NSG-430 Exam 1

psychosocial manifestations at end of life

-Altered decision making -Anxiety and fear about unfinished business -Decreased socialization -Fear of loneliness -Fear of meaninglessness of one's life -Fear of pain -Helplessness -Life review -Peacefulness -Restlessness -Saying goodbyes -Unusual communication -Vision-like experiences -Withdrawal -A variety of feelings and emotions affect the dying patient and the family at the end of life -Most patients and families struggle with a terminal diagnosis and the realization that there is no cure. -Patient and family may feel overwhelmed, fearful, powerless, and fatigued. -Family's response is dependent on: •Type and length of the illness •Relationship with the patient. -Patient's needs and wishes must be maintained. -Patients need time to think and express feelings. -Fatigue, weakness, and confusion may increase response time. Nursing Management: -Encourage the dying person and family to share their feelings of sadness, loss, forgiveness and to touch, hug, cry. -Allow the patient and family privacy to express their feelings and comfort one another. -Assess spiritual needs. Allow patient to express his or her spiritual needs. -Encourage visit by appropriate spiritual care service provider, chaplain, or family member. -Encourage the family to talk with and reassure the dying person. -Affirm the dying person's experience as a part of transition from this life. -Converse as though the patient were alert, using a soft voice and gentle touch. Anxiety and Depression: -Uncontrolled pain and dyspnea -Psychosocial factors from disease process or impending death -Altered physiologic states -Drugs used in increasing doses -Management: •Pharm and non-pharm interventions (relaxation, breathing, muscle relaxation, music, imagery) •Encouragement, support, and education Anger: -Anger is a common and normal response to grief -A grieving person cannot be forced to accept the loss. -Surviving family members may be angry with dying loved one who is leaving them. -You may sometimes be the target of anger and must understand what is happening and not react on a personal level. -Encourage expression of feelings, at the same time realizing how difficult it is to come to terms with loss. -You may remember reading about the five stages of death and dying, these are chronologically: denial, anger, bargaining, depression and acceptance. The model was first introduced by Swiss-American psychiatrist Elisabeth Kübler-Ross in her 1969 book On Death and Dying, and was inspired by her work with terminally ill patients. Hopelessness, Powerlessness, and Fear: -Feelings of hopelessness and powerlessness are common during the EOL period. -Allow patient and family to deal with what is within their control and help them to recognize what is beyond their control. -Encourage realistic hope within the limits of the situation -Decision making about care can foster a sense of control and autonomy -Four specific fears: 1.Pain 2.Shortness of breath 3.Loneliness and abandonment 4.Meaninglessness -Management: •Relaxation and coping strategies Fear of Pain: -Physiologically: no indication that death is always painful -Psychologically: pain may occur based on anxieties or separations related to dying -Many people assume that pain always accompanies death. -Terminally ill patients who do experience physical pain should have pain-relieving drugs available. -Assure the patient and family that drugs will be given promptly when needed and that side effects of drugs can and will be managed. -Re-assessment of pain after medications are given is an important nursing action. -Patients can participate in their own pain relief by discussing pain relief measures and their effects. -Most patients want their pain relieved without the side effects of grogginess or sleepiness -Pain relief measures do not need to deprive the patient of the ability to interact with others. Fear of Dyspnea: -Sensation of air hunger results in anxiety for patient and family -Respiratory distress and dyspnea are common near the EOL. -Anxiety-reducing agents (e.g., anxiolytics) may help produce relaxation. -Therapies depend on the cause and may include: •Opioids •Bronchodilators •Oxygen Fear of Loneliness and Abandonment: -Do not want to be alone -Fear abandonment -Presence of people provides comfort, support, and a sense of security -Many dying patients are afraid that loved ones who are unable to cope with the patient's imminent death will abandon them. -Holding hands, touching, and listening are important nursing interventions. -Life review -Intentions during life -Actions -Regrets about what might have been Communication: -Communication is essential -Use empathy: identification with and understanding of another's situation, feelings, and/or motives -Active listening: paying attention to what is said, observing nonverbal cues, and not interrupting. -Allow patients and families time to express their feelings and thoughts -Accept silence: may be related to overwhelming feelings experienced at the end of life. It can allow time to gather thoughts. -Listening conveys acceptance and comfort. -Consider ethnic, cultural, and religious backgrounds. -Prepare family for unusual patient communication -Patients and families may have difficulties expressing themselves emotionally. -Make time to listen and interact in a sensitive way to enhance the relationship among you, patient, and family. -A family conference can create a more conducive environment for communication. -Prepare family members for changes in emotional and cognitive function that occur at end of life. -Unusual communication may take place. -Patients may: •Speak to or about family or others who have predeceased them •Give instructions to those who will survive them •Speak of projects yet to be completed. -Listening carefully: •Helps identify specific communication patterns •Decreases risk for inappropriate labeling of behaviors.

acute respiratory distress syndrome (ARDS)

-An insult/injury/ infection causes the abnormal response leading to ARDS developing -Sudden progressive form of acute respiratory failure -Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid -10% of all ICU admissions; more than 200,000 cases per year in United States; mortality rate about 50% Etiology: -Predisposing Factors •Most common: sepsis •Other: multiple organ dysfunction syndrome (MODS) •Multiple risk factors means 3 to 4 times likely to develop ARDS -Direct lung injury •Common: pathogen in lungs; aspiration, virus, bacteria, or sepsis -Indirect lung injury •Common: problem (e.g., sepsis or massive trauma) from elsewhere in the body move toward favorable lung environment and proliferate, leading to acute lung injury Pathophysiology: 1)Injury or exudative phase: 24-72 hrs, edema, leaking alveoli, shunting from right to left side of heart unoxygenated, less surfactant, increased atelectasis, "stiff" lungs, increased WOB 2)Reparative or proliferative phase: 1-2 weeks, lung compliance continues to decline, hypoxemia worsens 3)Fibrotic or fibroproliferative phase: 2-3 weeks, diffuse scarring sets in, permanent changes and long term ventilation due to decreased functional lung volumes and PHTN Clinical Manifestations: -Initial presentation: 24 to 72 hours -Mild dyspnea, tachypnea, cough, restlessness -Chest auscultation may be normal or may reveal fine, scattered crackles -ABGs: mild hypoxemia and respiratory alkalosis from hyperventilation -Chest x-ray: may be normal or reveal diffusely scattered, minimal interstitial infiltrates, progresses till lungs appear "whited out" -ARDS progression 72+ hours: •Increased WOB, leading to respiratory distress •Tachypnea and intercostal and suprasternal retraction may be present •Tachycardia, diaphoresis, changes in mental status, cyanosis, pallor •Auscultate diffuse or coarse crackles with expiration •Chest x-ray (after 72 hours) showing diffuse and extensive bilateral interstitial and alveolar infiltrates: "whiteout" -Abnormal ABGs •"Refractory hypoxemia, despite 100% FIO2" (classic characteristic) •Hypercapnia (respiratory muscle fatigue) and hypoventilation Treatment: -Treat underlying cause -IV Fluids for stabilization of VS -Cardiac involvement may require Inotropic and vasopressor medications: •Norepinephrine •Dopamine •Dobutamine Complications: -Main Causes of Death: •MODS with sepsis; vital organs affected: lungs, kidneys, liver, and heart •Infection: catheter-related •Respiratory: O2 toxicity, barotrauma, PE, pulmonary fibrosis, ventilator-associated pneumonia •GI: hypermetabolic state, paralytic ileus, pneumoperitoneum, stress ulcer, hemorrhage •Renal: acute kidney injury •Cardiac: decreased cardiac output, dysrhythmias •Hematologic: anemia, DIC, thrombocytopenia, venous thromboembolism •Endotracheal tube: laryngeal ulceration; tracheal: malacia, stenosis, or ulceration •CNS and psychologic: delirium, PTSD, sleep deprivation -Barotrauma: rupture of overdistended alveoli during mechanical ventilation; high peak pressures causing pneumothorax, subcutaneous emphysema, pneumopericardium, and tension pneumothorax •Management: ventilate with smaller tidal volumes and varying amounts of PEEP to reduce risk -Stress ulcers: high risk - diversion of blood from GI tract •Management: GI prophylaxis antiulcer meds, early enteral nutrition -VTE blood clots: high risk - venous stasis, no elevation, •Management: intermittent pneumatic compression stockings, anticoagulants, early ambulation, -Acute kidney injury: decreased renal perfusion, oxygenation •Management: monitor input and output, daily BUN and creatinine, dialysis or continuous renal replacement therapy (CRRT) -Abnormal lung function: most recover within 6 months; normal or near normal lung function; persisting changes due to scarring can endure for years Ventilator-Associated Pneumonia (VAP): -Weakened host, invasive monitoring, aspiration of GI contents, prolonged mechanical ventilation -Implement ventilation bundle protocol -Strategies for prevention of VAP: •Good hand hygiene •Elevate HOB 30 to 45 degrees •Daily oral care with chlorhexidine (0.12%) solution •Daily assessment for readiness for extubation •Stress ulcer prophylaxis •Venous thromboembolism prophylaxis Best Practices (ARDSNet protocol): -O2 administration: hi-flow systems, keep PaO2 at least 60mmHg -Mechanical ventilation: special low pressure settings prevent alveolar rupture -Low tidal volume ventilation: avoids volutrauma and barotrauma -Permissive hypercapnia: PaCO2 up to 60 mmHg acceptable in early phase ARDS -Positive end expiratory pressure (PEEP): increased functional capacity; helps keep open/collapsed alveoli •Compromises venous return and decreased preload, CO, and BP; also watch for barotrauma -Prone positioning: up to 16 hours per day; facilitate secretion drainage and reduces atelectasis -Extracorporeal membrane oxygenation (ECMO): lung bypass to machine for "external" oxygenation

organ and tissue donation

-Any body part or the entire body may be donated -Decided by a person before death -With family permission after death -Follow specific legal guidelines for organ or tissue donation. -Some tissues must be used within hours after death so require immediate physician notification. -Provide information so that care outcomes are based on wishes and values. -Organ Donation: •Can be made by legally competent persons •Can be made by immediate family following death •Can be specified on donor cards or, in some states, on drivers' licenses •Handled by various agencies that differ by state and community (organ bank, organ-sharing network, organ-sharing alliance) •Follow specific legal guidelines for organ or tissue donation. •Some tissues must be used within hours after death so require immediate physician notification.

Graves' disease

-Autoimmune disease of unknown etiology characterized by diffuse thyroid enlargement and excess thyroid hormone secretion -The patient develops antibodies to the TSH receptor. These antibodies attach to the receptors and stimulate the thyroid gland to release T3, T4, or both -Accounts for up to 75% of the cases of hyperthyroidism -Women are 5 times more likely than men to develop it -Precipitating factors such as insufficient iodine supply, cigarette smoking, infection, and stressful life events may interact with genetic factors to cause it -The disease is characterized by remissions and exacerbations with or without treatment. -It may progress to destruction of the thyroid tissue, ultimately causing hypothyroidism. -Is associated with the presence of other autoimmune disorders, including rheumatoid arthritis, pernicious anemia, SLE, Addison's disease, celiac disease, and vitiligo. Clinical Manifestations: -Clinical manifestations of hyperthyroidism are related to the effect of excess circulating thyroid hormone. -It directly increases metabolism and tissue sensitivity to stimulation by the sympathetic nervous system. -Palpation of the thyroid gland may reveal a goiter. -When the thyroid gland is excessively large, a goiter may be noted on inspection. -Auscultating the thyroid gland may reveal bruits, a reflection of increased blood supply. -Visual of protruding eyes (exophthalmos) and enlarged thyroid in neck (goiter). -Hyperfunction of the thyroid gland can lead to cardiovascular manifestations -Patients with hyperthyroidism may experience dyspnea on mild exertion and have an increased respiratory rate -GI manifestations -Intolerance to heat -Elevated basal temperature -Lid lag, stare-unilateral/ bilateral -Eyelid retraction -Rapid speech Cardiovascular System: -Systolic hypertension -Bounding, rapid pulse; palpitations -↑ Cardiac output -Cardiac hypertrophy -Systolic murmurs -Dysrhythmias -Angina Respiratory System: -Dyspnea on mild exertion -Increased respiratory rate GI System: -Increased appetite, thirst -Weight loss -Diarrhea -Splenomegaly -Hepatomegaly Integumentary System: -Warm, smooth, moist skin -Thin, brittle nails -Hair loss -Clubbing of fingers; palmar erythema -Fine, silky hair; premature graying -Diaphoresis -Vitiligo -Pretibial myxedema (infiltrative dermopathy) Musculoskeletal System: -Fatigue -Weakness -Proximal muscle wasting -Dependent edema -Osteoporosis Nervous System: -Nervousness, fine tremors -Insomnia , exhaustion -Lability of mood, delirium •Personality changes of irritability, agitation •Depression, fatigue -Hyperreflexia of tendon reflexes -Inability to concentrate -Stupor, coma Reproductive System: -Menstrual irregularities -Amenorrhea -Decreased libido -Impotence/ erectile dysfunction -Gynecomastia in men -Decreased fertility

palliative care

-Care or treatment focusing on reducing the severity of symptoms -Begins during curative or restorative health care -Extends into end-of-life care -Bereavement care follows death Goals: -Regard dying as a normal process -Provide relief from symptoms, including pain -Affirm life and neither hasten nor postpone death -Support holistic patient care and enhance quality of life -Offer support to patients to live as actively as possible until death -Offer support to the family during the patient's illness and in their own bereavement -Indication: diagnosis of a life-limiting illness such as cancer, heart failure, COPD, dementia, or ESRD -Involves: -Interprofessional collaboration: includes physicians, nurses, social workers, pharmacists, chaplains, and others -Ongoing communication: important for optimal care -Care in multiple settings: home, long-term care, acute care, mental health facilities, rehabilitation centers, and prisons

special needs of nurses

-Caring for dying patients is -Challenging and rewarding -Intense and emotionally charged -Recognize your values, attitudes and feelings about death -When dealing with death and the dying you are not immune to feelings of loss, helplessness, and powerlessness. What are some strategies? -Many nurses who care for dying patients are passionate about providing quality EOL care. -A bond or connection may develop between you and the patient and/or family. -Be aware of how grief personally affects you. -When dealing with death and the dying you are not immune to feelings of loss, helplessness, and powerlessness. -Express feelings of sorrow, guilt, and frustration. -Recognize your own values, attitudes, and feelings about death. -Be aware of what you can and cannot control. •Realize it is OK to cry with the patient or family. •Focus on interventions to decrease your own physical and emotional stress. •Get involved in hobbies or other interests. •Schedule time for yourself. •Maintain a peer support system. •Develop a support system beyond the workplace. •Hospice agencies can provide care of their team with professionally assisted groups, informal discussion sessions, and flexible time schedules.

Cushing syndrome

-Caused by chronic exposure to excess corticosteroids, particularly glucocorticoid s: •Cortex hormones: glucocorticoid s, mineralcortic oids, andorgens •Medulla hormones-catecholamines: adrenaline, noradrenalin, dopamine -Common causes: •Iatrogenic administration of exogenous corticosteroids (e.g., prednisone) •ACTH-secreting pituitary adenoma-85% of endogenous cases •Adrenal tumors •Ectopic ACTH production by tumors (usually of the lung or pancreas) outside of the hypothalamic-pituitary-adrenal axis Clinical Manifestations: -Manifestations of Cushing syndrome occur in most body systems and are related to excess levels of corticosteroids. -Although signs of glucocorticoid excess usually predominate, symptoms of mineralocorticoid and androgen excess can occur. -Corticosteroid excess causes pronounced changes in physical appearance. -A rounded face ("moon facies") with thin, reddened skin -Weight gain, the most common feature, results from the accumulation of adipose tissue in the trunk (centripetal obesity), face ("moon face"), and cervical areas ("buffalo hump"). -Purplish red striae (usually depressed below the skin surface) appear on the abdomen, breast, or buttocks. -Truncal obesity; broad, purple striae; and easy bruising (left antecubital fossa). -Hyperglycemia occurs because of glucose intolerance (associated with cortisol-induced insulin resistance) and increased gluconeogenesis by the liver. -Muscle wasting causes weakness, especially in the extremities. -A loss of bone matrix leads to osteoporosis and back pain. -The loss of collagen makes the skin weaker, thinner, and more easily bruised. -Catabolic processes lead to a delay in wound healing. -Mineralocortic oid excess may cause hypokalemia from potassium excretion and hypertension secondary to fluid retention. -Adrenal androgen excess may cause severe acne, virilization in women, and feminization in men. -Menstrual disorders and hirsutism in women and gynecomastia and impotence in men are seen more commonly in adrenal cancers. Diagnostic Studies: -Plasma ACTH levels may be low, normal, or elevated, depending on the underlying cause of Cushing syndrome. -High or normal ACTH levels indicate Cushing disease (pituitary etiology), whereas low or undetectable levels indicate Cushing syndrome (an adrenal or medication etiology). -Hypokalemia and alkalosis are seen in ectopic ACTH syndrome and adrenal carcinoma Interprofessional Care: -The primary goal of treatment is to normalize hormone secretion. -The specific treatment is dependent on the underlying cause. -If the underlying cause is a pituitary adenoma, the standard treatment is surgical removal of the pituitary tumor via the transsphenoidal approach. -Radiation therapy is an option for patients who are not good surgical candidates. -Adrenalectomy is indicated when Cushing syndrome is caused by adrenal tumors or hyperplasia. -On occasion, bilateral adrenalectomy is necessary. -A laparoscopic approach is used unless a malignant adrenal tumor is suspected. -An open surgical adrenalectomy is usually performed for adrenal cancer. -Patients with ectopic ACTH-secreting tumors are best managed by locating and removing the tumor (usually lung or pancreas). This is usually possible when the tumor is benign. When a tumor is malignant and has already metastasized, surgical removal may not possible or successful. -If Cushing syndrome has developed during the course of prolonged administration of corticosteroids (e.g., prednisone), the following alternatives may be tried: •Gradually discontinuing corticosteroid therapy •Reducing the corticosteroid dose •Converting to an alternate-day regimen •Gradual tapering of the corticosteroids is necessary to avoid potentially life-threatening adrenal insufficiency. -An alternate-day regimen is one in which twice the daily dosage of a shorter-acting corticosteroid is given every other morning to minimize hypothalamic-pituitary-adrenal suppression, growth suppression, and altered appearance. -This regimen is not used when the corticosteroids are given as hormone therapy. Nursing Assessment: -Subjective data: •Patient health history: pituitary tumor; adrenal, pancreatic, or pulmonary neoplasms; GI bleeding; frequent infections •Medications: use of corticosteroids •Malaise •Weight gain •Anorexia •Polyuria •Prolonged wound healing •Easy bruising •Weakness, fatigue •Insomnia, poor sleep quality •Headache •Back, joint, bone, and rib pain •Poor concentration and memory •Negative feelings regarding changes in personal appearance •Amenorrhea •Impotence, decreased libido •Anxiety •Mood disturbances •Emotional lability •Psychosis -Objective Data: •Truncal obesity •Supraclavicular fat pads •Buffalo hump •Moon facies •Plethora •Hirsutism of body and face •Thinning of hair •Thin, friable skin •Acne •Petechiae, purpura •Hyperpigmentation •Purplish red striae on breasts, buttocks, and abdomen •Edema of lower extremities •Hypertension •Muscle wasting •Thin extremities •Awkward gait •Gynecomastia, testicular atrophy (in men) •Enlarged clitoris (in women) •↓ Potassium level •↑ Glucose level •Dyslipidemia •Polycythemia •Granulocytosis •Lymphocytopenia •Eosinopenia •↑ Serum cortisol level •High, low or normal ACTH levels •Abnormal dexamethasone suppression test •↑ Urine free cortisol and 17-ketosteroids •Glycosuria •Hypercalciuria •Osteoporosis on x-ray Nursing Diagnoses: -Risk for infection related to lowered resistance to stress and suppression of immune system -Risk for overweight related to increased appetite, high caloric content of foods, and inactivity -Disturbed body image related to change in appearance from disease process -Impaired skin integrity related to excess corticosteroids, immobility, and altered skin integrity (fragility) Patient Goals: 1. Experience relief of symptoms 2. Avoid serious complications 3. Maintain a positive self-image 4. Actively participate in the therapeutic plan Health Promotion: -Focused on identifying patients at risk for Cushing syndrome. -Patients receiving long-term, exogenous corticosteroids are at risk. -Teaching related to medication use and the monitoring of side effects are important preventive measures. -Patients with Cushing syndrome are seriously ill. -Because the therapy has many side effects, the focus of assessment is on signs and symptoms of hormone toxicity, drug toxicity, and complicating conditions (e.g., cardiovascular disease, diabetes mellitus, infection). Acute Care: -Monitor vital signs, daily weight, glucose level. -Assess for possible infection. •Because signs and symptoms of inflammation (e.g., fever, redness) may be minimal or absent, assess for pain, loss of function, and purulent drainage. •Monitor for signs and symptoms of thromboembolic events such as pulmonary emboli (e.g., sudden chest pain, dyspnea, tachypnea). Emotional Support: -Changes in appearance such as truncal obesity, multiple bruises, hirsutism in women, and gynecomastia in men can be distressing -Patient may feel unattractive, repulsive, or unwanted -Remain sensitive to patient's feelings and be respectful and accepting -Reassure patient that physical changes and emotional lability will resolve when hormone levels return to normal Preoperative Care: -If treatment involves surgical removal of a pituitary adenoma, an adrenal tumor, or one or both adrenal glands, nursing care will include preoperative and postoperative measures. -Before surgery, the patient's physical condition should be optimized. -Hypertension and hyperglycemia must be controlled. -Hypokalemia must be corrected with diet and potassium supplements. -A high-protein diet helps correct the protein depletion. -Preoperative teaching depends on the type of surgical approach planned (hypophysectomy or adrenalectomy) and should include information regarding the anticipated postoperative care. Postoperative Care: -↑ Risk of hemorrhage because adrenal glands are vascular -Manipulating glandular tissue during surgery may release large release of hormones into circulation, producing marked fluctuations in metabolic processes → instabilities in BP, fluid balance, and electrolyte levels -In the postoperative period for both laparoscopic and open adrenalectomy, the patient may have a nasogastric tube, a urinary catheter, IV therapy, central venous pressure monitoring, and leg sequential compression devices to prevent emboli. -High doses of corticosteroids (e.g., hydrocortisone [Solu-Cortef]) are given IV during and several days after surgery to ensure adequate responses to the stress of the procedure -If large amounts of endogenous hormone were released into the systemic circulation during surgery, the patient is likely to develop hypertension, which increases the risk of hemorrhage. -Increased risk for: •Problems with glycemic control •Susceptibility to infection •Delayed wound healing -The critical period for circulatory instability ranges from 24 to 48 hours after surgery. During this time, you must constantly be alert for signs of corticosteroid imbalance. -Report any rapid or significant changes in BP, respirations, or heart rate. -Monitor fluid intake and output carefully and assess for potential imbalances. -IV corticosteroids are given as ordered, and the dose and rate of flow are adjusted to the patient's clinical manifestations and fluid and electrolyte balance. Oral doses are given as tolerated. -Keep the IV line in place after IV corticosteroids are withdrawn to enable quick administration of corticosteroids or vasopressors. -Obtain morning urine samples (at the same time each morning) for cortisol measurement to evaluate the effectiveness of the surgery. -If corticosteroid dosage is tapered too rapidly after surgery, acute adrenal insufficiency may develop. •Vomiting, increased weakness, dehydration, and hypotension are signs of hypocortisolism •In addition, the patient may complain of painful joints, pruritus, or peeling skin and may experience severe emotional disturbances. •Report these signs and symptoms so drug doses can be adjusted as necessary. -The patient is usually maintained on bed rest until the BP stabilizes. -Be alert for subtle signs of postoperative infections because the usual inflammatory responses are suppressed. -To prevent infection, provide meticulous care when changing the dressing and during any other procedures that necessitate access to body cavities, circulation, or areas under the skin. Ambulatory Care: -Discharge instructions are based on the patient's lack of endogenous corticosteroids and resulting inability to react physiologically to stressors. -Consider a home health nurse referral, especially for older adults, because of the need for ongoing evaluation and educational needs. -Instruct the patient to wear a MedicAlert bracelet at all times and carry medical identification and instructions in a wallet or purse. -Teach the patient to avoid exposure to extremes of temperature, infections, and emotional disturbances. -Stress may produce or precipitate acute adrenal insufficiency because the remaining adrenal tissue cannot meet an increased hormonal demand. -Teach patients to adjust their corticosteroid replacement therapy in accordance with their stress levels. -Consult with the patient's HCP to determine the parameters for dosage changes if this plan is feasible. -If the patient cannot adjust his or her own medication or if weakness, fainting, fever, or nausea and vomiting occur, the patient should contact the HCP for a possible adjustment in corticosteroid dosage. -Many patients require lifetime replacement therapy. -However, it may take several months to adjust the hormone dose satisfactorily, and patients should be prepared accordingly. Expected Outcomes: -Experience no signs or symptoms of infection -Maintain weight appropriate for height -Verbalize acceptance of appearance and treatment regimen -Heal skin wounds and maintain intact skin

diabetic ketoacidosis (DKA)

-Caused by profound deficiency of insulin -Characterized by: •Hyperglycemia •Ketosis •Acidosis •Dehydration -Most likely to occur in Type 1 Diabetes -It is most likely to occur in people with type 1 diabetes but may be seen in people with type 2 diabetes in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin. -Remember looking at blood gas values, normal pH is 7.35-7.45 Normal PaCO2 is 35-45, Normal HCO3 is 22-26. -Think about skin turgor, dry mucous membranes, intake and output, vital signs, blood glucose > 250 Precipitating Factors: -Illness -Infection -Inadequate insulin dosage -Undiagnosed type 1 diabetes -Poor self-management -Neglect -Stress Clinical Manifestations: -Dehydration: •Poor skin turgor •Dry mucous membranes •Tachycardia •Orthostatic hypotension -Lethargy and weakness early -Skin dry and loose; eyes soft and sunken -When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel. -Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop. -Ketonuria is a process that occurs when ketone bodies are excreted in the urine. During this process, electrolytes become depleted as cations are eliminated along with the anionic ketones in an attempt to maintain electrical neutrality. -Insulin deficiency impairs protein synthesis and causes excessive protein degradation. This results in nitrogen losses from the tissues. -Insulin deficiency also stimulates the production of glucose from amino acids (from proteins) in the liver and leads to further hyperglycemia. -Because there is a deficiency of insulin, the additional glucose cannot be used and the blood glucose level rises further, adding to the osmotic diuresis. -If not treated, the patient will develop severe depletion of sodium, potassium, chloride, magnesium, and phosphate. -It is important to obtain electrolyte values before any treatment is started, typically an infusion of 0.45% NS or 0.9% saline is ordered at a rate to provide 30-60mL/hr urine output. Insulin is started at Regular insulin 0.1u/kg/hr. -Vomiting caused by the acidosis results in more fluid and electrolyte losses. -Eventually, hypovolemia will ensue and be followed by shock. -Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses. -Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis. If the condition is not treated, death is inevitable. -Abdominal pain, anorexia, nausea/vomiting -Kussmaul respirations: rapid, deep breathing associated with dyspnea; the body's attempt to reverse metabolic acidosis through the exhalation of excess carbon dioxide -Sweet, fruity breath odor (due to acetone) -Blood glucose level of ≥ 250 mg/dL -Blood pH lower than 7.30 -Serum bicarbonate level < 16 mEq/L -Moderate to high ketone levels in urine or serum Treatment: -Less severe form may be treated on outpatient basis -Hospitalize for severe fluid and electrolyte imbalance, fever, nausea/vomiting, diarrhea, altered mental state (considered unstable, often treated in ICU initially to stabilize), and nature of the cause of ketoacidosis -Patients with DKA who have an illness such as pneumonia or a urinary tract infection are usually admitted to the hospital -Also hospitalization may be required if communication with health care provider is lacking (less than every few hours) -Before the advent of self-monitoring of blood glucose, patients with DKA required hospitalization for treatment. -Today, hospitalization may not be required. -When fluid and electrolyte imbalances are not severe and blood glucose levels can be safely monitored at home, less severe forms of DKA may be managed on an outpatient basis Treatment: -Ensure patent airway; administer O2 via nasal cannula or non-rebreather mask -Establish IV access; begin fluid resuscitation -NaCl 0.45% or 0.9% at a rate to restore urine output to 30 to 60 mL/hr and to raise blood pressure -Add 5% to 10% dextrose when blood glucose level approaches 250 mg/dL to prevent hypoglycemia, as well as a sudden drop in glucose that can be associated with cerebral edema -Continuous regular insulin drip 0.1 U/kg/hr -It is important to prevent rapid drops in serum glucose to avoid cerebral edema. -A blood glucose reduction of 36 to 54 mg/dL (2 to 3 mmol/L) per hour will avoid complications. -Insulin allows water and potassium to enter the cell along with glucose and can lead to a depletion of vascular volume and hypokalemia; therefore, monitor the patient's fluid balance and potassium levels. -Potassium replacement as needed -Overzealous rehydration, especially with hypotonic IV solutions, can result in cerebral edema. -Monitor patients with renal or cardiac compromise for fluid overload. -Measure serum potassium level before starting insulin. If the patient is hypokalemic, insulin administration will further decrease the potassium levels, making early potassium replacement is essential. -Although initial serum potassium value may be normal or high, levels can decrease rapidly once therapy starts, as insulin drives potassium into the cells, leading to life-threatening hypokalemia. -IV insulin administration is therapy directed toward correcting hyperglycemia and hyperketonemia.

asthma and status asthmaticus

-Clinical course of asthma is unpredictable, ranging from periods of adequate control to exacerbations with poor control of symptoms. -Complex clinical manifestations with reversible expiratory airflow limitation or bronchial hyperresponsiveness -Affects about 18.8 million Americans -Women are 62% more likely to have asthma than men -Risk factors: genetics, male children, exercise, occupational exposure -Older adults may be undiagnosed -Gerontologic considerations: comorbidities, nonadherence, lack of access -Cultural considerations: higher rates in minorities with more morbidity and mortality due to lack of access, beliefs, lack of management Severe and Life-Threatening Exacerbations: -Respiratory rate >30/min -Dyspnea at rest, feeling of suffocation -Pulse >120/min -PEFR is 40% at best (or less than 150L) -Usually seen in ED or hospitalized -Too dyspneic to speak: often speaks in words, not sentences, because of the difficulty breathing -Perspiring profusely -Drowsy/ confused -PEFR <25% of personal best -Require hospital care and often admitted to ICU -The breath sounds may be very difficult to hear, and no wheezing is apparent as the airflow is exceptionally limited. Clinical Manifestations: -Unpredictable and variable: •Recurrent episodes of wheezing, breathlessness, cough, and tight chest •May be abrupt or gradual •Lasts minutes to hours -Triggers: •Allergens •Exercise •URI: major factor in acute attacks and exacerbations •Food •Emotions •NSAIDS •Beta blockers •ACEI -Early phase: initial inflammatory response -Late phase: 4-6 hours after initial attack, occurs in 50% of patients and lasts longer than 24 hours -Patient is often agitated (from hypoxemia) -During an acute attack, the person sits forward to maximize the diaphragmatic movement with prominent wheezing, a respiratory rate higher than 30 breaths/minute, and pulse greater than 120 beats/minute. Assessment: -Use of accessory muscles -Percussion of the lungs indicates hyperresonance -Auscultation of lungs indicates inspiratory or expiratory wheezing -Coughing produces thick, stringy mucus -Diaphoresis -Cyanosis -Lung sounds -Labs-ABGs, CBC, CMP -Pulse ox -Rule out infection -"RED" zone of asthma plan-seek immediate medical care -Obtaining a PEFR during a severe asthma attack is usually not possible. However, if it can be obtained, and it is less than 200 L/min, it indicates severe obstruction in all but very small adults. -Severely diminished breath sounds -Absence of wheeze after patient has been wheezing Diagnostic Studies: -Underdiagnosis of asthma is common. A detailed history is important to determine if a person has had similar attacks, which are often precipitated by a known trigger. -The peak expiratory flow rate (PEFR) measured by the peak flow meter (at home or in a health care setting) is an aid to diagnose and monitor asthma. -Spirometry (measured in a health care setting) is usually normal between asthma attacks if the patient has no other underlying pulmonary disease. -However, the patient with asthma may show an obstructive pattern including a decrease in forced vital capacity (FVC), FEV1, PEFR, and FEV1 to FVC ratio (FEV1/FVC). -Spirometry can be done before and after the administration of a bronchodilator to determine the degree of the response. -Chest x-ray is usually normal for asymptomatic patients, but can tell if something else (i.e., pneumonia, foreign body in the airway) could be causing symptoms similar to asthma. Plan of Care: -Monitor respiratory and heart rate, use of accessory muscles -PEFR to monitor airflow obstruction -O2 given via nasal cannula or mask to achieve a PaO2 of at least 60 mm Hg or O2 saturation greater than 90% -Continuous oxygen monitoring with pulse oximetry -Bronchodilator treatment -For any classification of asthma, in a "rescue plan" patients are instructed to take 2 to 4 puffs of albuterol every 20 minutes 3 times to gain rapid control of symptoms. -Management of the patient with acute exacerbations focuses on correcting hypoxemia and improving ventilation. -Moderate exacerbation: relief is provided with the SABA delivered as in the mild exacerbation, and oral corticosteroids are needed. The patient's symptoms may persist for several days even after the corticosteroids are started. Interprofessional Care: -Requires ED and possible ICU -IV magnesium sulfate -100% oxygen -Hourly or continuous nebulized SABA -IV corticosteroids Drug Therapy: -Corticosteroids:IV and inhaled (e.g., beclomethasone, budesonide) -Bronchodilators (SABA and LABA) -Anticholinergic drugs -ICSs are first-line therapy for patients with persistent asthma requiring step 2-6 therapy (see Fig. 28-4). -Usually, ICSs must be administered for 1 to 2 weeks before maximum therapeutic effects can be seen. -Some ICSs (e.g., fluticasone [Flovent], budesonide [Pulmicort]) begin to have a therapeutic effect in 24 hours. -Correct administration of drugs is a major factor in success Inhalation of drugs is preferable to avoid systemic side effects -MDIs, DPIs, and SVN -Acute episodes: nebulizers are devices used to inhale medications

culturally competent care

-Cultural beliefs affect: •Understanding of and reaction to death or loss •Treatment decisions -Cultural differences in relation to death and dying are varied -Rituals associated with dying are part of all cultures -Ensure adequate information for those who don't speak English -Pay attention to nonverbal cues -Culture and ethnicity are important considerations for patients who are receiving palliative and EOL care and their families. -In some groups, death and dying are private matters shared only with significant others. -Feelings are often repressed or internalized. -Beliefs include "toughing it out" and "being strong." -Some groups (African Americans and Hispanic/Latinos) easily express feelings and emotions. -Kinships are very strong in Hispanic cultures. -Both immediate and extended family provide support. -Expression of feelings is encouraged and accepted. -Rituals associated with dying are part of all cultures. -In certain cultures the family may want to keep constant vigil in the room of a dying patient or in the waiting area. For example, some Jewish Americans believe that the spirit should not be alone when it leaves the body at the time of death. Therefore someone who is terminally ill should never be left alone. The Jewish culture believes all body tissues must be buried with the individual. -Once a death has occurred, some cultures, such as the Puerto Rican American culture, may want to kiss and touch the body to say goodbye. -In the Islamic cultures the traditional rites of washing, shrouding, funeral prayers, and burial are done as soon as possible. -Families with non-English-speaking members are at risk for receiving less information about their family member's critical illness and prognosis. -Cultural variations also exist in symptom expression (e.g., pain expression) and use of health care services. -Providing culturally competent care requires assessment of nonverbal cues such as grimaces, body position, and decreased or guarded movements.

hospice

-Curative care is forgone -Requires physician certification that life expectancy is 6 months or less -Initiated only after the decision is made by the patient or a proxy not to pursue a cure

Addison's disease

-Primary: •Addison's disease •Lack of glucocorticoid s, mineralocorti coids, and androgens -Secondary: •Lack of pituitary ACTH •Lack of glucocorticoids and androgens -Adrenocortical insufficiency (hypofunction of the adrenal cortex) may be from a primary cause (Addison's disease) or a secondary cause (lack of pituitary ACTH secretion). -In Addison's disease, amounts of all three classes of adrenal corticosteroids (glucocorticoids, mineralocorticoids, and androgens) are reduced. -In secondary adrenocortical insufficiency, corticosteroid and androgen levels are deficient, but mineralocorticoid levels rarely are. -ACTH deficiency may be caused by pituitary disease or suppression of the hypothalamic-pituitary axis because of the administration of exogenous corticosteroids. -80% of cases caused by an autoimmune response: •Autoimmune adrenalitis causes the adrenal cortex to be destroyed by antibodies •Antibodies destroy adrenal cortex -Loss of : •Glucocorticoid •Mineralocorti coid •Adrenal androgen hormones Other Causes: -TB (not a common cause in United States) -Amyloidosis -Fungal infections (e.g., histoplasmosis) -AIDS -Metastatic cancer Clinical Manifestations: -Slow (insidious) onset -Anorexia, nausea, progressive weakness, fatigue, and weight loss. -The disease is often advanced before it is diagnosed because manifestations do not tend to become evident until 90% of the adrenal cortex is destroyed. -Abdominal pain -Diarrhea -Headache -Orthostatic hypotension -Salt craving -Joint pain -Irritability and depression may occur in primary adrenal hypofunction. -Patients with secondary adrenocortical hypofunction may have many signs and symptoms similar to those of patients with Addison's disease. -Hyperpigmen tation: because ACTH levels are high; bronze-colored skin -It is seen primarily in sun-exposed areas of the body, at pressure points, over joints, and in the creases, especially palmar creases. -The changes in the skin are most likely due to increased secretion of β-lipotropin (which contains melanocyte-stimulating hormone [MSH]) -This tropic hormone is increased because of decreased negative feedback and subsequent low corticosteroid levels. -Patients with secondary adrenocortical hypofunction usually do not have hyperpigmented skin because ACTH levels are low. Addisonian Crisis (Acute Care): -Patients with adrenocortical insufficiency are at risk for acute adrenal insufficiency (addisonian crisis), a life-threatening emergency caused by insufficient adrenocortical hormones or a sudden sharp decrease in these hormones. -Addisonian crisis is triggered by (1) stress (e.g., from infection, surgery, psychologic distress), (2) the sudden withdrawal of corticosteroid hormone therapy (which is often done by a patient who lacks knowledge of the importance of this therapy), (3) adrenal surgery, or (4) sudden pituitary gland destruction. Manifestations of Glucocorticoid and Mineralocorticoid Deficiencies: -Hypotension, tachycardia -Dehydration -Hyponatremia, hyperkalemia, hypoglycemia -↓ Sodium, ↑ potassium, ↓ glucose -Fever, weakness, confusion -Severe vomiting, diarrhea, pain -Pain may occur in the lower back or legs -Shock → circulatory collapse (hypotension) -Circulatory collapse associated with adrenal insufficiency is often unresponsive to the usual treatment (vasopressors and fluid replacement). Diagnostic Studies: -ACTH Stimulation Test: •Baseline levels of cortisol and ACTH •IV injection of synthetic ACTH (cosyntropin) •Levels rechecked after 30 and 60 minutes •↑ Blood cortisol levels is normal •Little or no ↑ in cortisol levels in Addison's disease •High ACTH level in primary adrenal insufficiency CRH Stimulation Test: -Done when there is an abnormal ACTH test response -IV injection of synthetic CRH -Blood drawn after 30 and 60 minutes: •High ACTH levels with no cortisol indicates Addison's disease •Absence of ACTH or delayed response common in secondary adrenal insufficiency -↑ Potassium -↓ Chloride, sodium, glucose -Anemia -↑ BUN -ECG changes: may show low voltage and peaked T waved caused by hyperkalemia -CT scan, MRI can identify causes other than autoimmune, including tumors, fungal infections, tuberculosis, or adrenal calcification Interprofessional Care: -Treatment of adrenocortical insufficiency focuses on managing the underlying cause when possible. -The mainstay is lifelong hormone therapy with glucocorticoids and mineralocorticoids. -Overall, patients who take their medications consistently can anticipate a normal life expectancy. -Hydrocortison e, the most commonly used form of hormone therapy, has both glucocorticoid and mineralocorticoid properties. •The dosage is increased in stressful situations to prevent addisonian crisis. -Mineralocortic oids are replaced with fludrocortisone (Florinef). -Women need androgen replacement with dehydroepiandrosterone (DHEA) as their only source of androgen production is the adrenal glands. -Increased salt is added to the diet. -Addisonian crisis is a life-threatening emergency necessitating aggressive management. •Treatment is directed toward shock management and high-dose hydrocortisone replacement. •Large volumes of 0.9% saline solution and 5% dextrose are given to reverse hypotension and electrolyte imbalances until BP returns to normal. Acute Care: -Frequent assessment necessary -When the patient with Addison's disease is hospitalized, nursing management focuses on monitoring the patient while correcting fluid and electrolyte balance. -Assess vital signs and neurologic status. -Monitor for signs of fluid volume deficit and electrolyte imbalance. -Obtain a daily weight and keep an accurate intake and output record. -Take a complete medication history to determine drugs that can potentially interact with corticosteroids. -These drugs include oral hypoglycemics, cardiac glycosides, oral contraceptives, anticoagulants, and NSAIDs. -Note changes in blood pressure, weight gain, weakness, or other manifestations of Cushing syndrome. -Guard the patient against exposure to infection, and assist with daily hygiene. -Protect the patient from noise, light, and environmental temperature extremes. -The patient cannot cope with these stresses because of the inability to produce corticosteroids. Patient Teaching: -As a nurse, you have an important role in the long-term management of Addison's disease. -The serious nature of the disease and the need for lifelong hormone therapy necessitate a comprehensive teaching plan. -Glucocorticoid s are usually given in divided doses: two thirds in the morning and one third in the afternoon. -Mineralocortic oids are given once daily, preferably in the morning. •This schedule reflects normal circadian rhythm in endogenous hormone secretion and decreases the side effects associated with corticosteroid therapy. -Teach patients using mineralocorticoid therapy (fludrocortisone) how to take their BP, increase salt intake, and report any significant changes to their HCP. -Patients with Addison's disease are unable to tolerate physical or emotional stress without additional exogenous corticosteroids. -Long-term care revolves around recognizing the need for extra medication and techniques for stress management. •Examples of situations necessitating corticosteroid adjustment are fever, influenza, tooth extraction, and rigorous physical activity, such as playing tennis on a hot day or distance running. -Provide written and verbal instructions on when to change the dose. -If vomiting or diarrhea occurs, as may happen with influenza, the patient should notify the HCP immediately because electrolyte replacement and parenteral administration of cortisol may be necessary. -Teach patients the signs and symptoms of corticosteroid deficiency and excess (Cushing syndrome) and to report these signs to their HCP so the drug dose can be adjusted. -It is critical that the patient wear an identification bracelet (Medic Alert) and carry a wallet card stating the patient has Addison's disease so that appropriate therapy can be started in case of an emergency. -The patient should carry an emergency kit at all times. The kit should consist of 100 mg of IM hydrocortisone, syringes, and instructions for use. -Teach the patient, caregiver, and significant others how to give an IM injection. Corticosteroid Therapy: -Corticosteroid s are effective in treating many diseases and disorders. -However, the long-term administration of corticosteroids at therapeutic doses often leads to serious complications and side effects. For this reason, corticosteroid therapy is not recommended for minor chronic conditions. -Therapy should be reserved for diseases that carry a risk of death or permanent loss of function and for conditions in which short-term therapy is likely to produce remission or recovery. -The potential benefits of treatment must always be weighed against the risks. -A beneficial effect of corticosteroids in one situation may be a harmful one in another. •For example, decreasing inflammation in arthritis is an important therapeutic effect, but increasing the risk for infection is a harmful effect. -Suppressing inflammation and the immune response may help save lives in persons with anaphylaxis and in those receiving an organ transplant, but it causes reactivation of latent tuberculosis and greatly reduces resistance to other infections and cancers. -The vasopressive effect of corticosteroids is critical in enabling a person to function in stressful situations, but this effect can produce hypertension when used for drug therapy. Corticosteroid Therapy Side Effects: -Hypokalemia may develop. -Hypocalcemia related to anti-vitamin D effect may occur. -Glucose intolerance predisposes to diabetes mellitus. -Blood pressure increases because of excess blood volume and potentiation of vasoconstrictor effects. Hypertension predisposes to heart failure. -Healing is delayed. There is increased risk for wound dehiscence. -Susceptibility to infection is increased. Infection develops more rapidly and spreads more widely. -Manifestations of inflammation, including redness, tenderness, heat, swelling, and local edema, are suppressed. -Predisposition to peptic ulcer disease develops. -Skeletal muscle atrophy and weakness occur. -Mood and behavior changes may be observed. -Fat from extremities is redistributed to trunk and face. -Protein depletion decreases bone formation, density, and strength, leading to predisposition to pathologic fractures, especially compression fractures of the vertebrae (osteoporosis). -Suppression of pituitary ACTH synthesis occurs. -Corticosteroid deficiency is likely if hormones are withdrawn abruptly. Taper corticosteroid doses to reduce risk for acute adrenal crisis Corticosteroid Therapy Patient Teaching: -Plan a diet high in protein, calcium (at least 1500 mg/day), and potassium but low in fat and concentrated simple carbohydrates such as sugar, honey, syrups, and candy. -Identify measures to ensure adequate rest and sleep, such as daily naps and avoidance of caffeine late in the day. -Develop and maintain an exercise program to help maintain bone integrity. -Recognize edema and ways to restrict sodium intake to less than 2000 mg/day if edema occurs. -Monitor glucose levels and recognize symptoms of hyperglycemia (e.g., polydipsia, polyuria, blurred vision). Report hyperglycemic symptoms or capillary glucose levels exceeding 120 mg/dL (10 mmol/L). -Notify health care provider if experiencing heartburn after meals or epigastric pain that is not relieved by antacids. -See an eye specialist yearly to assess for development of cataracts. -Use safety measures such as getting up slowly from bed or a chair, and use good lighting to avoid accidental injury. -Maintain good hygiene practices and avoid contact with persons with colds or other contagious illnesses to prevent infection. -Inform all health care providers about long-term corticosteroid use. -Patients receive corticosteroid therapy for many reasons. Detailed instruction is necessary to ensure patient adherence. -When corticosteroids are used as nonreplacement therapies, they are taken once daily or once every other day. They should be taken early in the morning with food to decrease gastric irritation. -Because exogenous corticosteroid administration may suppress endogenous ACTH and therefore endogenous cortisol (suppression is time and dose dependent), emphasize the danger of abrupt cessation of corticosteroid therapy to patients and caregivers. -Corticosteroids taken for longer than 1 week will suppress adrenal production, and oral cortiosteroids must be tapered. -Ensure that increased doses of corticosteroids are prescribed in acute care or home care settings in situations of physical or emotional stress. -Corticosteroid-induced osteoporosis is an important concern for patients who receive corticosteroid treatment for prolonged periods of time (longer than 3 months). Therapies to reduce bone resorption may include increased calcium intake, vitamin D supplementation, bisphosphonates (e.g., alendronate [Fosamax]), and institution of a low-impact exercise program.

progressive care units

-Progressive care units (PCUs), also called intermediate care or step-down units, provide a transition between the ICU and the general care unit or discharge -PCU clients are at risk for serious complications -Examples: ◦Awaiting stent placement ◦Awaiting heart transplant ◦Receiving stable doses of vasoactive IV drugs (e.g., diltiazem [Cardizem]) ◦Being weaned from prolonged mechanical ventilation -PCUs provide critical care nursing for an at-risk client population in a more cost-effective environment.

rapid response

-Provides rapid assessment and intervention -Non-ICU patients experiencing acute clinical deterioration -Reduce cardiopulmonary arrests outside ICU -Inclusion of increased standing orders for clients -Goal: Improve patient outcomes. Two Main Functions: -Recognize urgent unmet needs of patients: ◦Timely identification of clinical deterioration ◦Prompt activation of the team -Initiate response for assessment, intervention, and triage: ◦Activation of team members ◦You as the bedside nurse are part of this team, you have the information that necessitated the reason to call a rapid response (SBAR) Delays in Recognition: -Failure to monitor -Failure to recognize problems: ◦Physiologic changes ◦Diagnostic information ◦Clinical deviations from normal ◦Lack nurse intuition -Failure to escalate: ◦Lack of information ◦Scarcity of resources ◦Informal hierarchical culture ◦Fear of criticism ◦Calling covering provider before activating Team Members (varies by hospital): ◦ICU nurse or Swat Nurse- attends all activations, initial lead ◦Assigned client nurse- provides information ◦Respiratory Therapist-ventilation or supplemental oxygen ◦Nursing Supervisor- disposition of client, general support ◦Pharmacist: not all teams ◦Provider- hospitalist Protocols: -Begin treatment before provider arrives -Airway management: O2 -12 EKG -Lab -Medications -This is critical thinking in action Five Keys to Success: -Culture that supports client safety -Team structure and roles -Clinical expertise -Communication: debriefing, encouragement -Teamwork: shared purpose and collaboration Patient/Family Activation: -How involved should the family members be during a call for rapid response or code? -It's questionable whether it improves outcomes of the situation -It might result in a significant increase in unnecessary calls -It might overwhelm the staff and resources -It might decrease the risk of a lawsuit -It might result in acceptance of the situation

role of the nurse in end of life care

-Relieve suffering -Clarify misunderstanding about the use of pain medications -Addiction is not a concern when providing comfort for the terminally ill patient -The principle of double effect: morally permissible to give a medication that has the potential for harm if it is given with the intent of relieving pain and suffering and not intended to hasten death -The use of opioids for symptom management at the end of life is often misunderstood and feared by patients, families, and HCPs. For this reason, many patients will refuse to take the medications, which leads to physical and emotional suffering due to uncontrolled pain and symptoms. -Your moral obligation is to relieve suffering, which includes giving medications that have the potential of producing harm, such as with opioids. -As a nurse, your role is to teach the patient and family regarding addiction, tolerance, and dependence to medications. -The person with terminal illness should not be concerned with addiction when the goal of treatment is comfort.

resuscitation

-A common health care practice -Patients and families have the right to decide whether CPR will be used -Physician's orders should specify: •Full Code •Chemical Code •No Code - DNR or AND -CPR is given for respiratory or cardiac arrest unless otherwise ordered by a physician. -However, whether and to what extent CPR is used is no longer the sole decision of the physician. -The ANA supports patient's right to self-determination, and a primary role of nurses is supporting patient and family decisions. -Full code refers to use of complete and total heroic measures including CPR, drugs, and mechanical ventilation. -Chemical code involves use of drugs without CPR. -DNR indicates comfort measures only without interference of technology. -Some states have out-of-hospital DNR for patients being cared for out of acute care facilities. -Term being used to replace DNR is AND - Allow Natural Death: •More accurately conveys what actually happens. •Also referred to as "comfort measures only" status. •Comfort measures include pain control and symptom management. •Natural progression to death is not delayed or interrupted. •Care is not withheld. Care is supportive, providing comfort and dignity, while allowing nature to take its course.

postmortem care

-After death is pronounced, the nurse prepares or delegates preparation of the body for immediate viewing by the family -Close patient's eyes -Replace dentures -Wash and position body -Consideration must be given for: •Cultural customs •State law •Agency policy and procedure. -May be important to allow family to prepare or assist in preparing body in some cultures and some types of death -Remove tubes and dressings if appropriate. -Straighten the body, leaving the pillow to support the head and prevent pooling of blood and discoloration of the face. -In the case of an unexpected or unanticipated death, preparation of the patient's body for viewing or release to a funeral home depends on state law and agency policies and procedures. -Never refer to the deceased person as "the body." -Care of and discussion related to the person should continue to be respectful even after death. Needs of Caregivers: -Caregivers are important in meeting patient's physical and psychosocial needs. -Often face high levels of stress and emotional, physical, and economic consequences from caring for a dying member. -Responsibilities do not end when the person is admitted to an inpatient facility. -Allow family privacy and as much time as they need with deceased person -Maintain respect for patient and family -Role of family caregivers includes: •Working and communicating with the patient, other family members, and friends •Supporting patient concerns •Helping patient resolve any unfinished business -Family caregivers and other family members need encouragement to continue their usual activities as much as possible. -They need to discuss their activities and maintain some control over their lives. -Inform caregivers about appropriate resources for support, including respite care. -Resources such as community counseling and local support may assist some people in working through their grief. -Encourage caregivers to build a support system of extended family, friends, faith community, and clergy. The caregivers should have people to call on at any time to express any feelings they are experiencing.

thyrotoxicosis

-Also called thyrotoxic crisis, thyroid storm, and acute thyrotoxicosis -Physiologic effects/clinical syndrome of hypermetabolism -Results from increased circulating levels of T3, T4, or both -Hyperthyroidi sm and thyrotoxicosis usually occur together -An acute, severe, and rare condition that occurs when excessive amounts of thyroid hormones are released into the circulation. -Though considered a life-threatening emergency, death is rare when treatment is initiated early. -It is thought to result from stressors (e.g., infection, trauma, surgery) in a patient with preexisting hyperthyroidism •Patients undergoing thyroidectomy are at risk because manipulation of the hyperactive thyroid gland results in an increase in hormones released. Manifestations: -Severe tachycardia, heart failure -Shock -Hyperthermia (up to 106 degrees Fahrenheit or 41.1 degree Celsisus) -Agitation -Seizures -Abdominal pain, vomiting, diarrhea -Delirium, coma Diagnostic Studies: -The two primary laboratory findings used to confirm the diagnosis of hyperthyroidism are low or undetectable TSH levels (< 0.4 mIU/L) and elevated free thyroxine (free T4) levels. -Total T3 and T4 levels may also be assessed, but they are not as definitive. -Total T3 and T4 determine both free and bound (to protein) hormone levels. -The free hormone is the only biologically active form of these hormones. -The RAIU test is used to differentiate Graves' disease from other forms of thyroiditis. -The patient with Graves' disease will show a diffuse, homogeneous uptake of 35% to 95%, whereas the patient with thyroiditis will show an uptake of less than 2%. -The person with a nodular goiter will have an uptake in the high normal range. Interprofessional Care: Goals: -Block adverse effects of thyroid hormones -Suppress hormone over-secretion -Prevent complications Three Primary Treatment Options: -Antithyroid medications -Radioactive iodine therapy (RAI) -Surgery Drug Therapy: -Drugs used in the treatment of hyperthyroidism include antithyroid drugs, iodine, and β-adrenergic blockers. -These drugs are useful in treating thyrotoxic states, but they are not considered curative. Anti-thyroid Drugs: -The first-line antithyroid drugs are propylthiouracil and methimazole (Tapazole). -These drugs inhibit the synthesis of thyroid hormones. -Indications for use include Graves' disease in young patients, hyperthyroidism during pregnancy, and the need to achieve a euthyroid state before surgery or radiation therapy. -PTU is generally given to patients who are in the first trimester of pregnancy, who have had an adverse reaction to methimazole, or for whom a rapid reduction in symptoms is required. -PTU is also considered first line in thyrotoxic crisis as it also blocks the peripheral conversion of T4 to T3. -The advantage of PTU is that it achieves the therapeutic goal of a euthyroid state more quickly, but it must be taken three times per day. -In contrast, methimazole is given in a single daily dose. -Improvement usually begins 1 to 2 weeks after the start of drug therapy. -Good results are usually seen within 4 to 8 weeks. -Therapy is usually continued for 6 to 15 months to allow for spontaneous remission, which occurs in 20% to 40% of patients. -Emphasize to the patient the importance of adhering to the drug regimen. -Abruptly discontinuing drug therapy can result in a return of hyperthyroidism Iodine: -Iodine is available as saturated solution of potassium iodine (SSKI) and Lugol's solution. -Iodine is used with other antithyroid drugs to prepare the patient for thyroidectomy or for treatment of thyrotoxicosis. -Rapidly giving large doses of iodine inhibits synthesis of T3 and T4 and blocks the release of these hormones into circulation. -It also decreases the vascularity of the thyroid gland, making surgery safer and easier. -The maximal effect is usually seen within 1 to 2 weeks. -Because of a reduction in the therapeutic effect, long-term iodine therapy is not effective in controlling hyperthyroidism -Iodine is mixed with water or juice, sipped through a straw, and given after meals. -Assess the patient for signs of iodine toxicity such as swelling of the buccal mucosa and other mucous membranes, excessive salivation, nausea and vomiting, and skin reactions. -If toxicity occurs, discontinue iodine administration and notify the HCP B-Adrenergic Blockers: -Used for symptomatic relief of thyrotoxicosis. -These drugs block the effects of sympathetic nervous stimulation, thereby decreasing tachycardia, nervousness, irritability, and tremors. -Propranolol (Inderal) is usually given with antithyroid agents. -Atenolol (Tenormin) is the preferred β-adrenergic blocker for use in hyperthyroid patients with asthma or heart disease. Surgical Therapy: -Large goiter causing tracheal compression -Unresponsive to anti-thyroid therapy -Thyroid cancer -Not a candidate for RAI -Rapid reduction in T3 and T4 levels Subtotal Thyroidectomy: -A subtotal thyroidectomy is the preferred surgical procedure -It involves removing a significant portion (90%) of the thyroid gland. -Some patients may undergo minimally invasive endoscopic or robotic thyroidectomy. -Endoscopic thyroidectomy is an appropriate procedure for patients with small nodules (less than 3 cm) and no evidence of cancer. -Robotic surgery is best for those who are not overweight and have small nodules on only one side of the gland. -Advantages of endoscopic and robotic procedures over open thyroidectomy include less scarring, less pain, and a faster return to normal activity. -Post op risk: airway risk, bleeding, electrolyte changes

diabetes insipidus (DI)

-DI can be caused by a deficiency of production or secretion of ADH -Central: tumor, head injury, surgery, CNS infections -DI can be caused by a decreased renal response to ADH: Insensitivity •Lithium, renal damage, renal disease -Someone with DI does NOT require insulin Clinical Manifestations: -Decreased renal response -Fluid and electrolyte imbalances -Too much urine output -Very low specific gravity < 1.005 and urine osmolality of less than 100mOsm/kg (that means that serum osmolality is elevated, > 295mmol/kg due to hypernatremia, so these clients drink lots and lots of water) -Polydipsia -Polyuria 2 to 20L per day Diagnostic Studies: -Water Deprivation Test and administration of DDAVP -Measure the level of ADH after an analog of ADH is given Nursing and Interprofessional Management: -Maintain adequate hydration, IV or PO -Maintain electrolyte balance -Monitor BP, HR, LOC, I&O -Monitor specific gravity-urine or serum -Hormone replacement Medications: -DDAVP for central DI hormone replacement, monitor pulse -Dietary measures; low sodium diet -Thiazide diuretics reduce flow to the ADH sensitive nephrons -Indocine (NSAID) helps increase renal responsiveness to ADH

hypothyroidism/myxedema coma

-Deficiency of thyroid hormone -Causes general slowing of metabolic rate -More common in women than in men -Primary hypothyroidism is caused by destruction of thyroid tissue or defective hormone synthesis. -Secondary hypothyroidism is caused by pituitary disease with decreased TSH secretion or hypothalamic dysfunction with decreased thyrotropin-releasing hormone (TRH) secretion. -Hypothyroidism can be transient and related to thyroiditis or discontinuing thyroid hormone therapy. -Iodine deficiency is the most common cause of hypothyroidism worldwide. -In the United States, the most common cause of primary hypothyroidism is atrophy of the thyroid gland. -This atrophy is the end result of Hashimoto's thyroiditis or Graves' disease. -These autoimmune diseases destroy the thyroid gland. -Hypothyroidism also may develop after treatment for hyperthyroidism, specifically thyroidectomy or RAI therapy. -Drugs such as amiodarone (Cordarone) (which contains iodine) and lithium (which blocks hormone production) can cause hypothyroidism. -Hypothyroidism that develops in infancy (cretinism) is caused by thyroid hormone deficiencies during fetal or early neonatal life. All infants in the United States are screened for decreased thyroid function at birth. Clinical Manifestations: -Regardless of the cause, hypothyroidism has systemic effects characterized by a slowing of body processes. -Manifestations vary depending on the severity and the duration of thyroid deficiency, as well as the patient's age at the onset of the deficiency. -Symptoms may develop over months to years unless hypothyroidism occurs after a thyroidectomy, thyroid ablation, or during treatment with antithyroid drugs. -The patient is often fatigued, lethargic, and experiences personality and mental changes, including impaired memory, slowed speech, decreased initiative, and somnolence. -Many appear depressed. -Weight gain is most likely a result of a decreased metabolic rate. -In the older adult the typical manifestations of hypothyroidism (fatigue, cold and dry skin, hoarseness, hair loss, constipation, and cold intolerance) may be attributed to normal aging. -For this reason, the patient's symptoms may not raise suspicion of an underlying condition. -Older adults who have confusion, lethargy, and depression should be evaluated for thyroid disease. Cardiovascular System: -CV problems may be significant in patients with pre-existing cardiovascular disease -↓ Cardiac contractility and output -↑ Serum cholesterol and triglycerides and the accumulation of mucopolysaccharides in the intima of small blood vessels can result in coronary atherosclerosis -Anemia Respiratory System: -Low exercise tolerance -Shortness of breath on exertion Neurologic System: -Fatigue and lethargy -Personality and mood changes -Impaired memory, slowed speech, decreased initiative, and somnolence Gastrointestinal System: -Decreased appetite -Nausea and vomiting -Weight gain -Constipation -Distended abdomen -Enlarged, scaly tongue -Celiac disease Integumentary System: -Dry, thick, inelastic, cold skin -Thick, brittle nails -Dry, sparse, coarse hair -Poor turgor of mucosa -Generalized interstitial edema -Puffy face -Decreased sweating -Pallor Musculoskeletal System: -Fatigue, weakness -Muscular aches and pains -Slow movements -Arthralgia Reproductive System: -Prolonged menstrual periods or amenorrhea -Decreased libido, infertility Other: -Increased susceptibility to infection -Increased sensitivity to opioids, barbiturates, anesthesia -Intolerance to cold -Decreased hearing -Sleepiness -Goiter

acute complications of diabetes mellitus

-Diabetic ketoacidosis (DKA) -Hyperosmolar hyperglycemic syndrome (HHS) -Hypoglycemia -The acute complications of diabetes mellitus arise from events associated with hyperglycemia and hypoglycemia. -Hyperglycemia occurs when there is not enough insulin working, and hypoglycemia occurs when there is too much insulin working. -It is important for the HCP to distinguish between hyperglycemia and hypoglycemia because hypoglycemia worsens rapidly and is a serious threat if action is not immediately taken.

end of life

-Final phase of a patient's illness, when death is imminent -Diagnosis of a terminal illness to actual death varies depending on diagnosis and extent of disease -The period of time during which an individual copes with declining health from a terminal illness or from the frailties associated with advanced age even if death is not clearly imminent. -End-of-life care (EOL care) is the term used for issues and services related to death and dying. EOL care focuses on physical and psychosocial needs for the patient and family. Goals: -Provide comfort and supportive care during dying process -Improve quality of remaining life -Help ensure a dignified death -Provide emotional support to family -Uncertainty about how close at hand the end is adds to the challenge of answering patient and family questions including "how much time is left?" -Nurses spend more time with patients near the end of life than do any other health care professionals.

hypoxemic respiratory failure

-Four physiologic mechanisms* most common: 1. Ventilation (V) and perfusion (Q) mismatch: (V/Q mismatch) - ideally, V/Q ratio 1:1 or V/Q equals 1 - V/Q mismatch occurs when ratio is not 1:1 -Most common: COPD, pneumonia, asthma, pain, atelectasis, pulmonary embolus 2. Shunting: through heart by passing lungs OR through lungs without gas exchange -Most Common: ventricular septal defect, alveoli fill with fluid, for example, pneumonia 3. Diffusion limitation: gas exchange across alveolar-capillary membrane is compromised -Most common: pulmonary fibrosis, interstitial lung disease, ARDS, pulmonary edema, Hypoxemia present during exercise -Exchange of CO2 and O2 cannot occur because of the thickened alveolar-capillary membrane 4. Alveolar hypoventilation:atelectasis -Most common: CNS conditions, chest wall dysfunction, acute asthma, restrictive lung disease Oxygenation Failure: -Hypoxemia leads to hypoxia -Cells shift from aerobic to anaerobic metabolism, •Increased lactic acid and causing metabolic acidosis •Tissue and cell dysfunction and death (if not corrected) -Oxygen therapy: First step to reverse V/Q mismatch -Best: treat the underlying cause -Oxygen therapy with mechanical ventilation with high FiO2 may be needed Specific Manifestations of Hypoxemia: -Respiratory: dyspnea, tachypnea, prolonged expiration, nasal flaring, intercostal muscle retraction, use of accessory muscles, decreased SpO2 (less than 80%), paradoxic chest or abdominal wall movement with respiratory cycle (late), cyanosis (late) Nonspecific Manifestations of Hypoxemia: -CNS: agitation; confusion; disorientation; restless, combative behavior; delirium; decreased level of consciousness; coma (late) -Cardiovascular: tachycardia; hypertension; skin cool, clammy, and diaphoretic; dysrhythmias (late); hypotension (late) -Other: fatigue, inability to speak in complete sentences without pausing to breathe

acute respiratory failure (ARF)

-Hypoxemic: insufficient O2 transferred to blood •Causes involve respiratory or cardiac system disorders or diseases •Reflected in ABG: decreased PaO2 and SaO2 •Oxygenation failure •PaO2 less than or equal to 60 mmHg on greater than or equal to 60% oxygen •Main problem: inadequate exchange of O2 between the alveoli and pulmonary capillaries -Hypercapnic: inadequate CO2 removal •Causes involve respiratory system, CNS, chest wall, and neuromuscular system disorders or diseases •Reflected in ABGs: increased PaCO2 •Ventilatory failure •PaCO2 greater than 50 mm Hg with acidemia and pH less than 7.35 •Main problem: insufficient CO2 removal; the body is unable to compensate Clinical Manifestations: -Sudden or gradual onset -A sudden decrease in PaO2 or rapid increase in PaCO2 implies a serious condition or life-threatening emergency -Failure of compensatory mechanisms leads to respiratory failure -Frequent assessment is a priority -First sign of respiratory failure is a change in mental status -Decreased O2: restlessness, confusion, agitation -Increased CO2: morning headache, decreased RR, and decreased LOC -Early signs of compensation: •Heart and lungs: tachycardia, tachypnea, and mild HTN -Late signs of inadequate compensation: •Cyanosis (unreliable indicator) •PaO2 less than or equal to 45 mm Hg -Priority: immediate assessment of respiratory status: provide assistive measures •May require intubation and mechanical ventilation Observe/ Assess: -Position: lie down, sit upright, or tripod -Work of breathing (WOB); respiratory muscles effort needed to inhale/exhale -Breathing patterns •Rapid, shallow (hypoxemia); monitor for fatigue •Slow RR (hypercapnia) -Red Flag! Change from rapid to slow RR: severe muscle fatigue IMPENDING respiratory arrest -Ability to speak: full or partial sentences, 2 to 3 word dyspnea -Pursed-lip breathing: increased expiratory time; prevents small bronchial collapse -Retraction of intercostal spaces or supraclavicular area; use of accessory muscles -Paradoxical breathing: abdomen and chest move opposite of normal -Diaphoresis from increased WOB -Auscultate breath sounds: fine or coarse crackles, absent (consolidation), pleural rub Diagnostic Studies: Most Common: -Chest x-ray -ABG analysis/pulse oximetry Other: -CBC, serum electrolytes, urinalysis -12-lead ECG -Blood and sputum cultures -CT scan or V/Q scan -End tidal CO2 (with mechanical ventilation) Planning: -Independently maintain a patent airway -Absence of dyspnea or recovery to baseline breathing patterns -Effectively cough and able to clear secretions -Normal ABG values or values within patient's baseline -Breath sounds within patient's baseline Nursing Implementation: -Prevention!!! -Thorough history and physical assessment to identify at-risk patients and initiate early interventions -Deep breathing and coughing, incentive spirometry, and early ambulation -Frequent assessment of high-risk patients -Prevent: atelectasis, pneumonia, complications of immobility, and optimize hydration and nutrition Expected Outcomes: -Independently maintain a patent airway -Achieve normal or baseline respiratory system and function -Maintain adequate oxygenation as shown by normal or baseline ABGs -Have normal hemodynamic status Drug Therapy: -Reduce airway inflammation and bronchospasm: corticosteroids and bronchodilators-Relieve pulmonary congestion: IV diuretics, morphine, and mitroglycerine -Treat infections: IV antibiotics -Reduce anxiety, pain, and restlessness: benzodiazepines and opioids Nursing and Interprofessional Management: -Respiratory therapy: lowest possible FiO2, acid-base, improve oxygenation •Never withhold oxygen from a hypoxic patient •Observe response: monitor changes in mental status, RR, and ABGs -Oxygen therapy: high FiO2 for prolonged periods can lead to adverse effects •Oxygen toxicity (greater than 60% O2 for greater than 48 hours) -Delivery system should: be tolerated by the patient - claustrophobia? •Maintain PaO2 at 55 to 60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible Interventions to Mobilize Secretions: -Patient positioning- HOB 30, side lying if aspiration risk, frequent repositioning -Effective coughing- augmented (quad) coughing, huff coughing, staged coughing -Chest physiotherapy- postural drainage, percussion -Suctioning: complications- hypoxia, high ICP, low BP, HTN, PVCs/tachy/bradycardia -Humidification: thins secretions -Hydration: 2-3 L/day, IV fluids (check for overload) -If not successful—artificial ventilatory assistance needed -Respiratory therapy: positive pressure ventilation (PPV) -Noninvasive PPV must have spontaneous breathing -Provides O2: decreases WOB-must be awake, alert, stable VS -Contraindicated for decreased LOC, high O2 requirements, facial trauma, hemodynamic instability, or excess secretions -Two forms: •CPAP—continuous positive airway pressure •BiPAP—bilevel positive airway pressure -A mask is placed over the nose or nose and mouth. -Positive pressure from a mechanical ventilator aids the patient's breathing efforts, decreasing the work of breathing Medical Supportive Therapy: -Goals and interventions focus on improving oxygenation and ventilation to improve O2 delivery -Treat the underlying cause -Monitor hemodynamic status: CVP, ABP, SvO2 -Continuous monitoring for response to therapy -Optimize balance between rest and activity -Nutritional Therapy and Consult: -Critically ill: hypermetabolic state -Enteral or parenteral nutrition within 24 to 48 hours to avoid depletion and delayed recovery Gerontologic Considerations: -Risk factors for respiratory failure: •Decreased ventilatory capacity •Larger air spaces •Loss of surface area •Decreased elastic recoil, chest wall compliance, muscle strength -Tobacco use is a major risk factor -Poor nutritional status -Less cardiopulmonary physiologic reserve

chest tubes and pleural drainage

-If enough fluid or air accumulates in the pleural space, the negative pressure becomes positive and the lungs collapse. -As a result, chest tubes are inserted to drain the pleural space, reestablish negative pressure, and allow for proper lung expansion. -They may also be inserted in the mediastinal space to drain air and fluid postoperatively. -Chest tubes are approximately 20 inches (51 cm) long and vary in size from 12F to 40F. The size inserted is determined by the patient's condition. -Large (36F to 40F) tubes are used to drain blood, medium (24F to 36F) tubes are used to drain fluid, and small (12F to 24F) tubes are used to drain air. -Pigtail tubes are very small (10F to 14F) tubes with a curly end designed to keep them in place. They are a safe and effective alternative to larger bore chest tubes for treatment of pneumothorax. Chest Tube Insertion: -Insertion of a chest tube can take place in the emergency department (ED), in the operating room, or at the patient's bedside. -The patient is positioned with the arm raised above the head on the affected side to expose the midaxillary area, the standard site for insertion. -Elevate the patient's head 30 to 60 degrees, when possible, to lower the diaphragm and reduce the risk of injury. -Time permitting, a chest x-ray is used to confirm the affected side. -The area is cleansed with an antiseptic solution. The chest wall is infiltrated with a local anesthetic, and a small incision is made over a rib. -The area is first probed digitally to avoid injury with a sharp instrument. -A clamp is used to hold the chest tube and guide it into place. The tube is advanced up and over the top of the rib to avoid the intercostal nerves and blood vessels that are behind the rib inferiorly. -Once inserted, the tube is secured (sutured) in place, the incision is closed with sutures, and the tube is connected to a pleural drainage system -The wound is covered with an occlusive dressing. Most clinicians prefer to seal the wound around the chest tube with petroleum gauze. -Proper tube placement is confirmed by chest x-ray. -The insertion of a chest tube and its presence in the pleural space is painful. -Monitor the patient's comfort at frequent intervals and use the appropriate pain-relieving interventions. -Brisk bubbling of air often occurs in this chamber when a pneumothorax is initially evacuated and indicates an air leak. -Intermittent bubbling during exhalation, coughing, or sneezing (when the patient's intrathoracic pressure is increased) may be observed as long as air is in the pleural space. -Eventually, as the air leak resolves and the lung becomes more fully expanded, bubbling ceases. -Normal fluctuation of the water within the water-seal chamber is called tidaling. -This up-and-down movement of water in concert with respiration reflects intrapleural pressure changes during inspiration and expiration. -Investigate any sudden cessation of tidaling, as this may signify an occluded chest tube. -Gradual reduction and eventual cessation of tidaling is expected as the lung reexpands. Nursing Assessment: -Observe for air fluctuations (tidaling) and bubbling in the water-seal chamber. -If no tidaling is observed (rising with inspiration and falling with expiration in the spontaneously breathing patient), the drainage system is blocked, the lungs are reexpanded, or the system is attached to suction. If the chest tube is connected to suction, disconnect from wall suction to check for tidaling. -Observe for air leak in water-seal chamber. If bubbling increases, there may be an air leak in the drainage system or a leak from the patient (bronchopleural leak). Suspect a system leak when bubbling is continuous. -If leak persists, briefly clamp the chest tube at the patient's chest. If the leak stops, then the air is coming from the patient. -If the air leak persists, briefly and methodically move the clamps down the tubing away from the patient until the air leak stops. The leak will then be present between the last two clamp points. If the air leak persists all the way to the drainage unit, replace the unit. -Observe fluid levels in water-seal chamber. High fluid levels in the water-seal indicate residual negative pressure. -The chest system may need to be vented by using the high-negativity release valve available on the drainage system to release residual pressure from the system. -Do not lower water-seal column when wall suction is not operating or when patient is on gravity drainage. -Monitor the patient's clinical status. Assess vital signs, lung sounds, and pain. -Assess for manifestations of reaccumulation of air and fluid in the chest (↓ or absent breath sounds), significant bleeding (>100 mL/hr), chest drainage site infection (drainage, erythema, fever, ↑ WBC), or poor wound healing. Notify physician for management plan. -Evaluate for subcutaneous emphysema at chest tube site. -Encourage the patient to breathe deeply periodically to facilitate lung expansion and encourage range-of-motion exercises to the shoulder on the affected side. -Encourage use of incentive spirometry every hour while awake to prevent atelectasis or pneumonia. -Milking or stripping chest tube: •Not recommended •Can increase intrapleural pressures and damage lungs •Position tubing so that drainage flows freely to negate need for milking or stripping

lung transplant

-Indicated for end stage lung disease -Absolute contraindications: •Cancer malignancy (last s 2 years) •Chronic active Hep B •HIV •Liver or renal failure •Current smoker •Poor rehab potential •Psychiatric or support system challenges to keep up with management, medications -Post op care -ICU -Hemodynamic monitoring -Fluid and nutritional support -Immunosuppression -Detection of early rejection -Infection prevention: high risk due to immunosuppression therapy -Medications: -LIFELONG REGIMEN -3 meds specific to suppress immune system: •Mycophenolate Cellcept •Tacrolimus •Prednisone -Rejection signs and symptoms: •Fever, chills, fatigue, dyspnea, cough, low O2 sats, -NEVER MISS A MED--HOURS CAN MAKE A DIFFERNCE!

brain death

-Irreversible loss of all brain functions including the brainstem -Cerebral cortex stops functioning or is destroyed -Exact definition of death can be controversial -Technological developments in life support have led to questions about when death actually occurs: •When the whole brain (cortex and brainstem) ceases activity •Or when function of the cortex alone stops. -The American Academy of Neurology developed the diagnostic criteria that must be validated by a physician: •Coma or unresponsiveness •Absence of brainstem reflexes •Apnea -Currently legal and medical standards require that all brain function must cease for brain death to be pronounced and life support to be disconnected. -In some states and under specific circumstances, registered nurses are legally permitted to pronounce death. -Diagnosis of brain death is of particular importance when organ donation is an option.

hyperosmolar hyperglycemic syndrome (HHS)

-Life-threatening syndrome -Occurs with type 2 diabetes -Precipitating factors: •UTIs, pneumonia, sepsis •Acute illness •Newly diagnosed type 2 diabetes •Impaired thirst sensation and/or inability to replace fluids -Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion. -HHS is less common than DKA. It often occurs in patients older than 60 years with type 2 diabetes. -There is usually a history of inadequate fluid intake, increasing mental depression, and polyuria. Clinical Manifestations: -Enough circulating insulin to prevent ketoacidosis -Fewer symptoms lead to higher glucose levels (>600 mg/dL) -More severe neurologic manifestations (somnolence, coma, seizures, hemiparesis, aphasia) because of ↑ serum osmolality -Ketones absent or minimal in blood and urine Treatment: -HHS constitutes a medical emergency and has a high mortality rate. -The management of DKA and that of HHS are similar and includes immediate IV administration insulin and either 0.9% or 0.45% NaCl. -HHS usually necessitates greater volumes of fluid replacement. This should be accomplished slowly and carefully. -Patients with HHS are commonly older and may have cardiac or renal compromise, necessitating hemodynamic monitoring to avoid fluid overload during fluid replacement. -When blood glucose levels fall to approximately 250 mg/dL (13.9 mmol/L), IV fluids containing dextrose are administered to prevent hypoglycemia. -Electrolytes are monitored and replaced as needed. -Hypokalemia is not as significant in HHS as it is in DKA, although fluid losses may result in milder potassium deficits that necessitate replacement. -Assess vital signs, intake and output, tissue turgor, laboratory values, and cardiac monitoring to check the efficacy of fluid and electrolyte replacement. -This includes monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status. -Once the patient is stabilized, attempts to detect and correct the underlying precipitating cause should be initiated.

lung cancer

-Lung cancer is the leading cause of cancer-related deaths in the United States. -Lung cancer accounts for 28% of all cancer deaths, more than those caused by breast, prostate, and colon cancer combined. -Annually about 221,000 new cases of lung cancer are diagnosed and 158,000 Americans die. -Although associated with a high mortality and low cure rate, advances in medical treatment are improving the response to treatment. -Smoking is responsible for 80% to 90% of all lung cancers. -Tobacco smoke contains 60 carcinogens in addition to substances (carbon monoxide, nicotine) that interfere with normal cell development. -Exposure to tobacco smoke causes changes in the bronchial epithelium, which usually returns to normal when smoking is discontinued. -The risk of lung cancer gradually decreases with smoking cessation, reaching that of nonsmokers within 10 to 15 years of quitting. -The risk of developing lung cancer is directly related to total exposure to tobacco smoke, measured by total number of cigarettes smoked in a lifetime, age of smoking onset, depth of inhalation, tar and nicotine content, and the use of unfiltered cigarettes. Assessment: -Later manifestations include nonspecific systemic symptoms such as anorexia, fatigue, weight loss, and nausea and vomiting. -Hoarseness may be present as a result of involvement of the laryngeal nerve. -Unilateral paralysis of the diaphragm, dysphagia, and superior vena cava obstruction may occur because of intrathoracic spread of the malignancy. -Sometimes there are palpable lymph nodes in the neck or axilla. -Mediastinal involvement may lead to pericardial effusion, cardiac tamponade, and dysrhythmias. Planning: -Effective breathing pattern -Adequate airway clearance -Adequate oxygenation of tissues -Patient reports minimal to no discomfort -Realistic attitude about treatment and prognosis -Individualized care will depend on the plan for treatment. -Assessment and intervention in symptom management are pivotal, as well as teaching the patient to recognize signs and symptoms that may indicate progression or recurrence of disease. -Provide patient comfort, teach methods to reduce pain, monitor for side effects of prescribed medications, foster appropriate coping strategies for the patient and caregiver, assess smoking cessation readiness, and help patients to access resources to deal with the illness. Treatments: -Surgical Therapy -Radiation therapy -Stereotactic radiotherapy -Chemotherapy -Targeted therapy -Immunotherapy Diagnostic Studies: -A chest x-ray is the initial diagnostic test used for patients with suspected lung cancer. -The x-ray may initially be normal or identify a lung mass or infiltrate. -Evidence of metastasis to the ribs or vertebrae and the presence of pleural effusion may also be seen on chest x-ray. -CT scanning is used to further evaluate the lung mass. CT scans can identify the location and extent of masses in the chest, as well as any mediastinal involvement or lymph node enlargement. -Sputum cytology can identify malignant cells, but sputum samples are rarely used in diagnosing lung cancer because malignant cells are not always present in the sputum. -Biopsy is required for a definitive diagnosis. Cells for biopsy can be obtained by CT-guided needle aspiration, bronchoscopy, mediastinoscopy, or video-assisted thoracoscopy. -If a thoracentesis is performed to relieve a pleural effusion, the fluid is also analyzed for malignant cells. -Bone scans and CT scans of the brain, pelvis, and abdomen are used to determine if metastatic disease is present. -A complete history and physical examination, complete blood count (CBC) with differential, chemistry panel, liver function tests (LFTs), renal function tests, and pulmonary function tests are necessary. -Magnetic resonance imaging (MRI) and/or positron emission tomography (PET) may also be used to evaluate and stage lung cancer.

potassium imbalances

-Many complications including the heart -Keep balanced with IV and oral supplementation -Continuous ECG monitoring

physical manifestations at end of life

-Metabolism is decreased -Body function slows down until all function ends -Respiration generally ceases first -Heart stops beating within a few minutes Respiratory System: -Irregular breathing that gradually slows and becomes more shallow -Breath sounds may become wet and noisy, both audibly and on auscultation. -Cheyne-Stokes respiration: pattern of breathing characterized by alternating periods of apnea and rapid deep breathing -Inability to cough or clear secretions: grunting, gurgling, or noisy congested breathing ("death rattle") -Noisy, wet-sounding respirations, termed the death rattle or terminal secretions, are caused by mouth breathing and accumulation of mucus in the airways. Hearing, Touch: -Hearing is usually last sense to disappear -Decreased sensation -Decreased perception of pain and touch -The sense of touch is decreased first in the lower extremities because of circulatory alterations Taste, Smell, and Sight: -Blurring of vision -Blink reflex absent -Patient appears to stare -Eyelids remain half-open -Decreased sense of taste and smell Integumentary System: -Mottling on hands, feet, arms, and legs: looks faintly like purple and white leopard skin -Cold, clammy skin -Cyanosis of nose, nail beds, knees -"Waxlike" skin when very near death -The skin cools first on lower, then upper extremities and finally the torso unless a fever is present. Urinary System: -Gradual decrease in urinary output -Incontinent of urine -Unable to urinate Gastrointestinal System: -Slowing of digestive tract -Accumulation of gas -Distention and nausea -Loss of sphincter control -Bowel movement may occur before imminent death or at the time of death -Pain relieving drugs can accelerate the loss of GI function Musculoskeletal System: -Gradual loss of ability to move -Trouble holding body posture and alignment -Loss of facial muscle tone -Sagging of jaw -Difficulty speaking -Loss of gag reflex -Swallowing can become more difficult Cardiovascular System: -Increased heart rate -Later slowing and weakening of pulse -Irregular rhythm -Decreased BP -Delayed absorption of IM or SQ drugs

DKA/HHS nursing management

-Monitor: •IV fluids- to correct dehydration •Insulin therapy- to reduce blood glucose and serum acetone levels •Electrolytes- given to correct imbalance •Blood glucose •Urine for output and ketones •Laboratory data -Assess: •Renal status •Cardiopulmonary status •Level of consciousness -Assess for signs of potassium imbalance resulting from hypoinsulinemia and osmotic diuresis. -When treatment with insulin begins, serum potassium levels may decrease rapidly as potassium moves into the cells once insulin becomes available. This movement of potassium into and out of extracellular fluid influences cardiac functioning. -Cardiac monitoring is a useful aid in detecting hyperkalemia and hypokalemia because characteristic changes indicating potassium excess or deficit are observable on electrocardiographic tracings. -Assess vital signs often to determine the presence of fever, hypovolemic shock, tachycardia, and Kussmaul respirations

caring for unstable or "at-risk" adults

-Nurses care for clients with acute and unstable physiologic problems and can be anywhere in the healthcare or home setting -ICU care has expanded from delivering care in a standard unit to bringing ICU care to patients wherever they may be -A critical care nurse has in-depth knowledge of anatomy, physiology, pathophysiology, pharmacology, and advanced assessment skills, as well as the ability to use advanced technology -Specialization in critical care nursing requires formal education combined with a preceptored clinical orientation, often over several months Complexities of Unstable Clients: -1st: Physiologically unstable ◦Critical analysis and decision making -2nd: Risk of complications ◦Frequent assessment and treatments -3rd: IV polypharmacy-titration ◦Vasoactive, thrombolytics, sedation, insulin, nutrition -4th: Advanced technology/devices ◦Vents, ICP, SvO2, CCRT -Alteration in ventilated and immobile clients have an increased risk of developing other problems -Anxiety and pain, impaired communication and sensory-perceptual problems -Sleep and nutrition -Ethnics and culture -Quality and safety for complex care -Use technology wisely (ex: smart infusion pumps, alarms, frequent rounding) -Visitation policies: incorporate patient/family requests that reflect their culture -Purpose for care, current clinical picture, and picture of the outcome or result Family and Caregiver Concerns: -Caregivers play a valuable role in the patient's recovery -Advising-educating about decisions -Assist with ADLs -Communication with family members: ◦Daily routines disrupted ◦Long distances -Major needs of caregivers of critically ill patients include: ◦Information, reassurance, and access ◦Without these they feel powerless and will show signs of this

end of life nursing management

-Nurses spend more time with patients near the end of life than any other health care professionals -Respect, dignity, and comfort are important for patient and family -Nurses need to recognize their own needs when dealing with grief and dying -After the event debrief with a peer or the team. It is okay to feel the emotion, yes, you are human too, you may have a relationship with the family. -What Guides Our Care?: •Code of Ethics for Nurses-relieve suffering •Principle of beneficence-means that care is provided to benefit •Standard of care- used to define the nursing acts that are required for safe and competent nursing practice Assessment: -If patient is alert: •Brief review of body systems to detect signs and symptoms •Assess for discomfort, pain, nausea, or dyspnea -Follow specific legal guidelines for organ or tissue donation. -Some tissues must be used within hours after death so require immediate physician notification. -Assess coping abilities of patient and family -Promptly address discomfort. -Use evidence-based tools for symptom assessment including numeric scales or visual analog scales for pain rating. -Evaluate and manage co-morbid health care problems. -Gather information about abilities, intake, rest, and general response to the terminal illness and its prognosis. -Determine family's ability to manage and cope with the needed care and consequences of the illness. -Stability determines frequency of assessment -At least every 8 hours in the inpatient setting -More frequently as changes occur -Document -Monitor for system failure as death approaches -Attention to subtle physical changes requires vigilance -Neuro, circulation(CV), respiratory, I&O, integumentary -What type of changes/symptoms are seen? -Physical assessments are abbreviated and focused on changes that accompany terminal illness. -Assessment may occur weekly for patients cared for in their homes by hospice programs. -In the final hours of life, physical assessment may be limited to essential data. -Key elements of social assessment include: •Family relationships •Communication patterns •Differences in expectations •Interpersonal conflicts that may result in family disruptions during the dying process and after death •Patient and family goals -In the last hours of life: •Assessments should be limited to only those that are needed to determine patient comfort •More peaceful for patient and family to refrain from overstimulation that may occur from certain types of assessments, such as measuring BPs or checking for pupillary response •Pain level, respiratory status concerns should be addressed •Transition your efforts to emotional and comfort support for patient and family as death approaches rather than performing tasks that will have no impact on the patient's physical care Planning: -Involve patient and family -Advocate for: •Patient wishes •Comfort and safety •Care of emotional and physical needs •Where patient wants to die •Family conference may be helpful. •Develop a comprehensive plan to support, teach, and evaluate patients and families. •Nursing care goals may include determining where the patient would like to die and whether this is possible. For example, the patient may want to die at home, but the family may object. •Many factors contribute to the patient and family's decision. •Interprofessional EOL care that includes the physician, social worker, chaplain, as well as other members of the palliative and/or hospice care team is important. •Consult palliative care specialists for dealing with sudden or traumatic deaths such as those that occur in the ICU Implementation: -Ongoing information on disease, dying process, and care -Teaching of coping strategies for patients and families -Denial and grieving may be barriers to learning

death

-Occurs when all vital organs and body systems cease to function -Irreversible cessation of cardiovascular, respiratory, and brain function

legal and ethical issues

-Patients and families struggle with many decisions during the terminal illness and dying experience -Decisional capacity refers to the ability to consent or refuse care. It means that the individual has an understanding and appreciation of the information that is shared and has the capacity to engage in the reasoning process. -Organ and tissue donations -Advance directives -Resuscitation -Mechanical ventilation -Tube feeding placement

moving from "stable" to "unstable"

-Patients often exhibit early and subtle signs of deterioration (e.g., mild confusion, tachypnea) 6 to 8 hours before cardiac or respiratory arrest -Early critical care intervention has made significant contributions to reducing mortality rates -Frequent assessments to monitor trends (patterns) in the patient's physiologic parameters -Rapidly recognize and manage complications

flail chest

-Results from the fracture of several consecutive ribs, in two or more separate places, causing an unstable segment. -It can also be caused by fracture of the sternum and several consecutive ribs. -The resultant instability of the chest wall causes paradoxical movement during breathing. -The affected (flail) area will move in the opposite direction with respect to the intact portion of the chest. -During inspiration, the affected portion is sucked in, and during expiration, it bulges out. -This paradoxical chest movement not only prevents adequate ventilation but also increases the work of breathing. -The underlying lung may have a pulmonary contusion aggravating hypoxemia. -A flail chest is usually apparent on visual examination. -The patient manifests rapid, shallow respirations and tachycardia. -The patient moves air poorly, and movement of the thorax is asymmetric and uncoordinated. -The patient may also attempt to splint the chest to assist with breathing. -Observation of abnormal thoracic cavity movements, palpitation for crepitus near the rib fractures, and chest x-ray all assist in the diagnosis. -Initial therapy consists of ensuring adequate ventilation and supplemental oxygen therapy. -The goal is to facilitate lung expansion and ensure adequate oxygenation. -Analgesia is necessary to help promote adequate respiration. -Although many patients can be managed without the use of mechanical ventilation, intubation and ventilation may be necessary. -Surgical fixation of the flail segment may be used. -The lung parenchyma and fractured ribs will heal with time. Some patients continue to experience intercostal pain after the flail chest has resolved.

hyperthyroidism

-Since it may be precipitated by iodinated contrast media used in CT scans and other radiological studies, those who are at-risk should be monitored closely after iodinated contrast media exposure Subclinical: -Serum TSH level below 0.4mIU/L -Normal T4 and T3 levels Overt: -Low or undetectable TSH -Elevated T4 and T3 levels -Symptoms may or may not be present Subjective Data: -Impotence -Gynecomastia -Amenorrhea -Emotional lability, irritability, restlessness -Personality changes, delirium -Increased appetite, thirst -Nausea/ vomiting -Diarrhea, polyuria -Sweating -Dyspnea on exertion -Palpitations -Muscle weakness, fatigue -Insomnia -Chest pain -Nervousness -Heat intolerance, pruritus -Decreased libido -Family history -Iodine intake -Weight loss Objective Data: -Agitation -Rapid speech and body movements -Anxiety, restlessness -Hyperthermia -Enlarged or nodular thyroid gland -Exophthalmos -Eyelid retraction, infrequent blinking -Tachypnea, dyspnea on exertion -Tachycardia, bounding pulse -Systolic murmurs, dysrhythmias, hypertension, bruit over the thyroid gland -↑ Bowel sounds, ↑ appetite, diarrhea, weight loss -Hepatospleno megaly -Hyperreflexia -Diplopia -Fine tremors of hands, tongue, eyelids -Muscle wasting -Menstrual irregularities -Infertility -Impotence -Gynecomastia -↑ T3, ↑ T4 -↑ T3 resin uptake -↓ Or undetectable TSH -Chest x-ray showing enlarged heart -ECG findings of tachycardia Planning: -The overall goals are that the patient with hyperthyroidism will (1) experience relief of symptoms, (2) have no serious complications related to the disease or treatment, (3) maintain nutritional balance, and (4) cooperate with the therapeutic plan. Nursing Implementation: -Patients who have hyperthyroidism are usually treated in an outpatient setting. -However, those who develop acute thyrotoxicosis (thyroid storm) or undergo thyroidectomy require hospitalization and acute care. -Acute thyrotoxicosis is a systemic syndrome that necessitates aggressive treatment, often in an intensive care unit. -Administer medications (previously discussed) that block thyroid hormone production and the sympathetic nervous system. -Provide supportive therapy to the patient. This includes monitoring for cardiac dysrhythmias and decompensation, ensuring adequate oxygenation, and giving IV fluids to replace fluid and electrolyte losses. This is especially important in a patient who experiences fluid losses as a result of vomiting and diarrhea. -Ensuring adequate rest may be a challenge because of the patient's irritability and restlessness. -Provide a calm, quiet room because increased metabolism and sensitivity of the sympathetic nervous system causes sleep disturbances. -Other interventions may include placing the patient in a cool room away from very ill patients and noisy, high-traffic areas. -Use light bed coverings and changing the linen frequently if the patient is diaphoretic. -Encourage and assist with exercise involving large muscle groups (tremors can interfere with small-muscle coordination) to allow the release of nervous tension and restlessness. -It is important to establish a supportive, trusting relationship to help the patient who is irritable, restless, and anxious to cope. -If exophthalmos is present, there is a potential for corneal injury related to irritation and dryness. The patient may have orbital pain. -To relieve eye discomfort and prevent corneal ulceration, apply artificial tears to soothe and moisten conjunctival membranes. -Salt restriction may help reduce periorbital edema. -Elevate the patient's head to promote fluid drainage from the periorbital area. -The patient should sit upright as much as possible. -Dark glasses reduce glare and prevent irritation from smoke, air currents, dust, and dirt. -If the eyelids cannot be closed, they should be lightly taped shut for sleep. -To maintain flexibility, teach the patient to exercise the intraocular muscles several times a day by turning the eyes in the complete range of motion. -Good grooming can be helpful in reducing the loss of self-esteem that can result from an altered body image. -If the exophthalmos is severe, treatment options include corticosteroids, radiation of retroorbital tissues, orbital decompression, and corrective lid or muscle surgery. Evaluation: -The expected outcomes are that the patient with hyperthyroidism will: •Experience relief of symptoms •Have no serious complications related to the disease or treatment •Cooperate with the therapeutic plan

spiritual needs

-Spirituality: beliefs, values, practices that relate to the search for existential meaning and purpose -May or may not include a belief in a higher power -Does not necessarily equate to religion -Preferences should be noted -Question beliefs about a higher power, their own journey through life, religion, and an afterlife -Spirituality is associated with decreased despair at EOL -Spiritual distress may occur -A person may be of no particular faith but have a deep spirituality -Some patients may choose to pursue a spiritual path. Some may not. Their individual choice needs to be respected -The patient's and family's preferences related to spiritual guidance or pastoral care services should be assessed, and appropriate referrals made

thoracotomy

-Surgical incision into the chest cavity -Several different types of resections of the lung or pleura: decortication -Lobectomy: lung resection -Pneumonectomy: entire lobe removal -Video assisted thoracic surgery: less invasive, faster recovery Post-Op: -Pain -Chest tubes -Respiratory distress and effort -Daily CXRs for lung re-expansion -Pneumonectomies: area fills with fluid

physical care at end of life

-Symptom management and comfort -Physiologic and safety needs --Dying patients deserve and require the same care as people who are expected to recover -Pain, delirium, anxiety, dysphagia, fatigue, dehydration, dyspnea, myoclonus, skin breakdown, bowel changes, urinary incontinence, N/V, candida -Physical care focuses on the needs for oxygen, nutrition, pain relief, mobility, elimination, and skin care. -Skin integrity is difficult to maintain at the end of life because of immobility, urinary and bowel incontinence, dry skin, nutritional deficits, anemia, friction, and shearing forces. -If possible, it is important to discuss with the patient and family the goals of care before treatment begins. An advanced directive should be completed so that the patient and family wishes are followed.

unstable/complex care monitoring

-Technology available in the ICU or PCU is extensive: electrocardiogram (ECG), BP, O2 saturation, cardiac output (CO), intracranial pressure, temperature as well as focused ongoing assessments -Complex Care devices measure: cardiac index (CI), stroke volume (SV), stroke volume variation (SVV), ejection fraction (EF), end-tidal carbon dioxide (CO2), tissue O2 consumption, mechanical ventilators, intraaortic balloon pumps (IABPs), circulatory assist devices (CADs), dialysis machines PCU Monitoring Devices: -Continuous ECG -Arterial BP -O2 saturation -End-tidal CO2 -Ventilator care and monitoring

pulmonary embolism (PE)

-The blockage of one or more pulmonary arteries by a thrombus, fat or air embolus, or tumor tissue -Emboli are mobile clots that generally do not stop moving until they lodge at a narrowed part of the circulatory system -Consists of material that gains access to the venous system and then to the pulmonary circulation. -The embolus travels with the blood flow through ever-smaller blood vessels until it lodges and obstructs perfusion of the alveoli. -The lower lobes of the lung are most commonly affected. -Approximately 10% of patients with massive PE die within the first hour. -Treatment with anticoagulants significantly reduces mortality. Assessment: -The signs and symptoms in PE are varied and nonspecific, making diagnosis difficult. -Clinical manifestations depend on the size and extent of emboli. -Small emboli may go undetected or produce vague, transient symptoms. -Symptoms may begin slowly or suddenly. -Dyspnea is the most common presenting symptom, occurring in 85% of patients with PE. -A mild to moderate hypoxemia may be observed. -Other manifestations may include tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, and accentuation of the pulmonic heart sound -Massive emboli may produce a sudden change in mental status and hypotension Diagnostic Studies: -If a patient cannot have contrast media, a ventilation-perfusion (V/Q) scan is done. -The V/Q scan has two components and is most accurate when both are performed: 1.Perfusion scanning involves IV injection of a radioisotope. A scanning device images the pulmonary circulation. 2.Ventilation scanning involves inhalation of a radioactive gas such as xenon. -Scanning reflects the distribution of gas through the lung. -The ventilation component requires the cooperation of the patient and may be impossible to perform in the critically ill patient, particularly if the patient is intubated. -Pulmonary angiography is the most sensitive and specific test for PE. However, it is an expensive and invasive procedure that involves the insertion of a catheter through the antecubital or femoral vein, advancement of the catheter to the pulmonary artery, and injection of contrast medium. -The accessibility and accuracy of the spiral CT has greatly diminished the need for pulmonary angiography. -Arterial blood gases (ABGs) Plan of Care: -Begins with prevention of DVT. -DVT prophylaxis includes the use of sequential compression devices, early ambulation, and prophylactic use of anticoagulant medications. Interventions: -To reduce mortality risk, treatment is begun as soon as PE is suspected. -The objectives are to (1) prevent further growth or extension of thrombi in the lower extremities, (2) prevent embolization from the upper or lower extremities to the pulmonary vascular system, and (3) provide cardiopulmonary support if indicated. -Supportive therapy for the patient's cardiopulmonary status varies according to the severity of the PE. -O2 can be given via mask or cannula, and the concentration of FIO2 is determined by ABG analysis. -In some situations, endotracheal intubation and mechanical ventilation are necessary to maintain adequate oxygenation. -Respiratory measures such as turning, coughing, deep breathing, and incentive spirometry are important to help prevent or treat atelectasis (pulmonary toilet). -If manifestations of shock are present, IV fluids are administered followed by vasopressor agents as needed to support perfusion. -If heart failure is present, diuretics are used. -Pain resulting from pleural irritation or reduced coronary blood flow is treated with opioids. -Hemodynamically unstable patients with massive PE in whom thrombolytic therapy is contraindicated may be candidates for immediate pulmonary embolectomy. -Embolectomy, removal of emboli to help decrease right ventricular afterload, can be achieved via a vascular (catheter) or surgical approach. -Surgical outcomes have improved in recent years, in part due to rapid diagnosis and enhanced surgical procedures, with mortality rates decreasing from 30% to 19%. -To prevent further emboli, an inferior vena cava (IVC) filter may be the treatment of choice in patients who remain at high risk and for patients for whom anticoagulation is contraindicated. -This device, inserted percutaneously via the femoral vein, is placed at the level of the diaphragm in the inferior vena cava. -Once inserted, the stent expands and prevents migration of large clots into the pulmonary system. -Complications associated with this device are rare but include misplacement, migration, and perforation. Drug Therapy: -Immediate anticoagulation is required for patients with PE. -Subcutaneous administration of low-molecular-weight heparin (LMWH) (e.g., enoxaparin [Lovenox]) or fondaparinux has been found to be safer and more effective than unfractionated heparin. -It is the recommended choice of treatment for patients with acute PE, administered once daily. -Advantages of LMWH over unfractionated heparin include greater bioavailability, can be administered subcutaneously, longer duration of therapeutic effect, and monitoring the aPTT is not necessary or useful. -Unfractionated IV heparin can be as effective but is more difficult to titrate to therapeutic levels. -Warfarin (Coumadin), an oral anticoagulant, should also be initiated at time of diagnosis. -Warfarin should be administered for at least 3 months, and then reevaluated. -Alternatives to warfarin include apixaban (Eliquis), dabigitran (Pradaxa), and endoxaban (Savaysa). -Anticoagulant therapy may be contraindicated if the patient has complicating factors such as blood dyscrasias, hepatic dysfunction causing alterations in the clotting, overt bleeding, a history of hemorrhagic stroke, or heparin-induced thrombocytopenia (HIT). -Although not common, some HCPs use direct thrombin inhibitors in the treatment of PE. -Similarly, fibrinolytic agents, such as tissue plasminogen activator (tPA) or alteplase (Activase), may help dissolve the pulmonary embolus and the source of the thrombus in the pelvis or deep leg veins, thereby decreasing the likelihood of recurrent emboli. Nursing Management: -Nursing measures aimed at prevention of PE are similar to those for prophylaxis of DVT. -The prognosis of a patient with PE is good if therapy is promptly instituted. -Keep the patient on bed rest in a semi-Fowler's position to facilitate breathing. -Administer oxygen therapy as ordered. -Assess the patient's cardiopulmonary status with careful monitoring of vital signs, cardiac rhythm, pulse oximetry, ABGs, and lung sounds. -Maintain an IV line for medications and fluid therapy. -Monitor laboratory results to ensure therapeutic ranges of INR (for warfarin) and aPTT (for IV heparin). -Monitor the patient for complications of anticoagulant and fibrinolytic therapy (e.g., bleeding, hematomas, bruising). -Provide appropriate interventions related to immobility and fall precautions once the patient is permitted out of bed. -The patient is usually anxious because of pain, inability to breathe, and fear of death. -Carefully explain the situation, the medications, and provide emotional support and reassurance to help relieve the patient's anxiety. -Patient teaching regarding long-term anticoagulant therapy is critical. -Anticoagulant therapy continues for at least 3 months. -Patients with recurrent emboli may be treated indefinitely with anticoagulants. -INR levels are drawn at intervals, and warfarin dosage is adjusted. -Some patients are monitored by nurses in an anticoagulation clinic. -Discharge planning is aimed at preventing worsening of the condition and avoiding complications and recurrence. -Teach the patient measures to prevent DVT. -Reinforce the need for the patient to return to the HCP for regular follow-up examinations.

chest trauma

-The mechanism of injuries causing chest trauma are separated into two categories: blunt trauma and penetrating trauma. -Blunt trauma occurs when the chest strikes or is struck by an object. •The resultant impact can cause shearing and compression of thoracic structures. •The external injury may appear minor, but internally the organs may have severe injuries. •Rib and sternal fractures can lacerate lung tissue. •In a high-velocity impact, shearing forces can result in laceration or tearing of the aorta. •Compression of the chest may result in contusion, crush injury, and organ rupture. -Penetrating trauma is an injury in which a foreign object impales or passes through the body tissues, creating an open wound. •Examples include knife wounds, gunshot wounds, and injuries with other sharp objects. •Severity depends on location of penetration and affected organs/vessels. -Treatment of a pneumothorax depends on its severity and the nature of the underlying cause. -If the patient is stable, and has minimal air and/or fluid accumulated in the intrapleural space, no treatment may be necessary as the condition may resolve spontaneously. -The most definitive and common form of treatment of pneumothorax and hemothorax is to insert a chest tube and connect it to water-seal drainage. -Repeated spontaneous pneumothorax may need to be treated surgically by a partial pleurectomy, stapling, or pleurodesis to promote adherence of the pleurae to one another. -Tension pneumothorax is a medical emergency, requiring urgent needle decompression followed by chest tube insertion to water-seal drainage. Assessment: -Signs of respiratory distress include: •Dyspnea •Cough with or without hemoptysis •Cyanosis of mouth, face, nail beds, mucous membranes •Tracheal deviation •Audible air escaping from chest wound •Decreased breath sounds on side of injury •Decreased O2 saturation •Frothy secretions -Signs of cardiovascular compromise include: •Rapid, thready pulse •Decreased BP with narrowed pulse pressure and/or asymmetric readings •Narrowed pulse pressure •Asymmetric BP values in arms •Distended neck veins •Muffled heart sounds •Chest pain •Dysrhythmias Initial Interventions: -If unresponsive, assess circulation, airway, and breathing. -If responsive, monitor airway, breathing, and circulation. -Ensure patent airway. -Administer high flow O2 to keep SpO2 >90%. -Establish IV access with two large-bore catheters. Begin fluid resuscitation as appropriate. -Remove clothing to assess injury. -Cover sucking chest wound with nonporous dressing taped on three sides. -Additional interventions that need to be completed initially for patients with chest trauma include: •Stabilize impaled objects with bulky dressings. Do not remove object. •Assess for other significant injuries and treat appropriately. •Place patient in a semi-Fowler's position or position patient on the injured side if breathing is easier after cervical spine injury has been ruled out. •Administer small amounts of analgesia as necessary for pain and to help with breathing. •Prepare for emergency needle decompression if tension pneumothorax or cardiac tamponade present. -Ongoing Monitoring: •Monitor vital signs, level of consciousness, oxygen saturation, cardiac rhythm, respiratory status, and urinary output. •Anticipate intubation for respiratory distress. •Release dressing if tension pneumothorax develops after sucking chest wound is covered.

myxedema coma

-The mental sluggishness, drowsiness, and lethargy of hypothyroidism may progress gradually or suddenly to a notable impairment of consciousness or coma. -This situation, termed myxedema coma, is a medical emergency. -Precipitated by infection, drugs (especially opioids, tranquilizers, and barbiturates), cold, trauma -Characterized by: •Impaired consciousness •Subnormal temperature, hypotension, hypoventilation •Cardiovascular collapse-from hypoventilation, hyponatremia, hypoglycemia, and lactic acidosis -Treated with IV thyroid hormone Interprofessional Care: -Levothyroxine (Synthroid) -Start with low dose -Monitor for cardiovascular side effects (chest pain, dysrhythmias), weight loss, nervousness, tremors, insomnia -Increase dose in 4- to 6-week intervals as needed -Lifelong therapy Nursing Implementation: -Most outpatient therapy -Myxedema coma necessitates acute care: •Mechanical respiratory support •Cardiac monitoring •IV thyroid hormone replacement •Monitoring of core temperature

rib fractures

-The most common type of chest injury resulting from blunt trauma. -Ribs 5 through 9 are most commonly fractured because they are the least protected by chest muscles. -If the fractured rib is splintered or displaced, it may damage the pleura, lungs, and other internal organs. -Clinical manifestations of fractured ribs include pain at the site of injury, especially during inspiration and with coughing. -The patient splints the affected area and takes shallow breaths to try to decrease the pain. -Atelectasis and pneumonia may develop because of decreased chest wall movement and retained secretions. -Treatment: •NO strapping or binding chest •NSAIDs, opioids, nerve blocks •Patient teaching: deep breathing and coughing, incentive spirometry, appropriate use of analgesics

syndrome of inappropriate antidiuretic hormone (SIADH)

-The release of ADH despite normal or low plasma osmolarity -Disorder is characterized by fluid retention, dilutional hyponatremia, concentrated urine Clinical Manifestations: -Low urine output -Increased weight -Initially, thirst -Dyspnea on exertion -Fatigue -To identify these manifestations: I&O, daily weight, assess breath sounds, etc. Diagnosis: -Simultaneous measurement of urine and serum osmolality -Serum sodium <134 mEq/L -Urine specific gravity > 1.025 Pathophysiology: -Increased antidiuretic hormone -Increased water reabsorption in renal tubules -Increased intravascular fluid volume -Dilutional hyponatremia and decreased serum osmolality (the concentration of a solution expressed as the total number of solute particles per kilogram) Causes: -Malignant tumors, cancers -CNS disorders: head injuries, stroke, infection, Guillain-Barre, SLE -Drug therapy; Tegretol, general anesthesia, opioids, thiazides, SSRI, Chemotherapy -Miscellaneous; hypothyroid, COPD, HIV, and adrenal insufficiency Nursing Care Interventions and Interprofessional Management: -Monitor urine output and urine specific gravity -Daily weights, I&O, vital signs, monitor lab values -Monitor for seizures, headache, vomiting, and decreased neurological function -Provide frequent oral care -Fluid restriction -Loop diuretics Medications: -Demeclocycline: blocks the effect of antidiuretic hormone on renal tubules resulting in more dilute urine. -Vasopressor Receptor Antagonists: block the activity of antidiuretic hormone to treat hyponatremia -Loop Diuretics: promote diuresis -Sodium and Potassium Supplements: replace electrolytes

flutter (Heimlich) valve

-Used to evacuate air from the pleural space. -This device consists of a one-way rubber valve within a rigid plastic tube. It is attached to the external end of the chest tube. -During inspiration, when pressure in the chest is greater than atmospheric pressure, the valve opens. -During expiration, when intrathoracic pressure is less than atmospheric pressure, the valve closes. -The flutter valve can be used for small- to moderate-sized pneumothorax and for emergency transport. -It also allows for mobility of the patient, as the smaller drainage bag can be hidden under the clothes while the patient ambulates. -Drainage bags attached to the flutter valve must have a vent to the atmosphere in order to prevent a potential tension pneumothorax. -This can be accomplished by simply cutting a small slit in the top of any drainage bag that does not have a built-in vent. -Patients may go home with a Heimlich valve in place.

hypercapnic respiratory failure

-Ventilatory failure: increased CO2 levels better tolerated than decreased O2 levels -CO2 levels elevated due to: increase in CO2 production leading to decrease in alveolar ventilation -Consequences of hypercapnia: •Slow changes allow CO2 compensation •Arterial pH able to adjust •Treat primary cause or patient's condition will deteriorate Conditions Causing Impaired Ventilation: -CNS problems: suppress the drive to breathe, drug overdose, TBI/infarct (affecting medulla), spinal cord injuries -Neuromuscular conditions: respiratory muscle weakness or paralysis; retain CO2, Guillain-Barre, MS, toxins, muscle wasting -Chest wall abnormalities: prevent normal movement of chest wall or diaphragm and limit lung expansion, Kyphoscoliosis, severe obesity -Conditions affecting the airways and/or alveoli: airflow obstruction and air trapping lead to respiratory muscle fatigue and ventilator failure, asthma, COPD, cystic fibrosis Specific Manifestations of Hypercapnia: -Respiratory: dyspnea, tripod position, pursed-lip breathing, decreased RR or rapid rate with shallow respirations, decreased tidal volume, decreased minute ventilation Nonspecific Manifestations of Hypercapnia: -CNS: morning headache, disorientation, confusion, progressive somnolence, increased intracranial pressure, coma (late) -Cardiovascular: tachycardia, HTN, dysrhythmias, bounding pulse -Neuromuscular: muscle weakness, decreased deep tendon reflexes, tremors, seizures (late)