Critical Care of Patients With Shock PDF

34: Critical Care of Patients With Shock Nicole M. Heimgartner, and Maureen Bishop LEARNING OUTCOMES 1. Collaborate with the interprofessional team to coordinate high-quality care and promote perfusion in patients who are experiencing shock. 2. Teach adults how to decrease the risk for sepsis and sh...

34: Critical Care of Patients With Shock Nicole M. Heimgartner, and Maureen Bishop LEARNING OUTCOMES 1. Collaborate with the interprofessional team to coordinate high-quality care and promote perfusion in patients who are experiencing shock. 2. Teach adults how to decrease the risk for sepsis and shock. 3. Implement nursing interventions to help the patient and family cope with the psychosocial impact caused by shock or its complications. 4. Apply knowledge of anatomy and physiology to assess critically ill patients with respiratory problems affecting perfusion or infection. 5. Implement evidence-based nursing interventions to prevent complications of sepsis and shock. KEY TERMS anaphylaxis An extreme type of allergic reaction. multiple organ dysfunction syndrome (MODS) Progressive organ dysfunction in an acutely ill patient, such that homeostasis cannot be maintained without intervention. sepsis A life-threatening organ dysfunction caused by simultaneous systemic inflammation and coagulation in response to microbial infection. septic shock A subset of sepsis in which circulatory, cellular, and metabolic alterations are associated with a higher mortality rate than sepsis alone. shock Widespread abnormal cellular metabolism occurring when oxygenation and tissue perfusion needs do not maintain cell function. sympathetic tone A state of partial blood vessel constriction caused when nerves from the sympathetic division of the autonomic nervous system continuously stimulate vascular smooth muscle. Priority and Interrelated Concepts The priority concepts for this chapter are: Perfusion Infection The Perfusion concept exemplar for this chapter is Hypovolemic Shock. The Infection concept exemplar for this chapter is Sepsis and Septic Shock. The interrelated concepts for this chapter are: Clotting Gas Exchange Immunity Overview All organs, tissues, and cells need a continuous supply of oxygen to function properly. The lungs first bring oxygen into the body through ventilation and gas exchange, and the cardiovascular system (heart, blood, and blood vessels) delivers oxygen by perfusion to all tissues and removes cellular wastes. Shock is widespread abnormal cellular metabolism that occurs when gas exchange with oxygenation and tissue perfusion needs are not met sufficiently to maintain cell function (McCance & Huether, 2019). It is a condition rather than a disease and is the “whole-body” response that occurs when too little oxygen is delivered to the tissues. All body organs are affected by shock and either work harder to adapt and compensate for reduced gas exchange or perfusion or fail to function because of hypoxia. Shock is a “syndrome” because the problems resulting from it occur in a predictable sequence. Any problem that impairs perfusion and gas exchange to tissues and organs can start the syndrome of shock and lead to a life-threatening emergency. Shock is often a result of cardiovascular problems. Patients in acute care settings are at higher risk, but shock can occur in any setting. For example, older patients in long-term care settings are at risk for sepsis and septic shock related to urinary tract infections and pneumonia. When the body’s adaptive adjustments (compensation) or health care interventions are not effective or exhausted and shock progresses, it can lead to cell loss, multiple organ dysfunction syndrome (MODS), and death. Shock is classified by the type of impairment causing it into the categories of hypovolemic shock, cardiogenic shock, Key Features Shock Cardiovascular Symptoms Decreased cardiac output Increased pulse rate Thready pulse Decreased blood pressure Narrowed pulse pressure Postural hypotension Low central venous pressure Flat neck and hand veins in dependent positions Slow capillary refill in nail beds Diminished peripheral pulses Respiratory Symptoms Increased respiratory rate Shallow depth of respirations Decreased PaCO 2 initially then progressing to increased PaCO 2 Decreased PaO 2  Cyanosis, especially around lips and nail beds Gastrointestinal Symptoms Decreased motility Diminished or absent bowel sounds Nausea and vomiting Constipation Neuromuscular Symptoms Early Anxiety Restlessness Increased thirst Late Decreased central nervous system activity (lethargy to coma) Generalized muscle weakness Diminished or absent deep tendon reflexes Sluggish pupillary response to light Kidney Symptoms Decreased urine output Increased specific gravity Sugar and acetone present in urine Integumentary Symptoms Cool to cold Pale to mottled to cyanotic Moist, clammy Mouth dry; pastelike coating present  Decreased capillary refill Pa co 2, Partial pressure of arterial carbon dioxide; Pa o 2, partial pressure of arterial oxygen. distributive shock (which includes septic shock, neurogenic shock, and anaphylactic shock), and obstructive shock. Table 34.1 describes this classification and common causes of shock. Most signs and symptoms of shock are similar regardless of what starts the process or which tissues are affected first. Symptoms result from physiologic adjustments (compensatory mechanisms) that the body makes in the attempt to ensure continued perfusion of vital organs. Compensatory actions are triggered by the sympathetic nervous system’s stress response activating the endocrine and cardiovascular systems. Symptoms unique to any one type of shock result from specific tissue dysfunction. The common features of shock are listed in in the Key Features: Shock box. Review of Gas Exchange and Tissue Perfusion Gas exchange and perfusion depend on how much oxygen from arterial blood perfuses the tissue. Perfusion is related to mean arterial pressure (MAP). The factors that influence MAP include: Total blood volume (viscosity) Cardiac output (heart rate × stroke volume) Size and integrity of the vascular bed, especially capillaries Total blood volume and cardiac output are directly related to MAP, so increases in either total blood volume or cardiac output raise MAP. Decreases in either total blood volume or cardiac output lower MAP. The size of the vascular bed is inversely (negatively) related to MAP. This means that increases in the size of the vascular bed lower MAP and decreases raise MAP (Fig. 34.1). The small arteries and veins connected to capillaries can increase in diameter by relaxing the smooth muscle in vessel walls (dilation) or decrease in diameter by contracting the muscle (vasoconstriction). When blood vessels dilate and total blood volume remains the same, blood pressure decreases and blood flow is slower. When blood vessels constrict and total blood volume remains the same, blood pressure increases and blood flow is faster. Blood vessels are innervated by the sympathetic nervous system. Some nerves continuously stimulate vascular smooth muscle so the blood vessels are normally partially constricted, a condition called sympathetic tone. Increases in sympathetic stimulation constrict smooth muscle even more, raising MAP. Decreases in sympathetic tone relax smooth muscle, dilating blood vessels and lowering MAP. Perfusion to organs adjusts to changes in tissue oxygen needs. The body can selectively increase blood flow to some areas while reducing flow to others. The skin and skeletal muscles can tolerate low levels of oxygen for hours without dying or being damaged. Other organs (e.g., heart, brain, liver, pancreas) do not tolerate hypoxia, and a few minutes without oxygen results in serious damage and cell death. Types of Shock Types of shock vary because shock is a problem caused by a pathologic condition rather than a disease state (see Table 34.1). More than one type of shock can be present at the same time. For example, trauma caused by a car crash may trigger hemorrhage (leading to hypovolemic shock) and a myocardial infarction (leading to cardiogenic shock). Hypovolemic shock occurs when too little circulating blood volume decreases MAP, resulting in inadequate total body perfusion and gas exchange. Common problems leading to hypovolemic shock are dehydration and poor clotting with hemorrhage. A complete discussion of the pathophysiology and management of hypovolemic shock begins with the perfusion concept exemplar. Cardiogenic shock occurs when the heart muscle is unhealthy and pumping is impaired. Cardiogenic shock is most often associated with acute myocardial infarction (McCance & Huether, 2019). Other causes are listed in Table 34.1. Any type of pump failure decreases cardiac output and MAP. Chapter 35 discusses the pathophysiology and care for the adult with shock from myocardial infarction. Distributive shock occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot perfuse organs. It can be caused by blood vessel dilation, pooling of blood in venous and capillary beds, and increased capillary leak. All these factors decrease MAP and may be started either by nerve changes (neural induced) or by the presence of some chemicals (chemical induced). Septic shock is the most common cause of distributive shock (Gaieski & Mikkelsen, 2018). Anaphylaxis is an extreme type of allergic reaction. It begins within seconds to minutes after exposure to a specific allergen in a susceptible adult. The result is widespread loss of blood vessel tone, with decreased blood pressure and cardiac output. Chapter 18 describes the pathophysiology, prevention, and care of the patient with anaphylactic shock. TABLE 34.1 Causes and Types of Shock by Functional Impairment Hypovolemic Shock Overall Cause Total body fluid decreased (in all fluid compartments) Specific Cause or Risk Factors Hemorrhage Trauma GI ulcer Surgery Inadequate clotting Hemophilia Liver disease Cancer therapy  Anticoagulation therapy Dehydration Vomiting Diarrhea Heavy diaphoresis Diuretic therapy Nasogastric suction Diabetes insipidus Cardiogenic Shock Overall Cause Direct pump failure (fluid volume not affected) Specific Cause or Risk Factors Myocardial infarction Cardiac arrest Ventricular dysrhythmias Cardiomyopathies Myocardial degeneration Cardiac tamponade Distributive Shock Overall Cause Fluid shifted from central vascular space (total body fluid volume normal or increased) Specific Cause or Risk Factors Neural induced Pain Anesthesia Stress  Spinal cord injury Head trauma Chemical induced Anaphylaxis Sepsis Capillary leak Burns Extensive trauma Liver impairment Hypoproteinemia Obstructive Shock Overall Cause Cardiac function decreased by noncardiac factor (indirect pump failure); total body fluid not affected, although central volume is decreased Specific Cause or Risk Factors Cardiac tamponade Arterial stenosis Pulmonary embolus Pulmonary hypertension Constrictive pericarditis Thoracic tumors Tension pneumothorax FIG. 34.1 Interaction of blood volume and the size of the capillary bed affecting mean arterial pressure (MAP). Sepsis is life-threatening organ dysfunction brought on by a dysregulated response to infection (Singer et al., 2016). Septic shock is a subset of sepsis in which circulatory, cellular, and metabolic abnormalities substantially increase the risk of death over that associated with sepsis alone (Singer et al., 2016). A complete discussion of the pathophysiology, prevention, and care for the patient with sepsis and septic shock is located later in the chapter in the infection concept exemplar. Obstructive shock is caused by problems that impair the ability of the normal heart to pump effectively. The heart itself remains normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. The most common cause of obstructive shock is cardiac tamponade (see Table 34.1). Care of the adult with cardiac tamponade is presented in Chapter 32 (pericarditis) and Chapter 35. Although the causes and initial signs and symptoms associated with the different types of shock vary, eventually the effects of hypotension and anaerobic cellular metabolism (metabolism without oxygen) result in the common key features of shock as indicated in the Key Features: Shock box. Perfusion Concept Exemplar: Hypovolemic Shock Pathophysiology Review The basic problem of hypovolemic shock is a loss of vascular volume, resulting in a decreased mean arterial pressure (MAP) (see Fig. 34.1) and, in some cases, a loss of circulating red blood cells (RBCs). The reduced MAP slows blood flow, decreasing tissue perfusion. The loss of RBCs decreases the ability of the blood to oxygenate the tissue it does reach. These gas exchange and perfusion problems lead to anaerobic cellular metabolism. The main trigger leading to hypovolemic shock is a sustained decrease in MAP from decreased circulating blood volume. A decrease in MAP of 5 to 10 mm Hg below the patient’s normal baseline value is detected by pressure-sensitive nerve receptors (baroreceptors) in the aortic arch and carotid sinus. This information is transmitted to brain centers, which stimulate compensatory mechanisms to help ensure continued blood flow and oxygen delivery to vital organs while limiting blood flow to less vital areas. The movement of blood into selected areas while bypassing others (“shunting”) results in some shock symptoms. If the events that caused the initial decrease in MAP are halted now, compensatory mechanisms provide adequate gas exchange and perfusion without intervention. If events continue and MAP decreases further, some tissues function under anaerobic conditions. This condition increases lactic acid levels and other harmful metabolites (e.g., protein-destroying enzymes, oxygen free radicals) (McCance & Huether, 2019). These substances cause acidosis with tissue-damaging effects and depressed heart muscle activity. The effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. When shock conditions continue for longer periods without help, the resulting increased metabolites cause so much cell damage in vital organs that they are unable to perform their critical functions. When this problem, known as multiple organ dysfunction syndrome (MODS), occurs to the extent that vital organs die, recovery from shock is no longer possible (see the section Refractory Stage and Multiple Organ Dysfunction Syndrome). Table 34.2 summarizes the progression of shock. TABLE 34.2 Adaptive Responses and Events During Hypovolemic Shock Initial Stage Decrease in mean arterial pressure (MAP) of 5-10 mm Hg from baseline value Increased sympathetic stimulation Mild vasoconstriction Increased heart rate Compensatory Stage Decrease in MAP of 10-15 mm Hg from baseline value Continued sympathetic stimulation Moderate vasoconstriction Increased heart rate Decreased pulse pressure Chemical compensation Renin, aldosterone, and antidiuretic hormone secretion Increased vasoconstriction Decreased urine output Stimulation of the thirst reflex Some anaerobic metabolism in nonvital organs Mild acidosis Mild hyperkalemia Progressive Stage Decrease in MAP of >20 mm Hg from baseline value Anoxia of nonvital organs Hypoxia of vital organs  Overall metabolism is anaerobic Moderate acidosis Moderate hyperkalemia Tissue ischemia Refractory Stage Severe tissue hypoxia with ischemia and necrosis Release of myocardial depressant factor from the pancreas Buildup of toxic metabolites Multiple organ dysfunction syndrome (MODS) Death Stages of Shock The syndrome of shock progresses in four stages when the conditions that cause shock remain uncorrected and poor cellular oxygenation continues. These stages are: 1. Initial stage 2. Compensatory stage 3. Progressive stage 4. Refractory stage Initial Stage The initial stage is present when the patient’s baseline MAP is decreased by less than 10 mm Hg. Compensatory mechanisms are effective at returning systolic pressure to normal at this stage; thus oxygen perfusion to vital organs is maintained. Cellular changes include increased anaerobic metabolism in some tissues with production of lactic acid, although overall metabolism is still aerobic. The compensation responses of vascular constriction and increased heart rate are effective, and both cardiac output and MAP are maintained within the normal range. Because vital organ function is not disrupted, the indicators of shock are difficult to detect at this stage. Nursing Safety Priority Action Alert Be aware that increased heart and respiratory rates or a slight increase in diastolic blood pressure may be the only sign of this stage of shock. Compensatory Stage The compensatory stage of shock occurs when MAP decreases by 10 to 15 mm Hg from baseline. Kidney and hormonal compensatory mechanisms are activated because cardiovascular responses alone are not enough to maintain MAP and supply oxygen to vital organs. The ongoing decrease in MAP triggers the release of renin, antidiuretic hormone (ADH), aldosterone, epinephrine, and norepinephrine to start kidney compensation. Urine output decreases, sodium reabsorption increases, and widespread blood vessel constriction occurs. ADH increases water reabsorption in the kidney, further reducing urine output, and increases blood vessel constriction in the skin and other less vital tissue areas. Together these actions compensate for shock by maintaining the fluid volume within the central blood vessels. Tissue hypoxia occurs in nonvital organs (e.g., skin, GI tract) and in the kidney, but it is not great enough to cause permanent damage. Buildup of metabolites from anaerobic metabolism causes acidosis (low blood pH) and increased blood potassium levels. Signs and symptoms of this stage include changes resulting from decreased tissue perfusion. Subjective changes include thirst and anxiety. Objective changes include restlessness, tachycardia, increased respiratory rate, decreased urine output, falling systolic blood pressure, rising diastolic blood pressure, narrowing pulse pressure, cool extremities, and a decrease in oxygen saturation. Comparing these changes with the values and observations obtained earlier is critical to identifying this stage of shock. If the patient is stable and compensatory mechanisms are supported by interventions, he or she can remain in this stage for hours without having permanent damage. Stopping the conditions that started shock and providing supportive interventions can prevent the shock from progressing. The effects of this stage are reversible when nurses recognize the problem and coordinate the interprofessional health care team to start appropriate interventions. Progressive Stage The progressive stage of shock occurs when there is a sustained decrease in MAP of more than 20 mm Hg from baseline. Compensatory mechanisms are functioning but can no longer deliver sufficient oxygen, even to vital organs. Vital organs develop hypoxia, and less vital organs become anoxic (no oxygen) and ischemic (cell dysfunction or death from lack of oxygen). As a result of poor perfusion and a buildup of metabolites, some tissues die. Indications of the progressive stage include a worsening of changes resulting from decreased tissue perfusion. The patient may express a sense of “something bad” (impending doom) about to happen. He or she may be confused, and thirst increases. Objective changes are a rapid, weak pulse; low blood pressure; pallor to cyanosis of oral mucosa and nail beds; cool and moist skin; anuria; and a 5% to 20% decrease in oxygen saturation. Laboratory data may show a low blood pH, along with rising lactic acid and potassium levels. Nursing Safety Priority Action Alert The progressive stage of shock is a life-threatening emergency. Vital organs tolerate this situation for only a short time before development of multiple organ dysfunction syndrome (MODS) with permanent damage. Immediate interventions are needed to reverse the effects of this stage of shock. The patient’s life usually can be saved if the conditions causing shock are corrected within 1 hour or less of the onset of the progressive stage. Continuously monitor and compare with earlier findings to assess therapy effectiveness and determine when therapy changes are needed. NCLEX Examination Challenge 34.1 Safe and Effective Care Environment A client in the progressive stage of hypovolemic shock has all of the following signs, symptoms, or changes. Which signs will the nurse attribute to ongoing compensatory mechanisms? Select all that apply. A. Increasing pallor B. Increasing thirst C. Increasing confusion D. Increasing heart rate E. Increasing respiratory rate F. Decreasing systolic blood pressure G. Decreasing blood pH H. Decreasing urine output Refractory Stage and Multiple Organ Dysfunction Syndrome The refractory stage of shock occurs when too much cell death and tissue damage result from too little oxygen reaching the tissues. Vital organs have extensive damage and cannot respond effectively to interventions, and shock continues. So much damage has occurred with release of metabolites and enzymes that damage to vital organs continues despite interventions. The sequence of cell damage caused by the massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence becomes a vicious cycle as more dead cells open and release metabolites. These trigger small clots (microthrombi) to form, which block tissue perfusion and damage more cells, continuing the devastating cycle. Liver, heart, brain, and kidney functions are lost first. The most profound change is damage to the heart muscle. Signs are a rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation. Therapy, including fluid replacement, is not effective in saving the patient’s life, even if the cause of shock is corrected and MAP temporarily returns to normal. Etiology Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease that prevents total body perfusion and adequate gas exchange. Problems leading to hypovolemic shock are listed in Table 34.1. Hypovolemic shock from hemorrhage is common after trauma or surgery; and internal hemorrhage occurs with blunt trauma, GI ulcers, and poor control of surgical bleeding. Hemorrhage leading to hypovolemia also can be caused by any problem that reduces the levels of clotting factors (see Table 34.1). Hypovolemia from dehydration can be caused by any problem that decreases fluid intake or increases fluid loss (see Table 34.1). Incidence and Prevalence The exact incidence of hypovolemic shock is not known because it is a response rather than a disease. It is a common complication among hospitalized patients in emergency departments and after surgery or invasive procedures. Health Promotion and Maintenance Recognizing hypovolemic shock is a major nursing responsibility. Identify patients at risk for dehydration and assess for early signs and symptoms. This is especially important for those who have reduced cognition or mobility or who are on NPO status. Assess all patients with invasive procedures or trauma for obvious or occult bleeding from impaired clotting. Compare pulse quality and rate with baseline. Compare urine output with fluid intake; this includes monitoring trends in intake and output as well as changes in daily weight. Check vital signs of patients who have persistent thirst. Assess for shock in any patient who develops a change in mental status, an increase in pain, or an increase in anxiety. Teach patients who have invasive procedures about the signs and symptoms of shock. Stress the importance of seeking immediate help for obvious heavy bleeding, persistent thirst, decreased urine output, light-headedness, or a sense of impending doom. Interprofessional Collaborative Care Hypovolemic shock is an emergent problem that is usually managed in an acute care setting. If complications from the problem or its treatment are ongoing, patients may be cared for in a variety of community settings. Assessment: Recognize Cues History Ask about risk factors related to hypovolemic shock. If the patient is alert, question him or her directly. If the patient is not alert, collect information from family members. Ask about recent illness, trauma, procedures, or chronic health problems that may lead to shock (e.g., GI ulcers, general surgery, hemophilia, liver disorders, prolonged vomiting or diarrhea). Ask about the use of drugs such as aspirin, other NSAIDs, diuretics, and herbal supplements that may cause changes leading to hypovolemic shock. Ask about fluid intake and output during the previous 24 hours. Information about urine output is especially important because urine output is reduced during the first stages of shock, even when fluid intake is normal. Assess the patient for factors that can lead to shock. Areas to examine for poor clotting and hemorrhage include the gums, wounds, and sites of dressings, drains, and vascular accesses. Also check under the patient for blood. Observe for any swelling or skin discoloration that may indicate an internal hemorrhage. Physical Assessment/Signs and Symptoms Most signs and symptoms of hypovolemic shock are caused by the changes resulting from compensatory efforts. Shock may first be evident as changes in cardiovascular function. As shock progresses, changes in the renal, respiratory, integumentary, musculoskeletal, and central nervous systems become evident. Ensure that vital sign measurements are accurate, and monitor for trends indicating shock. A trend is indicated when any or all of the vital signs or other assessment findings move in a downward or upward direction over a period of 1 to 4 hours. Nursing Safety Priority Action Alert Assign a registered nurse (RN) rather than a licensed practical nurse/licensed vocational nurse (LPN/LVN) or assistive personnel (AP) to assess the vital signs of a patient who is suspected of having hypovolemic shock. The rapid progression associated with shock requires the interpretation of vital signs, which is included in the RN scope of practice. Remember to watch for trends in vital signs and in all other assessment parameters. Cardiovascular changes that occur with hypovolemic shock start with decreased mean arterial pressure (MAP) leading to compensatory responses. Assess the central and peripheral pulses for rate and quality. In the initial stage of shock, the pulse rate increases above the patient’s baseline to keep cardiac output and MAP at normal levels, even though the actual stroke volume (amount of blood pumped out from the heart) per beat is decreased. Increased heart rate is often the first sign of shock. Because stroke volume is decreased, the peripheral pulses are difficult to palpate and easily blocked. As shock progresses, peripheral pulses may not be palpable, and a Doppler may be needed. Nursing Safety Priority Action Alert Because changes in systolic blood pressure are not always present in the initial stage of shock, use changes in pulse rate and quality as the main indicators of shock presence or progression. With vasoconstriction, diastolic pressure increases but systolic pressure remains the same. As a result, the difference between the systolic and diastolic pressures (pulse pressure) is smaller or “narrower.” Monitor blood pressure for changes from baseline levels and for changes from the previous measurement. For accuracy, use the same equipment on the same extremity. Validate an abnormal electronic blood pressure reading with a manual blood pressure reading. Systolic pressure decreases as shock progresses and cardiac output decreases. A reduced systolic pressure narrows the pulse pressure even further. When shock continues and interventions are not adequate, compensation fails, both systolic and diastolic pressures decrease, and blood pressure is difficult to hear. Palpation or a Doppler device may be needed to detect the systolic blood pressure. Oxygen saturation is assessed through pulse oximetry. Pulse oximetry values between 90% and 95% occur with the compensatory stage of shock, and values between 75% and 80% occur with the progressive stage of shock. Any value below 70% is considered a life-threatening emergency and may signal the refractory stage of shock. Respiratory changes with shock are an adaptive response to help maintain gas exchange when tissue perfusion is decreased. Assess the rate and depth of respiration. Respiratory rate increases during shock to ensure that oxygen intake is increased so it can be delivered to critical tissues. Kidney and urinary changes occur with shock to compensate for decreased mean arterial pressure (MAP) by saving body water through decreased filtration and increased water reabsorption. Assess urine for volume, color, specific gravity, and the presence of blood or protein. Decreased urine output (less than 30 mL/hr or 0.5 mL/kg/hr) is a sensitive indicator of early shock. Measure urine output at least every hour. In severe shock, urine output may be absent. When hypoxia or anoxia persists beyond about an hour, patients are at risk for acute kidney injury (AKI) and kidney failure. Skin changes occur because of reduced blood flow in the skin. An early compensatory mechanism is skin blood vessel constriction, which reduces skin perfusion. This allows more blood to perfuse the vital organs, which cannot tolerate low oxygen levels. Assess the skin for temperature, color, and moisture. With shock, it feels cool or cold to the touch and is moist. Color changes appear first in oral mucous membranes and in the skin around the mouth. In dark-skinned patients, pallor or cyanosis is best assessed in the oral mucous membranes. Other color changes are noted first in the skin of the extremities and then in the central trunk area. The skin feels clammy or moist to the touch, not because sweating increases but because the normal fluid lost through the skin does not evaporate well on cool skin. As shock progresses, skin becomes mottled. Lighter-skinned patients have an overall grayish-blue color; and darker-skinned patients appear darker, without an underlying reddish glow. Evaluate capillary refill time by pressing on the patient’s fingernail until it blanches and then observing how fast the nail bed resumes color when pressure is released. Normally capillaries resume color as soon as pressure is released. With shock, capillary refill is slow or may be absent. Capillary refill is not a reliable indicator for peripheral blood flow in older patients or those with anemia, diabetes, or peripheral vascular disease. Central nervous system (CNS) changes with shock first manifest as thirst. Thirst is caused by stimulation of the thirst centers in the brain in response to decreased blood volume. Assess the patient’s level of consciousness (LOC) and orientation, which are sensitive to cerebral hypoxia. In the initial and nonprogressive stages, patients may be restless or agitated and may be anxious or have a feeling of impending doom. As hypoxia progresses, confusion and lethargy occur, which progress to loss of consciousness as cerebral hypoxia worsens. Skeletal muscle changes during shock include weakness and pain in response to tissue hypoxia and anaerobic metabolism, which are later indications. Weakness is generalized and has no specific pattern. Deep tendon reflexes are decreased or absent. Psychosocial Assessment Changes in mental status and behavior occur early in shock. Assess mental status by evaluating LOC and noting whether the patient is asleep or awake. If the patient is asleep, attempt to awaken him or her and document how easily he or she is aroused. If the patient is awake, determine whether he or she is oriented to person, place, and time. Avoid asking questions that can be answered with a “yes” or a “no” response. Consider these points during assessment: Is it necessary to repeat questions to obtain a response? Does the response answer the question asked? Does the patient have difficulty making word choices? Is the patient irritated or upset by the questions? Can the patient concentrate on a question long enough to answer, or is the attention span limited? Talk with the family to determine whether the patient’s behavior and cognition are typical or represent a change. Laboratory Assessment Although no single test confirms or rules out shock, changes in laboratory data may support the diagnosis. The Laboratory Profile: Hypovolemic Shock box lists laboratory changes occurring with hypovolemic shock. Laboratory Profile Hypovolemic Shock Test​ Normal Range for Adults​ Significance of Abnormal Findings pH (arterial)​ 7.35-7.45​ Decreased: insufficient tissue oxygenation causing anaerobic metabolism and acidosis Pao2​ 80-100 mm Hg​ Decreased: anaerobic metabolism Paco2​ 35-45 mm Hg​ Increased: anaerobic metabolism Lactic acid (lactate) (arterial)​ 3-7 mg/dL 0.3-0.8 mmol/L Increased: anaerobic metabolism with buildup of metabolites Hematocrit​ Females: 37%-47% (0.37-0.47 volume fraction) Males: 42%-52% (0.42-0.52 volume fraction) Increased: fluid shift, dehydration Decreased: hemorrhage Hemoglobin​ Females: 12-16 g/dL (120-160 g/L) Males: 14-18 g/dL (140-180 g/L) Increased: fluid shift, dehydration Decreased: hemorrhage Potassium​ 3.5-5.0 mEq/L or mmol/L​ Increased: dehydration, acidosis Pa co 2, Partial pressure of arterial carbon dioxide; Pa o 2, partial pressure of arterial oxygen. Data from Pagana, K., & Pagana, T. (2018). Mosby’s manual of diagnostic and laboratory tests (6th ed.). St. Louis: Elsevier; and Pagana, K., Pagana, T., & Pike-MacDonald, S. (2019). Mosby’s Canadian manual of diagnostic and laboratory tests (2nd ed.). St. Louis: Elsevier. Best Practice for Patient Safety & Quality Care The Patient in Hypovolemic Shock Ensure a patent airway. Insert an IV catheter or maintain an established catheter. A large-bore catheter is suggested. Administer oxygen to maintain O2 saturation at 92% to 96%; supplemental oxygen is no longer recommended if saturation is normal (Chu et al., 2018). Elevate the patient’s feet, keeping his or her head flat or elevated to no more than a 30-degree angle. Examine the patient for overt bleeding. If overt bleeding is present, apply direct pressure to the site. Administer drugs as prescribed. Increase the rate of IV fluid delivery. Do not leave the patient. As shock progresses, arterial blood gas values become abnormal. The pH decreases, the partial pressure of arterial oxygen (PaO 2) decreases, and the partial pressure of arterial carbon dioxide (PaCO 2) increases. Other laboratory changes occur with specific causes of hypovolemic shock. Hematocrit and hemoglobin levels decrease if shock is caused by hemorrhage from poor clotting or large open wounds. When shock is caused by dehydration or a fluid shift, hematocrit and hemoglobin levels are elevated. Analysis: Analyze Cues and Prioritize Hypotheses The priority collaborative problem for patients with hypovolemic shock is: Inadequate perfusion due to active fluid volume loss and hypotension Planning and Implementation: Generate Solutions and Take Action Interventions for patients in hypovolemic shock focus on reversing the shock, restoring fluid volume to the normal range, and preventing complications. Monitoring is critical to determine whether the patient is responding to therapy or whether shock is progressing and a change in intervention is needed. Surgery may be needed to correct some causes of shock. The Best Practice for Patient Safety & Quality Care: The Patient in Hypovolemic Shock box lists best practices for patients in hypovolemic shock. NCLEX Examination Challenge 34.2 Safe and Effective Care Environment The nurse is reviewing the laboratory profile of a client with hypovolemic shock. What laboratory value will the nurse anticipate? A. pH 7.51 B. PaO 2 106 mm Hg C. PaCO 2 49 mm Hg D. Lactate 0.4 mmol/L Nonsurgical Management The purposes of shock management are to maintain perfusion, increase vascular volume, and support compensatory mechanisms. Oxygen therapy, fluid replacement therapy, and drug therapy are useful. Oxygen therapy is used at any stage of shock and is delivered by mask, hood, nasal cannula, endotracheal tube, or tracheostomy tube. Maintain O2 saturations at 94% to 96%. Supplemental oxygen with normal oxygen saturations is no longer recommended, because it may be associated with increased mortality risk (Chu et al., 2018). Chapter 25 describes oxygen-delivery methods. IV therapy for fluid resuscitation is a primary intervention for hypovolemic shock. However, the type and amount of solution remain the subject of debate. Accordingly, the type of solution that is used is generally situation specific (Urden et al., 2018). Crystalloids and colloids are often used for volume replacement. Crystalloid solutions contain nonprotein substances (e.g., minerals, salts, sugars). Colloid solutions contain large molecules of proteins or starches (see Chapter 13). Crystalloid fluids help maintain an adequate fluid and electrolyte balance. Two common solutions are normal saline and Ringer’s lactate. Normal saline (0.9% sodium chloride in water) is a replacement solution used to increase plasma volume and can be infused with any blood product. Ringer’s lactate is considered a balanced salt solution containing sodium, chloride, calcium, potassium, and lactate. This isotonic solution expands volume, and the lactate buffers acidosis. Selection of specific fluid is based on the patient’s fluid and electrolyte status, acid-base status, and organ function (Procter, 2018; Urden et al., 2018). Nursing Safety Priority Action Alert Use only normal saline for infusion with blood or blood products because the calcium in Ringer’s lactate induces clotting of the infusing blood. Protein-containing colloid fluids help restore osmotic pressure and fluid volume. Blood products are used when shock is caused by blood loss. These fluids most often include packed red blood cells (PRBCs) and plasma. PRBCs increase hematocrit and hemoglobin levels along with some fluid volume. See Chapter 37 for nursing care during transfusion therapy. Drug therapy is used in addition to fluid therapy when volume loss is severe and the patient does not respond sufficiently to fluid replacement and blood products. Drugs for shock increase venous return, improve cardiac contractility, or improve cardiac perfusion by dilating the coronary vessels. See Common Examples of Drug Therapy: Hypovolemic Shock box for common drugs used to treat hypovolemic shock. Monitoring vital signs and level of consciousness is a major nursing action to determine the patient’s condition and the effectiveness of therapy. Monitor these patient responses: Pulse (rate, regularity, and quality) Blood pressure Pulse pressure Central venous pressure (CVP) Respiratory rate Skin and mucosal color Oxygen saturation Cognition Urine output Common Examples of Drug Therapy Hypovolemic Shock Drug Category​Nursing Implications Vasoconstrictors Improve mean arterial pressure by increasing peripheral resistance, increasing venous return, and increasing myocardial contractility. Norepinephrine Phenylephrine HCl Assess patient for chest pain because these drugs increase myocardial consumption and can cause angina or ischemia. Monitor urine output hourly because higher doses decrease kidney perfusion and urine output. Assess blood pressure every 15 min because hypertension is a symptom of overdose. Assess patient for headache because headache is an early symptom of drug excess. Assess every 30 min for extravasation; check extremities for color and perfusion because if the drug gets into the tissues, it can cause severe vasoconstriction, tissue ischemia, and tissue necrosis. Assess for chest pain because the drug can cause rapid onset of vasoconstriction in the myocardium and impair cardiac oxygenation. Inotropic Agents Directly stimulate beta-adrenergic receptors on the heart muscle, improving contractility. Dobutamine Milrinone Assess for chest pain because these drugs increase myocardial oxygen consumption and can cause angina or infarction. Monitor for transient hypotension as both drugs may cause vascular dilation. Assess blood pressure every 15 min because hypertension is a symptom of overdose. Agents That Enhance Myocardial Perfusion Improve myocardial perfusion by dilating coronary arteries rapidly for a short time. Sodium nitroprusside Nitroglycerin Protect drug container from light because light degrades the drug quickly. Assess blood pressure at least every 15 min because the drug can cause systemic vasodilation and hypotension, especially in older adults. Nursing Safety Priority Drug Alert Monitor the patient closely because drugs that dilate coronary blood vessels, such as nitroprusside and nitroglycerin, can cause systemic vasodilation and increase shock if the patient is volume depleted. Drugs that increase heart muscle contraction increase heart oxygen consumption and can cause angina or infarction. Assess these parameters at least every 15 minutes until the shock is controlled and the patient’s condition improves. Hemodynamic monitoring in critical care settings includes intra-arterial monitoring, mixed venous oxygen saturation (SvO 2), and pulmonary artery monitoring. Insertion of a CVP catheter allows pressure to be monitored in the patient’s right atrium or superior vena cava while providing venous access. A decrease in CVP from baseline levels reflects hypovolemic shock with reduced venous return to the right atrium. Intra-arterial catheters allow continuous blood pressure monitoring and are an access for arterial blood sampling. They are inserted into an artery (radial, brachial, or femoral). The catheter is attached to pressure tubing and a transducer, which converts arterial pressure into an electrical signal seen as a waveform on an oscilloscope and as a numeric value. NCLEX Examination Challenge 34.3 Safe and Effective Care Environment The nurse is caring for a client with hypovolemic shock who is bleeding from a traumatic injury to the upper chest wall. What is the priority nursing action? A. Insert a large-bore IV catheter. B. Administer supplemental oxygen. C. Elevate the client’s feet, keeping the head flat. D. Apply direct pressure to the area of overt bleeding. Surgical Management Surgical intervention in addition to nonsurgical management may be needed to correct the cause of shock. Such procedures include vascular repair, surgical hemostasis of major wounds, closure of bleeding ulcers, and chemical scarring (chemosclerosis) of varicosities. Care Coordination and Transition Management Hypovolemic shock is a complication of another condition and is resolved before patients are discharged from the acute care setting. Because surgery and many other invasive procedures now occur on an ambulatory care basis, more patients at home are at increased risk for hypovolemic shock. Teach patients and family members the early indicators of shock (increased thirst, decreased urine output, light-headedness, sense of apprehension) and to seek immediate medical attention if they appear. Evaluation: Evaluate Outcomes Evaluate the care of the patient with hypovolemic shock. The expected outcome is that the patient’s vascular volume will be restored with normal tissue perfusion.