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shock teaching for medical undergraduates

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  1. 1. SHOCKDr.sugunakar
  2. 2. DEFINITIONShock is simplydefined as perfusionthat is inadequate tomeet the bodysmetabolic needs.
  3. 3. EFFECTIVE TISSUEPERFUSION Cardiac Performance Vascular performance Cellular function Oxygen unloading and diffusion Energy generation
  4. 4. EncephalopathyRespiratory failure ArrhythmiasARDS IschemiaIschemic hepatitisCholestasis DIC ThrombocytopeniaIleusErosive gastritis HyperglycemiaPancreatitis HypoglycemiaCholecystitis Electrolyte abnormalitiesTransluminal bacterialtranslocation Cold extremities Thready pulse
  5. 5. CLINICAL RECOGNITION Mean arterial pressure < 65 mm Hg (in previously normotensive individual
  6. 6. TYPES OF SHOCK Hypovolemic Cardiogenic Obstructive Distributive
  7. 7. CAUSES Hemorrhagic: Don’t forget concealed Hemorrhagic bleeds: Abdomen Pelvis / Femoral Retroperitoneal Fluid depletion: Non-hemorrhagic Dehydration (Fluid depletion) Vomiting Diarrhea Burns Anaphylaxis Venodilation Venodilation: Sepsis Anaphylaxis Toxins / drugs Common with distributive shock
  8. 8.  small bowel obstruction, hypovolemic shock can develop as a result of shift of fluid into the bowel lumen. Patients with peritonitis after perforation of a duodenal ulcer accumulate several liters of inflammatory fluid in their peritoneal cavity, A reduction in intravascular volume is often a contributing factor to hypotension in patients with septic shock.
  9. 9.  Hemorrhagic shock can be categorized into three grades of severity based on the magnitude of blood loss: compensated shock, uncompensated shock, and lethal exsanguination
  10. 10. Patients with 20% to 40% of more than 40%less than a 20% their blood of their blooddeficit in blood volume volume andvolume profound cannot sustain hypotensionCan maintain mean aortic develops. With pressure by severelyOr restoreblood vasoconstriction reduced blood , have low flow to theirpressurewith ivfluids cardiac output, brain, these are subject to patients anaerobic become stress, and comatose within have acidemia minutes and die of cardiac BLOOD arrest.
  11. 11.  Hypovolemia! Preload! Diastolic Filling ! Cardiac Output ! MAP Shock MODS
  13. 13. causes Pump (CHF Ischemia1.infarction 1.bradycardia 1.Cardiomyopathy 2.tachycadia 2.Valve failure 3.Endocarditis 4.Acute massive pumonary emboli
  14. 14.  Hypovolemia Cardiogenic ! Preload ! Cardiac Output ! Diastolic Filling!  ! MAP Cardiac Output  Shock ! MAP  MODS Shock MODS
  16. 16. CAUSES Septic Toxic Shock Syndrome Anaphylactic / Anaphylactoid Neurogenic (Spinal Shock) Endocrinologic Adrenal Crisis Thyroid Storm Toxins
  17. 17.  Humans respond to invasive infection with an immune response that involves multiple mediators. These mediators enable the patients inflammatory processes to destroy the organisms at the site of infection. These same mediators can damage the individuals organs if they produce an exaggerated systemic inflammatory response syndrome
  19. 19.  Distributive Shock ! Systemic Vascular Resistance Maldistribution of flow ! Cardiac Output ! MAP Shock MODS Myocardial Suppression
  20. 20. SYSTEMIC INFLAMMATORYRESPONSE SYNDROME 36C < Fever > 38C Tachycardia > 90 Hypocapnia (PaCO2 > 32 mm Hg) / RR > 20 or use of mechanical ventilation 4000 < WBC > 12000 (or left shift) Sepsis Same criteria as for SIRS but with a clearly established focus of infection
  21. 21.  Severe sepsis - SIRS + Organ dysfunction…Indicators of hypoperfusion:▪ Systolic blood pressure <90 mm Hg ▪ >40 mm Hg fall from normal systolic blood pressure ▪ Lacticacidemia▪ Oliguria▪ Acute mental status changes Septic Shock - Severe sepsis + refractory hypotension despite adequate fluid & resuscitation
  22. 22. TREATMENT
  23. 23.  Management of a patient in shock is focused on the following: 1. Identifying the presence of shock 2. Searching for and treating immediately life- threatening conditions 3. Treating shock based on the underlying pathophysiology
  24. 24. THINK ABOUT... 2 large bore peripheral lines - iv fluids Central line - for CVP & vasopressors Arterial line - BP monitoring and repeated ABG Foley - urine output Nasogastric tube - maintain gut integrity
  25. 25. Hypovolemic Fluids---RINGER LACTATE BLOOD HEMOSTASISCardiogenic Cath Lab Inotropes IABPObstructive Remove obstructionDistributive Antibiotics Epinephrine
  26. 26.  A surgeon treating a patient in hypovolemic shock faces two concurrent challenges. First, the surgeon must restore intravascular volume to normal. Second, the surgeon must identify the cause of the patients hypovolemic shock and decide whether immediate surgical therapy is needed.
  27. 27. HEMORRHAGIC SHOCK Acidemia is used as a measure of the severity of hemorrhagic shock bicarbonate excess …-10 mEq/L or less in a hypovolemic patient is an indication that the patient has uncompensated shock and is at risk for death if resuscitation not done
  28. 28. HEMORRHAGIC SHOCK Adult patients who do not respond to 2 to 4 L of balanced electrolyte solution (children are given 20 mL/kg) and remain hypotensive usually require blood transfusions The surgeon must identify the potential sites of active hemorrhage in an irreversibly hypotensive patient and perform hemostatic interventions
  29. 29. HEMORRHAGIC SHOCK rapid resuscitation, timely hemostasis, and postresuscitation support of organ function.
  30. 30. TRETMENT OF CADIOGENICSHOCK The most common cause of cardiogenic shock is occlusion of a coronary artery in which a plaque in the coronary artery ruptures, combined with the formation of an intraluminal thrombus The key to improving survival of patients in cardiogenic shock is to promptly reestablish blood flow at the site of the coronary artery occlusion.[46] aspirin and a β-blocker , fibrinolysis, deployment of coronary artery stents, and surgery
  31. 31. SHOCK CAUSED BY CARDIACCONTUSION dobutamine, epinephrine, or dopamine may improve myocardial contraction in a patient with cardiac contusion and profound pump dysfunction. An intra-aortic balloon pump may provide temporary support while the contused cardiac muscle recovers
  32. 32. SHOCK CAUSED BY CARDIACTAMPONADE Acute cardiac tamponade is always suspected after gunshot or stab wounds to the chest in the vicinity of the sternum. Patients with acute cardiac tamponade have hypotension, distended neck veins pulsus paradoxus, pulsus paradoxus, immediate surgery to decompress the pericardium
  34. 34. SEPTIC SHOCK ….TREATMENT Culture relevant body fluids, including blood. Infuse a balanced electrolyte solution of 500 mL/15 min. Monitor the systolic blood pressure response. Insert a central venous or pulmonary artery catheter. ▪ If after a 500-mL bolus of saline the patient remains hypotensive and CVP is <8-12 mm Hg or PAWP is <8-12 mm Hg, infuse another 500-mL bolus of fluid
  35. 35. SEPTIC SHOCK ….TREATMENT IfCVP is >15 or PAWP is 15-20 and the patient remains hypotensive (<65 mm Hg), start an infusion of the inotropedobutamine or dopamine. The goal is a mean systemic pressure >65 mm Hg and a pulse rate <120 beats/min. Determine the cardiac index and systemic vascular resistance. ▪ If after infusion of fluid and inotropes SVR is <600, infuse avasopressor—either norepinephrine or vasopressin—to increase SVR
  36. 36. SEPTIC SHOCK ….TREATMENT Monitor mixed venous oxygen saturation and urine output as an indication that therapeutic interventions have improved perfusion. CVP, central venous pressure; PAWP, pulmonary artery wedge pressure; SVR, systemic vascular resistance.
  37. 37. SEPTIC SHOCK ….TREATMENT As a final consideration in the treatment of any patient in septic shock, resuscitation is often futile without effective treatment of the source of the sepsis. A patients survival from an episode of sepsis often hinges on prompt and effective performance of a surgical procedure.
  38. 38. MONITORING & GOALS...Hemodynamics Oxygen Organ Dysfunction1. MAP > 60 1. Hb > 10 1. Urine output2. CVP > 12 2. Sa O2 > 92 2. Mental3. CI > 2.2 L % Status4.PCWP 3. Mechanical 3. Lactate Ventilation levels 4.Serial blood 4. LFT gases
  39. 39.  AVOID HYPOTHERMIA, HYPERGLYCEMIA ,HYPERCHLOREMIC ACIDOSIS, ACTIVATED PROTEIN C, LOW DOSE STEROIDS IMPROVE SURVIVAL RATES. New therapeutic agents are still being tested for sepsis in multicentre trials.
  40. 40. THANK YOU