BASIC PRINCIPLES IN DISASTER NURSING N- ursing Plans should be integrated and coordinated U- pdate physical and Psychological preparedness

R- esponsible for Organizing, Teaching and Supervision S- timulate Community Participation E- xercise Competence The ED has typically been involved in both external (i.e., community) and internal (i.e., hospital) disaster planning. During a MCI, the ED serves as a central point for screening and the admission of critically ill or injured clients. They then institute a back-up plan to provide care to others. The entire hospital may be called into action to assist with providing care in the ED or expanding services throughout the institution. To help with emergency preparedness, the Centers for Disease Control and Prevention has developed a core set of competencies that include (1) understanding the necessary roles involved in responding to a disaster. (2) initiating and following the chain of command, and (3) activating the response plan. An ED nurse may help to coordinate responders and transfer clients; provide decontamination; deliver care for critically ill or injured clients admitted to ED; or be reassigned to other clinical areas that need additional nursing assistance. BASIC PRINCIPLES OF NURSING CARE FOR DISASTER VICTIMS A- daptation of Skills to Situation C- are for Disaster Victims C- ontinuous Awareness of the patients condition T- each AUXILLARY personnel S-election of Essential Care THE ROLE OF NURSING IN DISASTER RESPONSE PLANS The role of the nurse during a disaster varies. The nurse may be asked to perform outside his or her area of expertise and may take on responsibilities normally held by physicians or advanced practice nurses. For example, a critical care nurse may intubate a patient or even insert chest tubes. Wound debridement or suturing may be performed by staff registered nurses. A nurse may serve as the triage officer. Although the exact role of a nurse in disaster management depends on the specific needs of the facility at the time, it should be clear which nurse or physician is in charge of a given patient care area and which procedures each individual nurse may or may not perform. Assistance can be obtained through the incident command center, and nonmedical personnel can provide services where possible. For example, family members can provide nonskilled interventions for their loved ones. Nurses should remember that

nursing care in a disaster focuses on essential care from a perspective of what is best for all patients. New settings and atypical roles for nurses arise during a disaster: the nurse may provide shelter care in a temporary housing area, or bereavement support and assistance with identification of deceased loved ones. Individuals may require crisis intervention or the nurse may participate in counseling other staff members and in critical incident stress management (CISM). At-risk populations may also require special considerations during a disaster. SHOCK Shock is a life-threatening condition with a variety of underlying causes. It is characterized by inadequate tissue perfusion that, if untreated, results in cell death. The nurse caring for the patient with shock or at risk for shock must understand the underlying mechanisms of shock and recognize its subtle as well as more obvious signs. Rapid assessment and response are essential to the patients recovery. Shock can best be defined as a condition in which systemic blood pressure is inadequate to deliver oxygen and nutrients to support vital organs and cellular function (Mikhail, 1999). Adequate blood flow to the tissues and cells requires the following components: adequate cardiac pump, effective vasculature or circulatory system, and sufficient blood volume. When one component is impaired, blood flow to the tissues is threatened or compromised. Without treatment, inadequate blood flow to the tissues results in poor delivery of oxygen and nutrients to the cells, cellular starvation, cell death, organ dysfunction progressing to organ failure, and eventual death. Shock is commonly divided into three major classifications: (a) Hypovolemic (b) Cardiogenic (c) Distributive PHYSIOLOGIC RESPONSES TO SHOCK
A. Sympathetic nervous system (SNS) activation

a. As perfusion decreases, impulses are transmitted to the vasomotor center of the brain, causing SNS activation as a compensatory mechanism. b. SNS activation results in vasoconstriction of the arterial bed and increased cardiac inotropic and chronotropic activity. B. Tachycardia: abnormally rapid heart rate C. Skin color and temperature changes a. In the early stages of shock, blood is shunted to the brain and heart and away from the skin and other organs that tolerate ischemia well. b. As a result, the skin appears pale and feels cool.

D. Hypotension: occurs when compensatory mechanisms become inadequate E. Microcirculatory changes a. As shock progresses, the venous sphincters are less able to maintain vasoconstriction. b. Blood flow in the capillary beds becomes sluggish; eventually, microcirculation is blocked. F. Coagulation abnormablities a. Metabolic waste products and microaggregates of platelets and clotting factors accumulate in the capillary bed, resulting in clotting. b. Thrombocytopenia may also occur, particularly in septic shock. G. Hyperglycemia a. In response to the release of epinephrine, glycogen is broken down into glucose, which is released into the circulation. b. Lipolysis results in increased amounts of free fatty acids and increased levels of glucocorticoids, ocritsion, and cortisol, contributing to the production of more glucose. H. Hyperglycemia a. In response to the release of epinephrine, glycogen is broken down into glucose, which is released into the circulation. b. Lipolysis results in increased amopunts of free fatty acids and increased levels of glucocorticoids, cortisone, and cortisol, contributing to the production of more glucose. I. Fluid shifts a. To increase fluid retention and improve perfusion, renin is produced by the juxtaglomerular apparatus in the kidneys and antidiuretic hormone (ADH) is produced by the hypothalamus. b. In addition, activation of the renin-angiotensin system eventually results in further vasoconstriction in an attempt to raise blood pressure J. End organ damage, including: a. Impaired removal of waste products secondary to decreased renal function. b. Depression of the reticuloendothelial system resulting in impaired inflammatory and immune response. c. Pulmonary edema and adult respiratoyr distress syndrome (ARDS) d. Disseminated intravascular coagulation e. Hepatic dysfunction including fatty infiltrates and decreased clearance f. Gastrointestinal (GI) oriblems including ulcerations and enteritis g. Nutritional deficits secondary to impaired GI function h. Central nervous system (CNS) damage

EFFECTS OF SHOCK

Figure 1: Cellular effects of shock. The cell swells and the cell membrane becomes more permeable, and fluids and electrolytes seep from and into the cell. Mitochondria and lysosomes are damaged, and the cell dies. STAGES OF SHOCK
1.) Compensated or nonprogressive shock: Vital organs remain afequately

perfused because of compensatory mechanisms. or progressive shock: Vital organs become underperfused and compensatory mechanisms become ineffective, resulting in systemic manifestations. 3.) Irreversible shock: The extent of shock is so severe that therapeutic interventions become useless; death eventually occurs.
2.) Decompensated

CLINICAL FINDINGS IN STAGES OF SHOCK

TYPES OF SHOCK Shock can be categorized into four major types: a. Hypovolemic b. Cardiogenic c. Obstructive d. Distributive Hypovolemic shock is a state characterized by inadequate amounts of blood volume in the intravascular space. Cardiogenic shock is a condition in which myocardial damage renders the heart unable to pump enough blood to maintain adequate perfusion Obstructive shock occurs when blood flow is impeded by a mechanical or physical obstruction Distributive shock refers to conditions involving alterations in the distribution of intravascular volume. It includes three categories: a. Septic b. Neurogenic c. Anaphylactic HYPOVOLEMIC SHOCK A. Description: a state characterized by inadequate amounts of blood volume in the intravascular space B. Etiology a. Hypovolemic shock results from direct or indirect volume losses. b. Direct volume losses include: i. Frank bleeding ii. Diarrhea or vomiting iii. Diuresis iv. Loss of plasma through skin (eg, burns) c. Indirect volume losses include: i. Sequestration of fluid into third spaces (eg, ascites and abdominal obstruction)

ii. Internal volume losses (eg, hemothorax, hemorrhagic pancreatitis, and splenic rupture) iii. Internal fluid shifts (eg, addisonian crisis and hypopituitarism) C. Pathophysiologic processes and manifestations a. Hypovolemic shock can be categorized as mild, moderate, or devere; symptoms vary according to the severity of the volume deficit. b. Symptoms of mild Hypovolemic shock: i. Maximum volume loss is 10% ii. Cardiac output will be decreased, resulting in SNS activation. iii. SNS activation is sufficient to maintain normotensive blood pressure and heart rate. iv. Skin appears pale, feels cool and clammy because blood is shnted away from it and to vital organs. v. Mucosa is mildly dry vi. Skin turgor is decreased vii. Neurologic manifestations can include anxiety, restlessness, thirst, and weakness. c. Symptoms of moderate Hypovolemic shock: i. Volume loss reaches 15% to 40% ii. Cardiac output and blood pressure decrease dramatically iii. Arteriolar vasoconstriction results in decreased perfusion of the kidneys and GI organs. iv. Common manifestations include tachycardia, tachypnea, pallor, diaphoresis, hypotension, and CNS activation, including restlessness. v. Other symptoms can include thirst, poor skin turgor, and decreased urine output. vi. Although the bone marrow increases production of new blood products, the demand exceeds the ability to replace cells. d. Symptoms of severe Hypovolemic shock: i. Volume loss exceeds 45% ii. Compensatory mechanisms are functioning at maximum iii. Vital organs display evidence of impaired perfusion iv. Neurologic manifestations of underperfusion include decreased level of consciousness, confusion, and agitation. v. Metabolic alterations include hyperglycemia and lactic acidosis. vi. If shock continues, cell death and severe end organ damage will occur. D. Overview of Nursing Interventions

a. Institute fluid replacement therapy as prescribed. Fluid replacement should be with normal saline because all of the fluid stays in the intravascular space. b. Administer infusion of blood products, as ordered, for a patient who has experienced frank blood loss. c. Asess for the primary cause of shock in cases of third-space shifting to prevent further volume loss. d. Use military anti-shock trousers (MAST) with a patient who has experienced frank blood loss to cause venocompression and improve venous return. e. Assess hemodynamic status and all major body systems. f. Monitor the patients intake and output to ensure adequate fluid replacement. CARDIOGENIC SHOCK A. Description: a condition in which myocardial damage renders the heart unable to pump enough blood to maintain adequate perfusion B. Etiology a. Cardiogenic shock is a sequel of myocardial infarction (MI), occurring when 40 to 50% of the the myocardium has been destroyed. b. It also occurs secondary to valvular dysfunction (eg, mitral regurgitation, papillary muscle rupture, ventricular aneurysms, and severe dysrhythmias) or as a result of end-stage cardiomyopathies. C. Pathophysiologic processes and manifestations a. Impaired ventricular pumping ability reduces stroke volume and cardiac output. b. To compensate for decreased cardiac output, vascular resistance increases to maintain normotension. c. Increased resistance increases the workload on the ventricle as blood is forced to pump against increased pressure; this further decreases cardiac output. d. SNS activation results in the release of catecholamines, further increasing the afterload against which the ventricle must pump. e. The SNS also increases ventricular contractility, which may further exacerbate ischemia and failure. f. Left ventricular end diastolic pressure rises and the ventricle distends; this pressure extends to the pulmonary bed and can contribute to pulmonary edema. g. Hypoxemia and acidosis may occur. h. Manifestations of compensated shock include: i. Alterations in mentation ii. Restlessness iii. Weakness

iv. Decreased urine output v. Alterations in peripheral perfusion (eg, pallor, cool skin, jugular venous distention, and delayed capillary refill) vi. Hemodynamic manifestations, such as tachycardia, narrowed pulse pressure, mild hypotension or normal blood pressure, and altered pulmonary function (eg, tachypnea, orthopnea, and crackles) i. Manifestations of uncompensated shock include: i. Increased alterations in mentation ii. Oliguria iii. Frank hypotenion iv. Elevated central venous and pulmonary pressures v. Pulmonary deterioration (associated with a decrease in tidal volume, increasing pulmonary congestion, and cyanosis) j. Manifestations of irreversible shock include: i. Obtundation ii. Coma iii. Anuria or oliguria iv. Marked tachycardia v. Dysrhythmias vi. Severe hypotension vii. Deteriorated pulmonary status D. Overview of Nursing Interventions a. Assess hemodynamic and pulmonary systems b. Manage invasive monitoring equipment and monitor heart rhythm c. Administer vasopressors and diuretics as prescribed. d. Administer preload and afterload agents as prescribed (This condition cannot reverse unless appropriate amounts of medications are given.) e. Prepare patient for insertion of intraaortic balloon pump or ventricular assist device if necessary. f. Provide supportive care as indicated. OBSTRUCTIVE SHOCK A. Description: a condition in which blood flow is impeded by a mechanical or physical obstruction B. Etiology: causes include pulmonary emboli, tension pneumo-thorax, ruptured hemidiaphragm, dissecting aortic aneurysms, pericardial tamponade, and atrial myxoma. C. Pathophysiologic processes and manifestations a. Venous return decreases due to increased pressures around the right atrium or within the chest wall.

b. Decreased venous return results in less volume available for the ventricles to pump to end organs, causing inadequate perfusion. c. Manifestations of obstructive shock resemble those associated with Hypovolemic shock D. Overview of Nursing Interventions a. Prepare the patient for chest tube insertion, pericardial tap, or other surgical intervention. b. Replace volume with crystalloid or colloids. c. Provide supportive therapy as indicated. d. Provide swift and accurate care. SEPTIC SHOCK A. Description: a type of distributive shock, this condition occurs secondary to septicemia and is characterized by vascular collapse. B. Etiology a. The major cause of septic shock is Gram-negative bacteria. b. It also can be caused by Gram-positive bacteria, viruses, fungi, and rickettsiae. c. Mortality associated with septic shock is high because it results in multisystem organ failure. C. Pathophysiologic processes and manifestations a. Invading Gram-negative bacteria release toxins called endotoxins. b. Endotoxins are lipopolysaccharides that initiate a systemic inflammatory response syndrome (SIRS), activating a number of protein-based systems, including chemical, cellular, and immune or humoral mediators. The chemical mediators include the complement, clotting, kinin, and renin-angiotensin systems. c. The complement system increases the production of platelets, leukocytes, and mast cells and the release of anaphylatoxins. d. The vasoactive mediators histamine, prostaglandins, brady-kinin, and serotonin also are released, causing massive vasodilation and increased capillary permeability. e. The clotting system initiates the production of fibrin clots throughout the body; these clots impair blood flow and decrease perfusion. f. Activating the renin-angiotensin system results in the release of epinephrine, norepinepinephrine, and aldosterone, leading to increased sodium and water retention and improved myocardial contractility. In the early stages of septic shock, symptoms include those associated with SNS activation such as tachycardia, tachypnea, and increased cardiac output. g. Cellular mediators are involved with macrophage, granulocyte, and lymphocytic activity.

h. Immune or humoral mediators such as prostaglandins, tumor necrosis factors, interleukins, and myocardial depressant factors also contribute to cellular destruction and clinical deterioration. i. In the hyperdynamic phase, symptoms include: i. Decreased vascular resistance, while blood pressure is barely maintained ii. Peripheral vasodilation iii. Normal to high cardiac output iv. Hypotension or normotension v. Fever vi. Slight alterations in sensorium (eg, warm flushed peripheral skin and normal capillary refill) vii. Moderate tachycardia viii. Tachypnea with adventitious breath sounds ix. Normal urine output x. Hyperthermia j. In the hypodynamic phase, symptoms include: i. Profoundly impaired perfusion ii. Decreased cardiac output and increased resistance iii. Mental status changes, such as lethargy and coma iv. Clammy, pale skin v. Hemodynamic manifestations, including tachycardia, dysrhythmias, hypotension, and decreased cardiac output vi. Pulmonary congestion vii. Central cyanosis k. Decreased perfusion results in impaired oxygenation and clotting abnormalities, including disseminated intravascular coagulation (DIC). l. In the final stage, multiorgan dysfunction occurs. D. Overview of Nursing Interventions a. Administer appropriate antibiotics or antiviral agents as prescribed. b. Administer vasoactive agents as prescribed. c. Replace fluid with crystalloid. d. Provide supportive care of the pulmonary and cardiac systems as indicated. e. Monitor for evidence of end organ damage (associated with a high mortality rate). f. After killing the bacteria, manage any sequelae of the infection which are often serious conditions, such as renal failure, lifethreatening electrolyte disorders, or cardiac arrhythmias. g. Provide swift and accurate care as every body system is effected by the process. NEUROGENIC SHOCK

A. Description: (1) A type of distributive shock, neurogenic shock is characterized by a loss of SNS vasomotor function (2) This results in extreme vasodilation throughout the body, creating a maldistribution of blood volume. B. Etiology a. Neurogenic shock results from injury to the brain stem or to the spinal cord (high thoracic or low cervical); usually as a result of a traumatic event. b. It also has been associated with hypoxia, lack of glucose (or excessive insulin), and the depressant action of drugs (particularly anesthetic agents). C. Pathophysiologic processes and manifestations a. CNS system injury disrupts normal regulation of vasomotor tone, causing massive vasodilation throughout the body; this results in pooling of blood in the periphery. b. Venous return and cardiac output decrease. c. The decrease in cardiac output causes inadequate tissue perfusion. d. Common manifestations include: i. Alterations in mentation, ranging from confusion to coma ii. Alterations in peripheral perfusion, icnlduing cool and clammy skin above the lesion and warm, dry skin below( if a spinal cord lesion exists) iii. Normal capillary refill with palpable distal pulses. iv. Bradycardia v. Hypotension vi. Decreased pulse pressure vii. Tachypnea viii. Normal Urine Output D. Overview of Nursing Interventions a. Replace fluid with crystatalloid or colloids as ordered. b. Administer vasopressors and antiarrhythmics as prescribed. c. Administer steroids, as prescribed, depending on the causative injury. d. Maintain airway and provide pulmonary support. e. Provide supportive care ass indicated for the circulatory system. ANAPHYLACTIC SHOCK A. Description: (1) A type of distributive shock, anaphylactic shock is a severe, life-threatening allergic reaction to an antigen or other agent. (2) It is characterized by respiratory distress and vascular collapse; onset typically is sudden. B. Etiology a. Common causes of anaphylactic shock include: i. Reactions to drugs, such as penicillin and hormones

ii. Stings from insects, such as bees and wasps iii. Ingestion of certain foods, such as peanuts and shellfish b. Anaphylactic shock is considered a Type-I hypersensitivity response that most commonly involves Immunoglobulin E. C. Pathophysiologic process and manifestations a. After the first exposyre to an antigen or foreign agent, antibodies are made. b. Infrequently, the first exposure results in symptoms of anaphylaxis; typically, true anaphylactic shock occurs after the second exposure. c. In response to the antigen-antibody complex formation, vasoactive mediators such as histamine and leukotrines are relased. d. These mediators cause systemic vasodilation and alterations in capillary permeability. e. The resultant peripheral pooling of blood and decreased venous return and cardiac output cause cellular hypoperfusion. f. Swelling of the airway also can occur due to the inflammatory response, resulting in bronchoconstriction. g. Symptoms of anaphylactic shock include: i. Alterations in mentation, including restlessness progressing to coma ii. Cutaneous manifestations, including urticaria, pruritus, and angioedema iii. Bronchoconstriction, accompanied by tachypnea, wheezing, and use of accessory muscles. iv. Hemodynamic manifestations, including warm and flushed skin, tachycardia, dysrhythmias, angina, and hypotension. D. Overview of Nursing Interventions a. Ensure and maintain a patent airway. b. Prepare the patient for endotracheal intubation as indicated. c. Administer fluids and vasopressors as prescribed. d. Administer antihistamines (Benadryl) or epinephrine to promote vasoconstriction, as prescribed. e. Administer steroids, as prescribed, to reduce the inflammatory response associated with exposure to the allergen. f. Provide supportive care as indicated.