Nursing Care of Clients with Multisystem Problems PDF

# NURSING CARE OF CLIENTS WITH MULTISYSTEM PROBLEMS ## Introduction Shock is a life-threatening condition with a variety of underlying causes. It is characterized by inadequate perfusion that, if untreated, results in cell death. The progression of shock is neither linear nor predictable, and shoc...

# NURSING CARE OF CLIENTS WITH MULTISYSTEM PROBLEMS ## Introduction Shock is a life-threatening condition with a variety of underlying causes. It is characterized by inadequate perfusion that, if untreated, results in cell death. The progression of shock is neither linear nor predictable, and shock states, especially septic shock, comprise a current area of aggressive clinical research. Nurses caring for patients with shock and for those at risk for shock must understand the underlying mechanisms of shock and recognize its subtle as well as more obvious signs. Rapid assessment with early recognition and response to shock states are essential to the patient's recovery. ## Learning Outcome On completion of this module, the learners will be able to: 1. Compare and contrast different types of Shock. 2. Formulate nursing care plans to patients with Systemic Inflammatory Response Syndrome 3. Make a detailed pathophysiology of Multiple Organ Dysfunction Syndrome through a diagram ## Learning Content 1. Shock 2. Systemic Inflammatory Response Syndrome 3. Multi-organ Dysfunction Syndrome ## Shock Shock is a life-threatening condition that results from inadequate tissue perfusion. Many conditions may cause shock; irrespective of the cause, tissue hypoperfusion prevents adequate oxygen delivery to cells, leading to cell dysfunction and death. The progression of shock is neither linear nor predictable, and shock states, especially septic shock, comprise an area of aggressive clinical research. Nurses caring for patients with shock and those at risk for shock must understand the underlying mechanisms of the various shock states (i.e., hypovolemic, cardiogenic, obstructive, neurogenic, anaphylactic, and septic) and recognize the subtle as well as more obvious signs of each of these states. Rapid assessment with early recognition and response to shock states is essential to the patient's recovery. ## Overview Shock can best be defined as a clinical syndrome that results from inadequate tissue perfusion, creating an imbalance between the delivery of oxygen and nutrients needed to support cellular function (Maier, 2015; Moore, Dyson, Singer, et al., 2015). Adequate blood flow to the tissues and cells requires an effective cardiac pump, adequate vasculature or circulatory system, and sufficient blood volume. If one of these components is impaired, perfusion to the tissues is threatened or compromised. Without treatment, inadequate blood flow to the cells results in poor delivery of oxygen and nutrients, cellular hypoxia, and cell death that progresses to organ dysfunction and eventually death. Shock affects all body systems. It may develop rapidly or slowly, depending on the underlying cause. During shock, the body struggles to survive, calling on all its homeostatic mechanisms to restore blood flow. Any insult to the body can create a cascade of events resulting in poor tissue perfusion. Therefore, any patient with any disease state may be at risk for developing shock. The primary underlying pathophysiologic process and underlying disorder are used to classify the shock state (e.g., hypovolemic shock, cardiogenic shock, obstructive shock, distributive shock [i.e., neurogenic, anaphylactic, septic]). Regardless of the initial cause of shock, certain physiologic responses are common to all types of shock. These physiologic responses include hypoperfusion of tissues, hypermetabolism, and activation of the inflammatory response. The body responds to shock states by activating the sympathetic nervous system and mounting a hypermetabolic and inflammatory response. Failure of compensatory mechanisms to effectively restore physiologic balance is the final pathway of all shock states and results in end-organ dysfunction and death (Dellinger, Levy, Rhodes, et al., 2013; Maier, 2015; Wacker & Winters, 2014). ## SHOCK Signs and Symptoms | CHORD | ITEM| |:--|:--| | Cold, clammy skin | Hypotension | | Oliguria | Rapid, shallow breathing | | Drowsiness, confusion | Irritability | | Tachycardia | Elevated or reduced central venous pressure | | Multi-organ damage | | ## Nursing Management Nursing care of patients with shock requires ongoing systematic assessment. Many of the interventions required in caring for patients with shock call for close collaboration with other members of the health care team and rapid implementation of prescribed therapies. Nurses are in key positions to identify early signs of shock and anticipate rapid therapy. ## Physiology/Pathophysiology | Initial insult leading to shock state | |:--:| | Tissue perfusion and Oxygenation | Activation of homeostatic response | | | | |:--|:--:| | ↑ Sympathetic response (↑HR, ↑ BP, ↑ cardiac contractility), which leads to↑ cardiac output) | ↑ Respiratory rate to ↑ oxygen saturation and delivery | | ↑Renin-angiotensin activation, which leads to ↑ reabsorption of sodium and water, which leads to ↑preload and urine output | ↑ Catecholamines and cortisol to provide glucose for metabolism | | | Restoration of tissue perfusion and oxygenation | ## Stages of Shock Shock progresses along a continuum and can be identified as early or late, depending on the signs and symptoms and the overall severity of organ dysfunction. A convenient way to understand the physiologic responses and subsequent clinical signs and symptoms of shock is to divide the continuum into separate stages. ### Compensatory Stage In the compensatory stage of shock, the BP remains within normal limits. Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to maintaining adequate cardiac output. This results from stimulation of the sympathetic nervous system and subsequent release of catecholamines (e.g., epinephrine, norepinephrine). Patients display the often-described “fight-or-flight” response. The body shunts blood from organs such as the skin, kidneys, and gastrointestinal (GI) tract to the brain, heart, and lungs to ensure adequate blood supply to these vital organs. As a result, the skin may be cool and pale, bowel sounds are hypoactive, and urine output decreases in response to the release of aldosterone and ADH. ### Clinical Manifestations The result of inadequate perfusion is anaerobic metabolism and a buildup of lactic acid, producing metabolic acidosis. The respiratory rate increases in response to the need to increase oxygen to the cells and in compensation for metabolic acidosis. This rapid respiratory rate facilitates removal of excess CO2 but raises the blood pH and often causes a compensatory respiratory alkalosis. The patient may experience: - A change in affect, feel anxious, or be confused. If treatment begins in this stage of shock, the prognosis for the patient is better than in later stages. ### Medical Management Medical treatment is directed toward identifying the cause of the shock, correcting the underlying disorder so that shock does not progress, and supporting those physiologic processes that thus far have responded successfully to the threat. Because compensation cannot be maintained indefinitely, measures such as fluid replacement and medication therapy must be initiated to maintain an adequate BP and reestablish and maintain adequate tissue perfusion (Dellinger et al., 2013; Green, 2015). ## Nursing Management - Early intervention along the continuum of shock is the key to improving the patient's prognosis (Dellinger, 2015; Lee, 2015). - The nurse must systematically assess the patient at risk for shock, recognizing subtle clinical signs of the compensatory stage before the patient's BP drops. - Early interventions include identifying the cause of shock, administering intravenous (IV) fluids and oxygen, and obtaining necessary laboratory tests to rule out and treat metabolic imbalances or infection. Special considerations related to recognizing early signs of shock in the older adult patient. - Monitoring Tissue Perfusion -In assessing tissue perfusion, the nurse observes for subtle changes in level of consciousness, vital signs (including pulse pressure), urinary output, skin, respiratory rate, and laboratory values (e.g., base deficit, lactic acid levels). In the compensatory stage of shock, serum sodium and blood glucose levels are elevated in response to the release of aldosterone and catecholamines. If infection is suspected, blood cultures should be obtained prior to administration of prescribed antibiotics; both of these interventions should be given priority in the care of the patient (Dellinger, 2015; Green, 2015). - The nurse should monitor the patient's hemodynamic status and promptly report deviations to the primary provider, assist in identifying and treating the underlying disorder by continuous in-depth assessment of the patient, administer prescribed fluids and medications, and promote patient safety. Vital signs are key indicators of hemodynamic status, and BP is an indirect measure of tissue hypoxia. The nurse should report a systolic BP lower than 90 mm Hg or a drop in systolic BP of 40 mm Hg from baseline or a MAP less than 65 mm Hg (Cestero & Dent, 2015; Dellinger et al., 2013; Green, 2015). If the patient is concurrently diagnosed with an infection or if an infection is suspected, the nurse should promptly notify the primary provider if the patient exhibits any two of the three following signs (Antonelli, DeBacker, Dorman, et al., 2016) - Respiratory rate ≥22/min - Altered mentation - Systolic BP ≤100 mm Hg - Pulse pressure correlates well with stroke volume. Pulse pressure is calculated by subtracting the diastolic measurement from the systolic measurement; the difference is the pulse pressure. Normally, the pulse pressure is 30 to 40 mm Hg. Narrowing or decreased pulse pressure is an earlier indicator of shock than a drop in systolic BP (deWitt, Joshi, Meislin, et al., 2014; See, Mukhopadhyay, Lau, et al., 2015). Decreased or narrowing pulse pressure, an early indication of decreased stroke volume, is illustrated in the following example: - Systolic BP-Diastolic BP=Pulse pressure - Normal pulse pressure:120 mmHg-80mmHg= 40 mmHg - Narrowing of pulse pressure: 90 mmHg-70 mmHg= 20 mmHg - Elevation of the diastolic BP with release of catecholamines and attempts to increase venous return through vasoconstriction is an early compensatory mechanism in response to decreased stroke volume, BP, and overall cardiac output. - Continuous central venous oximetry (Scv–O2) monitoring may be used to evaluate mixed venous blood oxygen saturation and severity of tissue hypoperfusion states. A central catheter is introduced into the superior vena cava (SVC), and a sensor on the catheter measures the oxygen saturation of the blood in the SVC as blood returns to the heart and pulmonary system for reoxygenation. A normal Scv–O2 value is 70% (Cestero & Dent, 2015; Dellinger et al., 2013). Body tissues use approximately 25% of the oxygen delivered to them during normal metabolism. During stressful events, such as shock, more oxygen is consumed and the Scv-O2 saturation is lower, indicating that the tissues are consuming more oxygen. - Interventions focus on decreasing tissue oxygen requirements and increasing perfusion to deliver more oxygen to the tissues. For instance, sedating agents may be given to lower metabolic demands, or the patient’s pain may be treated with IV opioid agents to decrease metabolic demands for oxygen. Supplemental oxygen and mechanical ventilation may be required to increase the delivery of oxygen in the blood. Administration of IV fluids and medications supports BP and cardiac output, and the transfusion of packed red blood cells enhances oxygen transport. Monitoring tissue oxygen consumption with Scv-O2 is an invasive measure to more accurately assess tissue oxygenation in the compensatory stage of shock before changes in vital signs detect altered tissue perfusion (Dellinger et al., 2013). - Reducing Anxiety-Patients and their families often become anxious and apprehensive when they face a major threat to health and well-being and are the focus of attention of many health care providers. Providing brief explanations about the diagnostic and treatment procedures, supporting the patient during these procedures, and providing information about their outcomes are usually effective in reducing stress and anxiety and thus promoting the patient’s physical and mental well-being. Speaking in a calm, reassuring voice and using gentle touch also help ease the patient’s concerns. These actions may provide comfort for critically ill, frightened patients (Perrin & Kazanowski, 2015). - Promoting Safety-The nurse must be vigilant for potential threats to the patient’s safety, because a high anxiety level and altered mental status impair judgment. In this stage of shock, patients who were previously cooperative and followed instructions may now disrupt IV lines and catheters and complicate their condition. Close monitoring, frequent reorientation, hourly rounding, and implementing interventions to prevent falls (e.g., bed alarms) are essential. ### Progressive Stage In the second stage of shock, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits. Patients are clinically hypotensive; this is defined as a systolic BP of less than 90 mm Hg or a decrease in systolic BP of 40 mm Hg from baseline. The patient shows signs of declining mental status (Dellinger et al., 2013). ### Pathophysiology Although all organ systems suffer from hypoperfusion at this stage, several events perpetuate the shock syndrome. First, the overworked heart becomes dysfunctional, the body’s inability to meet increased oxygen requirements produces ischemia, and biochemical mediators cause myocardial depression (Dellinger et al., 2013; Moore et al., 2015). This leads to failure of the heart, even if the underlying cause of the shock is not of cardiac origin. Second, the autoregulatory function of the microcirculation fails in response to the numerous biochemical mediators released by the cells, resulting in increased capillary permeability, with areas of arteriolar and venous constriction further compromising cellular perfusion (Moore et al., 2015). At this stage, the prognosis worsens. The relaxation of precapillary sphincters causes fluid to leak from the capillaries, creating interstitial edema and decreased return to the heart. In addition, the inflammatory response to injury is activated, and proinflammatory and anti-inflammatory mediators are released, which activate the coagulation system in an effort to reestablish homeostasis (Levi & van der Poll, 2015). The body mobilizes energy stores and increases oxygen consumption to meet the increased metabolic needs of the underperfused tissues and cells. Anaerobic metabolism ensues, resulting in a buildup of lactic acid and disruption of normal cell function (Green, 2015). ### Clinical Manifestations Chances of survival depend on the patient’s general health before the shock state as well as the amount of time it takes to restore tissue perfusion. As shock progresses, organ systems decompensate. - **Respiratory Effects** - The lungs, which become compromised early in shock, are affected at this stage. Subsequent decompensation of the lungs increases the likelihood that mechanical ventilation will be needed. Respirations are rapid and shallow. Crackles are heard over the lung fields. Decreased pulmonary blood flow causes arterial oxygen levels to decrease and CO2 levels to increase. Hypoxemia and biochemical mediators cause an intense inflammatory response and pulmonary vasoconstriction, perpetuating pulmonary capillary hypoperfusion and hypoxemia. The hypoperfused alveoli stop producing surfactant and subsequently collapse. Pulmonary capillaries begin to leak, causing pulmonary edema, diffusion abnormalities (shunting), and additional alveolar collapse. This condition is called acute lung injury (ALI); as ALI continues, interstitial inflammation and fibrosis are common consequences, leading to acute respiratory distress syndrome (ARDS) (Silva, Pelosi, & Rocco, 2014). - **Cardiovascular Effects** - A lack of adequate blood supply leads to dysrhythmias and ischemia. The heart rate is rapid, sometimes exceeding 150 bpm. The patient may complain of chest pain and even suffer a myocardial infarction (MI). Levels of cardiac biomarkers (e.g., cardiac troponin I [cTn-I]) increase. In addition, myocardial depression and ventricular dilation may further impair the heart’s ability to pump enough blood to the tissues to meet increasing oxygen requirements. - **Neurologic Effects** - As blood flow to the brain becomes impaired, mental status deteriorates. Changes in mental status occur with decreased cerebral perfusion and hypoxia. Initially, the patient may exhibit subtle changes in behavior, become agitated, confused, or demonstrate signs of delirium. Subsequently, lethargy increases, and the patient begins to lose consciousness. - **Renal Effects** - When the MAP falls below 65 mm Hg (Zarbock, Gomez, & Kellum, 2014), the glomerular filtration rate of the kidneys cannot be maintained, and drastic changes in renal function occur. Acute kidney injury (AKI) is characterized by an increase in blood urea nitrogen (BUN) and serum creatinine levels, fluid and electrolyte shifts, acid-base imbalances, and a loss of the renal-hormonal regulation of BP. Urinary output usually decreases to less than 0.5 mL/kg per hour (or less than 30 mL per hour) but may vary depending on the phase of AKI. - **Hepatic Effects** - Decreased blood flow to the liver impairs the ability of liver cells to perform metabolic and phagocytic functions. Consequently, the patient is less able to metabolize medications and metabolic waste products, such as ammonia and lactic acid. Metabolic activities of the liver, including gluconeogenesis and glycogenolysis, are impaired. The patient becomes more susceptible to infection as the liver fails to filter bacteria from the blood. Liver enzymes (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase,) and bilirubin levels are elevated, and the patient develops jaundice. - **Gastrointestinal Effects** - GI ischemia can cause stress ulcers in the stomach, putting the patient at risk for GI bleeding. In the small intestine, the mucosa can become necrotic and slough off, causing bloody diarrhea. Beyond the local effects of impaired perfusion, Gl ischemia leads to bacterial translocation and organ dysfunction, in which bacterial toxins enter the bloodstream through the lymphatic system. In addition to causing infection, bacterial toxins can cause cardiac depression, vasodilation, increased capillary permeability, and an intense inflammatory response with activation of additional biochemical mediators. The net result is interference with healthy cellular functioning and the ability to metabolize nutrients (Dellinger et al., 2013). - **Hematologic Effects** - The combination of hypotension, sluggish blood flow, metabolic acidosis, coagulation system imbalance, and generalized hypoxemia can interfere with normal hemostatic mechanisms. In shock states, the inflammatory cytokines activate the clotting cascade, causing deposition of microthrombi in multiple areas of the body and consumption of clotting factors. The alterations of the hematologic system, including imbalance of the clotting cascade, are linked to the overactivation of the inflammatory response of injury (Levi & van der Poll, 2015; Moore et al., 2015). - Disseminated intravascular coagulation (DIC) may occur either as a cause or as a complication of shock. In this condition, widespread clotting and bleeding occur simultaneously. Bruises (ecchymoses) and bleeding (petechiae) may appear in the skin. Coagulation times (e.g., prothrombin time, activated partial thromboplastin time) are prolonged. Clotting factors and platelets are consumed and require replacement therapy to achieve hemostasis. ### Medical Management Specific medical management in the progressive stage of shock depends on the type of shock, its underlying cause, and the degree of decompensation in the organ systems. Medical management specific to each type of shock is discussed later in this chapter. Although medical management in the progressive stage differs by type of shock, some medical interventions are common to all types. These include the use of appropriate IV fluids and medications to restore tissue perfusion by the following methods: - Supporting the respiratory system - Optimizing intravascular volume - Supporting the pumping action of the heart - Improving the competence of the vascular system Other aspects of management may include early enteral nutritional support, targeted hyperglycemic control with IV insulin and use of antacids, histamine-2 (H2) blockers, or antipeptic medications to reduce the risk of Gl ulceration and bleeding. Tight glycemic control (serum glucose of 80 to 100 mg/dL) is no longer recommended, as hypoglycemic events associated with regulating tight control in critically ill patients have been found to result in adverse patient outcomes (Griesdale, DeSouza, VanDam, et al., 2009; Marik & Bellomo, 2013). Current evidence suggests that maintaining serum glucose less than 180 mg/dL with insulin therapy and close monitoring is indicated in the management of the critically ill patient (Dellinger et al., 2013). ## Nursing Management Nursing care of patients in the progressive stage of shock requires expertise in assessing and understanding shock and the significance of changes in assessment data. Early interventions are essential to the survival of patients; therefore, suspecting that a patient may be in shock and reporting subtle changes in assessment are imperative. - Patients in the progressive stage of shock are cared for in the intensive care setting to facilitate close monitoring (hemodynamic monitoring, electrocardiographic [ECG] monitoring, arterial blood gases, serum electrolyte levels, physical and mental status changes); rapid and frequent administration of various prescribed medications and fluids; and possibly interventions with supportive technologies, such as mechanical ventilation, dialysis (e.g., continuous renal replacement therapy), and intra-aortic balloon pump. - Working closely with other members of the health care team, the nurse carefully documents treatments, medications, and fluids that are given; recording the time; dosage or volume; and patient response. In addition, the nurse coordinates both the scheduling of diagnostic procedures that may be carried out at the bedside and the flow of health care personnel involved in the care of patients. The nurse also provides essential support through ongoing communication with the patient and the family. ## Preventing Complications - The nurse helps reduce the risk of related complications and monitors the patient for early signs of complications. - Monitoring includes evaluating blood levels of medications, observing invasive vascular lines for signs of infection, and checking neurovascular status if arterial lines are inserted, especially in the lower extremities. - Simultaneously, the nurse promotes the patient’s safety and comfort by ensuring that all procedures, including invasive procedures and arterial and venous punctures, are carried out using correct aseptic techniques and that venous and arterial puncture and infusion sites are maintained with the goal of preventing infection. - Nursing interventions that reduce the incidence of ventilator-associated pneumonia (VAP) must also be implemented. These include frequent oral care, aseptic suction technique, turning, elevating the head of the bed at least 30 degrees to prevent aspiration, and implementing daily interruption of sedation as prescribed to evaluate patient readiness for extubation (Dellinger et al., 2013; Hillier, Wilson, Chamberlain, et al., 2013; Makic, Rauen, Jones, et al., 2015). - The nurse must also be vigilant in assessing for acute delirium, characterized by an acute change in mental status, inattention, disorganized thinking, and altered level of consciousness. Delirium is potentially preventable (Barr, Fraser, Puntillo, et al., 2013). Critically ill patients with delirium have longer mechanical ventilation support needs, experience higher functional decline, and have higher rates of morbidity and mortality than those without delirium. ## Promoting Rest and Comfort - Efforts are made to minimize the cardiac workload by reducing the patient’s physical activity and treating pain and anxiety. Because promoting patient rest and comfort is a priority, the nurse performs essential nursing activities in blocks of time, allowing the patient to have periods of uninterrupted rest, which may prevent acute delirium, as noted previously (Barr et al., 2013; Makic, Rauen, Watson, et al., 2014). - To conserve the patient’s energy, the nurse should protect the patient from temperature extremes (e.g., excessive warmth or cold, shivering), which can increase the metabolic rate and oxygen consumption and thus the cardiac workload. ## Supporting Family Members - Because patients in shock receive intense attention by the health care team, families may be overwhelmed and frightened. Family members may be reluctant to ask questions or seek information for fear that they will be in the way or will interfere with the attention given to the patient. - The nurse should make sure that the family is comfortably situated and kept informed about the patient’s status. Often, families need encouragement from the health care team to get some rest; family members are more likely to take this advice if they feel that the patient is being well cared for and that they will be notified of any significant changes in the patient’s status. - A visit from the hospital chaplain may be comforting and provides some attention to the family while the nurse concentrates on the patient. Ensuring patient and family-centered care is central to the delivery of high-quality care. This helps meet the emotional well-being as well as the physiologic needs of the patient and the family (Giles & Hall, 2013). ## Irreversible Stage (Refractory Stage) - represents the point along the shock continuum at which organ damage is so severe that the patient does not respond to treatment and cannot survive. Despite treatment, BP remains low. Renal and liver dysfunction, compounded by the release of biochemical mediators, creates an acute metabolic acidosis. Anaerobic metabolism contributes to a worsening lactic acidosis. Reserves of ATP are almost totally depleted, and mechanisms for storing new supplies of energy have been destroyed. Respiratory system dysfunction prevents adequate oxygenation and ventilation despite mechanical ventilatory support, and the cardiovascular system is ineffective in maintaining an adequate MAP for tissue perfusion. Multiple organ dysfunction progressing to complete organ failure has occurred, and death is imminent. ## Medical Management Medical management during the irreversible stage of shock is similar to interventions and treatments used in the progressive stage. Although the patient may have progressed to the irreversible stage, the judgment that the shock is irreversible can be made only retrospectively on the basis of the patient’s failure to respond to treatment. Strategies that may be experimental (e.g., investigational medications, such as immunomodulation therapy) may be tried to reduce or reverse the severity of shock. ## Nursing Management As in the progressive stage of schock, - The nurse focuses on carrying out prescribed treatments, monitoring the patient, preventing complications, protecting the patient from injury, and providing comfort. - Offering brief explanations to the patient about what is happening is essential even if there is no certainty that the patient hears or understands what is being said. Simple comfort measures, including reassuring touches, should continue to be provided despite the patient’s nonresponsiveness to verbal stimuli (Hinkle et al., 2015). ## Types of Shock ### 1. Hypovolemic Shock - The most common type of shock, is characterized by decreased intravascular volume. - Body fluid is contained in the intracellular and extracellular compartments. Intracellular fluid accounts for about twothirds of the total body water. The extracellular body fluid is found in one of two compartments: intravascular (inside blood vessels) or interstitial (surrounding tissues). The volume of interstitial fluid is about three to four times that of intravascular fluid. - Hypovolemic shock occurs when there is a reduction in intravascular volume by 15% to 30%, which represents an approximate loss of 750 to 1,500 mL of blood in a 70-kg (154-lb) person (American College of Surgeons, 2012). ### 2. Cardiogenic shock - occurs when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and the tissues. The causes of cardiogenic shock are known as either coronary or noncoronary. Coronary cardiogenic shock is more common than noncoronary cardiogenic shock and is seen most often in patients with acute MI resulting in damage to a significant portion of the left ventricular myocardium (Tharmaratnam, Nolan, & Jain, 2013). - Patients who experience an anterior wall Ml are at greatest risk for cardiogenic shock because of the potentially extensive damage to the left ventricle caused by occlusion of the left anterior descending coronary artery. Noncoronary causes of cardiogenic shock are related to conditions that stress the myocardium (e.g., severe hypoxemia, acidosis, hypoglycemia, hypocalcemia, tension pneumothorax) as well as conditions that result in ineffective myocardial function (e.g., cardiomyopathies, valvular damage, cardiac tamponade, dysrhythmias). ### Distributive Shock ### 3. Septic shock - The most common type of distributive shock, is caused by widespread infection or sepsis. - is “a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality. | Risk Factors | | |:--|:--:| | Immunosuppression | Extremes of age (65 yrs) | | Malnourishment | Chronic illness | | Invasive procedures | Emergent and/or multiple surgeries | ### 4. Neurogenic Shock - vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation. Sympathetic stimulation causes vascular smooth muscle to constrict, and parasympathetic stimulation causes vascular smooth muscle to relax or dilate. The patient experiences a predominant parasympathetic stimulation that causes vasodilation lasting for an extended period, leading to a relative hypovolemic state. However, blood volume is adequate, because the vasculature is dilated; the blood volume is displaced, producing a hypotensive (low BP) state. The overriding parasympathetic stimulation that occurs with neurogenic shock causes a drastic decrease in the patient’s systemic vascular resistance and bradycardia. Inadequate BP results in the insufficient perfusion of tissues and cells that is common to all shock states. | Risk Factors: | | |:--|:--:| | Spinal cord injury | Spinal anesthesia | | Depressant action of medications | | ### 5. Anaphylactic Shock - is caused by a severe allergic reaction when patients who have already produced antibodies to a foreign substance (antigen) develop a systemic antigen-antibody reaction; specifically, an immunoglobulin E (IgE)- mediated response. This antigen-antibody reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin, and activates inflammatory cytokines, causing widespread vasodilation and capillary permeability. The most common triggers are foods (especially peanuts), medications, and insects (Muraro, Hoffmann-Sommergruber, Holzhauser, et al., 2014) | Risk Factors | | |:--|:--:| | History of medication sensitivity | Transfusion reaction | | History of reaction to insect bites/stings | Food allergies | | Latex sensitivity | | ## General Management Strategies in Shock - Support of the respiratory system with supplemental oxygen and/or mechanical ventilation to provide optimal oxygenation. - Fluid replacement to restore intravascular volume - Vasoactive medications to restore vasomotor tone and improve cardiac function - Nutritional support to address the metabolic requirements that are often dramatically increased in shock. ### Fluid replacement, also referred to as fluid resuscitation, is given in all types of shock. The type of fluids given and the speed of delivery vary; however, fluids are given to improve cardiac and tissue oxygenation, which in part depends on flow. The fluids given may include crystalloids (electrolyte solutions that move freely between intravascular compartment and interstitial spaces), colloids (large-molecule IV solutions), and blood components (packed red blood cells, fresh frozen plasma, and platelets). - **Crystalloid and Colloid Solutions** Fluid resuscitation should be initiated early in shock to maximize intravascular volume. Isotonic crystalloid solutions are often selected because they contain the same concentration of electrolytes as the extracellular fluid and, therefore, can be given without altering the concentrations of electrolytes in the plasma. IV crystalloids commonly used for resuscitation in hypovolemic shock include 0.9% sodium chloride solution (normal saline) and lactated Ringer's solution. Ringer's lactate is an electrolyte solution containing the lactate ion, which should not be confused with lactic acid. The lactate ion is converted to bicarbonate, which helps buffer the overall acidosis that occurs in shock. ### Complications of Fluid Administration Close monitoring of the patient during fluid replacement is necessary to identify side effects and complications. The most common and serious side effects of fluid replacement are cardiovascular overload, pulmonary edema, and ACS. - The patient receiving fluid replacement must be monitored frequently for adequate urinary output, changes in mental status, skin perfusion, and changes in vital signs. Lung sounds are auscultated frequently to detect signs of fluid accumulation. Adventitious lung sounds, such as crackles, may indicate pulmonary edema and ALI. ### Vasoactive Medication Therapy - Vasoactive medications are given in all forms of shock to improve the patient’s hemodynamic stability when fluid therapy alone cannot maintain adequate MAP. Specific medications are selected to correct the particular hemodynamic alteration that is impeding cardiac output. These medications help increase the strength of myocardial contractility, regulate the heart rate, reduce myocardial resistance, and initiate vasoconstriction. ### Nutritional Support - Nutritional support is an important aspect of care for critically ill patients. Increased metabolic rates during shock increase energy requirements and therefore caloric requirements. Patients in shock may require more than 3000 calories daily. The release of catecholamines early in the shock continuum causes rapid depletion of glycogen stores. Nutritional energy requirements are then met by breaking down lean body mass. In this catabolic process, skeletal muscle mass is broken down even when the patient has large stores of fat or adipose tissue. Loss of skeletal muscle greatly prolongs the patient’s recovery time. - Parenteral or enteral nutritional support should be initiated as soon as possible. Enteral nutrition is preferred, promoting Gl function through direct exposure to nutrients and limiting infectious complications associated with parenteral feeding (Blaser, Starkopf, Kirsimagi, et al., 2014). Implementation of an evidence-based enteral feeding protocol that is tolerant of increased gastric residual volumes ensures the delivery of adequate nutrition to critically ill patients (Blaser et al., 2014). Gastric residual volume does not predict a patient’s risk of aspiration (Blaser et al., 2014). Implementing early enteral nutrition has been found to promote gut-mediated immunity, reduce metabolic response to stress, and improve overall patient morbidity and mortality (Martindale & Warren, 2015). - Stress ulcers occur frequently in acutely ill patients because of the compromised blood supply to the Gl tract. Therefore, antacids, H2 blockers (e.g., famotidine [Pepcid]), and proton pump inhibitors (e.g., lansoprazole [Prevacid], esomeprazole magnesium [Nexium]) are prescribed to prevent ulcer formation by inhibiting gastric acid secretion or increasing gastric pH. ## Systemic Inflammatory Response Syndrome Systemic Inflammatory Response Syndrome (SIRS) is an exaggerated defense response of the body to a noxious stressor (infection, trauma, surgery, acute inflammation, ischemia or reperfusion, or malignancy, to name a few) to localize and then eliminate the endogenous or exogenous source of the insult. It involves the release of acute-phase reactants, which are direct mediators of widespread autonomic, endocrine, hematological, and immunological alteration in the subject. Even though the purpose is defensive, the dysregulated cytokine storm can cause a massive inflammatory cascade leading to reversible or irreversible end-organ dysfunction and even death. ### Cytokine storm syndrome - **Pro-inflammatory signaling molecules** - is a physiological reaction in humans and other animals in which the innate immune system causes an uncontrolled and excessive release of this molecule. - SIRS with a suspected source of infection is termed sepsis. Confirmation of infection with positive cultures is therefore not mandatory, at least in the early stages. Sepsis with one or more end-organ failure is called severe sepsis, and with hemodynamic instability despite intravascular volume repletion is called septic shock. Together they represent a physiologic continuum with progressively worsening Normally, cytokines are part of the body’s immune response to infection, but their sudden release in large quantities can cause multisystem organ failure and death. Both SIRS and sepsis could ultimately progress to multiple organ dysfunction syndrome. ### Etiologies | Damage Associated Molecular Pattern (DAMP) Non- Infectious/Auto immune Disorders Etiologies | | |:--|:--:| | Burns | Trauma | | Surgical procedure-related trauma | Acute aspiration | | Substance abuse and related intoxications | Acute end-organ ischemia | | Acute exacerbation of autoimmune vasculitis | Medication adverse reaction | | Intestinal ischemia and perforation | Hematologic malignancy | | Erythema multiforme | | | Pathogen Associated Molecular Pattern (PAMP) Infectious Etiologies | | |:--|:--:| | Bacterial infection | Viral syndrome-like influenza | | Disseminated fungal infection in immunosuppressed | Toxic shock syndrome derived from both exotoxins and endotoxins | ## Sepsis: SIRS Criteria | | | | |:--|:--|:--:| | Temperature | <36°C or >38°C | Systemic Inflammatory Response Syndrome ≥2 criteria | | Heart Rate | >90 beats per minute | Sepsis: SIRS plus confirmed or presumed infection | | Tachypnea | >20 breathes per minute or PaCO2 <32 mm Hg | Severe Sepsis: Sepsis plus organ dysfunction | | White Blood Cell Count | WBC <4,000/mm³ or WBC>12,000/mm³ or >10% immature (band) forms | Septic Shock: Severe sepsis plus refractory hypotension | | | | Multiple Organ Dysfunction Syndrome: Evidence of ≥ 2 organs failing | Objectively, SIRS is defined by the satisfaction of any two of the criteria below: - Body temperature over 38 or under 36 degrees Celsius. - Heart rate greater than 90 beats/minute - Respiratory rate greater than 20 breaths/minute or partial pressure of CO2 less than 32 mmHg - Leucocyte count greater than 12000 or less than 4000 /microliters ## Systemic Inflammatory Response Syndrome | | | |:--|:--:| |