Shock

Shock is a condition in which circulation fails to meet the nutritional needs of cells and at the same time fails to remove metabolic waste products.

1. School of Nursing & Midwifery Department of Adult Health Nursing 1 P.by: Habtemariam Mulugeta College of Medicine & Health Sciences

2. Presentation Outline Objectives Introduction Definition Incidence/Prevalence Rate Etiology Risk Factors Pathophysiology Stages of shock Clinical presentation Diagnosis Investigation Effect of shock Metabolic Changes In Shock Classification of shock Differential Diagnosis prognosis Nursing Process Summery Reference Acknowledgment 2

3. Objectives At the end of the session, you will be able to: Define Shock Explain the sign and symptom of Shock Differentiate the diagnostic modalities of Shock Discuss the management of Shock 3

4. INTRODUCTION Term “choc” – French for “push” or impact was first published in 1743 by the physician LeDran shock is a condition in which circulation fails to meet the nutritional needs of cells and at the same time fails to remove metabolic waste products. 4 ATLS - Student Course Manual (10 ed.). 2018 . pp. 43–52, 135.

5. Definition Shock is the state of insufficient blood flow to the tissues of the body as a result of problems with the circulatory system. 1 Shock also known as Circulatory Failure/ Circulatory Collapse/ circulatory shock / Hypovolemic Shock/ blood poisoning - septic shock. 2 5 International Trauma Life Support for Emergency Care Providers (8 ed .) 2018 . pp. 172–173. Tintinalli , Judith E. (2010). p . 168.

6. Cont. Shock is a life threatening situation due to poor tissue perfusion with impaired cellular metabolism, manifested in turn by serious pathophysiological abnormalities. 1 Shock is a term used to describe the clinical syndrome that develops when there is critical impairment of tissue perfusion due to some form of acute circulatory failure. 2 6 1. Bailey and love 2. Davidson’s

7. Cont. Shock may be defined as inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function. 1 The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then if prolonged, to irreversible cellular injury. 2 7 1. Schwartz’s 2. Kumar and Parrillo , 1995

8. Incidence/Prevalence Rate Shock from blood loss occurs in about 1–2% of trauma cases. 1 Up to 1/3 of people admitted to the ICU are in circulatory shock. 2 Of these, cardiogenic shock accounts for approximately 20%, hypovolemic about 20 %, and septic shock about 60% of cases. 3 8 Cherkas , David (Nov 2011). PMID 22164397 Vincent JL, De Backer D (October 2013. 369 (18): 1726–34 . Cecconi M, et al (December 2014). 40 (12): 1795–815.

9. Etiology Heart conditions (heart attack, heart failure ) Heavy internal or external bleeding, such as from a serious injury or rupture of a blood vessel Dehydration , especially when severe or related to heat illness. Infection (septic shock) Severe allergic reaction (anaphylactic shock) Spinal injuries (neurogenic shock) Burns Persistent vomiting or diarrhea 9 Elbers PW, Ince C (2006). 10 (4): 221.

10. Cont. 10 Elbers PW, Ince C (2006 ). PMC 1750971

11. Risk Factors Heart failure, Old age, Hypertension, 11 "Cardiogenic shock - Mayo Clinic. Retrieved 22 May 2020.

12. Pathophysiology 12

13. Stages of shock Deterioration of circulation in shock is a progressive & continuous phenomenon & compensatory mechanisms become progressively less effective Non-progressive (initial, compensated, reversible) shock Progressive decompensated shock Decompensated (irreversible) shock 14 Armstrong, D.J. (2004). The Adult. (2nd edition )

14. 15

15. 16 Non progressive shock

16. 17 Progressive decompensated shock

17. 18 Decompensated shock

18. 19 Armstrong, D.J. (2004). The Adult. (2nd edition )

19. Clinical Presentations Hypotension - Systolic BP<100mmHg and tachycardia - >100/min are the key signs of shock. Symptoms of all types of shock include: • Rapid , shallow breathing • Cold , clammy skin • Rapid , weak pulse • Dizziness or fainting • Weakness 20 International Trauma Life Support for Emergency Care Providers (8 ed .). 2018. pp. 172–173

20. Cont. Depending on the type of shock the following symptoms may also be observed: Eyes appear to stare Anxiety or agitation Seizures , Confusion or unresponsiveness Low or no urine output (Urine Output<30ml/hour ) Bluish lips and fingernails Sweating Chest pain Elevated or Reduced central venous pressure Multi-Organ Failure 21

21. 22

22. Diagnosis Initial Assessment – ABC Airway : Does patient have mental status to protect airway? GCS less than “eight” means “intubate” (E4 V5 M6) Airway is compromised in anaphylaxis Breathing : If patient is conversing, A & B are fine Place patient on oxygen Circulation : Vitals (HR, BP) IV, start fluids, put on continuous monitor 24 ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

23. Cont. In a trauma, perform ABCDE , not just ABC Deficit or Disability Assess for obvious neurologic deficit Movement of all four extremities? Pupils? Glasgow Coma Scale (V5, M6, E4) Exposure Loosening of clothing on trauma patients. 25

24. ATLS - Student Course Manual (10 ed.). 2018 . pp. 43–52, 135.

25. 29 In management of trauma patients, understanding the patterns of injury of the patient in shock will help direct the evaluation and management. Blood loss sufficient to cause shock is generally of a large volume (e.g. external, intrathoracic, intra-abdominal, retroperitoneal, and long bone fractures ). Cont. ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

26. 30 Diagnostic and therapeutic tube thoracotomy may be indicated in unstable patients based on clinical findings and clinical suspicion. Chest radiographs, pelvic radiography, diagnostic ultrasound or diagnostic peritoneal lavage. Cont. ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

27. Investigation CXR - consolidation FBC – WCC elevated or low CBC, ABG - hypoxia, acidosis, raised lactate ECG - low voltage, ST elevation, True Posterior MI Urgent Echo - LV dysfunction CT/MRI - to exclude constructive pericarditis Blood and urine culture 31 ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

28. Effect of shock CARDIOVASCULAR decrease of preload and afterload Baroreceptor response Release of catechol amines Tachycardia and vasoconstriction. RESPIRATORY Metabolic acidosis Inc. respiratory rate and excretion of carbon dioxide Results in compensatory resp. alkalosis. 32 Tintinalli , Judith E. (2010). pp . 174–175.

29. Cont. RENAL AND ENDOCRINE decreased urine output stimulation of renin angiotensin and aldosterone axis release of vasopressin from hypothalamus resulting vasoconstriction and increase Na+ and water reabsorption. 33

30. Cont. MICROVASCULAR Activation of immune and coagulation systems hypoxia and acidosis , activate complement and prime neutrophils oxygen free radicles and cytokine release damaged and endothelium fluids leak out and edema ensues. 34 Tintinalli , Judith E. (2010). pp . 174–175.

31. Cont. CELLULAR Cells switch from aerobic to anaerobic metabolism Decreased ATP production lactic acidosis Glucose exhausts and aerobic respiration ceases Na+/ K+ pump impaired Lysosomes release autodigestive enzymes mitochondria damage cell death . 35

32. Metabolic Changes In Shock CARBOHYDRATE METABOLISM Compensated shock : Hyperglycemia due to increased hepatic glycogenolysis . Decompensated shock : Hypoglycemia due to hepatic glycogen depletion & increased consumption of glucose by tissue . Anaerobic glycolysis occurs as assessed by high blood levels of lactate & pyruvate . 36

33. Cont. PROTEIN METABOLISM Increased intracellular protein catabolism Conversion of amino acids to urea. Increased blood non-nitrogen protein. FAT METABOLISM Increased endogenous fat metabolism. Rise of fatty acid level in blood . 37 Kumar, Vinay ; et al. (2007). pp . 102–103

34. Cont. WATER & ELECTROLYTE DISTURBANCES Failure of sodium pump  potassium leaves the cell ( hyponatremia )  causes cellular swelling. Shock due to loss of plasma only (in burns)  hemoconcentration 38 Kumar, Vinay ; et al. (2007). pp . 102–103

35. Cont. METABOLIC ACIDOSIS Hypoxia of kidney, renal function is impaired blood levels of acids like lactate, pyruvate, phosphate & sulfate rise causing metabolic acidosis. MORPHOLOGIC COMPLICATIONS Morphologic changes in shock are due to Hypoxia. resulting in degeneration & necrosis in various organ. Organs affected are : Brain, Heart, Lungs, Kidneys, Adrenals and GIT. 39

36. Cont. HYPOXIC ENCEPHALOPATHY Compensated shock results in cerebral ischemia which produce altered state of consciousness. However , if blood pressure falls below 50 mmHg as in systemic hypotension in prolonged shock & cardiac arrest, Brain suffers from serious ischemic damage with loss of cortical functions, coma,& vegetative state. 40

37. Cont. HEART IN SHOCK Two types of morphologic changes in Heart Hemorrhage's & Necrosis: Located in subepicardial & subendocardial region. Zonal Lesion: Opaque transverse contraction bands in a myocyte near an intercalated disc. 41

38. Cont. SHOCK LUNG Lungs have Dual blood supply & generally not affected by hypovolemic shock But in Septic shock  SHOCK LUNG seen as symptoms of ARDS including: congestion , interstitial & alveolar edema, interstitial lymphocytic infiltrate , alveolar hyaline membrane, Thickening & fibrosis of alveolar septa, fibrin & platelet thrombi in pulmonary microvasculature. 42 Kumar, Vinay ; et al. (2007). pp . 102–103

39. Cont. SHOCK KIDNEY Irreversible renal injury  Important complication of Shock. Renal ischemia following systemic hypotension is considered responsible for renal changes in Shock  End result is generally anuria & death. 43

40. Cont. ADRENALS IN SHOCK Adrenals show stress response in SHOCK. It includes Release of aldosterone in response to hypoxic kidney . Release of glucocorticoids from adrenal cortex & catecholamine like adrenaline from adrenal medulla. “ SEVERE SHOCK RESULTS IN ADRENAL HAEMORRHAGES ” 44

41. Cont. HYPOXIC ENCEPHALOPATHY Compensated shock results in cerebral ischemia which produce altered state of consciousness. However , if blood pressure falls below 50 mmHg as in systemic hypotension in prolonged shock & cardiac arrest, Brain suffers from serious ischemic damage with loss of cortical functions, coma,& vegetative state. 45

42. Cont. GIT Hypo perfusion of Alimentary tract  Mucosal & Mural infarction called “ HAEMORRHAGIC GASTROENTEROPATHY” In Shock due to burns, acute stress  ulcers of stomach/duodenum  “ CURLING’S ULCERS ” LIVER Hypoxia, VDM is released  Vasodilatation Others include focal necrosis, fatty change, impaired liver function . 46 Kumar, Vinay ; et al. (2007). pp . 102–103

43. 47

44. ISCHEMIC REPERFUSION SYNDROME It is the injury that occurs once the normal circulation is restored to the tissues Reasons : Ac i d an d potass i um l o ad bui lt u p leads to myocardial depression, vascular dilatation and hypotension. Neutrophils are flushed back into the circulation; causes further injury to the endothelial cells of lungs and kidneys. Results : Acute lung and renal injury Multiple organ failure Death 48 Kumar, Vinay ; et al. (2007). pp . 102–103

45. Classification of SHOCK Primary (INITIAL SHOCK) Secondary (TRUE SHOCK) Anaphylactic (Type I immunologic reaction) 49 Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th ed .).. pp. 278–288 .

46. Cont. Initial shock is a transient and usually benign vasovagal attack resulting from sudden reduction of venous return to the heart caused by neurogenic vasodilatation and consequent peripheral pooling of the blood . It can occur immediately following: Trauma Severe pain Emotional overreaction due to: Fear Sorrow and surprise Sight of blood 50

47. Cont. Primary shock can be labeled as a severe form of syncope because Clinically Patient develops, signs and symptoms similar to that of syncope: Unconsciousness Weakness Sinking Sensation Pale and Clammy limbs Weak and rapid pulse and Low Blood Pressure 51

48. Cont. True shock is circulatory imbalance between oxygen supply and oxygen requirements at cellular level; hence name CIRCULATORY SHOCK. occurs due to hemodynamic derangements with hypo perfusion of the cells. 52 Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th ed .).. pp. 278–288 .

49. Cont. Anaphylaxis  is a serious  allergic reaction  that is rapid in onset and may cause death.  It typically causes : an itchy rash, throat or tongue swelling,  SOB, vomiting, lightheadedness, and  low blood pressure .  These symptoms typically come on over minutes to hours. 53

50. Classification Based on Etiology HYPOVOLEMIC SHOCK CARDIOGENIC SHOCK SEPTIC SHOCK OTHER TYPES : TRAUMATIC NEUROGENIC HYPOADRENAL 54 Harsh Mohan 4 th ed

51. Cont. Due to low flow(reduced stroke volume) hypovolemic cardiogenic obstructive Due to low peripheral arteriolar resistance (vasodilatation) septic anaphylactic neurogenic Davidson’s 21st ed 55

52. Cont. 56 Vasovagal Psychogenic Neurogenic Hypovolemic Traumatic Burns Cardiogenic Septic (endotoxin ) : Anaphylactic hyper dynamic /warm hypovolemic hypo dynamic /cold (Bailey & Love’s short practice of surgery)

53. Proposed by HINSHAW and COX (1972) Hypovolemic shock Cardiogenic shock Extra cardiac obstructive shock Distributive shock Septic shock Anaphylactic shock Neurogenic shock 57

54. 58 Shock due to reduced blood volume (Hypovolemic shock or cold shock) Traumatic shock Hemorrhagic shock Surgical shock Burn shock Dehydration shock Proposed by HINSHAW and COX (1972)

55. SHOCK due to increased vascular capacity (Blood volume normal; occurs because of inadequate blood supply to the tissues due to increased vascular capacity): Neurogenic shock Anaphylactic shock Septic shock SHOCK due to diseases of the Heart (cardiogenic shock) SHOCK due to obstruction of blood flow. 59 Proposed by HINSHAW and COX (1972)

56. HYPOVOLEMIC SHOCK 61 Occurs from inadequate circulating blood volume Major effects are due to decreased cardiac output and low intra cardiac pressure Severity of clinical features depends on degree of blood volume lost ATLS - ( 10 ed.). 2018 . pp. 43–52, 135.

57. HYPOVOLEMIC SHOCK

58. PATHOP H YSIOLOGY 64 Hemorrhage from small venules & veins (50%) ↓ Decreased filling of right heart ↓ Decreased filling of pulmonary vasculature ↓ Decreased filling of left atrium & ventricle ↓ Left ventricular stroke volume decreases (Frank Starling ) ↓ Drop in arterial blood pressure & tachycardia ↓ Poor perfusion to pulmonary arteries ↓ Cardiac depression & pump failure

59. CLASSSIFICATION OF HYPOVOLEMIC SHOCK HEMORRHAGIC TRAUMA GASTROINTESTINAL BLEEDING NON-HEMORRHAGIC EXTERNAL FLUID LOSS DIARR H OEA VOMITING POLYUREA FLUID REDISTRIBUTION BURNS ANA P HYLA X S 65

60. CLASSIFICATION OF ACUTE BLOOD LOSS 66 Class I : blood loss up to 15% (≤1000ml)  mild clinical symptoms (compensated) Class II : blood loss 15-30% (1000-1500ml )  mild tachycardia, tachypnea, weak peripheral pulses and anxiety (mild ) Class III: blood loss 30-40% (1500-2000ml)  Hypotension , marked tachycardia [pulse >110 to 120 bpm], and confusion (moderate ) Class IV: blood loss >40% (>2000ml )  significant depression in systolic BP , very narrow pulse pressure (severe)

61. Class I Class II Class III Class IV Blood loss (mL) Up to 750 mL 750 – 1500 mL 1500- 2000mL >2000 mL Pulse rate & pulse pressure <100 normal or decreased >100 decreased >120 decreased >140 Decreased Blood pressure Normal Normal Decreased Decreased Respiratory rate 14 – 20 20 -30 30 - 40 35 Urine output mL/hr 30 20 -30 5 -15 Negligible Fluid rep l ac e ment Crystalloid Crystalloid & blood Crystalloid & blood Crystalloid 43

62. Bu r n s

63. Third Spacing .

64. Signs & Symptoms 72 Anxiety, restlessness, altered mental state Hypotension A rapid, weak, thready pulse Cool, clammy skin Rapid and shallow respirations Hypothermia Thirst and dry mouth Distracted look in the eyes

65. Compensatory Mechanisms 73 Adrenergic discharge Hyperventilation Vasoactive hormones Angiotensin ,Vasopressin, Epinephrine Collapse Re-absorption of fluid from interstitial tissue Resorption of fluid from intracellular to extracellular space Renal conservation of body water & electrolyte.

66. Clinical Monitoring 74 Blood pressure Respiration Urine output Central venous pressure ECG Swan-Ganz catheter cardiac output mixed venous oxygen level vascular pressure Pulmonary artery wedge pressure

67. 75

68. General Principles In Management Patients should be treated in ICUs preferably Continuous electrocardiographic monitoring Pulse oximetry A reduction of elevated serum lactate levels is one good indicator of successful resuscitation and is often used as a therapeutic goal 76

69. Medical & Surgical Management 77 OBJECTIVES Increase Cardiac Output Increase Tissue Perfusion The plan of action should be based on Primary problem Adequate fluid replacement Improving myocardial contractility Correcting acid base disturbances ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

70. Resuscitation Immediate control of bleeding: Rest, Pressure Packing, Operative Methods Extracellular fluid replacement: Infusion of fluid is the fundamental treatment Crystalloids , for initial resuscitation for most forms of hypovolemic shock. After the initial resuscitation, with up to several liters of crystalloid fluid, use of colloids. Drugs Sedatives Chronotropic agents Inotropic agents 78 Cont. ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

71. M AS T Crystalloid Colloid Blood

72. DISTRIBUTIVE SHOCK 80 As in hypovolemic shock, there is an insufficient intravascular volume of blood This form of "relative" hypovolemia is the result of dilation of blood vessels which diminishes systemic vascular resistance Examples of this form of shock : Septic shock Anaphylactic shock Neurogenic shock ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

73. TRAUMATIC SHOCK 81 Primarily due to hypovolemia from : Bleeding externally eg: open wounds, fractures Bleeding internally eg: ruptured liver, spleen Clinical features : Presence of peripheral & pulmonary edema. Infusion of large amount of fluid which is adequate in hypovolemic shock is inadequate here. ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

74. PATHOPHYSIOLOGY 82 Traumatic tissue activates the coagulation system ↓ Release of micro-thrombi into circulation ↓ Obstruction parts of pulmonary micro vasculature ↓ Increased pulmonary vascular resistance ↓ Increased right ventricular diastolic & right atrial pressure ↓ Humoral products of thrombi induce increase in capillary permeability ↓ Loss of plasma into interstitial tissue ↓ Depletion of Vascular volume

75. MANAGEMENT 83 Resuscitation Local treatment of trauma & control of bleeding , surgical debridement of ischemic & dead tissue & immobilization of fracture. Fluid replacement with Ringers lactate, Ringers acetate, Normal saline. Anticoagulation with one intravenous dose of 10,000 units of heparin

76. CARDIOGENIC SHOCK 84 Primary dysfunction of one ventricle or the other Dysfunction may be due to Myocardial infarction Chronic congestive heart failure Cardiac arrhythmias Pulmonary embolism Systemic arterial hypertension

77. Dysfunction of right ventricle  right heart unable to pump blood in adequate amount into lungs, filling of left heart decreases , so left ventricular out put decreases . Dysfunction of left ventricle  left ventricle unable to maintain adequate stroke volume , left ventricular output & systemic arterial blood pressure decreases ,there is engorgement of the pulmonary vasculature due to normal right ventricular output, but failure of left heart 86 Cont. Schumann, J: et al (29 January 2018).

78. Arises when heart is compressed from outside to decrease cardiac output , the cause may be Tension pneumothorax Pericardial tamponade Diaphragmatic rupture with herniation of the bowel into the chest. 87 Cardiogenic compressive shock:

79. CLINICAL FEATURES 88 Skin is pale & urine out put is low . Pulse becomes rapid & the systemic blood pressure is low . Right ventricular dysfunction, neck veins are distended & liver is enlarged. Left ventricular dysfunction , there are bronchial rales & third heart sound heard . Gradually, the heart also becomes enlarged.

80. 89

81. MANAGEMENT 90 Air way must be cleaned Initial measures include supplemental oxygen and, when systolic blood pressure permits, administration of i.v. nitroglycerin. Insertion of an intra-aortic balloon pump decreases ventricular after load, improving myocardial performance ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

82. Cont. Revascularization with either angioplasty or bypass surgery have suggested improved survival Vasodilators Beta-Blockers 91 ATLS - ( 10 ed .). 2018. pp. 43–52, 135.

83. Cardiogenic shock can also occur after prolonged cardiopulmonary bypass ; the stunned myocardium may require hrs or days to recover sufficiently to support circulation. Treatment consists of combination of inotropic agents In case of pulmonary embolus it should be treated with large doses of heparin, intravenously 92 Cont.

84. Cont . Pain ,if present should be controlled with sedatives like morphine Fulminant pulmonary edema should be controlled with diuretics. Drugs mainly employed are Inotrophic agents 93

85. EXTRACARDIAC OBSTRUCTIVE SHOCK 94 Flow of blood is obstructed, which impedes circulation and can result in circulatory arrest Several conditions result in this form of shock Cardiac tamponade Constrictive pericarditis Tension pneumothorax Massive pulmonary embolism Cotran , Ramzi S.; et al. (2005 ).. p. 141.

86. Tension Pneumothorax

87. Constrictive pericarditis

88.  Cardiac Tamponade

89. P ulmonary embolism

90. Aortic stenosis

91. Treatment of choice is pericardial drainage via surgery Pulmonary embolism is usually treated with systemic anticoagulation, but when massive pulmonary embolism causes right ventricular failure and shock, thrombolytic therapy should be strongly considered 102 Management

92. NEUROGENIC SHOCK 103 Primarily due to blockade of sympathetic nervous system  loss of arterial & venous tone with pooling of blood in the dilated peripheral venous system. The heart does not fill  the cardiac output falls. Neurogenic shock caused by: Paraplegia Quadriplegia. Trauma to Spinal cord. Spinal anesthesia .

93. syncope Holtz, Anders; Levi, Richard (6 July 2010). Spi ).. p. 63–4.

94. CLINICAL FEATURES : Warm skin, pink & well perfused Heart rate is rapid Blood pressure is low Urine output may be normal 106 Holtz, Anders; Levi, Richard (6 July 2010). Spi ).. p. 63–4.

95. Pathophysi o logy 107 Dilatation of the systemic vasculature ↓ Decreased systemic arterial pressure ↓ Pooling of blood in systemic venules & small veins ↓ The right heart filling & stroke volume decreases ↓ Decreased pulmonary blood volume & left heart filling ↓ Discharge of angiotensin & vasopressin though they fail to restore the cardiac output to normal

96. MANAGEMENT 108 Assuming Trendelenburg position - displaces blood from systemic venules into right heart & increases cardiac output. Administration of fluids. Vasoconstrictor drugs. Phenylephrine & Metaraminol Only type of shock safely treated with vasoconstrictor . Its prompt action saves patient from immediate damage to important organs like brain, heart & kidney. Holtz, Anders; Levi, Richard (6 July 2010). Spi ).. p. 63–4.

97. VASOVAGAL / VASOGENIC SHOCK 110 Part of neurogenic shock Pathophysiology : pooling of blood due to dilatation of peripheral vascular system particularly in the limb muscle & in splanchnic bed . Holtz, Anders; Levi, Richard (6 July 2010). Spi ).. p. 63–4.

98. Cont. This causes reduced venous return to the heart leading to low cardiac output & bradycardia , blood flow to brain is reduced causing cerebral hypoxia & unconsciousness. Management : Trendelenberg position - increases cerebral flow & consciousness is restored 111

99. PSYCHOGENIC SHOCK 112 Part of Neurogenic shock . Occurs following sudden fright from unexpected bad news or at the sight of horrible accident . Effect may vary in intensity from temporary unconsciousness to even sudden death.

100. SEPTIC SHOCK 113 Most often due to gram-negative & gram-positive septicemia. It occurs in cases of, -Severe septicemia -Cholangitis -Peritonitis -Meningitis etc. The common organisms that are concerned with septic shock are E.coli, klebsiella, aerobactor, proteus, pseudomonas, bacteroides, etc Singer M, et al . ( February 2016). JAMA . 315 (8): 801–10.

101.    Clinical features Hypotension – correct with pressors Elevated serum lactate Initially heart rate increase then decrease

102. GRAM POSITIVE SEPSIS AND SHOCK 117 It is usually caused by dissemination of a potent exotoxin liberated from gram positive bacteria without evidence of bacteremia. It is usually seen in Clostridium Tetany or Clostridium Perfringes infection. It is basically caused due to massive fluid losses. Arterial resistance falls but there is no fall in cardiac output. Urine output usually remains normal. Singer M, et al . ( February 2016). JAMA . 315 (8): 801–10.

103. GRAM NEGATIVE SEPSIS AND SHOCK 118 The most common cause of this infection is genito- urinary infection. Persons who have had operations of the genito-urinary tract are also susceptible. It may also be seen in patients who have undergone tracheostomy or those with gasterointestinal system infections .

104. The severity may vary from mild hypotension to fulminating septic shock which has a poor prognosis. The prognosis is more favorable when the infection is accessible to surgical drainage . The clinical manifestations of septic shock may be fulminating and rapidly fatal. It is recognized initially by the development of chills & fever of over 100 degrees. Two types are clearly defined -Early warm shock. -Late cold shock. 119 Cont.

105. EARLY WARM SHOCK 120 In this type there is cutaneous vasodilatation. Toxins increase the body temperature. To bring this down vasculature of the skin dilates. This increases the systemic vascular resistance. Arterial blood pressure falls but the cardiac output increases, because the left ventricle has minimal resistance to pump against .

106. Cont. Adrenergic discharge further Increases the cardiac output. The skin remains pink, warm & well perfused. The pulse is high & the blood pressure low. There are intermittent spikes of fever with bouts of chills . 121

107. LATE COLD SHOCK 122 There is increased vascular resistance due to release of toxic products. This leads to hypovolemia with decrease in right heart filling. There is decreased flow to pulmonary vasculature so the left heart filling & the cardiac output decreases. The knowledge of existence of a septic focus is the only factor that differentiates septic shock from traumatic & hypovolemic shock.

108. 123 The only way to reduce mortality in septic shock is by prompt diagnosis & treatment. It can be divided into two groups. Treatment of the infection. Treatment of the shock. Management Singer M, et al . ( February 2016). JAMA . 315 (8): 801–10.

109. Therapy of septic shock has 3 main components 1 st , the nidus of infection must be identified and eliminated 2 nd , adequate organ system perfusion and function must be maintained, guided by cardiovascular monitoring . 76 Cont.

110. Maintenance of blood Hb level, O 2 saturation are imp therapeutic guidelines. 3 rd therapeutic goal is to interrupt the pathogenic sequence leading to septic shock, achieved by inhibiting toxic mediators such as endotoxin, TNF, and IL-1 . 76 Cont.

111. It consists of: Fluid replacement. Debridement & drainage of the infection. Administration of the antibiotics. Mechanical ventilation. Steroids. Vasoactive drugs. Specific gamma globulins to bind the endotoxins. The antibiotic polymixin E also absorbs some of the endotoxin. 126 Cont.

112. ANAPHYLACTIC SHOCK 128 Etiology : The most common cause of anaphylaxis is the administration of penicillin. The other causes include anesthesia, dextrans, serum injections, stings, consumption of shell fish. Pathophysiology: The antigen combines with Ig E on the mast cell & basophils releasing large amounts of histamine and slow releasing substances of anaphylaxis.

113. Clinical features: It manifests as bronchospasm, laryngeal edema, respiratory distress, hypoxia, massive vasodilatation, hypotension and shock. The mortality rate is 10%. In the dental office this reaction can occur during or immediately following the administration of penicillin or LA to a previously sensitized patient. 129 Cont. Tintinalli , Judith E. (2010 ). pp. 174–175.

114. 130

115. 132

116. Mana g ement 134 Immediate & aggressive management is imperative if the patient is to survive. Step 1: Position the patient Place the patient in a supine position with the legs slightly elevated. Step 2: A-B-C Open the airway by tilting the head. Breathing & circulation should be established carrying BLS as needed. Step 3: Definitive care As soon as a systemic allergy is suspected emergency medical help is sought. Tintinalli , Judith E. (2010 ). pp. 174–175.

117. (A) Administration of epinephrine subcutaneously 0.3ml of 1:1000 for adults, 0.15 for children,0.075ml for infants. With decreased perfusion the absorption of epinephrine will be delayed. In such situations it can be administered sublingually or intralingually. If the respiratory or cardiovascular regions fail to improve within 5 minutes of administration, a 2 nd dose should be given. Subsequent doses can be given away 5-10 minutes as needed provided the patient is properly monitored. (B) Administration of oxygen Deliver oxygen at a flow of 5-6 liters per minute by nasal hood or full face mask at any time during the episode. 135 Cont. Tintinalli , Judith E. (2010 ). pp. 174–175.

118. (C) Monitoring of vital signs Monitoring the patients cardiovascular & respiratory status continuously. Record blood pressure & carotid heart rate at least every 5minutes & start closed chest compression if cardiac arrest occurs. ( D) Additional drug therapy After the administration of epinephrine, the other drugs to be administered are : Antihistamines, Corticosteroids. These drugs are administered only after clinical improvement is noted & are not be given during the acute phase as they are too slow in onset. Cont.

119. Prevention  Avoid Trigger  De s ensatizati o n

120. Nursing Management of Shock Check for a response. Give Rescue Breaths or CPR as needed. Lay the person flat, face-up, but do not move him or her if you suspect a head, back, or neck injury. Raise the person's feet about 12 inches. Use a box, etc. If raising the legs will cause pain or further injury, keep him or her flat. Keep the person still . 139 Sharma Asha , pp 1722- 1750

121. Cont. Do not raise the feet or move the legs if hip or leg bones are broken. Keep the person lying flat. Check for signs of circulation. If absent, begin CPR . Keep the person warm and comfortable. Loosen belt (s) and tight clothing and cover the person with a blanket . 140 Sharma Asha , pp 1722- 1750

122. Cont. NPO: Even if the person complains of thirst, give nothing by mouth. If the person wants water, moisten the lips. Reassure the person. Make him or her as comfortable. Fluid and blood replacement: Open IV line on both hands with two wide bore cannulas and start fluid rapidly as advised . 141 Sharma Asha , pp 1722- 1750

123. Cont. Administer oxygen via face mask. Identify the cause and treat accordingly. Vasoactive medications to improve cardiac contractility, i.e. Dopamine, Dobutamine , Noradrenaline . 142

124. Self-Care at Home Call for help and Stay with the person until help arrives, check the person's a irway, b reathing and c irculation (the ABCs ). Administer CPR if you are trained. If the person is breathing on his or her own, continue to check breathing every 2 minutes until help arrives. 143 Sharon Mantik 3 rd Ed pp. 740-757

125. Cont. Do NOT move a person who has a known or suspected spinal injury (unless they are in imminent danger of further injury). Have the person lie down on his or her back with the feet elevated above the head (if raising the legs causes pain or injury, keep the person flat) to increase blood flow to vital organs. Do not raise the head. 144

126. Cont. Keep the person warm and comfortable. Loosen tight clothing and cover them with a blanket. Do not give fluids by mouth, even if the person complains of thirst . There is a choking risk in the event of sudden loss of consciousness . Give appropriate first aid for any injuries. Direct pressure should be applied to any wounds that are bleeding significantly . 145

127. Differential Diagnosis Systemic inflammatory response syndrome (SIRS) Acute coronary syndrome (ACS) Aortic regurgitation Dilated cardiomyopathy Restrictive cardiomyopathy Congestive heart failure (CHF) and pulmonary edema 146 Alonso DR, et al . 1973 Sep. 48 (3):588-96.

128. Cont. Mitral regurgitation Pericarditis and cardiac tamponade Hypovolemic shock Papillary muscle rupture Acute valvular dysfunction 147 Alonso DR, et al . 1973 Sep. 48 (3):588-96.

129. Prognosis The prognosis varies with the origin of shock and its duration . Low volume, anaphylactic, and neurogenic shock are readily treatable and respond well to medical therapy. 80%-90% of young patients survive hypovolemic shock with appropriate management. 148

130. Cont. Cardiogenic shock associated with extensive myocardial infraction : (mortality rate up to 75 %) Septic shock, however has a mortality rate between 30 % and 80% while cardiogenic shock has a mortality rate between 70 % and 90%. 149

131. Cont. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Perfusion of the brain may be the greatest danger during shock. Therefore urgent treatment is essential for a good prognosis 150

132. NURSING PROCESS ASSESSMENT 1. Health Perception and Management Subjective Data c/c : SOB/chest pain/dizziness etc HPI: Mr. X is a 25yr old male married pt , presented with sob, weakness, fainting /2day… Hx Past: pt has Hx of HTN Rx in the past months…. Life style changes: sport, avoid salt, avoid smoking… Non/prescribed: penicillin He has visit to hospital in the past Objective Data Blood Pressure: 90/60 mmHg Heart Rate: 120bpm 2 appointment missed by the pt in the past Rx 151

133. 2. ACTIVITY AND EXERCISE 2.1 Mobility & Self Care Subjective Data Appropriate bathing, toileting, dressing, grooming, feeding . Good motor activities like sitting, standing, walking, and , opening doors . Good home maintenance skill Restriction of rigorous physical activity Objective Data Good balance, coordination, abnormal movements Good muscle tone, strength, bulk Good body position 152

134. 2. ACTIVITY AND EXERCISE 2.2 Respiration functioning Subjective Data Smoking cigarette Shortness of breath Objective Data Increased respiratory rate Decreased SpO2 Crackles in lungs No asymmetric expansion Tactile fremitus present No wheezing, rales , crackling, rhonchus sound 153

135. 2. ACTIVITY AND EXERCISE 2.3 Cardio vascular functioning Subjective Data Hx of smoking Hx Hypertension Fainting Dizziness Objective Data Blood Pressure: 90/60 mmHg (decreased bp ) Heart Rate: 120bpm (increased heart rate) Heart sounds muffled S3, S4 present JVD 154

136. 3. Nutrition & Metabolism Subjective Data Decreased food and fluid intake Nausea Vomiting Salty food intake restriction Objective Data BMI: with in normal range No edema No scars ,  stretch marks ,  lesions , dilated veins, or  rashes . No organomegaly 155

137. 4. ELIMINATION 4.1 Urinary elimination Subjective Data Small amount of urine Less frequent urination Objective Data Normal color of urine No bladder distension, tenderness 156

138. 4. ELIMINATION 4.2 Bowel Elimination Subjective Data Recent change in bowl movement Normal color of stool Hx of Bowel Surgery Objective Data No hemorrhoids, wart, sores or masses No masses or tenderness No enlargement of prostate 157

139. 5. Sleep & Rest Pattern Subjective Data Normal Hour of sleep: <8hr Nap during the day: present Satisfaction with sleep pattern: NO Objective Data Frequently yawning Decreased attention span. Dark circles or puffiness around the eyes. Continual dozing 158

140. 6. Cognition & Perception Subjective Data Orientation to place, person and time: absent Pain Fluid imbalance Decreased oxygen supply Inadequate blood flow Neurological impairment Systemic infection Medication toxicity Objective Data Shallow or rapid respiration/ SOB Abnormal cardiovascular function/ Hypotension History of HTN 159

141. 7. Self- Perception & Self- Concept Subjective Data The pt describe him self as good person Pt consider his illness as his weakness Pt. feels good most of the time Objective Data Good eye contact Personal grooming and appearance is good Posture and body movements is normal Mood and emotions are good Voice and speech pattern are normal 160

142. 8. Roles & Relationship Subjective Data Good financial status of the pt family The husband & the wife makes the decision of the house Family members support each others well No financial problem in the famil y Objective Data Good family interactions No behavioural signs of dysfunction like labile emotions, withdrawal, irritability, poor sleeping and eating, inability to concentrate, and dependency No indicators of physical abuse 161

143. 9. Coping & Stress Tolerance Subjective Data Praying relieve pt stress Pt talk when he is worried Little bad effect on the pt feeling due to illness Objective Data Pt has sympathetic stimulation for sudden stressors. 162

144. 10. SEXUALITY AND REPRODUCTION PATTERN Subjective Data No STI No change in sexuality Objective Data No abnormal findings in Examination of reproductive organs 163

145. 11. Values & Beliefs Pattern Subjective Data Praying, fasting are among the Religious practices that are important to the pt Significance of religion to the person is high No Impact of illness on the patient’s belief Objective Data Pt. Visit clergy Pt. seen praying 164

146. Nursing Diagnosis Ineffective breathing patter related to the disease process as evidenced by change in respiratory rate Anxiety related to the disease process as evidenced by dizziness and light headedness Risk of infection related to hospitalization 165

147. Nursing Plan Goal Return the Client breathing pattern to normal level Remove the Client anxiety completely Avoid the Client infection risk completely 166

148. Cont. Expected Outcome Client breathing pattern improved in 50% after 15min oxygenation Client anxiety decrease by half after 10 min health education Client risk of infection decrease by 75% after giving prophylactic ordered medication and CASH 167

149. Intervention Giving ordered medication and oxygenation Health Education And Reassurance Performing CASH Monitoring the client changes and treat accordingly 168

150. Evaluation Client condition Improved Proposed goal met 169

151. Shock is a life-threatening medical condition and is a medical emergency. Symptoms of septic shock include fever, nausea, vomiting, and dizziness or fainting. There are several types of shock: septic shock caused by bacteria, anaphylactic shock caused by hypersensitivity or allergic reaction , cardiogenic shock from heart damage, hypovolemic shock from blood or fluid loss, and neurogenic shock from spinal cord trauma . Treatment for shock depends on the cause. Tests will determine the cause and severity. Usually IV fluids are administered in addition to medications that raise blood pressure . 170 Summary

152. Cont. Septic shock is treated with antibiotics and fluids. Anaphylactic shock is treated with diphenhydramine ( Benadryl ), epinephrine (an " Epi -pen"), and steroid medications ( solu-medrol ). Cardiogenic shock is treated by identifying and treating the underlying cause. Hypovolemic shock is treated with fluids (saline) in minor cases, and blood transfusions in severe cases. Neurogenic shock is the most difficult to treat as spinal cord damage is often irreversible. Immobilization, anti-inflammatories such as steroids and surgery are the main treatments. Shock prevention includes learning ways to prevent heart disease , injuries, dehydration and other causes of shock. 171

153. Reference ATLS - Advanced Trauma Life Support - Student Course Manual (10 ed.). American College of Surgeons. 2018. pp. 43–52, 135. ISBN 978-78-0-9968267 International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018. pp. 172–173. ISBN 978-1292-17084-8. Tintinalli , Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine ( Tintinalli )). New York: McGraw-Hill Companies. p. 168. ISBN 978-0-07-148480-0. Cherkas , David (Nov 2011). "Traumatic Hemorrhagic Shock: Advances In Fluid Management“ (https://web.archive.org/web/20120118152838/http://www.ebmedicine.net/store.php?paction=showProduct&catid=8&pid=244). Emergency Medicine Practice. 13 (11). PMID 22164397 (https://pubmed.ncbi.nlm.nih.gov/22164397). Archived from the original (http://www.ebmedicine.net/store.php?paction=showProduct&catid=8&pid=244) on 2012-01-18. Vincent JL, De Backer D (October 2013). "Circulatory shock" (https://semanticscholar.org/paper/f8eb49085615fe6fac11777ae1f36786d161dfbe). The New England Journal of Medicine. 369 (18): 1726–34. doi:10.1056/NEJMra1208943 ( https://doi.org/10.1056%2FNEJMra1208943 ). PMID 24171518 ( https://pubmed.ncbi.nlm.nih.gov/24171518 ). Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, Jaeschke R, Mebazaa A, Pinsky MR, Teboul JL, Vincent JL, Rhodes A (December 2014). "Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239778). Intensive Care Medicine. 40 (12): 1795–815. doi:10.1007/s00134-014-3525-z (https://doi.org/10.1007%2Fs00134-014-3525-z). PMC 4239778 ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239778 ). PMID 25392034 (https://pubmed.ncbi.nlm.nih.gov/25392034 ). 172

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155. Cont. Armstrong, D.J. (2004). Shock . In: Alexander, M.F., Fawcett, J.N., Runciman , P.J. Nursing Schumann , J; Henrich , EC; Strobl , H; Prondzinsky , R; Weiche , S; Thiele, H; Werdan , K; Frantz, S; Unverzagt , S (29 January 2018). "Inotropic agents and vasodilator strategies for the treatment of cardiogenic shock or low cardiac output syndrome" (https://www.ncbi.nlm.nih.gov/p mc/articles/PMC6491099). The Cochrane Database of Systematic Reviews . 1 : CD009669. doi:10.1002/14651858.CD009669.pub3 (https://doi.org/10.1002%2F14651858.CD009669.pub 3). PMC 6491099 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6491099). PMID 29376560 (https://pubmed.ncbi.nlm.nih.gov/29376560). Singer M, Deutschman CS, Seymour CW, Shankar- Hari M, Annane D, Bauer M, et al. (February 2016). "The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968574). JAMA . 315 (8): 801–10. doi:10.1001/jama.2016.0287 (https://doi.org/10.1001%2Fjama.2016.0287). PMC 4968574 (http s://www.ncbi.nlm.nih.gov/pmc/articles/PMC4968574). PMID 26903338 (https://pubmed.ncbi.nl m.nih.gov/26903338). Sharma Asha , Lewis medical surgical nursing, Elsevier publication, page no 1722- 1750 Sharon Mantik Lewis Medical Surgical Nursing, Mosby's year book publication 3 rd Edition page no 740-757 174

156. Cont. Practice. Hospital and Home. The Adult. (2nd edition): Edinburgh: Churchill Livingstone. Tintinalli , Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine ( Tintinalli )) . New York: McGraw-Hill Companies. pp. 174–175. ISBN 978-0-07- Kumar, Vinay ; Abbas, Abul K.; Fausto , Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 102–103 ISBN 978-1-4160-2973-1 Guyton, Arthur; Hall, John (2006). "Chapter 24: Circulatory Shock and Physiology of Its Treatment". In Gruliow , Rebecca (ed.). Textbook of Medical Physiology (11th ed.). Philadelphia, Pennsylvania: Elsevier Inc. pp. 278–288. ISBN 978-0-7216-0240-0. Holtz, Anders; Levi, Richard (6 July 2010). Spinal Cord Injury (https://books.google.com/books? id= ZvCqdwWwGRsC&pg =PA63). Oxford University Press. p. 63–4. ISBN 978-0-19-970681-5. Cotran , Ramzi S.; Kumar, Vinay ; Fausto , Nelson; Nelso Fausto ; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease . St. Louis, Mo: Elsevier Saunders. p. 141. ISBN 0-7216-0187-1. 175

157. ACKNOWLEDGMENT First I would like to express my heartfelt gratitude to WU CMHS for giving me this chance to enhance my knowledge and skill. Secondly I would like to thank my instructor Mr. Wondwossen Yimam for sharing me his deep knowledge, experience and expertise. Last but not least I would like to thank my family and friends in helping me in ideas and material during my entire work. 176

158. Thank You 177