519
C HA P T E R 2 6
Shock, Sepsis, and Multiple Organ Dysfunction Syndrome
Beverly Carlson
SHOCK SYNDROME
FIG 26-1 Concept Map for Shock. (Concept map illustration created by Elaine Bishop Kennedy, EdD, RN.)
Maldistribution of circulating volume Loss of circulating volume
Invasion of microorganismsImmune cell activation Inability of the heart to pump
Loss of sympathetic tone
Etiologies Blood products Volume expanders Oxygen
Decreased Cardiac Output R/T alterations in preload
SHOCK Decreased cardiac output Activation of the renin response, retention of Na and water Compensatory failure and ineffective tissue perfusion Increased vascular permeability
Increased cellular death
Switch to aerobic metabolism with Increased lactic acid production Multiple Organ Dysfunction Syndrome (MODS)
Stimulation of anterior pituitary and adrenal glands with ACTH released to raise blood sugar and release of catecholamines
Increased heart rate, contractility, arterial and venous vasoconstriction, and shunting to vital organs Elevated serum lactate Base deficit Urinary output diminished or absent Serum creatinine elevated Systolic BP 90 mm Hg
Tachycardia Skin pale and cool Respiratory rate elevated Prolonged capillary refill Change in level of consciousness
causes causes
causescauses causescauses
leads toAssessment data Assessment data
Assessment data
leads to leads toleads to
Monitor intake and output Weigh daily Identify at-risk patients Assess for fluid overload Administer IV fluids as directed Prevent fluid loss Use large-bore IV needles Position flat with legs elevated and head and shoulders above chest Anti-ulcer Corticosteroids Epinephrine Antihistamines Vasodilators Oxygen Anti-infectives
Decreased Cardiac Output R/T alterations in afterload
Monitor response to drugs, blood, and blood products Prevent concomitant infections Postion in semi-Fowler’s Comfort measures for pruritis
Anticoagulants Vasopressors Atropine Oxygen
Decreased Cardiac Output R/T sympathetic blockade
Monitor neurologic status Frequent passive ROM Monitor for pulmonary embolism Antiembolic stockings Maintain body temperature Analgesics Sedatives Antidysrhythmics Inotropic agents Diuretics Oxygen
Decreased Cardiac Output R/T alterations in contractility
Assess respiratory function Limit myocardial oxygen demand Calm, quiet environment Position of comfort Limit activities
Pathophysiology
Etiology Nursing Diagnosis Nursing InterventionsAssessments
KEY Medication
ity,7,10-12 and management guided by lactate levels has been effective in improving outcomes.13-14 The base deficit derived from arterial blood gas (ABG) values also reflects global tissue acidosis and is useful to assess the severity of shock.6,9-11 Studies have demonstrated serum bicarbonate to be an equiv-alent alternative to arterial base deficit in predicting mortality in surgical and trauma patients.15-16 The use of mixed venous oxygen saturation (SVO2) measured by means of a pulmonary artery catheter or central venous oxygen saturation (SCVO2) measured with a central venous catheter allows assessment of the balance of oxygen delivery and oxygen consumption and the ratio of oxygen extraction.3,17-19 After years of recom-mended use to guide the care of patients with severe sepsis, this measure of global oxygen balance is being evaluated for use in other critically ill populations.17-21 Noninvasive indica- tors of regional tissue perfusion or oxygenation, such as sub-lingual capnometry and subcutaneous or skeletal muscle tissue oxygen saturation (StO2) measured with near-infrared spectroscopy, are also being evaluated.3,8,19 The sections on different types of shock discuss clinical assessment and diag-nosis of the patient in shock.
Medical Management
The major focus of the treatment of shock is the improvement and preservation of tissue perfusion. Adequate tissue perfu- sion depends on an adequate supply of oxygen being trans-ported to the tissues and the cell’s ability to use it. Oxygen transport is influenced by pulmonary gas exchange, CO, and hemoglobin level. Oxygen use is influenced by the internal metabolic environment and mitochondrial function. Man-agement of the patient in shock focuses on supporting oxygen delivery.1,3
Adequate pulmonary gas exchange is critical to oxygen transport. Establishing and maintaining an adequate airway are the first steps in ensuring adequate oxygenation. After the airway is patent, emphasis is placed on improving ventilation and oxygenation. Therapies include administration of supple-mental oxygen and mechanical ventilatory support.
An adequate CO and hemoglobin level are crucial to oxygen transport. CO depends on heart rate, preload, after-load, and contractility. A variety of fluids and medications are used to manipulate these parameters. The types of fluids used include crystalloids and colloids. The categories of medica-tions used include vasoconstrictors, vasodilators, positive inotropes, and antidysrhythmics.
Fluid administration is indicated for decreased preload related to intravascular volume depletion, and it can be accomplished by use of a crystalloid or colloid solution, or both. Crystalloids are balanced electrolyte solutions that may be hypotonic, isotonic, or hypertonic. Examples of crystalloid solutions used in shock situations are normal saline and lactated Ringer solution. Colloids are protein- or starch-containing solutions. Examples of colloid solutions are blood and blood components, such as albumin, and pharmaceuti-cal plasma expanders, such as hetastarch, dextran, and mannitol.
The quantity and choice of fluid is a subject of debate and depends on the situation.3,22-27 Excessive volume expansion, more than what increases preload and stroke volume (SV), worsens organ function and may produce coagulopathy, cytokine activation, and abdominal compartment syn-drome.3,24 Methods to measure preload responsiveness
Renal dysfunction develops as a result of renal vasoconstric-tion and renal hypoperfusion, leading to acute kidney injury (AKI). Gastrointestinal dysfunction occurs as a result of splanchnic vasoconstriction and hypoperfusion and leads to failure of the gut organs. Disruption of the intestinal epithe-lium releases gram-negative bacteria into the system, which further perpetuates the entire shock syndrome.5
During the refractory stage, shock becomes unresponsive to therapy and is considered irreversible. As the individual organ systems die, MODS—defined as failure of two or more body systems—occurs. Death is the final outcome. Regardless of the etiologic factors, death occurs from ineffective tissue perfusion because of the failure of the circulation to meet the oxygen needs of the cell.4
Assessment and Diagnosis
The patient with a mean arterial blood pressure (MAP) less than 60 mm Hg or with evidence of global tissue hypoperfu-sion is considered to be in a shock state.1,3 Because shock is a dynamic physiologic phenomenon, hypotension may occur late in the process or may normalize even when tissue perfu-sion is still inadequate.6-9 Clinical manifestations vary accord-ing to the underlying cause of shock, the stage of the shock, and the patient’s response to shock.
Compensatory mechanisms may produce normal hemo-dynamic values even when tissue perfusion is compro-mised.3,5,8,10-11 Global indicators of systemic perfusion and oxygenation include serum lactate, arterial base deficit, serum bicarbonate, and central or mixed venous oxygen saturation levels. Inadequate cellular oxygenation with anaerobic metab-olism and increased metabolic lactate production increase the serum lactate level.8,12 The level and duration of this hyperlactatemia are predictive of morbidity and
mortal-Cardiovascular
• Ventricular failure
• Microvascular thrombosis Neurologic
• Sympathetic nervous system dysfunction
• Cardiac and respiratory depression
• Thermoregulatory failure
• Coma Pulmonary
• Acute lung failure (ALF)
• Acute respiratory distress syndrome (ARDS) Renal
• Acute kidney injury (AKI) Hematologic
• Disseminated intravascular coagulation (DIC) Gastrointestinal
• Gastrointestinal tract failure
• Liver failure
• Pancreatic failure
BOX 26-1 Consequences of Shock
Nursing Management
The nursing management of a patient in shock is a complex and challenging responsibility. It requires an in-depth under-standing of the pathophysiology of the disease and the anticipated effects of each intervention, as well as a solid understanding of the nursing process. Later sections discuss specific interventions for the patient in shock.
The psychosocial needs of the patient and family dealing with shock are extremely important. These needs are based on situational, familial, and patient-centered variables.
Nursing priorities in managing the psychosocial stress of critical illness include 1) providing information on patient status, 2) explaining procedures and routines, 3) support-ing the family, 4) encouragsupport-ing the expression of feelsupport-ings, 5) facilitating problem solving and shared decision making, 6) individualizing visitation schedules, 7) involving the family in the patient’s care, and 8) establishing contacts with necessary resources. The consensus of all relevant pro-fessional organizations is that patients and families should be given the option of family presence during invasive proce-dures and resuscitation.47-50 Collaborative management of the patient with shock is outlined in Box 26-3.