Emergency lectures - Introduction to shock


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Emergency lectures - Introduction to shock

  1. 1. Introduction to Shock Is AllShock Alike? Barbie J. Barrett MD, FACEP Associate Professor Department of Surgery Division of Emergency Medicine Stanford University and Medical Center Palo Alto, California U.S.A.
  2. 2. Central Venous Pressure Training for MD
  3. 3. RN Education on SCVO2
  4. 4. Sepsis Class forParamedical Providers
  5. 5. Definition Shock is an imbalance between tissue oxygensupply and demand, resulting in inadequate tissue perfusion.- Shock may be present in the face of a: high, low or normal blood pressure High or Low Cardiac Output (CO)High or Low Systemic Volume Resistance (SVR)
  6. 6. Hypotension is a drop in systolic bloodpressure of > 40-50 mm HG from baseline. Systolic < 90 mm Hg MAP < 65 mm HgThe Surviving Sepsis Campaign recommends maintaining MAP at > 65.
  7. 7. PERFUSION is crucial Normal blood pressure may not equate to good flow
  8. 8. ARDS Adult Respiratory Distress SyndromeCA O2 Arterial Oxygen ContentCO Cardiac OutputEGDT Early Goal Directed TherapyMAP Mean Arterial PressureMODS Multi-organ Dysfunction SyndromePAC Pulmonary Artery Catheter
  9. 9. ScvO2 Central Venous Oxygen SaturationSvO2 Mixed Venous Oxygen SaturationSIRS Systemic Inflammatory Response SyndromeSVR Systemic Vascular ResistanceTO2 Tissue Utilization of OxygenTO2 crit Critical Oxygen Uptake to SupplyVO2 Ventilatory Oxygen Consumption
  10. 10. Classification by Etiology • Cardiogenic – Myocardial • Hypovolemic – Dysrrhythmia – Hemorrhage – Congenital Heart – Serum/Plasma loss Disease (Duct – Drugs Dependent) • Distributive • Obstructive – Pneumothorax, – Anaphylactic Tamponade, – Neurogenic Dissection – Septic • Dissociative – Heat, CO, Cyanide – Endocrine
  11. 11. The Chain of Survival Early and Early Appropriate Improved RapidDetection Disposition Outcomes Intervention
  12. 12. Right Atrium (RA) or CVP• Indicates preload• Crude example of fluid volume• Normal 2 – 8 mmHg
  13. 13. Right Ventricle (RV)• Normal systolic 15 – 25 mmHg• Normal diastolic 0–8 mmHg
  14. 14. Pulmonary Artery (PA)• Normal systolic 15 – 25 mmHg• Normal diastolic 8 – 15 mmHg• PAD correlates with the filling pressure of the left heart
  15. 15. Pulmonary Capillary Wedge Pressure (PCWP) • “Sees” what is in front of it left side of heart • Normal 8 – 12 mmHg
  16. 16. Mortality Septic Shock 30% - 45% (1 month mortality) Cardiogenic 60% - 90% Hypovolemic 30% - 40% Grater than 1 million cases of shock are seen in Emergency Departments annually EGDT = Early Goal Directed Therapy
  17. 17. Pathophysiology Oxygen supply and demand imbalance Conversion from aerobic to anaerobic metabolismLactic acidosis due to both appropriate and inappropriate response
  18. 18. • Cellular – Major third space fluid loss • Capillary Leak • Fluid & Electrolyte Imbalance – Diarrhea, Sweat, Vomit • Vasodilation – due to excessive activation of macrophages, neutrophils • Pro inflammatory mediators – Prostanoids, Nitric Oxide – Kinins and Pyrogens
  19. 19. Pathophysiology• Vascular Hyporeactivity – Adrenocortical Disruption – Decreased Response to Catecholamines• Cardiac – Profound Myocardial Depression – Excess Nitric Oxide – Release of Myocardial Depressant Factors
  20. 20. Pathophysiology Resultant Systemic Physiology-Cell Death-End Organ Dysfunction MODS = Multiorgan Dysfunction Sydrome
  21. 21. Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis CNS: Cardiovascular: Altered Tachycardia consciousness Hypotension Confusion Altered CVP + PAOP Respiratory: Tachypnea Renal: PaO2 Oliguria PaO2/FiO2 Anuria ratio Creatinine Hepatic: Hematologic: Jaundice, Platelets Liver PT/INR, aPTT enzymes Protein C Albumin D-dimer Metabolic: Metabolic acidosis Lactate level Lactate clearance Balk RA, Crit Care Clin, 2000-16.337.352 Keipell RM Crit Care Nurs Clin North Am 2003-15.27.34
  22. 22. Physiology• Characterized by three stages – Preshock (warm shock, compensated shock, cryptogenic shock) – Shock – End organ dysfunction
  23. 23. Physiology• Compensated shock – Low preload shock – tachycardia, vasoconstriction, mildly decreased BP – Low afterload (distributive) shock – peripheral vasodilatation, hyperdynamic state
  24. 24. Pathophysiology• Shock – Initial signs of end organ dysfunction • Tachycardia • Tachypnea • Metabolic acidosis • Oliguria • Cool and clammy skin
  25. 25. Physiology• End Organ Dysfunction – Progressive irreversible dysfunction • Oliguria or anuria • Progressive acidosis, CO • Agitation, obtundation, coma • Patient death
  26. 26. Shock Pathways Distributive Cardiogenic Obstructive Hypovolemic Decreased Myocardial Myocardial Pericardial Hemorrhage SVR Dysfunction Damage TamponadeBlood Flow Reduced ReducedMaldistribution Filling Preload Reduced Systolic High or Normal Function Cardiac Output Low Cardiac Output Decreased MAP Shock DEATH
  27. 27. Physical ExaminationVitals – Temperature may be or normal.General – Pale, WeakHEENT – Dry Mucous Membranes, Pale ConjunctivaNeck – Weak or Absent Carotid PulsesCardiovascular – Usually Tachycardia Late Bradycardia Exception – Athletes, Beta-blockers, Intra-abdominal Hemorrhage Hypoglycemia Cardiovascular drugs
  28. 28. Physical ExaminationRespiratory – Tachypnea Dead Space Bronchospasm Adult Respiratory Distress Syndrome (ARDS)Abdomen – ILEUS – low flow state GI Bleed Pancreatitis Acute Cholecystitis Mesenteric Ischemia
  29. 29. Physical ExaminationExtremities – Pulses Look for effusions, tracks, infections, septic joints, line infection,Skin – Pale Cyanosis Acrocyanosis Diaphoretic Capillary Refill Altered Temperature
  30. 30. Physical ExaminationGU – Genitourinary (Trauma, Blood Loss) Oliguria PolyuriaNeuro- Altered Mental Status Cord Signs Loss of cardiac sympathetic tone Paralysis MeningismusPsyche – Agitation Obtundation
  31. 31. Hypovolemic ShockHypovolemic Shock is an acute intravascular volume loss Results from decreased preloadEtiology Hemorrhage, Trauma, GI Bleed, and Ruptured AneurysmFluid loss Burns, Diabetic Ketoacidosis Diabetic Insipidus, Vomiting, and Diarrhea
  32. 32. Cardiogenic ShockCardiogenic Shock is decreased cardiac output (CO) despite adequate volume.Cardiogenic Shock is the leading cause of death in acute myocardial infarction.
  33. 33. Cardiogenic Shock Etiology Myocardial Infarction Cardiomyopathy Dysrhythmia Mechanical CHF (Congestive Heart Failure) Valve Contusion Extra cardiac (obstructive)
  34. 34. Cardiogenic Shock• Artioventricular valves – Tricuspid and Mitral – During diastole, the valves serve as a conduit from atria to ventricles• Semilunar Valves – Pulmonic and Aortic – After the end of systole, high pressure drops with the pulmonary artery and aorta, causing retrograde flow thus filling the aortic and pulmonary cusps with blood and snapping them shut. – Aortic valve is the valve most frequently replaced
  35. 35. Cardiogenic ShockClinical features Distended Neck Veins Weak or Absent Pulse Arrhythmia often Tachycardia Pulsus Paradoxus (if tamponade)
  36. 36. Distributive ShockDistributive Shock is a metabolic derangement that impairscellular respiration, due to severe decrease in SVR Vasodilation reduces after load. May be found with cardiac output (CO).
  37. 37. Bacteremia Pancreatiits Infection SEPSIS` SIRS Fungemia Trauma Parisitemia Viremia Burns Other OtherBone et al Chest 1992
  38. 38. Sepsis: Defining a Disease Continuum Septic Shock Lactic Acid < 4 Bone RC et al. Chest 1992, 101:1644-1655
  39. 39. Distributive ShockNeurogenic / High Spinal• Loss of cardiac sympathetic tone• Heart rate• Vascular dilitation• Warm skin
  40. 40. Distributive ShockSystemic Inflammation Pancreatitis Burns BiliaryToxic Shock SyndromeToxic Reactions (transfusion, drugs)Do not confuse spinal shock with neurogenic shock.
  41. 41. Distributive ShockAnaphylaxis & Anaphylactoid (Know the difference) Widespread vasodilatation due to release of histamine.Endocrine Addisonian Myxedema
  42. 42. Anaphylactic Reaction vs Anaphylactoid ReactionAnaphylactic AnaphylactoidPrevious No prior exposureexposer/sensitisation necessaryMediated by specific IgE No IgE antibody involvedantibodies Common reaction toCommon reaction to invenomations/insect, Nuts,contrast media Shell fish, Pharmaceuticals, LatexHistamine known responsible agent for most of manifestations
  43. 43. Anaphylaxis • Vasodilatation • Increased vascular permeability • Bronchoconstriction • Increased mucus production • Increased inflammatory mediators recruitment to sites of antigen interaction
  44. 44. AnaphylaxisClinic Presentation • Immediate response • Cutaneous manifestations – urticaria, erythema, pruritis, angioedema • Respiratory compromise – stridor, wheezing, bronchorrhea, resp. distress • Circulatory collapse – tachycardia, vasodilation, hypotension
  45. 45. Obstructive ShockObstructive Shock is extra cardiac obstruction toblood flow. Tension pneumothorax Cardiac tamponade Pulmonary embolus Aortic stenosis Can two or three different types of shock exist in one patient?
  46. 46. Dissociative Shock Heat Carbon Monoxide Cyanide Endocrine
  47. 47. EvaluationSimultaneous differential diagnosis thinking occurs intandem with your treatment.Targeted History & Physical What type(s) of shock am I dealing with?Full Laboratory Protocols & Evaluation What would you order? (don’t forget pregnancy) What Cultures would you obtain?
  48. 48. EvaluationOther Studies / Imaging EKG = Electrocardiogram) FAST = Focused Assessment with Sonography in Trauma CT = Computerized Tomography ECHO = Echocardiogram LP = Lumbar Puncture (if appropriate)
  49. 49. EvaluationMonitoring Vital signs including capnography Urine output CVP Central Venous Pressure Rectal probe Arterial line Pulmonary Artery (PA) catheterization Suspected etiology will direct studies.
  50. 50. Index of 2008 Recommendations• Initial resuscitation (first 6 hours) • Mechanical ventilation of sepsis –induced acute lung• Diagnosis injury ALI/ARDS (acute• Antibiotic therapy respiratory distress syndrome)• Source identification and • Sedation, analgesia, and control neuromuscular blockade in sepsis• Fluid therapy • Glucose control• Vasopressors • Renal replacement• Inotropic therapy • Bicarbonate therapy• Steroids • Deep vein thrombosis (DVT) prophylaxis• Recombinant human activated • Stress ulcer prophylaxis protein C (rhAPC) • Consideration for limitation• Blood production of support administration Dellinger RP, et al. Crit Care Med. 2008,36:296-327. (Updated 36:1394-1396)
  51. 51. EarlyGoal-DirectedTherapyN Engl J Med 2001; 345(19):1368-1377
  52. 52. Pearls and PitfallsPrecise diagnosis is often delayed but immediate treatment isessential.There is no single test that is diagnostic for sepsis.Young healthy patients may crash quickly due to theirabilities to compensate initially.Obtain pregnancy testing on all females of child bearing age. Don’t miss tension pneumothorax. Does the patient have a pneumothorax after your CVP (central venous pressure) line placement?Don’t miss cardiac tamponade in your cancer/dialysis patients.
  53. 53. Pearls and PitfallsCall for help.Check and recheck lines, monitors and infusionsDoes the patient arrive with any preexisting lines thatmay be infected.Up to 30% of shock patients can have adrenal insufficiencyIsolated intracranial injuries do not cause shock.Keep your code/resuscitation bay warm blood loss willcause hypothermia.Don’t assume there is only one cause for shock.
  54. 54. Is All Shock Alike?
  55. 55. References– Dellinger R, Carlet JM, Masur H, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004; 32(3): 858-873.– Dellinger R, Levy M, Carlet J, et al. Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock. Crit Care Med 2008;36(1):296-327.– Morris E, Light RB, Garber GE. Identifying patients with severe sepsis who should not be treated with drotrecogin alfa (activated). Am J Surgery 2002; 184: 19S-24S.– Nguygen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is associated with improved outcome in severe sepsis and septic shock. Crit Care Med 2004: 32(8): 1637-1642)– Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345(19):13681377.– Ruble, Cheryl RN, MICN, Alameida, Rich MD. Sepsis Workshop. 2011. Mills/Pensula Medical Center– Sherwin RL, M.D. Shock. Wayne State University. July 18th 2006. Presentation– Tintinalli JE. Tintinalli’s Emergency Medicine, A comprehensive Study Guide 7th ed. McGrawHill Med 2011. (165-182, 222-240, 1003-1014)– Vanhorebeek I, Van den Berghe G. The neuroendocrine response to critical illness is a dynamic process. Crit Care Clin 2006; 22: 1-15.