NURS 482 Exam 2 Questions and Complete Solutions Graded A+

NURS 482 Exam 2 Questions and Complete Solutions Graded A+ Acute GIB Risk Factors - Answer: smoking/alcohol use NSAIDs use infection of H. pylori comorbid disease in older adults Hallmarks of Acute GIB - Answer: hematemesis hematochezia melena Common Causes of Acute GIB - Answer: Esophageal source: -Varices -Esophagitis -Ulcers -Tumors -Mallory-Weiss tears Gastric sources: -Peptic ulcers -Gastrits -Tumors -Angiodysplasia -Dieulafoy lesions Duodenal Source -Peptic ulcers -Angiodysplasia -Crohn disease -Meckel diverticulum Labs for Acute GIB - Answer: Decreased hemoglobin and hematocrit Mild leukocytosis and hyperglycemia Elevated BUN Hypernatremia Hypokalemia Prolonged PT and PTT Thrombocytopenia Hypoxemia Acute GIB Nursing Interventions - Answer: -Maintain patent airway, elevate HOB, have suction available to prevent aspiration of emesis or blood. -Admin. O2 to treat hypoxia from decreased hemoglobin levels -Monitor pulse Ox -Signs of shock: restlessness, dim. peripheral pulses, cool/pale/moist skin, VS, output, hemodynamic values, SaO2 -Assess/document electrocardiographic monitoring and heart/lung/bowel sounds -Assist in placement of CVP (central venous pressure) cath. or pulmonary artery cath. -Maintain IV access/admin IV fluids/blood products -Insert NG and lavage as ordered -Monitor gastric pH. antacid admin. -Admin antisecretory meds (reduce gastric acid secretion). -Admin vasopressin or octreotide -Maintain accurate I's & O's every 1-2 hrs/PRN -Record urine/nasogastric drainage/emesis -Monitor electrolytes from loss of fluids or fluid shifts, report abnormal values -Mouth care as needed -Explain all procedures to patient -Prepare patient for diagnostic procedures/therapeutic interventions -Monitor for potential complications of endoscopy/colonoscopy (perforation, sepsis, pulmonary aspiration, induced bleeding) -Encourage smoking cessation/avoid alcohol. Esophageal Varices - Answer: -Portal hypertension usually develops as a result of cirrhosis, from increased resistance in the portal venous system caused by disruption of the normal liver lobular structure. -This resistance impedes blood flow into, through, and out of the liver. -In response to portal hypertension, collateral veins develop to bypass the increased portal resistance in an attempt to return blood to the systemic circulation. -As pressure rises in these veins, they become tortuous and distended, formic varicose veins or varices. Esophageal Varices Physical Examination - Answer: -Tachycardia, orthostatic hypotension indicate dehydration secondary to blood loss or vomiting. -Orthostatic hypotension, syncope, lightheadedness, and tachycardia suggest more than 15% blood volume loss. -Poor tissue perfusion: angina, cyanosis, altered mental status. -Baseline electrocardiogram is critical. -Signs of agitation/confusion indicate cerebral hypoperfusion. Sengstaken-Blakemore Tube - Answer: -Pressure is exerted on the cardia of stomach, against bleeding varices -Tube is instered at least 50 cm to ensure gastric intubation -Inflated to 250-300 mL air, traction is applied -Position confirmed by radiography -If chest pain, balloon is deflated immediately -If bleeding continues inflate esophageal tube 25-39 mmHg and maintain for 24-48 hrs -Nasogastric tube should be placed to aspirate oral and nasopharyngeal secretions that collect above the esophageal balloon Sengstaken-Blakemore Tube Nursing Interventions - Answer: -Explain procedure to patient -lubricate and chill tube as directed by manufacturer. Identify/label lumens on tube -Check patency of each lumen before insertion -Lavage stomach -Monitor patient during insertion -Elevate HOB to 30degrees to prevent reflux -Maintain balloon pressure/traction & position. -Clean/lubricate nostrils frequently -Irrigate nasogastric port every 2 hrs -Teach patient to avoid coughing/straining -Have second nasogastric tube, suction, scissors at bedside -Restrain patient's arms if patient is at risk for pulling out the tube -Assess for complications: rupture or deflating of the balloon, pulmonary aspiration, and esophageal rupture Acute Pancreatitis (AP) Etiology - Answer: -Gallstones are responsible for 40% of cases. Gallstones and biliary sludge may become lodged as they pass through the biliary system, blocking pancreatic secretions from emptying into the duodenum -Alcoholism is the second leading cause of pancreatitis and accounts for 35% of the cases of AP -Metabolic causes include hypercalcemia and hypertriglyceridemia -Many drugs include diuretics, sulfonamides, metronidazole, aminoscalicylates, and estrogen can precipitate AP as a result of toxic metabolites or a drug reaction -Idiopathic pancreatitis is associated with pregnancy, the administration of TPN, or major surgery Acute Pancreatitis (AP) Pathophysiology - Answer: -Pancreatic enzymes, vasoactive substances, hormones, and cytokines released from the injured pancreas cause a cascade of events that can lead to edema, vascular damage, hemorrhage, and necrosis -Systemic effects mediated by the immune system can lead to a SIRS, which can result in distant organ damage and MODS -The immune system response is independent of the event that causes AP but is responsible for the majority of the morbidity and mortality associated with it Acute Pancreatitis (AP) Diagnosis - Answer: diagnosis requires the presence of 2 of the 3 following features: abdominal pain consistent with pancreatitis, serum lipase at least three times or greater the upper limits or normal, and characteristic findings on CT, MRI, or US Acute Pancreatitis (AP) History - Answer: -History of biliary tract disease, alcohol intake, diabetes, and medication use should be elicited -A family history of AP may suggest hereditary cause. -Patient may report anorexia, weight loss, nausea, vomiting, or abdominal distention. -Assessment of the location, duration, quality, quantity, and precipitating factors of pain is important to identify potential causes Grey turner sign and Cullen sign - Answer: -Presence of bluish discoloration of the lower abdominal flanks -Or around the umbilical area -Indicates hemorrhagic pancreatitis and an accumulation of blood in these areas -Rare and don't appear till 48 hours after onset of symptoms Acute Pancreatitis (AP) Labs - Answer: No single lab is diagnostic however, elevations of serum amylase and lipase enzymes are often seen Acute Pancreatitis (AP) Nutrition - Answer: -NPO: no food until pain -For severe pancreatitis (TPN) -When diet is resumed: bland, high protein, low-fat diet with no stimulants (caffeine), small frequent meals -Administer antiemetic as needed -NG tube: gastric decompression -No alcohol -No smoking -Limit stress -Pain management Acute Pancreatitis (AP) Medications - Answer: -Opioid analgesics: Morphine or Hydromorphone (acute pain) *Ketorolac, an NSAID, mild/moderate pain -Antibiotics: Imipenem - clients who have acute necrotizing pancreatits -Histamine receptor antagonists: Ranitidine - decreases gastric acid secretion -Proton pump inhib: Omeprazole - Decreases gastric acid secretion -Pancreatic enzymes: Pancrelipase - Aid w/digestion of fats and proteins when taken with meals/snacks. Hepatitis C - Answer: Blood-borne virus: transmitted by blood transfusions (before 1992) and contaminated needles from illicit drug use/occupational needlestick exposure Cirrhosis Pathophysiology - Answer: -Develops over time, can cause severe alterations in the structural architecture of the liver and function of the hepatocytes. -Changes are characterized by inflammation and liver cell necrosis, which can be focal or diffuse. -Fibrous tissue and regenerative nodules develop over time, which distorts the normal architecture of the liver lobule and alters blood flow. -These fibrotic changes are irreversible, resulting in chronic liver dysfunction and eventual liver failure -The cause of fatty changes is unclear but it may be a response to alteration in enzymatic function responsible for normal fat metabolism. -Inflammation, fibrotic changes, and increases intrahepatic vascular resistance cause compression of the liver lobule, leading to increased resistance or obstruction of normal blood flow through the liver, which is normally a low pressure system. -Portal hypertension results in significant venous congestion and dilation. -Subsequently, nutrient rich blood from the GI tract is shunted away from the liver, the first site of metabolism for many nutrients, drugs, and toxins. -Pressure builds up in the systemic venous circulation, causing congestion where the portal and systemic venous systems connect. -Esophageal varices and gastric varices are of particular concern in the care of these patients because they are extremely friable. -Rupture from these varices can result in massive internal bleeding. Cirrhosis Assessment - Answer: -Altered carb metabolism can result in unstable blood glucose levels. -Altered fat metabolism can cause fatigue and decreased activity tolerance. -Altered protein metabolism results in a decreased synthesis of albumin. -Albumin is necessary for colloid osmotic pressure, which holds fluid in the intravascular space. -A decrease leads to interstitial tissue edema and decreased plasma volume. -A low grade DIC may develop. -Portal hypertension, ascites, and lower extremity edema cause hypotension. -Initially the patient may have flushed skin and bounding pulses from the vasodilation in the portal venous system which eventually leads to hypotension. Cirrhosis - Answer: -Goals include preventing additional stress on liver function and early recognition and treatment of complications. -Interventions include monitoring nutritional markers and providing nutrition; monitoring fluid balance, UP, electrolyte and chemistry studies, drug type, and dose requirements; monitoring bleeding times, platelet function, and hematocrit; and detecting signs of bleeding -Bowel cleansing regimens may be ordered. -Early recognition of complications include detecting signs of impending liver failure: changes in neurologic and mental status, increasing ascites, and HRS. -Maintaining fluid and electrolyte balance requires ongoing nursing assessment. -Monitor weight and CVT trends to help determine fluid retention and vascular loading. -Ascites is managed through bed rest, a low sodium diet of no more than 2 g/day, fluid restriction, and diuretic therapy. -Paracentesis is also used to treat ascites in patients not responding to salt restriction and maximal diuretic therapy. -A venous peritoneal shunt is used to relieve ascites that is resistant to other therapies. -A non surgical approach to managing ascites and acute vericeal hemorrhage is the TIPS Cirrhosis Medications - Answer: -Diuretics - decrease excessive fluid in the body -Beta-blocking agents: used for clients who have varices to prevent bleeding -Lactulose: used to promote excretion of ammonia from the body through the stool -Non Absorbable antibiotic: used in place of lactulose Hepatic Encephalopathy Pathophysiology - Answer: -A reversible decrease in neurologic function caused by liver disease. -The cause is thought to be related to the accumulation of toxic agents absorbed from the intestinal tract. -They accumulate because the liver cannot metabolize and detoxify the substances. -Elevated serum ammonia, is one of the neurotoxins. -If ammonia and other toxic agents can be reduced through effective therapy, the encephalopathy gradually clears. Hepatic Encephalopathy Clinical manifestations - Answer: -Subtle, with changes in memory, personality, concentration, and reaction times. -Can progress to more apparent neurologic cognitive changes, irritability or agitation, reversal of day and night schedules, somnolence, and eventually terminal coma if left untreated Hepatic Encephalopathy Treatment - Answer: -Generally targeted toward interventions that lower ammonia production and absorption with medications such as lactulose and/or rifaximin. -Lactulose is used to facilitate bowel movements and clearance of nitrogenous products and it also decreases the colonic pH to prevent the absorption of ammonia. -Antibiotics may be given to clear the gut of bacteria. -Bleeding from esophageal varices introduces nitrogenous load to the GI tract through the breakdown on RBCs. -Nursing measures to monitor for changes in mental status and provide a safe environment are a priority DIC Pathophysiology - Answer: -Inappropriate triggering of the coagulation cascade and a breakdown in the normal feedback mechanisms in the body that allow for the dissolution of clots -Instead of a localized response to tissue damage or vascular injury, there is systemic coagulation activity, resulting in diffuse intravascular fibrin formation and widespread intravascular clotting -Eventually, coagulation factors become depleted as the body attempts to dissolve the newly formed clots -Because of the rapidity of intravascular thrombin formation, clotting factors are used up at a rate exceeding factor replenishment Signs and Symptoms of Inappropriate Clotting - Answer: -Cyanosis, gangrene, mental status changes, altered level of consciousness, cerebrovascular accident, pulmonary embolus, bowel ischemia and infarction, and renal insufficiency or failure -Thrombosis may involve both arteries and veins Signs and Symptoms of Inappropriate Bleeding - Answer: Bleeding from the nose, gums, lungs, gastrointestinal tract, surgical sites, injection sites, and intravascular access sites, hematuria, petechial rashes, and purpura fulminans Nurse pt teaching r/t preventing burns - Answer: -prevent accidents in the home (smoke detector, kitchen safety, candles) -prevent accidents outside the home (fireworks, sunscreen, campfires) -if you get a burn, remove the source first Superficial Burn - Answer: -affect only the epidermis -cause the skin to become dry, red, and blanched, but blisters do not typically result -can be painful and itchy but heals quickly within 3-5 days -ex. sunburn Superficial Partial-Thickness Burn - Answer: -affects the epidermis and dermis -extends to the superficial dermis and causes the skin to become moist and reddened, blanched, blistered, and very painful -takes about 2-3 weeks to heal with minimal intervention -ex. grease, tar, chemical burns Deep Partial Thickness Burn - Answer: -extends to the deeper dermal layer and causes the skin to become slightly moist-to-dry, mottled, and no blanching -very painful and can cause scarring, contracture, and impaired function -heal more slowly and require excision and skin grafting surgeries if they are very large -ex. burns from hot solids, flames Full Thickness Burn - Answer: -third-degree burns, enter the subcutaneous tissue and even to connective tissue, muscle, and bonedestroy sweat glands, hair follicles, and other elements of the epidermal and dermal layers -can look white, red, brown, or black, do not blanch, and may only cause a feeling of pressure as the sensory receptors have been destroyed -can also appear sunken due to fat and muscle destruction, and blood vessels and capillaries may be visible -ex. prolonged flame or hot object exposure, chemicals, or high-voltage electricity "Rule of Nines" - Answer: -divides the body into parts that equal roughly 9% body surface area -head is roughly 9% (4.5% for the front of the head and 4.5% for the back of the head) -each arm is 9% (again, 4.5% for anterior aspect and 4.5% for posterior aspect) -front and back torso each count for 18% -front of each leg is 9%, and the back of each leg is 9% -groin accounts for the other 1% surface area -palm, including their fingers, is estimated as 1% body surface area Systemic Response for Burns - Answer: -release of vasoactive substances -initiate SIRSpotent mediators and cytokines deplete intravascular volume and decrease blood flow to kidneys and GI tract -relaxes smooth muscle and produces vasodilation, hypotension, depress myocardial function and block platelet aggregation/adhesion -tissue inflammation, increases vessel permeability, and causes hypotension, vasodilation and further depresses myocardial function -vasoconstriction and fever -increased formation of oxygen free radicals, which lead to injury of the lung, GI tract and kidneys -increased cytokine productioninitial hyperglycemia, followed by hypoglycemia, hypotension, metabolic acidosis, coagulopathy and activation of coagulation cascade Pulmonary Complications - Answer: -Occurs within 24 to 48 hours of the injury -Secondary to the inhalation of combustible products, or may be the result of inhaled superheated air -Carbon Monoxide Toxicity and Inhalation Inury Carbon Monoxide Toxicity - Answer: -Nonirritating, odorless, colorless gas that is formed as a result of the incomplete combustion of any carbon fuel -Sources of carbon monoxide include hot water heaters, furnaces, tobacco smoke, and exhaust from vehicles -Carbon monoxide affinity for hemoglobin is 200 to 300 times higher than oxygen, carbon monoxide readily displaces the oxygen, leading to the formation of carboxyhemoglobin and a reduction in system arterial oxygen content Carbon Monoxide Toxicity Signs and Symptoms - Answer: The patient with a clear history of exposure to carbon monoxide is usually found in a closed environment in the presence of combusted gases, such as smoke, automobile exhaust, or fumes from a faulty furnace Carboxyhemoglobin 10% -No symptoms Carboxyhemoglobin 20% -Headache, nausea/vomiting, dyspnea on exertion Carboxyhemoglobin 30% -Confusion, lethargy, tachypnea Carboxyhemoglobin 40%-60% -Seizure, coma, changes on electrocardiogram Carboxyhemoglobin more than 60% -Death Carbon Monoxide Toxicity Management - Answer: -100% high-flow oxygen is administered -The patient should be maintained on 100% oxygen until carboxyhemoglobin level is less than 10% and neurologic symptoms resolve -Serial carboxyhemoglobin level measurements are the most accurate way to assess responsiveness to oxygen therapy -The analysis and trending of arterial blood gas levels for acid-base balance, lactate levels, and bicarbonate are helpful to manage carbon monoxide poisoning with lactic or metabolic acidosis Inhalation Injury - Answer: -Thermal injury to the airway can result from smoke inhalation -Pulmonary damage from inhalation injury has historically been seen in less than 10% of the total burn cases but accounts for 20% to 84% of burn mortality and is a significant factor in increasing the hospital stay of length Three stages of injury have been described: -Acute pulmonary insufficiency may occur during the first 36 hours -Pulmonary edema occurs in 5% to 30% of patients with burns between 6 and 72 hours after injury -Bronchopneumonia appears in 15% to 60% of patients with burns 3 to 10 days after injury Inhalation Injury Signs and Symptoms - Answer: -Upper airway injury is the result of inhalation of superheated air, which may cause blisters and edema in the supraglottic area around the vocal cords -May cause airway obstruction and edema -Hoarseness, stridor, dyspnea, carbonaceous sputum, and tachypnea indicate airway compromise, which must be addressed immediately -Early intubation may prevent these occurences Inhalation Injury History and Physical Assessment - Answer: -History of incident occurring in a confined area -Singed nasal or facial hairs -Burns of the oral or pharyngeal mucous membranes -Burns in the perioral area or neck -Carbonaceous sputum -Change in voice -Change in level of consciousness Inhalation Injury Diagnostic - Answer: -Serial ABG evaluations show a decreasing arterial oxygen tension -The admission chest film appears normal because changes are not reflected until 24 to 48 hours after the burn -Sputum specimen is obtained for culture and sensitivity studies -Laryngoscopy and bronchoscopy may be of value in determining the presence of extra mucosal carbonaceous material (the most reliable sign of inhalation injury) and the state of mucous (blistering, edema, erythema) -More specific confirmation of inhalation injury is achieved with the use of fiberoptic bronchoscopy, which permits direct examination of the proximal airway, and xe-non-133 scintigraphy Infection - Answer: -Most common cause of death in patients with burns after the first 5 to 7 days -Frequent and meticulous hand washing alone prevents infection more than any other single action Primary Survey - Answer: Airway Maintenance with cervical spine protection Breathing and Ventilation Circulation with hemorrhage control Disability (assess neurologic deficit) Exposure (completely undress the patient, but maintain temperature) Airway Maintenance - Answer: -Must be assessed immediately -Compromised airway can be controlled by a chin lift, jaw thrust, insertion of an oropharyngeal airway in an unconscious patient, or endotracheal intubation Breathing and Ventilation - Answer: -Ventilation requires adequate functioning of the lungs, chest wall, and diaphragm -Listen to the chest and verify breath sounds in each lungs, assess adequacy of rate and depth of respiration, administer high flow oxygen at 15 L/min using a nonbreathing mask, and assess for circumferential full thickness burns of the chest that may impair ventilation Circulation - Answer: -Assessment of circulation includes a measurement of blood pressure and heart rate -Special attention to the distal pulses of any extremity with circumferential burns -IV cannulation is performed by inserting two large bore catheters into the skin that is unburned, if possible -Central venous catheter should be inserted when indicated -Doppler ultrasonography can be used to asses for pulses RISK FACTORS FOR IMPAIRED CIRCULATION -Progressive diminution of pulses despite adequate resuscitation -Decreased capillary refill -Decreased sensation -Progressive worsening of pain -Paresthesia -Pallor of extremity Disability - Answer: -In the presence of burns alone, the patient will be alert and oriented -If this is not the case, associated injuries, such as inhalation injury, head trauma, substance abuse, or preexisting medical conditions, should be considered -The assessment is initiated by determining the patients level of consciousness using the AVPU method: A lert, responds to V erbal stimuli, responds to P ainful stimuli, U nresponsive Exposure - Answer: -All the patients clothing and jewelry are removed to complete the primary and secondary survey -The environment should be warmed, because the burn patient has lost significant capacity to maintain body temperature -After the examination, the patient is covered with a clean, dry sheet and warm blankets to prevent evaporative cooling -IV fluid may be warmed Secondary Survey - Answer: -Every attempt is made to determine exactly what happened -A detailed neurologic examination is completed, and initial radiographic and laboratory studies are done -Resuscitative measures are ongoing and constantly evaluated -A complete history and physical examination are the hallmarks to the secondary survey -It is not uncommon for patient to have comorbid diseases -Preexisting diseases, such as diabetes, hypertension, asthma, cancer, and stroke, should be documented -A medication list is obtained from the patient if possible, or a family member is asked to provide the information -Any allergies, the person's tetanus immunization history, and the time of the person's last meal should be documented -Burn depth and burn size are assessed LABORATORY AND DIAGNOSTIC STUDIES *CBC *Comprehensive chemistry panel, including blood urea nitrogen *Creatinine levels *Urinalysis *ABG values to include carboxyhemoglobin determination *Electrocardiogram *Chest radiograph -If the patient has a high-voltage electrical burn or if cardiac changes are noted, continuous cardiac monitoring is indicated -If the patient has a chemical burn, the area is immediately flushed with large amounts of water to remove the chemical, and all contaminated clothing is removed and bagged -If the patient is transferred to a burn center, initiation of fluid resuscitation, insertion of a nasogastric tube, and insertion of an indwelling urinary catheter may be carried out during the secondary assessment Hemodynamic Support and Fluid Resuscitation - Answer: -Therapy for burn shock is aimed at supporting the patient through the period of hypovolemic shock until capillary integrity is restored -Fluid resuscitation is the primary intervention in the resuscitative phase in the intensive care unit to maintain tissue perfusion and end organ function -Lactated Ringer solution is the crystalloid of choice GOALS OF FLUID RESUSCITATION -Correct fluid, electrolyte, and protein deficits -Replace continuing losses and maintain fluid balance -Prevent excessive edema formation -Maintain and hourly urinary output in adults of 30 to 50 mL/h Pulmonary Interventions to Prevent Complications - Answer: -Goals for the successful treatment of inhalation injury include improving oxygenation and decreasing interstitial edema and airway occlusion -Humidified oxygen is administered to prevent drying and sloughing of the mucosa -Upper airway edema peaks 24 to 48 hours after injury -If the injury is mild or moderately severe, placing the patient in high fowlers position and administering aerosolized racemic epinephrine may be sufficient to limit further edema formation -Severe upper airway obstruction may require endotracheal intubation to protect the airway until the edema subsides -In patients with mild tracheobronchial injury, atelectasis may be prevented by frequent pulmonary toilet, using a high Fowler position, coughing and deep breathing, chest physiotherapy, repositioning, frequent tracheal suctioning, and incentive spirometry -In patients with more severe inhalation injury, more frequent suctioning may be necessary, and bronchoscopic removal of debris may be appropriate *These patients usually require endotracheal intubation and mechanical ventilatory support *The objective of ventilatory support is to provide adequate gas exchange at the lowest possible inspired oxygen concentration and airway pressure, in an attempt to reduce the incidence of oxygen toxicity and pulmonary barotrauma *The use of volumetric diffusive respiration (VDR) appears to offer advantages over conventional mechanical ventilation *In VDR, subtidal volume breaths accumulate and build to a set airway pressure, which is then followed by passive exhalation *Throughout the ventilatory cycle, high-frequency pulsations of air are continuously administered *This method of inspiration appears to aid in ventilation and recruitment of partially obstructed alveoli -Patients with bronchospasm are treated with aerosolized or intravenously administered bronc Nutrition - Answer: -The rationale for enteral feedings within the first 24 hours of injury is that the presence of food in the gut lumen reduces the rate of microbial translocation -Parenteral nutrition can be used for patients who do not tolerate enteral feedings because of paralytic ileus of the intestine or prolonged diarrhea -Wound repair depends on amino acids, which are the building blocks of protein -The type of amino acids used in enteral feedings varies -The amino acids arginine and glutamine have immune-enhancing properties, improve nitrogen retention, and maintain lean body mass -Formulas containing arginine supplements have been reported to reduce infections in trauma patients and to reduce length of stay of critically ill patients Musculoskeletal Support - Answer: -Range of motion exercises prevention tendon shortening and restriction of joint motion by burn scar contractures -As patients begin to recover and participate actively in therapy, exercises are designed to increase muscle strength and endurance -A return to activities of daily living frequently takes months Managing pain - Answer: -All narcotics are given intravenously because absorption of the drug is unpredictable when given IM or subcutaneously -Patients are given anxiolytics for anxiety related to appearance, procedures, and fear -Patient-controlled analgesia (PCA) is ideal for patients who are awake, sufficiently oriented, and physically able to use the pump -PCA pumps can provide a continuous pain medication with a dose available every 6 to 8 minutes for intermittent pain -The nurse can give the patient a bolus dose before procedures such as dressing changes and physical therapy -Recommended narcotics include morphine, fentanyl, and hydromorphone Pathophysiology of Shock - Answer: -Although shock states have different causes and different clinical presentations, some features, such as hypoperfusion, hypercoagulability, and activation of the inflammatory response, are common to all shock states -Once a shock state develops, the subsequent course of illness is less dependent on the initial cause and more significantly influenced by the physiologic response to shock, including activation of the sympathetic nervous system, the inflammatory response, and the immune system -Shock can be considered as a derangement of compensatory mechanisms that results in further circulatory and respiratory dysfunction with subsequent multiple organ damage Compensatory Mechanisms used by the body during shock - Answer: -Respiratory: increase RR; increase depth of respirations -Endocrine: increase ADH release and renin-angiotensin-aldosterone activity -Circulatory: increase cardiac output; arterial vasoconstriction increases SVR and BP and shunts blood from less vital organs (stomach/intestines) to heart/lungs/brain -Kidneys: activate RAAS to increase vasoconstriction of arterioles/veins to increase SVR and BP; conserve sodium and water -May result to anaerobic metabolism to produce enough ATP SIRS criteria - Answer: TWO OR MORE OF THESE CONDITIONS -Temperature: less than 36 C or greater than 38 C -Heart rate: greater than 90 bpm -Respiratory rate: greater than 20 breaths/min -PaCO2: less than 32 mm Hg -WBC count: less than or equal to 4000 cell/mm3, greater than or equal to 12000 cell/mm3, or greater than 10% immature (band) forms Stage 1 of Shock - Answer: -Initial, nonprogressive stage, compensatory mechanisms are effective in maintaining relatively normal vital signs and tissue perfusion -Shock is poorly diagnosed and frequently goes unrecognized -If SIRS criteria are recognized, early shock may be successful recognized and treated and the patient may make a full recovery Stage 2 of Shock - Answer: -Intermediate, progressive phase, compensatory mechanisms than maintain normal perfusion begin to fail, metabolic and circulatory derangements become more pronounced, and activated of the inflammatory and immune responses may fully develop -Signs of failure in one or more organs may become apparent -Interventions that target both the cause of the shock and the resultant metabolic, circulatory, and inflammatory responses may result in salvage of the patient Stage 3 of Shock - Answer: -Final, irreversible stage, cellular and tissue injury is so severe that correction of metabolic, circulatory, and inflammatory derangements is difficult or impossible, and cellular hypoxia and death ensue -MODS develop, often resulting in the demise of the patient Hypovolemic shock etiology - Answer: -A result of inadequate circulating volume -Caused by sudden blood loss or severe dehydration -Acute fluid volume loss does not allow the normal compensatory mechanisms to restore and appropriate circulating volume rapidly enough Hypovolemic shock pathophysiology - Answer: -A sudden loss of intravascular volume decreased venous return to the heart and results in reduced CO -Compensatory mechanisms are initiated to increase the circulating volume through the activation of the sympathetic nervous system and neurohormonal responses -Existing blood volume is shunted to the vital organs (heart, lungs, brain) causing hypoperfusion to other organs such as liver, stomach, and kidneys -If volume is not replaced, compensatory mechanisms eventually become ineffective Hypovolemic shock RISK FACTORS - Answer: Fluid loss, hemorrhage, trauma, burns, dehydration, diarrhea Hypovolemic shock physical findings - Answer: -Altered mentation, ranging from lethargy to unresponsiveness -Rapid and deep respirations, which gradually become labored and more shallow as the patients condition deteriorates -Cool and clammy skin, with weak and thready pulses -Tachycardia from activation of the sympathetic nervous system -Hypotension -Decreased urine output, urine is darker and more concentrated because the kidneys are conserving fluid Hypovolemia shock management - Answer: -Focuses on restoring circulating volume and resolving the cause of volume loss -First line therapy for volume resuscitation is typically crystalloid solution *Isotonic solutions (lactated ringer, or 0.9% normal saline) are preferred over hypotonic solutions (5% dextrose solution) -Blood and blood products are administered to replace red blood cells, platelets, and clotting factors lost with severe bleeding -Other colloid solutions (albumin and synthetic volume expanders) may be used to assist in the resuscitation process, especially if blood loss is the primary cause *Use of colloid solutions is controversial because it could worsen the hypovolemia Hypovolemia shock nursing management - Answer: -Focuses on the restoring of circulating volume through volume administration -Obtaining and maintaining adequate IV access is essential -Large volumes of fluids given too quickly may cause pulmonary congestion and inhibit adequate ventilation, further compromising DaO2 to the tissues -Fluids should also be warmed during infusion to limit negative effects of hypothermia -Frequent monitoring and documentation of blood pressure, heart rate, respiratory rate and depth, oxygen saturation, urine output, and mentation, as well as laboratory results and interventions Cardiogenic shock etiology - Answer: -Most common cause is an extensive left ventricular myocardial infarction -Results from loss of contractile function of the heart -Usually diagnosed by the presence of systemic and pulmonary hemodynamic alternations, which result from inadequate CO and tissue perfusion Risk Factors for Inpatient Development of Cardiogenic Shock - Answer: -Increased age -Left ventricular ejection fraction less than 35% on hospital admission -Large myocardial infarction -Previous myocardial infarction -Presence of chronic comorbidities (DM, HTN) -Altered mental status -Hemodynamic instability Cardiogenic shock pathophysiology - Answer: -Caused by loss of ventricular contractile force, which results in decreased stroke volume and decreased CO -Neuroendocrine compensatory mechanisms are activated to improve perfusion by increasing preload and afterload -Stimulation of the RAAS and the sympathetic nervous system causes vasoconstriction and increased afterload -Although vasoconstriction increases blood pressure, the increase in afterload causes increased myocardial workload, intraventricular filling pressures, and myocardial oxygen requirements -Elevated afterload therefore reduces effective contraction and inhibits ejection -Ventricular filling pressures increase because of the increased preload, but lack of contractility prevent complete ejection -The ventricle becomes distended, further impairing effective contraction, and CO continues to decrease Cardiogenic shock physical findings - Answer: Hemodynamic findings -SBP less than 90 mm Hg -MAP less than 70 mm Hg -Cardiac index less than 2.2 L/min/m2 -Pulmonary artery occlusion pressure greater than 18 mm Hg -SVR greater than 1400 dynes/s/cm5 Noninvasive findings -Thready, rapid pulse -Narrow pulse pressure -Distended neck veins -Dysrhythmias -Chest pain -Cool, pale, moist skin -Oliguria -Decreased mentation Pulmonary findings -Dyspnea -Increased respiratory rate -Inspiratory crackles, possible wheezing -Arterial blood gas measures show a decrease in PaO2 -Respiratory alkalosis Radiographic findings -Enlarged heart -Pulmonary congestion Cardiogenic shock laboratory findings - Answer: -Creatine phosphokinase and cardiac troponin I are released in the bloodstream by dying cardiac cells -Brain natriuretic peptide and N-terminal pro-brain natriuretic peptide are produced and released by the ventricle when it is stretched owing to increased intraventricular pressure Cardiogenic shock management - Answer: -Aimed at increasing myocardial DaO2, maximizing CO, and decreasing left ventricular workload -The goals of treatment are to protect and preserve myocardium and improve tissue perfusion -Reversing hypoxemia due to pulmonary congestion and metabolic acidosis can improve the response to other therapies -Left ventricular filling pressures are often elevated, therefore reducing preload with diuretics or nitrate infusion may be indicated -Vasodilators and intra-aortic balloon pumps are interventions directed at reducing afterload, thus improving left ventricular emptying and reducing myocardial workload Cardiogenic shock nursing management - Answer: -Centers on conserving myocardial energy and decreasing the workload of the heart -Nurses need to provide physical care and periods of rest to minimize myocardial energy expenditure -Use of opioids analgesics and sedatives to minimize the sympathetic nervous system response can increase venous capacitance and decrease resistance to ejection -Supplemental oxygen is necessary to optimize arterial oxygen content and diffusion, this may require mechanical ventilation -The critical care nurse must obtain, follow, and carefully interpret the patient's hemodynamic parameters to achieve the goal of optimizing CO -Diuresis should be used to reduce the pressure: left ventricular filling pressures, pulmonary artery pressures, and pulmonary artery occlusion pressures -If the left ventricular filling pressure is too low, fluids may be used but they must be stopped when filling pressures increase without a subsequent increase in CO Neurogenic shock etiology - Answer: -Results from loss or disruption of sympathetic tone, which causes peripheral vasodilation and subsequent decreased tissue perfusion -Most common cause is a spinal cord injury above the level of T6 -Other causes include spinal analgesia, drugs, or other central nervous system problems Neurogenic shock pathophysiology - Answer: -Characterized by hypotension, bradycardia, and hypothermia -When sympathetic tone is lost, unopposed parasympathetic response results in uncontrolled arterial vasodilation and a decrease in SVR -Simultaneous venous vasodilation results in blood pooling and decreases preload -Unopposed parasympathetic stimulation leads to bradycardia, even in the presence of falling blood pressure -Disruption of the sympathetic nervous system inhibits the stimulation of baroreceptors in the aortic arch and carotid sinus -The decrease in both stroke volume (from decreased preload) and heart rate leads to decreased CO, resulting in inadequate tissue perfusion -Hypothermia results from uncontrolled heat loss from excessive vasodilation Neurogenic shock assessment - Answer: -Patients demonstrate decreased central venous pressure, CO, and SVR combined with bradycardia -Skin is warm owing to massive vasodilation Neurogenic shock management - Answer: -Prevention and treatment of hypotension through careful fluid resuscitation is a high priority *Vasopressors may be added if fluid resuscitation does not work -The goal of pharmacology in neurogenic shock is to mimic the sympathetic nervous system *The use of agents with a-adrenergic activity, such as norepinephrine, promotes vasoconstriction, while b-adrenergic agonists, such as dopamine, increase heart rate and contractility Anaphylactic shock - Answer: -Results from an allergic reaction to a specific allergen that evokes a life-threatening hypersensitivity response -Most common causes: foods, insect stings, and medications -If left untreated vascular collapse can occur, resulting in greatly decreased tissue perfusion and death Anaphylactic shock etiology - Answer: May be either immunoglobulin E (IgE) mediated or non-IqE mediated -IgE mediated anaphylaxis occurs as a result of the immune response to a specific antigen *The first time the immune system is exposed to the antigen, a very specific IgE antibody is formed and circulates in the blood *When a second exposure to this antigen occurs, the antigen binds to this circulating IgE, which then activates mast cells and basophils, triggering release of histamine, prostaglandins, leukotrienes, and other biochemical mediators that initiate anaphylaxis -Non-IqE mediated (anaphylactoid) reactions occur without the presence of IgE antibodies *It is thought that direct activation of mediators causes this response *One common anaphylactoid reaction is associated with NSAIDS *If there has been anaphylactoid reaction to one agent, restrictions should include all NSAIDS Anaphylactic shock pathophysiology - Answer: Antibody-antigen reaction causes antibody-specific mast cells and basophils, triggering release of histamine, prostaglandins, leukotriene, eosinophil chemotactic substance, heparin, neutrophil chemotactic substance, and platelet-activating factor -Cause systemic vasodilation, increased capillary permeability, bronchoconstriction, coronary vasoconstriction, and urticaria (hives) -Some cause a continued downward spiral by causing myocardial depression, inflammation, excessive secretion of mucus, and peripheral vasodilation -Initial symptoms including itching, urticaria, and some difficulty breathing due to bronchoconstriction -Death from circulatory collapse or extreme bronchoconstriction may occur within minutes to hours Anaphylactic shock physical findings - Answer: -Initially, generalized erythema, urticaria and pruritus may occur in response to the antigen -Anxiety and restlessness, dyspnea, wheezing, chest tightness, warm feeling, nausea and vomiting, angioedema, abdominal pain -Severe respiratory manifestations: laryngeal edema or severe bronchoconstriction with stridor, may develop -Hypotension from vasodilation soon occurs and leads to circulatory collapse -As circulatory collapse or hypoxemia related to severe bronchoconstriction progresses, the level of consciousness deteriorates to unresponsiveness Anaphylactic shock management - Answer: -Therapeutic goals include removal of the offending antigen, reversal of effects of the biochemical mediators, and restoration of adequate tissue perfusion -If the symptoms are mild, immediate therapy includes oxygen ad subcutaneous IV administration of an antihistamine, such as diphenhydramine (Benadryl) to block the effects of histamine -Any patient with life-threatening changes in airway, breathing, or circulation should immediately receive epinephrine *Adrenergic agonist: reverses the vasodilation and bronchoconstriction *If the patient does not respond to epinephrine, rapid infusion of crystalloids fluids is essential Anaphylactic shock nursing management - Answer: -Maintaining adequate airway and monitoring patient response to the antigen -Monitors respirations, heart rate, blood pressure, and level of anxiety, and institutes comfort measures -Patient education regarding prevention and treatment is critical Sepsis Classification - Answer: SIRS plus a known or suspected infection Severe sepsis - Answer: Sepsis associated with organ dysfunction, hypoperfusion, or hypotension. Hypoperfusion and perfusion abnormalities may include but are not limited to: -Altered mental status -Lactate greater than 4 mmol/L -Urine output less than 0.5 mL/kg/h for more than 2 hours -Acute lung injury PaO2/FiO2 less than 200 with pneumonia, less than 250 without pneumonia -Platelet count less than 100000 uL Septic shock - Answer: Severe sepsis with hypotension, despite adequate fluid resuscitation. Patients who are on inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured Risk Factors for Sepsis - Answer: Host factors -Extremes of age -Malnutrition -General debilitation -Chronic debilitation -Chronic illness -Drug or alcohol abuse -Neutropenia -Splenectomy -Multiple organ failure Treatment related factors -Use of invasive catheters -Surgical procedures -Traumatic or thermal wounds -Invasive diagnostic procedures -Mechanical ventilation -Drugs (antibiotics, cytotoxic agents, steroids) Sepsis Bundle 1 Hour - Answer: -Measure lactate level *Remeasure lactate if initial lactate elevated (>2 mmol/L) -Obtain blood cultures before administering antibiotics -Administer broad spectrum antibiotics -Rapidly administer 30 mL/kg crystalloid for hypotension or lactate > or equal to 4 mmol/L -Apply vasopressors if hypotension during or after fluid resuscitation to maintain a mean arterial pressure > or equal to 65 mm Hg Sepsis Physical Findings - Answer: tachycardia, increased respiratory rate, abnormal WBC count, and either fever or hypothermia--reflect the SIRS Lactic Acid - Answer: elevated levels indicate inadequate perfusion and utilization of anaerobic metabolism to meet cellular energy requirements What are the goals of treatment in sepsis - Answer: -Maximize DaO2 to meet cellular oxygen demand requirements -Halt the exaggerated inflammatory response MODS Pathophysiology - Answer: -It appears to result from a cascade of bacterial factors, endothelial injury, inflammatory mediatory release, disturbed hemostasis, and microcirculatory failure -Presence of altered organ function in an acutely ill patient such that hemostasis cannot be maintained without intervention MODS Nursing Management - Answer: Prevention strategies include enforcement of measures to prevent nosocomial infections, such as proper positioning (head of bed elevated during mechanical ventilation), oral care, turning and skin care, invasive catheter care, and wound care Norepinephrine (Levophed) - Answer: the gold standard vasopressor in the treatment of sepsis and septic shock. Norepinephrine (Levophed) Pharmacokintetics - Answer: -Administered via IV route -Immediate onset of action with vasopressor duration of 1 to 2 minutes Norepinephrine (Levophed) Action - Answer: -Is a pharmaceutical preparation of the naturally occurring catecholamine norepinephrine -It has a predominant alpha-receptor agonist effects and results in potent peripheral arterial vasoconstriction -It increases blood pressure more than it increases heart rate, force of contraction, or cardiac output -This drug is useful in cardiogenic and septic shock, but reduced renal blood flow limits its prolonged use Norepinephrine (Levophed) Use - Answer: Used to treat severe hypotension and shock that persists after adequate fluid volume replacement Norepinephrine (Levophed) Adverse Effects - Answer: -Possible diminished renal perfusion and decreased urine output due to vasopressor action -Possible decreased perfusion to the liver, with subsequent liver damage due to vasopressor action -Possible irritable cardiac dysrhythmias due to beta1 activity -Possible increase in myocardial oxygen requirement due to beta1 activity -Hyperglycemia, hypokalemia, and hypophosphatemia due to beta1 activity -Severe hypertension and reflex bradycardia -Limb ischemia due to profound vasoconstriction Extravasation at infusion site Norepinephrine (Levophed) Contraindications - Answer: -Cardiac dysrhythmias, angina pectoris, hypertension, hyperthyroidism and cerebrovascular disease, stimulation of the sympathetic nervous system worsens these conditions -Narrow-angle glaucoma because the drug results in mydriasis, closure of the filtration angle of the eye, and increased intraocular pressure -Hypersensitivity Norepinephrine (Levophed) Patient Teaching - Answer: -Frequent cardiac monitoring and checks of flow rate, blood pressure, and urine output are necessary -Report adverse effects such as fast pulse, palpitations, and chest pain Epinephrine - Answer: -the adrenergic drug of choice for relief of anaphylactic shock -naturally occurring catecholamine produced by the adrenal glands -administered IV, instant onset, peak of 20 minutes, duration of 20 to 30 minutes -produces an increase in blood pressure, positive inotropic and positive chronotropic effect on the myocardium hyperglycemia, bronchodilation, and vasoconstriction of arterioles in the skin, mucosa, and most viscera Dopamine - Answer: -Useful in hypovolemic and cardiogenic shock -Naturally occurring precursor of norepinephrine and epinephrine, functions as a neurotransmitter Dobutamine - Answer: -Cardiogenic and Septic Shock -Most useful in cases of shock that require increased cardiac output without the need for blood pressure support -Caution is warranted when administering the drug in patients with moderate to severe hypotension because the peripheral vasodilation may cause a further fall in blood pressure Phenylephrine - Answer: -Septic Shock -Synthetic adrenergic drug that stimulates alpha-adrenergic receptors to produce vasoconstriction -Vasoconstriction decrease cardiac output and renal perfusion and increases peripheral vascular resistance and blood pressure -May be given to increase blood pressure in hypotension and shock