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CHAPTER 26 Shock, Sepsis, and Multiple Organ Dysfunction Syndrome Copyright © 2012, 2008, 2004, 2000, 1996, 1992 by Mosby, an imprint of Elsevier Inc. OBJECTIVES Describe generalized shock response and systemic inflammatory response. List the etiologies of hypovolemic, cardiogenic, anaphylactic, neurogenic, and septic shock and multiple organ dysfunction syndrome (MODS). Explain the pathophysiology of the five forms of shock and MODS. (continued) OBJECTIVES (CONTINUED) Identify the clinical manifestations of the five forms of shock and MODS. Outline the important aspects of the medical management of hypovolemic, cardiogenic, anaphylactic, neurogenic, and septic shock and multiple organ dysfunction syndrome. Summarize the nursing priorities for managing a patient with each type of shock or MODS. SHOCK SYNDROME Description Often results in MODS Etiology Four classifications: Hypovolemic Cardiogenic Distributive Septic, anaphylactic, or neurogenic PATHOPHYSIOLOGY OF SHOCK SYNDROME Four stages: Initial stage Compensatory stage Progressive stage Refractory stage CONSEQUENCES OF SHOCK Cardiovascular Ventricular failure Microvascular thrombosis Neurological Sympathetic nervous system dysfunction Cardiac and respiratory depression Thermoregulatory failure Coma (continued) CONSEQUENCES OF SHOCK (CONTINUED) Pulmonary Acute respiratory failure Acute lung injury (ALI) Renal Acute tubular necrosis (ATN) (continued) CONSEQUENCES OF SHOCK (CONTINUED) Hematological Disseminated intravascular coagulation (DIC) Gastrointestinal Gastrointestinal Hepatic tract failure failure Pancreatic failure ASSESSMENT AND DIAGNOSIS OF SHOCK SYNDROME Clinical assessment SBP <90 mm Hg Accompanied by: Tachycardia Altered mental status Varies with specific shock syndromes Global indicators of systemic perfusion and oxygenation Serum lactate Base deficit levels MEDICAL MANAGEMENT OF SHOCK SYNDROME Improvement and preservation of tissue perfusion Adequate pulmonary gas exchange Adequate cardiac output Preload Volume resuscitation Afterload Contractility Adequate hemoglobin level Optimal metabolic environment Nutritional support Glucose control NURSING MANAGEMENT OF SHOCK SYNDROME Nursing priorities in managing the patient’s psychosocial needs: Providing information on patient status Explaining procedures and routines Supporting the family Encouraging the expression of feelings Facilitating problem solving and decision making Involving the family in the patient’s care Establishing contacts with necessary resources COLLABORATIVE MANAGEMENT Support oxygen transport Establish a patent airway Initiate mechanical ventilation Administer oxygen Administer fluids (crystalloids, colloids, blood and other blood products) Administer vasoactive medications Administer positive inotropic medications Ensure sufficient hemoglobin and hematocrit (continued) COLLABORATIVE MANAGEMENT (CONTINUED) Support oxygen use Identify and correct cause of lactic acidosis Ensure adequate organ and extremity perfusion Initiate nutritional support therapy Identify underlying cause of shock and treat accordingly Provide comfort and emotional support Maintain surveillance for complications QUESTION Sodium bicarbonate is recommended in the treatment of shock-related lactic acidosis. A. B. True False ANSWER B. False Sodium bicarbonate is not recommended in the treatment of shock-related lactic acidosis. No overall benefit has been found. Risks associated with its use include shifting of the oxyhemoglobin dissociation curve to the left, rebound increase in lactic acid production, development of hyperosmolar state, fluid overload resulting from excessive sodium, and rapid cellular electrolyte shifts. HYPOVOLEMIC SHOCK Description Inadequate fluid volume in the intravascular space Etiology Absolute Relative Pathophysiology Loss of circulating blood volume PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK FIGURE 26-1 The pathophysiology of hypovolemic shock. ASSESSMENT AND DIAGNOSIS OF HYPOVOLEMIC SHOCK Clinical manifestations Based on severity of fluid loss Class I Class II Class III Class IV Hemodynamic assessment Varies by stage MEDICAL MANAGEMENT OF HYPOVOLEMIC SHOCK Medical management Correct hypovolemia Restore tissue perfusion NURSING DIAGNOSIS PRIORITIES HYPOVOLEMIC SHOCK Deficient fluid volume related to active blood loss Deficient fluid volume related to interstitial fluid shift Decreased cardiac output related to alterations in preload Imbalanced nutrition: less than body requirements related to increased metabolic demands or lack of exogenous nutrients (continued) NURSING DIAGNOSIS PRIORITIES HYPOVOLEMIC SHOCK (CONTINUED) Risk for infection Anxiety related to threat to biological, psychological, and/or social integrity Compromised family coping related to a critically ill family member NURSING MANAGEMENT OF HYPOVOLEMIC SHOCK Nursing priorities are directed toward: Minimizing fluid loss Administering volume replacement Promoting comfort and emotional support Maintaining surveillance for complications CARDIOGENIC SHOCK Description Failure of heart to pump blood effectively Etiology Primary ventricular ischemia Structural problems Dysrhythmias PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK Pathophysiology Impaired ability of ventricle to pump blood Leads to a decrease in stroke volume and an increase in the blood left in the ventricle at the end of systole Decreased cellular oxygen supply Ineffective tissue perfusion Caused by a “heart” problem PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK FIGURE 26-2 The pathophysiology of cardiogenic shock. ASSESSMENT AND DIAGNOSIS OF CARDIOGENIC SHOCK Clinical manifestations Low CO and low BP Compensatory mechanisms develop Hemodynamic assessment Decreased cardiac output with a cardiac index <2.2 L/min/m2s MEDICAL MANAGEMENT OF CARDIOGENIC SHOCK Correct underlying cause of pump failure Identify etiological factors Enhance the effectiveness of the pump Pharmacological management Improve tissue perfusion Intubation and mechanical ventilation Early revascularization Intraaortic balloon pump (IABP) or ventricular assist device (VAD) NURSING DIAGNOSIS PRIORITIES CARDIOGENIC SHOCK Ineffective cardiopulmonary tissue perfusion related to acute myocardial ischemia Decreased cardiac output related to alterations in contractility Decreased cardiac output related to alterations in heart rate Imbalanced nutrition: less than body requirements related to increased metabolic demands or lack of exogenous nutrients (continued) NURSING DIAGNOSIS PRIORITIES CARDIOGENIC SHOCK (CONTINUED) Risk for infection Disturbed body image related to functional dependence on life-sustaining technology Compromised family coping related to a critically ill family member NURSING MANAGEMENT OF CARDIOGENIC SHOCK Nursing priorities are directed toward: Limiting myocardial oxygen demand Enhancing myocardial oxygen supply Providing comfort and emotional support Maintaining surveillance for complications ANAPHYLACTIC SHOCK Description Distributive shock Etiology Antigen-antibody reaction PATHOPHYSIOLOGY OF ANAPHYLACTIC SHOCK Immunological stimulation of mast cells results in release of biochemical mediators Histamine Eosinophil chemotactic factor of anaphylaxis Neutrophil chemotactic factor of anaphylaxis Platelet-activating factor Proteinases Heparin, serotonin, leukotrienes Prostaglandins (continued) PATHOPHYSIOLOGY OF ANAPHYLACTIC SHOCK (CONTINUED) Activation of biochemical mediators causes: Vasodilation Increased capillary permeability Bronchoconstriction Excessive mucus secretion Coronary vasoconstriction Inflammation Cutaneous reactions Constriction of smooth muscle in intestinal wall, bladder, and uterus PATHOPHYSIOLOGY OF ANAPHYLACTIC SHOCK FIGURE 26-3 The pathophysiology of anaphylactic shock. ASSESSMENT AND DIAGNOSIS OF ANAPHYLACTIC SHOCK Clinical manifestations Affects multiple body systems Hemodynamic assessment Decreased cardiac output–cardiac index Vasodilation leads to decrease in systemic vascular resistance QUESTION Clinical manifestations of anaphylactic shock include: A. B. C. D. chest pain and crackles. decreased urine output and narrowing pulse pressure. bradycardia and warm dry skin. pruritus and hypotension. ANSWER D. Pruritus and hypotension. Chest pain and crackles are symptoms of cardiogenic shock. Decreased urine output and narrowing pulse pressure are symptoms of hypovolemic shock. Bradycardia and warm dry skin are symptoms of neurogenic shock. MEDICAL MANAGEMENT OF ANAPHYLACTIC SHOCK Immediate and direct approach Remove antigen Reverse effects of biochemical mediators Promote adequate tissue perfusion Fluid replacement Oxygen Epinephrine Benadryl NURSING DIAGNOSIS PRIORITIES ANAPHYLACTIC SHOCK Deficient fluid volume related to relative loss Decreased cardiac output related to alterations in preload Decreased cardiac output related to alterations in afterload Ineffective breathing pattern related to decreased lung expansion Impaired gas exchange related to ventilation/ perfusion mismatching or intrapulmonary shunting (continued) NURSING DIAGNOSIS PRIORITIES ANAPHYLACTIC SHOCK (CONTINUED) Imbalanced nutrition: less than body requirements related to increased metabolic demands or lack of exogenous nutrients Risk for infection Ineffective coping related to situational crisis and personal vulnerability Compromised family coping related to a critically ill family member NURSING MANAGEMENT OF ANAPHYLACTIC SHOCK Nursing priorities are directed toward: Facilitating ventilation Administering volume replacement Providing comfort and emotional support Maintaining surveillance for complications NEUROGENIC SHOCK Description Distributive shock Etiology Disruption (SNS) of sympathetic nervous system PATHOPHYSIOLOGY OF NEUROGENIC SHOCK Loss of sympathetic tone results in: Massive peripheral vasodilation Inhibition of the baroreceptor response Impaired thermoregulation PATHOPHYSIOLOGY OF NEUROGENIC SHOCK FIGURE 26-4 The pathophysiology of neurogenic shock. ASSESSMENT AND DIAGNOSIS OF NEUROGENIC SHOCK Clinical manifestations Hypotension Bradycardia Warm dry skin Hypothermia Hemodynamic assessment Decreased cardiac output/cardiac index Decrease in systemic vascular resistance due to vasodilation MEDICAL MANAGEMENT OF NEUROGENIC SHOCK Careful approach Remove cause of neurogenic shock Prevent cardiovascular instability Promote optimal tissue perfusion NURSING DIAGNOSIS PRIORITIES NEUROGENIC SHOCK Deficient fluid volume related to relative loss Decreased cardiac output related to sympathetic blockade Hypothermia related to exposure to cold environment trauma or damage to the hypothalamus Imbalanced nutrition: less than body requirements related to increased metabolic demands or lack of exogenous nutrients (continued) NURSING DIAGNOSIS PRIORITIES NEUROGENIC SHOCK (CONTINUED) Risk for infection Anxiety related to threat to biological, psychological, or social integrity Compromised family coping related to a critically ill family member NURSING MANAGEMENT OF NEUROGENIC SHOCK Nursing priorities are directed toward: Treating hypovolemia Maintaining normothermia Monitoring for dysrhythmias Providing comfort and emotional support Maintaining surveillance for complications SEVERE SEPSIS AND SEPTIC SHOCK Description Occurs when microorganisms invade the body and initiate a systemic inflammatory response Host response results in perfusion abnormalities with organ dysfunction (severe sepsis) and eventually hypotension (septic shock) Primary mechanism of shock is maldistribution of blood flow to the tissues ETIOLOGY OF SEVERE SEPSIS AND SEPTIC SHOCK Caused by a wide variety of microorganisms Gram-negative and gram-positive aerobes Anaerobes Fungi Viruses Source of microorganisms Exogenous Endogenous Intrinsic and extrinsic precipitating factors PATHOPHYSIOLOGY OF SEVERE SEPSIS AND SEPTIC SHOCK Complex system response Initiated when a microorganism enters the body Stimulates inflammatory/immune system Release of toxins and other substances activated the plasma enzyme cascades as well as platelets, neutrophils, monocytes, and macrophages (continued) PATHOPHYSIOLOGY OF SEVERE SEPSIS AND SEPTIC SHOCK (CONTINUED) Hallmarks of severe sepsis Endothelial damage Coagulation dysfunction PATHOPHYSIOLOGY OF SEVERE SEPSIS AND SEPTIC SHOCK FIGURE 26-5 The pathophysiology of septic shock. ASSESSMENT AND DIAGNOSIS OF SEVERE SEPSIS AND SEPTIC SHOCK Effective treatment depends on timely recognition Diagnosis based on identification of three conditions Known or suspected infection Two or more of the clinical indicators of the systemic inflammatory response Evidence of at least one organ dysfunction MEDICAL MANAGEMENT OF SEVERE SEPSIS AND SEPTIC SHOCK Multifaceted approach Goals of treatment Reverse pathophysiological responses Control and eliminate infection Promote metabolic support SEVERE SEPSIS AND SEPTIC SHOCK MANAGEMENT GUIDELINES Initial resuscitation Diagnosis Antibiotic therapy Source identification and control Fluid therapy Vasopressors Inotropic therapy Steroids (continued) SEVERE SEPSIS AND SEPTIC SHOCK MANAGEMENT GUIDELINES (CONTINUED) Recombinant human activated protein C Blood product administration Mechanical ventilation of sepsis-induced ALI/ARDS Sedation, analgesia, and neuromuscular blockade in sepsis Glucose control Renal replacement (continued) SEVERE SEPSIS AND SEPTIC SHOCK MANAGEMENT GUIDELINES (CONTINUED) Bicarbonate therapy Deep Vein thrombosis prophylaxis Stress ulcer prophylaxis Consideration for limitation of support NURSING DIAGNOSIS PRIORITIES SEVERE SEPSIS AND SEPTIC SHOCK Deficient fluid volume related to relative loss Decreased cardiac output related to alterations in preload Decreased cardiac output related to alterations in afterload Decreased cardiac output related to alterations in contractility Impaired gas exchange related to ventilation/perfusion mismatching or intrapulmonary shunting (continued) NURSING DIAGNOSIS PRIORITIES SEVERE SEPSIS AND SEPTIC SHOCK (CONTINUED) Imbalanced nutrition: less than body requirements related to increased metabolic demands or lack of exogenous nutrients Risk for infection Anxiety related to threat to biological, psychological, or social integrity Compromised family coping related to a critically ill family member NURSING MANAGEMENT OF SEVERE SEPSIS AND SEPTIC SHOCK Prevention is one of the primary responsibilities of the critical care nurse Nursing priorities are directed toward: Early identification of the sepsis syndrome Administering prescribed fluids and medications Providing comfort and emotional support Maintaining surveillance for complications MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS) Description MODS results from progressive physiological function of two or more separate organ systems Trauma patients are particularly vulnerable Other high-risk patients include those who have experienced: Infection Shock episodes Ischemia-reperfusion events Acute pancreatitis Burns ETIOLOGY OF MODS Primary MODS Occurs as a direct consequence of the insult Secondary MODS Manifests latently and involves organs not affected in the initial insult Systemic inflammatory response syndrome (SIRS) PATHOPHYSIOLOGY OF MODS FIGURE 26-6 Pathogenesis of multiple organ dysfunction syndrome. GI, gastrointestinal; MDF, myocardial depressant factor; MODS, multiple organ dysfunction syndrome; PAF, platelet activating factor; WBCs, white blood cells. (From Cheek DJ, et al: Shock, multiple organ dysfunction syndrome, and burns in adults. In McCance KL, Huether SE, editors: Pathophysiology: the biologic basis for disease in adults and children ed 6, St Louis, 2010, Mosby.) PATHOPHYSIOLOGY OF MODS INFLAMMATORY MEDIATORS Inflammatory cells Neutrophils Macrophages or monocytes Mast Lymphocytes Endothelial (continued) PATHOPHYSIOLOGY OF MODS INFLAMMATORY MEDIATORS (CONTINUED) Biochemical mediators Reactive oxygen species Superoxide radical Hydroxyl radical Hydrogen peroxide Tumor necrosis factor Interleukins Platelet activating factor (continued) PATHOPHYSIOLOGY OF MODS INFLAMMATORY MEDIATORS (CONTINUED) Arachidonic acid metabolites Prostaglandins Leukotrienes Thromboxanes Proteases Plasma protein systems Complement Kinin Coagulation ASSESSMENT AND DIAGNOSIS OF MODS Clinical manifestation of organ dysfunction GI dysfunction Hepatobiliary dysfunction Pulmonary dysfunction Renal dysfunction Cardiovascular dysfunction Coagulation dysfunction QUESTION The primarily mechanism of bacterial translocation has been associated with: A. B. C. D. gastrointestinal mucosal edema. dysfunction of Kupffer cells. intestinal bacterial overgrowth. colonization of the oropharynx. ANSWER C. Intestinal bacterial overgrowth. The gastrointestinal tract harbors organisms that present an inflammatory focus when translocated from the gut into the portal circulation and are inadequately cleared by the liver. The primary mechanism of bacterial translocation has been associated with intestinal bacterial overgrowth. MEDICAL MANAGEMENT OF MODS Interdisciplinary collaboration in clinical management Goals of medical management include: Prevention and treatment of infection Maintenance of tissue oxygenation Nutritional and metabolic support Comfort and emotional support Support for individual organ function COLLABORATIVE MANAGEMENT OF MODS Support oxygen transport: Establish a patent airway Initiate mechanical ventilation Administer oxygen Administer fluids (crystalloids, colloids, blood and other blood products) Administer vasoactive medications Administer positive inotropic medications Administer antidysrhythmic medications Ensure sufficient hemoglobin and hematocrit (continued) COLLABORATIVE MANAGEMENT OF MODS (CONTINUED) Support oxygen use: Identify and correct cause of lactic acidosis Ensure adequate organ and extremity perfusion Decrease oxygen demand: Administer sedation or paralytics Administer antipyretics and external cooling measures Administer pain medications (continued) COLLABORATIVE MANAGEMENT OF MODS (CONTINUED) Identify the underlying cause of inflammation and treat accordingly Remove infected organs or tissue Administer antibiotics Initiate nutritional support Treat individual organ dysfunction Gastrointestinal Hepatobiliary Pulmonary (continued) COLLABORATIVE MANAGEMENT OF MODS (CONTINUED) Treat individual organ dysfunction (continued) Renal Cardiovascular Coagulation system Maintain surveillance for complications Infection Provide comfort and emotional support NURSING DIAGNOSIS PRIORITIES MODS Decreased cardiac output related to alterations in preload Decreased cardiac output related to alterations in afterload Decreased cardiac output related to alterations in contractility Impaired gas exchange related to ventilation/perfusion mismatching or intrapulmonary shunting (continued) NURSING DIAGNOSIS PRIORITIES MODS (CONTINUED) Ineffective renal tissue perfusion related to decreased renal blood flow Ineffective cardiopulmonary tissue perfusion related to decreased coronary blood flow Imbalanced nutrition: less than body requirements related to increased metabolic demands or lack of exogenous nutrients Risk for infection (continued) NURSING DIAGNOSIS PRIORITIES MODS (CONTINUED) Acute pain related to transmission and perception of cutaneous, visceral, muscular, or ischemic impulses Acute confusion related to sensory overload, sensory deprivation, and sleep pattern disturbance Anxiety related to threat to biological, psychological, or social integrity Compromised family coping related to a critically ill family member NURSING MANAGEMENT OF MODS Nursing priorities are directed toward: Preventing development of infections Facilitating tissue oxygen delivery and limiting tissue oxygen demand Facilitating nutritional support Providing comfort and emotional support Maintaining surveillance for complications
