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Interventions for clients with shock

June 25, 2024

Interventions for clients with shock. Care plan II

Shock, the whole-body response to poor tissue oxygenation, is a condition rather than a disease state. Any situation that impairs oxygen delivery to tissues and organs can start a syndrome of shock and lead to a life-threatening emergency. Clients in acute care settings are at high risk for conditions that lead to shock, but shock can occur in any setting. When compensation or interventions are ineffective and shock progresses, extensive hypoxiacan lead to the complication of multiple organ dysfunction syndrome (MODS) and death. Table 37-1 lists important concepts related to shock.

OVERVIEW Body organs, tissues, and cells need a continuous supply of oxygen for proper metabolism and function. The pulmonary system initially supplies oxygen to the body. The cardiovascular system delivers oxygen to all tissues and removes cellular wastes. The units of the cardiovascular system are the blood, blood vessels, and heart. When any component of the cardiovascular system does not function properly for any reason, shock can result.

Shock, a pathologic condition, is started by abnormal cellular metabolism that occurs when too little oxygen is delivered to the tissues (Guyton & Hall, 2000). Shock used to be classified as hypovolemic, cardiogenic, vasogenic, or septic, which indicated the origin of the problem causing the shock. Shock is now classified by the specific functional impairment caused: hypovolemic shock, cardiogenic shock, distributive shock, and obstructive shock (Effron & Chernow, 1992).

Table 37-2 compares the old and new classification systems and common conditions causing each category of shock. The functional classification is used by researchers and guides clinicians and therefore is used in this chapter.

Many clinical manifestations of shock are similar regardless of what starts the process or which tissues are affected first. These common clinical manifestations are due to physiologic compensatory mechanisms. Manifestations unique to any one type of shock result from specific tissue dysfunction. The common clinical features of shock are listed in Chart 37-1.

Physiology Review

Oxygenation of any organ or tissue depends on how much oxygenated arterial blood perfuses the organ or tissue. Organ perfusion is related to mean arterial pressure (MAP). Because the cardiovascular system is a closed but continuous circuit, the factors that influence MAP include the following:

• Total blood volume

• Cardiac output

• Size of the vascular bed

Total blood volume and cardiac output are directly related to MAP—increases in either total blood volume or cardiac output usually raise MAP. Decreases in either total blood volume or cardiac output eventually lower MAP. The size of the vascular bed is inversely (negatively) related to MAP—increases in the size of the vascular bed lower MAP, and decreases raise MAP (Figure 37-1). Blood vessels, especially small arteries and veins connected directly to cap- illaries, can increase in diameter by relaxing the smooth muscle in vessel walls (dilating) 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 contaierves from the sympathetic division of the autonomic nervous system. Some nerves continuously stimulate vascular smooth muscle so that the blood vessels are normally partially constricted. This state of partial blood vessel constriction is called sympathetic tone. An increase in sympathetic stimulation causes the smooth muscle of the blood vessels to constrict further, raising MAP; a decrease in sympathetic stimulation causes the smooth muscle of the blood vessels to relax, dilating them and lowering MAP.

Blood flow to body organs varies and adjusts to changes in tissue oxygeeeds. The body can selectively increase blood flow to some areas while reducing blood flow to others. Some organs, such as the skin and skeletal muscles, can tolerate low levels of oxygen for hours without dying or being damaged. Other organs (e.g., heart, brain, and liver) tolerate hypoxic conditions (low levels of tissue oxygenation) poorly, and even just a few minutes without adequate oxygen results in serious or permanent damage.

Pathophysiology The underlying problems common to all types of shock, regardless of cause, are the effects of anaerobic cellular metabolism (metabolism without oxygen). These effects result from inadequate tissue oxygenation and cause adverse changes in tissue function. The body begins to compensate in an attempt to maintain or restore tissue perfusion and oxygenation—even while the causes of shock are still present.

When the conditions that cause shock remain uncorrected, shock progresses through the following predictable stages:

1. Initial stage

2. Nonprogressive stage

3. Progressive stage

4. Refractory stage

The stages of shock are identified on the basis of the following:

• How well the client’s compensatory mechanisms are working

• The severity of the clinical manifestations

• Whether tissue damage is reversible

The main trigger leading to the recognizable picture of shock is a sustained decrease in mean arterial pressure (MAP) that results from decreased cardiac output, decreased circulating blood volume, or expansion of the vascular bed. A decrease in MAP of 5 to 10 mm Hg below the client’s baseline value is immediately detected by pressure-sensitive nerve receptors (baroreceptors) in the aortic arch and carotid sinus (Guyton & Hall, 2000). This information is transmitted to brain centers, which stimulates compensatory mechanisms. These mechanisms ensure continued blood flow and oxygen delivery to vital organs while limiting blood flow to less vital areas. Moving blood into selected areas while bypassing others (shunting) causes the physiologic changes and clinical manifestations of shock.

If the events that caused the initial decrease in MAP are halted at this point, the compensatory mechanisms can return the body to a normal perfused and oxygenated state, even without outside intervention. However, if the initiating events continue and MAP decreases further, some tissues function under anaerobic conditions. This condition creates an increase in lactic acid levels and other harmful metabolites (e.g., protein-destroying enzymes and oxygen radicals). These substances cause electrolyte and acid-base imbalances that have generalized, tissue-damaging effects and depress cardiac activity. Such effects are temporary and reversible if the cause of shock is corrected within 1 to 2 hours after onset. When such conditions continue for longer periods without help, the resulting acid-base imbalance, electrolyte imbalances, and increased levels of toxic metabolites cause so much cell damage in vital organs that multiple organ dysfunction syndrome (MODS) occurs and full recovery from shock is no longer possible. Table 37-3 summarizes the progression of shock.

INITIAL STAGE OF SHOCK (EARLY STAGE)

The initial (early) stage of shock is present when any condition causes MAP to decrease from the client’s baseline level by less than 10 mm Hg. During this stage, active compensatory mechanisms are so effective at returning MAP to normal levels that oxygenated blood flow to all vital organs is maintained. Cellular changes in this stage are decreased aerobic metabolism and increased anaerobic metabolism with a production of lactic acid; overall cellular metabolism is still aerobic. Compensation (vascular constriction and increased heart rate) is effective, and both cardiac output and MAP are maintained within the normal range. Because vital organ function is not disrupted, the signs and symptoms of shock are difficult to detect. An increase in heart rate from the client’s baseline level or a slight increase in diastolic blood pressure may be the only objective manifestation of this early stage of shock.

NONPROGRESSIVE STAGE OF SHOCK (COMPENSATORY STAGE)

The nonprogressive (compensatory) stage of shock occurs when conditions decrease MAP 10 to 15 mm Hg from baseline. Kidney and chemical compensatory mechanisms need to be activated because cardiovascular compensation alone is not enough to maintain MAP and supply needed oxygen to the vital organs. The kidneys and baroreceptors sense an ongoing decrease in MAP and cause the release of renin, antidiuretic hormone (ADH), aldosterone, epinephrine, and norepinephrine. Kidney compensation occurs through the actions of renin, aldosterone, and ADH. Renin, which is secreted by the kidney, starts the reactions that eventually cause decreased urine output, increased sodium reabsorption, and widespread vasoconstriction. ADH is secreted by the posterior pituitary gland. ADH increases water reabsorption in the kidney and causes blood vessel constriction in the skin and other less vital tissue areas. Together, these actions attempt to compensate for shock by maintaining the volume in the central blood vessels (Guyton & Hall, 2000). Tissue hypoxia is present ionvital organs and in the kidney but is not great enough to cause severe symptoms or permanent damage. Because some metabolism is anaerobic, acid-base and electrolyte changes occur in response to the buildup of metabolites. Changes include acidosis (low blood pH) and hyperkalemia (increased blood potassium level). If the client’s condition is stable and compensatory mechanisms are supported by medical and nursing interventions, he or she can remain in this stage for hours without experi encing permanent damage. Stopping the conditions that started the shock and providing supportive interventions can prevent the shock from progressing and reverse the effects of this stage.

PROGRESSIVE STAGE OF SHOCK (INTERMEDIATE STAGE) The progressive stage of shock results when there is a sustained decrease in MAP of more than 20 mm Hg from baseline. In this stage, compensatory mechanisms are functioning but are no longer able to deliver sufficient oxygen, even to vital organs. Compensatory mechanisms use large amounts of oxygen in certain tissues, which worsens the problem of general inadequate oxygenation. Vital organs develop hypoxia, and less vital organs experience anoxia (no oxygen) and ischemia (cell dysfunction or death from lack of oxygen). As a result of inadequate oxygenation and a buildup of toxic metabolites, some tissues experience extensive cell damage and ultimately die. The progressive stage of shock is a life-threatening emergency. Vital organs can tolerate this situation for only a short time before being permanently damaged. Immediate interventions are needed to reverse the effects of this stage of shock. Tolerance varies from person to person and depends greatly on pre-existing health. Usually the client’s life can be saved if the conditions causing shock are corrected within 1 hour of the onset of the progressive stage.

REFRACTORY STAGE OF SHOCK (IRREVERSIBLE STAGE) Formerly called the irreversible stage, the refractory stage of shock occurs when too much cell death and tissue damage results from too little oxygen reaching the tissues. As a result, the vital organs experience overwhelming changes. This stage is termed refractory because the body is unable to respond effectively to interventions, and the syndrome of shock continues. The remaining cells perform their metabolic functions anaerobically. Therapy is ineffective in saving the client’s life, even if the underlying cause of shock is corrected and MAP temporarily returns to normal. So much tissue damage has occurred, causing widespread release of toxic metabolites and destructive enzymes, that cell deterioration in vital organs continues

MULTIPLE ORGAN DYSFUNCTION SYNDROME 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 of events becomes a vicious cycle as more dead or dying cells break open and release more harmful metabolites. The metabolites cause the formation of small clots (microthrombi); this blocks tissue oxygenation and damages more cells, thus continuing the devastating cycle. MODS occurs first in the liver, heart, brain, and kidney. In sepsis-induced distributive shock, the lungs also are affected. The most profound change is deterioration of the heart muscle. One contributing factor is the release of myocardial depressant factor (MDF) from the ischemic pancreas.

Etiology Because shock is a manifestation of a pathologic condition rather than a disease state, its causes vary. Specific conditions leading to hypovolemic, cardiogenic, distributive, and obstructive shock are listed in Table 37-4. More than one type of shock can be present at the same time. For example, trauma caused by an automobile accident may trigger hemorrhage (leading to hypovolemic shock) and a myocardial infarction (leading to cardiogenic shock).

HYPOVOLEMIC SHOCK Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease so that the body’s total need for tissue oxygenation is not met. The most common conditions leading to hypovolemic shock are hemorrhage (external or internal) and dehydration. Hypovolemic shock caused by external hemorrhage is common after trauma, wounds, and surgery. Hypovolemic shock caused by internal hemorrhage occurs with blunt trauma, gastrointestinal (GI) ulcers, and poor control of surgical bleeding. External and internal hemorrhage can be caused by any health problem that reduces the levels of clotting factors (see Table 37-4). Hypovolemia as a result of dehydration can be caused by any condition that decreases fluid intake or increases fluid loss (see Table 37-4).

CARDIOGENIC SHOCK Cardiogenic shock occurs when the actual heart muscle is unhealthy and contraction is directly impaired. Table 37-4 lists the common causes of direct pump failure. These conditions decrease cardiac output and afterload, thus reducing MAP.

DISTRIBUTIVE SHOCK Distributive shock is caused by a loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased blood vessel permeability (leak). All of these factors can decrease mean arterial pressure (MAP) and may be induced either neurogenically or chemically.

NEURAL-INDUCED DISTRIBUTIVE SHOCK. Neural-induced loss of MAP occurs when sympathetic stimulation of the nerves controlling blood vessel smooth muscle is decreased and the smooth muscles of blood vessels relax, causing vasodilation. This blood vessel dilation can be a normal local response to injury, but shock results when the vasodilation is widespread or systemic. Common conditions that can cause a systemic loss of sympathetic tone are listed in Table 37-4.

CHEMICAL-INDUCED DISTRIBUTIVE SHOCK. Chemical-induced distributive shock has three common origins: anaphylaxis, sepsis, and capillary leak syndrome. Chemical-induced distributive shock occurs when certain chemicals or foreign substances within the blood and blood vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock can be induced by substances normally found in the body (endogenous).

ANAPHYLAXIS. Anaphylaxis is one result of type I allergic reactions. It usually begins within seconds to minutes after exposure to a specific allergen. However, it is termed delayed because this type of reaction rarely occurs the first time a person encounters the allergen. It occurs on repeated exposure to the same allergen (Guyton & Hall, 2000). Table 23-2 lists common allergens that can cause anaphylaxis. Anaphylaxis is due to an antigen-antibody reaction that occurs in blood vessels throughout the body in response to contact with a substance to which the person has a severe allergy (hypersensitivity). This widespread reaction involves the interaction of the allergen, immunoglobulin E (IgE), basophils, and mast cells. It occurs within the walls of blood vessels, heart muscle cells, and bronchial tubes. Anaphylaxis damages cells and causes the release of large amounts of histamine and other inflammatory chemicals. These substances move rapidly throughout the circulatory system, causing massive blood vessel dilation and increased capillary permeability. These responses result in severe hypovolemia and vascular collapse. Decreased cardiac contractility and dysrhythmias occur during anaphylaxis. These symptoms may be the direct result of heart muscle changes induced by the antigen-antibody reaction, or they may result from the profound hypovolemia. Antigen-antibody reactions in the bronchial tissues cause severe edema and pulmonary obstruc- tion, which greatly reduce gas exchange. The pulmonary problems, together with inadequate circulation, cause extreme whole-body hypoxia. Without intervention, this condition results in death.

SEPSIS. Sepsis leading to distributive shock occurs when microorganisms are present in the blood. This form of shock is most commonly called septic shock in clinical situations. Sepsis is often associated with disseminated intravascular coagulation (DIC). Distributive shock (septic shock) is more often associated with bacterial infection and has also been reported among clients with viral and yeast sepsis. Organisms often causing sepsis include gram-negative bacteria {Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae) and gram-positive bacteria (Staphylococcus and Streptococcus). Table 37-5 lists some of the conditions that put the client at risk for septic shock (sepsis-induced distributive shock). Septic shock results when large amounts of toxins and endotoxins produced by bacteria are secreted into the blood, causing a whole-body inflammatory reaction. These toxins and endotoxins react with blood vessels and cell membranes. Through the activity of white blood cells, the resulting reactions start inflammatory and immune events known as the systemic inflammatory response syndrome (SIRS). These toxin-host interactions activate complement, alter microcirculation within the vital organs (including selective coagulation and thrombus formation), increase capillary permeability (leakiness), cause cell injury, and increase cell metabolism (in combination with a decreased ability of some cells to take up needed oxygen). Metabolism becomes anaerobic because of decreased MAP, clot formation in capillaries, and poor cell uptake of oxygen.

CAPILLARY LEAK SYNDROME. Capillary leak syndrome leading to distributive shock occurs when there is a fluid shift from the blood to the interstitial space. Such shifts are caused by increased capillary permeability, loss of plasma osmolarity, and increased hydrostatic pressure in the blood. Specific conditions causing fluid shifts include severe burns, bullous skin disease, liver disorders, abdominal ascites, acute peritonitis, paralytic ileus, severe malnutrition, surgical wounds, hyperglycemia, kidney disease, hypoproteinemia, and trauma.

OBSTRUCTIVE SHOCK Obstructive shock is caused by conditions that affect the ability of the normal heart muscle to pump effectively. The heart itself is normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. Common causes of obstructive shock are listed in Table 37-4.

Incidence/Prevalence The exact incidence of shock is not known because it is a response rather than a separate disease entity. Some degree of shock is a common complication among hospitalized clients. Hypovolemic shock is the most common type experienced by clients in emergency departments and after surgery or invasive procedures. Cardiogenic shock is the most common complication of myocardial infarction in clients who experience damage to 40% or more of the heart muscle. The frequency of distributive shock as a result of sepsis, which has a 40% to 85% mortality rate, is increasing among clients who are immunocompromised or have infections (Ackerman, 1994; Clochesy, 1996). This chapter presents the collaborative management of clients experiencing hypovolemic shock caused by hemorrhage and distributive shock caused by sepsis.

COLLABORATIVE MANAGEMENT: HYPOVOLEMIC SHOCK

The Concept Map addresses assessment and nursing care issues related to clients with hypovolemic shock.

Assessment

HISTORY The nurse collects data on risk factors and causative factors related to hypovolemic shock. Age is important because hypovolemic shock associated with trauma is more common in young adults, whereas sepsis is more common among older adults. Clients are asked specific questions about recent illness, trauma, procedures, or chronic conditions that may lead to shock. Such conditions include gastrointestinal ulcers, general surgery, hemophilia, liver disorders, prolonged vomiting, and prolonged diarrhea. Medications such as aspirin, diuretics, and antacids may cause changes leading to hypovolemic shock or may indicate the presence of a problem that can contribute to hypovolemic shock. The nurse asks about fluid intake and output during the previous 24 hours. Information about urine output is especially important because the first stages of shock are characterized by a reduced urine output, even when fluid intake is normal. The nurse assesses the client and the immediate environment for obvious signs of factors leading to shock. Areas to examine for signs of hemorrhage include the gums, wounds, and sites of dressings, drains, and vascular access. The nurse observes for any swelling, skin discoloration, or manifestations of pain that may indicate an internal hemorrhage.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS

Most of the visible signs of hypovolemic shock are caused by the changes resulting from compensatory efforts. Compensation or compensatory mechanisms are physiologic responses that try to keep an adequate blood flow to vital organs. Signs of shock are first evident as changes in cardiovascular function. As shock progresses, changes in the kidney, respiratory, integumentary, musculoskeletal, and central nervous systems become evident.

CARDIOVASCULAR MANIFESTATIONS. Shock involves a decrease of mean arterial pressure (MAP), and the resulting early compensation is cardiovascular. Therefore the earliest clinical signs of hypovolemic shock are also cardiovascular.

PULSE. The nurse or assistive nursing personnel assesses the central and peripheral pulses for rate and quality. In the initial stage of hypovolemic shock, the pulse rate increases 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 usually decreased. Because stroke volume is decreased, the peripheral pulses are more difficult to palpate and are easily blocked with light pressure. As hypovolemic shock progresses, superficial peripheral pulses may be absent.

BLOOD PRESSURE. Changes in systolic blood pressure are not always present in the initial stage of hypovolemic shock. When assessing the blood pressure of a client at risk for shock, the nurse considers the client’s normal baseline blood pressure level. Although a blood pressure of 90/50 may indicate severe shock in one person, it may be the normal blood pressure value for another healthy adult. When vasoconstriction is present, diastolic pressure increases but systolic pressure remains the same. As a result, the pulse pressure, or the difference between the systolic and diastolic pressures, is smaller. The blood pressure is monitored for changes from baseline levels and for changes from the previous measurement. For accuracy, the same equipment is used on the same extremity. When possible, the nurse measures blood pressure with the client in the lying, sitting, and standing positions. Systolic pressure decreases as shock progresses and cardiac output decreases; this reduces the pulse pressure even further. When shock continues and interventions are not adequate, compensation fails and systolic and diastolic pressures decrease. At this stage, blood pressure is difficult to hear. Palpation or a Doppler device may be needed to detect the systolic blood pressure.

OXYGEN SATURATION. Peripheral oxygen saturation is assessed through pulse oximetry. Hemoglobin oxygen saturation values between 90% and 95% are associated with the nonprogressive stage of shock, and values between 75% and 80% are associated with the progressive stage of shock. Any value below 70% is considered a life-threatening emergency and may signal the refractory stage of shock.

INTEGUMENTARY MANIFESTATIONS. Skin changes occur in shock because of decreased perfusion. An early compensatory mechanism for hypovolemic shock is vasoconstriction in the skin, which results in minimal perfusion. This allows more blood to circulate to the vital organs, which cannot tolerate low oxygen levels. The skin is assessed for temperature, color, and degree of moisture. It feels cool or cold to the touch, and the color is pale to cyanotic. Color changes are first evident in the mucous membranes and in the skin around the mouth. Pallor or cyanosis may be difficult to observe in many areas in darkskinned clients, and the nurse particularly assesses color changes in oral mucous membranes. As shock progresses, color changes in clients with lighter skin are noted first in the extremities and then in the central trunk area. The skin also feels clammy or moist to the touch, not because sweating increases but because the normal fluid lost through the skin does not evaporate quickly on cold skin. Capillary refill time is evaluated by pressing on the client’s fingernail until it blanches and then observing how fast the nail bed resumes color when pressure is released. Normally the nail bed capillaries resume color as soon as pressure is released. With shock, capillary refill is usually slow and is sometimes absent.

RESPIRATORY MANIFESTATIONS. The nurse assesses the rate, depth, and ease of respiration and also auscultates the lungs for abnormal breath sounds. Respiratory rate increases during hypovolemic shock. This increase is a compensatory mechanism to provide adequate oxygen to the critical tissues. When shock progresses to the stage at which lactic acidosis is present, the depth of respiration also increases.

KIDNEY/URINARY MANIFESTATIONS. The renal system compensates for decreased MAP by conserving body water through decreased filtration and increased water reabsorption. Urine is assessed for color, specific gravity, and the presence of blood or protein. The nurse or assistive nursing personnel measures urine output every hour. In severe shock, urine output is decreased (compared with fluid intake) or even absent. Of the four vital organs (heart, brain, liver, and kidney), only the kidney can tolerate hypoxia and anoxia for up to 1 hour without permanent damage. When hypoxic or anoxic conditions persist beyond this time, clients are at grave risk for acute tubular necrosis (ATN) and renal failure.

CENTRAL NERVOUS SYSTEM MANIFESTATIONS. Clients in hypovolemic shock are thirsty. This sensation is caused by stimulation of the osmoreceptors in the brain in response to decreased blood volume. The nurse assesses the client’s level of consciousness (LOC) and orientation to person, time, and place. Most causes of hypovolemic shock do not interfere with the transmission of nerve impulses. The central nervous system manifestations of hypovolemic shock are instead associated with cerebral hypoxia. In the initial and nonprogressive stages, clients may be restless or agitated and may be anxious or have a feeling of impending doom that has no obvious cause. As hypoxia progresses, clients become confused and lethargic. Lethargy progresses to somnolence and loss of consciousness as cerebral hypoxia worsens.

MUSCULOSKELETAL MANIFESTATIONS. Tissue hypoxia, anaerobic metabolism, and lactic acidosis cause weakness and pain in skeletal muscle. This weakness is generalized and has no specific pattern. The electrolyte disturbances in the progressive and refractory stages of shock worsen muscle weakness by interfering with action potentials. In this situation, deep tendon reflexes are decreased or absent. The nurse assesses muscle strength by having the client squeeze the nurse’s hand and try to keep the arms flexed while the nurse pulls downward on the lower arms. Deep tendon reflexes are assessed by lightly tapping the patellar tendons and Achilles tendons with a reflex hammer and observing the degree of reflexive movement.

PSYCHOSOCIAL ASSESSMENT Changes in mental status and behavior may be early signs of hypovolemic shock. The nurse observes the client closely and documents behavior. The nurse assesses current mental status by evaluating LOC and noting whether the client is asleep or awake. If the client is asleep, the nurse attempts to awaken him or her and documents how easily he or she is aroused. If the client is awake, the nurse establishes whether he or she is oriented to person, time, and place.

Questions that can be answered with a “yes” or a “no” response are avoided. The following points are considered during evaluation:

• Is it necessary to repeat questions to obtain a response?

• Does the response answer the question asked?

• Does the client have difficulty making word choices?

• Is the client irritated or upset by the questions?

• Can the client concentrate on a question long enough to answer appropriately, or is attention span limited?

If possible, the nurse questions family members or a significant other to determine whether the client’s behavior and mental status are typical.

LABORATORY ASSESSMENT Although no single laboratory finding confirms or rules out the presence of shock, changes in laboratory data may support the diagnosis of hypovolemic shock. (Chart 37-2 lists the common laboratory findings associated with hypovolemic shock.)

As shock progresses, arterial blood gas values become abnormal. The pH usually decreases, the partial pressure of arterial oxygen (Pao2) decreases, and the partial pressure of arterial carbon dioxide (Paco2) increases. Changes in other laboratory values may be associated with specific causes of hypovolemic shock. Hematocrit and hemoglobin concentrations decrease if hypovolemic shock is caused by hemorrhage. When hypovolemic shock is the result of dehydration or a fluid shift, hematocrit and hemoglobin values are elevated.

Interventions Interventions for clients in hypovolemic shock are focused on reversing the shock, restoring fluid volume, and preventing ischemic complications through supportive and drug therapies. Surgery may be necessary to correct the underlying problem leading to hypovolemic shock. Chart 37-3 summarizes best practices for clients in hypovolemic shock. Chart 37-4 lists selected interventions based on the Nursing Interventions Classification (NIC) for clients with hypovolemic shock.

NONSURGICAL MANAGEMENT. The goals of intervention are to maintain tissue oxygenation, increase body fluid compartment volumes to normal ranges, and support operating compensatory mechanisms. Oxygen therapy, intravenous (IV) therapy, fluid replacement therapy, and drug therapies are the management choices for this problem.

OXYGEN THERAPY.

VIDEO

Oxygen therapy is useful whenever shock is present. Oxygen can be administered by mask, hood, nasal cannula, nasopharyngeal tube, endotracheal tube, and tracheostomy tube. Oxygen is administered in liters per minute (for administration via cannula) or concentration by percentage (for administration by mask), as specified by the health care provider’s order.

INTRAVENOUS THERAPY. Colloids and crystalloids are the two types of fluids commonly used for volume replacement during hemorrhagic hypovolemia. IV colloid solutions are used to restore plasma volume and colloidal osmotic pressure and contain large molecules (usually proteins or starches). IV crystalloid solutions are given for fluid and electrolyte replacement and contaionprotein substances (e.g., minerals, salts, and sugars). A current controversy involves the infusion rate of fluids when hypovolemia is a result of hemorrhage that has not yet been controlled. A consideration is that the rapid infusion of large-volume IV fluids can increase blood pressure and may actually increase the rate of blood loss (see the Evidence-Based Practice for Nursing box on p. 781).

Colloid Fluid Replacement. Protein-containing colloid fluids are good for restoring vascular osmotic pressure and fluid volume. Blood and blood products are often used for this purpose and are the treatment of choice for hypovolemia caused by blood loss. These products include whole blood, packed red blood cells, plasma, plasma fractions, and synthetic plasma expanders. Whole blood and packed red blood cells increase hematocrit and hemoglobin concentrations as well as vascular fluid volume. Whole blood is used to replace large volumes of blood loss because it provides increased intravascular volume while improving the oxygen-carrying capacity of the blood. Packed red cells are given for moderate blood loss because they replenish the red blood cell deficit and improve oxygencarrying capacity without adding excessive fluid volume. Chapter 40 discusses nursing care issues in blood and blood product administration. Human plasma, an acellular blood product containing some clotting factors, is given to correct plasma deficits and restore osmotic pressure when hematocrit and hemoglobin levels are withiormal ranges. Plasma protein fractions (e.g., Plasmanate) and synthetic plasma expanders (e.g., hetastarch [hydroxyethyl starch, Hespan]) increase plasma volume and are often used as early treatment for hypovolemic shock before a cause has been established.

Crystalloid Fluid Replacement. Crystalloid solutions are given to help establish and maintain an adequate fluid and electrolyte balance. Two common crystalloid solutions are Ringer’s lactate and normal saline. Ringer’s lactate contains physiologic concentrations of sodium, chloride, calcium, potassium, and lactate dissolved in water. This isotonic solution is a good volume expander, and the lactate is a buffer in the presence of acidosis. Normal saline (0.9% sodium chloride in water) is a fluid replacement used to increase plasma volume when there has beeo loss of red blood cells.

DRUG THERAPY. Medications may be necessary if the volume deficit is severe and the client does not respond sufficiently to the replacement of fluid volume and blood products. The actions of drugs for shock increase venous return, improve cardiac contractility, or ensure adequate cardiac perfusion through dilation of the coronary vessels. Chart 37-5 lists the drugs commonly used to treat hypovolemic shock.

Vasoconstricting Agents. Many drugs stimulate venous return by causing vasoconstriction and decreasing venous pooling of blood. These actions increase cardiac output and mean arterial pressure (MAP), which helps to improve tissue perfusion and oxygenation. Examples of such agents include dopamine (Intropin, Reviminc) and norepinephrine (Levophed). Most of these drugs produce serious side effects, and their dosages must be carefully calculated on the basis of the client’s size and degree of response (see Chart 37-5).

Agents Enhancing Myocardial Contractility. Some drugs directly stimulate adrenergic receptor sites on the heart muscle (especially beta, receptors) and increase the contraction of the cardiac muscle cells. Other agents enhance cardiac contractility—they slow heart rate by altering electrical conduction and allowing the left ventricle a longer filling time. When filling time is increased, more blood enters the left ventricle and stretches the muscle fibers. Thus greater recoil is achieved, and more blood leaves the left ventricle during contraction. Some of these drugs also stimulate the ventricles. Agents with these types of actions include digoxin (Lanoxin) and dobutamine (Dobutrex).

Agents Enhancing Myocardial Perfusion. The treatment of shock includes giving agents that cause systemic vasoconstriction to help enhance venous return and increase MAP. It is important to ensure that the heart is well perfused so that aerobic metabolism is maintained in the cardiac cells and maximum contractility can be achieved. Agents that dilate coronary blood vessels while causing minimal systemic vasodilation are used for this purpose. A common agent with this action is sodium nitroprusside (Nitropress, Nipride). Care is taken because higher dosages can cause some systemic vasodilation and increase shock.

MONITORING. A major nursing responsibility in caring for the client in hypovolemic shock is monitoring his or her vital signs and level of consciousness (LOC).

On the acute nursing unit, the nurse monitors the client’s:

Ø Pulse

Ø Blood pressure

Ø Pulse pressure

Ø Central venous pressure

Ø Respiratory rate

Ø Skin and mucosal color

Ø Oxygen saturation

These parameters are assessed at least every 15 minutes until the shock is under control and the client’s condition improves. More extensive monitoring of cardiac output (hemodynamic monitoring) occurs in critical care settings and includes intra-arterial monitoring, mixed venous oxygen saturation (Svo2), and pulmonary artery wedge pressures. Clients in shock are transported to a critical care unit if they require more invasive monitoring such as central venous pressure (CVP), pulmonary artery pressure (PAP), and pulmonary artery wedge pressure (PAWP). Table 37-6 compares the changes in hemodynamic patterns seen with different types of shock.

Insertion of a CVP catheter allows pressure to be monitored in the client’s right atrium or superior vena cava while providing venous access. Changes in CVP reflect hypovolemic shock. As circulating volume decreases, the amount of blood returning to the right atrium also decreases, causing the CVP to decrease from baseline levels. Intra-arterial catheter placement provides a means of monitoring blood pressure continuously and serves as an access for arterial blood sampling. Intra-arterial catheters are inserted into an artery (radial, brachial, femoral, or dorsalis pedis). The arterial catheter is attached to pressure tubing and a transducer. The transducer converts pressure in the artery (mechanical energy) into an electrical signal that is expressed as a visible waveform on an oscilloscope, and a digital numeric value is displayed.

SURGICAL MANAGEMENT. The nurse monitors fluid loss and uses the nonsurgical interventions described on pp. 779-781 to stabilize the client’s hemodynamic status. After a cause has been established, surgical intervention may be necessary to correct the underlying problem. Such interventions include vascular repair or revision, surgical hemostasis of major wounds, closure of bleeding ulcers, and chemical scarring (chemosclerosis) of varicosities.

COLLABORATIVE MANAGEMENT: SEPSIS-INDUCED DISTRIBUTIVE SHOCK (SEPTIC SHOCK)

Assessment Distributive shock caused by sepsis does not resemble other types of shock in that it has two distinctive phases (Figure 37-2).

The first phase is relatively long, often lasting from hours to a day or longer. The clinical manifestations during this phase are subtle. The chance for recovery is good when the client is recognized as being in the first phase of septic shock and the appropriate interventions are made. The second phase of septic shock has a sudden onset and a rapid downhill course. If septic shock progresses without intervention to the second phase, chances for recovery are slim. Identification of the first phase of sepsis-induced distributive shock can make the greatest difference in survival.

HISTORY The nurse collects data about risk factors and causative factors related to septic shock. Age is important because sepsis can develop more easily among older, debilitated people with any degree of immunosuppression. Chart 37-6 lists some of the factors that increase the older adult’s risk for shock.

Clients are asked specific questions about recent illness, trauma, or procedures or chronic conditions that may lead to sepsis and distributive shock. The use of some medications may directly cause changes leading to shock. A medication regimen may also indicate a disease or problem that can contribute to septic shock. Such medications include aspirin and aspirin-containing drugs, antibiotics, and chemotherapeutic agents.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS Many of the clinical manifestations of the first phase are unique to septic shock and are often opposite from those associated with all other types of shock. Chart 37-7 summarizes the clinical manifestations of the first (hyperdynamic) phase of septic shock. These findings result from the body’s reaction to endotoxins and affect the cardiovascular, integumentary, pulmonary, immune, and hematologic systems.

CARDIOVASCULAR MANIFESTATIONS. Endotoxins in the blood interact with white blood cells and blood vessel walls to trigger an inflammatory reaction. Some endotoxins ap- pear to stimulate the heart muscle directly. As a result, cardiac output actually increases during the first phase of septic shock.

This phase is hyperdynamic and also may be called the highoutput or warm-shock phase. Increased cardiac output is reflected by tachycardia, increased stroke volume, a normal-to-elevated systolic blood pressure, and a normal CVP. Increased cardiac output and vasodilation cause good perfusion of the skin so that it appears normal in color with pink mucous membranes and may feel warm to the touch. This situation is temporary, and eventually the cardiac output greatly diminishes in clients in septic shock. As septic shock progresses, disseminated intravascular coagulation (DIC) may occur. The endotoxins and inflammatory reactions stimulate the activation of complement. These actions cause thousands of small clots to form in the tiny capillaries of vascular organs (e.g., liver, kidney, brain, spleen, and heart). These small clots interfere with oxygenation in those organs, causing hypoxia and ischemia and making overall metabolism anaerobic. This enormous number of small clots uses clotting factors and fibrinogen faster than they can be regenerated by the liver, which makes clients much more susceptible to hemorrhage. These occurrences mark the beginning of the second phase of septic shock. Because some of the blood has already clotted, most of the clotting factors are gone, and the blood vessels are dilated. Clients are hypovolemic in this phase of septic shock. Cardiac output, systolic blood pressure, and pulse pressure decrease dramatically.

This phase is called the hypodynamic, lowoutput, or cold-shock phase of septic shock. The clinical manifestations of this phase resemble those of the later stages of all forms of shock.

RESPIRATORY MANIFESTATIONS. In the hyperdynamic phase of septic shock, respiratory rate and depth are increased. Clients often experience a respiratory alkalosis. When septic shock progresses to the hypodynamic phase, the possible life-threatening pulmonary complication of acute respiratory distress syndrome (ARDS) may occur. Although this complication has many causes, ARDS in cases of sepsis is thought to be related to the formation of oxygen free radicals, which damage the pulmonary cells. Oxygen free radicals can form as a result of oxygen therapy and in response to cellular destruction and the subsequent release of oxidizing enzymes. The presence of ARDS in a client with septic shock is an ominous clinical sign and is associated with a high mortality rate.

INTEGUMENTARY MANIFESTATIONS. Clients in the hyperdynamic phase of septic distributive shock often are not recognized as having a problem. The appearance of the skin and mucous membranes leads health care professionals to believe that circulation is unimpaired. Clients feel warm to the touch, and their lips and mucous membranes appear well oxygenated. When septic shock progresses so that circulation is compromised in the hypodynamic phase, the skin is cool and clammy, and pallor or cyanosis is present. In clients with DIC, petechiae and ecchymoses can occur anywhere. Blood may ooze from the gums, other mucous membranes, and venipuncture sites, as well as around IV catheters.

PSYCHOSOCIAL ASSESSMENT The indicator that all is not well with clients at the beginning of septic shock is often a change in affect or behavior. The nurse compares the client’s presenting behavior, verbal responses, and general affect with those assessed earlier in the day or the day before and notes changes. Clients may seem just slightly different in their reactions to greetings, comments, or jokes. They may be less patient than usual or act restless or fidgety. They may verbalize feelings such as, “I feel as if something is wrong, but I don’t know what.” If this behavior represents a change from prior assessments, the nurse always considers the possibility of sepsis and shock.

LABORATORY ASSESSMENT The presence of bacteria in the blood and other extracellular fluids supports the diagnosis of sepsis. The nurse obtains specimens of urine, blood, sputum, and any drainage for culture to identify the causative organisms for both diagnostic and therapeutic purposes. Other abnormal laboratory findings associated with septic shock include changes in the white blood cell count; the differential leukocyte count may demonstrate a left shift (see Chapter 20). Changes in hematocrit and hemoglobin levels usually are not evident until late in septic shock, when the client is hemorrhaging. At that point, the hematocrit and hemoglobin levels, fibrinogen levels, and platelet count are low

Analysis A common collaborative problem for clients with septic shock is Potential for Multiple Organ Dysfunction Syndrome (MODS).

Planning and Implementation

PLANNING: EXPECTED OUTCOMES. The client in septic shock is expected to have normal arterial blood gases, maintain a urine output of at least 20 mL/hr, and have a mean arterial blood pressure within 10 mm Hg of baseline.

INTERVENTIONS. Interventions for the client experiencing septic shock focus on correcting the conditions causing shock and on preventing complications. Chart 37-8 summarizes the best practices for clients experiencing septic shock. Control of fluid volume deficit associated with septic shock is accomplished through supportive and drug therapies. IV therapy is the same as for hypovolemic shock.

OXYGEN THERAPY. Oxygen therapy is useful whenever inadequate tissue perfusion and inadequate oxygenation are present, such as during distributive shock. Oxygen therapy for septic shock is administered in the same ways as for hypovolemic shock.

DRUG THERAPY. The same agents used to enhance cardiac output and restore vascular volume in hypovolemic shock are used for septic shock. A major focus is the administration of antibiotics to combat sepsis. In addition, agents to counteract disseminated intravascular coagulation (DIC) may be required. Septic shock and DIC have two distinctly different phases, and the drug therapies for each phase of septic shock are different. Drug therapy in the first phase is aimed at preventing coagulation and usually consists of heparin administration. Drug therapy in the second, late phase of septic shock is aimed at increasing the blood’s ability to clot and usually consists of the administration of clotting factors, plasma, platelets, or other blood products.

ANTIBIOTICS. Although sepsis and distributive shock can be caused by any microorganism, the most common agents are gram-negative bacteria. When blood cultures have identified specific bacteria, IV antibiotics with known activity against the bacteria are administered. Multiple agents with wide activity are prescribed when the causative agent is not known. A common “triple-antibiotic” regimen includes vancomycin, one of the aminoglycosides (e.g., amikacin, streptomycin, kanamycin, gentamicin), and a systemic penicillin or cephalosporin.

ANTIBODIES. Antibodies against the body’s mediators for inflammation are being tested for their effectiveness in septic shock. Antibodies have been developed against the different substances produced by white blood cells to stimulate the inflammatory response. The mediators thought to start the inflammatory responses in blood vessels and lead to the cascade of septic shock are interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF). This experimental therapy shows promise in reducing the extensive mortality associated with septic shock (Clochesy, 1996; Workman, 1995).

ANTICOAGULANTS. When clients are identified as being in the early phase of septic shock and are beginning to form numerous small clots, heparin is given to limit unnecessary clotting and to prevent the consumption of clotting factors.

CLOTTING FACTORS AND BLOOD PRODUCTS. When septic shock progresses to the point that small clots have formed to such an extent that the client no longer has sufficient clotting factors to prevent hemorrhage, clotting factors are given intravenously. These factors are obtained from pooled human serum. Infusing fresh frozen plasma also helps to replace clotting factors. In addition, platelets or other blood products may be needed.

PROVIDING A SAFE ENVIRONMENT. Primary prevention is possible for some types of shock by identifying clients at risk for conditions and complications leading to sepsis and preventing those complications. Strict adherence to aseptic technique during invasive procedures and during the manipulation of nonintact skin and mucous membranes in immunocompromised clients can help to prevent or limit sepsis and septic shock. Early detection of the clinical manifestations of shock is a major nursing responsibility. Because shock is a common complication of many conditions found in acute care settings, the nurse always considers the possibility of septic shock. For early detection, the nurse frequently assesses vital signs for specific changes from normal values or from baseline levels. After distributive shock is recognized, health care providers rapidly take action to halt or change the conditions contributing to shock, to support the physiologic compensatory mechanisms, and to prevent life-threatening complications.

Community-Based Care For most clients, shock is a complication of another condition and is resolved before they are discharged from the emergency department or acute care setting. Because more clients are receiving treatment on an outpatient basis and are being discharged earlier from acute care settings, more

HOME CARE MANAGEMENT The nurse or home care aide evaluates the home environment for safety regarding infection hazards. General cleanliness is noted, and particular attention is given to the kitchen and bathrooms. Chart 37-10 lists focused client and environmental assessment data to obtain during a home visit.

Evaluation: Outcomes The nurse evaluates the care of the client with sepsis-induced distributive shock. The expected outcomes are that the client:

• Maintains oxygen saturation (as measured by pulse oximetry) of at least 85%

• Maintains a urine output of at least 20 mL/hr Has arterial blood gas values within the normal range

• Has a mean arterial pressure within 10 mm Hg of baseline

• Does not experience multiple organ dysfunction syndrome (MODS)

• Correctly states measures to reduce the risk for sepsis

Signs and symptoms

The presentation of shock is variable with some people having only minimal symptoms such as confusion and weakness.^[2] While the general signs for all types of shock are low blood pressure, decreased urine output, and confusion these may not always be present.^[2] While a fast heart rate is common, those on β-blockers, those who are athletic and in 30% of cases those with shock due to intra abdominal bleeding may have a normal or slow heart rate.^[5] Specific subtypes of shock may have additional symptoms.

Hypovolemic

Hemorrhage classes^[6]

Class

Blood loss

Response

Treatment

<15 %(0.75 l)

min. fast heart rate, normal blood pressure

minimal

15-30 %(0.75-1.5 l)

fast heart rate, min. low blood pressure

intravenous fluids

III

30-40 %(1.5-2 l)

very fast heart rate, low blood pressure, confusion

fluids and packed RBCs

>40 %(>2 l)

critical blood pressure and heart rate

aggressive interventions

Hypovolemia is a direct loss of effective circulating blood volume leading to:

· A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia

· Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction

· Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis

· Hypothermia due to decreased perfusion and evaporation of sweat

· Thirst and dry mouth, due to fluid depletion

· Cold and mottled skin (Livedo reticularis), especially extremities, due to insufficient perfusion of the skin

The severity of hemorrhagic shock can be graded on a 1-4 scale on the physical signs. This approximates to the effective loss of blood volume.

Cardiogenic

Symptoms of cardiogenic shock include:

· Distended jugular veins due to increased jugular venous pressure

· Weak or absent pulse

· Arrhythmia, often tachycardic

· Pulsus paradoxus in case of tamponade

Distributive

Systemic inflammatory response syndrome^[7]

Finding

Value

Temperature

<36 °C (96.8 °F) or >38 °C (100.4 °F)

Heart rate

>90/min

Respiratory rate

>20/min or PaCO2<32 mmHg (4.3 kPa)

WBC

<4×10⁹/L (<4000/mm³), >12×10⁹/L (>12,000/mm³), or 10% bands

Distributive shock includes infectious, anaphylactic, Endocrine and neurogenic causes. The SIRS features typically occur in early septic shock.^[2]

Pathophysiology

Effects of inadequate perfusion on cell function.

There are four stages of shock. As it is a complex and continuous condition there is no sudden transition from one stage to the next.^[8] At a cellular level shock is the process of oxygen demand becoming greater than oxygen supply.^[2]

Initial

During this stage, the state of hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform lactic acid fermentation. Since oxygen, the terminal electron acceptor in the electron transport chain is not abundant, this slows down entry of pyruvate into the Krebs cycle, resulting in its accumulation. Accumulating pyruvate is converted to lactate by lactate dehydrogenase and hence lactate accumulates (causing lactic acidosis).

Compensatory

This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of theacidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO₂). CO₂indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release ofepinephrine and norepinephrine. Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. Renin–angiotensin axis is activated and arginine vasopressin (Anti-diuretic hormone; ADH) is released to conserve fluid via the kidneys. These hormones cause the vasoconstriction of the kidneys,gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the Renin–angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock.^[^{citation needed}^]

Progressive

Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body’s metabolic acidosis, the arteriolar smooth muscle and precapillarysphincters relax such that blood remains in the capillaries.^[9] Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and proteininto the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.^[9] If the bowel becomes sufficiently ischemic, bacteria may enter the blood stream, resulting in the increased complication of endotoxic shock.^[3][9]

Refractory

At this stage, the vital organs have failed and the shock cao longer be reversed. Brain damage and cell death are occurring, and death will occur imminently. One of the primary reasons that shock is irreversible at this point is that much cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid. Because cells can only produce adenosine at a rate of about 2% of the cell’s total need per hour, even restoring oxygen is futile at this point because there is no adenosine to phosphorylate into ATP.^[3]

Septic shock

· Systemic leukocyte adhesion to endothelial tissue^[9]

· Reduced contractility of the heart^[9]

· Activation of the coagulation pathways, resulting in disseminated intravascular coagulation^[9]

· Increased levels of neutrophils^[9]

Main manifestations are produced due to massive release of histamine which causes intense vasodilation.

Diagnosis

The first changes seen in shock is an increased cardiac output followed by a decrease in mixed venous oxygen saturation (SmvO2) as measured in the pulmonary artery via a pulmonary artery catheter. Central venous oxygen saturation (ScvO2) as measured via a central line correlates well with SmvO2 and are easier to acquire. If shock progresses anaerobic metabolism will begin to occur with an increased blood lactic acid as the result. While many laboratory tests are typically performed there is no test that either makes or excludes the diagnosis. A chest X-ray or emergency department ultrasound may be useful to determine volume state.^[2][5]

Differential diagnosis

Shock is a common end point of many medical conditions.^[1] It has been divided into four main types based on the underlying cause: hypovolemic, distributive, cardiogenic and obstructive.^[10] A few additional classifications are occasionally used including: endocrinologic shock.^[1]

Hypovolemic

Hypovolemic shock is the most common type of shock and is caused by insufficient circulating volume.^[2] Its primary cause is hemorrhage (internal and/or external), or loss of fluid from thecirculation. Vomiting and diarrhea are the most common cause in children.^[1] With other causes including burns, environmental exposure and excess urine loss due to diabetic ketoacidosis anddiabetes insipidus.^[1]

Cardiogenic

Cardiogenic shock is caused by the failure of the heart to pump effectively.^[2] This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include dysrhythmias, cardiomyopathy/myocarditis, congestive heart failure (CHF), contusio cordis, or cardiac valve problems.^[1]

Obstructive

Obstructive shock is due to obstruction of blood flow outside of the heart.^[2] Several conditions can result in this form of shock.

· Cardiac tamponade^[1] in which fluid in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.

· Tension pneumothorax^[1] Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return).

· Pulmonary embolism is the result of a thromboembolic incident in the blood vessels of the lungs and hinders the return of blood to the heart.

· Aortic stenosis hinders circulation by obstructing the ventricular outflow tract

Distributive

Distributive shock is due to impaired utilization of oxygen and thus production of energy by the cell.^[2] Examples of this form of shock are:

· Septic shock is the most common cause of distributive shock.^[1] Caused by an overwhelming systemic infection resulting in vasodilation leading to hypotension. Septic shock can be caused by Gram negative bacteria such as (among others) Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces adverse biochemical, immunological and occasionally neurological effects which are harmful to the body, and other Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive bacterial toxins. Septic shock also includes some elements of cardiogenic shock. In 1992, the ACCP/SCCM Consensus Conference Committee defined septic shock: “. . .sepsis-induced hypotension (systolic blood pressure < 90 mmHg or a reduction of 40 mmHg from baseline) despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include, but are not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Patients who are receiving inotropic or vasopressor agents may have a normalized blood pressure at the time that perfusion abnormalities are identified.”

· Anaphylactic shock Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation, leading to hypotension and increased capillary permeability.

· High spinal injuries may cause neurogenic shock.^[11] The classic symptoms include a slow heartrate due to loss of cardiac sympathetic tone and warm skin due to dilation of the peripheral blood vessels.^[11] (This term can be confused with spinal shock which is a recoverable loss of function of the spinal cord after injury and does not refer to the haemodynamic instability per se.)

Endocrine

Based on endocrine disturbances such as:

· Hypothyroidism (Can be considered a form of Cardiogenic shock) in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.

· Thyrotoxicosis (Cardiogenic shock)

· may induce a reversible cardiomyopathy.

· Acute adrenal insufficiency (Distributive shock) is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.

· Relative adrenal insufficiency (Distributive shock) in critically ill patients where present hormone levels are insufficient to meet the higher demands

Management

The best evidence exists for the treatment of septic shock in adults and as the pathophysiology appears similar in children and other types of shock treatment this has been extrapolated to these areas.^[1] Management may include securing the airway via intubation to decrease the work of breathing, oxygen supplementation, intravenous fluids and a passive leg raise (not Trendelenburg position), and blood transfusions.^[2] It is important to keep the person warm as well as adequately manage pain and anxiety as these can increase oxygen consumption.^[2]

Fluids

Aggressive intravenous fluids are recommended in most types of shock (e.g. 1-2 liter normal saline bolus over 10 minutes or 20ml/kg in a child) which is usually instituted as the person is being further evaluated.^[12] Which intravenous fluid is superior, colloids or crystalloids, remains undetermined.^[2] Thus as crystalloids are less expensive they are recommended.^[13] If the person remains in shock after initial resuscitation packed red blood cells should be administered to keep the hemoglobin greater than 100 gms/l.^[2]

For those with hemorrhagic shock the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension).^[14] Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70-90 mmHg,^[2][15] or until their adequate mentation and peripheral pulses.^[15]

Medications

Vasopressors may be used if blood pressure does not improve with fluids. There is no evidence of superiority of one vasopressor over another.^[16] Vasopressors have not been found to improve outcomes when used for hemorrhagic shock from trauma^[17] but may be of use in neurogenic shock.^[11] Activated protein C (Xigris) while once aggressively promoted for the management of septic shock has been found to improve survival and is associated with a number of complications, thus recommended.^[18] The use of sodium bicarbonate is controversial as it has not been shown to improve outcomes.^[19] If used at all it should only be considered if the pH is less than 7.0.^[19]

Treatment goals

The goal of treatment is to achieve a urine output of greater than 0.5 ml/kg/h, a central venous pressure of 8-12 mmHg and a mean arterial pressure of 65-95 mmHg. In trauma the goal is to stop the bleeding which in many cases requires surgical interventions.

Epidemiology

Hemorrhagic shock occurs in about 1-2% of trauma cases.^[15]

Prognosis

The prognosis of shock depends on the underlying cause and the nature and extent of concurrent problems. Hypovolemic, anaphylactic and neurogenic shock are readily treatable and respond well to medical therapy. Septic shock however, is a grave condition with a mortality rate between 30% and 50%. The prognosis of cardiogenic shock is even worse.

This phase is called the hypodynamic, lowoutput, or cold-shock phase of septic shock. The clinical manifestations of this phase resemble those of the later stages of all forms of shock.

Analysis A common collaborative problem for clients with septic shock is Potential for Multiple Organ Dysfunction Syndrome (MODS).

Planning and Implementation

Evaluation: Outcomes The nurse evaluates the care of the client with sepsis-induced distributive shock. The expected outcomes are that the client:

• Maintains oxygen saturation (as measured by pulse oximetry) of at least 85%

• Maintains a urine output of at least 20 mL/hr Has arterial blood gas values within the normal range

• Has a mean arterial pressure within 10 mm Hg of baseline

• Does not experience multiple organ dysfunction syndrome (MODS)

• Correctly states measures to reduce the risk for sepsis

This phase is called the hypodynamic, lowoutput, or cold-shock phase of septic shock. The clinical manifestations of this phase resemble those of the later stages of all forms of shock.

Analysis A common collaborative problem for clients with septic shock is Potential for Multiple Organ Dysfunction Syndrome (MODS).

Planning and Implementation

DRUG THERAPY.

The same agents used to enhance cardiac output and restore vascular volume in hypovolemic shock are used for septic shock. A major focus is the administration of antibiotics to combat sepsis. In addition, agents to counteract disseminated intravascular coagulation (DIC) may be required. Septic shock and DIC have two distinctly different phases, and the drug therapies for each phase of septic shock are different. Drug therapy in the first phase is aimed at preventing coagulation and usually consists of heparin administration. Drug therapy in the second, late phase of septic shock is aimed at increasing the blood’s ability to clot and usually consists of the administration of clotting factors, plasma, platelets, or other blood products.