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  1. 1. SHOCK
  2. 2. Definition Shock is a state of inadequate perfusion, which does notsustain the physiologic needs of organ tissues. A physiological state characterized by a significant,systemic reduction in tissue perfusion, resulting in decreasedtissue oxygen delivery and insufficient removal of cellular metabolicproducts, resulting in tissue injury.
  3. 3. SRUP• Inadequate tissue perfusion• Decreased oxygen supply• Anaerobic metabolism• Accumulation metabolic waste
  4. 4. Pathophysiology Alteration in hemodynamic results in a drop in arterial bloodpressure by one of these mechanisms:• Decrease in cardiac output (ability of heart to supply adequatecirculation)• Decrease in circulating blood volume• Increase in size of vascular bed
  5. 5. Vicious cycle of shock
  6. 6. Stage of shock
  7. 7. Early reversible and compensatory shock• Mean arterial pressure drops 10 -15 mmHg• Decrease in circulating blood volume (25-35%) 1000ml• Sympathetic nervous system stimulated; release ofcatecholamine
  8. 8. Early reversible and compensatory shockFindings• Increase in heart rate and contractility• Increase in peripheral vasoconstriction• Circulation maintained, but can only be sustained short timewithout harm to tissues• Underlying cause of shock must be addressed and corrected orwill progress to next stage
  9. 9. Intermediate or progressive shock• Further drop in MAP (20%)• Increase in fluid loss (1800 – 25400 ml)• Vasoconstriction continues and leads to oxygen deficiency• Body switches to anaerobic metabolism forming lactic acid as awaste product
  10. 10. Intermediate or progressive shockFindings• Body increases heart rate and vasoconstriction• Heart and brain become hypoxic• More severe effects on other tissues which become: ischemicand anoxic• State of acidosis with hyperkalemia develops Needs rapid treatment
  11. 11. Refractory or irreversible shock• Tissues are anoxic, cellular death widespread• Even with restoration of blood pressure and fluid volume there istoo much damage to restore homeostasis of tissues• Cellular death leads to tissue death; vital organs fail and deathoccurs
  12. 12. Effects of Shock on Body Systems
  13. 13. Cardiovascular system• Initially: slight tachycardia, normal blood pressure• Progresses to weak, rapid pulse with dysrhythmias• Progressive decrease in systolic and diastolic blood pressureswith narrowing of pulse pressure; blood pressure becomesinaudible
  14. 14. Respiratory system• Initially: Increased respiratory rate, but gas exchange isimpaired; leads to anaerobic metabolism and development ofacidosis• Acute Respiratory Distress Syndrome (ARDS): complication ofdecreased lung perfusion
  15. 15. Gastrointestinal and Hepatic• GI organs become ischemic, with blood circulation shunted toheart and brainComplications :• Stress Ulcers• Paralytic Ileus• Altered liver metabolism: hypoglycemia, fat breakdown leads toketones and metabolic acidosis
  16. 16. • Neurologic systemDevelops cerebral hypoxia Restlessness initially, then altered level of consciousness,lethargy, coma ,Thirsty from dehydration• Renal Decreased kidney perfusion leads to oliguria (urine output< 0.5 ml/kg/hr)• Skin Skin: cool, pale, hypothermic
  17. 17. Causes of Shock [-]• Severe or sudden blood loss• Large drop in body fluids• Myocardial infarction• Major infections• High spinal injuries• Anaphylaxis• Extreme heat or cold
  18. 18. Clinical Markers of Shock• Brachial systolic blood pressure: < 110mmHg• Sinus tachycardia: > 90 beats/min• Respiratory rate: < 7 or > 29 breaths/min• Urine Output: < 0.5 cc/kg/hr• Metabolic acidemia: [HCO3] < 31mEq/L or base deficit > 3mEq/L• Hypoxemia: 0-50yr: < 90 mmHg; 51-70 yr: < 80mmHg; > 71yo < 70mmHg• Cutaneous vasoconstriction vs. vasodilatation.• Mental Changes: anxiousness, agitation, indifference, lethargy, obtundation
  19. 19. Classification of Shock• Hypovolemic shock• Septic/Inflammatory shock• Cardiogenic shock• Neurogenic shock• Anaphylactic shock• Obstructive shock• Traumatic shock
  20. 20. Hypovolemic Shock A medical or surgical condition in which rapid fluid lossresults in multiple organ failure due to inadequate circulatingvolume and subsequent inadequate perfusion. Most often,hypovolemic shock is secondary to rapid blood loss(hemorrhagic shock).
  21. 21. SRUP• Hemorrhage: Overt or occult• Reduction in circulating volume• Reduction in venous return and CO• O2 supply-demand imbalance• Lactic acidosis• Reduction in venous oxygen saturation• Non hemorrhagic hypovolemic – Severe burns, vomiting and diarrhea
  22. 22. • Decreased preload->small ventricular end-diastolic volumes -> inadequate cardiac generation of pressure and flow• Causes: -- bleeding: trauma, GI bleeding, ruptured aneurysms, hemorrhagic pancreatitis -- protracted vomiting or diarrhea -- adrenal insufficiency; diabetes insipidus -- dehydration -- third spacing: intestinal obstruction, pancreatitis, cirrhosis
  23. 23. Cause• Acute external blood loss secondary to penetrating trauma and severe GI bleeding disorders are 2 common causes of hemorrhagic shock.• Hemorrhagic shock can also result from significant acute internal blood loss into the thoracic and abdominal cavities• Two common causes of rapid internal blood loss are solid organ injury and rupture of an abdominal aortic aneurysm.• Hypovolemic shock can result from significant fluid (other than blood) loss. Two examples of hypovolemic shock secondary to fluid loss include refractory gastroenteritis and extensive burns
  24. 24. Pathophysiology:• The human body responds to acute hemorrhage by activating the following major physiologic systems:• The hematologic• Cardiovascular• Renal• Neuroendocrine systems.
  25. 25. The hematologic• The hematologic system responds to an acute severe blood loss by activating the coagulation cascade and contracting the bleeding vessels (by means of local thromboxane A2 release).• In addition, platelets are activated (also by means of local thromboxane A2 release) and form an immature clot on the bleeding source.• The damaged vessel exposes collagen, which subsequently causes fibrin deposition and stabilization of the clot.• Approximately 24 hours are needed for complete clot fibrination and mature formation.
  26. 26. Cardiovascular• The cardiovascular system initially responds to hypovolemic shock by increasing the heart rate, increasing myocardial contractility, and constricting peripheral blood vessels.• This response occurs secondary to an increased release of norepinephrine and decreased baseline vagal tone (regulated by the baroreceptors in the carotid arch, aortic arch, left atrium, and pulmonary vessels).• The cardiovascular system also responds by redistributing blood to the brain, heart, and kidneys and away from skin, muscle, and GI tract.
  27. 27. Renal• The renal system responds to hemorrhagic shock by stimulating an increase in renin secretion from the juxtaglomerular apparatus.• Renin converts angiotensinogen to angiotensin I, which subsequently is converted to angiotensin II by the lungs and liver• Angiotensin II has 2 main effects, both of which help to reverse hemorrhagic shock, vasoconstriction of arteriolar smooth muscle, and stimulation of aldosterone secretion by the adrenal cortex.• Aldosterone is responsible for active sodium reabsorption and subsequent water conservation.
  28. 28. Neuroendocrine systems• The neuroendocrine system responds to hemorrhagic shock by causing an increase in circulating antidiuretic hormone (ADH).• ADH is released from the posterior pituitary gland in response to a decrease in BP (as detected by baroreceptors) and a decrease in the sodium concentration (as detected by osmoreceptors).• ADH indirectly leads to an increased reabsorption of water and salt (NaCl) by the distal tubule, the collecting ducts, and the loop of Henle.
  29. 29. Clinical Signs of Acute Hemorrhagic Shock Parameter Class I Class II Class III Class IVBlood loss (%) <15 15-30 30-40 >40Blood loss (ml) <750 750-1500 1500-2000 >2000Heart rate (bpm) <100 >100 >120 >140Blood pressure Normal Orthostatic Hypotension Severe hypotensionCNS symptom Normal Anxious Confused Obtunded
  30. 30. Signs of Shock• Cold, clammy and pale skin• Rapid, weak pulse• Shallow, rapid breathing• Oliguria• Reduction in MAP• Cyanosis• Loss of consciousness
  31. 31. The 4 areas in which life-threateninghemorrhage can occur are as follows: chest,abdomen, thighs, and outside the body.
  32. 32. • The chest should be auscultated for decreased breath sounds, because life-threatening hemorrhage can occur from myocardial, vessel, or lung laceration• The abdomen should be examined for tenderness or distension, which may indicate intraabdominal injury
  33. 33. • The thighs should be checked for deformities or enlargement (signs of femoral fracture and bleeding into the thigh).• The patients entire body should then be checked for other external bleeding
  34. 34. • Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lactic acid and PCWP• Treatment: ABCs, IVF (crystalloid), Transfusion Stem ongoing Blood Loss
  35. 35. Treatment of Shock **Increase tissue perfusion and oxygenation status• Maintain airway• Control bleeding• Baseline vital signs• Level of consciousness
  36. 36. Treatment of Shock• Positioning• ABCD approach• Fluid therapy• Drug therapy• Keep patient at normal temperature – Prevent hypothermia – Minimize effect of shock• On-going assessment - every 10-15 minutes
  37. 37. • Crystalloid solutions for intravascular volume replenishment are typically isotonic (e.g. 0.9% saline or Ringers lactate [RL]).• Both 0.9% saline and RL are equally effective; RL may be preferred in hemorrhagic shock because it somewhat minimizes acidosis.
  38. 38. • Colloid solutions (e.g. hydroxyethyl starch, albumin, dextrans) are also effective for volume replacement during major hemorrhage.• Despite theoretical benefits over crystalloid, no differences in survival have been proven.• Both dextrans and hydroxyethyl starch adversely affect coagulation when > 1.5 L is given.
  39. 39. • Blood typically is administered as packed RBCs, which should be cross-matched, but in an urgent situation, 1 to 2 units of type O Rh-negative blood is an acceptable alternative.• When > 1 to 2 units are transfused (e.g. in major trauma), blood is warmed to 37° C.• Patients receiving > 8 to 10 units may require replacement of clotting factors with infusion of fresh frozen plasma or cryoprecipitate and platelet transfusion
  40. 40. Route and Rate of Administration• Standard, large (eg, 14- to 16-gauge) peripheral IV catheters are adequate for most fluid resuscitation.• With infusion pump they typically allow infusion of 1 L of crystalloid in 10 to 15 min and 1 unit of packed RBCs in 20 min.
  41. 41. • For patients at risk of exsanguination, a large (eg, 8.5 French) central venous catheter provides more rapid infusion rates; a pressure infusion device can infuse 1 unit packed RBCs in < 5 min.
  42. 42. • Patients in shock typically require and tolerate infusion at the maximum rate. Adults are given 1 L of crystalloid (20 mL/kg in children) or, in hemorrhagic shock, 5 to 10 mL/kg of colloid or packed RBCs, and the patient is reassessed.• An exception is a patient with cardiogenic shock who typically does not require large volume infusion.
  43. 43. Specific measures• Hypovolaemia: Blood transfusion• Electrolyte/acid base imbalance• Sepsis: Antibiotics, ?steroids• Neurogenic: Steroids• Anaphylactic: Adrenalin
  44. 44. Invasive monitoring• Essential in the definitive treatment• Direct arterial pressure• Central venous pressure• Cardiac output
  45. 45. • The actual endpoint of fluid administration in shock is normalization of DO2.• However, this parameter is not often measured directly. Surrogate endpoints include clinical indicators of end organ perfusion and measurements of preload.• Adequate end organ perfusion is best indicated by urine output of > 0.5 to 1 mL/kg/h
  46. 46. • Heart rate, mental status, and capillary refill may be affected by the underlying disease process and are less reliable markers.• Because of compensatory vasoconstriction, mean arterial pressure (MAP) is only a rough guideline; organ hypoperfusion may be present despite apparently normal values
  47. 47. • Because urine output does not provide a minute-to-minute indication, measures of preload may be helpful in guiding fluid resuscitation for critically ill patients• Central venous pressure (CVP) is the mean pressure in the superior vena cava, reflecting right ventricular end-diastolic pressure or preload.
  48. 48. • Normal CVP ranges from 2 to 7 mm Hg (3 to 9 cm H20). A sick or injured patient with a CVP < 3 mm Hg is presumed to be volume depleted and may be given fluids with relative safety.
  49. 49. Septic shock
  50. 50. Criteria for Four Categories of the Systemic Inflammatory Response Syndrome1. Systemic Inflammatory Response Syndrome (SIRS)Two or more of the following: – Temperature (core) >38°C or <36°C – Heart rate >90 beats/min – Respiratory rate of >20 breaths/min for patients spontaneously ventilating or a PaCO2 <32 mm Hg – White blood cell count >12,000 cells/mm3 or <4000 cells/mm3 or >10% immature (band) cells in the peripheral blood smear
  51. 51. Criteria for Four Categories of the Systemic Inflammatory Response Syndrome2. Sepsis Same criteria as for SIRS but with a clearly established focus of infection3. Severe Sepsis Sepsis associated with organ dysfunction and hypoperfusionIndicators of hypoperfusion: - Systolic blood pressure <90 mmHg - > 40 mmHg fall from normal systolic blood pressure - Lactic acidemia - Oliguria - Acute mental status changes
  52. 52. Phases of Septic Shock• Warm Phase (early): skin flushed, warm due to vasodilatation• Cold Phase (late): skin cool due to fluid deficit with shock
  53. 53. Sign & symptom• Lactic acidosis • Oliguria• Renal failure • Hypotension• Altered mentation • Decrease cardiac output• DIC • Hypoxia • Respiratory failure• Bleeding
  54. 54. Risk factors– Diabetes– Diseases of the genitourinary system, biliary system, or intestinal system– Immunocompromised host such as AIDS , Leukemia , steroid medications– Indwelling catheters– Recent surgery or medical procedure
  55. 55. Septic Shock in trauma patients• Develops 2 - 5 days after injury occurs• Carries a poor prognosis• Assess for: – Penetrating abdominal injuries – Signs of infection – Warm pink skin and dry elevated body temperature – Tachycardia – Wide pulse pressures
  56. 56. Septic shock management
  57. 57. Anaphylactic shock
  58. 58. Anaphylactic shock• DEFINITION – Anaphylaxis is a sudden-onset, life-threatening type I hypersensitivity• Anaphylaxis results from sudden release into the systemic circulation of histamine, tryptase, and other inflammatory mediators from basophiles and mast cells.
  59. 59. Diagnosis• Anaphylaxis remains a clinical diagnosis• directly challenging the patient with the suspected agent
  61. 61. Management of anaphylaxis• Assessment of airway, breathing, circulation• Epinephrine is the drug of choice – IM every 5 to 15 minutes to control symptoms and blood pressure• Oxygen administration• Fluid replacement – Normal saline is preferred, because lactated Ringers may contribute to metabolic acidosis
  62. 62. • Vasopressors – should be administered if epinephrine injections fail to alleviate hypotension – Dopamine increases the force and rate of myocardial contractions while maintaining or enhancing renal and mesenteric blood flow• Antihistamines• Inhaled B2 agonists• Corticosteroids
  63. 63. References• Schwartz’s .Principle of surgery.8th edition• Sabiston.Textbook of surgery.18th edition• ตาราศัลยศาสตร์ .คณะแพทยศาสตร์ จฬาลงกรณ์มหาวิทยาลัย พิมพ์ครังที่ 11 ุ ้• สรี รวิทยา 2.คณะแพทยศาสตร์ ศิริราชพยาบาล
  64. 64. Anaphylactic Shock• Rapid onset• Primary systems: – Cardiovascular, Respiratory – Skin, Gastrointestinal, coagulation• Face, pharynx and laryngeal oedema• Adrenaline is life saving
  65. 65. Anaphylactic Shock• Diffuse vasodilatation• Increase size of vascular bed• Blood is trapped in small vessels and viscera• Temporary loss in total circulatory volume• Sudden severe allergic reaction to: – Drugs, Toxins, Foods, Plants
  66. 66. Symptoms• Apprehension and flushing• Wheezing or shortness of breath & cough• Rapid, weak pulse• Cyanosis• Generalized itching or burning• Watering and itching of the eyes• Hypotension• Coma
  67. 67. Evaluation of Shock• Internal or external hemorrhage• Underlying cardiac problems• Sepsis• Trauma to spine cord• Contact with known allergic substance• Determine amount of blood loss• How long has casualty been bleeding?
  68. 68. Obstructive Shock
  69. 69. Obstructive Shock•Tension pneumothorax •Air trapped in pleural space with 1 way valve, air/pressure builds up •Mediastinum shifted impeding venous return •Chest pain, decreased breath sounds •Rx: Needle decompression, chest tube
  70. 70. Obstructive Shock•Cardiac tamponade •Blood in pericardial sac prevents venous return to and contraction of heart •Related to trauma, pericarditis, MI •Beck’s triad: hypotension, muffled heart sounds, JVD •Diagnosis: large heart CXR, echo •Rx: Pericardiocentisis
  71. 71. Treatment• airway and ventilation• fluid resuscitation and restoration of intravascular volume• vasoconstrictors will improve peripheral vascular tone, decrease vascular capacitance, and increase venous return• dopamine• phenylephrine
  72. 72. • Management of acute spinal cord injury -blood pressure -oxygenation -hemodynamics
  73. 73. Obstructive Shock•Pulmonary embolism •Virscow triad: hypercoaguable, venous injury, venostasis •Signs: Tachypnea, tachycardia, hypoxia •Rx: Heparin, thrombolytics
  74. 74. Obstructive Shock•Aortic stenosis •Resistance to systolic ejection causes decreased cardiac function •Chest pain with syncope •Systolic ejection murmur •Diagnosed with echo •Rx: Valve surgery
  75. 75. Etiology & Hemodynamic Changes in ShockEtiology of shock example CVP CO SVR VO2 satpreload hypovolemic low low high lowcontractility cardiogenic high low high lowafterload Hyperdynamic Low/Hi High Low High Septic gh Hypodynamic Low/Hi Low High Low/High Septic gh Neurogenic Low Low Low Low Anaphylactic Low Low Low Low