NUR 445 Exam 1 PDF

Diabetes insipidus - Classified as either central (caused by a decreased secretion of ADH from the posterior pituitary gland) or nephrogenic (occurs when the kidneys are resistant to ADH and are unable to concentrate urine, and this type of DI is observed in patients with chronic rena...

Diabetes insipidus - Classified as either central (caused by a decreased secretion of ADH from the posterior pituitary gland) or nephrogenic (occurs when the kidneys are resistant to ADH and are unable to concentrate urine, and this type of DI is observed in patients with chronic renal insufficiency, hypercalcemia, hypokalemia, and interstitial disease of the renal tubules.) Clinical manifestations: - Polyuria, polydipsia, and nocturia are the primary clinical manifestations seen in patients with DI. - Hypotension - Tachycardia - Hypovolemia - Signs of fluid deficits (skin tenting, thirst) Diagnosis: - serum and urine electrolytes, serum and urine osmolality, urine specific gravity (decreased), and CT or MRI of the head - Hematocrit (increased) - Serum sodium increased Fluid management and medications: - Hypotonic solutions (0.45% NS) - Desmopressin (synthetic analog of ADH) - Vasopressin (less expensive) - require frequent monitoring of fluid status, serum electrolytes, and urine output. Nursing actions: - IV access and administer IV fluids - Daily weight - Administer meds - Mouth care and oral fluids - Teach about clinical manifestations of fluid overload Hypopituitarism - hyposecretion of hormones from the anterior pituitary gland. - In children before the closure of the epiphyses, dwarfism (small stature) develops. - osteoporosis (reduction in bone density) may develop. Clinical manifestations - Diagnosis - ACTH stimulation test - Measurements of TSH, FSH, LH, prolactin, and growth hormones Medications - Hormone replacement (corticosteroids, thyroid hormone, testosterones, or estrogen) - Vitamin D and calcium intake - PT Hyperpituitarism - hypersecretion of hormones from the anterior pituitary gland. - An increase in prolactin may lead to hypogonadism, galactorrhea (milky nipple discharge), and increased body fat. - acromegaly (thickening of bones, particularly of the hands, feet, and facial bones) Clinical manifestations -  Medications - Dopamine agonists (bromocriptine mesylate \[Parlodel\]) inhibit the release of anterior pituitary hormones. - Medications that inhibit release of growth hormone include somatostatin analogs and growth hormone receptor blockers. Surgical management - transsphenoidal hypophysectomy: 1. The graft aids in healing and prevents cerebrospinal fluid (CSF) rhinorrhea (CSF draining from the nose). 2. Monitor the patient for ICP 3. The patient is instructed to avoid activities that could increase pressure at the incision site, for example, coughing, sneezing, and bending over.  4. Signs of meningitis Syndrome of inappropriate antidiuretic hormone secretion (SIADH) - Disorder related to an increase in ADH - Characterized by water overload and resultant hyponatremia and hypoosmolality caused by hemodilution. - decreased urine output with an increase in the concentration (increased urine specific gravity) and osmolality of the urine. Clinical manifestations: - Hyponatremia - Anorexia - Nausea - Malaise - Decreased urine output (increased urine concentration) - Headache, irritability, confusion, and weakness Diagnosis: - Scant urine output and elevated urine specific gravity but a decrease in serum sodium and osmolality. Fluid management and medications: - Fluid restriction (monitor weight and I/O's - Severe hyponatremia may require 3% NS - Vasopressin, diuretics, and demeclocycline - IV mannitol Complications: - Seizures and coma (start seizure precautions) Nursing actions and teachings: - Restrict fluids - Administer meds as ordered - Administer 3% NS via central IV - Implement seizure precautions - Teach about signs fluid overload Adrenal cortical insufficiency (Addison\'s disease) - decreased secretion of ACTH from the anterior pituitary gland (secondary insufficiency), or dysfunction of the hypothalamus (tertiary insufficiency). Clinical manifestations: - Weakness - Weight loss - Fatigue - Nausea - Abdominal pain - Darkened, bronzed hyperpigmentation that accompanies the increased secretion of adrenocorticotropic hormone (ACTH) is observed in adrenal insufficiency. - Changes in mood - Loss of sodium (at risk for dehydration and hypotension) - Hyponatremia and hyperkalemia Diagnosis - Cortisol decreased; Glucose decreased; Potassium increased - Sodium decreased - CT and MRI - Corticotropic (Cortrosyn) stimulation test - Insulin tolerance test Fluid and medication management: - Replacement of cortisol (administration of glucocorticoids-hydrocortisone and dexamethasone) - IV fluids and glucose - Kayexalate (potassium excreting agents) Complications: - Addisonian crisis 1. Risk factors: patients who have underlying adrenal hypofunction and who undergo stressful events such as trauma, surgery, and infections. 2. At risk for hyperkalemia and hypoglycemia is associated with lack of both mineralocorticoids and glucocorticoids. 3. Patients with primary adrenal insufficiency need additional doses of glucocorticoid during stress periods like surgery, trauma, or infection. Nursing actions and teachings - Ensure vascular access for administration of IV fluids containing sodium and glucose. - Administer corticosteroid as prescribed. - Maintain safety precautions such as placing the patient's bed in the lowest position and always aiding when the patient is getting out of bed. - Always wear a medical alert bracelet. - Potential need for increased salt intake in hot weather Adrenal cortex hyperfunction (Cushing\'s syndrome) - condition caused by excessive hormone production from an anterior pituitary tumor (70%) producing excessive ACTH or excess hormone secretion from a primary tumor of the adrenal cortex (15%). - Excessive circulating glucocorticoid (cortisol) from the adrenal glands Clinical manifestations - virilization (male sexual characteristics developing in female individuals) - Hyperglycemia - Increased risk of infection Diagnosis: - Assessment of cortisol levels - Results of suppression tests - Serum electrolytes Nursing actions and teachings - Administer medications that interfere with production/secretion of cortisol. - Head of bed elevated 45 degrees - Turn patient frequently and protect skin from injury. - Modify salt and fluid intake as directed by provider (due to fluid overload) Pheochromocytoma - Catecholamine-secreting tumors of the adrenal medulla and are usually unilateral. Clinical manifestations - tachycardia, hypertension, severe headaches, palpitations, hyperhidrosis (excessive sweating), hypermetabolism, and hyperglycemia. - Paroxysmal (sudden onset) hypertension (excess of 250/140) Diagnosis - Sudden elevation of blood pressure - Imaging studies (CT/MRI) - Measurements of urine and plasma levels of catecholamines Medications: - Hypertension, tachycardia (require bed rest and HOB elevated) - alpha-adrenergic blocking agents or smooth muscle relaxants. Surgical management - Adrenalectomy is the definitive treatment for pheochromocytoma - open anterior transabdominal 1. preparation focuses on lowering the BP and HR (starts 7-10 days before procedure) 2. fluid management 3. during procedure patient is at risk of hypertensive crisis (administer nitroprusside or alpha-adrenergic blockers) 4. post op: monitoring blood pressure, heart rate, hypovolemia, hypoglycemia, and blood glucose levels 5. Patients with bilateral pheochromocytomas require bilateral adrenalectomy, and this necessitates lifelong adrenal cortex hormone replacements. Nursing actions and teachings: - Administer sodium nitroprusside (hypertensive crisis) - Administer alpha-adrenergic blocking agents (lowers BP) - Administer beta-adrenergic blocking agents (lowers HR) - Bedrest with head of bed elevated - Administer glucocorticoid the morning of surgery for adrenalectomy. - Maintain calm, quiet environment. Hypothyroidism - Hashimoto's thyroiditis is the most common type of hypothyroidism and is caused by an autoimmune response that leads to destruction of the thyroid gland by immunological processes. - Hypothyroidism is a major cause of goiter (enlargement of the thyroid gland. Risk factors: - female individuals between the ages of 30 and 60 Clinical manifestations - Decreased energy, increased sleep, fatigue, weight gain, decreased appetite, and susceptibility to cold temperatures. - Myxedema, a condition resulting from an increased deposition of glycosaminoglycans (a type of polysaccharide) in cells and tissues (causes an osmotic edema and a fluid collection that is associated with a generalized nonpitting edema) - Decreased T3/T4  Myexedema Diagnosis - T3/T4 (low), and TSH (elevated) Medications - Levothyroxine (medication is started at a low dose and increased as needed to treat symptoms of hypothyroidism, medication should be taken in the morning at the same time every day and it is a lifelong therapy) Complications - Myxedema coma is characterized by hypoxia and carbon dioxide retention (secondary to hypoventilation), fluid and electrolyte imbalances, and hypothermia. Nursing actions and teachings - Administer thyroid replacement therapy at the same time every day. - Administer narcotics and sedatives with caution (metabolism of the medication is slower and respiratory compromise may occur with normal dosages) - Provide warming blankets as needed. - Watch for signs of hyperthyroidism Hyperthyroidism - Graves' disease is the most common cause of hyperthyroidism and is an autoimmune disorder involving antibodies (thyroid-stimulating immunoglobulins) that bind to the thyroid gland, resulting in the enlargement of the thyroid gland and subsequent hypersecretion of thyroid hormone. Risk factor - Female individuals between the ages of 20 and 40 years Clinical manifestations - Elevated heart rate, cardiac dysrhythmias, and increased heart sounds - Thyroid bruit secondary to increased blood flow - Heat intolerance - Increased gastric activity resulting in increased bowel movements - Increased appetite - Weight loss - Fatigue - Nervousness - Insomnia - Light to absent menses - Hair loss - Exophthalmos (protrusion of the eyeball) and goiter Diagnosis - Elevated serum T3, elevated serum T4, and decreased TSH - Elevations in RAIU Non-surgical treatment - treatment focuses on ensuring adequate fluid intake because insensible losses are greater secondary to the hypermetabolic state, monitoring for cardiovascular complications, and promoting a quiet, non-stressful environment. - Propylthiouracil (PTU), methimazole (Tapazole), and lithium carbonate (Lithonate). In the inpatient setting, if a patient receives radioiodine I-131 for treatment of hyperthyroidism (or thyroid cancer), the following precautions are needed: - Place the patient in a private room. - Place a "Caution---Radioactive Material" sign on the door. - Nursing staff always wear dosimeter badges when interacting with the patient to measure the amount of exposure. - Staff are to limit direct contact with patients to 30 minutes per 8-hour shift. - Staff are rotated to minimize radiation exposure. - Pregnant staff are not to be assigned patients receiving radioiodine therapy. - Encourage patients to complete as much of their care as tolerated. Surgical management - Total or subtotal thyroidectomy are performed (monitoring for airway compromise, hemorrhage, hypocalcemia secondary to removal of all parathyroid gland tissue, and damage to the laryngeal nerve.) - Position patient in a semi-fowler's position, suction equipment, and supplemental oxygen the 1^st^ 48 hrs (humidified air) - Changes in voice quality such as hoarseness or husky tone (laryngeal nerve damage) - A tracheostomy tray is maintained at the bedside because of the risk of respiratory compromise secondary to postoperative swelling, tetany (intermittent muscle spasms), and laryngeal damage. - A table with a list of medical procedures Description automatically generated with medium confidence -  Complications - Thyroid storm or thyrotoxicosis: tachycardia, fever, systolic hypertension, abdominal pain, tremors, and changes in level of consciousness. Nursing actions and teachings - Administer antithyroid medications as ordered. - Administer iodine preparations. - Administer beta-adrenergic blocking agents as prescribed. - Implement cooling measures with elevated temperature. - Administer eye lubricant. Thyroid cancer Risk factors - Women (40s or 50s) Clinical manifestations - painless, palpable, solitary thyroid nodule often discovered during a routine examination of the neck. The patient may also report hoarseness, dysphagia, feeling of fullness of the neck, and swollen lymph nodes. Diagnosis: - Fine needle aspiration biopsy - Ultrasound - Radioiodine - CT/MRI - TSH Treatment: - Radioiodine I-131 (check out precautions box) - Radiation/chemotherapy - Cabozantinib (treatment of locally advanced or metastatic differentiated thyroid cancer that progressed after treatment with VEGF (vascular endothelial growth factor--targeted therapy). Surgical management: - Surgical excision is the primary treatment for thyroid cancers - Following surgery, the patient usually is treated with radioiodine I-131 to destroy any remaining cancer. After total thyroidectomy, the patient is required to take levothyroxine for life to prevent hypothyroidism. Nursing actions and teachings - Administer levothyroxine as prescribed. - Prepare patient for surgery (as indicated). - Postoperative surgical thyroidectomy care (see thyroidectomy care for patients with hyperthyroidism) Hypoparathyroidism - Hypocalcemia is the primary disorder associated with hypoparathyroidism. Because of a lack of parathyroid hormone (PTH), calcium is not mobilized from the bones, conserved in the kidneys, or absorbed in the small intestines. Clinical manifestations: - numbness and tingling around the mouth or in the hands and feet, severe muscle cramps, spasms of the hands and feet, and tetany. - Chvostek sign and trousseau sign - Prolonged QT interval - A close-up of a person\'s face Description automatically generated Diagnosis: - low serum calcium levels, high serum phosphate levels, and low serum PTH levels. -  Treatments: - Intravenous calcium (usually calcium gluconate or calcium chloride) is administered to the patient presenting with acute hypocalcemia and then followed up with oral calcium and vitamin D supplementation. Nursing actions and teachings: - Administer calcium replacements (over 10-15 minutes) - Administer vitamin D - Eat foods high in calcium but low in phosphorus. - A list of foods that are used in the treatment of hypopathy Description automatically generated Hyperparathyroidism - hypercalcemia secondary to its actions on bone, kidneys, and the bowel. The action of PTH on bone leads to osteoclastic (breakdown of bone) activity and bone demineralization, which causes pathological fractures and bone lesions Clinical manifestations: - some may be asymptomatic - Elevated ionized and serum calcium levels - Decreased serum phosphorus levels - Muscle weakness and atrophy - Low-back pain - Increased incidence of pathological fractures - Prolonged PR interval - Shortened QT interval - Constipation, anorexia, and nausea and vomiting - Renal stones Diagnosis: - serum calcium, albumin, phosphorus, and ionized calcium levels - Direct measurement of intact PTH Treatment: - consumption of calcium-containing antacids and vitamin D. Nursing actions and teachings: - Increase fluid intake to 3,000 mL/day (renal calculi) - Administer furosemide (Lasix) as ordered. - Administer calcium chelators. - Use a lift sheet in patients with chronic hyperparathyroidism to prevent bone injury. - Strain urine with suspected renal calculi. - Low-calcium diet - Increase fluids and fiber to decrease complications of constipation. Type 1 diabetes mellitus Patho - typically triggered by an autoimmune process in which the insulin-producing beta cells of the pancreas are destroyed, resulting in an absolute lack of insulin. Clinical manifestations - Polyuria - Polydipsia - Polyphagia - Fatigue - Weight loss - Glucosuria Diagnosis - H1AC (measures the average blood glucose concentration over time (6-12 weeks) by measuring the amount of glucose that binds to red blood cells (RBCs). - Fasting blood glucose (no caloric intake for at least 8 hours) - Two-hour postprandial (after meals) or the oral glucose tolerance test (OGTT) (consuming a beverage containing glucose load, blood samples are taken before consuming the drink and then 1-2hrs after) -  Pharmacological interventions: - Oral administration of insulin is not effective because it is broken down and rendered ineffective during the digestive process. - The goal of treatment is to maximize glycemic control, the maintenance of blood glucose levels within normal ranges, in an effort to prevent the complications of hyperglycemia. - A table with a list of blood pressure Description automatically generated with medium confidence - Insulin pumps provide rapid-acting insulin in continuous incremental dosages to match the patient's variable needs throughout the day, thus eliminating the need for a separate basal insulin. -  - Continuous glucose monitoring (CGM) systems use a tiny sensor inserted under the skin to check glucose levels in the interstitial fluid. The sensor stays in place for 6 to 14 days and then is replaced. Complications - Diabetic ketoacidosis (DKA), there is inadequate insulin for cells to obtain adequate glucose for normal metabolism. Causes of DKA - Intentional or unintentional missed or reduced doses of insulin - Inadequate insulin due to increased insulin needs secondary to stress or infection - New onset of type 1 DM Clinical manifestations - Blood glucose level greater than 250 mg/dL (however, rarely a person may develop DKA at glucose levels lower than 250 mg/dL) - Ketonuria (ketones in the urine) - Arterial pH of less than or equal to 7.3 - Serum bicarbonate level of less than or equal to 18 mEq/L - Positive anion gap - Kussmaul respirations (rapid, deep respirations that occur as a compensatory mechanism for the acidosis.) - Treatment - Fluid replacement with isotonic normal saline - Correction of electrolyte imbalances, focusing on monitoring and correction of decreased or increased potassium level if necessary, before insulin administration - Insulin administration, most effective by intravenous delivery Prevention - Monitoring glucose to be aware of rising levels - Patient education on the signs and symptoms of DKA - Insulin instruction on how to cover glucose elevations - Following "Sick Day Rules" - Care must be taken to monitor potassium levels before treating the hyperglycemia with insulin.  Hypoglycemia - defined as a blood glucose level of less than 65 mg/dL, results when there is more circulating insulin than is needed to handle the amount of circulating glucose. Clinical manifestations -  Anxiety -  Hunger -  Palpitations -  Circumoral paresthesia (numbness around lips) -  Sweating -  Shakiness -  Irritability - Difficulty thinking -  Dizziness -  Fatigue -  Sleepiness -  Slurred speech -  Weakness/lack of coordination Management - Conscious patients (Juice, soda, honey, jelly, bread, or crackers) - Unconscious (IV dextrose, 25 to 50 mL of 50% dextrose solution (D50) - No IV access (1 mg of intramuscular glucagon injection should be administered.) Dawn phenomenon and Somogyi effect - result in increased blood glucose levels in the early morning. They occur more commonly in the patient with type 1 DM but are also known to occur in patients with type 2 DM. The increased blood glucose levels of the dawn phenomenon result from the naturally occurring release of hormones, such as glucagon, cortisol, and growth hormone, in the early morning.  Typer 2 diabetes mellitus Risk factors - BMI - Physical inactivity - HDL less than 35 and triglyceride greater than 250 - Metabolic syndrome - Family Hx - HTN - HGBA1C greater than 5.7% - PCOS Clinical manifestations - Polyuria - Polydipsia - Polyphagia - Fatigue - Poor wound healing - Cardiovascular disease - Visual disturbances - Renal insufficiency - Recurring infection -  Hyperosmolar hyperglycemic state (HHS) - characterized by hyperglycemia, hyperosmolality, and dehydration without significant ketoacidosis. (Above 600 mg/dL) Diagnosis -  Blood glucose level of 600 mg/dL or greater -  Serum osmolality of 320 mOsm/kg or greater -  Profound dehydration -  Serum pH greater than 7.4 -  Bicarbonate concentration greater than 15 mEq/L -  Low ketonuria and absent to low ketonemia -  Alteration in level of consciousness Treatment - priorities include standard care for dehydration with IV fluid and treatment for altered mental status, including airway management as appropriate. Patients may respond to fluids alone, but IV insulin may be necessary to correct hyperglycemia. Prolonged hyperglycemia effects - Vascular - Neurological - Peripheral neuropathy - Autonomic neuropathy Respiratory disorders Pulmonary embolism - the obstruction of one or more of the branches of the pulmonary artery (PA) by particulate matter that has an origin elsewhere in the body. - A pulmonary embolus is most caused by a thrombus. - ventilation--perfusion mismatch (V/Q mismatch), a decreased blood flow to functioning alveoli or areas of the lung where gas exchange can take place if perfusion is adequate. Risk factors - DVT - Virchow's triad of venous stasis, vessel wall damage, and hypercoagulability - Obesity - Smoking - Fracture (hip or leg) - Hip or knee replacement - Major trauma What does it prevent? - Prevents gas exchange at the alveolar level (leading to hypoxemia- low blood oxygen levels) - inadequate tissue perfusion and hypoxia (inadequate oxygenation at the cellular level) Clinical manifestations - A screenshot of a medical chart Description automatically generated Diagnosis - ECG - inverted T waves and ST changes (Ischemic changes) - CT with IV contrast (most ordered test) - Angiography (most definitive study for PE) Lab testing - Plasma D-dimer (A positive D-dimer indicates the presence of a clot but requires further testing.) - If respiratory distress is present an ABG is performed Treatment - Anticoagulation meds (helps reduce the formation of other clots) - Asymptomatic (oral factor Xa inhibitor) - Symptomatic (hospitalized and is started on heparin therapy- bleeding risk should also be initiated and monitor aPTT) - Patients need to be on anticoagulation at least 3 months post-discharge (warfarin when they go home and to monitor INR) - If a patient is hemodynamically compromised, thrombolytic therapy (alteplase) should be considered (concerns for older people is cerebral hemorrhage) - Intravenous isotonic fluid is used to decrease the viscosity of the blood. Medications used - Heparin (unfractionated) - Low molecular weight heparin (no lab monitor required) - Vitamin K antagonist - Xa inhibitors (rivaroxaban) - Thrombolytics (alteplase- dissolves clots)  Surgical management - embolectomy, or physical removal of the clot. There are two types of embolectomies, catheter or surgical. - Inferior vena cava (IVC) filters are placed to prevent recurrent Pes (active bleeding that disqualifies anticoagulation therapy, recurrent PE despite adequate anticoagulation therapy, or evidence that hemodynamic or respiratory dysfunction) allows for blood passage, but blocks. Any emboli from the lower extremities. Complications: filter migration, erosion of the vena cava wall, obstruction due to filter thrombosis, and procedural complications. Nursing actions and patient teachings - Elevate HOB - Administer IV fluids - Administer anticoagulation meds as ordered - Initiate bleeding precautions - Be prepared to intubate or resuscitate - Aerobic exercise - Cardiac-prudent diet and smoking cessation Acute respiratory failure - when one or both gas-exchange functions of the lungs are compromised. A chart of medical information Description automatically generated with medium confidence Clinical manifestations - Hypercapnia (headache, confusion, and a decreased level of consciousness or increased somnolence.) - Tachycardic, tachypneic, and may also appear dizzy and flushed, with a pink coloring to the skin. - Hypoxemia (increases in heart rate, respiratory rate, and blood pressure to increase oxygenation and perfusion.) -  Diagnosis - ABGs - Venous oxygen saturation - Hemoglobin/hematocrit - Chest c-ray - Sputum cultures Types of oxygen - Nasal cannula or venturi mask - Nonrebreather mask with 100% FIO2 (for patients who have not responded to traditional methods) - High-flow nasal cannula (up to 60L/minute) - Noninvasive positive-pressure ventilation (BiPAP and CPAP) - Invasive positive-pressure ventilation (Endotracheal tube, tracheostomy tube, and mechanical ventilation) - Medications - inhaled bronchodilators, inhaled steroids, diuretics, sedation, and antibiotics - The combination of bronchodilators and steroids provides a more therapeutic response than either medication alone. This is known as a synergistic response. - Diuretics are used to decrease pulmonary congestion, especially in cases where pulmonary edema is the underlying cause of failure. Nursing actions and teachings - Administer oxygen (with humidity) as ordered - Medication administration - Administer sedation as ordered (typically only in mechanically ventilated patients). - Elevate the head of the bed; sit the patient up in a chair. - Position patient with the "good lung down."(V/Q ratio) - Chest physical therapy and suctioning; ambulate as able. - Smoking cessation Acute respiratory distress syndrome - acute onset of less than 7 days, refractory hypoxemia, and bilateral infiltrates ruling out cardiac pulmonary edema as the cause. - PaO2/FIO2 ratio, the ratio of the partial pressure of oxygen over the fraction of inspired oxygen. -  3 phases: - The exudative phase typically occurs within 24 to 48 hours after injury (ACM becomes dilated due to the inflammatory mediators, and this disturbance allows fluid to move from the capillaries into the interstitial space and into the alveoli.) 1. Clinical manifestations of this phase: hyperventilation and tachycardia as a compensatory response to hypoxemia. - In the proliferative phase, neutrophils and other inflammatory mediators cross the damaged ACM and release toxic mediators that further damage both the alveolar and capillary epithelium. 1. Clinical manifestations: hypercarbia and worsening hypoxemia. - In the fibrotic phase, there is diffuse fibrosis and scarring, resulting in greatly impaired gas exchange and compliance. 1. Clinical manifestations: decreased left-heart preload due to the right heart failure and reduced capacity of the right ventricle to deliver blood to the lungs and on to the left side of the heart. Diagnosis - Chest X-ray (ground-glass appearance and snow-screen effect" or whiteout effect) Lab testing - ABGs - CBC - Liver function test Treatment - Mechanical ventilation (primary treatment for the refractory hypoxemia of ARDS.) - The most common is lung-protective ventilation using reduced tidal volumes and higher PEEP. - APRV utilizes an inverse inspiratory/expiratory ratio (longer inspiration than expiration) to facilitate oxygenation and gas exchange. - Another treatment to support gas exchange in severe ARDS is extracorporeal membrane oxygenation (ECMO). Medications - Antibiotics (broad spectrum then narrow spectrum after pathogen is identified) - Corticosteroids - Neuromuscular blocking agents or paralytics (mechanically ventilated patients) Complications - infection-related ventilator-associated complication (IVAC) - noninfectious ventilator-associated complication (VAC) - ventilator-associated pneumonia (VAP) Actions - Airway suctioning when indicated by the presence of secretions to ensure that the ETT is clear - Patient positioning/activity - Range-of-motion (ROM) exercises Chest trauma - Chest trauma is divided into two types: blunt-force and penetrating trauma. (Blunt chest trauma is the result of a blunt object hitting the chest) - Penetrating trauma is the result of sharp objects such as knives or bullets entering the chest and causing damage to internal structures or organs. - A pneumothorax may result from severe blunt or penetrating chest trauma. a hemothorax is the presence of blood in the pleural space. Clinical manifestations -  Tachypnea/hyperventilation -  Tachycardia -  Shortness of breath -  Decreased oxygenation -  Decreased level of consciousness -  Decreased or absent lung sounds -  Asymmetrical chest excursion (in the case of a flail chest) -  Subcutaneous emphysema (air under a layer of the skin) Diagnosis - Chest X-ray - Ultrasonography (also known as focused assessment with sonography in trauma (FAST), is a valuable tool for a quick assessment in an emergency situation.) - Chest CT Lab testing -  ABGs -  Serum lactate -  Hemoglobin/hematocrit -  CBC and complete metabolic profile, coagulation studies, and a type and crossmatch if the patient needs a blood transfusion Treatment - Airway - Breathing - Circulation  Medications - Analgesics (morphine) Complications - Tension pneumothorax may occur if air or blood collects in the pleural space and is not removed. If this is left untreated, the positive pressure in the pleural cavity increases, and the affected lung collapses. - Cardiac tamponade is caused by excessive air, fluid, or blood collecting in the pericardial sac. When this occurs, the heart cannot adequately fill or contract because of the compression of the ventricles. It can manifest as hypotension with narrow pulse pressure, muffled heart sounds, and distended neck veins, which are known collectively as Beck's triad. Surgical management - thoracotomy, a surgical excision to the chest wall, is an option if the chest trauma has resulted in damaged organs or major vessels. Actions - Apply oxygen as ordered. - Anticipate and prepare for intubation. - Elevate the head of the bed. - Encourage deep breathing and coughing, every 1 to 2 hours. - Keep the collection apparatus below the level of the chest; keep tubing free from kinks or loops. - NEVER CLAMP THE CHEST TUBE! - When the chest tube is removed, immediately apply a sterile occlusive petroleum jelly dressing. - Administer pain medications; encourage the use of patient-controlled analgesia before ambulation and pulmonary toileting. Teaching - Use of pain medications Importance of: Coughing and deep breathing Ambulation Splinting with pillow while coughing