Final Exam Review Crabb PDF
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This document reviews fluid and electrolyte balance, covering topics such as water content, fluid compartments, electrolytes, mechanisms of fluid and electrolyte balance, and osmotic movement of fluids. It's a good study guide for nursing students or anyone studying the body's fluid balance. The document is not a traditional past paper but a review for a final exam, and not enough information is provided to accurately determine the exam board, year, or school.
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Final Exam Review Crabb Chapter 17: Fluid & Electrolytes 1. Importance of Fluids & Electrolytes a. Maintain homeostasis b. Compositions of fluids and electrolytes is kept within narrow limits of normal i. Body fluids deliver dissolved nutrients an...
Final Exam Review Crabb Chapter 17: Fluid & Electrolytes 1. Importance of Fluids & Electrolytes a. Maintain homeostasis b. Compositions of fluids and electrolytes is kept within narrow limits of normal i. Body fluids deliver dissolved nutrients and electrolytes to all organs, tissues, and cells ii. Carry waste away from cells iii. Any changes in the amount of water or electrolytes can alter these functions 2. Water Content of the Body a. Human body is made up of mostly water b. Accounts for about 50-60% of body weight in the adult c. Water content varies with age, gender, and fat content 3. Fluid Compartments a. Intracellular fluid (ICF) i. Fluid found within the cells ii. Approximately ⅔ of body water is located in the ICF b. Extracellular fluid (ECF) i. Fluid found outside the cells ii. Approximately ⅓ of the body water is located in the ECF iii. Interstitial 1. Fluid located between the cells & lymph 2. Where “third spacing” occurs iv. Intravascular 1. Fluid portion of blood (plasma) v. Transcellular 1. Fluids found in specialized areas of the body vi. Lymph 4. Calculation of Fluid Gain or Loss a. 1 L of water weighs 2.2 pounds (1 kg) b. Body weight change is an excellent indicator of overall fluid volume loss or gain 5. Electrolytes a. Substances whose molecules dissociate into ions when placed in water i. Cations: positively charged ii. Anions: negatively charged b. Concentration of electrolytes is expressed in milliequivalents (mEq)/L c. Intracellular Fluid (ICF) i. Prevalent cation is Potassium (K+) ii. Prevalent anion is Bicarbonate (PO43-) d. Extracellular Fluid (ECF) i. Prevalent cation is Sodium (Na+) ii. Prevalent anion is Chloride (Cl-) 6. Mechanisms of Fluid and Electrolyte Balance a. The movement of fluid & electrolytes between the ICF and ECF to maintain homeostasis involves many different processes i. Simple diffusion 1. Movement of molecules across a permeable membrane from high to low concentration 2. Movement of molecules stops when the concentrations are equal in both areas 3. Requires no external energy ii. Facilitated diffusion 1. Requires the use of a protein carrier in the cell membrane 2. Combines with a molecule too large to pass by easily across the membrane alone 3. Requires no external energy iii. Active transport 1. Molecules move against the concentration gradient 2. Requires use of external energy a. Adenosine triphosphate (ATP) 3. Example: Sodium-potassium pump 4. Concentrations of sodium and potassium vary between the ICF and ECF 5. To maintain concentration difference, the cell uses active transport to move sodium out of the cell and potassium into the cell iv. Osmosis 1. Movement of water “down” concentration gradient from a region of low solute concentration to one of high solute concentration across a semipermeable membrane a. Requires no outside energy sources b. The concentration of the solution determines the strength of the osmotic pull i. > the concentration, the greater a solution’s pull or osmotic pressure b. Water moves as driven by two forces i. Hydrostatic pressure 1. Force of fluid in a compartment 2. Blood pressure caused by plasma proteins ii. Osmotic pressure 1. Amount of pressure required to stop osmotic flow of water 2. Determined by concentration of solutes in a solution 3. May be referenced as either fluid osmolarity or osmolality a. Osmolarity or Osmolality i. Osmolality measure the total milliosmoles/L of a solution 1. Concentration of molecules per volume of a solution ii. Osmolality measures the number of milliosmoles per kg of water 1. Concentration of molecules per weight of water a. Preferred measurement to evaluate the concentration of plasma, urine, and other body fluids b. Measurement i. Calculate the plasma osmolality 1. Plasma osmolality= (2xNa)+(BUN/2.8)+(glucose/18) ii. Normal plasma osmolality is between 280 and 295 mOsm/kg 1. Greater than 295 mOsm/kg= water deficit 2. Less than 275 mOsm/kg= water excess 7. Osmotic Movement of Fluids a. The osmolality of the fluid surrounding cells affects them i. Isotonic- same as cell interior 1. Solutions in which the solutes are the same concentration on the inside of the cell as the outside of the cell 2. Treatment For: a. Blood loss b. Dehydration (vomiting/diarrhea) c. Surgical patients 3. Examples: a. 0.9% Sodium Chloride (NS) b. Lactated Ringers c. 5% Dextrose in Water (later becomes hypotonic due to metabolism of dextrose) ii. Hypotonic- solutes less concentrated than in cells/ hypoosmolar 1. Solutions in which there is a lower solute concentration on the outside of the cell, than on the inside of the cells 2. Treatment For: a. Diabetic Ketoacidosis (DKA) b. Hyperosmolar Hyperglycemia 3. Contraindications a. INCREASED INTRACRANIAL PRESSURE/HEAD INJURY b. BURN PATIENTS c. TRAUMA PATIENTS 4. Examples: a. 0.45% Normal Saline b. 0.225% Normal Saline c. 0.33% Normal Saline iii. Hypertonic- solutes more concentrated than in cells/ hyperosmolar, outside the cell 1. Solutions in which there is a higher concentration of solutes on the outside of the cell, than on the inside of the cell 2. Treatment For: a. Severe hyponatremia b. Increased intracranial pressure 3. Caution a. Can cause severe hypernatremia b. Fluid volume overload 4. Examples: a. TPN b. 3% Normal Saline c. 5% Dextrose in 0.45% Normal Saline d. 5% Dextrose in Lactated Ringers e. 10% Dextrose 8. Fluid Movement in Capillaries a. Amount and direction of movement determined by: i. Capillary hydrostatic pressure ii. Plasma oncotic pressure iii. Interstitial hydrostatic pressure iv. Interstitial oncotic pressure 9. Fluid Shifts a. Edema is caused by: i. Shifts of plasma to interstitial fluid ii. Elevation of venous hydrostatic pressure iii. Decrease in plasma oncotic pressure iv. Elevation of interstitial oncotic pressure 10. Fluid Spacing a. First spacing- normal distribution in ICF and ECF b. Second spacing- abnormal accumulation of interstitial fluid (edema) c. Third spacing- fluid is trapped where it is difficult or impossible for it to move back into cells or blood vessels 11. Fluid Balance: Intake & Output a. Fluid balance is maintained through fluid intake and fluid loss i. Fluid intake is regulated through the thirst drive 1. Daily intake of water is 2000mL-3000mL for a healthy adult ii. Fluid output is maintained by several systems: 1. The kidneys are the most important and sensitive fluid loss route because it is regulated and adjustable a. The minimum amount of urine output (UOP) per day needed to excrete toxic waste is 400-600mL b. A more specific measure indicates patients should excrete 0.5-1 mL/kg/hr (e.g., a 60 kg patient should have a UOP of 30-60 mL/hr) 12. Regulation of Water Balance a. Hypothalamic-Pituitary Regulation i. Osmoreceptors in hypothalamus sense fluid deficit or increase ii. Deficit stimulates thirst and antidiuretic hormone (ADH) release iii. Decreased plasma osmolality (water excess) suppresses ADH release b. Renal Regulation i. Kidneys are the main organ for regulating fluid and electrolyte balance ii. Adjusting urine volume 1. Selective reabsorption of water and electrolytes 2. Renal tubules are sites of action of ADH and aldosterone c. Adrenal Cortical Regulation i. Releases hormones to regulate water and electrolytes ii. Glucocorticoids 1. Cortisol 2. Anti-inflammatory effect and increase serum glucose levels iii. Mineralocorticoids 1. Aldosterone 2. Enhances sodium retention & potassium excretion, increasing water reabsorption 3. Nicknamed the “water-and-sodium-saving hormone” d. Renin-Angiotensin-Aldosterone-System (RAAS) i. RAAS is a hormone system that regulates BP through vasoconstriction and fluid retention 1. Normally activated when there is a drop in BP or a loss of volume 2. For adequate perfusion and cellular function, the blood volume (plasma volume) and fluid inside the cell (intracellular fluid) must remain in balance 3. e. Cardiac Regulation i. Natriuretic peptides are antagonists to the RAAS ii. Hormones made by the cardiomyocytes in response to increased atrial pressure iii. They suppress secretion of aldosterone, renin, and ADH to decrease blood volume and pressure\ f. Gastrointestinal Regulation i. Oral intake accounts for most water ii. Small amounts of water are eliminated by GI tract in feces iii. Diarrhea and vomiting can lead to significant fluid and electrolyte loss g. Older Adult Considerations i. 13. Fluid Volume Imbalances a. Fluid Volume Deficit (Hypovolemia) i. Abnormal loss of body fluids, inadequate fluid intake, or plasma to interstitial fluid shift ii. Dehydration 1. Loss of pure water without corresponding loss of sodium iii. Assessment 1. Cardiovascular- decreased bp, increased heart rate, orthostatic hypotension 2. Vascular- flat neck and hand veins 3. Respiratory- increased respirations 4. Integumentary- poor skin turgor, cool and clammy skin iv. Treatment 1. Correct the underlying cause and replace water and electrolytes a. Orally b. Blood products c. Isotonic IV solutions 2. Daily weights 3. Frequent I&O b. Fluid Volume Excess (Hypervolemia) i. Excess fluid intake, abnormal fluid retention, or interstitial-to-plasma fluid shift ii. Clinical manifestations related to excess fluid volume 1. Weight gain is the most common iii. Assessment 1. Cardiovascular- increased BP & HR, bounding pulses 2. Vascular- jugular neck vein distention 3. Respiratory- shortness of breath, crackles 4. Integumentary- pitting edema, cool & pale skin iv. Treatment 1. Remove fluid without changing electrolyte composition or osmolality of ECF a. Diuretics b. Fluid restriction c. Possible restriction of sodium intake d. Removal of fluid to treat ascites or pleural effusion e. Daily weights f. Frequent I&O 2. Diuretic Effects on Electrolyte Excretion a. b. LOOP diuretics (Furosemide (Lasix)) increase excretion of all electrolytes, when kidney function is normal c. Thiazide diuretics (Hydrochlorothiazide (HCTZ)) tend to spare calcium d. Potassium sparing diuretics (Spironolactone (Aldactone)) spare all electrolytes but sodium c. Nursing Management i. Daily weights 1. Same time every day 2. Empty all drainage bags first 3. Only use minimal limits ii. I&O iii. Rehydration 1. IV/PO challenge iv. Cardiovascular care 1. Monitor vitals 2. Telemetry v. Respiratory care 1. Assess lung sounds and pulse oximetry vi. Patient safety 1. Fall risk vii. Skin care 1. Skin breakdown 2. Turn & reposition q 2 hours 3. Monitor edema and skin turgor 4. Keep skin clean and dry 14. Electrolytes a. Sodium (Na+): 135-145 mEq/L i. Maintains extracellular fluid osmolarity, regulated by kidneys, because water follows sodium changes can lead to fluid shifting ii. Major cation in the extracellular fluid (ECF) and maintains osmolality iii. Important in generating and transmitting nerve impulses, muscle contractility, and acid-base balance iv. Sodium levels and movement influence water balance 1. “Where salt goes, water follows” v. Hypernatremia (>145 mEq/L) 1. Causes: a. Inadequate water intake b. Diabetes insipidus c. Excess water loss 2. Signs & Symptoms: a. Altered mental status, seizures b. Intense thirst c. Postural hypotension d. Muscle cramps 3. Treatment: a. Primary water deficit i. Fluid replacement (hypotonic/isotonic) b. Excessive sodium intake i. Diuretics ii. Sodium restrictions c. Seizure precautions 4. Nursing Implications: a. Serum sodium level should not decrease more than 8-15 mEq/L in an 8-hour period due to risk for cerebral edema and neurological complications vi. Hyponatremia (5.0 mEq/L) 1. Causes: a. Impaired renal excretion b. Renal failure 2. Signs & Symptoms: a. Life-threatening arrhythmias b. EKG changes (tall, peaked T wave) c. Weak or paralyzed skeletal muscles d. Respiratory arrest 3. Treatment: a. Increase K+ excretion (thiazide diuretics, dialysis) i. Sodium polystyrene sulfonate (Kayexalate) b. Force K+ from ECF to ICF by IV regular insulin with dextrose and a beta-adrenergic agonist or sodium bicarbonate c. Stabilize cardiac cell membrane by administering calcium chloride or calcium gluconate IV 4. Nursing Implications: a. Use continuous EKG monitoring ix. Hypokalemia (10.5 mEq/L) 1. Causes: a. Hyperparathyroidism b. Cancers c. Thyrotoxicosis 2. Signs & Symptoms: a. Weakness b. Dysrhythmias c. Bone pain d. Depressed reflexes e. Kidney stones 3. Treatment: a. Low calcium diet b. Hydration with isotonic saline solution c. Bisphosphonates- gold standard 4. Nursing Implications: a. Use continuous EKG monitoring b. Educate patient about use of digoxin and signs of toxicity i. Confusion, lethargy, anorexia, nausea, vomiting, vision changes xiii. Hypocalcemia (4.5 mEq/L) 1. Causes: a. AKI or CKD Hypoparathyroidism 2. Signs & Symptoms: a. Tetany b. Muscle cramps c. Paresthesia d. Dysrhythmias e. Calcified deposits in soft tissue (causes organ dysfunction) 3. Treatment: a. Oral phosphate-binding agents (calcium carbonate) b. Hemodialysis c. Volume expansion and forced diuresis 4. Nursing Implications: a. Use continuous EKG monitoring viii. Hypophosphatemia (2.1 mEq/L) 1. Causes: a. Renal insufficiency/ failure 2. Signs & Symptoms: a. Hypotension, facial flushing b. Nausea and vomiting c. Muscle paralysis d. Respiratory and cardiac arrest 3. Treatment: a. IV calcium gluconate b. Fluids and diuretics to promote urinary excretion c. Dialysis 4. Nursing Implications: a. Use continuous EKG monitoring ix. Hypomagnesemia (0.5 cm in diameter ii. Examples: 1. Psoriasis, seborrheic and actinic keratoses d. Pustule i. Elevated, superficial lesion filled with purulent fluid ii. Examples: 1. Acne, impetigo e. Vesicle i. Circumscribed, superficial collection of serous fluid. 0.5 cm, it is a bulla ii. Examples: 1. Varicella (chickenpox), herpes zoster (shingles), second-degree burn f. Wheal i. Firm, edematous, irregularly shaped area. Size varies. May only last a few hours ii. Examples: 1. Insect bite, urticaria, angioedema 7. Secondary Skin Lesions a. Atrophy i. Depression in skin resulting from thinning of the epidermis or dermis ii. Examples: 1. Aged skin, striae b. Excoriation i. Linear erosion caused by scratching, rubbing, or picking. Area in which epidermis is missing, exposing the dermis ii. Examples: 1. Abrasion, scratch 2. Lichenification c. Fissure i. Linear crack or break from the epidermis to the dermis. Dry or moist ii. Examples: 1. Athlete’s foot, chapping, eczema d. Scale i. Heaped-up keratinized cells, flakey exfoliation, irregular, thick or thin, dry or oily, and variable in size. Excess, dead epidermal cells made by abnormal keratinization and shedding ii. Examples: 1. Flaking of skin after a drug reaction or sunburn, psoriasis e. Scar i. Scars are areas of fibrosis, become thickened and raised. Abnormal formation of connective tissue that replaces normal skin ii. Examples: 1. Surgical incision, healed wound f. Ulcer i. Loss of the epidermis and dermis. Crater-like, irregular shape. Heals with scarring ii. Examples: 1. Pressure injury, chancre 8. Types of Skin Biopsies a. Punch biopsy i. Most common technique used ii. Local anesthetic is used to numb the area. A circular cutting device is used to remove a 2-6 mm plug of tissue; may or may not require sutures b. Shave biopsy i. Remove only the area of skin with a scalpel or razor blade using a parallel cut that rises above the surrounding tissue after an injection of a local anesthetic is given ii. Usually indicated for superficial or raised lesions iii. Suturing is not required c. Excisional biopsy i. Deep excision with a scalpel and closed with sutures 1. Can be painful throughout healing process d. Patient Education i. Keep dressing clean and dry ii. Clean the site daily and as needed once dressing is removed iii. Apply new dressing or leave open to air iv. If gauze is dried to wound or if crusting is present, use tap water or normal saline to remove v. May apply antibiotic ointment if ordered vi. Educate patient about infection signs and symptoms and when to call provider vii. May need to return to office for suture removal in 7-10 days Chapter 25: Integumentary Problems 1. Environmental Hazards a. Sun exposure i. Visible light and ultraviolet (UV) light 1. UVA- responsible for tanning 2. UVB- responsible for sunburn 3. Damage caused by UV rays is cumulative a. Causes premature aging and degenerative changes in the dermis ii. Prolonged and repeated sun exposure increases risk for: 1. Actinic keratosis a. Most common precancerous skin lesions b. Affect most of the older white population c. Sun exposure is the key factor d. Impossible to tell from squamous cell cancer i. Treatment should be aggressive e. Characteristics: i. Irregularly shaped, flat, pinkish/red papule with indistinct borders f. Treatment: i. Excision, topical medications (fluorouracil), photodynamic therapy 2. Basal Cell Carcinoma a. Arises from the basal cell layer of the epidermis b. Found on the head, neck, extremities, and trunk c. UV exposure is the most common cause d. Most common type of skin cancer e. Least deadly f. Middle-aged to older adults g. Characteristics: i. Red, pearly, defined, slightly elevated plaques h. Treatment: i. Surgical incision, curettage, radiation, targeted therapy 3. Squamous Cell Carcinoma a. Cancer arising from the keratinizing epidermal cells b. Aggressive and potential to metastasize c. Main risk factors are sun exposure and immunosuppression after organ transplant d. Pipe, cigar, and cigarette smoking contribute to SCC on mouth and lips e. Characteristics: i. Thin, scaly plaques with indistinct borders and ulcerations f. Treatment: i. Surgical excision, radiation, curettage, fluorouracil, immunotherapy 4. Melanoma a. Tumors arising from melanocytes b. Causes most skin cancers c. Sun exposure is the greatest risk factor d. May start as benign mole with changes, itching/bleeding e. Highly metastatic; survival depends on early diagnosis and treatment f. Characteristics: i. Irregular color, surface, border ii. Flat or elevated g. Treatment: i. Excision, lymph node dissection (may be necessary) ii. Immunotherapy and targeted therapy (early) iii. Chemotherapy h. Risk Factors: i. Red or blonde hair ii. Blue or light-colored eyes iii. Light-colored skin that freckles iv. Chronic UV exposure v. Family history vi. ABCDE Rule: 1. Asymmetry 2. Border irregularity 3. Color change 4. Diameter greater than 6mm 5. Evolving in appearance 5. Atypical/Dysplastic Nevus a. Nevi larger than normal i. Irregular borders ii. Various shades of color b. May have same ABCDE characteristics but less pronounced c. Increased risk of developing melanoma iii. Health Promotion 1. Most effective way to prevent skin cancer is avoiding or reducing exposure to the sun or tanning beds a. Sunscreen, hats, umbrellas, canopies 2. Educate about self-screenings and when to contact provider a. ABCDE method 2. Skin Infections and Infestations a. Bacterial infections i. Can occur as either primary or secondary infection ii. Staphylococcus aureus and group a b-hemolytic streptococci most common iii. Viral infections 1. Create lesions that can be hard to treat b. Infestation and insect bites i. Allergy to the venom ii. Reaction to infestation of eggs, feces, parasite c. Fungal infections i. Easy to diagnose ii. Affect skin, hair, and nails iii. Candidiasis common 3. Bacterial Infections a. Folliculitis i. Inflammation of the hair follicles found primarily on the scalp and extremities ii. Symptoms: 1. Areas of redness with pustules or papules 2. Infectious agents a. Bacteria, viruses, or fungi 3. Noninfectious agents a. Trauma, plugged hair follicle, poor hygiene, prolonged skin moisture, occlusive clothing iii. Treatment: 1. Teach proper hygiene methods 2. Keep skin folds clean and dry 3. Topical antibiotics 4. Warm compresses b. Furuncles i. Also called “boils” ii. Staphylococcus aureus bacteria iii. Inflammation of the hair follicle 1. Buttocks, thighs, abdomen, posterior neck regions, and axillae iv. Symptoms: 1. Painful deep, red, firm nodule v. Treatment: 1. Warm compresses 2. Systemic antibiotics 3. If abscess develops, will need incision and drainage c. Carbuncles i. Collection of infected hair follicles 1. Back of neck, upper back, lateral thighs ii. Symptoms: 1. Firm lesion that is red, painful, and swollen, drainage present 2. Abscess may be present iii. Treatment: 1. Warm compress 2. Systemic antibiotics 3. If abscess develops, will need incision and drainage d. Cellulitis i. Dermal and subcutaneous tissue infection 1. Staphylococcus, community-acquired methicillin resistant staphylococcus aureus (CA-MRSA), or group b streptococci 2. Can occur anywhere a. Often develops from another wound 3. Symptoms: a. Infected area is red, warm to touch, painful, swollen b. Can extend to lymph nodes and blood 4. Treatment: a. Systemic treatment of antibiotics are necessary e. Impetigo i. Infection from streptococci, staphylococcus, or both ii. Primary or secondary infection iii. Contagious iv. Symptoms: 1. Vesiculopustular lesions that develop thick, honey-colored crust 2. Itching 3. Face is the most common site v. Treatment: 1. Antibiotics, wound care 2. Good personal hygiene f. Methicillin-resistant staphylococcus aureus (MRSA) i. Can range from mild to extensive 1. Life-threatening if wound infection erupts or MRSA enters the bloodstream 2. Contact isolation 3. Treatment: a. IV antibiotics b. Hospitalization c. Possible surgery 4. Preventing the spread 4. Viral Infections a. Herpes Simplex i. Grouped vesicles with a reddened base ii. Herpes Simplex Type 1 1. Found primarily on the face (cold sore) iii. Herpes Simplex Type 2 1. Primarily found on the genitalia iv. Symptoms: 1. Vesicles may become pustules and burst, weep, then crust 2. Lesions last 2-6 weeks 3. Itch, painful, stinging sensation v. Treatment: 1. Topical or oral antivirals may be given 2. Can be transmitted to others a. Avoid contact with lesions 3. Infections will return to same skin area 4. Type 1 and 2 can be found in either area where inoculation has occurred b. Herpes Zoster i. Lesions are similar to herpes simplex and progress with weeping and crusting ii. Symptoms: 1. Lesions are unilateral and follow nerve route 2. Anterior/posterior trunk, face, eye 3. Very painful; pain after infection has resolved is common in older adults iii. Treatment: 1. Antivirals (acyclovir) should be given within 72 hours of eruption 2. Vaccination in adults over 60 a. Shingrix should only be given once; zostavax is a live vaccine and can’t be given to immunocompromised 3. Supportive care 4. Gabapentin may be prescribed for neuralgia 5. Parasitic Infections a. Pediculosis (lice) i. Lice infection of either the head, body, or pubic area ii. Most common symptom is itching iii. Observe hair for nits iv. Pubic lice causes severe itching of the vulvar or perirectal area 1. Can be contracted through bed linens or during sexual intercourse with infected person v. Treatment: 1. Use of topical sprays, creams, and shampoos a. Over-the-counter lice kits b. Topical permethrin cream or malathion lotion c. Oral ivermectin d. Wash contaminated linens and personal items in hot water with detergent b. Scabies i. Contagious skin infection caused by mite infestation ii. Characteristics of linear or curved ridge, intense itching worse at night iii. Transmitted through close contact with an infected individual or bedding/clothing 1. Common in nursing homes, other crowded living areas, and those with poor hygiene iv. Infestation is confirmed with scraping of a lesion v. Treatment: 1. Scabicides (topical permethrin or oral/topical ivermectin) 2. Launder all clothing and personal items in hot water with detergent c. Bedbugs i. Common parasite with infestations increasing due to travel and resistance to pesticides ii. Live in mattresses, fabrics, and cracks/crevices of furniture iii. Feed on human blood; don’t live on humans 1. Bites resemble mosquito bites 2. Resolve on own 3. Hydrocortisone cream/oral antihistamine to help with itching iv. Preventative measures 1. Examine hotel room, bedding especially box springs 2. Place luggage away from bed when traveling 3. Soiled clothing goes in sealed plastic bag when traveling 4. Observe and clean items bought at garage sales, thrift shops other resellers before bringing items into the home v. Eradicate infestation 1. Usually requires an exterminator d. Bees and wasps i. Symptoms: 1. Intense burning with local pain 2. Swelling and itching 3. May cause anaphylaxis ii. Treatment: 1. Cool compresses 2. Application of antipruritic 3. Antihistamines 6. Fungal Infections a. Candidiasis i. Found in moist areas of skin folds, axillae, under breasts, perineal/perianal regions ii. Oral mucosa (thrush) iii. Symptoms: 1. Red, moist, itchy, painful areas 2. Oral mucosa has white plaques iv. Treatment: 1. Antifungal medications (PO,topical,IV) 2. Keep areas clean and dry b. Tinea i. Can occur anywhere on the body ii. Athlete's foot, nail fungus, ringworm iii. Symptoms: 1. Depend of cause iv. Treatment: 1. Keep feet clean and dry 2. Wear shoes in public shower, locker rooms, pool 3. Avoid sharing footwear and clothing 7. Irritation Conditions a. Pruritus i. Also called itching ii. Localized or generalized; rash may or may not be present iii. Caused by stimulation of itch-specific nerve fibers 1. Physical or chemical agents either activate nerve fibers or stimulate the release of chemical mediators (histamine) a. Medications, lotions, soaps, detergents, insect bites, humidity, poison ivy/oak/sumac iv. Scratching can cause infection 1. Keep fingernails short v. Treatment: 1. Identify cause and eliminate it 2. Topical or oral medications 3. Prevention of dry skin b. Urticaria i. Also called hives ii. Rash of white or red raised areas (wheals) iii. Release of histamine iv. Treatment: 1. Identify cause and remove it 2. Oral antihistamine 3. Avoid behavior(s) that could cause vasodilation v. Usually caused by exposure to allergens 1. Drugs, extreme temperature, food, infection, disease, cancer, insect bites 8. Inflammatory Conditions a. Most often related to allergic immune response i. Specific cause not always known b. Corticosteroids may be prescribed to decrease inflammation c. Antihistamines may help with itching d. Comfort measures i. Cool, moist compresses ii. Lukewarm baths will colloidal oatmeal 9. Life-Threatening Skin Conditions a. Steven-Johnson Syndrome i. Life-threatening skin reaction from a drug 1. Allopurinol, Carbamazepine, Lamotrigine, Phenobarbital, Phenytoin, NSAIDs, Sulfonamides ii. Fever, extensive necrosis, epidermal detachment, and mucous membrane involvement iii. Disorders are classified by percentage of affected body surface 1. Skin detachment of less than 10% of body surface iv. Treatment: 1. Stop medication immediately 2. Supportive care 3. Antibiotics, corticosteroids b. Toxic Epidermal Necrolysis i. Life-threatening skin reaction from a drug 1. Allopurinol, Carbamazepine, Lamotrigine, Phenobarbital, Phenytoin ii. Fever, extensive necrosis, epidermal detachment, and mucous membrane involvement iii. Disorders are classified by the percentage of affected body surface 1. Skin detachment of more than 30% of the body surface iv. Treatment: 1. Stop medication immediately 2. Supportive care 3. Antibiotics, corticosteroids 4. Usually treated in ICU in reverse isolation 10. Benign Skin Problems a. Acne b. Skin tags c. Lentigo (age spots) d. Lipoma e. Nevi (moles) f. Psoriasis i. Chronic autoimmune disorder marked by exacerbations and remissions of the disorder 1. Underlying dermal inflammation from the abnormal growth of epithelial cells ii. Hyperproliferative state 1. Plaques on the skin secondary to rapid division and shedding of epithelial cells (every 4 days) iii. Triggers: 1. Environment, stress, illness, medications, skin injuries, smoking, obesity, and alcohol iv. May also develop psoriatic arthritis v. Develop a thorough patient/family history related to disorder 1. Strong genetic connection vi. 5 types of psoriasis 1. Plaque psoriasis 2. Guttate psoriasis 3. Inverse psoriasis 4. Pustular psoriasis 5. Erythrodermic psoriasis vii. There is no cure, disease management viii. Treatment is individualized 1. Topical corticosteroids and emollients to moisturize skin are most common topical treatments 2. Anthralin, tar-like substance applied to plaques for short periods of time a. Suppress cell division and reduce inflammation b. Can cause chemical burns 3. Light therapy 4. Oral systemic medications a. Methotrexate, folic acid, and retinoids (vitamin A derivatives) i. Vitamin A derivatives can have teratogenic effects b. Biologic agents i. Stop use and notify physician if signs and symptoms of illness occurs while taking g. Rosacea 11. Treatment of Dermatologic Problems a. Phototherapy b. Radiation therapy c. Laser technology d. Dru therapy i. Antibiotics ii. Corticosteroids iii. Antihistamines iv. Topical fluorouracil v. Immunomodulators 12. Diagnostic and Surgical Therapy a. Skin scraping b. Electrodesiccation c. Electrocoagulation d. Curettage e. Punch biopsy f. Cryosurgery g. Excision- Mohs surgery 13. Cosmetic Procedures a. Topical procedures b. Injection c. Surgical therapies i. Laser surgery ii. Face lift iii. Liposuction d. Nursing Management i. Preoperative 1. Informed consent 2. Realistic expectations 3. Patient teaching ii. Postoperative 1. Pain management 2. Monitor for signs of infection and adequate circulation 14. Skin Grafts a. Uses b. Types i. Free grafts 1. Autograft and isograft 2. Reconstructive microsurgery ii. Skin flaps iii. Soft tissue expansion iv. Engineered skin substitutes Chapter 26: Burns 1. Burns a. Occur when there is injury to the skin or other tissues of the body caused by heat, chemicals, electrical current, or radiation b. Injury severity can range from mild to life-threatening c. Burn injury affects many body systems d. Risk of infection is high e. Most burn accidents are preventable f. Complications i. Impaired gas exchange ii. Fluid and electrolyte imbalances iii. Altered perfusion to affected limbs iv. Risk for malnutrition v. Risk for immobility vi. Risk for infection is constant vii. Anxiety/PTSD viii. Disfigurement 2. Types of Burn Injury a. Thermal burns i. Most common type of burn injury ii. Exposure to external heat sources such as hot metals, scalding liquids, steam, or flames iii. Severity of injury depends on 1. Temperature of burning agent 2. Duration of skin contact 3. Contact with acids, alkalis, or organic compounds 4. Amount of skin exposed iv. Dangerous chemicals are in homes, businesses, and industries 1. Lye and sulfuric acid, common chemicals used to unclog sinks in homes 2. Wet cement, oven cleaners, and heavy industrial cleaners 3. Organic compounds include phenols and petroleum products b. Chemical burns i. Contact with acids, alkalis, and organic compounds ii. Dangerous chemicals are in homes, businesses, and industries 1. Lye and sulfuric acid, common chemicals used to unclog sinks in homes 2. Wet cement, oven cleaners, and heavy industrial cleaners 3. Organic compounds include phenols and petroleum products 4. Severity of the injury depends on: a. Duration of contact b. Concentration of chemical used c. Chemical’s action d. Amount of skin exposed c. Smoke inhalation injury i. Can occur during inhalation ii. Orofacial burns can cause swelling that impairs breathing iii. Assess for cough, shortness of breath, or hoarseness as this may indicate smoke inhalation iv. Always assess the mouth, throat, and nose for signs of scoot v. Signs and symptoms: 1. Facial burns; flaring nostrils; stridor, wheezing, and dyspnea; hoarseness; tachycardia d. Electrical burns i. Tissue injury occurs when an electrical current enters the body and converts to heat injury ii. Extent of injury depends on the voltage, pathway of current, local tissue resistance, surface area in contact with the current and duration of contact iii. The longer the electricity is exposed to the body, the greater the damage iv. Electrical injury puts the patient at risk for respiratory arrest, severe metabolic acidosis, and myoglobinuria v. Can cause immediate cardiac arrest or ventricular fibrillation vi. Myoglobin from injured muscle and hemoglobin from damaged RBCs travel to kidneys; may block renal tubules leading to acute kidney injury vii. Contact with an electric current can cause muscle contractions strong enough to fracture the long bones and vertebrae e. Radiation burns i. Occurs with prolonged exposure to the sun, or radiation ii. Individuals that work in the nuclear industry are at risk for radiation burns associated with cancer due to exposure to ionizing radiation f. Cold thermal injury (frostbite) 3. Classification of Burn Injury a. Severity of injury is determined by: i. Depth of burn 1. Burns are defined by degrees (first, second, third, and fourth) 2. The ABA classifies burns according to depth of skin destruction a. Partial-thickness burn i. Superficial-Thickness Burn 1. Involves injury to the epidermis; blood supply to the dermis is still intact 2. Mild to severe erythema, NO BLISTERS 3. Skin blanches with pressure 4. Burn is painful, tingling sensation, pain is eased with cooling 5. Discomfort lasts about 48 hours; healing occurs in about 3 to 6 days 6. No scarring occurs and skin grafts are not required ii. Superficial Partial-Thickness Burn 1. Involves injury deeper into the dermis; blood supply is reduced 2. Large blisters may cover an extensive area 3. Edema is present 4. Mottled pink to red base and broken epidermis, with a wet, shiny, weeping surface 5. Burn is painful and sensitive to cold air 6. Heals in 10-21 days with no scarring; minor pigment changes may occur 7. Grafts may be used if the healing process is prolonged iii. Deep Partial-Thickness Burn 1. Extends deeper into skin dermis 2. Blister formation does not occur 3. Wound surface is red and dry with white areas in deeper parts 4. May or may not blanch, moderate edema present 5. Generally heals in 3 to 6 weeks, scar formation develops and skin grafting may be necessary b. Full-thickness burn i. Full-Thickness Burns 1. Involves injury and destruction of the epidermis and dermis 2. Appears as a dry, hard, leathery eschar 3. Color may be waxy white, deep red, yellow, brown, or black 4. Injured surface appears dry 5. Edema present under eschar 6. Sensation is reduced or absent 7. Eschar requires removal 8. Grafting may be required ii. Deep Full-Thickness Burn 1. Injury extends beyond skin into underlying fascia and tissues, muscle, bone, and tendons 2. Injured area is black, sensation is completely absent 3. Eschar is hard and inelastic 4. Lack of pain 5. Healing takes months 6. Grafting is required ii. Extent of burn in percent of TBSA 1. 2 common tools for determining the total body surface area a. Lund-Browder chart i. Considered more accurate b. Rule of Nines i. Used for initial adult assessment c. Sage Burn Diagram iii. Location of the burn 1. Severity of burn is influenced by location of burn injury a. Face, neck, circumferential torso i. May interfere with gas exchange b. Circumferential eschar i. Restrict chest movement c. Hands, feet, joints i. Limit mobility and function ii. Decreased perfusion below burn injury d. Ears, nose, buttocks, perineum i. High risk for infection iv. Pre-existing health 1. Pre-existing heart, lung, or chronic diseases contribute to poorer prognosis 2. Diabetes and peripheral vascular disease put patient at high risk for delayed healing v. Associated injuries 4. Prehospital and Emergency Care a. Scene safety is a priority b. Remove person from source od burn and stop burning process i. Wounds flushed with copious amounts of water ii. Minimizes depth of injury c. Wrap a person in a dry, clean sheet or blanket i. Prevents wound contamination and provides warmth ii. Moist dressings can reduce pain but may cause hypothermia d. Burn patient may have other injuries that are priority over burn e. First responders must fully explain injures to ED i. Any hazardous chemicals involved ii. Traumatic injury (e.g., fall) 5. Phases of Burn Management a. Resuscitation/Emergent i. Health care team prioritizes life-threatening problems ii. Last up to 72 hours after the initial injury iii. Priority nursing concerns 1. Fluid and electrolyte shifts 2. Gas exchange iv. Fluid and electrolyte shifts 1. Greatest threat is burn shock a. Combination of distributive and hypovolemic shock b. Increased capillary permeability causes a massive shift of fluids from intravascular to interstitial spaces 2. Loss of intravascular fluid can cause burn shock a. Hypotension b. Tachycardia c. Tachypnea 3. Acute kidney injury and ultimately death if not resuscitated sufficiently 4. Hemolysis of RBCs from circulating factors released at time of injury from the burned tissue 5. Thrombosis in capillaries of burned tissue causes loss of circulating RBCs 6. High hematocrit caused by hemoconcentration 7. K+ shift develops first because injured cells and hemolyzed RBCs release K+ into circulation 8. Na+ rapidly moves to interstitial spaces and stays there until edema formation ends v. Inflammation and Healing 1. Burn injury causes coagulation necrosis 2. Neutrophils and monocytes accumulate at site of injury 3. Fibroblasts and newly formed collagen fibrils begin wound repair within first 6 to 12 hours after injury vi. Immunologic Changes 1. Immune system is challenged when burn injury occurs a. Skin barrier is destroyed b. Bone marrow depression occurs c. Circulating levels of immune globulins decrease d. Defects occur in WBCs i. Inflammatory cytokine cascade ii. Patient at greater risk for infection vii. Clinical Manifestations 1. Normally alert and able to answer questions a. Monitor cognition b. Altered mental status usually result of hypoxia 2. Frightened and need reassurance 3. Shivering from heat loss, anxiety, pain a. Provide warming blankets, heat lamps b. Increase room temperature 4. Pain with partial-thickness burns viii. Complications 1. Respiratory a. Inhalation injuries i. 3 types 1. Injury from exposure to toxic gases including carbon monoxide and/or cyanide 2. Above the glottis injury from direct heat or chemicals causing severe mucosal edema 3. Below the glottis injury causing airway inflammation and edema resulting in edema, atelectasis, and pneumonia ii. Need fiberoptic bronchoscopy and carboxyhemoglobin blood levels iii. Examine sputum for carbon particles iv. Watch for signs of respiratory distress v. Patients with pre-existing lung disease are more likely to develop a respiratory infection 2. Cardiovascular a. Impaired circulation to extremities with circumferential burns i. Tissue ischemia ii. Paresthesia iii. Necrosis b. Escharotomy will i. Restore circulation to compromised extremities ii. Improve chest expansion c. Risk for venous thromboembolism i. Age, obesity, extensive or lower extremity burns ii. Concomitant lower extremity trauma, and prolonged immobility iii. Prophylaxis with low-molecular-weight heparin (enoxaparin) or low-dose unfractionated heparin iv. Apply SCDs if the patient is immobile 3. Renal a. Acute kidney injury (AKI) b. If patient becomes hypovolemic, blood flow to kidneys will decrease causing renal ischemia i. If this continues, AKI will develop c. With full-thickness and major electrical burns, released myoglobin (from muscle cell breakdown) can block renal tubules d. Monitor adequacy of fluid replacement ix. Nursing and Interprofessional Management 1. Airway management a. High fowler’s position b. 100% oxygen, aerosolized heparin, N-acetylcysteine, and albuterol c. Deep breathing, coughing, repositioning d. Suctioning e. ABGs, telemetry, pulse oximetry, capnography f. Early endotracheal intubation 2. Fluid therapy a. 2 large-bore IV lines for greater than 20% TBSA b. For burns greater than 20% TBSA central line may be considered c. Parkland formula for fluid replacement i. 4mL/kg of body weight for each percent of TBSA burned ii. ½ is given within the first 8 hours and then the other ½ will be given over the remaining 16 hours d. Insert an indwelling catheter for patients with burns greater than 20% TBSA 3. Wound care a. When burn wounds are exposed, staff should wear PPE i. Disposable hats ii. Masks iii. Gowns iv. Non-sterile gloves to remove dressings 1. Use sterile gloves to apply antimicrobial ointment and sterile dressings b. Cleansing and gentle debridement i. Shower cart or shower ii. Scissors or forceps to remove loose burn tissue and blisters iii. Dressings applied c. Extensive surgical debridement i. Occurs in the OR d. Dressings i. Antimicrobial creams, hydrocolloids, alginates, hydrogels, collagen, and hyaluronic acid ii. Type of dressing based on burn depth, bacterial count, cost iii. Dressing changes continue once or twice a day iv. Specific specialty dressings may be changed every 5 to 7 days v. Application of Silver Sulfadiazine to Moistened Gauze e. Other care measures i. Facial Care 1. Covered with ointment and gauze 2. Not wrapped to limit pressure ii. Eye Care 1. Eye exam on admission 2. Artificial tears for moisture, comfort 3. Periorbital edema may frighten patient iii. Keep ears free from pressure 1. No use of pillows 2. Raise patient’s head with rolled towel iv. For neck burns hyperextend the neck to prevent contractures v. Hands and arms should be extended and elevated on pillows or foam wedges 1. Patient will evaluate and provide splints 2. Work with PT and OT for ROM exercises vi. Keep patient’s perineum clean and dry 1. Remove indwelling catheter as soon as possible 2. Fecal diversion device if loose stools vii. Drug Therapy 1. Analgesics and sedatives a. Morphine b. Hydromorphone (Dilaudid) c. Haloperidol (Haldol) d. Lorazepam (Ativan) e. Midazolam 2. IV pain medication for fastest onset of action 3. Tetanus immunization a. Given routinely to all burn patients viii. Nutrition Therapy 1. Hypermetabolic state a. Resting metabolic expenditure may be increased by 50% to 100% above normal b. Core temperature is increases c. Catecholamines release stimulates catabolism and heat production d. Massive catabolism occurs with protein breakdown and increased gluconeogenesis 2. Early nutrition support within hours of burn injury a. Can reduce complications and mortality b. Optimizes burn wound healing c. Minimizes negative effects of hypermetabolism and catabolism d. Supplements or enteral feeding promotes optimal conditions for wound healing e. High protein, high carbohydrate diet needed f. Supplemental vitamins may be given b. Resuscitative c. Acute i. Begins with mobilization of interstitial fluid and subsequent diuresis ii. Continues until wounds are nearly healed iii. May take weeks or months iv. Oxygenation problems may resolve but sometimes inhalation injuries will not resolve for many days, weeks, or months v. Vital signs are more stable vi. Wound healing begins vii. With major burns complications may occur during this phase viii. Clinical Manifestations 1. Partial-thickness wounds begin to hea; at the wound margins a. Epithelial buds eventually close wound b. Healing is spontaneous i. Occurs within 10-21 days ii. Often more pain during this time c. Surgical procedures continue for extensive debridement and skin grafting ix. Laboratory Values 1. Sodium a. Hyponatremia can develop from i. Excessive GI suction ii. Diarrhea b. Dilutional hyponatremia i. From excess water intake ii. Offer juices, nutrition supplements c. Assess for clinical manifestations of hyponatremia d. Hypernatremia may occur after i. Successful fluid resuscitation with hypertonic solutions ii. Tube feedings (EN) iii. Inappropriate fluid administration e. Assess for clinical manifestations of hypernatremia f. Restrict sodium in IVs and EN feedings 2. Potassium a. Hyperkalemia may occur if a patient has i. Renal failure ii. Adrenocortical insufficiency iii. Massive deep muscle injury b. Large amounts of potassium are released from damaged cells c. Assess for clinical manifestations of hyperkalemia d. Hypokalemia occurs with i. Vomiting, diarrhea ii. Prolonged GI suction iii. IV therapy without potassium supplementation iv. Through burn wounds e. Assess for manifestations of hypokalemia x. Complications 1. Infection a. Burn would colonized by patient’s flora b. WBCs have functional deficit c. Patient is immunosuppressed for many months d. Watch for signs and symptoms of systemic infection i. Hypothermia or hyperthermia ii. Increased heart and respiratory rate iii. Decreased BP iv. Decreased urine output e. Causative organism of sepsis usually gram-negative bacteria f. Fungal infections may develop in the patient’s mucous membranes due to systemic antibiotic therapy 2. Cardiovascular and respiratory a. Same complications can present in emergent phase and may continue into acute phase b. New problems might arise, requiring prompt intervention 3. Neurologic a. May result due to severe hypoxia from respiratory injuries or as a complication from electrical injuries b. Disorientation c. Withdraw or become combative d. Hallucinations e. Frequent nightmare-like episodes f. Delirium i. More acute at night ii. Occurs more often in the older patient iii. Usually transient iv. Some complications can last for years 4. Musculoskeletal a. ROM may be affected b. Skin and joint contractures 5. Gastrointestinal a. Paralytic ileus b. Diarrhea c. Constipation d. Curling’s ulcer 6. Endocrine a. Transient increased blood glucose levels i. Stress-mediated cortisol and catecholamine release ii. Increased mobilization of glycogen stores iii. Gluconeogenesis b. Increased insulin production i. Insulin effectiveness decreases due to insulin insensitivity c. High glucose levels may also be be caused by high caloric intake needed xi. Nursing and Interprofessional Management 1. Wound care a. Gently cleanse wounds b. Topical antimicrobial therapy c. Graft care, donor site care d. Collagenase is used for enzymatic debridement of burn wounds i. Promotes removal of nonviable tissue from the healthy wound bed 2. Excision and grafting a. Eschar is surgically removed down to subcutaneous tissue or fascia b. Hemostasis is achieved c. Autograft is placed on clean, viable tissue d. Donor skin is taken with a dermatome e. Choice of dressings varies f. Grafts are attached with i. Sutures or staples ii. Negative pressure wound therapy g. Outer occlusive dressings apply just enough pressure to i. Promote adherence of the graft ii. Help control bleeding h. Cultured epithelial autografts i. Grown from biopsies obtained from the patient’s unburned skin ii. Used in patients with a large body surface burn area or those with limited skin for harvesting i. Dermal substitutes i. Life-threatening full-thickness or deep partial-thickness wounds where conventional autograft is not available or advisable ii. Also is used in reconstructive burn surgery procedures iii. Consists of both dermal and synthetic elements 3. Pain management a. Patients experience 2 kinds of pain i. Continuous background pain 1. IV administration of opioid 2. Slow-release, twice-a-day oral opioid 3. Patient-controlled anesthesia 4. Anxiolytics and adjuvant analgesics ii. Treatment-induced pain 1. Premedicate with analgesic and anxiolytic 2. Non Drug strategies may also be used a. Relaxation breathing b. Visualization, guided imagery c. Hypnosis d. Biofeedback e. Music therapy 4. Physical and occupational therapy a. Good time for exercise is during dressing changes b. Passive and active ROM c. Splints should be custom-fitted 5. Nutrition therapy a. Caloric needs regularly calculated by dietitian b. High-protein, high-carbohydrate foods c. Antioxidant protocol may be beneficial d. Monitor laboratory values e. Weigh weekly d. Rehabilitative i. The rehabilitation phase begins when 1. Wounds have nearly healed 2. Patient is engaging in some level of self-care 3. Goals of the patient are a. Work toward resuming a functional role in society b. Rehabilitate from any functional and cosmetic postburn reconstructive surgery 4. Burn wounds heal either by spontaneous re-epithelialization or by skin grafting 5. Layers of keratinocytes begin rebuilding the tissue structure 6. Collagen fibers add strength to weakened areas 7. In about 4 to 6 weeks, area becomes raised and hyperemic 8. Mature healing is reached about 12 months 9. Pink or red color has fades to a slightly lighter hue than the surrounding unburned tissue 10. Discoloration of scar fades somewhat with time 11. Scar contour elevates and enlarges 12. Newly healed areas can be more or less sensitive to cold, heat, and touch 13. Complications a. Skin and joint contractures i. Most common complications during rehab phase ii. Develops because of shortening of scar tissue in flexor tissues of point iii. Encourage proper positioning, splinting 14. Nursing and Interprofessional Management a. Encourage both patient and caregiver to take part in care i. Wound care instructions ii. Demonstrate dressing changes iii. Scar management, moisturizing, sun protection b. Need for reconstructive surgery is reviewed during follow-up appointments c. Ongoing pain management d. Nutrition needs e. PT and OT exercises f. Encouragement and reassurance 6. Carbon Monoxide Poisoning a. Carbon monoxide is a colorless, odorless, and tasteless gas i. 1-10: normal level ii. 11-20 (mild): headache, flushing, decreased visual acuity, decreased cerebral functioning, and slight breathlessness iii. 21-40 (moderate): headache, n/v, drowsiness, vertigo and tinnitus, confusion and stupor, pale to reddish-purple skin, decreased blood pressure iv. 41-60 (severe): coma, seizures, cardiopulmonary instability v. 61-80 (fatal): death Chapter 36: Hypertension 1. Hypertension a. Most important modifiable risk factor to prevent CVD b. ~45% adults in United States meet diagnosis criteria for HTN i. Heart disease associated with HTN leads leads to 23.7% of deaths in United States c. As BP increases, so does the risk of: i. MI ii. Heart Failure iii. Stroke iv. Renal Disease v. Retinopathy d. Most people need a combination of medication and lifestyle modification i. 71% do not have their BP in control ii. 49% of those with uncontrolled HTN are untreated e. National guidelines are designed to apply to all racial and ethnic groups f. BP control is strongly impacted by social determinants of health i. Lack of access to healthcare ii. Poverty iii. Chronic stress g. Blacks i. Highest prevalence ii. More resistant HTN iii. Develop at younger age iv. Female greater than male v. More nocturnal non-dipping BP (increased CVD risk) vi. More end-organ damage vii. Highest death rate h. Hispanics i. Are less likely to receive treatment for hypertension than Whites and Non-Hispanic Blacks ii. Have lowest rates of BP control iii. Have lowest levels of awareness of hypertension and its treatment i. Gender Differences i. Men-more common before middle age ii. Women 1. Increased 2-3x with oral contraceptives 2. Preeclampsia- possible early sign 3. More common after menopause 4. Harder control in older women j. Clinical Manifestations i. “Silent killer”- asymptomatic until severe and target organ disease occurs 1. Fatigue 2. Dizziness 3. Palpitations 4. Angina 5. Dyspnea ii. Hypertensive crisis 1. May experience severe headaches, dyspnea, and nosebleeds k. Complications i. Target organ diseases occur most frequently in: 1. Heart a. Coronary artery disease; atherosclerosis b. Left ventricular hypertrophy c. Heart failure 2. Brain-cerebrovascular disease a. TIA/Stroke; atherosclerosis b. Hypertensive encephalopathy; changes in autoregulation 3. Peripheral Vascular Disease a. Atherosclerosis leads to PVD, aortic aneurysm, aortic dissection b. Intermittent claudication 4. Kidney a. Nephrosclerosis leads to chronic kidney disease (CKD) 5. Eyes- retinal damage a. Blurry or loss of vision; retinal hemorrhage b. Damaged retinal vessels indicate concurrent damage to vessels in heart, brain, and kidneys l. Diagnostic Studies i. Basic lab studies done to 1. Identify or rule out causes of secondary hypertension 2. Evaluate target organ disease 3. Determine overall cardiovascular risk 4. Establish baseline levels before starting therapy 5. Measurement of BP 6. Renal function, U/A, BMP, CBC, serum lipid profile, uric acid, ECG, ophthalmic exam 7. Echocardiogram 8. Liver function tests 9. Thyroid stimulating hormone m. Interprofessional Care i. Achieve and maintain goal BP ii. Reduce cardiovascular risk factors and target organ disease iii. Lifestyle modifications iv. AHA Life’s Simple 7 1. Manage BP 2. Control cholesterol 3. Reduce blood sugar 4. Get active 5. Eat better 6. Lose weight 7. Stop smoking n. Health Promotion i. Healthy people 2020 goals to decrease cardiovascular mortality related to hypertension 1. Promote weight loss and reducing calories & increase physical activity a. Aerobic exercise, resistance training b. Implement dietary approaches to stop hypertension (DASH) diet c. High in fruits, vegetables and low-fat dairy d. Enhance intake of potassium, calcium, magnesium, and fiber 2. Reduce intake of dietary sodium, optimal goal is less than 1500 mg/day 3. Educate patients about modifiable risk factors for hypertension 4. Complementary supplements a. Garlic, fish oil, coenzyme Q-10 i. Educate patients to speak with providers about using complementary supplements as they can interfere with other medications o. Drug Therapy i. Patient with stage 1 hypertension- non-pharmacological treatment + 1 first line pharmacologic drug ii. Patient with stage 2 hypertension- non-pharmacological treatment + 2 antihypertensives from two different classifications 1. If a drug is not tolerated, then another classification will be used 2. Monthly follow-up visits until at goal BP; then 3 to 6 months 3. Stage 2 hypertension or comorbidities- more frequent iii. Angiotensin Converting Enzyme (ACE) Inhibitors 1. Medications ending in “pril” a. Lisinopril 2. Prevent angiotensin I from converting to angiotensin II 3. Dry, nagging cough most common side effect iv. Angiotensin II Receptor Blockers (ARBs) 1. Medications ending in “sartan” a. Losartan 2. Selectively block binding of angiotensin II but not inhibit ACE 3. Great alternative for ACE Inhibitor v. Beta Blockers 1. Medications ending in “olol” a. Propranolol 2. Block beta I receptors vi. Calcium Channel Blockers 1. Medications ending in “pines” a. Amlodipine 2. Vasodilation vii. Diuretics 1. Lasix, spironolactone, thiazides (HCTZ) 2. Electrolyte imbalances viii. Side Effects 1. Orthostatic hypotension- feel dizzy or faint when change position a. BP and HR after supine for 5 minutes b. Assist to standing c. Measure BP and HR at 1 minute and 3 minutes of position change i. Normal: SBP decreased (less than 10 mm Hg) 1. DBP and HR increased slightly ii. Abnormal: SBP decreased 20 mm Hg or more 1. DBP decreased 10 mm Hg or more 2. HR increased 20 beats/min or more 3. Report of lightheadedness or dizzy 2. Sexual problems- reduced libido or erectile dysfunction a. Sensitive subject b. Plan for treating HTN needs to be acceptable to patient 3. Dry mouth- sugarless gum or candy 4. Frequent voiding- take diuretic early in the day to avoid getting up at night p. Nursing Assessment i. Subjective Data 1. Health history a. Hypertension, cardiovascular, cerebrovascular, renal, or thyroid disease b. Diabetes mellitus, pituitary disorders, obesity, dyslipidemia c. Menopause or hormone replacement 2. Drugs: prescription, OTC, herbals, illicit ii. Objective Data 1. Cardiovascular a. Blood pressure readings, orthostatic changes, abnormal heart sounds, pulses, edema 2. Gastrointestinal a. Body measurements 3. Neurologic a. Mental status changes 4. Diagnostic study results q. Patient Education i. Educate patient about importance of medication competence 1. Taking medication as prescribed 2. Side effects, indications, drug interactions a. Report unpleasant side effects to pcp 3. Decrease sodium intake 4. Stress management 5. Limit alcohol 6. Obtain personal BP monitor to use at home 7. Obtain weight scale a. Record all findings to take to pcp 2. Normal Regulation of Blood Pressure a. Blood pressure (BP)- force exerted by blood against walls of blood vessels i. Involves both systemic factors and local peripheral vascular effects ii. Important to maintain tissue perfusion during activity and rest b. Systemic vascular resistance- force opposing the movement of blood within the blood vessels i. Arteries and arterioles principle factor determining SVR ii. Narrowing of artery increases resistance to blood flow iii. Dilation or artery decreases resistance to blood 3. Classification of Hypertension (age >18) a. The higher measurement when either SBP or DBP are outside a range determines the classification i. SBP increases with age ii. DBP rises until about age 55, then declines b. BP classification is based on i. 2 or more readings ii. Accurately performed on both arms iii. On 2 separate occasions iv. Normal 180 mmHg and/or DBP >120 mmHg i. Hypertensive emergency 1. Target organ damage 2. Requires hospitalization 3. Very severe problems can result if prompt recognition and treatment is not obtained 4. Manifestations: encephalopathy, intracranial or subarachnoid hemorrhage, HF, MI, renal failure, dissecting aortic aneurysm or retinopathy 5. Untreated= 79% mortality in one year b. Hospitalization- HTN emergency i. Treatment related to BP and evidence of target organ disease ii. IV drugs: slow titration; MAP 110 to 115 mmHg 1. MAP= (SBP + 2DBP)/3 2. Drugs: vasodilators (sodium nitroprusside), adrenergic inhibitors, calcium channel blockers 3. Drugs have rapid onset; monitor HR and BP every 2 to 3 minutes 4. Special considerations: aortic dissection, acute ischemic stroke, poststroke patients iii. Monitor cardiac and renal function iv. Frequent neurologic checks v. Bed rest for those on IV drugs vi. Determine cause vii. Education to avoid future crisis c. Hypertensive urgency- more common i. No evidence of target organ disease ii. Hospitalization usually not required iii. Associated with chronic stable disorders 1. Stable angina, chronic HF, prior MI or CVA iv. Hypertensive crisis 1. History of HTN; not adherent or undermedicated 2. Cocaine, amphetamines, PCP, LSD, leads to seizures, stroke, MI, or encephalopathy Chapter 37: Coronary Artery Disease and Acute Coronary Syndrome 1. Coronary Artery Disease a. Coronary artery disease is the most common type of cardiovascular disease b. Leading cause of death in the United States c. Patients with CAD may be asymptomatic or develop chronic stable angina (chest pain) d. May evolve to more serious conditions of unstable angina and MI e. Coronary artery disease is a type of blood vessel disorder caused by atherosclerosis i. Atherosclerosis is the deposit of fat along the arterial wall that hardens over time ii. “Hardening of the arteries” iii. Atherosclerosis can occur in any artery iv. Endothelial injury and inflammation play a key role in developing atherosclerosis v. Stages of Atherosclerosis 1. Chronic Endothelial Injury a. Caused by: i. Hypertension ii. Tobacco use iii. Hyperlipidemia iv. Hyperhomocystinemia v. Diabetes vi. Infections vii. Toxins 2. Fatty streak a. Earliest lesion; lipid filled smooth muscle cells; appears yellow b. Start- age 20 and increase as age c. Treatment that lower low-density lipoproteins (LDL) may slow process 3. Fibrous plaque a. Beginning of progressive change in endothelium; age 30 b. LDLs and growth factors stimulate smooth muscle proliferation and arterial wall thickens c. Cholesterol and other lipids move into intima d. Collagen covers and forms grayish or whitish fibrous plaque with smooth or rough, jagged edges e. Narrowed vessel lumen reduces distal blood flow 4. Complicated lesion a. Fibrous plaque grows; continued inflammation leads to plaque instability, ulceration, and rupture b. Platelets accumulate leading to thrombus that further narrows or occludes artery c. Activation of platelets causes expression of glycoprotein llb/llla receptors to bind fibrinogen resulting in increased size of thrombus f. Effects of Coronary Artery Disease i. CAD- profound effect on perfusion ii. Perfusion depends on the heart’s ability to generate enough cardiac output (CO) to distribute blood to all body tissues iii. Significant CAD negatively affects heart function; impaired CO and decreased perfusion g. Developmental Stages of Coronary Artery Disease i. Progressive disease that develops over many years ii. Patient becomes symptomatic once disease process is well advanced h. Clinical Manifestations of Coronary Artery Disease i. Angina Pectoris- (chest pain) transient pain caused by ischemia ii. Acute myocardial infarction- when ischemic intracellular changes become irreversible and necrosis results iii. Sudden cardiac death- unexpected death from cardiac causes i.Nonmodifiable Risk Factors For CAD i. Age ii. Gender iii. Ethnicity iv. Family history v. Genetics j. Modifiable Risk Factors For CAD i. High serum lipids 1. Cholesterol >200 mg/dL 2. High-density lipoproteins (HDL) 150 mg/dL a. High levels increase risk for CAD ii. Hypertension (HTN) iii. Tobacco use iv. Diabetes- 2-4x greater incidence of CAD v. Metabolic syndrome vi. Physical inactivity vii. Obesity 1. BMI >30 2. “Apple” figure >CAD than “pear” figure viii. Psychological states ix. Substance use k. Interprofessional and Nursing Care: Health Promotion i. Identifying high-risk persons 1. Health history, including family history 2. Presence of cardiovascular symptoms 3. Lifestyle patterns 4. Psychosocial history 5. Employment history 6. Attitudes and beliefs about health and illness; education and literacy 2. PREVENTION IS KEY! a. Increase Physical Activity i. FITT formula: 1. Frequency, Intensity, Type and Time 2. 30 minutes most days plus weight training 2 days/week ii. Regular physical activity helps with 1. Weight reduction 2. Reduction of systolic BP 3. Increase in HDL cholesterol b. Nutritional Therapy i. Focus on lowering LDL cholesterol