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Published by: jefroc on Apr 02, 2010
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Chapter 67: Nursing Management: Shock, Systemic Inflammatory ResponseSyndrome, and Multiple Organ Dysfunction Syndrome
is a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism resulting in an imbalance between the supply of and demand for oxygen andnutrients.
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 pumpingaction 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, cardiactamponade, 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, anarrowed pulse pressure, tachypnea, pulmonary congestion, cyanosis, pallor, cool andclammy skin, 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, hyperglycemia, or diuresis.
Relative hypovolemia
results when fluid volume moves out of the vascular space intoextravascular 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 aspinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks, or inresponse to spinal anesthesia.
Clinical manifestations include hypotension, bradycardia, temperature dysregulation(resulting in heat loss), dry skin, and
(taking on the temperature of theenvironment).
Anaphylactic Shock 
Anaphylactic shock 
is an acute and life-threatening hypersensitivity (allergic) reaction to asensitizing substance (e.g., drug, chemical, vaccine, food, insect venom).
Immediate reaction causes massive vasodilation, release of vasoactive mediators, and anincrease in capillary permeability resulting in fluid leaks from the vascular space into theinterstitial space.
Clinical manifestations can include anxiety, confusion, dizziness, chest pain, incontinence,swelling of the lips and tongue, wheezing, stridor, flushing, pruritus, urticaria, andangioedema.
Septic Shock 
is a systemic inflammatory response to a documented or suspected infection. Severesepsis is sepsis complicated by organ dysfunction.
Septic shock 
is the presence of sepsis with hypotension despite fluid resuscitation alongwith the presence of tissue perfusion abnormalities.
In severe sepsis and septic shock, the initiated body response to an antigen is exaggeratedresulting 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-activatingfactor.
Platelet-activating factor results in the formation of microthrombi and obstruction of the microvasculature resulting in damage to the endothelium, vasodilation, increasedcapillary permeability, neutrophil and platelet aggregation, and adhesion to theendothelium.
Clinical presentation for sepsis is complex and no single or group of symptoms are specificto the diagnosis.
Patients will usually experience a hyperdynamic state characterized by increased COand decreased SVR.
Persistence of a high CO and a low SVR beyond 24 hours is ominous and oftenassociated with hypotension and multiple organ dysfunction syndrome (MODS).
Initially patients will hyperventilate as a compensatory mechanism, resulting inrespiratory alkalosis followed by respiratory acidosis and respiratory failure.
Other clinical signs include 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.
compensatory stage
is clinically apparent and involves neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasingconsequences of anaerobic metabolism and to maintain homeostasis.
 progressive stage
of shock begins as compensatory mechanisms fail and aggressiveinterventions are necessary to prevent the development of MODS.
In the final stage of shock, the
refractory stage,
decreased perfusion from peripheralvasoconstriction and decreased CO exacerbate anaerobic metabolism and the patient willdemonstrate 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, physicalexamination, 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 organsfrom dysfunction; and (5) provision of multisystem supportive care.
General management strategies for a patient in shock begin with ensuring that the patienthas 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 theappropriate fluid.
It is generally accepted that isotonic crystalloids, such as normal saline, are used in theinitial resuscitation of shock. If the patient does not respond to 2 to 3 L of crystalloids, bloodadministration 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.
Sympathomimetic drugs cause peripheral vasoconstriction and are referred to asvasopressor 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.
The goal of vasodilator therapy, as in vasopressor therapy, is to maintain MAP at 60to 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 inshock and nutrition is vital to decreasing morbidity from shock.
Enteral nutrition should be initiated within the first 24 hours. Parenteral nutrition is usedif enteral feedings are contraindicated or fail to meet at least 80% of the patient’s caloricrequirements.
Serum protein, nitrogen balance, BUN, serum glucose, and serum electrolytes are allmonitored to assess nutritional status.
Collaborative Care: Specific Measures

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