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GOOD MORNING

GOOD MORNING. Moderator : Dr.Vikram Mahajan. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Shock. “A rude unhinging of the machinery of life”. “A brief pause in the act of dying”. Shock. Inadequate peripheral perfusion leading to failure of tissue oxygenation

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GOOD MORNING

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  1. GOOD MORNING Moderator : Dr.Vikram Mahajan www.anaesthesia.co.in anaesthesia.co.in@gmail.com

  2. Shock “A rude unhinging of the machinery of life” “A brief pause in the act of dying”

  3. Shock Inadequate peripheral perfusion leading to failure of tissue oxygenation  may lead to anaerobic metabolism

  4. Clinically • Hypotension (ie. SBP < 90mmHg or MAP <60mmHg or reduced by >30% for last 3min) • Oliguria (Urine output20ml/hr or 0.3ml/kg/hr for 2 consecutive hours) • Poor peripheral perfusion (eg. Skin is cool and clammy; demonstrates poor capillary refill). With cardiogenic/septic, Skin exhibits cyanosis mottling which occurs first over knees.

  5. Etiology of shock Cardiogenic • Acute myocardial infarction (implies >40% LV muscle loss)Shock accompanies 6-20% of all acute MI’s ;more common with patients with ant. MI • Dilated cardiomyopathy • Acute myocarditis

  6. Mechanical • Mitral regurgitation • Ventricular septal defect • Left ventricular aneurysm • Left ventricular outflow obstruction • Metabolic and pharmacologic myocardial depression • Arrhythmias

  7. Extra cardiac obstructive • Massive pulmonary embolism • Severe pulmonary hypertension • Pericardial obstruction • Tension pneumothorax

  8. Oligemic: _ Hemorrhagic Volume depletion Adrenal insufficiency Distributive • Septic • Toxic agents including adverse reaction to medications and certain drug overdose • Anaphylaxis • Neurogenic

  9. The Stages Compensated • 15-25% of fluid loss from the vessels • Signs are subtle • Patient may show signs of an adrenaline rush Decompensated • 25-35% of fluid loss from the vessels • The body cells are profoundly hypoxic • Classic signs of shock Irreversible • > 35% fluid loss from the vessels • Body cells die • All vital signs bottom out

  10. Pathophysiology

  11. Compensated Shock • Baroreceptors sense a drop in pressure in the arteries • Medulla is stimulated • Sympathetic NS Response Clammy and pale skin Increased HR • Cells receive less oxygen as a result of a loss of RBC by the vomiting of blood • Pre-capillary sphincter closes in periphery and Blood shunted to the core

  12. Sympathetic NS response continues Adrenal hormones released Chemoreceptors sense changes in CO2 and oxygen concentrations Medulla stimulated again Increase in RR HR continues to rise Cellular Ischemic Phase Cells transition from aerobic to anaerobic metabolism Lactic acid begins to build Blood begins to coagulate behind the closed precapillary sphincter Post-capillary sphincter closes. Compensated Shock (cont)

  13. Less blood flow and oxygen delivery impact more of the body Tissues in the core become hypoxic • More shifts to anaerobic metabolism • Organ function slows Capillary Stagnation Phase • Lactic acid build in the cells and leak into the capillaries • Cell function drops dramatically Continued closure of postcapillary sphincters reduce preload Cardiac output drops Blood pressure begins to fall Decompensated Shock

  14. The medulla stops working Sympathetic nervous system stimulation ceases Heart function drops Drop in heart rate and contractility Vessels dilate No more energy to constrict Capillary Washout Phase Cell functions cease and cells die Potassium, acid dumps into the capillaries Large accumulations of acid force the opening of the capillary sphincters Sludge, clots and acid circulates throughout the entire body Other organ systems die off from this wave of destruction Irreversible Shock

  15. General Management • Initial Approach to patient in shock ABC • Airway • Indications for intubation in patients with shock • Severe hypoxemia • In appropriately high pCo2 • Obtundation (ensure protection of airway) • Vital organ Hypoperfusion Resting ventilatory muscles will permit diversion of cardiac output to other hypoperfused organs

  16. Breathing oxygen • Circulation a. Immediate determination of relative intravascular volume status is required. • Physical Examin- sufficient to distinguish shock with volume overload (ie. Cardiogenic shock) with pulmonary edema from shock with inadequate volume / eg. Septic shock with low cardiac filling pressures. • Unless there are signs of intravascular volume overload initial resuscitation with IV fluids is generally indicated. b. Vasopressor medications should be selected based on the cause of shock

  17. Management of cardiogenic shock Definition • Clinical • Poor cardiac output • Tissue hypoxemia 1. Oliguria 2. Cyanosis 3. Altered mentation 4 . Cool extremities • Adequate blood volume

  18. 2. Hemodynamic • systolic hypotension (< 90 mm or 30mm below baseline) • Increased arterial venous oxygen difference >5.5ml/dl • Low cardiac index (<2.2) • Elevated PCWP (>18) • The LV ejection fraction can be misleading and in one case study of patients with cardiogenic shock the avg LVEF was 31% (circulation 2003/107:279-84)

  19. Management (Cardiogenic ) • Establish Airway and ensure ventilation if necessary • Assessment • Identify and correct rhythm disturbances • Exchange other frequent mimics of cardiogenic shock (PE, Sepsis, Aortic dissection, Ruputred Aortic Aneurysm pericardial tamponade)

  20. Assess Volume Status • An adequate pre load is prerequisite to successful resuscitation • Clinical assessment is often in accurate • CVP, PCWP is many circumstances. • Insertion of Swan Ganz catheter is indicated in patient with hypotension unresponsive to fluid administration or if fluids are contraindicated (circulation 2004;110)

  21. Replace volume • In the absence of clinical evidence of pulmonary edema, an immediate fluid challenge is indicated. • Often small volume of fluid can mean the difference between inadequate LV filling pressure and pulmonary edema. • Frequent small volume 250cc saline bolus are preferable in cardiogenic shock resuscitation.

  22. Vasopressors Dobutamine • Dose- 2.5-20g/kg/min • First line drug if shock is mild with relatively pressured blood pressure. Dopamine • Dosage- 2.5-20g/kg/min • In moderate – severe cardiogenic shock dopamine is drug of 1st choice.

  23. Norepinephrine • Dosage- 0.05 - 1g/kg/min • Use is primarily reserved for patients failing to respond to dopamine. Phenylephrine • Dose 0.5 - 10g/kg/min • Use is primarily reserved for patients with septic shock with high cardiac output refractory to nor epinephrine,dopamine

  24. Vasodilators (Rarely useful in acute cardiogenic shock) • Nitroprusside useful only if cardiogenic shock accompanied by in appropriately high after load acute mitral regurgitation acute aortic regurgitation acute ventricular septal defect Dosage- 10mcg/min (0.6ml/hr) increase by 10mcg/min every 5-10 min to achieve optimal effect b. Nitroglycerin useful only if cardiogenic shock accompanied by in appropriately high preload. Dosage-10mcg/min 6ml/hr increase by 10mcg/min every 5-10 min to achieve optimal effect.

  25. Intra Aortic Balloon counter pulsation • Indications • Cardiogenic shock not responding promptly to pharmacologic therapy • Right ventricular infarction with shock not responding to volume infusion. • Refractory post infraction angina for stabilization before and during angiography. • Use as bridge to the surgical correction of mechanical complication of acute myocardial infarction. • Intractable recurrent tachycardia accompanied by hemodynamic compromise. • IABP can enhance diastolic coronary artery blood flow thus reducing ischemia to ‘Stunned’ myocardium

  26. Thrombolytics • In one small uncontrolled study of 8 patients, if BP could first be raised with vasopressors subsequent in fusion of t-PA was effective (CanJ Cardial 1995;11:30-6) • Reasonable to try unless contra- indications exist and if angioplasty is not available.

  27. Identify correctable causes of cardiogenic shock Approx 8% of pts. With cardiogenic shock will have surgically correctable cause, usually MR or vs rupture (circulation 1995;91:873-81) • Acute mitral regurgitation (J Am loll cardiol 1986;8:558) • Ventricular Aneurysm (NEJM 1984;311:1001-6) • Acute VSD (Chest 1989; 95:292-98) • Ruptured ventricle (Chest 1987; 92:219-223)

  28. Role of Interventional Cardiac Catheterization • Coronary angiography should be considered in all patients in cardiogenic shock after myocardial infarction • Results of the shock study (should we emergently revascularize Occluded Coronary for cardiogenic shock) indicated that patients who underwent emergent coronary revascularization with either PTCA or CABG had improved 1 – year survival compared to patients who unwent thrombolysis and/or intra-aorticballoon counterpulsation (46.7% surviva versus 33.6% survival) (JAMA 2001;285:190-2)

  29. Indications for Emergent Surgical Intervention In patients with cardiogenic shock. • Papillary muscle rupture • Acute ventricular septal defect • LV aneurysm with pump failure • Intractable ventricular tachycardia • Pump failure with cardiogenic shock (angioplasty usually attempted first)

  30. The special case of right ventricular infarction 1. Pathogenesis: • Usually right coronary artery occlusion • More frequent interior infarctions 2. Exam may reveal: • Hypotension • Clear lungs • Elevated jugular venous pressure • Kussmaul’s sign (jugular venous distension with inspiration

  31. 3. Hemodynamics: • Right atrial pressure>10 mm • Right atrial pressure within 5 mm of PCWP 4. Frequent EKG findings: • RBBB • Complete heart block • 1 mm ST elevation in lead V4R (very specific)

  32. 5. Treatment: • IV volume loading with saline • Avoid nitrates, morphine, and diuretics • Correct arrythmias • Dobutamine if shock persists • IABP • Vasodilators • Consider angioplasty (or thrombolysis if angioplasty not immediately available)

  33. Management of Extracardiac Obstructive shock • Pulmonary Embolus • Thrombolytics • Pericardial Tamponade • Intravenous fluids • Pericardiocentesis • Pneumothorax • Chest tube • Pulmonary hypertension • Vasodilators

  34. OLIGEMIC SHOCK • In a 70kg adult male • Class1: 500-750ml(10-15%)BV loss; no cinical features • Class2: 750-1500ml(15-30%)BV loss; postural hypotension • Class3: 1500-2000ml(30-40%)BV loss; hypotesion,tachycardia • Class4: >2000ml(40%)BV loss;severe shock

  35. Managementof oligemic shock • Operative control of blood loss is the major consideration in patients with continuing hemorrhage • Passive leg raising to increase central blood volume during resucitation

  36. Management of oligemic shock (Crit care 2004; 8:373-81) Protect/ensure patent airway and provide ventilation if necessary • Establish Adequate Venous Access • Flow dependent on catheter diameter plus catheter length • Flow through a small (2 inch) wide bore (16 gauge) peripheral IV is far better than through a central line port • optimally, place 2 wide bore peripheral IVs

  37. Volume replacement 1. Solutions: • Saline (140 mEq Na, 140 mEq Cl) • Lactated Ringer’s solution (130 nEg Na, 4mEq k, 10g mEq cl, 28mEq lactate) • Albumin • Dextran • Hydorxyethyl starch • Packed red blood cell 2. Volume expansion equivalents: • 6 liters D5W = 2 liters saline/Ringer’s =1 liter albumin = 1 unit PRBCs

  38. SEPSIS • Clinical syndrome with infection along with two criteria of systemic inflammatory response markers of inflammation: changes in temperature(>38 ̊c<36̊c),tachycardia(>90 per minute) , tachypnea (>20 per minute) changes in wbc count in peripheral bld (<4000or>12000cells per µL ,or immature forms of granulocytes

  39. SEPTIC SHOCK • Severe sepsis is diagnosed by presence of tissue hypoperfusion (elevated lactate or altered mental status), arterial hypotension or other organ dysfunction due to systemic manifestations of infection. • Once BP remains low, despite adequate fluid resucitation, progression of sepsis to shock

  40. Management of septic shock • Pathophysiology of sepsis: 1. Invasive factors • Endotoxins (lipopolysaccharide; LPS) • Exotoxins • Other microbial antigens 2. Host factors • Tumor necrosis factor – many pro-inflammatory effects • Interleukin-1 – many pro-inflammatory effects • Interleukin -8 – neutrophil recruitment • Complement – many pro-inflammatory effects • Platelet activating factor – many pro-inflammatory effects • Endorphins – myocardial depression • Nitric oxide (endothelium-derived) – vasodilator • Histamine-vasodilation

  41. i. Atrial natriuretic factors – vasodilation • Catecholamines – variable • Serotonin – vasodilation • Prostacyclin – vasodilation • Thomboxane A2 – vasoconstriction • Angiotensin – vasoconstriction • Vasopressin - vasoconstriction • Kinins – vasodilation • Genetics: TNF2 polymorphism is associated with an increase in the risk of death from septic shock

  42. B. Pathophysiology of Multiple Organ Dysfunction Syndrome • Changes in oxygen uptake – oxygen delivery curves • Altered blood flow distribution & shunt • Endothelial injury • Mitochondrial dysfunction

  43. C. Clinical Findings • Temperature • Hemodynamic changes • Early: normal BP, low SVR, increased CO • Intermediate: low BP, normal SVR, low Co • Late: very low BP, normal SVR, low CO

  44. ABG Changes Early : respiratory alkalosis Intermediate: respiratory alkalosis + metabolic acidosis Late: metabolic acidosis

  45. 4.Adult respiratory distress syndrome (ARDS) • Vascular “leak” • Exudative pulmonary edema • Alveolar neutrophil accumulation • Microatelectasis • Shunt physiology

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