor more………………………. and not corrected with one liter rapidly infused crystalloid: 1. Temperature < 36° C 4. Cool extremities or or 96.8 ° F skin mottling 2. RR > 20 bpm 5. Oliguria < 30 cc/hour • Altered mental status 6. Lactic Acid > 2.0 or BE < -5 mmol/L of the following Normotension
Shock confirmatory criteria Required one of the following: • Administration of > 4 liters of fluid in first 24 hours • Lactic acid > 2 mmol/L • Use of vasoconstrictors • Death as a result of hemodynamic instability SCREENING CRITERIA + CONFIRMATORY = INCLUSION CRITERIA
In Shock with pos criteria Pos criteria and in shock Pos criteria and not in shock Sensitivity & Specificity of Shock Screening Criteria
Types of Shock • Hypovolemic - low circulating blood volume i.e GI bleed, severe dehydration. • Obstructive - obstructed blood flow i.e pulmonary embolism, cardiac tamponade, tension pneumothorax • Cardiogenic - muscle, valve or rhythm problem causing significant drop in cardiac output.
Types of Shock • Septic or Distributive - vasodilation loss of arterial tone with redistribution of vol to tissues, viens i.e. infection, pancreatitis orother sources of tissue injury • Anaphylactic – same as distributive shock i.e reaction to drug or environmental agent • Hypoxic – not considered a classic form of shock - but is a is the most rapidly progressive and fatal case of global inadequate delivery of oxegen; if not reversed
Hemodynamics Of Shock BP = CO X SVR(HR x SV)
Hypovolemic Shock Decreased Preload i.e., GI Bleed BP = CO X SVR or
Septic / Distributive Shock BP = CO after fluid x SVR Sepsis Pancreatitis Anaphylaxis
Cardiogenic / Obstructive Shock NLBP = CO x SVR A.M.I. Valve Failure P.E. Tamponade or
Why a Shock Educational Program and System • A standardized and systematic approach to shock will lead to: • Early Recognition • Early Initiation of Best Practice Improved Outcomes !
Medical Emergency Teams AShock Team In A General Hospital Edward D. Frank, M.D. Department of Surgery Harvard Medical School Published in Anesthesia and Analgesia November - December 1967
Portable Monitoring Equipment at Bedside Edward David Frank, MD
Confused, Shock Appearance Cool, Moist Flow Sheet Used for Shock Patients Blood Pressure Heart Rate Respiratory Rate Temperature Urinary Output Fluid Balance HCT Cardiac Output CVP Arterial Blood Gases Whole Blood Treatment Pressor Drug IV Cooling Blanket Antibiotic Treatment Time
Shock (Septic) Mortality • None reported 1967 by Dr Frank • 70% septic shock in 1970s • 50% in 1990s • 40 to 30% in 2000-2005 • 30% to 27% in 2015 to present • 10% reported with a dedicated Shock program and team in 2005
Shock Program and Team Effect of a Rapid Response System for Patients in Shock on Time to Treatment and Mortality During 5 Years CC Med 2007 Frank Sebat, MS, MD, FCCP, FCCM; Amjad A. Musthafa, FCCP; David Johnson, MD; Andrew A. Kramer, PhD; Debbie Shoffner; Mark Eliason, BSN; Kristen Henry, BSN; Bruce Spurlock, M • Mortality of septic shock decreased from 50% (2000) to 10% (2005) • Decreased time from when shock could have been recognized till administration of Key interventions - 310 min to 80 min
Shock - Why such high fatality rates? • Frequently not recognized early • When recognized often have the onset of end organ damage (MOF) AND
ALL SHOCK Leads to cardiogenic shock
Coronary Artery Blood Flow F L O W Target BP 120 60 MAP
Shock leads to positive feedback death spiral • Decreased cerebral perfusion - Decreased airway protection and resp compensation • Decreased CA perfusion • Resulting lower CO to Resp muscle, CNS and other organs- worsing their dysfunction Over time Code Blue
Cycle of Critical Illness / Shock Respiratory Failure Acute Change in Neurologic Status S H O C K • Hypoxic • Hypovolemic • Septic • Cardiogenic • Anaphylactic Blood Flow (C.O.) or Blood Pressure or Oxygen delivery Death Organ Perfusion UNTREATED SHOCK IS 100% FATAL Multiorgan Failure Neurologic, Respiratory, and Cardiovascular Function Blood Flow or Pressure EARLIER RECOGNITION AND EARLY GOAL DIRECTED THERAPY WILL INTERRUPT THIS CYCLE
How to prevent the shock death spiral? Early Recognition!!! Frequently obvious, but can be subtle • ALOC, anxiety, apathy stupor • Cool extremities, poor cap refill • Tachypneaalmost always present, but non specific
Recognition of Shock Frequently obvious, but can be subtle • Hypotension--frequently, but not always present or worse not detected • Oliguria--takes time to assess • Metabolic acidosis/LA may take time to develop or wash out of the tissues
How Do We Recognize Shock Sooner? • Learn the manifestations • Have a high index of suspicion • Once the question of shock is raised, go through the drill, i.e., Hx, exam, lab, repeat observation • Burden of proof on the caregiver i.e., • prove to yourself the patient is not in shock !
Apathy Lethargy / Stupor Coma C.N.S. Manifestations of Shock Anxiety
ALL SHOCK LEADS TO CARDIOGENIC SHOCK Cardiac Manifestations of Shock Dysrhythmias Myocardial ischemia, chest pain Myocardial depression
1st Hour/Kidney Oliguria 1st 24 Hours/Bowel Ileus 24-72 Hours ATN, increasing LFTs Day 3-21 occult abdominal problems • Ischemic bowel, acalculus cholecystitis leading to multi organ failure Abdominal Manifestations of Shock Our window to the abdomen
CAPILLARY REFILL TIME Critical Care Medicine. 37(3):934-938, March 2009 50 consecutive adults admitted to ICU When cap refill > 4.5 sec, 77% vs. 23% progressed to worsening organ function (p < 0.05) Subjective assessment of peripheral perfusion can identify patients at-risk for severe organ dysfunction and higher lactate levels
Metabolic Manifestations of Shock Acid accumulation in the body BE < -5 meq/L Lactic Acid > 2.0 meq/L
Coagulation Manifestations of Shock • Decreasing platelet count • Endothelial injury with consumption in lung, liver, bowel • DIC • Increasing protime • Decrease synthesis of coagulation factor by the liver • Increase consumption of clotting factors
Shock If Crtieria Met Then What?
?CALL ALERT? RRT
Goals for Shock Resuscitation • SaO2 > 93% • Decrease work of breathing (BIPAP or Early intubation) • Aggressive volume resuscitation, CVP >12 • MAP > 70, if above not effective then pressors (Levophed) • UO > .5 ml/kg/hr • Cap refill < 3 sec • SvO2> 60 Dobutamine if needed • Decreasing LA
Standardized Best Practice:V. I. P.P. S. Approach to Bedside Management of Shock Weil MH; Shubin H. JAMA 1969 Jan 13 S V entilation/oxygenation I nfusion of VOL ressors / Pump P P harmacy pecific
Treatment - V. I. P. P. S. Approach entilation / oxygenation • Supplemental Oxygen • Early Intubation • Adequate Hemoglobin V
Prospective Study of the Treatment of Septic Shock The Lancet, June 3, 1978 113 patients over 3 years
Treatment - V. I. P. P. S. Approach nfusion of VOL • 2 16 ga IVs • Central line • Up to two liters of Crystalloid • 500 cc of Colloid up to 1,000 cc • Packed red blood cells for Hgb < 9, < 10 for sepsis I
Treatment - V. I. P. P. S. Approach P ressors / Pump • MAP < 60 • With Dopamine or Levophed for Cardiogenic Shock • Levophed for Septic Shock • Treat dysrhythmia • Rule out tamponade, ischemia, PE, or valvular abnormality
Treatment - V. I. P. P.S. Approach P harmacy • Antibiotics, Hydrocortisone for pressor dependent sepsis • Albuterol, steroids and H1, H2 blockers for anaphylaxis • Dobutamine / Nipride for cardiogenic shock, MAP > 60 • Thrombolytics for PE • Other
Treatment - V. I. P. P.S. Approach S pecific • Endoscopy for upper GI bleed • O.R. for ruptured Abdominal Aortic Aneurysm or perforated viscus • Pericardiocentesis for tamponade • Activated protein C for toxic shock
Key Points of Shock Program • Early recognition • Rapid Response by Team • Early / Aggressive Application of Best Practice • Rapid transfer to ICU or O.R.
Study Methods • Control Group were patients who came into Redding Medical Center between 1998 and June 2000 who qualified by inclusion / exclusion criteria • Intensive education and implementation of protocols and mock shock alerts during June 2000 • Treatment Group were all patients who qualified by inclusion/exclusion criteria starting July 1, 2000
Identification of Patients in Shock • Control 86 /20,976 or 1/244 Admissions • Protocol 103/9,120 or 1/89 Admissions • p < 0.001 Increased the identification of shock by 300%
Discharge Location SNF HOME REHAB OTHER CONTROL GROUP TREATMENT GROUP