Chapter 67: Nursing Management: Shock, Systemic Inflammatory Response Syndrome, and Multiple Organ Dysfunction Syndrome

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.

Shock can be classified as low blood flow (cardiogenic and hypovolemic shock) or maldistribution of blood flow (septic, anaphylactic, and neurogenic shock).

Cardiogenic Shock • Cardiogenic shock occurs when either systolic or diastolic dysfunction of the pumping action of the heart results in compromised cardiac output (CO). • Precipitating causes of cardiogenic shock include myocardial infarction (MI), cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary hypertension, cardiac tamponade, and myocardial depression from metabolic problems. Hemodynamic profile will demonstrate an increase in the pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance. Clinical manifestations of cardiogenic shock may include tachycardia, hypotension, a narrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool and clammy skin, decreased capillary refill time, anxiety, confusion, and agitation.

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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, hyperglycemia, or diuresis. Relative hypovolemia results when fluid volume moves out of the vascular space into extravascular space (e.g., interstitial or intracavitary space) and this is called third spacing. The physiologic consequences of hypovolemia include a decrease in venous return, preload, stroke volume, and CO resulting in decreased tissue perfusion and impaired cellular metabolism. 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, 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 (taking on the temperature of the environment).

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 tissue perfusion abnormalities. In severe sepsis and septic shock, the initiated body response to an antigen is exaggerated resulting in an increase in inflammation and coagulation, and a decrease in fibrinolysis. Endotoxins from the microorganism cell wall stimulate the release of cytokines and other proinflammatory mediators that act through secondary mediators such as platelet-activating factor. o Platelet-activating factor results in the formation of microthrombi and obstruction of the microvasculature resulting in damage to the endothelium, vasodilation, increased capillary permeability, neutrophil and platelet aggregation, and adhesion to the endothelium. Clinical presentation for sepsis is complex and no single or group of symptoms are specific to the diagnosis. o Patients will usually experience a hyperdynamic state characterized by increased CO and decreased SVR. o Persistence of a high CO and a low SVR beyond 24 hours is ominous and often associated with hypotension and multiple organ dysfunction syndrome (MODS). o Initially patients will hyperventilate as a compensatory mechanism, resulting in respiratory alkalosis followed by respiratory acidosis and respiratory failure. o Other clinical signs include alteration in neurologic status, decreased urine output, and GI dysfunction.

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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 MODS.

In the final stage of shock, the refractory stage, decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism and the patient will demonstrate profound hypotension and hypoxemia, and organ failure. In this final stage, recovery is unlikely.

Diagnostic Studies • The process begins with a thorough history and physical examination. • • Evaluation of serum lactate and a possible base deficit. Other diagnostic studies include a 12-lead 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 patient’s 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. It is generally accepted that isotonic crystalloids, such as normal saline, are used in the initial resuscitation of shock. If the patient does not respond to 2 to 3 L of crystalloids, blood administration and central venous monitoring may be instituted. Two major complications of fluid resuscitation are hypothermia and coagulopathy. The primary goal of drug therapy for shock is the correction of decreased tissue perfusion. o Sympathomimetic drugs cause peripheral vasoconstriction and are referred to as vasopressor drugs (e.g., epinephrine, norepinephrine).  The goals of vasopressor therapy are to achieve and maintain a mean arterial pressure (MAP) of 60 to 65 mm Hg and the use of these drugs is reserved for patients unresponsive to other therapies. o The goal of vasodilator therapy, as in vasopressor therapy, is to maintain MAP at 60 to 65 mm Hg or greater.  Vasodilator agents most often used are nitroglycerin (in cardiogenic shock) and nitroprusside (in noncardiogenic shock). Protein-calorie malnutrition is one of the primary manifestations of hypermetabolism in shock and nutrition is vital to decreasing morbidity from shock. o Enteral nutrition should be initiated within the first 24 hours. Parenteral nutrition is used if enteral feedings are contraindicated or fail to meet at least 80% of the patient’s caloric requirements. o Serum protein, nitrogen balance, BUN, serum glucose, and serum electrolytes are all monitored to assess nutritional status.

Collaborative Care: Specific Measures

Cardiogenic Shock • 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. o Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss). Septic Shock • Patients in septic shock require large amounts of fluid replacement, sometimes as much as 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids, to restore perfusion. ο Hemodynamic monitoring and arterial pressure monitoring are often necessary. • Vasopressor drug therapy may be added and vasopressin may be given to patients refractory to vasopressor therapy. • Intravenous corticosteroids are recommended for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP. • Antibiotics are early component of therapy and are started after obtaining cultures (e.g., blood, wound exudate, urine, stool, sputum). • Drotrecogin alpha (Xigris), a recombinant form of activated protein C, has demonstrated promise in treating patients with severe sepsis. Bleeding is the most common serious adverse effect. • Glucose levels should be maintained at less than 150 mg/dl.

• Stress ulcer prophylaxis with histamine (H2)-receptor blockers and deep vein thrombosis prophylaxis with low dose unfractionated heparin or low molecular weight heparin are recommended.

Neurogenic Shock • Treatment of neurogenic shock is dependent on the cause. o In spinal cord injury, general measures to promote spinal stability are initially used. o Definitive treatment of the hypotension and bradycardia involves the use of vasopressors and atropine respectively. o Fluids are administered cautiously as the cause of the hypotension is generally not related to fluid loss. o The patient is monitored for hypothermia. Anaphylactic Shock

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Epinephrine is the drug of choice to treat anaphylactic shock. Diphenhydramine is administered to block the massive release of histamine.

• Maintaining a patent airway is critical and the use of nebulized bronchodilators is highly effective. • • Endotracheal intubation or cricothyroidotomy may be necessary. Aggressive fluid replacement, predominantly with colloids, is necessary.

• Intravenous corticosteroids may be helpful in anaphylactic shock if significant hypotension persists after 1 to 2 hours of aggressive therapy. Nursing Management: Shock Nursing Assessment • The initial assessment is geared toward 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) assurance 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 • Health Promotion o To prevent shock, the nurse needs to identify patients at risk (e.g., patients who are older, those with debilitating illnesses, those who are immunocompromised, surgical or accidental trauma patients). o Planning is essential to help prevent shock after a susceptible individual has been identified (e.g., monitoring fluid balance to prevent hypovolemic shock, maintenance of hand washing to prevent spread of infection). • Acute Intervention o The role of the nurse in shock involves (1) monitoring the patient’s ongoing physical and emotional status to detect subtle changes in the patient’s condition; (2) planning and implementing nursing interventions and therapy; (3) evaluating the patient’s response to therapy; (4) providing emotional support to the patient and family; and (5) collaborating with other members of the health team when warranted by the patient’s condition. o Neurologic status, including orientation and level of consciousness, should be assessed every hour or more often. o Heart rate/rhythm, BP, central venous pressure, and PA pressures including continuous cardiac output (if available) should be assessed at least every 15 minutes and PAWP every 1 to 2 hours.  Trends in these parameters yield more important information than individual numbers.  Trendelenburg (head down) position during hypotensive crisis is not supported by research and may compromise pulmonary function and increase intracranial

pressure.  The patient’s ECG should be continuously monitored to detect dysrhythmias that may result from the cardiovascular and metabolic derangements associated with shock. Heart sounds should be assessed for the presence of an S3 or S4 sound or new murmurs. The presence of an S3 sound in an adult usually indicates heart failure. The frequency of this monitoring is decreased as the patient’s condition improves. o The respiratory status of the patient in shock must be frequently assessed to ensure adequate oxygenation, detect complications early, and provide data regarding the patient’s acid-base status.  Pulse oximetry is used to continuously monitor oxygen saturation.  Arterial blood gases (ABGs) provide definitive information on ventilation and oxygenation status, and acid-base balance.  Most patients in shock will be intubated and on mechanical ventilation. o Hourly urine output measurements assess the adequacy of renal perfusion and a urine output of less than 0.5 ml/kg/hour may indicate inadequate kidney perfusion.  BUN and serum creatinine values are also used to assess renal function. o Tympanic or pulmonary arterial temperatures should be obtained hourly if temperature is elevated or subnormal, otherwise every 4 hours. o Capillary refill should be assessed and skin monitored for temperature, pallor, flushing, cyanosis, diaphoresis, or piloerection. o Bowel sounds should be auscultated at least every 4 hours, and abdominal distention should be assessed.  If a nasogastric tube is inserted, drainage should be checked for occult blood as should stools. o Oral care for the patient in shock is essential and passive range of motion should be performed three or four times per day. o Anxiety, fear, and pain may aggravate respiratory distress and increase the release of catecholamines. The nurse should talk to the patient, even if the patient is intubated, sedated, and paralyzed or appears comatose. If the intubated patient is capable of writing, a “magic slate” or a pencil and paper should be provided.  Family and significant others (1) link the patient to the outside world; (2) facilitate decision-making and advise the patient; (3) assist with activities of daily living; (4) act as liaisons to advise the health care team of the patient’s wishes for care; and (5) provide safe, caring, familiar relationships for the patient. Family time with the patient should be facilitated, provided this time is perceived as comforting by the patient. • Ambulatory and Home Care o Rehabilitation of the patient who is recovering from shock necessitates correction of the precipitating cause and prevention or early treatment of complications.  Complications may include decreased range of motion, decreased physical endurance, chronic kidney disease following acute tubular necrosis, and the development of fibrotic lung disease as a result of ARDS.  Patients may require diverse services (e.g., transitional care [for mechanical ventilation weaning], rehabilitation, home health care).

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. Multiple organ dysfunction syndrome (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 ARDS. o Cardiovascular changes include myocardial depression and massive vasodilation in response to increasing tissue demands. o Neurologic dysfunction commonly manifests as mental status changes with SIRS and MODS. o Acute renal failure (ARF) is frequently seen in SIRS and MODS. o In the early stages of SIRS and MODS, blood is shunted away from the GI mucosa, making it highly vulnerable to ischemic injury.  Risk for ulceration and GI bleeding.  Potential for bacterial translocation from the GI tract into circulation. o Both syndromes trigger a hypermetabolic response.  Catecholamines and glucocorticoids are released and result in hyperglycemia and insulin resistance.  Net result is a catabolic state, and a reduction in lean body mass (muscle).  May see liver dysfunction as a result of hypermetabolic state. o Failure of the coagulation system manifests as DIC. o Electrolyte imbalances, which are common, are related to hormonal and metabolic changes and fluid shifts.  These changes exacerbate mental status changes, neuromuscular dysfunction, and dysrhythmias.  The release of antidiuretic hormone and aldosterone results in sodium and water retention.

Nursing and Collaborative Management: SIRS and MODS • The prognosis for the patient with MODS is poor and the most important goal is to prevent the progression of SIRS to MODS. • • A critical component of the nursing 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. Prevention and treatment of infection: o Aggressive infection control strategies are essential to decrease the risk for nosocomial infections. o Once an infection is suspected, interventions to control the source must be instituted.

Maintenance of tissue oxygenation: o Interventions that decrease oxygen demand are essential and may include sedation, mechanical ventilation, analgesia, paralysis, and rest. o Oxygen delivery may be optimized by maintaining normal levels of hemoglobin and PaO2, using individualized tidal volumes with positive end-expiratory pressure, increasing preload or myocardial contractility to enhance CO, or reducing afterload to increase CO. Nutritional and metabolic needs: o Hypermetabolism in SIRS or MODS can result in profound weight loss, cachexia, and further organ failure. o Total energy expenditure is often increased 1.5 to 2 times the normal metabolic rate. o Plasma transferrin and prealbumin levels are monitored to assess hepatic protein synthesis. o The goal of nutritional support is to preserve organ function and the use of the enteral route is preferable to parenteral nutrition. Support of failing organs: o Support of any failing organ is a primary goal of therapy (e.g., the patient with ARDS requires aggressive oxygen therapy and mechanical ventilation, DIC should be treated appropriately [e.g., blood products], renal failure may require dialysis).

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