Summer 2920 Final Exam Review

Summer 2920 Final Exam Review Case Study Options: GI Bleed, DKA, Preeclampsia Emergency Principles A-B-Cs Airway, Breathing, Circulation Prioritization of patients (Still use A-B-Cs) Adventitious breath sounds (identify types) Breath Sound Description When It Occurs Causes Crackles (Rales) Fine or coarse popping sounds; Mostly during like Velcro or Rice Krispies inspiration Wheezes High-pitched, musical sounds Mostly during expiration Narrowed airways: asthma, COPD, bronchospasm Rhonchi Low-pitched, snoring or gurgling sound During inspiration/expiration Mucus or secretions in large airways: bronchitis, COPD Stridor Loud, high-pitched crowing sound (upper airway) During inspiration Upper airway obstruction: croup, foreign body, laryngeal edema (EMERGENCY) Inspiration & expiration Pleural inflammation: pleuritis, pleural effusion, pneumonia Pleural Grating, creaky leather sound Friction Rub (like walking on snow) NCLEX Tip: Stridor = emergency (airway obstruction) Crackles = think fluid overload or alveoli collapse Wheezes = think asthma or bronchoconstriction Rhonchi = may clear with coughing Pleural rub = does not go away with coughing Fluid in alveoli: CHF, pneumonia, pulmonary edema, atelectasis Neurological Pain – PCA assessment and evaluation, PCA troubleshooting: PCA is a medication delivery system that allows clients to self-administer safe doses of opioids. Small, frequent dosing ensures consistent plasma levels. Clients have less lag time between identified need and delivery of medication, which increases their sense of control and can decrease the amount of medication they need. Morphine and hydromorphone are typical opioids for PCA delivery. Clients should let the nurse know if using the pump does not control the pain. To prevent inadvertent overdosing, the client is the only person who should push the PCA button. Complications Undertreatment of pain is a serious complication and can lead to increased anxiety with acute pain and depression with chronic pain. Assess clients for pain frequently and intervene as appropriate. Sedation, respiratory depression, and coma can occur as a result of overdosing. Sedation always precedes respiratory depression. QS Identify high-risk clients (older adult clients). G ??????? Carefully titrate doses while closely monitoring respiratory status. Stop the opioid and give the antagonist naloxone if respiratory rate is below 8/min and shallow, or the client is difficult to arouse. The nurse should closely monitor the client following administration of naloxone. The duration of the certain opioids can last longer than the effectiveness of the naloxone creating a need for additional doses. Identify the cause of sedation. Use a sedation scale in addition to a pain rating scale to assess pain, especially when administering opioids. Stroke – how to differentiate hemorrhagic and ischemic: Ischemic is the most common type of stroke (further classified as thrombotic or embolic) that accounts for 87% of all strokes. This is caused by a blockage of circulation to the brain. It can be reversed with fibrinolytic therapy using alteplase, also known as tissue plasminogen activator (tPA), if given within 3 to 4.5 hr of the initial manifestations (unless contraindicated by factors [presence of active bleeding]). Common risk factors for ischemic stroke include: High blood pressure (hypertension) Atherosclerosis (build-up of plaque in the arteries) Diabetes Smoking High cholesterol Atrial fibrillation (an irregular heart rhythm) biggest risk factor Heart disease Obesity Family history of stroke Symptoms of an ischemic stroke can vary depending on the location and extent of the blocked blood vessel. Common signs and symptoms include sudden: Weakness or numbness, often on one side of the body Difficulty speaking or slurred speech. Confusion Visual disturbances Severe headache Trouble with coordination and balance Dizziness or loss of consciousness A hemorrhagic stroke is caused by bleeding into the brain tissues, ventricles, or subarachnoid space. It can be caused by hypertension, an aneurysm, or an arteriovenous malformation. A sudden, severe thunderclap headache is an expected initial manifestation of a hemorrhagic stroke. Described as the worst headache of my life. If hemorrhage is large, hematoma and clot form; may expand in first 24 hours, worsening symptoms. Eventually, immune response and scar tissue form There are two primary types of hemorrhagic strokes. Intracerebral Hemorrhage (ICH): This type of hemorrhagic stroke occurs when a blood vessel within the brain itself ruptures and blood leaks into the surrounding brain tissue. ICH is often associated with conditions such as high blood pressure, arteriovenous malformations (abnormal blood vessel connections), or the use of blood-thinning medications. Subarachnoid Hemorrhage (SAH): Subarachnoid hemorrhage is characterized by bleeding into the space between the arachnoid membrane (one of the layers of the meninges surrounding the brain) and the pia mater (the delicate innermost layer). SAH is commonly caused by the rupture of an aneurysm, a weakened or bulging blood vessel in the brain. Trauma, bleeding disorders, or vascular malformations can also lead to SAH. Common risk factors for hemorrhagic stroke include: High blood pressure (hypertension) Aneurysms Arteriovenous malformations (AVMs) Blood clotting disorders Head trauma Illicit drug use (such as cocaine or amphetamines) Use of anticoagulant medications Symptoms of a hemorrhagic stroke can vary depending on the location and extent of the bleeding but often include sudden: Severe headache (often described as "the worst headache of my life") Thunderclap Headache Nausea and vomiting Altered consciousness. Weakness or numbness, typically on one side of the body Seizures Visual disturbances Difficulty speaking or slurred speech. Dysphasia – interventions and education Dysphagia can result from neurologic involvement of the cranial nerves that innervate the face, tongue, soft palate, and throat. As a result, the client’s risk of aspiration is great. QS The client is at risk for developing aspiration pneumonia because of these findings. Not all clients who have experienced a stroke have dysphagia, but all should be evaluated prior to reestablishing oral nutrition and hydration. Nursing Actions Keep the client completely NPO until evaluated by the SLP. When resuming intake, provide the client with the prescribed diet and liquid-consistency and observe closely for choking. Have suction equipment available but use with caution because nasotracheal suctioning increases ICP. QEBP An RN should provide the initial feeding and intervene if choking occurs. Some clients require an eating environment without distractions to prevent choking. Client Education Use recommended techniques for eating and adhere to instructions regarding prescribed consistency of liquids and solid foods. Sit upright and flex the head forward when swallowing to decrease the risk of choking. Spinal cord injury complications and assessments for complications Remember to prevent skin breakdown if unable to move turning schedule every 2 hours, keep the heels off the bed, keep the skin dry and minimize exposure to moisture. Do not use lotions or powders as it may cause additional skin breakdown. Complications Pneumonia and septicemia Respiratory complications and infections are among the leading causes of death in clients who have SCI. Nursing Actions Assist the client to cough and deep breath and use an incentive spirometer if able. Provide oral and nasal suctioning as needed to clear secretions. Monitor the client’s respirations, temperature, and pulse oximeter. Turn and reposition the client every 2 hrs Orthostatic hypotension Occurs when clients change position due to the interruption in functioning of the automatic nervous system and pooling of blood in lower extremities when in an upright position. Nursing Actions Change the client’s positioning slowly and place the client in a wheelchair that reclines. Use thigh-high elastic hose or elastic wraps to increase venous return. Elastic wraps might need to extend all the way up the client’s legs and include the client’s abdomen. Spinal shock Spinal shock is the spinal cord’s response to the inflammation caused by the injury. Manifestations include ?accid paralysis, loss of re?ex activity below the level of injury, and paralytic ileus due to the loss of autonomic function. Keeping mean arterial pressure at least 85 mm Hg can prevent further damage to the spinal cord. Neurogenic shock Neurogenic shock is a common response of the spinal cord following an injury. Manifestations of bradycardia, hypotension, dependent edema, and loss of temperature regulation are caused by a sudden loss of communication within the sympathetic nervous system that maintains the normal muscle tone in blood vessel walls. Nursing Actions: Treat adverse findings with prescribed medications (vasopressors or atropine) and IV fluids. Autonomic dysreflexia Occurs secondary to the stimulation of the sympathetic nervous system and inadequate compensatory response by the parasympathetic nervous system. Clients who have lesions below T6 do not experience dysreflexia because the parasympathetic nervous system is able to neutralize the sympathetic response. Sympathetic stimulation is usually caused by a triggering stimulus in the lower part of the body. (See Nursing Actions). Stimulation of the sympathetic nervous system causes extreme hypertension, sudden severe headache, pallor below the level of the spinal cord’s lesion dermatome, blurred vision, diaphoresis, restlessness, nausea, and piloerection (goose bumps). Stimulation of the parasympathetic nervous system causes bradycardia, flushing above the corresponding dermatome to the spinal cord lesion (?ushed face and neck), and nasal stuffiness. Nursing Actions Sit the client up to decrease blood pressure secondary to postural hypotension. Notify the provider. Determine and treat the cause. QEBP ??????? Distended bladder is the most common cause (kinked or blocked indwelling urinary catheter, urinary retention, urinary calculi). Insert a catheter for distended bladder using anesthetic ointment on the catheter tip, or check existing catheter for kinks, and irrigate if needed. Remove fecal impaction (use anesthetic ointment prior to removal). Adjust the room temperature and block drafts. Remove tight clothing. Assess for injury (lower extremity fracture, kidney/bladder infection). Monitor vital signs for severe hypertension and bradycardia. Administer antihypertensives (nitrates or hydralazine). Client Education Understand and prevent potential causes of dysreflexia. If fluid intake is temporarily increased, drink a little more at various times throughout the day rather than all at once. Keep a list of actions to take if an episode of dysreflexia occurs. Halo fixation – education Client Education If going home with a halo fixation device on, follow instructions for pin and vest care. Report indications of infection and skin breakdown. Halo on for 8 to 12 weeks The screws are not to be adjusted except by the provider. Pin loosing is a complication and should be reported to the provider immediately. Respiratory Bleeding varices – balloon placement and interventions (ABC) Esophagogastric balloon tamponade Rarely used but can be used to temporarily control bleeding until another measure can be implemented. Risks: Tube migration, which can lead to airway obstruction; aspiration of gastric contents into lungs. Clients often require endotracheal intubated to protect the airway. Can cause necrosis of tissue if left in place for an extended period of time . Balloon should be in place no longer than 12 hr. Nursing Actions Check balloons for leaks prior to insertion. Monitor placement of the tube and observe for possible obstruction of airway. Monitor for aspiration into the lungs and secretions or blood from the esophagus. Provide oral suction as needed. Maintain balloon pressure at prescribed pressure for prescribed time to decrease risk of esophageal or gastric necrosis from ischemia. Monitor the client who has decreased mentation or confusion and who might pull on the tube. Status Asthmaticus interventions and prioritization in interventions This is a life-threatening episode of airway obstruction that is often unresponsive to common treatment. It involves extreme wheezing, labored breathing, use of accessory muscles, distended neck veins, and creates a risk for cardiac and/or respiratory arrest. Nursing Actions Prepare for emergency intubation. Administer IV fluids, oxygen, bronchodilators, and epinephrine. Initiate systemic steroid therapy. Hypoxemia Hypoxemia is an inadequate level of oxygen in the blood. Hypovolemia, hypoventilation, and interruption of arterial flow can lead to hypoxemia. Hypoxia is a decrease in tissue oxygenation. Client Presentation Tachypnea Tachycardia Restlessness Pale skin and mucous membranes Elevated blood pressure Findings of respiratory distress (use of accessory muscles, nasal flaring, tracheal tugging, and adventitious lung sounds) Confusion and stupor Cyanotic skin and mucous membranes Bradypnea Bradycardia Hypotension Cardiac dysrhythmias Considerations Preparation of the client Explain all procedures to the client. Place the client in semi-Fowler’s or Fowler’s position to facilitate breathing and promote chest expansion. Ensure that all equipment is working properly. Ongoing care Provide oxygen therapy at the lowest flow that will correct hypoxemia. Assess/monitor respiratory rate, rhythm and effort, lung sounds, and SaO 2 to determine the client’s need for supplemental oxygen. Manifestations of hypoxemia are shortness of breath, anxiety, tachypnea, tachycardia, restlessness, pallor or cyanosis of the skin or mucous membranes, adventitious breath sounds, and confusion. Manifestations of hypercarbia (elevated levels of CO 2 ) are restlessness, hypertension, and headache. Monitor diagnostic reports that show information related to oxygenation, including ABGs. Promote good oral hygiene and provide as needed. Promote turning, coughing, deep breathing, use of incentive spirometer, and suctioning. Promote rest and decrease environmental stimuli. QPCC Provide emotional support for clients who appear anxious. Assess nutritional status. Provide supplements as prescribed. Assess/monitor skin integrity. Provide moisture and pressure-relief devices as indicated. Assess/monitor and document the client’s response to oxygen therapy. Titrate oxygen to maintain prescribed oxygen saturation. Discontinue supplemental oxygen gradually. Interventions Monitor for manifestations of respiratory depression, such as decreased respiratory rate and decreased level of consciousness. Notify the provider if findings are present. Respiratory distress Position the client for maximum ventilation (Fowler’s or semi-Fowler’s position). Complete a focused respiratory assessment. Promote deep breathing. Use supplemental oxygen as prescribed. Stay with the client and provide emotional support to decrease anxiety. Promote airway clearance by encouraging coughing and oral/oropharyngeal suctioning if necessary. Complications Oxygen toxicity Oxygen toxicity can result from high concentrations of oxygen (typically above 50%), long durations of oxygen therapy (typically more than 24 to 48 hr ), and the client’s degree of lung disease. Manifestations include a nonproductive cough, substernal pain, nasal stuffiness, nausea, vomiting, fatigue, headache, sore throat, and hypoventilation. Nursing Actions Use the lowest level of oxygen necessary to maintain the prescribed SaO 2 . Monitor ABGs. Notify the provider if results are outside the expected or prescribed ranges. Use an oxygen mask with continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP) if prescribed to help decrease the amount of oxygen needed. Use positive end expiratory pressure (PEEP) as prescribed while the client is receiving mechanical ventilation to help decrease the amount of needed oxygen. Oxygen-induced hypoventilation Oxygen-induced hypoventilation can develop in clients who have COPD and chronic hypoxemia with hypercarbia. Nursing Actions Monitor respiratory rate and pattern, level of consciousness, and SaO 2 . Provide oxygen therapy at the lowest flow rate that manages hypoxemia. If the client tolerates it, use a Venturi mask to deliver precise oxygen levels. Notify the provider of findings of respiratory depression, such as a decreased respiratory rate or a decreased level of consciousness. TB – expected findings, isolation: Expected Findings Persistent cough lasting longer than 3 weeks Purulent sputum, possibly blood-streaked Fatigue and lethargy Weight loss and anorexia Night sweats and low-grade fever in the afternoon Nursing Care Place the client in a negative airflow room and implement airborne precautions . Chest tube – normal/abnormal findings A disposable three-chamber drainage system is most often used. First chamber: drainage collection Second chamber: water seal Third chamber: suction control (can be wet or dry) Water seals are created by adding sterile fluid to a chamber up to the 2 cm line. While this is the minimum amount required for functioning, recommended amounts can vary by manufacturer. The water seal allows air to exit from the pleural space on exhalation and stops air from entering the lungs with inhalation. To maintain the water seal, always keep the chamber upright and below the chest tube insertion site . Routinely monitor the water level due to the possibility of evaporation. Add fluid as needed to maintain the manufacturer’s recommended water seal level. Wet suction: The height of the sterile fluid in the suction control chamber determines the amount of suction transmitted to the pleural space. A suction pressure of -20 cm H 2 O is commonly prescribed. The level of water in the suction control chamber determines the suction pressure. The system is attached a suction source, and suction initiated until gentle bubbling begins in the suction chamber. Dry suction: When a dry suction control device is used, the provider prescribes a level of suction for the device, typically -20 cm H 2 O. When connected to wall suction, the regulator on the chest tube drainage system is set to the manufacturer’s recommendation. Tidaling (movement of the fluid level with respiration) is expected in the water seal chamber. With spontaneous respirations, the fluid level will rise with inspiration (increase in negative pressure in lung) and will fall with expiration. With positive-pressure mechanical ventilation, the fluid level will rise with expiration and fall with inspiration. Cessation of tidaling in the water seal chamber signals lung re-expansion or an obstruction within the system. Continuous bubbling in the water seal chamber indicates an air leak in the system. When the tubes are inserted to remove air from the pleural space, intermittent bubbling is expected; it is common to see bubbling during exhalation, sneezing, or coughing. In this case, when bubbling is no longer seen, it indicates that all the air has been removed. When tubes are in the mediastinal space (such as following open heart surgery), bubbling and tidaling are not expected; pulsations in the fluid level might be seen. Fatty emboli – late vs early signs Early manifestations of fatty emboli – tachypnea, dyspnea, hypoxemia, anxiousness Late manifestations of fatty emboli – petechia, neurological changes (associated with hypoxemia), tachycardia. Pancuronium (-ronium drugs) ( P ancuronium ) are neuromuscular blockade agents that are used to induce paralysis in patients. This suppresses a patient’s respiratory effort allowing the vented patient to rely on the vent to breath and helps to overcome poor lung compliance . Reversal agent: neostigmine Therapeutic Uses Neuromuscular blocking agents are used as adjuncts to general anesthesia to promote muscle relaxation. These agents are used to control spontaneous respiratory movements in clients receiving mechanical ventilation. These agents are used as seizure control during electroconvulsive therapy. Neuromuscular blocking agents are used during endotracheal intubation and endoscopy. Complications Respiratory arrest Atracurium Hypotension Malignant hyperthermia ARDS interventions Proning is a therapeutic technique used in the management of acute respiratory distress syndrome (ARDS) to improve oxygenation and ventilation. Here's an explanation of how proning works and its benefits: Cardiovascular Unstable angina – medications and instructions Management of Angina: Lifestyle Modifications: Healthy diet, regular exercise, smoking cessation, and weight management. Medications: Nitroglycerin, beta-blockers, calcium channel blockers, and antiplatelet agents may be prescribed. ASPIRIN is given as an antiplatelet aggregate (it stops it from accumulating and sticking together) (Nitro 3 every 5 min, if the pt calls and takes 1 nitro have the pt call 911 and take another nitro. MI – meds and why, labs to assess. Morphine, Oxygen, Nitrate, Aspirin. The administration of aspirin upon arrival, beta-blocker within 24 hours, and thrombolytic within 30 minutes MORPHINE is the medication of choice for pain and anxiety of acute MI because it will reduce the preload and afterload thus decreasing the work of the heart. Medications: Aspirin, nitroglycerin, and anticoagulants may be administered. MONA = Morphine, Oxygen, Nitro, Aspirin. Nitrates: vasodilators (opens all vasculature) Aspirin: decrease platelet adherence (limits clotting) Beta blockers: decrease myocardial oxygen demand . Calcium antagonists: arteriole dilation (decreased systemic vascular resistance) ACE inhibitors: decrease BP and resistance (prevents further remodeling of the heart for heart failure patients) Labs: Troponin is a contractile protein (cardiac enzyme) that is released from the cardiac muscle when it has a mismatch between oxygen demand and oxygen supply. If there is an ischemic event for some reason. We must evaluate a baseline and serial troponins over time to see if the level is changing (in the case an ischemic event is developing). Troponin I <0.03 g/L is normal. Above that is considered elevated "high" lab value. Troponins are proteins found in skeletal and cardiac muscle fibers, and they play a crucial role in muscle contraction. When it comes to heart problems, the troponins primarily assessed are cardiac troponins, specifically troponin I (cTnI) and troponin T (cTnT). These troponins are released into the bloodstream when there is damage to the heart muscle, and their levels are measured as diagnostic markers for various cardiac conditions, particularly myocardial infarction (heart attack). Troponin I (cTnI): Troponin I is a subtype of troponin specific to cardiac muscle. It is not normally found in the bloodstream under normal conditions. When there is damage to cardiac muscle, such as during a heart attack, troponin I is released into the bloodstream. Elevated levels of troponin I in the blood are a highly sensitive and specific marker for acute myocardial infarction (AMI). Troponin T (cTnT): Troponin T is another subtype of troponin specific to cardiac muscle. Similar to troponin I, troponin T is not normally present in the bloodstream. Its release into the blood is indicative of cardiac muscle injury or damage. Elevated levels of troponin T are used as a diagnostic marker for myocardial infarction. Troponin I is higher with MI’s while Troponin T is often higher in patient with stable conditions like atrial fibrillation. This helps to differentiate. Troponin Complex: Troponin I and troponin T, along with troponin C, together form the troponin complex. The troponin complex is involved in regulating the contraction of cardiac muscle fibers. CPK creatine phosphokinase, is an enzyme that is elevated in the presence of muscle injury. This is not specific for myocardial damage; it is used in conjunction with other diagnostic tests to support a diagnosis of myocardial infarction. CK-MB is a test of myocardial cell injury (this is a CPK isoenzyme) and increases 3-6 hours post-injury and peaks at 12-24 hours. It returns to normal within 48 hours. CK-MB should be <4-5% of total creatine kinase (CK). Above that is considered elevated "high" lab value. While CK-MB has been historically used as a cardiac biomarker, troponins (specifically troponin I and troponin T) have become the preferred markers due to their higher sensitivity and specificity. Troponins are released earlier than CK-MB and persist in the bloodstream for a longer duration. Myoglobin indicates myocardial injury. This will significantly increase within approximately 3 hours following myocardial infarction. This is used in conjunction with other diagnostic tests. Heart failure – identify and compare symptoms right/left, orders to question and why Left-sided failure Dyspnea, orthopnea (shortness of breath while lying down), nocturnal dyspnea Fatigue Displaced apical pulse (hypertrophy) S3 heart sound (gallop) Pulmonary congestion (dyspnea, cough, bibasilar crackles) Frothy sputum (can be blood-tinged) Altered mental status Manifestations of organ failure, such as oliguria (decrease in urine output) Nocturia Right-sided failure Jugular vein distention Ascending dependent edema (legs, ankles, sacrum) Abdominal distention, ascites Fatigue, weakness Nausea and anorexia Polyuria at rest (nocturnal) Liver enlargement (hepatomegaly) and tenderness Weight gain Questions fluid intake. Maintain dietary restrictions as prescribed (restricted fluid intake, restricted sodium intake). Question Digoxin orders. For a client taking digoxin, take the apical heart rate for 1 min. Hold the medication if apical pulse is less than 60/min, and notify the provider. For some clients, the provider might allow the heart rate to be as low as 50/min. Laboratory Tests Heart Failure Cardiac Labs BNP – B-type natriuretic peptide causes natriuresis (excretion of sodium in the urine) and is released from the ventricles. This test is used to determine if heart failure is present. Ideal lab to distinguish between cardiac and respiratory causes of shortness of breath. (BNP is looking at the heart failure), does not tell you were, but does tell you that there has been damage in the heart) Shock – identify types, assessment findings: Type of Shock Underlying Cause Expected Findings Key Difference Cardiogenic Hypotension (late), Chest pain Tachycardia, Failure of the heart to pump Cool, clammy skin Dyspnea, pulmonary Crackles + chest pain + effectively due to a cardiac congestion/crackles, Weak, thready pulses - signs of poor pump factor (MI, HF, dysrhythmias, Decreased urine output function valvular rupture) Hypovolemic Loss of 25–30% of intravascular volume (hemorrhage, burns, dehydration) Hypotension, Tachycardia, Cool, clammy skin - Thirst, dry mucous membranes Weak, thready pulses - Decreased urine output - Rapid breathing Obstructive Mechanical blockage of blood Hypotension, Tachycardia, Chest pain, flow (cardiac tamponade, dyspnea, Distended neck veins (JVD), tension pneumothorax, Possible muffled heart sounds (tamponade) pulmonary embolism) or tracheal deviation (tension pneumothorax) JVD + specific obstructive signs (muffled heart sounds or tracheal deviation) Neurogenic (Distributive) Loss of sympathetic tone (spinal cord injury, head trauma, epidural) - Bradycardia (unique) - Hypotension Warm, dry skin (initially) - Poikilothermia (cannot regulate body temp) Bradycardia + warm dry skin instead of cool clammy Septic (Distributive) Massive vasodilation from infection (usually gramnegative bacteria) Warm, flushed skin early ? cool as it progresses, Fever, chills, Tachycardia, Hypotension (late) Tachypnea, Altered mental status Fever and warm flushed skin early Anaphylactic (Distributive) Antigen-antibody reaction (allergic reaction to meds, food, latex, bee sting) Airway swelling (laryngeal edema), Wheezing, bronchospasm Dyspnea, Urticaria, itching, flushing, Hypotension, Anxiety Respiratory distress + hives/urticaria Thirst and signs of fluid loss Digoxin, Furosemide Digoxin decreases the heart rate, so the nurse should count the apical pulse for at least 1 min before administering. The nurse should hold the medication and notify the provider if the client's heart rate is below 60/min or if a change in heart rhythm is detected. High-ceiling loop diuretics Furosemide Purpose Expected Pharmacological Action High-ceiling loop diuretics work in the loop of Henle. Block reabsorption of sodium and chloride and prevent reabsorption of water Cause extensive diuresis even with severe renal impairment Increase kidney excretion of water, potassium, sodium, chloride, magnesium, calcium Therapeutic Uses High-ceiling loop diuretics are used when there is an emergent need for rapid mobilization of fluid. Pulmonary edema caused by heart failure Conditions not responsive to other diuretics (edema caused by liver, cardiac, or kidney disease) Hypertension (torsemide) Unlabeled use: Hypercalcemia Complications Dehydration Nursing actions Assess/monitor for manifestations of dehydration: dry mouth, increased thirst, oliguria, and lethargy and report findings to the provider. Report urine output less than 30 mL/hr. Notify provider of findings (may need to withhold medication). Minimize the risk for dehydration by monitoring the client's weight daily and checking the prescribed dose of medication (therapy is generally initiated with a low dose of medication). Hypotension Nursing actions Monitor blood pressure. Advise clients to avoid sudden changes of position and arise slowly from lying down or sitting. Client Education Monitor for manifestations of postural hypotension (light-headedness, dizziness). If these occur, sit or lie down. Ototoxicity Transient with furosemide and irreversible with ethacrynic acid Nursing actions: Avoid use with other ototoxic medications (aminoglycoside antibiotics [gentamicin]). Client Education: Notify the provider of tinnitus, which can indicate ototoxicity. Hypokalemia K+ less than 3.5 mEq/L Nursing actions Monitor cardiac status and potassium levels. Report a decrease in potassium level (K+ less than 3.5 mEq/L). Client education Teach clients to consume high-potassium foods (bananas, potatoes, dried fruits, nuts, spinach, citrus fruit). Teach clients to observe and report manifestations of hypokalemia (nausea, vomiting, fatigue, leg cramps, and general weakness). Contraindications/Precautions Contraindicated in clients who have anuria (no urine output). Use cautiously in clients who have, severe liver disease, diabetes mellitus, dehydration, electrolyte depletion, and gout. Use cautiously in clients taking digoxin, lithium, ototoxic medications, NSAIDs, or antihypertensives. Administration to clients who have hypoproteinemia can result in ototoxicity. Interactions Digoxin toxicity (ventricular dysrhythmias) can occur in the presence of hypokalemia. Nursing actions Parts of EKG (what do they represent and where are they located) P wave – the depolarization of the atria (0.06-0.12 seconds) PR interval – from the onset of the P wave to the QRS, time is 0.12 - 0.20 seconds, this is the time it takes for the atria to depolarize and travel through the fibers to the ventricles . QRS complex – the depolarization of the ventricles (also the repolarization of the atria but much smaller so hidden in the QRS complex), time is less than 0.12 seconds . ST segment from the end of the QRS to the start of the T wave, this is the time it takes for early ventricular repolarization . T wave – the repolarization of the ventricles QT interval – from the start of the QRS to the end of the T wave (0.34-0.43 seconds) this is the time it takes for the ventricles to depolarize and repolarize . U wave – repolarization of Purkinje fibers, or due to imbalance of electrolytes. One of the most common causes of U waves is hypokalemia, which is a lower-than-normal level of potassium in the blood. Brady dysrhythmias, slower heart rates can alter the normal repolarization sequence and result in the appearance of U waves. Drugs that prolong the QT interval may contribute to U waves. They are of concern if they are new, prominent, or associated with cardiac symptoms. VTach – interventions and symptoms Ventricular Tachycardia with a rate of 140-150. What do you do first? Check your patient! DO they have a pulse? Symptoms: hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest, causes decreased CO due to decreased ventricle refill time and may lead to VFib Treatment: treat the underlying causes such as electrolyte and MI, medications (Monomorphic -lidocaine, procainamide, amiodarone, Polymorphic - magnesium), elective cardioversion if awake and responsive. If the client is unstable or in pulseless VTach you would defibrillate, CPR, epinephrine, treat underlying cause, amiodarone/lidocaine) Defibrillation is performed to correct life-threatening cardiac arrhythmias including UNSTABLE VT. In cardiac emergencies, defibrillation should be performed immediately after identifying the client is experiencing an arrhythmia. The client in the question is awake and reporting sudden heart palpitations. There is no indication the client is unstable. Elective cardioversion is the priority intervention when the client is awake and responsive. Ventricular tachycardia might not be an immediate threat to the client, but it does require intervention to prevent long-term cardiac impairment. Pacemaker and EKGs Permanent pacemaker After insertion the nurse should assess the incisional site for bleeding and hematoma post implantation. The dressing over the site should remain clean and dry. The nurse should closely monitor the client’s EKG rhythm following permanent pacemaker insertion to ensure that the pacemaker is preventing bradycardia. The nurse should assess for hiccups which can indicate the generator is pacing the diaphragm. ~ They should not lift their arm above their shoulder for 1-2 weeks and nothing over 10 lbs for 4 weeks. ~ The batter on a permanent pacemaker is expected to last approximately 10 years. The pacer spike, a vertical line, should be followed by a P wave (atrial pacing) or QRS complex (ventricular pacing). A client with a pacemaker will show pacer spikes. The pacemaker fires, showing a spike on the monitor strip, which stimulates the ventricle, and the QRS complex appears, indicating that depolarization has occurred. This is used to increase the speed of contraction. The client may be internally (surgically placed pacemaker), endovascular pacing, or transcutaneous pacing. Hematological Thrombocytopenia: Platelets Platelet transfusion Platelets do not need to match the client blood type. Platelet infusion bags contain 200 to 300 mL. Nursing Actions Platelets are fragile and must be immediately infused once brought to the client’s room, and given over 15 to 30 min using a special transfusion set with a small filter and short tubing. Vital signs are taken before the infusion, 15 min after the infusion starts, and upon completion. Secondary to disease and/or treatment; greatly increases the client’s risk for bleeding. The greatest risk is at platelet counts less than 50,000/mm3, and spontaneous bleeding can occur at less than 20,000/mm 3 . QS Nursing Actions Monitor for petechiae, ecchymosis, bleeding of the gums, nosebleeds, and occult or frank blood in stool, urine, or vomitus. Institute bleeding precautions. (Avoid IVs and injections; apply pressure for approximately 10 min after blood is obtained; and handle client gently and avoid trauma.) Minimize the risk of trauma (safe environment). Administer blood products (platelets) if platelet count is less than 20,000/mm3. Anemia assessment findings Physical Assessment Findings Shortness of breath/fatigue, especially upon exertion Tachycardia and palpitations, orthostatic hypotension Dizziness or syncope upon standing or with exertion . Pallor of the nail beds and mucous membranes Cold intolerance: skin is cool to the touch . Nail bed deformities (spoon-shaped nails) when chronic . Smooth, sore, bright-red tongue (vitamin B 12 deficiency) Paresthesia in hands and feet with possible loss of balance (vitamin B 12 deficiency) Sickle cell anemia teaching Defective Hgb (sickle-cell disease): RBCs become malformed during periods of hypoxia and obstruct capillaries in joints and organs . If lacking intrinsic factor or have an irreversible malabsorption syndrome, this therapy must be continued for the rest of their life. Receive vitamin B 12 injections monthly. Drink plenty of fluid. Fluid/Electrolyte/Acid-Base IV assessment problems and interventions Infiltration or Extravasation IV solution or medication leaks into the subcutaneous tissue. Infiltration is the leak of a non-vesicant; extravasation is the leak of a vesicant solution which can damage the tissues. With extravasation, prior to regular treatment, the nurse should withdraw the solution from the client’s IV catheter and might need to administer an antidote prior to discontinuing the IV access. Findings include pallor, local swelling at the site, decreased skin temperature around the site, damp dressing, or slowed rate of infusion. Treatment Stop the infusion and remove the catheter. Elevate the extremity. Encourage active range of motion. Apply a warm or cold compress depending on the solution infusing. Restart the infusion proximal to the site or in another extremity. Prevention Carefully select the site and catheter. Secure the catheter. Phlebitis or Thrombophlebitis Edema; throbbing, burning, or pain at the site; increased skin temperature; erythema; a red line up the arm with a palpable band at the vein site; slowed rate of infusion. Treatment Promptly discontinue the infusion and remove the catheter. Elevate the extremity. Apply warm compresses 3 to 4 times/day. Restart the infusion in a different vein proximal to the site or in another extremity. Obtain a specimen for culture at the site and prepare the catheter for culture if drainage is present. Prevention Change the IV site at least every 72 hr or sooner according to the facility’s policy. Avoid inserting an IV into the lower extremities. Use hand hygiene. Use surgical aseptic technique. Fluid Overload Distended neck veins, increased blood pressure, tachycardia, shortness of breath, crackles in the lungs, edema, additional findings varying with the IV solution. Treatment Decrease the IV flow rate. and notify the provider of the change. Raise the head of the bed. Measure vital signs and oxygen saturation. Adjust the rate after correcting fluid overload. Administer diuretics. Prevention Use an infusion pump. Monitor I&O. Transfusion reactions and interventions Acute hemolytic transfusion reaction Onset: Immediate or can manifest during subsequent transfusions Findings Results from a transfusion of blood products that are incompatible with the client’s blood type or Rh factor. Can occur following the transfusion of as few as 10 mL of a blood product. Can be mild or life-threatening, resulting in disseminated intravascular coagulation (DIC) or circulatory collapse. Findings include chills, fever, low-back pain, tachycardia, hypotension, chest tightening or pain, tachypnea, nausea, anxiety, hemoglobinuria, and an impending sense of doom. Nursing Actions Stop the transfusion. Remove the blood tubing from the IV access. Avoid infusing further blood products into the circulatory system. Initiate an infusion of 0.9% sodium chloride using new tubing. Monitor vital signs and fluid status. Send the blood bag and administration set to the lab for testing. Febrile transfusion reaction Onset: Commonly occurs within 2 hr of starting the transfusion Findings Results from the development of anti-WBC antibodies. Can be seen when the client has received multiple transfusions. Findings include chills, increase of 1° C (2° F) or greater from the pretransfusion temperature, hypotension, and tachycardia. Nursing Actions Use WBC filter for administration to catch the WBCs and prevent the reaction from occurring. Stop the transfusion and administer antipyretics. Initiate an infusion of 0.9% sodium chloride using new tubing. Allergic transfusion reaction Onset: During or up to 24 hr after transfusion Findings Results from a sensitivity reaction to a component of the transfused blood products. Findings are usually mild and include itching, urticaria, and flushing. The client can develop an anaphylactic transfusion reaction resulting in bronchospasm, laryngeal edema, hypotension, and shock. Nursing Actions Mild reaction Stop the transfusion. Initiate an infusion of 0.9% sodium chloride using new tubing. Administer an antihistamine, such as diphenhydramine. If the provider prescribes to restart the transfusion, do so slowly. Anaphylactic reaction Stop the transfusion. Administer epinephrine, corticosteroids, vasopressors, oxygen, or CPR if indicated. Remove the blood tubing from the client’s IV access. Initiate an infusion of 0.9% sodium chloride using new tubing. Bacterial transfusion reaction Onset: During or up to several hours after transfusion Findings Results from a transfusion of contaminated blood products. Findings include wheezing, dyspnea, chest tightness, cyanosis, hypotension, and shock. Nursing Actions Stop the transfusion. Administer antibiotics and an IV infusion of 0.9% sodium chloride using new tubing. Send a blood culture specimen to the lab for analysis. Circulatory overload Onset: Can occur any time during the transfusion Findings Results from a transfusion rate that is too rapid for the client. Older adult clients or those who have a preexisting increased circulatory volume are at an increased risk. Findings include crackles, dyspnea, cough, anxiety, jugular vein distention, and tachycardia. Manifestations can progress to pulmonary edema. Nursing Actions Slow or stop the transfusion depending on the severity of manifestations. Position the client upright with feet lower than the level of the heart. Administer oxygen, diuretics, and morphine as prescribed. Hypokalemia (<3.5) results from increased loss of potassium from the body or shifting of potassium into the cells; may cause cardiac standstill. Causes: Actual loss: overuse of diuretics, digitalis, corticosteroids; increased aldosterone secretion, Cushing’s syndrome, Loss through GI tract (vomiting, diarrhea, NG tube suctioning, excessive laxative use or tap water enema (hypotonic), NPO, kidney disease that impairs reabsorption of potassium . Relative loss (shifting): alkalosis, hyperinsulinism, hyperalimentation, TPN, water intoxication . Symptoms may include shallow respirations from weak accessory muscles, orthostatic hypotension due to cardiovascular changes, constipation due to decreased peristalsis, hyporeflexia and slow tendon response. Hypokalemia: Flattened T waves, prominent U waves, prolonged QT interval, ventricular arrhythmias. Adic-Base imbalance – numbers, expected findings for metabolic acidosis: pH and Acidosis: Normal blood pH is between 7.35 and 7.45. In metabolic acidosis, the pH drops below 7.35 due to an excess of acid or loss of bicarbonate (a base). Bicarbonate (HCO??): Bicarbonate is a base that helps neutralize acids in the blood. In metabolic acidosis, bicarbonate levels are usually low, either due to its consumption in buffering excess acid or loss from the body. The signs and symptoms of metabolic acidosis can vary depending on the underlying cause and the severity of acidosis. Common manifestations include: Kussmaul Respirations: Deep and labored breathing, often seen in severe acidosis, as the body attempts to compensate by exhaling more CO?. Fatigue and Weakness: Due to the body’s impaired ability to maintain normal cellular function in an acidic environment. Confusion or Lethargy: Acidosis can affect brain function, leading to altered mental status. Nausea and Vomiting: As the body tries to rid itself of excess acid. Decreased Blood Pressure: Caused by vasodilation and decreased heart function in severe cases. Gastrointestinal Appendicitis – assessment: Subjective (What the Patient Reports): Abdominal pain: Starts as vague, periumbilical ? localizes to right lower quadrant (RLQ) (McBurney’s point) Pain worsens with movement, coughing, or sneezing . Nausea and vomiting Loss of appetite (anorexia) Low-grade fever Constipation or diarrhea Feeling of needing to pass gas, but unable to Objective (What the Nurse Assesses): Sign Description McBurney’s point tenderness Pain located ? the distance from the anterior superior iliac spine to the navel Rebound tenderness Increased pain when pressure is released from RLQ Guarding Tensing of abdominal muscles during palpation Rigidity Board-like abdomen ? may indicate rupture or peritonitis Rovsing’s sign RLQ pain when LLQ is palpated Psoas sign RLQ pain when patient extends right leg against resistance Obturator sign RLQ pain when the hip is flexed and rotated internally Fever, tachycardia Common systemic signs Elevated WBCs Often seen on labs (noted in assessment documentation) Cholecystitis – expected findings (ex. Urine), cholecystectomy: laparoscopic vs open nursing actions: Expected Findings Sharp pain in the right upper quadrant, often radiating to the right shoulder Pain with deep inspiration during right subcostal palpation (Murphy’s sign) Intense pain (increased heart rate, pallor, diaphoresis) with nausea and vomiting after ingestion of high-fat food caused by biliary colic Rebound tenderness (Blumberg’s sign performed by the provider or advanced practice nurse) Dyspepsia, eructation (belching), and flatulence Fever Physical assessment findings Jaundice, icterus (yellow discoloration of the sclera), clay-colored stools, steatorrhea (fatty stools), dark urine, and pruritus (accumulation of bile salts in the skin) can manifest in clients who have chronic cholecystitis (due to biliary obstruction). Older adult clients can have atypical presentation of cholecystitis (absence of pain or fever). Delirium might be the initial manifestation, or the client might have localized tenderness. Removal of the gallbladder: traditional (large abdominal incision) or laparoscopic (small incisions) requires proper positioning after surgery to encourage lung expansion and support the wound (semi-fowlers). For laparoscopic the nurse should also encourage ambulation as soon as fully away to encourage the absorption of the carbon dioxide that was used during the surgery. This will minimize discomfort form trapped CO2. Lift no more than 2.3 kg (5 lb) and following surgery. Offer foods low in fat to prevent nausea and vomiting. (Gas stays after surgery to get rid of the carbon dioxide from surgery) TPN – complications At risk for Hypoglycemia manifestations shakiness and diaphoresis. Renal Dialysis adverse complications and interventions, what to report to provider (peritoneal dialysis) Peritonitis (infection in peritoneum): cloudy or discolored output, fever, purulent drainage, redness and swelling, tender abdomen. Site infection – must maintain aseptic technique. May have wet appearance at site, leaking fluids, purulent drainage, redness of site, swelling at site Peritoneal dialysis can remove protein from the blood as well as excess fluid, wastes, and electrolytes. Hyperglycemia can result from glucose in the dialysate. The blood can absorb glucose from the dialysate. Hyperlipidemia can also occur from long-term therapy and lead to hypertension. Disequilibrium Syndrome is a rare but serious neurological complication that occurs when dialysis removes solutes from the blood too quickly, leading to cerebral edema. It typically happens in patients who are new to hemodialysis or those who have had a long delay between treatments. Signs & Symptoms include: Headache, confusion, restlessness, dizziness, seizures, coma, Nausea, vomiting, Muscle cramps, twitching, Hypertension, bradycardia, loss of consciousness Monitor Neurological Status: Perform frequent neuro checks (e.g., Glasgow Coma Scale, pupil reactions, LOC to check for cerebral edema). Monitor Vital Signs: Watch for hypertension, bradycardia, and respiratory changes (signs of cerebral edema). Bleeding & AV shunt rupture Medical emergency where the arteriovenous access site (either AV fistula or AV graft) experiences a break in integrity, leading to severe bleeding, hemodynamic instability, and potential limb ischemia. AKI – Oliguric phase Oliguric Phase: Oliguria is a hallmark of the oliguric phase and is characterized by low glomerular filtration rate (GFR) and a lack of urine output (<400ml/day). Nephrons are filled with WBCs and overloaded. The kidneys are unable to effectively filter and eliminate waste products and excess fluids, leading to fluid overload. Common manifestations include fluid retention, electrolyte imbalances, elevated blood pressure, and uremic symptoms. Close monitoring of fluid status, electrolyte levels, and hemodynamic stability is crucial during this phase. UTI/Pyelonephritis and pregnancy concerns The most common organism is E. coli UTI treatment with antibiotics. Ciprofloxacin carries a risk of tendon rupture. Fluoroquinolone antibiotics are associate with an increased risk of tendon rupture. Instruct the client to report any tendon swelling or inflammation immediately. Risk factors: Most often seen in females ages 20-30. Kidney stones (frequent) increase risk. Reflux (the backward flow of urine from the bladder into the kidney) and pregnancy also increase risk. Males over 65 years have increased risk due to prostatitis and hypertrophy of the prostate. Bladder tumors, chronic urinary stones. Neurogenic bladder (chronic). Chronic illness (diabetes mellitus, hypertension, chronic cystitis) Signs/Symptoms – chills, abdominal pain (colicky), nausea, malaise/fatigue, urinary tract infection symptoms, CVA tenderness (costovertebral angle tenderness), flank and back pain, fever, tachycardia, tachypnea, hypertension, vomiting. Reproductive HIV/AIDS Stages of HIV Infection: Acute HIV Infection: This stage occurs within the first few weeks after infection. Some people may experience flu-like symptoms, while others may have no symptoms at all. Chronic HIV Infection: This stage can last for many years, during which the virus replicates in the body, but the immune system is still functional. AIDS (acquired immunodeficiency syndrome): AIDS is the final stage of HIV infection, characterized by a severely damaged immune system and a range of opportunistic infections and cancers. An individual is diagnosed with AIDS when their CD4 cell count falls below a certain level and/or they develop an AIDS-defining illness. Symptoms: The symptoms of HIV can vary widely and may include fever, fatigue, swollen lymph nodes, sore throat, rash, and more. However, these symptoms are not specific to HIV and can be caused by other illnesses. Treatment: Antiretroviral therapy (ART) is the standard treatment for HIV. ART helps suppress the virus, preserve immune function, and reduce the risk of complications and transmission to others. Patients are subject to opportunistic infections when CD4-T cell count is low! Ex. Candidiasis: oral candidiasis can affect anyone, it occurs most often in infants, toddlers, older adults, and clients whose immune systems have been compromised by illness, such as AIDS, or medications. HSV-2 assessment findings and symptoms Symptoms of genital herpes develop 3 to 7 days after skin to skin contact with and infected person. The nurse should expect the client to have influenza like symptoms, along with genital herpes lesion which appear as small blisters on the genitals. Other symptoms can include painful urination, vaginal discharge, and enlarged lymph nosed in the groin. Medications Acyclovir The best for diagnosis of Herpes is not a blood test. They are unreliable to detect the type of herpes. An essay swab is best. Musculoskeletal Traction – interventions and meds for muscle spasms Nursing Interventions/Actions: Assess neurovascular status of the affected body part every hour for 24 hr and every 4 hr after that. Maintain body alignment and realign if the client seems uncomfortable or reports pain. Avoid lifting or removing weights. Ensure that weights hang freely and are not resting on the floor. If the weights are accidentally displaced, replace the weights. If the problem is not corrected, notify the provider. Ensure that pulley ropes are free of knots, fraying, loosening, and improper positioning at least every 8 to 12 hr. Notify the provider if the client experiences severe pain from muscle spasms unrelieved with medications or repositioning. Move the client in halo traction as a unit, without applying pressure to the rods. This will prevent loosening of the pins and pain. Routinely monitor skin integrity and document. Use heat/massage as prescribed to treat muscle spasms. Use therapeutic touch and relaxation techniques. Baclofen and dantrolene: Administered to clients who have severe muscle spasticity. Monitor for drowsiness and muscle weakness. Baclofen may be administered intrathecally to reduce the sedative effects. Flail chest As a result of the free-floating rib segments, the lung below the flail segment caves in on inhalation and balloons out on exhalation. The portion of the lung below the flail segment cannot participate in gas exchange, so oxygenation is compromised. Assessment Risk Factors Multiple rib fractures from blunt chest trauma (often caused by motor-vehicle crash or as a result of cardiopulmonary resuscitation on older adults) Expected Findings Unequal chest expansion (the unaffected side of the chest will expand, while the affected side can appear to diminish in size or remain stationary) Paradoxical chest wall movement (inward movement of segment during inspiration, outward movement of segment during expiration) Tachycardia Hypotension Dyspnea Cyanosis Anxiety Chest pain Patient-Centered Care Nursing Care Administer humidified oxygen. Monitor vital signs and SaO 2 . Review findings of pulmonary function tests, periodic chest x-rays, and ABGs. Assess lung sounds, color, and capillary refill. Promote lung expansion by encouraging deep breathing and proper positioning. Maintain mechanical ventilation in the event of severe injury to establish adequate gas exchange and stabilize the injury. (Flail chest is usually stabilized by positive-pressure ventilation.) Suction trachea and endotracheal tube as needed. Administer pain medication. Patient-controlled analgesia or an epidural block commonly is used. Administer IV fluids as prescribed. Monitor intake and output. Offer support and reassurance by explaining all procedures. Traumatic amputation Traumatic amputation caused by crashes, war, or other injury is the primary cause of upper extremity amputations. Management of traumatic amputation Activate the medical emergency system (EMS). Apply direct pressure using gauze, if available, or clean cloth to prevent life-threatening hemorrhage. Elevate the extremity above the heart to decrease blood loss. Wrap the severed extremity in dry sterile gauze (if available) or in a clean cloth, and place in a sealed plastic bag. Submerge the bag in ice water (one part ice and three parts water ), and send with the client. Nursing care Prevent postoperative complications (hypovolemia, pain, infection). Assess surgical site for bleeding. Monitor vital signs frequently. Monitor tissue perfusion of end of residual limb. Palpate residual limb for warmth. Heat can indicate infection. Compare pulse most proximal to incision with pulse in other extremity. QPCC ??????? Monitor for manifestations of infection and non-healing of incision. Infection can lead to osteomyelitis. Amputation might not heal if performed below the level of adequate tissue perfusion. Administer antibiotics and change dressings as prescribed if open amputation was performed. Record characteristics of drainage (amount, color, and odor). Pain Monitor and treat pain. Differentiate between phantom limb and incisional pain. Incisional pain is treated with analgesics. Phantom limb pain The sensation of pain in the location of the extremity following the amputation Related to severed nerve pathways and is a frequent complication in clients who experienced chronic limb pain before the amputation Can be experienced immediately after surgery, up to several weeks, or indefinitely Occurs less frequently following traumatic amputation Often described as deep and burning, cramping, shooting, or aching Treated much differently than incisional pain Administration of calcitonin during the first week of after having an amputation can decrease phantom limb pain. Administering beta blockers (propranolol) can relieve the continual dull, burning sensation associated with the amputated limb. Administering antiepileptics (gabapentin or pregabalin) can relieve sharp, stabbing, and burning phantom limb pain. Some clients can have relief from antispasmodics (baclofen) and antidepressant medication. The nurse should recognize the pain is real and manage it accordingly. Alternative treatment for phantom limb pain can include nonpharmacological methods (massage, heat, transcutaneous electrical nerve stimulation [TENS], ultrasound therapy, biofeedback, acupuncture, relaxation therapy). Teach the client how to push the residual limb down toward the bed while supported on a soft pillow. This helps reduce phantom limb pain and prepare the limb for a prosthesis. Integumentary Burns - Priority interventions, fluids used Slide 48 - Fluid Imbalance: Watch for shock or overload. The initial fluid for resuscitation is Lactated Ringers because it is a crystalloid solution that most resembles plasma. Clients who have a large percentage of burned body surface area require critical care and accurate monitoring. Hemodynamic monitoring – burns, which is “acceptable” and which is most accurate for measuring both left and right heart pressure The pulmonary artery pressure provides an accurate assessment of the cardiovascular system by detecting changes in both right and left heart pressure which can indicate possible development of pulmonary edema, as well monitor overall fluid status. Rule of 9s calculation To calculate the amount of fluid required for resuscitation in the first 24 hours of a major burn you will utilize the Parkland Formula. 1/2 of the total fluid will be administered in the first 8 hours after the burn and the other 1/2 of the fluid will be administered in the next 16 hours. The Parkland Formula (mls) = 4 (mls) X weight (kg) X TBSA (%) Example: Client weighs 80kg and is burned on 30% of the body. 4 X 80 X 30 = 9,600 mls total 1/2 in the first 8 hours = 4,800 mls 1/2 in the next 16 hours = 4,800 mls Endocrine DKA – manifestations Slide 5 – With metabolic acidosis the nurse would expect a pH below 7.35, bicarb below 21, normal PaO2 80-100, and PaCO2 below 35. Because of the lack of insulin, the body is unable to use glucose and instead breaks down fats resulting in excessive ketones. The large amount of ketones causes the body to become acidotic and causes a fruity, or acetone odor to the breath. Additionally, the nurse should expect Kussmaul breathing (rapid and deep), hyperglycemia and associated symptoms. Polyuria: Osmotic diuresis resulting in excess urine production Polydipsia (excess thirst): Osmotic diuresis causing excess loss of fluids resulting in dehydration and increased thirst. Polyphagia: Cell starvation due to inability to receive glucose resulting in increased appetite Weight loss: Cells are unable to use glucose because of insulin deficiency. The body is placed in a catabolic state. GI effects (nausea, vomiting, abdominal pain): Increased ketones and acidosis lead to nausea, vomiting, and abdominal pain Blurred vision, headache, weakness: Fluid volume depletion caused from osmotic diuresis resulting in dehydration. Orthostatic hypotension: Fluid volume depletion caused by osmotic diuresis resulting in dehydration. Fruity odor of breath: Elevated ketone bodies (small fatty acids) used for energy that collect in the blood, which leads to metabolic acidosis. Kussmaul respirations: Deep rapid respirations occur in an attempt to excrete carbon dioxide and acid when in metabolic acidosis. Metabolic acidosis: Breakdown of stored glucose, protein, and fat to produce ketone bodies. Mental status changes: Lack of glucose circulating to the brain can cause neuron dysfunction and even cell death of the brain. The brain cannot produce or store glucose. SIADH manifestations Slide 48 - The nurse should expect a client who has developed SIADH to manifest oliguria. The decrease in urine output can be dramatic with output less than 20 mL/hr. Additionally, the nurse should expect hyponatremia, weight gain, and a lowering of thirst. If SIADH is present, the client can have disorientation, headache, vomiting, muscle weakness, decreased LOC, irritability, loss of thirst, and weight gain. If severe or untreated, this condition can cause seizures and a coma. Treatment consists of fluid restriction, administration of oral conivaptan, and treatment of hyponatremia, with 3% hypertonic saline solution for severe cases. Monitor for hyponatremia and low blood osmolality. SIADH causes the body to retain water. This results in a dilution of electrolytes (such as sodium) in the blood. It is often associated with lung and brain cancers. Key findings include nausea and vomiting (early); lethargy, hostility, seizures, and coma. Nursing Actions Monitor for hyponatremia and low blood osmolality. Administer furosemide, 0.9% sodium chloride IV, and hypertonic sodium chloride solution as prescribed for severe hyponatremia. Monitor vital signs and blood sodium level because furosemide promotes sodium excretion and hypertonic sodium chloride can cause fluid overload. Addison’s Disease and Crisis – assessments to monitor for risk of developing crisis (how do you know they have developed crisis): Slide 36 - Clients who have Addison's disease are prone to hypoglycemia. They should follow a high-protein, highcarbohydrate diet to ensure adequate caloric intake and avoid weight loss, which is common with Addisonian crisis. Clients are prone to dehydration so the nurse should encourage fluid intake as well. Slide 47 – Dehydration is a precipitating factor for Addisonian crisis. Daily weights would assist in identifying if the client has impending crisis Addison’s disease is an adrenocortical insufficiency. It is caused by damage or dysfunction of the adrenal cortex. With Addison’s disease, the production of mineralocorticoids and glucocorticoids is diminished, resulting in decreased aldosterone and cortisol. Acute adrenal insufficiency, also known as Addisonian crisis, has a rapid onset. It is a medical emergency. If it is not quickly diagnosed and properly treated, the prognosis is poor. Older adult clients are less able to tolerate the complications of Addison’s disease and acute adrenal insufficiency and need more frequent monitoring. G??????? Produced by the adrenal cortex Mineralocorticoids: Aldosterone increases sodium absorption and causes potassium excretion in the kidney. Glucocorticoids: Cortisol affects glucose, protein, and fat metabolism; the body’s response to stress; and the body’s immune function. Sex hormones: Androgens and estrogens Assessment Risk Factors Causes of primary Addison’s disease Idiopathic autoimmune dysfunction (majority of cases) Tuberculosis Histoplasmosis Adrenalectomy Metastatic cancers (breast, lung, colon, melanoma Radiation therapy of the abdomen Causes of secondary Addison’s disease Steroid withdrawal Hypophysectomy Pituitary neoplasm High dose radiation of pituitary gland or entire brain Acute adrenal insufficiency is a life-threatening event in which the need for cortisol is greater than the body’s supply and if left untreated can lead to death. Factors that precipitate acute adrenal insufficiency are the following: Sepsis Trauma Stress (myocardial infarction, surgery, anesthesia, hypothermia, volume loss, hypoglycemia) Adrenal hemorrhage Steroid withdrawal Expected findings Manifestations of chronic Addison’s disease develop slowly, and manifestations of acute adrenal insufficiency develop rapidly. Weight loss Craving for salt Hyperpigmentation of the skin and mucous membranes Weakness and fatigue Nausea, anorexia, and vomiting Abdominal pain Constipation or diarrhea Severe hypotension (acute adrenal insufficiency) Hypovolemia Hyponatremia Hyperkalemia Hypoglycemia Hypercalcemia Acute adrenal insufficiency (Addisonian crisis) occurs when there is an acute drop in adrenocorticoids due to sudden discontinuation of glucocorticoid medications or when induced by severe trauma, infection, or stress. QEBP Nursing Actions Establish an IV access and initiate a rapid infusion of 0.9% sodium chloride or dextrose 5% in normal saline. Administer hydrocortisone sodium as IV bolus, initially and then as a continuous infusion. It can be administered IM as well. Administer insulin and dextrose to move potassium into cells. Administer calcium to counteract the effects of hyperkalemia and protect the heart; and sodium polystyrene sulfonate, a resin that absorbs potassium. If acidosis occurs, administer sodium bicarbonate to promote alkalinity and increase uptake of and move potassium into cells. Loop or thiazide diuretics are used to manage hyperkalemia. Monitor vital signs. Monitor for manifestations of hyperkalemia (bradycardia, heart block, and peaked T waves). Monitor electrolytes. Administer an H2 antagonist (famotidine, cimetidine) intravenously for ulcer prevention. Position the client in a recumbent position with legs elevated. Administer vasopressors to increase blood pressure. Client Education Notify the provider of any infection, trauma, or stress that can increase the need for adrenocorticoids. Do not discontinue the medication abruptly. Immune Neutropenia, Leukopenia, Leukocytosis Leukopenia is a total WBC count less than 4,000/mm3. It can indicate drug toxicity, autoimmune disease, bone marrow failure, and some overwhelming infections. Leukocytosis is a total WBC count greater than 10,000/mm3. It can indicate inflammation, infection, some malignancies, trauma, dehydration, stress, steroid use, and thyroid storm. The WBCs involved in inflammation are neutrophils, macrophages, eosinophils, monocytes, and basophils. A client who has had a splenectomy can have a persistently increased WBC count. Older adult clients can have a severe bacterial infection without leukocytosis. Manifestations of infection, such as fever, can be absent in an older adult who has an infection. The nurse should monitor older adult clients carefully for infection risks. G Neutropenia is a neutrophil count less than 2,000/mm3. Neutropenia occurs in clients who have viral infections, overwhelming bacterial infections, or are undergoing radiation or chemotherapy. A client who has neutropenia is at an increased risk for infection. The absolute neutrophil count (ANC) of a client who has neutropenia can help determine severity of the client’s risk for infection. Multiplying the total WBC count by the percentage of neutrophils plus the percentage of bands determines the ANC. An ANC less than 1,000 means that neutropenic precautions are essential. Neutropenic precautions (a protective environment) include the following. Restricting visitors. Prohibiting visits by people who have an infection. Restricting exposure to live (cut or potted) plants. Ensuring that all fruits and vegetables are well washed prior to eating. Avoiding contamination from the client’s own bacterial flora by avoiding the measurement of rectal temperature and administering IM injections. Q Lupus – priority concerns vs normal assessment findings, Physical Assessment Findings QEBP??????? Fever (also a major indication of exacerbation) Anemia Lymphadenopathy Pericarditis (presence of a cardiac friction rub or pleural friction rub) Raynaud’s phenomenon (arteriolar vasospasm in response to cold/stress) Erythematous “butterfly” rash on the nose and cheeks (raised, dry, scaly) Discoid: coin shaped lesions on body areas exposed to sun (face, scalp) Oral lesions Few to no manifestations if lupus is in remission . With exacerbation of lupus, multiple body systems are often affected (kidney, heart, lungs, gastrointestinal tract, vasculature) Complications Lupus nephritis Clients whose SLE cannot be managed with immunosuppressants, and corticosteroids can experience chronic kidney disease, resulting in the possible need for a kidney transplant. Lupus nephritis is the leading cause of death related to SLE. Nursing Actions: Monitor for periorbital and lower extremity swelling and hypertension. Monitor renal status (creatinine, BUN). Client Education Take immunosuppressants and corticosteroids as prescribed. Avoid stress and illness . HIV/AIDS – initial symptoms, precautions with care, HIV infection is one continuous disease process with three stages. Progression of HIV infection Manifestations occur within 2 to 4 weeks of infection. Manifestations are similar to those of influenza and can include a rash and a sore throat. Manifestations of acute HIV infection can include the following: fever, night sweats, chills, headaches, muscle aches, sore throat, and rash. The findings are temporary and resolve with the client returning to previous level of health. This stage is marked by a rapid rise in the HIV viral load, decreased CD4+ cells, and increased CD8 cells. The resolution of manifestations coincides with the decline in viral HIV copies. Lymphadenopathy persists throughout the disease process. Health Promotion and Disease Prevention Teach the client how the virus is transmitted and ways to prevent infection, such as the use of condoms, abstinence, and avoiding sharing needles. (Refer to Fundamentals for Nursing Review Module: chapter 34: Self Concept and Sexuality.) Encourage the client to maintain up-to-date immunizations, including yearly seasonal influenza and pneumococcal polysaccharide vaccine. Providers should use standard precautions when caring for the client. Wilms tumor precautions Is a neoplasm of the kidney (nephroblastoma). This tumor is encapsulated, and palpation can cause it to rupture, which would allow seeding of the tumor into the pelvic cavity. (DO NOT PALPATE) Perioperative Anesthesia problems with different types Spinal anesthesia: when spinal fluid is lost through a leak at the puncture site around the spinal column, a severe headache can occur, which may last several days. This finding is a complication of the anesthesia. Expected outcomes include an absence of the urge to void and numbness in the legs. The postoperative surgical client may need supplemental oxygen in order to maintain normal blood oxygen levels. The effectiveness of oxygenation is monitored using pulse oximetry and arterial blood glasses. PACU priority (ABCs) Sit them up, chin lift for airway problem, Breathing they may need oxygen (can be caused by too much opioid meds which causes respiratory depression) Maternal Newborn Placenta previa Placenta implants in the lower part of the uterus, partly or completely obstructing the cervical os (outlet of the vagina) Bright red, painless vaginal bleeding occurs in the second and third trimester. Risk Factors Previous placenta previa Uterine scarring (previous cesarean birth, curettage, endometritis) Maternal age greater than 35 years Multifetal gestation Multiple gestations Smoking Expected Findings Painless, bright red vaginal bleeding during the second or third trimester Uterus soft, relaxed, and nontender with normal tone Fetus in a breech, oblique, or transverse position Reassuring FHR Vital signs within normal limits Decreasing urinary output, which can be a better indicator of blood loss . Placenta Abruption Separation of the placenta from the site of uterine implantation before delivery of the fetus. When the placenta separates prematurely, there is internal bleeding, which is painful, and the uterus is non-relaxed or becomes rigid as the separation advances. Refrain from performing vaginal exams (can exacerbate bleeding). (A CLIENT WITH PLACENTA PREVIA WILL REQUIRE CESAREAN SECTION FOR DELIVERY) Risk Factors Maternal hypertension (chronic or gestational) Blunt external abdominal trauma (motor-vehicle crash, maternal battering) Cocaine use resulting in vasoconstriction. Previous incidents of abruptio placentae Cigarette smoking or other nicotine use Pre labor rupture of membranes Multifetal pregnancy Expected Findings Sudden onset of intense localized uterine pain with dark red vaginal bleeding Area of uterine tenderness can be localized or diffuse over uterus and board-like Contractions with hypertonicity Fetal distress Clinical findings of hypovolemic shock Magnesium administration uses, assessment, concerns: Magnesium sulfate Classification and Therapeutic Intent: A commonly used tocolytic that is a central nervous system depressant and relaxes smooth muscles, thus inhibiting uterine activity by suppressing contractions. Magnesium sulfate reduces the severity and risk of fetal neuroprotection in surviving infants if administered when birth is anticipated before 32 weeks’ gestation. Nursing Actions Contraindications for tocolysis include active vaginal bleeding, intrauterine infection, greater than 34 weeks of gestation, and acute fetal distress. Do not use concurrently with nifedipine. Do not give to clients who have myasthenia gravis. Monitor the client closely. Discontinue tocolytic therapy immediately if the client exhibits manifestations of pulmonary edema, which includes chest pain, shortness of breath, respiratory distress, audible wheezing and crackles, and a productive cough containing blood-tinged sputum. Monitor for adverse effects (hot flashes, diaphoresis, burning at IV site, nausea, vomiting, drowsiness, blurred vision, headache, non-reactive nonstress test, reduced fetal heart rate variability). Monitor for magnesium sulfate toxicity and discontinue for any of the following adverse effects: loss of deep tendon reflexes, urinary output less than 30 mL/ hr or 100 mL/4 hr , respirations less than 12/min, pulmonary edema, severe hypotension, or chest pain. QS Administer calcium gluconate or calcium chloride as an antidote for magnesium sulfate toxicity . ???????Client Education: Notify the nurse of blurred vision, headache, nausea, vomiting, or difficulty breathing. Magnesium Sulfate: Magnesium sulfate is administered to prevent seizures (eclampsia) and promote vasodilation to lower blood pressure is an added benefit. A loading dose is given (the bolus causes the patient to feel flushed and they do not feel well), followed by a maintenance dose. Close monitoring of magnesium levels is crucial to prevent toxicity. Normal Magnesium lab values are 1.3-2.1 mEq/ L Mag levels for preeclampsia therapeutic levels are 4.8-8.4 mEq/ L Hypermagnesemia leads to muscle flaccid paralysis, decreased respiratory rate, hypotension, bradycardia with prolonged P-R interval (cardiac), an Atrial-Ventricle Block, lethargy. Nursing Considerations: Regularly assess blood pressure, signs, and symptoms (such as headache, vision changes, epigastric pain). Monitor heart rate, oxygenation, lung sounds, reflexes, and edema. Assess for hyperreflexia (measured both in upper and lower extremities) and clonus (rapid rhythmic contractions of a muscle). Lower extremities are likely to be affected by epidural and spinal anesthesia . Frequent monitoring of intake and output (I&O). Magnesium Toxicity: Watch for signs of magnesium toxicity using the BURP acronym: B lood pressure decrease. U rine output decrease. REPORT URINE OUTPUT <30ML/HR & DISCONTINUTE USE R espiratory rate less than 12 breaths per minute. P atellar reflexes absent or decreased deep tendon reflexes (DTRs). Cord pro-lapse interventions and priority: Nursing Care Call for assistance immediately. Do not leave the client. Notify the provider. Using a sterile-gloved hand, insert two fingers into the vagina, and apply finger pressure on either side of the cord to the fetal presenting part to elevate it off of the cord. Stay in this position until the birth of the baby. QS Reposition the client in a knee-chest, Trendelenburg, or modified lateral semi-prone recumbent position with a rolled towel under the client’s right or left hip to relieve pressure on the cord. QEBP Apply a warm, sterile, saline-soaked towel to the visible cord to prevent drying and to maintain blood flow. Provide continuous electronic monitoring of FHR for variable decelerations, which indicate fetal asphyxia and hypoxia. Administer oxygen via face mask if prescribed by the provider or indicated according to agency policy. Initiate IV access and administer IV fluid bolus. Prepare for an immediate vaginal birth if cervix is fully dilated or cesarean birth if it is not. Inform and educate the client and their partner about the interventions. Ectopic pregnancy -identify symptoms, what do we observe for “blood in the abdomen” (hint – this is not just for ectopic pregnancy, but any blood in the abdomen) Unilateral stabbing pain and tenderness in the lower-abdominal quadrant Menses that is delayed (1 to 2 weeks), lighter than usual, or irregular . Scant, dark red, or brown vaginal spotting 6 to 8 weeks after last normal menses; red, vaginal bleeding if rupture has occurred . Referred shoulder pain due to blood in the peritoneal cavity irritating the diaphragm or phrenic nerve after tubal rupture . Findings of hemorrhage and shock ( hypotension, tachycardia, pallor, dizziness ) if a large amount of bleeding has occurred . Hyperemesis gravidarum expected findings: Hyperemesis gravidarum is excessive nausea and vomiting (possibly related to elevated hCG levels) that is prolonged throughout the pregnancy or that is excessive and causes weight loss, dehydration, nutritional deficiencies, electrolyte imbalances, and ketonuria. There is a risk to the fetus for intrauterine growth restriction, small for gestational age, or preterm birth if the condition persists. Expected Findings Physical Assessment Findings Excessive vomiting for prolonged periods Dehydration with possible electrolyte imbalance Weight loss Increased pulse rate Decreased blood pressure . Poor skin turgor and dry mucous membranes Decelerations – identify causes and interventions: Late decelerations stem from decreased blood perfusion to the placenta or compression of the placenta. A position change should increase perfusion or decrease compression, and it is the first intervention the nurse should try. The greatest risk to the client is fetal hypoxia, so the priority action is the one that has the best chance of improving fetal perfusion. Causes/Complications Uteroplacental insufficiency causing inadequate fetal oxygenation . Maternal hypotension, placenta previa, abruptio placentae, uterine tachysystole with oxytocin Preeclampsia Late- or post-term pregnancy Maternal diabetes mellitus Nursing Interventions Place client in side-lying position. Insert an IV catheter if not in place and increase rate of IV fluid administration. Discontinue oxytocin if being infused. Elevate the client’s legs. Notify the provider. Prepare for an assisted vaginal birth or cesarean birth. The provider may prescribe oxygen via facemask, or it may be indicated by agency policy, especially if other interventions have been unsuccessful. Newborn – hyperinsulemia and respiratory distress High levels of maternal glucose increase the production of fetal insulin. High fetal insulin levels interfere with the production of surfactant. This may lead to a newborn with respiratory distress syndrome. Interventions for post-partum hemorrhage Patient-Centered Care Nursing Care Determine QBL immediately following birth. Weigh all blood saturated items and clots, measure fluids in suction cannisters, and subtract any irrigation fluids. Firmly massage the uterine fundus. Monitor vital signs. Assess for source of bleeding. Assess fundus for height, firmness, and position. If uterus is boggy, massage fundus to increase muscle contraction. Assess lochia for color, quantity, and clots. Assess for clinical findings of bleeding from lacerations, episiotomy site, or hematomas. Assess bladder for distention. Insert an indwelling urinary catheter to assess kidney function and obtain an accurate measurement of urinary output. Maintain or initiate IV fluids to replace fluid volume loss with IV isotonic solutions, such as lactated Ringer’s or 0.9% sodium chloride; colloid volume expanders, such as albumin; and blood products (packed RBCs and fresh frozen plasma). Provide oxygen at 10 to 12 L/min via nonrebreather facemask and monitor oxygen saturation. Elevate the client’s legs to a 20° to 30° angle to increase circulation to essential organs. Medications Oxytocin Classification: Uterine stimulant Therapeutic intent: Promotes uterine contractions. Nursing Actions Assess uterine tone and vaginal bleeding. Monitor for adverse reactions of water intoxication (lightheadedness, nausea, vomiting, headache, malaise). These reactions can progress to cerebral edema with seizures, coma, and death. Methylergonovine Classification: Uterine stimulant Therapeutic intent: Controls postpartum hemorrhage Nursing Actions Assess uterine tone and vaginal bleeding. Do not administer to clients who have hypertension. Monitor for adverse reactions, including hypertension, nausea, vomiting, and headache. Misoprostol Classification: Uterine stimulant Therapeutic intent: Controls postpartum hemorrhage. Nursing Actions: Assess uterine tone and vaginal bleeding. Carboprost tromethamine Classification: Uterine stimulant Therapeutic intent: Controls postpartum hemorrhage Nursing Actions Assess uterine tone and vaginal bleeding. Monitor for adverse reactions, including fever, hypertension, chills, headache, nausea, vomiting, and diarrhea.??????? Tranexamic Acid Classification: antifibrinolytics Therapeutic intent: Works to improve blood clotting Nursing actions: Monitor vaginal bleeding and it is recommended to administer to clients who experience postpartum hemorrhage within 3 hrs of birth.