Lewis: Medical-Surgical Nursing, 8th Edition

Chapter 67: Nursing Management: Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome Key Points Printable SHOCK Shock is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply of and demand for oxygen and nutrients. The four main categories of shock are cardiogenic, hypovolemic, distributive (includes septic, anaphylactic, and neurogenic shock), and obstructive. Cardiogenic Shock Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in reduced cardiac output (CO). Causes of cardiogenic shock include acute myocardial infarction (AMI), cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, and myocardial depression from metabolic problems. Clinical manifestations include tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, diaphoresis, decreased capillary refill time, anxiety, confusion, and agitation. Hypovolemic Shock Hypovolemic shock occurs when there is a loss of intravascular fluid volume. Absolute hypovolemia results when fluid is lost through hemorrhage, gastrointestinal (GI) loss (e.g., vomiting, diarrhea), fistula drainage, diabetes insipidus, or diuresis. Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space, such as with sepsis and burns. Clinical manifestations depend on the extent of injury or insult, age, and general state of health and may include anxiety; an increase in heart rate, CO, and respiratory rate and depth; and a decrease in stroke volume, pulmonary artery wedge pressure (PAWP), and urine output. Neurogenic Shock Neurogenic shock is a hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or in response to spinal anesthesia. Clinical manifestations include hypotension, bradycardia, temperature dysregulation (resulting in heat loss), dry skin, and poikilothermia.

Anaphylactic Shock Anaphylactic shock is an acute and life-threatening hypersensitivity (allergic) reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect venom). Immediate reaction causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permeability resulting in fluid leaks from the vascular space into the interstitial space. Clinical manifestations can include anxiety, confusion, dizziness, chest pain, incontinence, swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria, and angioedema. Septic Shock Sepsis is a systemic inflammatory response to a documented or suspected infection. Severe sepsis is sepsis complicated by organ dysfunction. Septic shock is the presence of sepsis with hypotension despite fluid resuscitation along with the presence of inadequate tissue perfusion. In severe sepsis and septic shock, the bodys response to infection is exaggerated, resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis. Septic shock has three major pathophysiologic effects: vasodilation, maldistribution of blood flow, and myocardial depression. Patients often have hypotension, respiratory failure, alteration in neurologic status, decreased urine output, and GI dysfunction. Stages of Shock The initial stage of shock that occurs at a cellular level is usually not clinically apparent. The compensatory stage is clinically apparent and involves neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis. The progressive stage of shock begins as compensatory mechanisms fail and aggressive interventions are necessary to prevent the development of multiple-organ dysfunction system (MODS). In the irreversible stage, decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism. The patient will demonstrate profound hypotension and hypoxemia, as well as organ failure; at this stage, recovery is unlikely. Diagnostic Studies There is no specific diagnostic study to determine shock. The diagnosis depends on the history and physical. Studies that assist in diagnosis include a serum lactate, base deficit, 12lead ECG, continuous cardiac monitoring, chest x-ray, continuous pulse oximetry,

and hemodynamic monitoring. Collaborative Care: General Measures Successful management of the patient in shock includes the following: (1) identification of patients at risk for the development of shock; (2) integration of the patients history, physical examination, and clinical findings to establish a diagnosis; (3) interventions to control or eliminate the cause of the decreased perfusion; (4) protection of target and distal organs from dysfunction; and (5) provision of multisystem supportive care. General management strategies for a patient in shock begin with ensuring that the patient has a patent airway and oxygen delivery is optimized. The cornerstone of therapy for septic, hypovolemic, and anaphylactic shock is volume expansion with the administration of the appropriate fluid. The primary goal of drug therapy for shock is the correction of decreased tissue perfusion. Vasopressor or vasodilator therapy is used according to patient needs to maintain the mean arterial pressure at the appropriate level. Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in shock; nutrition is vital to decreasing morbidity from shock. Collaborative Care: Specific Measures Cardiogenic Shock The overall goal is to restore blood flow to the myocardium by restoring the balance between oxygen supply and demand. Definitive measures include thrombolytic therapy, angioplasty with stenting, emergency revascularization, and valve replacement. Care involves hemodynamic monitoring, drug therapy (e.g., diuretics to reduce preload), and use of circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device). Hypovolemic Shock The underlying principles of managing patients with hypovolemic shock focus on stopping the loss of fluid and restoring the circulating volume. Septic Shock Patients in septic shock require large amounts of fluid replacement; the goal is to achieve a target central venous pressure (CVP) of 8 to 12 mm Hg. Vasopressor drug therapy may be added once CVP is 8 mm Hg; vasopressin may be given to patients refractory to vasopressor therapy. Intravenous corticosteroids are only recommended for patients who cannot maintain an adequate blood pressure (BP) with vasopressor therapy, despite fluid resuscitation. Antibiotics are an important component of therapy and should be started within the first hour of septic shock. Neurogenic Shock

The treatment of neurogenic shock is dependent on the cause. In spinal cord injury, general measures to promote spinal stability are initially used. Treatment of hypotension and bradycardia involves the use of vasopressors and atropine, respectively. Fluids are administered cautiously; the patient is monitored for hypothermia.

Anaphylactic Shock Epinephrine is the drug of choice to treat anaphylactic shock. Maintaining the airway is critical; endotracheal intubation or cricothyroidotomy may be necessary. Aggressive fluid replacement, predominantly with colloids, is necessary. Obstructive Shock The primary strategy in treating obstructive shock is early recognition and treatment to relieve or manage the obstruction. NURSING MANAGEMENT: SHOCK Nursing Assessment The initial assessment focuses on the ABCs: airway, breathing, and circulation. Further assessment focuses on the assessment of tissue perfusion and includes evaluation of vital signs, peripheral pulses, level of consciousness, capillary refill, skin (e.g., temperature, color, moisture), and urine output. Planning The overall goals for a patient in shock include (1) evidence of adequate tissue perfusion, (2) restoration of normal BP, (3) return/recovery of organ function, and (4) avoidance of complications from prolonged states of hypoperfusion. Nursing Implementation Your role in shock involves (1) monitoring the patients ongoing physical and emotional status, (2) identifying trends to detect changes in the patients condition, (3) planning and implementing nursing interventions and therapy, (4) evaluating the patients response to therapy, (5) providing emotional support to the patient and caregiver, and (6) collaborating with other members of the health team to coordinate care. The patient in shock requires frequent assessment of heart rate/rhythm, BP, CVP, and pulmonary artery (PA) pressures; neurologic status; respiratory status, urine output, and temperature; capillary refill; skin for temperature, pallor, flushing, cyanosis, diaphoresis, or piloerection; and bowel sounds and abdominal distention. Rehabilitation of the patient who is recovering from shock necessitates correction of the precipitating cause and prevention or early treatment of complications.

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME AND MULTIPLE ORGAN DYSFUNCTION SYNDROME Systemic inflammatory response syndrome (SIRS) is a systemic inflammatory response to a variety of insults, including infection (referred to as sepsis), ischemia, infarction, and injury. SIRS is characterized by generalized inflammation in organs remote from the initial insult and can be triggered by mechanical tissue trauma (e.g., burns, crush injuries), abscess formation, ischemic or necrotic tissue (e.g., pancreatitis, myocardial infarction), microbial invasion, and global and regional perfusion deficits. MODS results from SIRS and is the failure of two or more organ systems such that homeostasis cannot be maintained without intervention. o The respiratory system is often the first system to show signs of dysfunction in SIRS and MODS, often culminating in acute respiratory distress syndrome (ARDS). o Cardiovascular changes, neurologic dysfunction, acute renal failure, DIC, GI dysfunction, and liver dysfunction are common. Nursing and Collaborative Management: SIRS and MODS The prognosis for the patient with MODS is poor; the most important goal is to prevent the progression of SIRS to MODS. A critical component of your role is vigilant assessment and ongoing monitoring to detect early signs of deterioration or organ dysfunction. Collaborative care for patients with MODS focuses on (1) prevention and treatment of infection, (2) maintenance of tissue oxygenation, (3) nutritional and metabolic support, and (4) appropriate support of individual failing organs.