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Other Acute Problems 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: Shock 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 heart 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 LWBK1620-C54_p1507-1531.indd 1508 11/12/17 10:36 PM CHAPTER 54 NURSING MANAGEMENT: SHOCK AND MULTISYSTEM FAILURE 1509 BOX 54-1 strategy for the management of hyperglycemia (also Classifications of Shock called stress hyperglycemia) in patients who are • Hypovolemic shock occurs when there is a decrease in critically ill with and without diabetes is unknown; the intravascular volume. Hypovolemia 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, • Cardiogenic shock 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. • Distributive shock 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 Septic shock is technically considered a “distributive” type edema results from the increased prohibited.intracellular sodium and of shock. Sepsis 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 signs and symptoms 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) LWBK1620-C54_p1507-1531.indd 1509 11/12/17 4:29 PM 1510 UNIT 15 OTHER ACUTE PROBLEMS 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
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