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ch 37 shock

Terms in this set (54)

types of shock
hypovolemic cardiogenic, distributive
cardiovascular manifestations of shock
• 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 Manifestations
• Increased respiratory rate
• Shallow depth of respirations
• Increased Paco2
• Decreased Pao2
• Cyanosis, especially around lips and nail beds
Gastrointestinal Manifestations
• Decreased motility
• Diminished or absent bowel sounds
• Nausea and vomiting
• Constipation
Paco2, Partial pressure of arterial carbon dioxide; Pao2, partial pressure of arterial oxygen.
Neuromuscular Manifestations
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
Integumentary Manifestations
• Cool to cold
• Pale to mottled to cyanotic
• Moist, clammy
• Mouth dry; pastelike coating present
risk factors for hypovolemic shock
• 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-pump failure risks (fluid volume not affected)
• Myocardial infarction
• Cardiac arrest
• Ventricular dysrhythmias
• Cardiac amyloidosis
• Cardiomyopathies
• Myocardial degeneration
Distributive Shock
Fluid shifted from central vascular space (total body fluid volume normal or increased).
• Neural-induced
• Pain
• Anesthesia
• Stress
• Spinal cord injury
• Head trauma
• Chemical-induced
• Anaphylaxis
• Sepsis
• Capillary leak
• Burns
• Extensive trauma
• Liver impairment
• Hypoproteinemia
Obstructive Shock
Cardiac function decreased by noncardiac factor (indirect pump failure). Total body fluid is not affected although central volume is decreased.
• Cardiac tamponade
• Arterial stenosis
• Pulmonary embolus
• Pulmonary hypertension
• Constrictive pericarditis
• Thoracic tumors
• Tension pneumothorax
Perfusion is related to mean arterial pressure (MAP). The factors that influence MAP include:
mean arterial pressure (MAP). The factors that influence MAP include:
• Total blood volume
• Cardiac output
• 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.
Blood vessels are innervated by the sympathetic nervous system.
blood vessels are normally partially constricted, a condition called sympathetic tone. Increases in sympathetic stimulation constrict smooth muscle even more, raising MAP
Types of shock vary because shock is a manifestation of a pathologic condition rather than a disease state
More than one type of shock can be present at the same time.
Cardiogenic shock
occurs when the heart muscle is unhealthy and pumping is impaired. Myocardial infarction is the most common cause of direct pump failure.
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 mean arterial pressure (MAP) and may be started either by nerve changes (neural-induced) or by the presence of some chemicals (chemical-induced).
Neural-induced distributive shock
loss of MAP that occurs when sympathetic nerve impulses are decreased and blood vessel smooth muscles relax, causing vasodilation and poor perfusion.
Chemical-induced distributive shock has three common origins:
anaphylaxis, sepsis, and capillary leak syndrome. It occurs when certain body chemicals or foreign substances in the blood and vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock also can be induced by substances normally found in the body, such as excessive amounts of histamine.
Sepsis is a widespread infection that triggers whole-body inflammation. It leads to distributive shock when infectious microorganisms are present in the blood and is most commonly called septic shock
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Capillary leak syndrome is the response of capillaries to the presence of body chemicals that enlarge capillary pores and allow fluid to shift from the capillaries into the interstitial tissues. Once in the interstitial tissue, these fluids are stagnant and cannot deliver oxygen or remove tissue waste products. Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, large wounds, kidney disease, hypoproteinemia, and trauma.
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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
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hypovolemic shock is a loss of blood volume from the vascular space, resulting in a decreased mean arterial pressure (MAP)
loss of RBCs decreases the ability of the blood to oxygenate the tissue it does reach
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.
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. Nonprogressive stage
3. Progressive stage
4. Refractory stage
Initial Stage of Shock.
The initial (early) stage of shock is present when the patient's baseline MAP is decreased by less than 10 mm Hg. Compensatory mechanisms are so effective at returning systolic pressure to normal during this stage that oxygen perfusion to vital organs is maintained. The cellular change in this stage is 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, manifestations of shock are difficult to detect at this stage. A heart and respiratory rate increased from the patient's baseline level or a slight increase in diastolic blood pressure may be the only manifestation of this stage of shock.
Nonprogressive Stage (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. Acid-base and electrolyte changes occur in response to the buildup of metabolites. Changes include acidosis (low blood pH) and hyperkalemia
nonprogressive
Manifestations 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 2% to 5% decrease in oxygen saturation. Comparing these changes with the values and manifestations obtained earlier is critical to identifying this stage of shock.
Progressive Stage of Shock
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.
Progressive Stage of Shock
Manifestations of the progressive stage of shock 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 seem 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 at this stage may show a low blood pH, along with rising lactic acid and potassium levels.
Manifestations of the progressive stage of shock 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 seem 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 at this stage may show a low blood pH, along with rising lactic acid and potassium levels.
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Refractory Stage of Shock and Multiple Organ Dysfunction Syndrome.
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 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 and dying 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 function are lost first. The most profound change is damage to the heart muscle.
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Manifestations are a rapid loss of consciousness; nonpalpable pulse; cold, dusky extremities; slow, shallow respirations; and unmeasurable oxygen saturation. Therapy is not effective in saving the patient's life, even if the cause of shock is corrected and MAP temporarily returns to normal.
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 BP reading with a manual BP reading.
Pulse oximetry values between 90% and 95% occur with the nonprogressive 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 oxygenation 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 that it can be delivered to critical tissues. When shock progresses to the stage at which lactic acidosis is present, the respiratory depth also increases
Kidney and urinary changes occur with shock to compensate for decreased 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 is a sensitive indicator of early shock. Measure urine output at least every hour. In severe shock, urine output may be 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 hypoxia or anoxia persists beyond this time, patients are at risk for acute kidney injury (AKI) and kidney failure.
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.
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
CNS changes with shock are caused by 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 that has no obvious cause. As hypoxia progresses, confusion and lethargy occur. Lethargy progresses to somnolence and loss of consciousness as cerebral hypoxia worsens with shock progression.
Skeletal muscle changes during shock include weakness and pain in response to tissue hypoxia and anaerobic metabolism, which are later manifestations. Weakness is generalized and has no specific pattern. Deep tendon reflexes are decreased or absent.
Changes in mental status and behavior occur early in shock. Observe the patient closely, and document behavior. 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.
no single test confirms or rules out shock, changes in laboratory data may support the diagnosis. Chart 37-2 lists laboratory changes occurring with hypovolemic shock. As shock progresses, arterial blood gas values become abnormal. The pH decreases, the partial pressure of arterial oxygen (Pao2) decreases, and the partial pressure of arterial carbon dioxide (Paco2) increases. Other laboratory changes occur with specific causes of hypovolemic shock.
Hematocrit and hemoglobin levels decrease if shock is caused by poor clotting and hemorrhage. When shock is 747caused by dehydration or a fluid shift, hematocrit and hemoglobin levels are elevated.
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 (arterial) 3-7 mg/dL Increased: anaerobic metabolism with buildup of metabolites
0.3-0.8 mmol/L
Hematocrit Females: 37%-47%
Males: 42%-52% Increased: fluid shift, dehydration
Decreased: hemorrhage
Hemoglobin Females: 12-16 g/dL
Males: 14-18 g/dL Increased: fluid shift, dehydration
Decreased: hemorrhage
Potassium 3.5-5.0 mEq/L or mmol/L Increased: dehydration, acidosis
The priority NANDA-I nursing diagnoses and collaborative problems for patients with hypovolemic shock include:
• Hypoxia related to hypovolemia
• Inadequate perfusion related to active fluid volume loss and hypotension
• Anxiety related to potential for death and decreased cerebral perfusion (NANDA-I)
• Acute Confusion related to decreased cerebral perfusion (NANDA-I)
Medical and nursing 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
Medical and nursing 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
• Ensure a patent airway.
• Insert an IV catheter, or maintain an established catheter.
• Administer oxygen.
• 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.
purposes of shock management are to maintain tissue oxygenation, 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
IV therapy for fluid resuscitation is a primary intervention for hypovolemic shock. Crystalloids and colloids are often used for volume replacement. Crystalloid solutions contain nonprotein substances (e.g., minerals, salts, sugars)
IV therapy for fluid resuscitation is a primary intervention for hypovolemic shock. Crystalloids and colloids are often used for volume replacement. Crystalloid solutions contain nonprotein substances (e.g., minerals, salts, sugars)
Protein-containing colloid fluids help restore osmotic pressure and fluid volume. Blood and blood products are used when shock is caused by blood loss. These fluids include whole blood, packed red blood cells, and plasma.
Whole blood and packed red blood cells (PRBCs) increase hematocrit and hemoglobin levels along with fluid volume. PRBCs are given for moderate blood loss because they restore 748the red blood cell deficit and improve oxygen-carrying capacity without adding excessive fluid volume. Massive transfusion therapy, defined as 10 units of PRBCs given within the first 6 hours of severe hemorrhage, can improve outcomes and prevent death from acute traumatic coagulopathy
Plasma, an acellular blood product containing clotting factors, is given to restore osmotic pressure when hematocrit and hemoglobin levels are normal. Plasma protein fractions (e.g., Plasmanate) and synthetic plasma expanders (e.g., hetastarch [hydroxyethyl starch, Hespan]) increase volume and are used for hypovolemic shock before a cause is identified.
Drug therapy is used in addition to fluid therapy when the volume lost 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.
Vasoconstrictors
Dopamine (Intropin, Revimine image)
Norepinephrine (Levophed)
Phenylephrine HCl
Improve mean arterial pressure by increasing peripheral resistance, increasing venous return, and increasing myocardial contractility.
Assess patient for chest pain. Drugs increase myocardial oxygen consumption.
Monitor urine output hourly. Higher doses decrease kidney perfusion and urine output.
Assess blood pressure every 15 min. Hypertension is a manifestation of overdose.
Assess the patient for headache. Headache is an early manifestation of drug excess.
Assess every 30 min for extravasation; check extremities for color and perfusion. If the drug gets into the tissues, it can cause severe vasoconstriction, tissue ischemia, and tissue necrosis.
Assess for chest pain. Drug can cause rapid onset of vasoconstriction in the myocardium and impair cardiac oxygenation.
Inotropic AgentsDobutamine (Dobutrex)
Milrinone (Primacor)
Directly stimulate beta adrenergic receptors on the heart muscle, improving contractility
Assess for chest pain. Drugs increase myocardial oxygen consumption and can cause angina or infarction.
Assess blood pressure every 15 min.
Hypertension is a manifestation of overdose.
Agents Enhancing Myocardial Perfusion
Sodium nitroprusside (Nitropress, Niprid
Improve myocardial perfusion by dilating coronary arteries rapidly for a short time.
Protect drug container from light. Light degrades drug quickly.
Assess blood pressure at least every 15 min.
Drug can cause systemic vasodilation and hypotension, especially in older adults.
Drug Alert
Monitor the patient closely because drugs that dilate coronary blood vessels, such as nitroprusside, 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.
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 vital signs:
• Pulse (rate, regularity, and quality)
• Blood pressure
• Pulse pressure
• Central venous pressure (CVP)
• Respiratory rate
• Skin and mucosal color
• Oxygen saturation
• Cognition
• Urine output
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 (Svo2), pulmonary artery monitoring, and pulmonary capillary wedge pressures
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, femoral, or dorsalis pedis). 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.
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Sepsis leading to septic shock is a complex type of distributive shock that usually begins as a bacterial or fungal infection and progresses to a critical emergency over a period of days. The progression of sepsis to septic shock is outlined in Fig. 37-3. As progression occurs, the pathologic problems occur faster and to a greater degree. Thus control of sepsis and prevention of severe sepsis and septic shock are easier to achieve early in the process. Failure to recognize and intervene in early sepsis is a major factor for progression to septic shock and death.
local infection
systemis infection (early sepsis)
Sirs systemic inflammatoryresponse system
organ failure-severe sepsis
Mods- septic shock
death
(WBCs) in the area of invasion secrete cytokines to trigger local inflammation and bring more WBCs to kill the invading organisms. The results of this response constrict the small veins and dilate the arterioles in the area, which increases perfusion to locally infected tissues.
Capillary leak occurs, allowing plasma to leak into the tissues. This response causes swelling. The duration of inflammation depends on the size and severity of the infection, but usually it subsides within a few days, when the infection has been managed by these responses. A benefit of inflammation is that it is limited only to the area of infection and stops as soon as it is no longer needed. The patient does not have fever, tachycardia, decreased oxygen saturation, or reduced urine output.
Sepsis is the presence of infection systemic manifestations (Dellinger et al., 2013). Infectious organisms have entered the bloodstream. As their numbers increase, widespread inflammation, known as systemic inflammatory response syndrome (SIRS), is triggered as a result of infection escaping local control. With the organisms and their toxins in the bloodstream and entering other body areas, inflammation is an enemy, leading to extensive hormonal, tissue, and vascular changes and oxidative stress that further impair oxygenation and tissue perfusion. The WBCs produce many pro-inflammation cytokines
As a result, there is widespread vasodilation and blood pooling (Schell-Chaple & Lee, 2014). The patient has mild hypotension, a low urine output, and an increased respiratory rate. These responses result in a hypodynamic state with decreased cardiac output. Body temperature varies depending on the duration of the sepsis and on WBC function. Some patients have a low-grade fever and others have a high fever. Still others may have a below-normal body temperature. Fever and hypotension result from SIRS.
Inappropriate clotting with microthrombi forming in some organ capillaries causes hypoxia and reduces organ function. This problem is hard to detect, but if sepsis is stopped at this point, the organ damage is completely reversible. The microthrombi increase hypoxic conditions, which then generate more toxic metabolites. These damage more cells and increase the production of pro-inflammatory cytokines, leading to an amplification of SIRS and a vicious repeating cycle of poor oxygenation and perfusion (Fig. 37-4). Although these manifestations are subtle, they indicate sepsis and SIRS and will progress unless intervention begins now.
Sepsis with Systemic Inflammatory Response Syndrome (SIRS) Criteria
• Temperature of more than 101° F (38.3° C) or less than 96.8° F (36° C)
• Heart rate of more than 90 beats per minute
• Respiratory rate of more than 20 breaths per minute
• Abnormal WBC count (>12,000/mm3 or <4000/mm3)
• Normal WBC count with >10% bands
• Plasma C-reactive protein >2 standard deviations above normal
• Plasma prolactin >2 standard deviations above normal
• Arterial hypotension (SBP <90 mm Hg; MAP <70 mm Hg)
• Arterial hypoxemia (Pao2/Fio2 <300)
• Urine output <0.5 mL/kg/hr for 2 hours despite adequate fluid resuscitation
• Creatinine increase >0.5 mg/dL
• INR >1.5 or aPTT >60
• Absent bowel sounds
• Platelet count <100,000/mm3
• Total bilirubin >4 mg/dL
• Elevated lactic acid (lactate) levels
• Decreased capillary refill or presence of mottling
• Hyperglycemia (plasma glucose >140 mg/dL or 7.7 mmol/L) in absence of diabetes
• Unexplained change in mental status
• Significant edema or positive fluid balance
Notify the health care provider or the Rapid Response Team for any patient who has vital signs or other conditions that meet the sepsis with SIRS criteria.
Severe sepsis is sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion (Dellinger et al., 2013). It represents the progression of sepsis with an amplified SIRS (see Fig. 37-4). All tissues are involved and are hypoxic to some degree. Some organs are experiencing cell death and dysfunction at this time. Microthrombi formation is widespread with clots forming where they are not needed. This process uses up or consumes much of the available platelets and clotting factors, a condition known as disseminated intravascular coagulation (DIC). The amplified SIRS and cytokine release increase capillary leakiness, injure cells, and increase cell metabolism. Damage to endothelial cells reduces anticlotting actions and triggers the formation of even more small clots, increasing DIC. Anaerobic metabolism continues, and cell uptake of oxygen is poor. The continued stress response triggers the continued release of glucose from the liver and causes hyperglycemia. The more severe the response, the higher the blood glucose level (Kleinpell et al., 2013; Schell-Chaple & Lee, 2014).
Despite the severity of this stage and the fact that it may be present for 24 hours or more, it is often missed. One of the reasons it may be missed is that the cardiac function is hyperdynamic in this phase. The pooling of blood and the widespread capillary leak stimulate the heart, and cardiac output is increased 751with a more rapid heart rate and an elevated systolic blood pressure. In addition, the patient's extremities may feel warm and there is little or no cyanosis. Even though the patient may "look" better, the pathologic changes occurring at the tissue level are serious and have caused significant damage. The WBC count at this time may no longer be elevated.
Clinical manifestations of this stage include a lower oxygen saturation, rapid respiratory rate, decreased to absent urine output, and a change in the patient's cognition and affect. Appropriate and aggressive interventions at this stage can still prevent septic shock, although mortality after a patient reaches this stage is much higher than for sepsis and SIRS. At this point, the down-hill course leading to septic shock is extremely rapid.
Septic shock is sepsis-induced hypotension persisting despite adequate fluid resuscitation. It is the stage of sepsis and SIRS when multiple organ dysfunction syndrome (MODS) with organ failure is evident and poor clotting with uncontrolled bleeding occurs (see Fig. 37-4). Even with appropriate intervention, the death rate among patients in this stage of sepsis is very high (Dellinger et al., 2013). Severe hypovolemic shock and hypodynamic cardiac function are present as a result of an inability of the blood to clot because the platelets and clotting factors were consumed earlier. Vasodilation and capillary leak continue from vascular endothelial cell disruption, and cardiac contractility is poor from cellular ischemia. The clinical manifestations resemble the late stage of hypovolemic shock.
Conditions Predisposing to Sepsis and Septic Shock
• Malnutrition
• Immunosuppression
• Large, open wounds
• Mucous membrane fissures in prolonged contact with bloody or drainage-soaked packing
• GI ischemia
• Exposure to invasive procedures
• Cancer
• Older than 80 years
• Infection with resistant microorganisms
• Receiving cancer chemotherapy
• Alcoholism
• Diabetes mellitus
• Chronic kidney disease
• Transplantation recipient
• Hepatitis
• HIV/AIDS
Because sepsis can be a complication of many conditions found in acute care settings, always consider its possibility. 752Early detection of sepsis before progression to septic shock is a major nursing responsibility. The nurse is the health care professional most in contact with the patient and is in a unique position to detect subtle changes in appearance and behavior that can indicate sepsis. Use the assessment techniques described below for changes in vital signs, laboratory findings, appearance, and behavior to identify early any characteristics of sepsis and sepsis progression at least every shift for potentially infected, seriously ill patients (Kleinpell & Schorr, 2014). Using an evidence-based protocol to identify patients in the emergency department who may be in early sepsis on admission can improve the timing of implementing an appropriate sepsis bundle intervention (
Early detection can be made by patients and families, as well as by health care personnel. This is especially important for patients discharged to home after invasive procedures or surgery. Teach patients the manifestations of local infection
Risk Factors for Shock
Hypovolemic Shock
• Diuretic therapy
• Diminished thirst reflex
• Immobility
• Use of aspirin-containing products
• Use of complementary therapies such as Ginkgo biloba
• Anticoagulant therapy
Cardiogenic Shock
• Diabetes mellitus
• Presence of cardiomyopathies
Distributive Shock
• Diminished immune response
• Reduced skin integrity
• Presence of cancer
• Peripheral neuropathy
• Strokes
• Being in a hospital or extended-care facility
• Malnutrition
• Anemia
Obstructive Shock
• Pulmonary hypertension
• Presence of cancer
although the hallmark of sepsis is an increasing serum lactate level, a normal or low total white blood cell (WBC) count, and a decreasing segmented neutrophil level with a rising band neutrophil level (left shift, see Chapter 17).
Another indicator of sepsis and septic shock is a low blood level of activated protein C. Protein C is an enzyme that prevents inappropriate clot formation. It is activated when it binds to healthy vascular endothelial cells. In severe sepsis, the injured endothelial cells cannot activate protein C and thousands of small clots form in the capillaries of vascular organs. Decreasing levels of activated protein C indicate the beginning of severe sepsis even before other manifestations are evident.
With appropriate interventions, the patient with sepsis or septic shock is expected to have normal aerobic cellular metabolism. Indicators include:
• Arterial blood gases (pH, Pao2, and Paco2) within the normal range
• Maintenance of a urine output of at least 20 mL/hr
• Maintenance of mean arterial blood pressure within 10 mm Hg of baseline
• Absence of multiple organ dysfunction syndrome (MODS)
Surviving Sepsis Care Bundle
Within the first 3 hours of suspecting severe sepsis:
1. Measure serum lactate levels.
2. Obtain blood cultures before administering antibiotics.
3. Administer broad-spectrum antibiotics.
4. If either hypotension or a serum lactate level greater than 4 mmol/L (36 mg/dL) is present, administer 30 mL/kg crystalloids intravenously.
Within 6 hours of initial manifestations of suspected septic shock:
5. Administer prescribed vasopressors for hypotension that does not respond to initial fluid resuscitation measures to maintain MAP ≥65 mm Hg.
6. If arterial hypotension persists despite fluid volume resuscitation (indicating septic shock) or lactic acid remains ≥4 mmol/L (36 mg/dL), institute these assessments:
• Measure central venous pressure.
• Measure central venous oxygen saturation.
7. Re-measure lactic acid (lactate) level if initial value was elevated.
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