Unit Fifteen

Other Acute Problems

prohibited. An 80-year-old patient is in acute kidney failure and has is been diagnosed with multiple organ dysfunction syndrome (MODS). She underwent a right hip replacement 2 days ago and currently has a temperature of 102.6°F. publisher the Kluwer.of

What are treatment measures to reverse MODS? Wolters permission What patient populations are at increased risk for developing MODS? Discuss nursing care of patients with MODS. Copyrightexpress ©

without

reproduction or

Use

LWBK1620-C54_p1507-1531.indd 1507 11/12/17 4:29 PM Chapter 54 Nursing Management: and Multisystem Failure Linda Honan • Philip R. Martinez, Jr. • Kelly S. Grimshaw

Learning Objectives After reading this chapter, you will be able to: 1. Describe shock and its underlying pathophysiology. 2. Compare clinical findings of the preshock, shock, and end-organ damage stages of shock. 3. Describe similarities and differences in hypovolemic, cardiogenic, distributive, and prohibited. obstructive shock states. is 4. Identify medical and nursing management priorities in treating patients in shock. 5. Identify vasoactive medications used in treating shock, and describe nursing implications associated with their use. publisher the Kluwer.of Shock is a life-threatening condition with a variety of under- ­inadequate blood flow to the tissues results in poor delivery lying causes. The progression of shock is neither linear nor of oxygen and nutrients to the cells, cellular starvation, cell predictable. Nurses caring for patients with shock and forWolters death, organ dysfunction progressing to organ failure, and those at risk for shock must understand the underlying mech- permissioneventual death. anisms of shock and recognize its subtle as well as more Shock affects all body systems. It may develop rapidly or obvious signs. Rapid assessment and response are essential slowly, depending on the underlying cause. During shock, to the patient’s recovery. the body struggles to survive, utilizing a variety of homeo- Copyrightexpress © static, compensatory mechanisms to restore blood flow. Any insult to the body can create a cascade of events resulting Overview in poor tissue perfusion, which means that nurses should be without vigilant about watching for signs of shock in all patients, Shock can best be defined as a condition in which tissue regardless of their primary problem or diagnosis. perfusion is inadequate to deliver oxygen and nutrients to support vital organs and cellular function. This definition differs from more traditional views of shock because it does Pathophysiology not depend on absolute criteria for parameters, such as blood pressure (BP). reproduction Tissue perfusion is determined by cardiac output (CO) and or systemic vascular resistance (SVR). CO is the amount of Nursing Alert blood pumped by the in liters per minute (usual CO Use By the time BP drops, damage has already is about 4 to 6 L/min but varies greatly depending on the been occurring at the cellular and tissue metabolic needs of the body). CO depends on stroke volume, levels. Therefore, the patient at risk for shock must be determined by ventricular preload (volume), and heart rate, assessed and monitored closely before the BP falls. which is controlled in large part by the autonomic nervous system. Afterload is related closely to, and often equated Adequate blood flow to the tissues and cells requires the with, the aortic pressure. It depends on the contractility of following components: adequate cardiac pump, effective the right or left side of the heart and SVR (the resistance to vasculature and circulatory system, and sufficient blood the flow of blood out from the ventricles and a key determi- volume. If one component is impaired, perfusion to the nant of aortic pressure). It is helpful to think of SVR as a vise tissues is threatened or compromised. Without treatment, grip on the aorta. If the vise is tightened, the SVR and aortic 1508

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BOX 54-1 strategy for the management of hyperglycemia (also Classifications of Shock called ) in patients who are • occurs when there is a decrease in critically ill with and without diabetes is unknown; the intravascular volume. can be the result of however, maintaining the glucose of 140 to 180 mg/dL an imbalance of intake and output, such as in patients with avoids marked hyperglycemia while minimizing the dehydration or hemorrhage. risk of iatrogenic hypoglycemia (Stapleton & Heyland, • occurs when the heart has an 2016). impaired pumping ability; it may be of coronary or noncor- onary event origin. As the hypoxemia progresses, cellular metabolism becomes • Obstructive shock occurs when there is decreased ­oxygen anaerobic, which causes the lactic acid level to rise. Excess delivery due to an obstructive cause, such as pericardial levels of lactic acid limit the amount of adenosine triphos- tamponade, tension pneumothorax, PE, or abdominal com- phate (ATP) produced, and normal cell function cannot be partment syndrome. • is caused by alterations in vascular maintained. Recall ATP which is in every cell is responsi- smooth muscle tone, caused by nervous system injury, ble for storing and supplying needed energy to the cell. The + + inflammatory release causing vasodilation, or complications impaired Na /K and ATP membrane pump function results in + associated with medications such as epidural anesthesia. intracellular accumulation of sodium and loss of K . ­Cellular is technically considered a “distributive” type edema results from the increased prohibited.intracellular sodium and of shock. is a complex condition, caused by an increased capillary permeability,is further decreasing the CO. infection with profound vasodilation. As the cell membrane becomes more permeable, allowing electrolytes and fluids to seep out of and into the cell, cell structures, primarily the mitochondria, are damaged; and cell death results. pressure rise, and now it requires more work for the ventricle publisher to pump blood out. In contrast, if the vise grip is released from the aorta, there is little resistance to the outflow of Pathophysiologythe Alert blood and the work required of the heart muscle is dimin- Kluwer.Shockof often affects the mitochondria within ished. Conventionally, the primary underlying pathophysi- the cell, which normally function at the lowest

ologic process is used to classify the shock state (Box 54-1 oxygen tensions in the body (mitochondrial pO2 is provides classifications). When considering possible causes about 5 mm Hg). However, they consume almost of shock and potential interventions, nurses should remem-Woltersall the oxygen used by the body. More than 95% of ber that the interplay of these two factors (CO and SVR) is permissionaerobic chemical energy comes from mitochondrial what determines the extent of the course of shock and the work (aka oxidative phosphorylation), and the oxygen- prognosis of the patient. dependent combustion of fuel substrates (primarily In all types of shock, the cells lack an adequateCopyright bloodexpress sup - fats, amino acids, carbohydrates, ketones) into carbon ply and are inadequately oxygenated; therefore,© they must dioxide (CO2), water, and ATP. Because of this oxygen produce energy through anaerobic metabolism. This results dependence, the mitochondria of patients in shock in an acidotic intracellular environment, along with a host can be referred to as “canaries in the coal mine” since of electrolyte derangements. In stress stateswithout such as shock, often they are affected first during inadequate tissue catecholamines, cortisol, glucagon, and inflammatory cyto- perfusion. Historically miners would carry canaries into kines and mediators are released, causing hyperglycemia the mine tunnels since the buildup of gases such as and insulin resistance in an effort to mobilize glucose for carbon monoxide would kill the canary before killing cellular metabolism. the miners, thus it was a warning to get out! Similarly, reproduction without sufficient oxygen, ATP is generated by potential Nursing Alert mitochondrial fuels that are anaerobic. Thus lactic acid or Tight glycemic control (blood glucose, 80 accumulates in the blood (Jones & Kline, 2014). to 110Use mg/dL) was considered to reduce morbidity and mortality of patients who were acutely ill. While a higher blood glucose concentration has Stages of Shock been associated with adverse outcomes in a variety of clinical settings, recent research studies reveal Shock is believed to progress along a continuum. One way inconsistent results, suggesting that, in patients who to understand the physiologic responses and subsequent are critically ill, a less aggressive glycemic target clinical is to divide the continuum into is appropriate (e.g., a blood sugar of less than or separate stages: equal to 120 mg/dL was an independent risk factor associated with an increased mortality in patients who • A nonprogressive stage (also called the compensated were nondiabetic) (Chan et al., 2016). The optimal stage or preshock)

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Table 54-1 Clinical Findings in Stages of Shock Stage

Finding Nonprogressive stage; Progressive stage; Uncompensated Irreversible stage or Compensated stage or Stage or Shock End-Organ Dysfunction Preshock

Blood pressure Near normal Systolic below 80–90 mm Hg; Mean Requires mechanical or arterial pressure (MAP) less than pharmacologic support 65 mm Hg

Heart rate Over 100 bpm 100–150 bpm Erratic or asystole

Respiratory status Fewer than 20 breaths/min Rapid, shallow respirations; crackles May require assisted ventilation

Skin Cold, clammy Mottled, petechiae Jaundice

Urinary output Mildly decreased Severely decreased Anuric, requires dialysis

Mentation Confusion Lethargy Unresponsive prohibited. Acid–base balance Respiratory alkalosis Metabolic acidosis Profound acidosis is

• A progressive stage (also called the uncompensated stage Anxiety, along with feelings of doom, are common signs of or shock) shock during this earlypublisher phase and often are not recognized • An irreversible stage (also called End-organ dysfunction in patients or attributed to something other than developing which results in irreversible organ damage) shock. the of The earlier on this continuum that shock is recognized Kluwer. and interventions are initiated, the greater the patient’s Medical and Nursing Management chance of survival. Table 54-1 compares clinical findings in At this nonprogressive stage, treatment is directed toward the different stages of shock. Woltersidentifying the cause of shock, correcting the underlying permissiondisorder, and initiating aggressive measures aimed at sup- Nonprogressive Stage porting the body’s compensatory mechanisms. Because (Compensated Stage or Preshock) compensation cannot be maintained indefinitely, measures Pathophysiology Copyrightexpress such as fluid replacement and medication therapy must be © initiated early to maintain an adequate BP and reestablish In preshock, or the compensatory stage of shock, the BP and maintain adequate tissue perfusion. Early interven- often remains within normal limits. Compensatory responses, tion along the continuum of shock is the key to improving such as vasoconstriction, increased heart rate, and increased without the patient’s prognosis. Therefore, the nurse must assess contractility of the heart, contribute to maintaining ade- the patient at risk for shock systematically to recognize the quate CO and SVR. This results from stimulation of the subtle clinical signs of the compensatory stage before the sympathetic nervous system and subsequent release of cat- patient progresses to uncompensated shock. Box 54-2 high- echolamines (epinephrine and norepinephrine). Patients lights considerations for recognizing shock in older patients. display the often-described “fight-or-flight” response. Thus, The role of the nurse at this stage is to monitor the or a modest reproductionchange in systemic blood pressure patient’s hemodynamic status and promptly report devia- (increase or decrease)or may be the only clinical sign of early tions to the provider, to assist in identifying and treating the shock. Adult patients can often compensate for up to a 10% underlying disorder by continuous in-depth assessment of total volume lossUse through normal homeostatic mechanisms. the patient, to administer prescribed fluids and medications, Conversely, patients who have other medical problems or and to promote patient safety. In assessing tissue perfusion, who take certain medications (such as beta blockers or the nurse specifically observes for changes in level of con- ­calcium channel blockers) may have a diminished ability sciousness, vital signs, urinary output, skin, and laboratory to compensate. values. Constant reassessment is warranted at this stage. Nurses should try to maintain a calm environment for both Clinical Manifestations and Assessment the patient’s and family’s sake and also ensure that assess- Despite a near-normal BP, the patient may show other clin- ments and interventions are rapid and ongoing. Providing ical signs indicating inadequate organ perfusion. Tachycar- brief explanations about the diagnostic and treatment pro- dia, peripheral vasoconstriction, and anxiety are common. cedures, supporting the patient during these procedures, and

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increased oxygen requirements produces ischemia, and bio- BOX 54-2 chemical mediators cause myocardial depression. This leads Gerontologic Considerations to failure of the cardiac pump, even if the underlying cause Recognizing Shock in Older Patients of the shock is not of cardiac origin. The systemic impact of hypotension, and thus hypoper- The physiologic changes associated with aging, coupled with fusion, on the kidneys results in decreased urine output. In pathologic and chronic disease states, place older people at increased risk for developing a state of shock and possibly addition, the inflammatory response to injury is activated, and multiple organ dysfunction syndrome (MODS). Elderly peo- proinflammatory and anti-inflammatory cytokines and medi- ple can recover from shock if it is detected and treated early ators are released, which, in turn, activate the coagulation with aggressive and supportive therapies. Nurses play an system in an effort to reestablish homeostasis. At the same essential role in assessing and interpreting subtle changes in time, acidosis impairs all enzymatic functions, including older patients’ responses to illness. coagulation. A cascade of progressive organ failure resulting • During hypovolemic states, medications such as beta- from poor tissue perfusion is illustrated in ­Figure 54-1. Thus blocking agents (metoprolol [Lopressor]) used to treat hyper- it is common for a systemic inflammatory response, coined tension may mask tachycardia, a primary compensatory SIRS, to occur in patients with shock (see section on Septic mechanism to increase CO. Shock, page 1521). • The aging immune system may not mount a truly febrile Even if the underlying cause of the shock is reversed, the response (temperature over 40°C or 104°F), but an increasing prohibited. trend in body temperature should be addressed. sequence of compensatory responsesis to the decrease in tis- • The heart does not function well in hypoxemic states, and sue perfusion perpetuates the shock state, and a vicious cycle the aging heart may respond to decreased myocardial ensues. It is believed that the body’s appropriate or inappro- oxygenation with arrhythmias that may be misinterpreted priate response in this stage of shock may be the primary as a normal part of the aging process. factor determining the patient’s survival. publisher • Changes in mentation may be inappropriately misinter- preted as dementia. Older people with a sudden change in Clinical Manifestationsthe and Assessment mentation should be aggressively treated for the presence Kluwer.of of infection and organ hypoperfusion. Clinical manifestations that may be seen include symptom- atic tachycardia, dyspnea, restlessness, diaphoresis, meta- bolic acidosis, hypotension, prolonged capillary refill (more providing ­information about their outcomes reduces stressWolters than 2 seconds), decreasing pressure, and oliguria. The and anxiety and thus promotes the patient’s physical and permissionmost frequent neurologic finding in patients with shock is mental well-being. Speaking in a calm, reassuring voice and alteration in the level of consciousness, ranging from con- using gentle touch also help ease the patient’s concerns. fusion to coma (Rivers, 2016, p. 673). Skin changes will depend on the type of shock and may include cool, clammy Copyrightexpress Nursing Alert © skin (related to vasoconstriction) or warm, pink skin (related For patients experiencing shock, if perfusion to peripheral vasodilation of distributive shock). does not improve despite aggressive interventions, the nurse recognizes thatwithout the body will Nursing Alert shunt blood from organs such as the skin, kidneys, Although BP readings alone are unreliable and gastrointestinal (GI) tract to the brain and heart to indicators of circulatory status, a single ensure adequate blood supply to these vital organs. episode of systolic BP of less than 80 mm Hg is As a result, the skin is cool and clammy, bowel sounds associated with an 18% increase in hospital mortality are hypoactive, and urinereproduction output decreases. (Rivers, 2016). or Progressive Stage Nursing Alert (UncompenUsesa ted Stage or Shock) Pulse pressure is the difference between the systolic and diastolic pressure; for example, In the progressive stage, the patient loses the ability to com- for a BP of 120/80, the pulse pressure is 40 mm Hg. pensate for the insult, infection, or injury. It is during this Pulse pressure rises when the stroke volume increases stage that clinical signs become more obvious. and narrows when resistance to outflow decreases (Porth, 2015). The pulse pressure may decrease Pathophysiology before the systolic pressure decreases, and in patients The heart and kidneys are among the first organs to show with shock pulse pressure is less than 25 mm Hg. signs of dysfunction. Up until now on the continuum, the Nurses are key to identifying narrowing pulse myocardium has kept pace by increasing CO, but this can pressures in patients early in the course of shock and only go on for a limited time. The body’s inability to meet should immediately report a pulse pressure of less

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Central nervous system deficits due to hypoxia

Multisystem organ failure Immune deficiency

Adult respiratory distress syndrome

Myocardial depression Disseminated intravascular coagulation Lactic acidosis Liver failure Acute renal prohibited.failure is Stress ulcers

Paralytic ileus publisher the Kluwer.of

Wolters permission

Copyrightexpress Figure 54-1 Multiorgan system effects© of shock.

than 25 mm Hg to the provider, even if other signs of • provide access for strict measurement of intake and shock have not yet manifested. without ­output (Foley catheter may be inserted, and urine output should be measured vigilantly: A urine output of less than Medical and Nursing Management 30 mL/hr or 0.5 mL/kg/hr is indicative of renal hypoper- fusion and/or hypovolemia); and possibly Early and aggressive interventions are essential to the sur- • provide interventions with supportive technologies, such as vival of patients in shock; therefore, identifying patients who , dialysis, extracorporeal membrane may be in shock and reportingreproduction subtle changes in assessment oxygenation (ECMO), and intra-aortic balloon pump. are imperative. Initially,or two large-bore peripheral IVs (at least 16 gauge) are inserted to prepare for fluid administra- Nursing care of patients in shock requires expertise in tion (Rivers, 2016).Use Two IV lines allow simultaneous admin- assessing and understanding shock and the significance of istration of fluid, medications, and blood component therapy changes in assessment data. if required. Patients in shock are often cared for in the inten- Specific management of shock depends on the type of sive care (ICU) setting in order to shock and its underlying cause, but, in general, care is aimed at achieving the following goals using the acronym ASSESS: • facilitate close (hemodynamic monitoring, arte- rial line insertion, electrocardiographic [ECG] monitoring, A: Assess frequently the body’s response to shock arterial blood gases [ABGs], oxygen saturation, serum S: Support the pumping action of the heart electrolyte levels, physical and mental status changes); S: Support the respiratory system • allow for rapid and frequent administration of various E: Encourage patient and family involvement in care, par- prescribed medications and fluids; ticularly in end-of-life discussions

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S: Strengthen the competence of the vascular system unlikely to survive, the family must be informed about the S: Significantly optimize intravascular volume prognosis and likely outcome. Clear, honest communication is imperative as families may not understand what is hap- Irreversible Stage (End-Organ pening with the patient. Opportunities should be provided, Dysfunction) throughout the patient’s care, for the family to see, touch, and talk to the patient. Close family friends or spiritual advi- Pathophysiology sors may be of comfort to the family members in dealing If adequate tissue perfusion is not restored in a timely fash- with the inevitable death of their loved one. Whenever pos- ion, irreversible end-organ damage ensues. This represents sible, the patient’s family should be approached regarding the point along the shock continuum where end-organ dam- any living wills, advance directives, or other written or ver- age is so severe that the patient does not respond to treat- bal wishes the patient may have shared in the event that he ment and cannot survive. As the damage increases, acidosis or she became unable to participate in end-of-life decisions. may become so severe that even aggressive therapies such as In some cases, ethics committees may assist families and vasopressor support may not work. For example, kidney and health care teams in making difficult decisions. liver failure, compounded by the release of necrotic tissue toxins, will create an overwhelming metabolic acidosis. If the integrity of the gut barrier is compromised, bacteria and General Managementprohibited. their toxins can be translocated into the bloodstream. With Strategies in Shockis severe hypoperfusion of the liver, massive elevations in the enzyme aminotransferase and extensive hepatocellular dam- As described previously, and in the discussion of types of age occurs. Anaerobic metabolism contributes to a worsening shock to follow, management in all types and all phases of lactic acidosis. Respiratory system failure prevents adequate shock includes the following:publisher oxygenation and ventilation despite mechanical ventilatory support, and the cardiovascular system is ineffective in main- • Optimization theof systemic oxygen delivery to improve ­tissue oxygenation taining an adequate mean arterial pressure (MAP; MAP = Kluwer.of [(2 × diastolic pressure + systolic pressure)/3]) for tissue per- • Fluid replacement to restore intravascular volume fusion. Multiple organ dysfunction progressing to complete • Vasoactive medications to restore vasomotor tone and organ failure has occurred, and death is imminent. Multiple improve cardiac function organ dysfunction can occur as a progression along the shockWolters • Nutritional support to address the metabolic requirements continuum or as a syndrome unto itself and is described in permissionthat are often dramatically increased in shock more detail on page 1528. Therapies described in this section require collaboration among all members of the health care team to ensure that the Nursing Alert Copyrightexpress manifestations of shock are quickly identified and that ade- To optimize end-organ perfusion,© the nurse quate and timely treatment is instituted to achieve the best monitors the MAP. Although a specific MAP outcome possible (see Fig. 54-2). goal has not been established for all shock states, an without MAP of at least 60 to 65 mm Hg is a reasonable goal Optimize Oxygen Delivery (Rivers, 2016). The first step is to assess oxygenation and provide sup- plemental oxygen as needed. Oxygen is administered to Medical and Nursing Management increase the amount of oxygen carried by available hemo- Specific therapies in thisreproduction stage are usually the same as for globin in the blood. A patient who is confused may feel shock. Although the patient may have progressed from shock apprehensive with an oxygen mask or cannula in place, or to irreversible end-organ damage, the judgment that the shock and frequent explanations about the need for the mask may is irreversible canUse be made only retrospectively, on the basis reduce some of the patient’s fear and anxiety. Frequent of the patient’s failure to respond to treatment. As in shock, assessment of the respiratory status is warranted since many the nurse focuses on carrying out prescribed treatments, mon- patients with severe shock will require intubation and ven- itoring the patient, preventing complications, protecting the tilatory support. Continuous oxygen saturation monitoring patient from injury, and providing comfort. is expected. It is important to consider that intubation and Offering brief explanations to the patient about what mechanical ventilation not only provides for delivery of is happening is essential even if there is no certainty that oxygen and removal of carbon dioxide but also reduces the the patient hears or understands what is being said. Simple work of breathing, which, in the patient with hypoperfusion, comfort measures, including reassuring touches, should con- further exacerbates lactic acidemia (Rivers, 2016). Nurses tinue to be provided despite the patient’s nonresponsiveness understand that when patients are “working to breathe,” this to verbal stimuli. As it becomes obvious that the patient is strenuous use of accessory respiratory muscles can increase

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Hypotension

Hypodynamic Hyperdynamic Low CO (narrow PP) Low SVR (wide PP)

Pulmonary edema?

No Yes

JVD?

No Yes

Hypovolemia RV failure Cardiogenic shock Distributive shock Hemorrhage Obstructive MI Sepsis prohibited. Dehydration PE Valvular disease is Tamponade PTX Liver failure Figure 54-2 Shock diagnosis, treatment, Medications and monitoring. CO, cardiac output; PP, pulse pressure; SVR, systemic vascular resistance; JVD,publisher jugular venous distention; PE, pulmonary Fluids embolism; PTX, pneumothorax; MI, myocardial Fluids Fluids Inotropes Vasopressors theinfarction; Tx, treatment; IABP, intra-aortic bal- Blood Inotropes IABP EGDTx of loon pump; EGDTx, early goal-directed therapy; Hemostasis Revascularize Treat causeKluwer. Specific Tx SvO2, mixed venous oxygen saturation (percent of oxygenated hemoglobin in blood returning to the right heart). (Reprinted with permission from Lawrence, P., Bell, R., Dayton, M., & Hebert, J. Base deficit Wolters (2012). Essentials of general surgery (5th ed.). Lactate SvO2 permission Philadelphia, PA: Lippincott Williams & Wilkins.)

oxygen consumption­ by 50% to 100% and decrease cerebral dependent on the type of shock and on the specific patient blood flow by 50% (Jones & Kline, 2014). Copyrightexpress presentation. For example, in patients with septic shock, © crystalloid fluid remains the IV fluid of choice (Dellinger et al., 2013). Conversely, Hespan, a type of colloid fluid, has Fluid Replacement been shown to cause increased organ damage and mortality The fluids administered vary but may includewithout crystalloids in patients who are critically ill, including those with shock (electrolyte solutions that move freely between intravascular (Rivers, 2016). Blood should be given for hypovolemic shock and interstitial spaces), colloids (large-molecule IV solu- due to trauma and/or hemorrhage, although initially crystal- tions), and blood components (Table 54-2). The best fluid to loids may be given to patients to restore intravascular volume treat shock remains controversial. In emergencies, the “best” while waiting for blood products to transfuse. fluid is often the fluid thatreproduction is readily available and is depen- Common crystalloid fluids used for in hypo- dent on the type of shock and patient presentation. Fluid volemic shock include 0.9% sodium chloride solution (normal or resuscitation should be initiated early and aggressively in saline) and LR solution. LR is an electrolyte solution contain- patients with shockUse to maximize intravascular volume. For ing the lactate ion, which should not be confused with lactic example, in patients with septic shock, an intravenous fluid acid. The exogenous lactate is converted to bicarbonate by the challenge (20 to 30 mL/kg) may be given rapidly of crys- liver, thus assisting in treatment of the acidosis. It is important talloid IV fluid to improve intravascular volume (Dellinger to assess for liver disease when using this solution as the aci- et al., 2013; Ferri, 2016). A bolus of 500 mL titrated to MAP dosis may worsen when LR is administered to patients with or measurement of preload is recommended according to severe liver dysfunction. Additionally, because each liter con- Rivers (2016), and repeated based on the absence of pulmo- tains 4 mEq of potassium per liter, it should not be given to nary edema and evidence of improving tissue perfusion. Both patients with severe hyperkalemia. Care also must be taken crystalloids (e.g., saline and lactated Ringer’s [LR] solution) when administering normal saline rapidly as large volumes and colloids (e.g., albumin) may be administered to restore result in hyperchloremic metabolic acidosis and coagulop- intravascular volume. However, IV fluid choice remains athy (Rivers, 2016). If colloids are administered, the nurse

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Table 54-2 Fluid Replacement in Shock Fluids Advantages Disadvantages

Crystalloids

0.9% sodium chloride (normal Widely available, inexpensive Requires large volume of infusion; can saline solution) cause hyperchloremic metabolic acidosis, pulmonary edema

Lactated Ringer’s (LR) Lactate ion helps buffer metabolic Requires large volume of infusion; can cause acidosis pulmonary edema; should not be used in patients with severe hyperkalemia or patients with severe liver dysfunction

Hypertonic saline (3%, 5%, 7.5%) Small volume needed to restore Danger of hypernatremia, central pontine intravascular volume myelinolysis, and increased serum osmolality

Colloids

Albumin (5%, 25%) Rapidly expands plasma volume Expensive; requires human donors; limited supply; can cause heartprohibited. failure is Dextran (40, 70) Synthetic plasma expander Interferes with platelet aggregation; not recommended for patients with hemorrhagic shock

Hetastarch Synthetic; less expensive than albumin; Prolongspublisher bleeding and clotting times effect lasts up to 36 hours the ­understands that they expand intravascular volume by exerting what Kluwer.is actuallyof pumped out by the left ventricle; oncotic pressure, thereby pulling fluid into the intravascular thus the nurse considers parameters such as urinary space. Colloidal solutions have the same effect as hypertonic output (increasing), MAP, and lactate concentrations solutions in increasing intravascular volume, but less volume (decreasing) as measures of improved hemodynamic of fluid is required than with crystalloids. Albumin is a col-Woltersresponse to treatment. loid that is commonly ordered to treat hypovolemic shock. The permission disadvantage of colloids is their high cost, and outcomes of With newer technologies, catheters can be placed that patients with hypovolemic shock are equivalent regardless if allow the monitoring of intravascular pressures and venous they are given crystalloids or albumin (Rivers, 2016).Copyright expressRegard - oxygen levels. Assessment of mixed venous oxygen satura- less of the solution administered it is important© to avoid “over tion (SvO2) or ScvO2 (central venous oxygen saturation) is resuscitation” and thus causing fluid volume excess. done with a CVP line or from a special pulmonary artery The patient receiving fluid replacement in the context of catheter that has fiber optics capable of calculating the oxy- without shock must be monitored frequently for adequate urinary gen saturation of hemoglobin. SvO2 reflects the balance output, changes in mental status, skin perfusion, and changes between oxygen delivery and oxygen consumption. Know-

in vital signs. Lung sounds are auscultated frequently to ing the SvO2 in conjunction with pulse oximetry is helpful in detect signs of fluid accumulation. evaluating the adequacy of oxygenation; newer technology

Often, a central venous line is inserted in order to measure allows for continuous SvO2/ScvO2 measurements similar to (CVP).reproduction In addition to physical assess- the pulse oximetry. A normal SvO2/ScvO2 is 70% to 80% ment, the CVP helps in monitoring the patient’s response to (i.e., when the blood is returning to the right side of the heart, or fluid resuscitation. A normal CVP is 2 to 8 mm Hg. Several it has lost only 20% to 30% of its oxygen). An SvO2/ScvO2 readings are obtainedUse to determine a range, and fluid replace- of 50% to 70% reveals that more oxygen is being extracted ment is continued to achieve a CVP of 8 to 12 mm Hg; higher- from the RBCs; when the SvO2/ScvO2 is at 30% to 50% the than-“normal” CVPs readings are desired since ventricles oxygen extraction is becoming exhausted and lactic acido- tend to stiffen during shock (Jones & Kline, 2014). sis begins, and at 25% to 30%, severe lactic acidosis exists.

SvO2/ScvO2 below 25% is associated with cellular death Nursing Alert (Reyer, 2013). When the SvO2 drops, it reflects the increased The nurse understands that the CVP consumption of oxygen and the need for intervention. represents the volume in the right atrium and, Knowing the CVP assists in evaluating the intravascular therefore, is reflective of the amount of preload to the volume. Also the BP, urine output, and base deficit all are right ventricle. But in patients with shock, because of suggestive of intravascular volume status. Hemodynamic the stiffening of the ventricles, the CVP cannot predict monitoring with arterial and pulmonary artery lines may be

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implemented to allow close monitoring of the patient’s per- down lean body mass. In this catabolic process, skeletal fusion and cardiac status, as well as response to therapy. For muscle mass is broken down even when the patient has large additional information about hemodynamic monitoring, see stores of fat or adipose tissue. Loss of skeletal muscle greatly Chapter 55. prolongs the patient’s recovery time. Parenteral or enteral nutritional support should be initiated as soon as possible, Vasoactive Medication Therapy with some form of enteral nutrition always administered. The integrity of the GI system depends on direct exposure Vasoactive medications can be used in patients with all to nutrients. Stress ulcers occur frequently in patients who forms of shock to improve the patient’s hemodynamic stabil- are acutely ill because of the compromised blood supply to ity when fluid therapy alone cannot maintain adequate MAP. the GI tract. Therefore, antacids (e.g., Carafate), H blockers Different medications work on different aspects of CO, and 2 (e.g., famotidine [Pepcid], ranitidine [Zantac]), and/or pro- specific medications are selected depending on the under- ton pump inhibitors (e.g., lansoprazole [Prevacid]) are pre- lying cause (see Chapter 55, Table 55-9). Although most of scribed to prevent ulcer formation by inhibiting gastric acid the medications have several effects, these medications are secretion or increasing gastric pH. used to (1) increase the strength of myocardial contractility, (2) regulate the heart rate, (3) reduce myocardial resistance, and (4) initiate vasoconstriction. Receptors in the sympathetic nervous system are known Types of Shock prohibited. as alpha-adrenergic and beta-adrenergic receptors. Beta-­ is adrenergic receptors are further classified as beta-1 and Hypovolemic Shock beta-2 adrenergic receptors. When alpha-adrenergic recep- Hypovolemic shock, the most common type of shock, is tors are stimulated, blood vessels constrict in the cardiore- characterized by a decreased intravascular volume. Intracel- spiratory and GI systems, skin, and kidneys. When beta-1 lular fluid accountspublisher for about two thirds of the total body adrenergic receptors are stimulated, heart rate and myocar- water. The remainingthe one third of fluid is in the extracellular dial contraction increase. When beta-2 adrenergic receptors space that is divided into two compartments: intravascular of are stimulated, vasodilation occurs in the heart and skeletal spaceKluwer. (IVS, inside blood vessels) or interstitial space (ISS, muscles, and the bronchioles relax. The medications used in surrounding tissues). Approximately three quarters of the treating shock consist of various combinations of vasoactive extracellular fluid is in the ISS, and the remaining one quar- medications to maximize tissue perfusion by stimulating orWolters ter is in the IVS. Thus, the normal intravascular volume is blocking the alpha- and beta-adrenergic receptors. permission4 to 6 L. Hypovolemic shock occurs when there is a reduction When vasoactive medications are administered, the nurse in intravascular volume by 15% to 25%, which represents a must monitor vital signs frequently (at least every 15 minutes loss of 750 to 1,500 mL of blood in a 70-kg (154-lb) person. until stable, or more often if indicated). Vasoactive medica- Copyright tions should be administered through a central venousexpress line © Pathophysiology because infiltration and extravasation of some vasoactive medications can cause tissue necrosis and sloughing. An IV Hypovolemic shock can be caused by sudden fluid losses, such as hemorrhage, or by a gradual deficit in I&O, such as pump must be used to ensure that the medicationswithout are deliv- ered safely and accurately. Often, invasive monitoring using dehydration. See Chapter 56, Table 56-1 for further informa- an is used to titrate medications accurately. Indi- tion on hemorrhagic shock. Figure 54-3 depicts the sequence vidual medication dosages are usually titrated by the nurse, of events in hypovolemic shock. Box 54-3 discusses risk fac- who adjusts drip rates based on the prescribed dose and the tors for hypovolemic shock. patient’s response. Dosages are changed to maintain the MAP at a physiologic levelreproduction that ensures adequate tissue per- Medical Management fusion (usually aboveor 65 mm Hg). Vasoactive medications Major goals in the treatment of hypovolemic shock are (1) to should be tapered when possible, and the patient should be restore intravascular volume, (2) to reverse the sequence of weaned from medicationUse with frequent monitoring of BP (at events leading to inadequate tissue perfusion, and (3) to cor- least every 15 minutes). rect the underlying cause of the fluid loss as quickly as pos- sible. Depending on the severity of shock and the patient’s Nutritional Support condition, it is likely that efforts will be made to address all Nutritional support is an important aspect of care for patients three goals simultaneously. with shock. Increased metabolic rates during shock increase If the patient is hemorrhaging, efforts are made to stop the energy requirements and, therefore, caloric requirements. bleeding. This may involve applying pressure to the bleeding The release of catecholamines early in the shock continuum site or a surgery or procedure to stop internal bleeding. If the causes depletion of glycogen stores in about 8 to 10 hours. cause of the hypovolemia is diarrhea or vomiting, medica- Nutritional energy requirements are then met by breaking tions to treat diarrhea and vomiting are administered while

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the ­intracellular or interstitial compartment. Blood products Decreased blood volume may need to be administered, particularly if the cause of the hypovolemic shock is hemorrhage. Packed red blood cells are administered to replenish the patient’s oxygen-carrying capacity, in conjunction with other fluids that will expand Decreased venous return volume. Plasma and platelet transfusions can help with fluid resuscitation and also treat other underlying problems. The need for transfusions is based on the patient’s individual per- Decreased stroke volume fusion needs, which are determined by vital signs, blood gas values, and clinical appearance rather than an arbitrary labo- ratory value. An area of active research is the development of synthetic forms of blood (i.e., compounds capable of carrying Decreased cardiac output oxygen in the same way that blood does) as potential alterna- tives to blood component therapy. Risks inherent to adminis- tering blood include the possibility of a transfusion reaction. Commonly, positioning the patient with his or her head Decreased tissue perfusion down, known as the Trendelenburg positionprohibited., has been thought to increase blood flow to vital organsis by increasing preload. Figure 54-3 Pathophysiologic sequence of events in hypovolemic This practice has not been found to be supported by evidence shock. and, in fact, may worsen pulmonary gas exchange and risk of aspiration (Rivers, 2016). An alternative is to elevate the patient’s legs slightly to improve cerebral circulation and pro- efforts are made to identify and treat the cause. In elderly publisher patients, dehydration is a common cause of hypovolemia. mote venous return to the heart, but this position is contrain- If the underlying cause of the hypovolemia is dehydra- dicated for patientsthe with head injuries. tion, medications are also administered to reverse the cause Kluwer.of of the dehydration. For example, insulin is administered if Nursing Management dehydration is secondary to hyperglycemia, and desmo- Primary prevention of shock is an essential focus of nursing pressin (DDAVP) is administered for patients with diabetesWolters insipidus. care. Hypovolemic shock can be prevented in some instances permission Beyond reversing the primary cause of the decreased by closely monitoring patients who are at risk for fluid defi- intravascular volume, fluid replacement (also referred to cits and assisting with fluid replacement before intravascu- as fluid resuscitation) is of primary concern. At least two lar volume is depleted. In other circumstances, nursing care large-gauge IV lines are inserted to establish accessCopyright forexpress fluid focuses on assisting with treatment targeted at the cause of administration. Because the goal of the fluid© replacement is the shock and restoring intravascular volume. to restore intravascular volume, it is necessary to adminis- General nursing measures include ensuring safe adminis- ter fluids that will remain in the intravascular compartment, tration of prescribed fluids and medications and documenting without to avoid fluid shifts from the intravascular compartment into their administration and effects. Another important nursing role is monitoring for signs of complications and side effects of treatment and reporting these signs early in treatment. BOX 54-3 Administering blood transfusions safely is a vital nursing Risk Factors for Hypovolemic Shock role. In emergency situations, it is important to acquire blood External: Fluid losses: reproduction specimens quickly, to obtain a baseline complete blood • Trauma count, and to type and cross-match the blood in anticipation or • Surgery of blood transfusions. A patient who receives a transfusion • Vomiting Use of blood products must be monitored closely for adverse • Diarrhea effects (see Chapter 20). • Diuresis Fluid replacement complications can occur, often when large • Diabetes insipidus volumes are administered rapidly. Therefore, the nurse moni- • NPO status tors the patient closely for cardiovascular overload and edema. Internal: Fluid shifts: The risk of these complications is increased in the elderly and • Hemorrhage in patients with pre-existing cardiac disease. Hemodynamic • Burns • Ascites pressure, vital signs, ABGs, serum lactate levels, hemoglobin • Peritonitis and hematocrit levels, and fluid I&O are among the parame- • Dehydration ters monitored. Temperature should also be monitored closely to ensure that rapid fluid­ resuscitation does not ­precipitate

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­hypothermia. IV fluids may need to be warmed during the administration of large volumes. Physical assessment focuses Decreased cardiac on observing the jugular veins for distention and monitoring contractility CVP. CVP is typically low in hypovolemic shock; it increases with effective treatment, and is significantly increased with fluid overload and heart failure. The nurse must monitor car- diac and respiratory status closely and report to the provider Decreased stroke any changes in BP, pulse pressure, heart rate and rhythm, and volume and lung sounds. cardiac output

Cardiogenic Shock Pulmonary Decreased Decreased congestion systemic coronary artery Cardiogenic shock occurs when the heart’s ability to con- tissue perfusion perfusion tract and to pump blood is impaired and the supply of oxy- gen is inadequate for the heart and tissues. Cardiogenic Figure 54-4 Pathophysiologic sequence of events in cardiogenic shock is seen most often in patients with myocardial infarc- shock. prohibited. tion (MI). Other causes of cardiogenic shock are related to is conditions that stress the myocardium (e.g., severe hypox- myocardium and (2) to improve the cardiac function by emia, acidosis, hypoglycemia, and hypocalcemia), as well in­creasing cardiac contractility, decreasing ventricular after- as in conditions that result in ineffective myocardial function load, or both. In general, these goals are achieved by increas- (e.g., cardiomyopathies, valvular damage, and arrhythmias). ing oxygen supply topublisher the heart muscle while reducing oxygen demands. Pathophysiology the As with all forms of shock, the underlying cause of car- of In cardiogenic shock, CO, which is a function of stroke vol- diogenicKluwer. shock must be corrected. It is necessary first to treat ume and heart rate, is compromised. When stroke volume the oxygenation needs of the heart muscle to ensure its con- and heart rate decrease or become erratic, BP falls (systolic tinued ability to pump blood to other organs. In the case of blood pressure is less than 90 mm Hg or there is a decreaseWolters cardiogenic shock due to ischemia or infarction, the patient from baseline of more than 30 mm Hg for more than 30 min- permissionmay require thrombolytic therapy, angioplasty, coronary utes), and systemic tissue perfusion is compromised (urine artery bypass graft surgery, intra-aortic balloon pump ther- output decreases, skin becomes cool and mottled, mental sta- apy, ventricular assist device (VAD), or some combination tus changes [sensorium becomes clouded], anxiety is obvi- of these treatments. General interventions for cardiogenic Copyright ous, capillary refill is delayed). Blood supply for theexpress heart shock include supplemental oxygen, controlling , © muscle itself is inadequate, resulting in further decreases in providing selected fluid support, administering vasoactive CO (cardiac index is less than 2.2 L/min/m2). Additionally, medications, controlling heart rate with medication or pace- diastolic dysfunction increases left atrialwithout pressure, which maker, and using a mechanical assist device if needed. Serial leads to pulmonary congestion and hypoxemia that can fur- laboratory markers for ventricular dysfunction (e.g., BNP) ther exacerbate myocardial ischemia and impair ventricular and cardiac enzyme levels (i.e., troponin-I) are measured, performance (pulmonary capillary wedge pressure is greater serial 12-lead ECGs are obtained, and frequently an echo- than 18 mm Hg). This can occur rapidly or over a period cardiogram is ordered to assess the degree of myocardial of days. Patients in cardiogenic shock may experience the damage or dysfunction. pain of and developreproduction arrhythmias and hemodynamic instability. Figure 54-4or depicts the pathophysiology of car- Pharmacologic Therapy diogenic shock. Use Oxygen In the early stages of shock, supplemental oxygen is admin- Nursing Alert istered at a rate sufficient to achieve an oxygen saturation In the case of heart failure resulting in exceeding 90%. Monitoring of ABG values and pulse oxim- cardiogenic shock, the nurse assesses for etry values helps determine whether the patient requires a jugular vein distention (JVD), rales, shortness of more aggressive method of oxygen delivery. breath, and S3 gallop. Analgesia Medical Management If a patient experiences chest pain, an IV analgesic (com- The goals of management in cardiogenic shock are (1) to monly morphine sulfate) is administered for pain relief. limit further myocardial damage and preserve the healthy In addition to relieving pain, morphine dilates the blood

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­vessels. This reduces the workload of the heart by both If tissue perfusion remains inadequate, inotropic ther- decreasing the cardiac filling pressure (preload) and reduc- apy may be considered with dobutamine, which predomi- ing the pressure against which the heart muscle has to eject nantly affects beta-1 adrenergic receptors (increases the blood (afterload). strength of myocardial activity and improves CO). Dobuta- mine enhances the strength of cardiac contraction, improv- Antiplatelet Agents and Beta Blockers ing stroke volume ejection and overall CO. Because it also Antiplatelet agents, such as aspirin, should be given in the has some beta-2 properties, vasodilation occurs (decreased case of a patient with acute MI. In addition, a beta blocker is afterload), and the bronchioles relax. The nurse is aware that used to decrease workload of the heart and preserve cardiac dobutamine may exacerbate hypotension is some patients muscle. The use of these medications in the case of a patient (related to vasodilatory effects) and can precipitate tachyar- with cardiogenic shock can be complicated since beta block- rhythmias (Hollenberg, 2016). ers will decrease BP. See Chapter 14 for acute treatment of IV nitroglycerin in low doses acts as a venous vasodila- chest pain and MI. tor and, therefore, reduces preload. At higher doses, nitro- glycerin causes arterial vasodilation and reduces afterload Nursing Alert as well. These actions, in combination with dobutamine, During an acute MI, aspirin may be ordered increase CO while minimizing cardiac workload. In addi- to prevent worsening thrombosis in the tion, vasodilation enhances blood flowprohibited. to the myocardium, coronary arteries. When administering aspirin in this improving oxygen delivery to theis weakened heart muscle. A acute situation, the nurse should ask the patient to combination of medications may be prescribed, depending chew aspirin (162 to 325 mg) rather than swallow a on the patient’s response to treatment. All vasoactive med- whole enteric-coated aspirin. Chewing aspirin allows ications have adverse effects, making specific medications for a more rapid absorption rate than does swallowing more useful than others at different stages of shock. publisher it whole (Anderson, 2016; Feldman & Cryer, 1999). Nursingthe Alert Vasoactive Medications Kluwer.Vasoactiveof medications should never be Vasoactive medication therapy consists of multiple pharma- stopped abruptly because this could cause cologic strategies to restore and maintain adequate CO. In severe hemodynamic instability, perpetuating the cardiogenic shock, the aims of vasoactive medication ther- shock state. apy are to improve cardiac contractility, optimize preloadWolters and afterload, reduce myocardial oxygen demand, and sta- permissionDiuretics bilize heart rate and rhythm. Medications commonly used Diuretics such as furosemide (Lasix) may be administered to treat cardiogenic shock include dobutamine, dopamine, to reduce the workload of the heart by reducing fluid accu- and nitroglycerin. See Table 55-9 for a reviewCopyright of commonexpress mulation. Diuretics must be used cautiously since they can vasoactive medications. © lead to hypovolemia. In addition, aggressive diuresis can lead to metabolic alkalosis, often referred to as a contraction Nursing Alert alkalosis. The use of diuretics can also lead to electrolyte The nurse is vigilant in observingwithout the patient’s abnormalities, the most common of which is hypokalemia. response to vasoactive agents because of the potential of worsening myocardial ischemia by Antiarrhythmic Medications increasing cardiac work. Multiple factors, such as hypoxemia, electrolyte imbalances, and acid–base imbalances, contribute to serious cardiac Dopamine is a sympathomimeticreproduction agent. It acts as an ino- arrhythmias in all patients with shock. In addition, as a com- trope and a vasopressor (at higher doses). It may be used or pensatory response to decreased CO and BP, the heart rate with dobutamine and nitroglycerin to improve tissue per- increases beyond normal limits. This impedes CO further by fusion. SympathomimeticUse agents must be used with cau- shortening diastole and thereby decreasing the time for ven- tion in patients with cardiogenic shock since they increase tricular filling. Consequently, antiarrhythmic medications myocardial oxygen demand and can worsen failure. Also, in are required to stabilize the heart rate. For a full discussion patients with severe metabolic acidosis, which occurs in the of cardiac arrhythmias, as well as commonly prescribed later stages of shock, the effectiveness of dopamine is dimin- medications, see Chapter 17. ished. Norepinephrine also may be considered as a first-line agent for hypotension in patients with cardiogenic shock; it Fluid Status is a vasoactive agent that acts primarily as a vasoconstric- tor, has a mild inotropic effect, and increases coronary flow Appropriate fluid administration is also necessary in the treat- while having less of an effect on heart rate in patients with ment of cardiogenic shock. Administration of fluids must be tachycardia (Hollenberg, 2016). monitored closely to detect signs of fluid overload.­ Incremental

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IV fluid boluses are cautiously administered to determine opti- The nurse must be knowledgeable about the desired effects, mal filling pressures for improving CO. Nurses should use as well as the side effects, of medications. For example, it caution when administering fluids rapidly because rapid fluid is important to monitor the patient for decreased BP after administration in patients with cardiac failure may result in administering morphine or nitroglycerin. Patients receiving acute pulmonary edema. Fluid overload and pulmonary edema thrombolytic therapy must be monitored for bleeding. Arte- are risks because of ineffective cardiac function and accumula- rial and venous puncture sites must be observed for bleeding, tion of fluid in the pulmonary tissues. and pressure must be applied at the sites if bleeding occurs. Neurologic assessment is essential after the administration of Mechanical Assistive Devices thrombolytic therapy to assess for the potential complication If CO does not improve despite supplemental oxygen, vaso- of cerebral hemorrhage associated with the therapy. IV infu- active medications, and fluid boluses, mechanical assistive sions must be observed closely because tissue necrosis and devices can sometimes be used temporarily to improve the sloughing may occur if vasopressor medications infiltrate the heart’s ability to pump. Intra-aortic balloon counterpulsation tissues. Urine output, blood urea nitrogen (BUN), and serum or left and right ventricular assist devices and total tempo- creatinine levels are monitored to detect decreased kidney rary artificial are means of providing temporary cir- function secondary to the effects of cardiogenic shock or its culatory assistance and are reviewed in Chapters 16 and 55. treatment. prohibited. Nursing Management Enhancing Safety and Comfortis Preventing Cardiogenic Shock Throughout care, the nurse must take an active role in safe- guarding the patient, enhancing comfort, and reducing anx- In many circumstances, identifying at-risk patients early, iety. This includes administering medication to relieve chest promoting adequate perfusion of the heart muscle, and pain, preventing infectionpublisher at the multiple arterial and venous decreasing cardiac workload can prevent cardiogenic shock. line insertion sites, protecting the skin, and monitoring respi- Risk factors include advanced age, anterior MI or previous the ratory and kidney function. Proper positioning of the patient MI, diabetes, hypertension, multivessel CAD, and peripheral Kluwer.of promotes effective breathing without decreasing BP and may vascular and cerebrovascular diseases (Hollenberg, 2016). also increase patient comfort while reducing anxiety. Patients who have decreased ejection fractions, larger infarc- Brief explanations about procedures that are being per- tions, and echo results that demonstrate a lack of hyperkine- Woltersformed and the use of comforting touch often provide reassur- sis in the myocardial remote from the infarction should be ance to the patient and family. The family is usually anxious considered at risk for cardiogenic shock (Hollenber­ g, 2016). permission and benefits from opportunities to see and talk to the patient. Minimizing patient risk can be accomplished by conserving Explanations of treatments and the patient’s responses are the patient’s energy, promptly relieving angina, and admin- often comforting to family members. istering supplemental oxygen, aspirin, and betaCopyright blockers.express When cardiogenic shock is present, nursing© management includes working with other members of the health care team to prevent shock from progressing and to restore ade- Distributive Shock without quate cardiac function and tissue perfusion. Distributive shock, also sometimes called circulatory shock, Monitoring Hemodynamic Status occurs when the body’s ability to adjust vascular tone is impaired, and thus blood volume is abnormally displaced in A major role of the nurse is monitoring the patient’s hemo- the vasculature (e.g., when blood volume pools in peripheral dynamic and cardiac status. Arterial lines and ECG moni- reproduction blood vessels). The displacement of blood volume causes toring equipment must be well maintained and functioning a relative hypovolemia because not enough blood returns or properly. The nurse anticipates the medications, IV fluids, to the heart, which leads to subsequent inadequate tissue and equipment that might be used and is ready to assist in Use perfusion. The vascular tone is determined both by central implementing these measures. Changes in hemodynamic, regulatory mechanisms, as in BP regulation, and by local cardiac, pulmonary, and renal status and laboratory values are regulatory mechanisms, as in tissue demands for oxygen and documented and reported promptly. In addition, adventitious nutrients. Therefore, distributive shock can be caused either breath sounds, changes in cardiac rhythm, and other abnor- by a loss of sympathetic tone or by release of biochemical mal physical assessment findings are reported immediately. mediators from cells. The varied mechanisms leading to the initial vasodilation Administering Medications in distributive shock further subdivide this classification of The nurse documents and records medications and treat- shock into three types: (1) septic shock, (2) neurogenic ments that are administered, as well as the patient’s response shock, and (3) anaphylactic shock. Other causes of dis- to treatment. tributive shock are rare but include ,

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BOX 54-4 ­vancomycin-resistant enterococci (VRE), penicillin-resistant Risk Factors for Distributive Shock Streptococcus pneumoniae, and resistant gram-­negative bacilli Septic shock: are seen (Russell, 2016). Additional risk factors are age, immu- • Immunosuppression nocompromise due to malnutrition, alcoholism, malignancy, • Extremes of age (under 1 year of age and over 65 years of diabetes mellitus, and AIDS; invasive procedures and indwell- age) ing medical devices; and the increased number of resistant • Malnourishment microorganisms. Elderly patients continue to be at particular • Chronic illness risk for sepsis because of decreased physiologic reserves and • Invasive procedures an aging immune system. The incidence of septic shock can Neurogenic shock: be reduced by carrying out infection control practices, includ- • Spinal cord injury ing the use of meticulous aseptic technique, properly cleaning • Spinal anesthesia and maintaining equipment, and using thorough hand hygiene • Depressant action of medications techniques. • Glucose deficiency Anaphylactic shock: Pathophysiology • Penicillin sensitivity • Transfusion reaction When microorganisms invade body tissues, patients exhibit an • Bee sting allergy immune response. This immune responseprohibited. provokes the activa- • Latex sensitivity tion of biochemical cytokines andis mediators associated with • Severe allergy to some foods or medications an inflammatory response and produces a complex cascade of physiologic events that leads to poor tissue perfusion. Wide- spread endothelial injury leads to increased capillary per- drug overdose, neurogenic insults, addisonian crisis, and meability, which triggerspublisher seepage of protein-rich fluid from myxedema coma (Rivers, 2016). In all types of distributive the capillaries, and vasodilation, which occurs when injured shock, massive arterial and venous dilation allows blood to the endothelial cells release nitric acid (a potent vasodilator). pool peripherally. The different types of shock cause varia- TheseKluwer. two effectsof interrupt the ability of the body to provide tions in the pathophysiologic chain of events. Risk factors adequate perfusion, oxygen, and nutrients to the tissues and for distributive shock are summarized in Box 54-4. cells. In addition, proinflammatory and anti-inflammatory cytokines released during the inflammatory response activate Septic Shock Wolters permissionthe coagulation system, which begins to form clots in areas Septic shock, the most common type of distributive shock, where a clot may or may not be needed, further compromising is caused by widespread, overwhelming infection in combi- tissue perfusion. The imbalance of the inflammatory response nation with a dysregulated host immune response. Because and the clotting and fibrinolysis cascades are considered crit- Copyright of the increased sophistication of antibiotic therapyexpress and ical elements of the devastating physiologic progression that © improved recognition of sepsis and initiation of inten- is present in patients with severe sepsis. To illustrate, the sive care management, the incidence of septic shock has increased permeability within the lung is a key component of declined. Approximately 750,000 cases ofwithout severe sepsis or acute lung injury (ALI), whereas increased permeability in the septic shock occur annually in the United States, with mor- intestine can lead to translocation of intestinal bacteria. tality rates of about 25 to 35%, which is down from rates of 70% in 2010 (Russell, 2016). Finding and aggressively treat- Clinical Manifestations and Assessment ing the source of infection, as well as providing aggressive Sepsis is defined by presence of at least two of the four signs cardiopulmonary support, are important determinants of the of the systemic inflammatory response syndrome: (1) fever clinical outcome. reproduction (above 38°C) or hypothermia (below 36°C); (2) tachycar- or dia (more than 90 beats/min); (3) tachypnea (more than Risk Factors Use 20 breaths/min), hypocapnia (partial pressure of carbon Nosocomial infections (infections occurring in the hospital) dioxide less than 32 mm Hg), or the need for mechanical in patients who are critically ill that may progress to septic ventilatory assistance; and (4) leukocytosis (more than shock commonly originate in the lungs (pneumonia) and uri- 12,000 cells/μL), leukopenia (fewer than 4,000 cells/μL), or nary (pyelonephritis) and GI tract (peritonitis, intra-abdominal­ a left shift (more than 0% immature band cells) in the circu- abscess, cholangitis), although they can originate anywhere lating white blood cell differential and suspected or proven in the body (refer to Table 54-3 for common sites related infection plus a documented or suspected infection (Russell, to sepsis). Organisms include gram-positive or negative bac- 2016, p. 685). teria, fungi, and, rarely, protozoa or rickettsiae are associated Systemic inflammatory response syndrome (SIRS) with septic shock; commonly gram-positive bacteria, espe- presents clinically like sepsis. The only difference between cially methicillin-resistant Staphylococcus aureus (MRSA), SIRS and sepsis is that an identifiable causative infectious

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Table 54-3 Common Sites and Diseases Associated with Sepsis/Systemic Inflammatory Response Syndrome (SIRS) Organ System Location Disease

Respiratory Upper respiratory tract Sinusitis Mastoiditis Lower respiratory tract Pneumonia Lung abscess Empyema

Gastrointestinal Mediastinum Esophageal rupture/perforation Hepatobiliary Hepatic abscess Intra-abdominal Cholangitis Cholecystitis Intestinal infarction/perforation Pancreatitis Intra-abdominal/diverticular abscess

Cardiovascular Mediastinum Postoperative mediastinitis Native or prosthetic cardiac valve Endocarditis prohibited. Genitourinary Kidney, ureter, and bladder Perinephric abscessis Pyelonephritis Cystitis

Neurologic Brain and meninges Meningitis Intracranialpublisher abscess Dermatologic Traumatic wound, surgical wound, or burn sitethe Soft tissue abscess Necrotizing fasciitis Kluwer.of Infected decubitus ulcer Full and partial thickness burn

Prosthetic Central/peripheral venous catheter Catheter infection Arterial catheter Wolters Infected prosthesis Ventriculoperitoneal shunt Dialysis catheter permission Articular prosthetic device Dialysis graft/shunt

Other Vascular system Copyrightexpress Septic thrombophlebitis © Reprinted with permission from Stenbit, A., & Serio, A. (2010). Sepsis. In R. Irwin & J. Rippe (Eds.), Manual of intensive care management (Chapter 123). Philadelphia, PA: Lippincott Williams & Wilkins. without agent is established in the latter. SIRS/sepsis results in an having two phases, a hyperdynamic (warm) and a hypody- inflammatory and immunologic response that is over- namic (cold) phase. Although the division into phases may whelming, thought to be caused in large part by an array of promote understanding of sepsis, its actual progression into inflammatory cytokines, including but not confined to tumor severe sepsis and septic shock is not always easy to recog- necrosis factor (TNF). Thereproduction inflammatory response also leads nize clinically. Initially, a hyperdynamic response occurs; it to increased coagulation, and coagulation triggers inflamma- is characterized by a high CO with systemic vasodilation. or tion; a positive feedback loop is at play that has the potential The BP may remain within normal limits, or the patient to disrupt essentialUse kidney, cardiovascular, and respiratory may be hypotensive but responsive to fluids. The heart rate function (Russell, 2016). Any overwhelming insult can stim- increases, progressing to tachycardia. Fever, with warm, ulate SIRS and may progress to sepsis; noninfectious disor- flushed skin and bounding , is evident. The respiratory ders include pancreatitis and drug intoxication. Therefore, rate is elevated. Urinary output may remain at normal levels despite an absence of infection, antibiotic agents still may or decrease. GI status may be compromised, as evidenced be administered because of the possibility of unrecognized by nausea, vomiting, diarrhea, or decreased bowel sounds. infection. Additional therapies directed to support patients Signs of hypermetabolism include increased serum glucose with SIRS are similar to those for sepsis. If the inflammatory and insulin resistance. Subtle changes in mental status, such process progresses, septic shock may develop. as confusion or agitation, may be present. Sepsis is an evolving process, without a predictable linear As the sepsis progresses, tissues become more under- progression. In the past, septic shock has been described as perfused and acidotic, compensation begins to fail, and the

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BOX 54-5 Definitions in Sepsis Bacteremia: The presence of bacteria in the blood • Areas of mottled skin Infection: The presence of microorganisms that trigger an • Capillary refill of more than 3 seconds inflammatory response • Decreased urinary output (less than 0.5 mg/kg for 1 hour) Systemic inflammatory response syndrome (SIRS): A syn- (oliguria) drome resulting from a severe clinical insult that initiates an • Lactate greater than 2 mmol/L (lactic acidosis) overwhelming inflammatory response by the body; defined • Abrupt change in mental status (decreased Glasgow as two or more of the following conditions: Coma Scale) • Temperature greater than 38.5°C or less than 35.0°C • Platelet count of less than 100,000 or disseminated • Heart rate of more than 90 bpm intravascular coagulation (DIC) (thrombocytopenia)

• Respiratory rate of more than 20 breaths/min or PaCO2 • Acute lung injury or acute respiratory distress syndrome of less than 32 mm Hg (ARDS) (hypoxemia) • White blood cell count of more than 12,000 cells/mL, • Cardiac dysfunction less than 4,000 cells/mL, or greater than 10% immature Septic shock: Shock associated with sepsis; defined as severe (band) forms sepsis, plus one of the following: Sepsis: A systemic response to infection; may occur after a burn, • Mean arterial pressure (MAP) of less than 60 after fluid surgery, or serious illness and is defined as the presence of resuscitation; systolic blood pressureprohibited. less than 90 mm Hg SIRS, plus the presence of an infectious source (either by or a decrease from baseline thatis is greater than 40 mm Hg, documented culture or by visualizing focal infection) despite adequate fluid resuscitation. Severe sepsis: Defined as sepsis, plus at least one of the fol- • Need for vasoactive medication in order to maintain MAP lowing signs of organ hypoperfusion: of greater than 60.

Adapted from Annane, D., & Cavaillon, J. M. (2005). Septic shock. Lancet, 365(9453), 63–78; Sommers, M.publisher S. (2003). The cellular basis of septic shock. Clinics of North America, 15(1), 13–26. the of patient becomes more hypodynamic. The cardiovascular sys- productsKluwer. may be administered to increase intravascular vol- tem also begins to fail, the BP does not respond to vasoactive ume. IV fluids boluses (in the range of 20 to 40 mL/kg) may agents and fluid resuscitation, and signs of end-organ damage be ordered to improve intravascular volume (Rivers, 2016). are visible (e.g., kidney failure, pulmonary failure, hepaticWolters The CVP, MAP, urinary output, and SvO2 are used to guide failure). As sepsis progresses to septic shock, the BP drops, permissiontherapy. and the skin becomes cool and pale. Temperature may be Oxygen is administered and guided by the pulse oximeter,

normal or below normal. Heart and respiratory rates remain SvO2, and clinical presentation. Many patients will require rapid. Urine output decreases, and multiple organ dysfunc- mechanical ventilation, with a lower tidal volume (typically Copyright tion syndrome (MODS) develops (discussed on pageexpress 1528). greater than 6 mL/kg of ideal body weight [IBW]), which © In an effort to promote recognition and earlier treatment has been associated with decreased mortality from ALI and of patients with sepsis, the Society of Critical Care Medi- acute respiratory distress syndrome (ARDS). ARDS and cine defined a common set of terms and withoutcues for clinicians ALI are discussed in Chapter 10. (Box 54-5). Preventing the progress from sepsis to septic shock neces- sitates early diagnosis and aggressive resuscitation. The Medical Management patient’s responses to treatment are closely monitored, and resuscitation is continued until CVP is greater than 8, MAP is Current treatment of septic shock involves identification and greater than 65 mm Hg, urine output is 0.5 mL/kg/hr or more, elimination of the cause of infection and aggressive cardio- reproduction and SvO is greater than 70%. This approach is associated pulmonary support to prevent or limit end-organ damage 2 or with a decreased mortality and should be considered standard and death. Specimens of blood, sputum, urine, and wound of care in the management of septic shock. drainage are collectedUse for culture using aseptic technique. Any potential routes of infection must be eliminated. IV Pharmacologic Therapy lines may need to be removed and reinserted at other body sites; the patient will require scrupulous sterile techniques Antibiotics for the insertion of catheters, with consideration of the use of Before antibiotic therapy is initiated, it is important that all cul- antibiotic-impregnated catheters (Russell, 2016). If possible, tures be obtained. However, if obtaining cultures is delayed, urinary catheters are removed or replaced. Any abscesses are the nurse is aware that antimicrobials should be administered drained, and necrotic areas are surgically débrided. within 1 hour of identification of septic shock. The nurse Fluid replacement must be instituted to correct the hypo- anticipates the need for blood, sputum, urine, and wound cul- volemia that results from the incompetent vasculature and tures, and, depending on the site of the expected infection, the inflammatory response. Crystalloids, colloids, and blood additional cultures may be obtained from the cerebrospinal­

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fluid (in the case of suspected meningitis) or pleural space (if nutrition in surgical patients who are critically ill. Regarding empyema is suspected). If the infecting organism is unknown, glycemic control, intense insulin therapy increases the risk of empiric broad-spectrum antibiotics are started. When culture higher rates of hypoglycemia and perhaps increased mortality and sensitivity reports become available, the antibiotic agents and, therefore, is not recommended (Russell, 2016). However, can be changed to those that are more specific to the infecting the nurse assesses and alerts the team when the patient’s blood organism and less toxic to the patient. glucose level is outside the range of 140 to 180 mg/dL.

Nursing Alert Nursing Management It is important for the nurse to consider all possible sources of the infection. Symptoms Nurses caring for patients in any setting must keep in mind such as cough, sputum production, adventitious the risks of sepsis and the high mortality rate associated with lung sounds and increased work of breathing sepsis, severe sepsis, and septic shock. All invasive proce- suggests pneumonia; pleuritic chest pain, decreased dures must be carried out with aseptic technique after care- fremitus, and a dull, flat sound on percussion ful hand hygiene. In addition, IV lines, arterial and venous suggests empyema; dysuria and costovertebral angle puncture sites, surgical incisions, traumatic wounds, urinary tenderness suggests pyelonephritis; erythema and catheters, and pressure ulcers must be monitored for signs of drainage and warmth from IV lines suggests line infection in all patients. Nurses shouldprohibited. identify patients who sepsis; whereas headache and stiff neck suggest are at particular risk for sepsis andis septic shock (i.e., elderly meningitis. and immunosuppressed patients and those with extensive trauma, burns, or diabetes), keeping in mind that these high- Vasopressors risk patients may not develop typical or classic signs of infection and sepsis. For example, confusion may be the first Therapy with vasopressors (e.g., norepinephrine, epinephrine) publisher is expected if a mean arterial blood pressure of greater than sign of infection and sepsis in elderly patients. 65 mm Hg is not achieved by IV hydration alone. The nurse Monitoring andthe constant reassessment are primary nurs- ing tasks when caring for a patient with septic shock. Vital monitors the MAP, the CVP, O2 saturation, and SvO2, as well Kluwer.of as the hourly urine output (aim is greater than 0.5 mL/kg/hr) signs, hemodynamics (CVP, SvO2, SVR, CO), urinary out- to assess evidence of improving perfusion (improved mental put, mental status, and physical assessment findings must be status, peripheral perfusion). reported accurately and in a timely fashion so that interven- Wolterstions can be instituted. When caring for a patient with sep- permission Glucocorticoids tic shock, the nurse collaborates with other members of the Glucocorticoids have been used in the treatment of septic health care team to identify the site and source of sepsis and shock with varying effect for decades. The general concept the specific organisms involved. Appropriate specimens for is that, since septic shock represents a significantCopyright physiologicexpress culture and sensitivity are often obtained by the nurse. stress, dysfunction of the hypothalamic–pituitary–adrenal© Elevated body temperature (hyperthermia) is common axis may be one factor that leads to increased mortality. in patients with sepsis and raises the patient’s metabolic Several studies have attempted to investigate the effect of rate and oxygen consumption. Fever is one of the body’s without administering steroids to septic patients. Drawbacks to natural mechanisms for fighting infections. Therefore, steroid administration include increased infection rate and elevated temperatures may not be treated unless they increased risk of superinfections, worsening glycemic con- reach dangerous levels (greater than 40°C [104°F]) or trol, and impaired wound healing. High-dose corticosteroids unless the patient is uncomfortable. Efforts may be made do not improve outcomes in the full spectrum of patients to reduce the temperature by administering acetamin- with sepsis or ARDS, andreproduction the evidence supporting the use of ophen or applying a hypothermia blanket. During these therapies, the nurse monitors the patient closely for shiv- low-dose corticosteroidsor in septic shock remains controver- sial (Russell, 2016, p. 690). If the patient has not responded ering, which increases oxygen consumption. Efforts to to vasopressor support,Use corticosteroids may be considered. increase comfort are important if the patient experiences fever, chills, or shivering. The nurse administers prescribed IV fluids and medi- Nutritional Therapy and Glycemic Control cations, including antibiotic agents and vasoactive medi- Aggressive nutritional supplementation is critical in the man- cations, to restore vascular volume. Because of decreased agement of patients with septic shock because malnutrition perfusion to the kidneys and liver, serum concentrations of further impairs the patient’s compensatory mechanisms. antibiotic agents that are normally cleared by these organs Nutritional supplementation should be initiated as soon as may increase and produce toxic effects. Therefore, the nurse possible. Enteral feeding, rather than parental nutrition, is monitors blood levels (antibiotic agent, peak and trough lev- associated with improved outcomes, although reasons­ for els of antibiotics (if available), BUN, creatinine, white blood this remain unclear. Evidence is particularly strong for enteral cell count, hemoglobin, hematocrit, platelet le­ vels, coagu-

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lation studies) and reports changes to the provider. Daily warm skin rather than the cool, moist skin seen in hypo- weights and close monitoring of serum prealbumin levels volemic shock. Another characteristic is hypotension with help determine the patient’s protein requirements. Addition- , rather than the tachycardia that characterizes ally, the nurse expects that deep vein thrombosis (DVT) and other forms of shock. prophylaxis will be instituted. Medical Management Neurogenic Shock Treatment of neurogenic shock involves IV fluid or plasma Pathophysiology expanders, vasopressors, and restoring sympathetic tone, either through the stabilization of a spinal cord injury or, in In neurogenic shock, vasodilation occurs as a result of a loss the instance of spinal anesthesia, by positioning the patient of balance between parasympathetic and sympathetic stim- properly. Specific treatment depends on cause of the shock. ulation. Sympathetic stimulation causes vascular smooth Further discussion of management of patients with a spi- muscle to constrict, and parasympathetic stimulation causes nal cord injury is presented in Chapter 45. If hypoglycemia the vascular smooth muscle to relax or dilate. The patient (insulin shock) is the cause, glucose is rapidly administered. experiences a predominant parasympathetic stimulation that Hypoglycemia and the insulin reaction are described further causes vasodilation lasting for an extended period because in Chapter 30. Current guidelines recommend maintaining of acute interruption of sympathetic function. It is important an MAP of 85 to 90 mm Hg for 1 prohibited.week post injury to pro- to understand that the blood volume is adequate, but because mote spinal cord perfusion (Hickey,is 2014, p. 400). the vasculature is dilated, the blood volume is displaced, pro- ducing a hypotensive (low BP) state (see Box 54-1, p. 1509). Nursing Management Thus, this is a situation where blood volume is stable, but the drastic dilatation of the vasculature causes a relative hypo- In suspected spinal publishercord injury, neurogenic shock may be volemia. The overriding parasympathetic stimulation that prevented by carefully immobilizing the patient to prevent occurs with neurogenic shock causes a severe decrease in further damagethe to the spinal cord. The nurse is aware that the patient’s SVR and sometimes bradycardia. Inadequate orthostaticKluwer. hypotensionof caused by loss of vasomotor tone BP results in the insufficient perfusion of tissues and cells below the level of the spinal cord lesion can occur with posi- that is common to all shock states. tion changes. Even slightly raising the head of the bed for a new tetraplegic patient can result in a drastic hypotension Wolters Nursing Alert (Hickey, 2014). The nurse understands that the preganglionic permissionNursing interventions are directed toward supporting car- axons of the SNS have origins in the diovascular and neurologic function until the usually tran- thoracolumbar region of the spinal cord. Thus, patients sient episode of neurogenic shock resolves. Apply sequential with spinal cord injuries in the cervical or upperCopyright express compression devices since pooled blood increases the risk for thoracic spinal cord are at risk for neurogenic© shock. thrombus formation. The nurse must check the patient daily Without the tonic sympathetic input to the systemic for any lower extremity pain, redness, tenderness, unilateral vasculature, the vagal response of bradycardia and edema, and warmth of the calves. If the patient complains without decreased SVR are unopposed and culminate in of pain, and objective assessment of the calf is suspicious, hypotension. Prompt recognition and treatment is the patient should be evaluated for DVT. Administration of essential to avoid potential organ damage. heparin or low–molecular-weight heparin (Lovenox) may prevent thrombus formation. Passive range of motion of the Neurogenic shock can be caused by spinal cord injury immobile extremities also helps promote circulation. (commonly above the levelreproduction of T6), spinal anesthesia, or ner- A patient who has experienced a spinal cord injury may vous system damage. orIt may also result from the depressant not report pain caused by internal injuries. Therefore, in the action of medications or from lack of glucose (e.g., insu- immediate postinjury period, the nurse must monitor the lin reaction or shock).Use Neurogenic shock may have a pro- patient closely for signs of internal bleeding that could lead longed course (spinal cord injury) or a short one (syncope or to hypovolemic shock. In hemorrhagic shock, the nurse is fainting). Normally, during states of stress, the sympathetic aware that tachycardia will be present versus bradycardia stimulation causes the BP and heart rate to increase. In neu- with neurogenic shock. rogenic shock, the sympathetic system is not able to respond to body stressors. Anaphylactic Shock Anaphylactic shock occurs rapidly and is life-threaten- Clinical Manifestations and Assessment ing. Annual mortality rates of 1,500 to 2,000 deaths in the The clinical characteristics of neurogenic shock are signs United States per year are attributed to systemic anaphylaxis of parasympathetic stimulation. It is characterized by dry, (Schwartz, 2016). Medications (e.g., antibiotics, NSAIDs,

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contrast media, and blood products) are triggers in 55% of to the heart, and subsequent hypotension; activation of cases, while food (26%) and insect bites (19%) are other fre- multiple inflammatory pathways causes fluid extravasa- quent causes; combined they are the most common causes of tion, seen as angioedema, tissue edema, and hypovolemia; anaphylaxis (Brown & Turner, 2017; Ferri, 2016). Approx- whereas the smooth muscle contraction is associated with imately 6% of children and 3% to 4% of adults have food bronchospasm and abdominal and pelvic cramps. Thus the allergy (Brown & Turner, 2017). nurse observes for generalized hives, pruritus or flushing, Because anaphylactic shock occurs in patients already angioedema, swelling of the tongue and/or uvula, dyspnea, exposed to an antigen and who have developed antibodies wheezing, stridor, hypoxemia, and reduced blood pres- to it, it can sometimes be prevented. Patients with known sure. GI symptoms, including nausea, vomiting, abdominal allergies should understand the consequences of subsequent cramps, and diarrhea, may precede the more generalized exposure to the antigen and should wear medical identifi- clinical manifestations described previously after ingestion cation that lists their sensitivities. This could prevent inad- of an antigen (Haupt & Grandhi, 2017, p. 437). Serum mast vertent administration of a medication that would lead to cell tryptase (MCT) is the only widely available assay used anaphylactic shock. In addition, patients and families need to confirm the diagnosis of anaphylaxis (Brown & Turner, instruction about emergency use of medications for treat- 2017, p. 354). ment of anaphylaxis. Medical Management prohibited. Nursing Alert is Latex allergies are a risk for health care Treatment of anaphylactic shock requires removing the workers and patients who have multiple causative antigen (e.g., discontinuing an antibiotic agent) mucosal exposures to latex. Nurses should use and administering medications that restore vascular tone. nonlatex gloves when possible, and patients at risk In addition, the health care team will need to provide emer- publisher (patients with spina bifida, spinal cord injuries, and gency airway support, position the patient in supine (see congenital abnormalities of the genitourinary tract) Alert below), administerthe oxygen, provide ventilation support should be catheterized when needed with nonlatex (endotrachealKluwer.of intubation or tracheotomy may be necessary equipment. to establish an airway), perform external chest compressions if cardiac arrest occurs, and prepare for early administration Pathophysiology of epinephrine. Epinephrine is usually given intramuscularly Woltersin the thigh in a dose of 0.01 mg/kg with a usual dose of 0.2 Anaphylactic shock is caused by a severe allergic reaction permissionto 0.5 mg for adults (maximum dose of 0.6 mg), which can when patients who have already produced antibodies to a be repeated every 5 to 30 minutes if the response is inade- foreign substance (antigen) develop a systemic antigen– quate. Epinephrine is given for its vasoconstrictive action as antibody reaction. This reaction provokes mast cells and Copyright well its effect of reducing bronchospasm (Brown & Turner, basophils to release potent vasoactive substances, expresssuch as © 2017). When epinephrine is given early (before the onset histamine or bradykinin, causing widespread vasodilation, of shock), systemic absorption of IM epinephrine is rapid, capillary permeability, and potentially catastrophic vascular with a response seen in minutes. IV epinephrine carries more collapse. Mast cells in any organ system may be involved, without risks, and incorrect dosing has been associated with serious depending on the distribution of the instigating stimulus; in adverse events (Brown & Turner, 2017). However, in patients general the principal targets include the cardiovascular, cuta- with severe anaphylaxis, the nurse considers that decreased neous, respiratory, and GI systems (where mast cells are most perfusion to the muscle may result in slow absorption of epi- abundant) (Schwartz, 2016, p. 1698). An equally important nephrine into the circulation; therefore, IV epinephrine may feature of anaphylactic shock is the onset of severe broncho- be necessary. Diphenhydramine (Benadryl), given intramus- spasm, which causes airwayreproduction compromise (stridor, wheezing, cularly or intravenously, may be administered to reverse the shortness of breath) andor urticaria. A delayed recurrence of urticaria and pruritus but is not likely to reduce the hypo- the reaction, without re-exposure to the allergen, can some- tension of tissue edema (Schwartz, 2016). Nebulized med- times occur. ThisUse has been termed a biphasic reaction and ications, such as albuterol (Proventil), may also be given to most commonly occurs 8 to 10 hours after the first symp- reverse histamine-induced bronchospasm. Glucocorticoids toms; therefore, patients with severe reactions are generally may be considered to prevent a rebound, biphasic reaction, observed for at least 10 hours. although it is unlikely to be beneficial acutely because of the slow onset of action (Ferri, 2016; Schwartz, 2016). IV lines Clinical Manifestations and Assessment are inserted to provide access for administering fluids and The clinical manifestations are related to the potent vaso- medications. Aggressive IV fluid resuscitation is expected active and smooth muscle contractile actions due to mast with hypotension. The patient’s cardiac status is monitored, cell release of vasoactive substances. For example, the and the electrocardiogram is assessed because anaphylaxis vasodilatation results in erythema, decreased venous return and treatments can be associated with arrh­ ythmias and

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­cardiac ischemia. Pulse oximetry is also expected to mon- tests. These include patients with a known allergy to iodine itor oxygenation status and response to treatment. Anaphy- or fish and those who have had previous allergic reactions laxis and specific chemical mediators are discussed further to contrast agents. This information must be conveyed to in Chapter 38. the staff at the diagnostic testing site, including radiology staff. The nurse anticipates that “pre-medication” regimens Nursing Alert are likely to be administered in patients with known contrast It is important to note that Fowler’s (upright) allergies. or semi-Fowler’s (semi recumbent) position has been associated with fatal anaphylaxis. Changing Nursing Alert the patient’s position to one that is upright reduces Pre-medication with steroids and Benadryl venous return to the heart and is proposed to may be recommended for patients who have exacerbate the pathophysiologic processes occurring had a previous reaction to contrast agent (gadolinium- in anaphylaxis; therefore, keeping a patient flat is based contrast or iodinated contrast) and a similar suggested to improve venous return to the heart, a key contrast will be administered (ACR, 2016). aspect of the initial response to anaphylaxis (Brown & Turner, 2017). The nurse must be knowledgeable about the clinical signs of anaphylaxis, must take immediateprohibited. action if signs Nursing Alert and symptoms occur, and must beis prepared to begin cardio- Nurses understand that epinephrine is typically pulmonary resuscitation if cardiopulmonary arrest occurs. In supplied as 1 mg/mL (1:1,000 dilution). Most addition to monitoring the patient’s response to treatment, authorities recommend that 0.3 to 0.5 mg of the 1:1,000 the nurse assists with intubation if needed, monitors the hemodynamic status, ensures IV access for administration of solution (0.3 to 0.5 mL) be given intramuscularly in the publisher anterolateral aspect of the thigh. medications, administers prescribed medications and fluids, and documents thetreatments and their effects. Nursing Management Kluwer.of Nursing Alert The nurse plays an important role in preventing anaphylac- If IV epinephrine is required, the nurse tic shock. The nurse must assess all patients for allergies carefully titrates the medication to prevent or previous reactions to antigens (e.g., medications, bloodWolters a hypertensive surge. Symptoms of tachycardia, products, foods, contrast agents, latex) and communicate permissionpallor, diaphoresis, and arrhythmias in a patient with the existence of these allergies or reactions to others. In normal or raised blood pressure are indicative of addition, the nurse assesses the patient’s understanding of epinephrine toxicity. The provider should be notified previous reactions and the steps taken by theCopyright patientexpress and and the infusion rate reduced (Brown & Turner, 2017). family to prevent further exposure to antigens.© When new Additionally, the nurse observes carefully the effect allergies are identified, the nurse advises the patient to wear of epinephrine in patients with cerebrovascular or or carry identification that names the specific allergen or coronary artery disease, hypertension, diabetes, antigen. without hyperthyroidism, cardiomyopathy, or narrow-angle When administering any new medication, the nurse glaucoma, in whom adverse events, such as MI, observes all patients for allergic reactions. This is espe- stroke, or pulmonary edema, can be precipitated cially important with IV medications. Allergy to penicillin (Schwartz, 2016, p. 1702). is one of the most common causes of anaphylactic shock. Patients who have a penicillinreproduction allergy may also develop an Community health and home care nurses who admin- allergy to similar medications. For example, they may react ister medications, including antibiotic agents, in the or to cefazolin sodium (Ancef) because it has a similar anti- patient’s home or other settings, must be prepared to microbial actionUse of attaching to the penicillin-binding pro- administer epinephrine subcutaneously or intramuscularly teins found on the walls of infectious organisms. Previous in the event of an anaphylactic reaction. Prescriptions adverse drug reactions increase the risk that the patient will for prefilled epinephrine syringe (EpiPen or EpiPen Jr.) develop an undesirable reaction to a new medication. If the should be given, and the patient and significant others are patient reports an allergy to a medication, the nurse must be instructed on how to administer the EpiPen and that the aware of the risks involved in the administration of similar patient needs to carry it on his or her person at all times. medications. After recovery from anaphylaxis, the patient and family In the hospital and outpatient diagnostic testing sites, the require an explanation of the event. Furthermore, the nurse nurse must identify patients who are at risk for anaphylactic provides instruction and counseling about avoiding future reactions to the contrast agents (radiopaque, dye-like sub- exposure to antigens and administering emergency medi- stances that may contain iodine) that are used for diagnostic cations to treat anaphylaxis.

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Obstructive Shock more ­sensitive. A chest tube or needle decompression is the primary procedure to relieve tension pneumothorax. Cardiac Obstructive shock is caused by a physical obstruction to tamponade is diagnosed similarly, with echocardiography blood flow, either in the heart or major blood vessels. This being the most effective. Pericardiocentesis is the treatment causes a decrease in CO and thus a decrease in tissue perfu- for and involves inserting a needle into sion. Common causes of obstructive shock include cardiac the pericardium to draw off fluid or blood. tamponade, tension pneumothorax, and pulmonary embolism The treatment of PE is usually aimed toward prevent- (PE). Obstructive shock is common in the setting of trauma. ing clot expansion, although if the patient is experiencing obstructive shock, then other treatment, such as thrombo- Pathophysiology lytic drugs or surgical embolectomy, may be considered. Depending on the severity of the PE, mechanical ventilation In the case of tension pneumothorax or hemothorax, air or and hemodynamic support may be needed to stabilize the blood has entered the pleural space and caused a restriction patient. PE is usually diagnosed using a CT angiogram, but in lung expansion. If enough air is trapped, then eventually other imaging and laboratory tests can be used as well. pressure builds up and compresses the vessels and myocar- dium. This compression reduces preload (volume of blood) and increases afterload, in addition to restricting the expan- Nursing Management sion of the myocardium during filling. Clinical presentation prohibited. Because patients with tension ispneumothorax and cardiac may include JVD, crepitus (with pneumothorax), dyspnea, tamponade who are experiencing obstructive shock will chest pain, tachycardia and tachypnea, tracheal shifting need an emergent procedure, nurses should focus on facil- away from the tension pneumothorax, and decreased breath itating that process. This includes collecting and setting sounds on the affected side. Tension pneumothorax is com- up equipment, communicating effectively with staff, and publisher mon in trauma but can also develop spontaneously or as a helping gain consent from the patient and/or family. Care- complication from a procedure such as central line place- ful monitoring theof the patient prior to, during, and after the ment. Patients who are mechanically ventilated are at higher procedureKluwer. isof essential. If a chest tube is placed, then a chest risk of developing a clinically significant pneumothorax due drainage system (e.g., Pleuravac) will need to be set up and to increased ventilatory pressures. connected to suction as ordered. The chest tube setup needs Cardiac tamponade results from excessive blood or fluid to be monitored to ensure that it is functioning correctly and inside the pericardium, the sac that surrounds the heart. ThisWolters also to record output. A postprocedure chest radiograph will can result from a traumatic or infectious cause with a resul- permissionbe ordered, and the results should be followed closely. tant restriction on the pumping ability of the heart. Signs and Nursing care of a patient with a PE that is causing symptoms of cardiac tamponade include narrowing pulse obstructive shock involves monitoring and initiating ven- pressure (difference between the systolic and diastolic pres- Copyright tilatory and hemodynamic support similar to what is done sure; normally 40 mm Hg), chest pain, distant or expressmuffled © for patients with other types of shock. A primary function , JVD, hypotension, and tachycardia. of the nurse in this situation is to facilitate diagnostic testing A PE is a clot that gets lodged in the pulmonary vasculature and imaging and then institute treatment in a timely manner. and causes ischemia to the capillary beds. Ifwithout large enough, the Patients with a PE large enough to cause obstructive shock embolism interferes significantly with pulmonary blood flow, have a very high mortality and often die within an hour of which causes blood to back up into the right side of the heart. presentation. As the clot increases the pressure in the pulmonary artery, Patients who experience obstructive shock are often quite the right heart must beat faster and harder to overcome the suddenly acutely ill. This affects the entire health care team pressure. Overall, CO is decreased as the patient goes into as decisions need to be made quickly, and the nurse should reproduction right-sided heart failure. Clots that have traveled from the work hard to maintain a calm environment. Since obstruc- or lower extremities cause most PEs. Signs and symptoms of PE tive shock usually has a sudden onset, families are quite include pleuritic chest pain, shortness of breath, tachycardia, Use often surprised when given news about massive PE or other and hypoxia (refer to Chapter 10 for more details). causes of obstructive shock. Having other support personnel in place, such as a social worker or a chaplain, to provide Medical Management support is advised. In the case of cardiac tamponade and tension pneumotho- rax, a procedure done by a qualified clinician should be performed immediately to relieve the obstruction. If the Multiple Organ Dysfunction patient is experiencing obstructive shock, then these pro- Syndrome cedures are done emergently at the bedside. A chest radio- graph is often used to diagnose a pneumothorax, although MODS is altered organ function in patients who are acutely computed tomography (CT) scans and even ultrasound are ill that requires medical intervention to support continued

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organ function. It is another phase in the progression of acronym stands for Sequential (Sepsis-related) shock states. The actual incidence of MODS is difficult to Organ Failure Assessment (SOFA) and includes

determine because it develops with acute illnesses that com- parameters such as the PaO2/FiO2 ratio (respiratory promise tissue perfusion. It is defined as severe organ dys- system), the platelet count (coagulation), bilirubin function of two or more organ systems lasting at least 24 to level (hepatic system), MAP (cardiovascular system), 48 hours in the setting of sepsis, trauma, burns, or severe (CNS system), and creatinine inflammatory conditions (Tiesi et al., 2016). It is important and urine output (renal system). A higher SOFA to note that the definition includes the number of dysfunc- score is associated with an increased probability of tional organs and duration. Mortality rates when two organ mortality (Singer et al., 2016). systems are involved are 40%; and persistent dysfunction (more than 72 hours) present in three organ systems can result in a mortality risk of 80%. Pathophysiology The inflammation, tissue injury, and other sequelae asso- Nursing Alert ciated with MODS are thought to be caused by an unreg- Clinicians may use the SOFA scale to ulated host response. MODS may result from any form of rapidly identify adult patients with organ shock because of inadequate tissue perfusion. As previously dysfunction and risk for poor outcomes. The described, in patients with shock, prohibited.all organ systems suffer is

Systemic Central Venous Pulmonary Cardiac Systemic Vascular Diagnosis Blood Pressure Heart Rate Pressure (CVP) Artery Pressure Output (CO) Resistance (SVR) publisher Cardiogenic: Myocardial the Infarction (MI), Cardiac Kluwer.of Tamponade, Pulmonary Emboli

Hypovolemic: Wolters Hemorrhage, permission Diarrhea, Burns, Dehydration

Copyrightexpress © Septic: Severe Infection without

Anaphylactic: Type 1 Hypersensitivity Reaction reproduction or

Use

Neurogenic: Brain Damage, Spinal Cord Injury

Figure 54-5 Types of shock. Shock results from (1) an inability of the heart to pump adequately (cardiogenic shock); (2) decreased effective blood volume as a consequence of severely reduced blood or plasma volume (hypovolemic shock); or (3) widespread vasodilation (septic; anaphylactic or neurogenic shock). Increased vascular permeability may complicate vasodilation by contributing to reduced effective blood volume. (Adapted from Lawrence, P., Bell, R., Dayton, M., & Hebert, J. (2012). Essentials of general surgery (5th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.)

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damage from a lack of adequate perfusion, which can result Medical Management in organ failure. Prevention remains the top priority in managing MODS. Elderly patients are at increased risk for MODS because of Clinical Manifestations and Assessment the lack of physiologic reserve associated with aging and the natural degenerative process, especially immune com- Various causes of MODS have been identified, including promise. Early detection and documentation of initial signs dead or injured tissue, infection, and perfusion deficits. of infection are essential in managing MODS in elderly However, it is not possible as yet to predict which patients patients. Subtle changes in mentation and a gradual rise in will develop MODS, partly because much of the organ dam- temperature are early warning signs. Other patients at risk age occurs at the cellular level and, therefore, cannot be for MODS are those with chronic illness, malnutrition, directly observed or measured. The most common types of immunosuppression, or surgical or traumatic wounds. organ dysfunction seen with MODS are acute kidney failure If preventive measures fail, treatment measures to reverse and ARDS. However, organ failure can affect the other body MODS are aimed at (1) controlling the initiating event, systems: (2) promoting adequate organ perfusion, and (3) providing • Hepatic: jaundice, elevated liver function tests (LFTs), nutritional support. decreased albumin and elevated PT • Hematologic: decreased platelets, elevated PT/APTT, Nursing Management prohibited. increased D-dimer is The general plan of nursing care for patients with MODS is • Central nervous system (CNS): altered level of con- the same as that for patients in septic shock. Primary nursing sciousness (LOC), confusion, psychosis interventions are aimed at early and aggressive hemodynamic • Respiratory: tachypnea, hypoxemia, PaO /FiO greater 2 2 support until primary organ insults are halted. Providing than 300 (see Chapter 10) publisher information and support to family members is a critical role • Cardiovascular: tachycardia, hypotension, altered CVP of the nurse. It isthe important that the health care team address and pulmonary artery pressure (PAP) readings end-of-lifeKluwer. decisionsof to ensure that supportive therapies are Advanced age, malnutrition, and coexisting diseases congruent with the patient’s wishes (see Chapter 3). appear to increase the risk of MODS in patients who are Refer to Figure 54-5 for a review of the various forms of acutely ill. shock. Wolters permission

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Critical Thinking Exercises without and his heart rate is 124. What type of shock is this patient most likely in? What led you to that conclusion? Name 1. You administer an antibiotic to a patient before he goes some interventions that would help this patient. to surgery. The patient’s chart states that he has no known drug allergies. After 15 minutes, the patient complains of 4. You are taking care of a patient in the ICU with a spinal anxiety, shortness of breath, and chest discomfort. He is cord injury. His BP has not been responsive to repeated flushed and visibly uncomfortable.reproduction What are your nursing fluid boluses. What type of shock is he mostly likely priorities in providing care to this patient? What clinical experiencing? Name some appropriate interventions. or signs and symptoms would you look for to determine if he is experiencing anaphylactic shock? What nursing inter- Use NCLEX-Style Review Questions ventions and medical treatments would you anticipate? 1. During a conversation about a patient, a new nurse states 2. An elderly woman is admitted to the medical floor for a to the charge nurse, “His BP is 92/50, so he can’t be in urinary tract infection. You notice that she has become shock.” Which response by the charge nurse indicates steadily more tachycardic and her urine output has that the new nurse does not completely understand the dropped to 15 cc for the last hour. How would you assess symptoms of shock? this patient for the possibility of sepsis? a. Patients can have a near-normal BP, yet still have 3. While working in the emergency department, you see a inadequate tissue perfusion. victim of a motor vehicle accident brought in by ambu- b. The cutoff for shock is a systolic pressure of 100 mm lance. His pelvis appears deformed, he is pale, ­diaphoretic, Hg.

LWBK1620-C54_p1507-1531.indd 1530 11/12/17 4:29 PM Chapter 54 Nursing Management: Shock and Multisystem Failure 1531

c. Shock is determined by mean arterial pressure. 4. In early goal-directed therapy for shock, the nurse knows d. Shock is determined by a heart rate of over 100. that which parameter is the highest priority when evalu- ating effectiveness of therapy? 2. A patient with a GI bleed arrives at the emergency a. Heart rate and BP department with the following vital signs: Temperature b. SvO and O saturation 37.4°C, HR 112, RR 26, BP 88/44. The nurse recognizes 2 2 c. Base deficit and hematocrit that this patient is most likely experiencing or at risk for d. SvO and CVP which type of shock? 2 a. Anaphylactic 5. A patient develops low BP and tachycardia and is b. Neurogenic very agitated. The nurse remembers that a central line c. Hypovolemic was placed 3 hours ago. The patient’s lung sounds are d. Septic decreased on one side, and tracheal deviation is present. The nurse realizes that this patient is most likely experi- 3. A patient comes in to the urgent care center complain- encing which type of shock? ing of shortness of breath and dizziness after being stung a. Hypovolemic by a bee. The patient loses consciousness in the waiting b. Obstructive room. The receptionist has called 911. The nurse antici- c. Anaphylactic pates that which medication will be considered first? d. Neurogenic prohibited. a. Diphenhydramine (Benadryl) is b. Phenytoin (Dilantin) c. Epinephrine IV d. Epinephrine IM References and publisherSelected Readings Try these additional resources, available at the References and selected readings http://thepoint.lww.com/Honan2e, to enhance associatedKluwer. ofwith this chapter can be found on the website your learning and understanding of this chapter: that accompanies the book. Visit http://thepoint. • NCLEX-Style Student Review Questions lww.com/Honan2e to access the references and other • Journal Articles additional resources associated with this chapter. Wolters permission

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