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NURSING N490 Medical Surgical Final Exam Blueprint (65 Q&A from all the topics)OCR100% Guaranteed Pass.

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N490 SPRING Final Exam Blueprint 65 questions on the following topics: GENETICS In all nursing practice settings, nurses have five main tasks: • Help collect and interpret relevant family... and medical histories • Identify patients and families who need further genetics evaluation and counseling and refer them to appropriategenetics services • Offer genetics information and resources to patients and families • Collaborate with genetics specialists • Participate in the management and coordination of care of patients with genetic conditions. Genetics-related nursing practice involves the care of people who have genetic conditions, those who may be predisposed to develop or pass on genetic conditions, and those who are seeking genetics information and referral for additional genetics services. Nurses support patients and families with genetics related and genomics-related health concerns by ensuring that their health choices are informed ones and by advocating for the privacy and confidentiality of genetic and genomic information and for equal access to genetic testing and treatments BONE MARROW TRANSPLANT Peripheral Stem Cell Transplantation – effective, lifesaving procedures for treatment of number of malignant or nonmalignant diseases - Safe use of high doses of chemotherapy agents and radiation therapy in patients whose tumor developed resistance or failed to respond to standard doses - GOAL IS TO CURE – if it can’t be achieved, it can result in period of remission - Commonly used to treat leukemia and lymphoma and also other cancers - Treatment is very damaging to bone marrow – without donation the patient can DIE TYPES OF DONOR STEM CELLS - ALLOGENEIC: a donor with matching HLA tissue typing o Can be from parents, siblings and unrelated matching donor o More at risk for graft vs. host - SYNGENEIC: stem cell from identical twin – perfect match o Graft vs. Host does not occur - AUTOLOGOUS: Most common – donation from self, stored and frozen for later use PROCEDURE - Harvesting: Two different methods o Harvesting stem cell residing in bone marrow ▪ Aspiration with large bore needle from ILIAC CREST OR STERNUM ▪ Takes 1-2 hours, can be discharged after recovery ▪ Pain may last for 7 days o Harvesting with cell separator equipment ▪ Takes 2-4 hours, but might take longer ▪ Would need drugs for mobilization of stem cells (see chart above) – harvested after 4-5 days - Conditioning phase: o Total body irradication of all malignant cells and create space in bone marrow for engraftment of new marrow - Transplantation: o Stem cell infusion administered BY IV SLOWLY INTO CENTRAL LINE o Usually 2-4 weeks required for transplanted marrow to start producing hematopoietic blood cells o RISK FOR PANCYTOPENIA – protect from sun exposure and supply them with electrolytes, nutrition and blood transfusion if needed ▪ Usually required patient to stay in hospital for 2-4 weeks to prevent infection COMPLICATIONS - INFECTIONS – need to use prophylactic antibiotic therapy - GRAFT VS. HOST – immunosuppressive therapy - Phlebitis – may occur 1 month after transplant – Need to monitor for jaundice, abdominal pain and liver. LYMPHOMA TWO TYPES: HODGKINS and NON-HODGKINS - Hodgkins – REED-STERNBERG, spreads in orderly fashion – upper body, cervical mantle region (NECK) - Non-Hodgkins – enlarged lymph nodes from multiple sites and extra nodal locations HODGKIN’S LYMPHOMA - Malignant condition characterized by proliferation of abnormal giant, multinucleated cells located in lymph nodes – REED- STERNBERG CELLS – know this! - Occurs mostly in 15-35 years of age and above 50 – more common in men WHAT IS THIS REALLY? - Cause is unknown, factors include Epstein-Barr Virus, genetics and exposure to toxins - Incidence increase among HIV patients - Disease arise from one location and spread to adjacent lymphatic – FROM CERVICAL LYMPH NODES - Eventually infiltrates to other organs – LUNGS, SPLEEN, LIVER o Above diaphragm – remains confine to lymph node for variable time o Below diaphragm – frequently spread to extra lymphoid sites such as LIVER WHAT CAN WE SEE? - Onset of symptoms usually insidious – PAINLESS lymph nodes enlargement usually in the NECK o IF PAINLESS SWELLING IS >1 INCH AND LASTS >6 WEEKS – CALL PROVIDER - Initial development most often in cervical, axillary, or inguinal; mediastinal node mass is 2nd most common location - Patient may notice weight loss, fatigue, weakness, fever, chills, tachycardia and night sweats - 2 types of staging symptoms o STAGE A: Asymptomatic o STAGE B: Unexplained weight loss >10% in 6 months, FEVER, and night sweats - Further down the road – Hepatomegaly and splenomegaly DIAGNOSTIC AND STAGING STUDIES - Peripheral blood analysis, excisional lymph nodes biopsy and bone marrow examination - PET SCAN – can detect malignant tumor in cells in the body o A small amount of radioactive glucose injected into vein and then scanner rotates around the body taking pictures o More glucose is metabolized by malignant tumor cells than normal – will be brighter in the scan - COTSWOLD STAGING CLASSIFICATION: o STAGE I: CONFINED TO ONE NODE REGION OR LYMPHOID STRUCTURE o STAGE II: 2 OR MORE NODAL REGIONS/SAME SIDE OF DIAPHRAGM o STAGE III: LYMPHOID REGIONS ON BOTH SIDE OF DIAPHRAGM o STAGE IV: EXTRA NODAL SITES – LIVER, BONE MARROW - STAGING can be classified with STAGE A and B symptoms HOW DO WE TREAT THIS? Treatment depends on the stage of Hodgkin’s disease: SURVIAL RATE IS GOOD - Stage I & II: o Chemotherapy with/without radiation therapy o 95% - complete remission o 90 – 95% have 5 year survival & 20 years for 70-80& - Stage III & IV: o Chemotherapy o Partial remission o Follow up with radiation drugs o 90% have 5 year survival rate - Chemotherapy and radiation: LOOK AT OTHER SECTION - Drugs: o Standard chemotherapy is AVBD – ADRIAMYCIN, BLEOMYCIN, VINBLASTINE, DACARBAZINE o A common regimen is BE A COPP ▪ BLEOMYCIN, ETOPOSIDE, ADRIAMYCIN, CYCLOPHOSPHAMIDE, ONCOVIN, PROCARBAZINE, PREDNISONE ▪ Take the prednisone in the morning! COMPLICATIONS - Late effects: thyroid, heart and lungs and also increase risk for other cancers o May appear years later: important for them to have regular follow-ups - NEED TO MANAGE PANCYTOPENIA - Fertility issues: need to address this concern (sperm bank, or have another dude nail your wife?) NON-HODGKIN’S LYMPHOMA – MORE COMMON THAN HL - Heterogeneous group of malignant neoplasms of primarily B, T or natural killer cell origin affecting all ages - Two types: o Low-grade: indolent – SILENT o Intermediate and high grade – aggressive WHAT IS THIS REALLY? SAME THING AS HL EXCEPT: - Multiple possible virus and bacteria include: o HTLV-1, EBV, HPV, HEP B and C, H. PYLORI, and BIG BACTERIA NAMES probably not on exam – BET ON IT! - Environmental involves chemicals and air pollution - Inherited syndromes or chemotherapy drugs - Involves lymphocytes arrested in various stages of development and mimics leukemia - BURKITT’s LYMPHOMA – high aggressive disease from B-cell blasts in lymph nodes WHAT DO WE SEE? - NO PATTERN, UNPREDICTABLE , most common is PAINLESS lymph node enlargement - LYMPHADENOPATHY – related to obstruction - Can manifest into more complications: Airway obstruction, spinal cord compression, hyperuricemia, tumor lysis syndrome and pericardial tamponade - Also similar staging as HL DIAGNOSTIC STUDIES - Almost the same as HL (PET), but more studies o MRI to rule out CNS or bone marrow infiltration o Barium enema o Upper endoscopy o CT to suspect GI involvement - Prognosis for NHL is based on HISTOPATHOLOGY SO…WE DO THE SAME THING AS HL? - Involves chemotherapy and radiation therapy o Indolent lymphoma have naturally long course but are difficult to effectively treat – may live 10 years without treatment - Infection lymphomas may be treated with antibiotics or antiviral therapy - Drug: Rituximab o Monitor patient for signs of severe hypersensitivity infusion reactions, AFTER FIRST INFUSION o S/Sx: hypotension, bronchospasm, dysrhythmias, angioedema and cardiogenic shock o Screen patient for history of hepatitis - Complete remission uncommon – but majority respond with improvement of symptoms - Psychosocial considerations are important: o Help family understand the disease, treatment and expected side effects – encourage expression of feelings and relaxation techniques o Identify infections related to bone marrow suppression o Body image disturbance – advise wig use or long sleeve shirts to cover skin changes ▪ GOT TO GIVE THEM CONTROL – let them cut hair themselves o Reproductive issues – sperm banking CHEMOTHERAPY AND VESICANTS - Chemotherapy usually administered by IV, but major concern is EXTRAVASATION – infiltration of drugs into tissue surrounding infusion site causing local tissue damage o Irritant – will damage veins, causing phlebitis and sclerosis BUT REVERSIBLE o VESICANTS – infiltrated into the skin, causing NECROSIS LIST OF VESICANTS Akylating Agents Anthracyclines (DNA) Mitomycin C (DNA) Vinca Alkaloid (non- Taxanes (Non-DNA) (DNA) Doxorubicin DNA) Docetaxel Bendamustine Daunorubicin Vincristine Paclitaxel Mechorlethamine Epirubicin Vinblastine THE PATIENT IS ACTING UP! WHAT DO I DO?!! - Identify the signs and take immediate action o WHEN PATIENT SAYS – SHEEEEEIT!!! MY HAND IS BURNING!!!! o Pain, but sometimes no pain is indicated o Swelling, redness and vesicles on the skin o After few days, ulceration and necrosis o Complications – sepsis, scarring, contractures, joint pain and nerve loss - SO NOW WHAT? o STOP INFUSION IMMEDIATELY o ASPIRATE THE CHEMO AGENT – DO NOT REMOVE IV YET o DO NOT FLUSH THE LINE! – can buffer with sodium bicarbonate o Remove needle and apply compression – BUT DON’T APPLY TOO MUCH, CAN CAUSE MORE DAMAGE o Mark the extravasation site and monitor - USE OF HOT AND COLD COMPRESSION o HOT – vasodilation/Disperse - vinca alkaloids, Taxanes, NON-DNA DRUGS o COLD – Vasoconstriction/Localize – Anthracyclines, mitomycin C, DNA DRUGS - To minimize physical discomforts, infections, IV can be given by central venous access device HEPATITIS Inflammation of the liver - NOTE: HEP A and E – ORAL FECAL – AMERICAN EAGLE - NOTE: MUST HAVE HEP B to HAVE HEP D – USE THE BATHROOM TO TAKE A DUMP HEP A - RNA virus transmitted through ORAL-FECAL route - Caused by dirty foods or water, crowded situations, DAYCARES, or cooks who don’t wash hands - Can lead to acute liver failure - Can be transmitted by people who have undetectable subclinical infections o Greatest risk of transmission occurs before clinical symptoms are apparent o HAV found in feces 2 or more weeks before onset of symptoms and up to 1 week after onset of jaundice - HEP A IgM – INDICATES ACUTE HAV - HEP A IgG – INDICATES PAST INFECTION - WASH HANDS BEST MEASURE TO PREVENT OUTBREAK HEP B - DNA virus – INFECTED BLOOD OR BODY FLUIDS enters someone’s body who has no vaccination 5 o Perinatally by mothers with HBV o IV drugs, needles, or unprotected sex(gay sex is most common) o Kissing can spread HBV by saliva o No evidence that urine, non-GI bleeding stools, tears, breast milk can transmit HBV - HBV can live on dry surface for up to 7 DAYS! More infectious than HIV! - HBsAg INDICATES INFECTION - Anti-HBs INDICATES IMMUNITY HEP C - Can be both acute and chronic, can be asymptomatic and difficult to detect - MOST COMMON CAUSE – DRUG USE, GAY SEX FROM HIV + MEN o People at risk for HCV also at risk for HBV and HIV - 20-30% chance of developing cirrhosis and is the most common cause of chronic liver disease o NEED LIVER TRANSPLANT o NO VACCINATION HEP D - Defective single stranded RNA virus that cannot survive on its own – NEED HEP B TO REPLICATE - Transmitted percutaneously – can cause asymptomatic chronic carrier state to acute liver failure - ALSO NO VACCINE! HEP E - RNA virus – THE OTHER FECAL ORAL ONE - Can get it from dirty water – usually occurs in developing countries CLINICAL MANIFESTATIONS - ACUTE PHASE – 1 to 4 months o Incubation period: Malaise, anorexia, weight loss, fatigue, N/V, and RUQ discomfort o May find food repugnant/smokers might think cigarettes are disgusting? o PERIOD OF MAXIMAL INFECTIVITY - Acute phase maybe icteric (JAUNDICE) or anicteric o Yellow like The Simpsons – alteration in bilirubin metabolism or flow of bile o Urine may be dark – excess bilirubin being excreted o IF BILIRUBIN CAN’T FLOW OUT OF LIVER – POOP WILL BE LIGHT OR CLAY COLOR o Pruritis can occur with jaundice - Convalescent phase: Jaundice fades and lasts for 2 to 4 months o Malaise and easily fatigued o Hepatomegaly, but splenomegaly subsides COMPLICATIONS - Most with acute hepatitis recover completely, HOWEVER complications occur including acute liver failure, chronic hepatitis, and cancer o HEP A – viral relapse after 2-3 months o Disappearance of jaundice does not mean patient has recovered o Chronic HBV more likely to develop in infant born to infected mothers and those who acquire infection before 5 years old o HCV more likely to become chronic ▪ RISK FACTORS: DRINKING, MALE, HIGH CHOLESTEROL, OBESITY and DM DIAGNOSTIC STUDIES - DEFINITIVE WAY – testing patient’s blood for specific antigen or antibody - HVC testing – if antibody testing is positive: HCV RNA test for chronic infection o May be helpful for immunocompromised patients - VIRAL GENOTYPE TESTING – for HBV and HCV patients undergoing drug therapy - Physical assessment – palpate liver – one hand on right ribcage and the other pressing down GENTLY COLLABORATIVE CARE - Most patients can be managed at home: MAIN GOAL IS REST AND NUTRITION – promotes liver healing - AVOID ALCOHOL – STOP DRINKING DRUG THERAPY - No drug therapy for Hepatitis A - Treatment for Acute Hepatitis B – only patients with severe hepatitis and liver failure - Acute Hepatitis C – PEGYLATED INTERFERON WITHIN FIRST 12 to 24 WEEKS – decrease chance of becoming chronic - Chronic Hepatitis B o To decrease viral load and liver enzymes – slowing the rate of disease progression – PREVENT CIRRHOSIS, LIVER FAILURE and CANCER o FIRST LINE OF DRUG: INTERFERON AND NUCELOSIDE ▪ Interferon – blocks viral entry to cells, synthesizes the viral proteins • Standard: Intron A – short half life – given 3 time a week • Pegylated: Long-acting – subcut. 1 times a week – BETTER WITH LONG DOSE • Effect: reduction in HBV DNA levels, normalize ALT and loss of HBeAg = response to treatment depends on viral genotype • CBC and LFTs done every 4 to 6 weeks! ▪ Nucleoside and Nucleotide Analogs: • Tricks HBV into thinking they are normal building blocks for DNA; thus virus not able to reproduce • Medications: lamivudine (Epivir), adefovir (Hepsera), entecavir (Baraclude), telbivudine (Tyzeka), and tenofovir (Viread • BENEFICIAL for lowering vial dose, decreasing liver damage and decreasing enzymes • LFTs for several month after medication is stopped o Chronic Hepatitis C ▪ PEGYLATED INTERFERON WITH RIBAVIRIN (REBETOL, COPEGUS) • RIVAVIRIN: MAKE SURE THE PATIENT ISNT PREGNANT – HARMFUL TO NEONATES! ▪ Careful when giving HIV patients – can lower their CD4 counts – WATCH FOR ANEMIA AND LEUKOPENIA ▪ ALSO WATCH FOR MOOD CHANGES – DEPRESSION NUTRITIONAL THERAPY - No special diet – BUT ATI SAYS – LOW CARB, LOW FAT, LOW PROTEIN, FREQUENT MEALS – promotes healing - VITAMIN K if needed - If anorexia, N/V are severe – IV solutions of glucose HEALTH PROMOTION - CONTROL AND PREVENT - HEP A: o HAND WASHING – IMPORTANT – AFTER TAKING A DUMP o Vaccination is BEST PROTECTION – IM IN DELTOID – Booster 6-12 months after primary dose o Isolation NOT required – private room if patient has crazy poop or personal hygiene o IG effective in preventing if given within 2 weeks of exposure - Hepatitis B o Best way to reduce: SCREENING, AND VACCINATION o GOOD HYGEINE – don’t share razors, toothbrush or cucumbers, USE CONDOMS o VACCINE IS BEST PREVENTION: 3 IM injections ▪ First dose: within one month of birth ▪ Recommended for chronic kidney disease patients – keep their antibody titers for dialysis o Postexposure prophylaxis – HBIG ▪ Used incase of needle stick injuries, or sexual exposures for infant born to mothers who are positive HBsAG - Hepatitis C o NO VACCINES!!!!! Primary measure is screening of blood, organs and tissue donors o After exposure: have anti-HCV testing done, baseline ALT levels should be measures with follow-up 4-6 months o Testing HCV RNA – 4-6 weeks ACUTE INTERVENTIONS - ASSESS FOR JAUNDICE o Fair skin people: sclera of eye or skin o Dark skin people: hard palate of mouth, inner canthus of eues o Urine may be dark brown – bilirubin being pissed out - Ensure adequate nutrition o Small frequent meals, and give them what they enjoy o Avoid hot drinks and soda o FLUID – 2.5 to 3 L/day is important! AMBULATORY CARE - Assess knowledge of nutrition and provide teaching - Vital to teach them how to prevent transmission to others - Assess foe manifestation of complications: o Bleeding with increasing PT values, symptoms of encephalopathy, or elevated LFTs - AVOID ALCOHOL!!!!! - Adhere to medication regimen - Make sure patients with positive HBsAg or HCV antibodies can’t donate blood… LAB VALUES FOR LIVER FUNCTION - ATI VALUES TEST NORMAL VALUES ABNORMAL FINDINGS INDICATION OF WHAT? Alanine aminotransferase ALT 3 to 35 IU/L INCREASED Liver cell injury Aspartate aminotransferase AST 5 to 40 units/L INCREASED Liver cell injury Gamma glutamyl transpeptidase GGT 0 to 45 units/L INCREASED Liver cell injury Alkaline phosphatase 44 to 147 IU/L INCREASED Impaired excretory function of liver Gamma globulin 3 to 12% of total proteins INCREASED Impaired clearance from liver Serum albumin 3.5 to 5g/dL DECREASED Liver cell damage Serum bilirubin 0.1 to 1.0 mg/dL INCREASED Liver cell damage Serum protein 6 to 8 g/dL DECREASED Lack of hepatic synthesis Prothrombin 11 to 12.5 seconds PROLONGED Decreased PT production by liver Ammonia 11 to 32 umol/L INCREASED Cirrhosis HEPATITIS TITERS (PRESENT AND PAST INFECTIONS) HEPATITIS LETTERS PRESENT INFECTION PAST INFECTIONS HEP A Anti-HAV IgM – ACUTE INFECTION Anti-HAV IgG – PREVIOUS INFECTION or immunization HEP B HBsAg – in acute or chronic infection, + in chronic carriers HBeAg – HIGH INFECTIVITY Anti-HBc IgM – ACUTE – blank after vaccination Anti-HBc IgG – ONGOING or PAST HBV DNA quanitation – active ongoing viral replication, indicates the effectiveness of therapy Anti-HBs – previous or immunization – MARKER OF POSITIVE RESPONSE TO VACCINATION! Anti-HBe – low viral load or infectivity in chronic HBV Anti-HBc IgG – Previous infection HEP C Anti-HCV – acute/chronic infection HCV RNA quantitation – active ongoing viral replication HEP D Anti-HDV – PRESENT/PAST HDV Ag – present within few days of infection Anti-HVD HEP E Anti-HEV igM and IgG – 1 week to 2 months after illness onset HEV RNA quantitation – active ongoing viral replication HIV/AIDS A retrovirus that causes immunosuppression - Can be transmitted: o UNPROTECTED Sexual activity with infected partner – blood, semen, vaginal secretions – GAY MEN SEX AT MOST RISK! o CONTACT WITH BLOOD PRODUCTS – NEEDLE SHARING, JUNKIES, BLOOD BROTHERS, VAMPIRES ▪ Puncture wound most common in work related HIV – AS AN RN – WE WASH WITH SOAP WITH WATER AND QUICKLY REPORT TO SUPERVISOR TO EMPLOYEE HEALTH • Given antivirals as option and stay on pills on 9 months until cleared -3 months each test o Perinatal transmissions - can be infected during pregnancy, deliver or breastfeeding - Variables that influence whether infection will establish after an exposure includes: o Duration and frequency of contact with organism o Volume, virulence, and concentration of organism o Host immune status ANYWAY, WHAT IS HIV? - It is an RNA virus – reverse transcriptase – killing off CD4+ T cells - Clinical symptoms may not appear for a long time – can go 10 years with no symptoms - NORMAL CD4 COUNT – 800-1200 o Normal lifespan if CD4 is 100 days, but in HIV it dies in 2 DAYS - Immune problems starts when it drops below 500 - <200 would indicate AIDS WHAT DO WE SEE? Important to remember that disease progression is highly individualized so the prognosis is unpredictable - ACUTE INFECTIONS: o Fever, SWOLLEN LYMPH NODES, sore throat, headache, malaise, nausea, muscle and joint pain, diarrhea or rash(SEROCONVERSION) o Neurologic complications – aseptic meningitis, peripheral neuropathy, facial palsy, Guillian-Barre syndrome o Can be mistaken sometimes as a bad flu - CHRONIC HIV INFECTIONS: o Often asymptomatic – CD4 remains about 500 ▪ Fatigue, headache, low grade fever, night sweats and lympadenopathy ▪ Patient might not be aware they are infected o Symptomatic infection: CD4 drops around 200-500 ▪ Persistent fever, frequent night sweats, chronic diarrhea, recurrent headaches, fatigue ▪ MOST COMMON – ORAL CANDIDIASIS or THRUSH ▪ Other infection include: shingles, vaginal candida infection, herpes, Kaposi sarcoma ▪ Oral hairy leukoplakia – painless, white, raised lesions on tongue AIDS - <200 CD4 count - Organisms that do not cause severe diseases in normal people can cause debilitating, disseminated and life threatening infections during this stage DIAGNOSTIC STUDIES - Test for HIV antibodies or antigen in blood – oral or blood specimen o Can take several week after the infection before antibody can be detected on screen test – WINDOW PERIOD - Rapid HIV antibody can be done in office and results in 20 minutes o Can also be done at home - A positive test should be followed by WESTERN BLOT test o EIA positive – REPEAT, if positive again, WESTERN BLOT - Lab tests measures viral levels and provides an assessment of disease progression o If undetectable – does not mean virus has been eliminated – can still transmit HIV to others - Two types of resistance test can be determines if patient’s HIV is resistant to ART therapy o Genotype assay detects drug resistant viral mutation that are present in reverse transcriptase and protease genes o Phenotype assay measure the growth of HIV in various concentration of antiretroviral drugs HOW DO WE CARE FOR THIS TYPE OF PATIENT? Collaborative care focuses on: - Monitoring HIV disease progression and immune function - Initiating and monitoring ART - Preventing the development of opportunistic diseases - Detecting and treating opportunistic diseases - Managing symptoms - Preventing or decreasing complications of treatment - Preventing further transmission of HIV Initial patient visit provide opportunity to gather baseline data to start establishing rapport - Remember: Newly diagnosed people won’t listen – MUST BE CLEAR DRUG THERAPY - Goal is to: o Decrease viral load, maintain or increase CD4 count, prevent HIV related symptoms and opportunistic diseases, delay diseas progression and prevent HIV transmission - Antiretroviral therapy – HIV CAN’T BE CURE , but ART can delay disease progression by deceasing viral replication o Major advantage of using different classes of drugs – can inhibit viral replication making it difficult for virus to recover and decreasing likelihood of drug resistance o Drugs has LETHAL INTERACTION with OTC drugs and herbs – ST. JOHN WORTs - SUSTIVA!!!!!! o Don’t use in pregnant ladies, large does can be fatal to babies o Once a day dose should be taken at bed time to cope with side effects – dizziness and confusion o Common to have bizarre dreams - Drug therapy for opportunistic diseases: o Prophylactic medicines can significantly decrease morbidity and mortality rate - Preventing transmission of HIV o Preexposure prophylaxis (PrEP) – reduce risk of sexually acquired HIV in adults at high risk ▪ Safe sex practice, risk reduction counseling and regular HIV testing o Emtricitabine and tenofovir can be used for PrEP ▪ Truvada is the first drug approved to reduce the risk of HIV infection in uninfected individual who are at high risk of HIV infection and who may engage in sexual activity with HIV infected partners ▪ Truvada is currently used in combination with other antiretroviral agents for the treatment of HIV-infected people. NURSING MANAGEMENT - Assessment: o Identify behaviors for people at risk o Basic questions you can ask: ▪ Have you ever had a blood transfusion or used clotting factor? ▪ Have you ever shared needles with another person ▪ Have you ever had sexual experience in which your sexual organs touched other person’s sexual organs? ▪ Have you ever had a sexually transmitted infection? NURSING IMPLEMENTATION Health promotion: - PREVENTION IS ONLY WAY TO CONTROL EPIDEMIC - Encourage early detection and if primary prevention has failed, early intervention initiated - Prevention of HIV Infection: o Goal is to develop safer, healthier and less risky behavior - condoms and decreasing number of sex partners - Decreasing risk related to sexual intercourse: o Abstinence is the most effective way – listened by no one ever o Limiting sexual behaviors which the penis, mouth, vagina, or ass does not come into contact with partner’s same organs – eliminates contact with blood, semen or secretions o Safe activities – Masturbation, mutual masturbation – “hand job” – whoever wrote this in the textbook must be laughing his/her ass off. o USE CONDOM – PROMOTE IT – EXPENSIVE? THERE ARE FREE ONES! - Decreasing risk related to drug use: o Alcohol and tobacco is harmful – again listened by no one ever ▪ Can cause immunosuppression, poor nutrition and mental problems ▪ Major risk is sharing needles, not the drug itself o Basic risk reduction includes: ▪ DO NOT DO DRUGS ▪ IF DOING DRUGS, DON’T SHARE NEEDLES ▪ Do not have sex while on drugs o Safest way: DON’T DO DRUGS, but if you REALLY NEED TO – sterile equipment… - Decreasing risk of perinatal transmission: o Best way to prevention infection in infants is to prevent HIV infection in women o Ask them about their reproductive desires o Optimal ART therapy and counseling helps - Decreasing Risk at work: o Should exposure occur, PrEP with combination of ART can significantly decrease the risk of infection o Need for timely treatment and counseling make it even more critical for nurses to report all blood exposures – REPORT TO SUPERVISOR ASAP!!! - HIV testing: o Many people don’t know that they are infected o CDC recommends, universal, voluntary testing for all ages 13- 64 regardless of status o Goal: normalize the test and decrease new case of infection o ALSO, it is a crime not to tell your partners that you are infected with HIV ACUTE INTERVENTION - Early detection of symptoms, opportunist diseases and mental problems - Initial response to diagnosis of HIV: o Anxiety, fear, depression, denial, hopelessness, anger and guild - Antiretroviral Therapy: o ART can significantly slow clinical progression of HIV. However, this is very expensive and can cause problems with adherence to treatment. o Interventions include teaching about: ▪ Advantages and disadvantages of new treatment ▪ Dangers of poor adherence to therapeutic regimens ▪ How and when to take each drug ▪ Drug interactions to avoid ▪ Side effects that must be reported to health care provider o Issues to consider when selecting an initial drug regimen: ability of patient’s HIV to resist specific drug, potential medication side effects, existing co-morbidities and dosing schedule ▪ Critical because first treatment regimen is generally the patient’s best chance for success ▪ Most important is patient readiness ▪ Adherence to ART is critical component of successful drug therapy for people with HIV infection • MISSING ONE DOES CAN LEAD TO DRUG RESISTANCE!!!!! • Need reminders, beepers, timer pillboxes and calendar • IF MISS FOR ANY REASON, REPORT TO PCP 13 o Group support and individual counseling can help – best approach to learn about patient’s life and assist with problem solving related to taking medication within the confines of life. - Delaying Disease Progression o Useful interventions for delaying HIV ▪ Getting nutritional support to maintain lean body mass and ensure appropriate levels of vitamins and micronutrients – MILKSHAKE? ▪ Moderating or eliminating alcohol, tobacco and drugs ▪ Keeping up to date with recommended vaccines ▪ Getting adequate rest and exercise ▪ Avoiding exposure to new infectious agents ▪ Accessing mental health counseling ▪ Getting involved in support groups and community activities ▪ Developing a consistent relationship with healthcare providers, including attendance at regular appointment o Teach patient to recognize signs and symptoms that may indicate disease progression or drug side effects (CHART ABOVE) - Acute Exacerbations o Best way to prevent opportunistic disease is to ensure that patient is adhering to effective ART regimen, and taking prophylactic medications ▪ If a person has PNEOMOCYSTIS PNEUMONIA (PCP), nursing intervention can ensure adequate oxygenation ▪ If the patient has crytococcal meningitis, an important nursing concern is maintaining a safe environment for a confused patient AMBULATORY AND HOME CARE - Many cases HIV leads to death because of no cure - Affects the entire range of person’s life from physical health to social, emotional, economic, and spiritual well being - Stigma of HIV o HIV infected patients share problems experienced by all individuals with chronic diseases, but these problems are exacerbated by negative social constructs surrounding HIV o Some people may believe they brought HIV upon themselves, immoral (homosexuality), or illegal (drug use) o There is constant fear that HIV may spread to other people o HIV stigma is a global problem often more severe for women o Discrimination can lead to social isolation, dependence, frustration, low self image, loss of control, and economic pressures - Disease and Drug Side effects: o Patients on ART for a long time can develop metabolic disorders that changes their body shape because of lipodystrophy, hyperlipidemia, insulin resistance and hyperglycemia, osteoporosis, lactic acidosis and renal and cardiovascular diseases o Management: early detection, dealing with symptoms, and helping with patients cope with emerging problems and change to treatment regimens - End of Life Care o Keep patient comfortable, facilitating emotional and spiritual acceptance of finite nature of life, helping patients significant other deal with loss and maintaining a safe environment GERENTOLOGICAL CONSIDERATIONS - HIV on the rise – need to assess them carefully because they might be too ashamed to admit infection CUSHING SYNDROME Results from chronic exposure to excess corticosteroids, particularly glucocorticoids CAUSES - iatrogenic administration of exogenous corticosteroids e.g. prednisone - ACTH-secreting pituitary adenoma (Cushing disease) - adrenal tumors - ectopic ACTH production by tumors (usually of the lung or pancreas) Cushing disease and primary adrenal tumors are more common in women between 20s and 40s Ectopic ACTH production is more common in men MANIFESTATIONS - accumulation of adipose tissue in the trunk, face, and cervical spine area  weight gain - cortisol-induced insulin resistance and gluconeogenesis by the liver  hyperglycemia - muscle wasting  muscle weakness - loss of bone matrix  osteoporosis, back pain - loss of collagen  weak and thin skin, easily bruised - catabolic processes  delay in wound healing - mineralocorticoid excess  HTN - adrenal androgen excess  severe acne, virilization in women, feminization in men - first indication of Cushing syndrome may be truncal or generalized obesity, moon face w/ facial plethora, purplish red striae, hirsutism and menstrual disorders in women, HTN, and unexplained hypokalemia DIAGNOSTIC - plasma cortisol levels may be ↑ w/ loss of diurnal variation - collect a 24-hr urine collection for free cortisol - urine cortisol > 80 to 120 mcg/24 hr = Cushing syndrome - if results are borderline  low-dose dexamethasone suppression test - false-positive results can occur in pts with depression and those taking certain meds, including phenytoin, rifampicin - urine levels of 17-ketosteroids may be ↑ - high or normal ACTH levels = Cushing disease - low or undetectable ACTH levels = adrenal or med etiology COLLABORATIVE CARE - if cause is pituitary adenoma  surgical removal of pituitary tumor using the transphenoidal approach or radiation - if adrenal tumors or hyperplasia  adrenalectomy (laparascopic if benign, open surgery if cancer) - if poor candidate for surgery  drugs - ketoconazole (Nizoral), aminoglutethimide (Cytadren), mitotane (Lysodren) o often toxic at the dosages needed to ↓ cortisol secretion - hydrocortisone or prednisone o may be needed to avoid adrenal insufficiency - mifepristone (Korlym) o may be used to control hyperglycemia in pts w/ DM-2 - if cause is corticosteroid therapy  o gradual discontinuance of CS therapy o or reduction of CS dose o or conversion to alternate-day regimen ▪ twice the daily dosage of a shorter-acting CS every other morning NURSING MANAGEMENT - focus on s/sx of hormone and drug toxicity and complicating conditions e.g. CV disease, DM, infection - assess and monitor VS, daily weight, glucose, and possible infection - s/sx of inflammation may be minimal or absent - monitor s/sx of abnormal thromboembolic events such as PE - emotional support - Preoperative care o pt should be brought to optimal physical condition o preop teaching - Postoperative care o adrenal glands are vascular  high risk of hemorrhage o may have NG tube, urinary catheter, IV catheter, CVP monitoring, and leg sequential compression devices to prevent emboli o manipulation of glandular tissue during surgery may release large amts of hormones into the circulation  marked fluctuations in the metabolic processes  unstable BP, fluid balance and electrolyte levels o high doses of CS e.g. hydrocortisone are administered IV during surgery and for several days afterward to ensure adequate responses to the stress of the procedure  ↑ susceptibility to infection and delay wound healing o large amts of endogenous hormones in circulation  HTN, ↑ risk of hemorrhage o critical period for circulatory instability ranges from 24 to 48 hrs postop o keep IV line open for quick admin of CS or vasopressors o obtain AM urine samples (at the same time each AM) for cortisol measurement to evaluate surgery’s effectiveness o tapering CS too rapidly  acute adrenal insufficiency  hypocortisolism (vomiting, ↑ weakness, dehydration, hypotension), painful joints, pruritus, peeling skin, severe emotional disturbances o after surgery, pt is usually maintained on bed rest until BP stabilizes o prevent infection AMBULATORY & HOME CARE - consider home health nurse referral - wear Medic Alert bracelet at all times and carry medical identification and instructions - avoid exposure to extreme temperatures, infections, and emotional disturbances - teach pt to adjust their CS replacement therapy in accordance w/ their stress level - many pts require lifetime replacement therapy - prepare pt to take several months to adjust the hormone dose satisfactorily ADDISON’S DISEASE ETIOLOGY & PATHO - causes adrenocortical insufficiency (hypofunction of the adrenal cortex) - ↓ glucocorticoids, mineralocorticoids, and androgens - most common cause is autoimmune (most common in white females) - adrenal tissue is destroyed by antibodies against the pt’s own adrenal cortex - other causes: o infarction o fungal infections e.g. histoplasmosis o AIDS o metastatic cancer o iatrogenic may be due to adrenal hemorrhage - adrenal insufficiency most often occurs in adults < 60 yrs MANIFESTATIONS - evident when adrenal cortex is 90% destroyed - insidious onset - progressive weakness - fatigue - weight loss - anorexia - ↑ ACTH  bronze-colored skin hyperpigmentation – primarily seen in sun-exposed areas, pressure points, over joints, and in the creases, esp palmar creases - orthostatic hypotension - hyponatremia - salt craving - hyperkalemia - N/V/D - irritability, depression – primary adrenal hypofunction COMPLICATIONS - Addisonian crisis o acute adrenal insufficiency o triggered by: ▪ stress e.g. infection, surgery, psychologic distress ▪ sudden withdrawal of corticosteroid hormone therapy ▪ adrenal surgery ▪ sudden pituitary gland destruction o severe manifestations of glucocorticoid and mineralocorticoid deficiencies includeing hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, confusion o hypotension may lead to shock o circulatory collapse associated with adrenal insufficiency is often unresponsive to usual tx (vasopressors and fluid replacement) o GI manifestations: severe vomiting, diarrhea, and pain abdomen o pain may occur in lower back or legs DIAGNOSTICS - depressed serum and urinary cortisol levels - ↓ urine level of aldosterone - ACTH ↑ in primary adrenal insufficiency and ↓ in secondary disease - primary disease if cortisol levels fail to rise over basal levels with an ACTH stimulation test - secondary disease if a positive response to ACTH stimulation test indicates a functioning adrenal gland - ↑ K, BUN - ↓ Cl, Na, glucose - anemia - ECG may show low voltage and peaked T waves caused by hyperkalemia - CT and MRI scans to identify other causes e.g. tumor, fungal infections, TB, or adrenal calcification COLLABORATIVE CARE - hormone therapy o glucocorticoid ▪ hydrocortisone – has both glucocorticoid and mineralocorticoid properties ▪ during stressful situations, ↑ dose to prevent addisonian crisis ▪ dosage is given 2/3 in the morning and 1/3 in the afternoon o mineralocorticoid ▪ fludrocortisone (Florinef) daily, preferably AM (reflect normal circadian rhythm and ↓ side effects) - ↑ salt in diet - Addisonian crisis o shock management o high-dose hydrocortisone replacement o large volumes of 0.9% saline and 5% dextrose NURSING MANAGEMENT - if pt is hospital o monitor and correct fluid & electrolyte balance o assess VS and signs of fluid volume deficit o monitor serum glucose, Na, K o establish baseline data for mental status, VS, and weight o obtain a complete med hx to determine potential interactions (oral hypoglycemic, cardiac glycosides, oral contraceptives, anticoagulants, NSAIDs) o note s/sx of Cushing syndrome (changes in BP, weight gain, weakness, etc) o protect against infection o assist w/ daily hygiene o protect from noise, light, and env’t temp extremes AMBULATORY & HOME CARE - stress management - teach s/sx of corticosteroid deficiency and excess (Cushing syndrome) and to report to MD to adjust dose - wear Medic Alert and carry a wallet card stating the pt has Addison’s - meds that cause a need to ↑ glucocorticoid dose – phenytoin, barbiturates, rifampin, antacids, etc - meds that cause a need to ↓ glucocorticoid dose – estrogen, etc - carry emergency kit that contains 100 mg of IM hydrocortisone, syringes, and instructions for use TRANSPHENOIDAL HYPOPHYSECTOMY - offers the best chance for a cure - surgery produces an immediate reduction in GH levels followed by a drop in IGF-1 levels w/in a few weeks - when the entire pituitary gland is removed  permanent loss of all pituitary hormones - replace with essential hormones instead (glucocorticoids, thyroid hormone, and sex hormones) - hormonal therapy for life - large tumors or if GH > 45 ng/mL  adjuvant radiation or drug therapy - can treat Cushing syndrome that is caused by pituitary adenoma - Surgical removal of the hypophysis (pituitary gland) – best option for a cure for small adenomas - POST-SURGERY EDUCATION! o Elevating HOB 30 degrees – decreases headaches and pressure on sella turcica o Monitor pulillary response, speech patterns and extremity strength – detect neurologic complications o MOUTH CARE Q4H o AVOID BRUSHING TEETH FOR 10 DAYS – PROTECT SUTURE LINES o Observe for any signs of bleeding o AVOID HARD COUGHING OR SNEEZING OR POOPING TOO HARD – prevent CFS leakage ▪ CLEAR nasal drainage need to be tested for glucose - >30mg/dL INDICATES CSF LEAKAGE! IS AT RISK FOR MENINGITIS o BUT! CSF leakage usually resolves within 72 hours when head elevated and bed rest. o CHECK URINE OUTPUT! PHEOCROMOCYTOMA A rare condition caused by a tumor in the adrenal medulla affecting the chromaffin cells  excess production of catecholamines (epinephrine, norepinephrine) MANIFESTATIONS - most dangerous immediate effect is severe hypertension o if left untreated, may lead to hypertensive encephalopathy, DM, cardiomyopathy, and death - most common in young to middle-aged adults - may be inherited in persons with multiple endocrine neoplasia - severe, episodic HTN accompanied by classic manifestations of severe, pounding headache; tachycardia with palpitations, profuse sweating, and unexplained abdominal or chest pain - attacks may be provoked by many meds, including antihypertensives, opioids, radiologic contrast media, and TCA – attacks may last from a few mins to several hrs DIAGNOSIS - is often missed - uncommon cause of HTN - the simplest and most reliable test is measurement of urinary fractionated metanephrines (catecholamine metabolites) and fractionated catecholamines and Cr – usually done as a 24-hr urine collection o values are elevated in 95% of the pts - serum catecholamines may be elevated during an attack - CT scans and MRI to diagnose for tumors - avoid palpating abdomen of pt suspected with pheochromocytoma as this may cause sudden release of catecholamines and severe HTN! TREATMENT & NURSING MANAGEMENT - primary tx is surgical removal of the tumor - give α and β-adrenergic receptor blockers preop to control BP and prevent intraoperative hypertensive crisis - α-adrenergic receptor blocker (phenoxybenzamine [Dibenzyline]) is given 7 to 10 days preop to ↓ BP and alleviate other sc of catecholamine excess - then, β-adrenergic blockers (e.g. propranolol) are used to ↓ tachycardia and other dysrhythmias o if β blockers are started too early, unopposed α-adrenergic stimulation could precipitate hypertensive crisis - they can cause orthostatic hypotension - surgery is usually done laparoscopically - alternative option is giving metyrosine (Demser) to ↓ catecholamine production by the tumor o adverse effect is orthostatic hypotension - identify classic triad of sx: severe pounding headache, tachycardia, and profuse sweating - pt need rest, nourishing food, and emotional support - HTN may persist even after tumor removal BRAIN ATTACK (look at Hauck’s outline) - PREVENTIVE DRUG THERAPY - antiplatelet drugs for pts who have had a TIA: o Aspirin (81 to 325 mg/day) o ticlopidine (Ticlid) o clopidogrel (Plavix) o dipyridamole (Persantine) o combined dipyridamole and aspirin (Aggrenox) - statins for pts w/ hx of TIA - anticoagulants for pts who have A Fib: o warfarin o rivaorxaan (Xarelto) o dabigatran etexilate (Pradaxa) ACUTE CARE FOR ISCHEMIC STROKE - Most important is the time of onset of symptoms!!! - Goals: preserving life, preventing further brain damage, reducing disability - Acute care begins with ABC - Need baseline neurologic assessment - ~25% of pts worsen in the first 24 to 48 hrs - ↑ BP is common immediately after a stroke and may be a protective response to maintain cerebral perfusion – but it can be detrimental! o ↓ BP if markedly increased (systolic BP > 220 or diastolic > 120) and if pt is NOT on fibrinolytic therapy o if pt IS on fibrinolytic therapy, then BP needs to be < 185/110 and then maintained at or below 180/105 for at least 24 hrs after fibrinolytic therapy o IV antihypertensives such as labetalol and nicardipine are preferred - Correct hypotension and hypovolemia if present, but unlikely - Control fluid and electrolyte balance carefully o keep pt adequately hydrated via IV, oral, or tube feeding to promote perfusion – priority! o overhydration may increase cerebral edema o monitor urine output to prevent dehydration - if ADH ↑  urine ouput ↓ and fluid is retained  hyponatremia - AVOID IV solutions of glucose and water b/c they are hypotonic and may further ↑ cerebral edema and ICP o prevent hyperglycemia - ↑ ICP o more likely with hemorrhagic stroke o usually peaks in 72 hrs and may cause brain herniation o prevent by elevating HOB, maintaining head alignment, and avoiding hip flexion, managing hyperthermia, drug therapy to prevent seizures, pain management, avoidance of hypervolemia, and management of constipation o drain CSF DRUG THERAPY FOR ISCHEMIC STROKE Recombinant tissue plasminogen activator (tPA) - produce localized fibrinolysis by binding to the fibrin in the thrombi - other fibrinolytic agents CANNOT be substituted for tPA - administered IV to reestablish blood flow thru a blocked artery to prevent cell death in pts with acute onset of ischemic stroke - must be administered within 3 to 4 ½ hrs of onset of clinical signs of ischemic stroke - Screening: o noncontrast CT or MRI scan to rule out hemorrhagic stroke o blood tests for glucose level and coagulation disorders o recent hx of GI bleeding, stroke, or head trauma w/in the past 3 months, or surgery w/in 14 days - insert a urinary catheter, NG tube, and multiple IVs before tPA administration - during infusion, closely monitor VS and neurologic status - control of BP is critical during tx and for 24 hrs following!!!! - intraarterial infusion of tPA o can be administered up to 6 hrs after onset of stroke sx o neurovascular specialist inserts a thin, flexible catheter into an artery (usually femoral artery) and guides to area of clot by angiogram o tPA is administered thru catheter and immediately targets the clot o less tPA is needed Anticoagulants generally NOT recommended after an ischemic stroke due to risk for intracranial hemorrhage - anticoagulants and platelet inhibitors can be used if pt is stabilized and stroke is caused by thrombi and emboli - platelet inhibitors = aspirin, ticlopidine, clopidogrel, dipyridamole - for pts with A fib – warfarin, rivaroxaban, and dabigatran etexilate Asprin 325 mg may be initiated within 24 to 48 hrs after onset of ischemic stroke – beware of hx of PUD Statins SURGICAL THERAPY FOR ISCHEMIC STROKE - stent retrievers e.g. Solitaire FR, Trevo - mechanical embolus removal in cerebral ischemia (MERCI) retriever ACUTE CARE FOR HEMORRHAGIC STROKE Drug Therapy - anticoagulants and antiplatelet inhibitors are CONTRAINDICATED - main drug therapy is management of HTN with oral or IV agents to maintain normal BP - seizure prophylaxis in acute period after intracerebral and subarachnoid hemorrhage is situation specific Surgical Therapy - immediate evacuation of aneurysm-induced hematomas or cerebellar hematomas larger than 3 cm - if arteriovenous malformation (AVM) ruptures  tx with surgical resection and/or radiosurgery - tx aneurysms by clipping or coiling to prevent rebleeding NURSING INTERVENTIONS Respiratory - risk of aspiration pneumonia is high b/c of impaired consciousness or dysphagia - dysphagia after stroke is common - airway obstruction from chewing and swallowing, food pocketing, and tongue falling back - may require ET intubation or mechanical ventilation initially o oral care at least q 2 hr to reduce risk of ventilator-assisted pneumonia - enteral tube feedings place pt at risk for aspiration pneumonia - screen all pts for ability to swallow and keep NPO until dysphagia is ruled out 1) frequently assess airway patency and function, 2) provide oxygenation, 3) suction, 4) promote pt mobility, 5) position pt to prevent aspiration, and encourage deep breathing Neurologic - National Institutes of Health Stroke Scale (NIHSS) – measures stroke severity, predictor of short- and long-term outcomes of stroke pts - closely monitor VS - neurologic assessment - ↓ LOC may indicate ↑ ICP Cardiovascular - Aimed at maintaining homeostasis - Cardiac efficiency may be further compromised by fluid retention, overhydration, dehydration, or BP variations - CVP, PAP, or hemodynamic monitoring may be used as indicatiors of fluid balalnce or cardiac function in the CCU 1) Monitor VS frequently, 2) monitor cardiac rhythms, 3) calculate I&O and noting imbalances, 4) regulate IV infusions, 5) adjust fluid intake to individual needs, 6) monitor lung sounds for crackles and rhonchi indicating pulmonary congestion, 7) monitor heart sounds for murmurs or for S3 or S4 - monitor for orthostatic hypotension before ambulating pt for the first time - pt is at risk for VTE – keep pt moving! – assess for signs of VTE Musculoskeletal - prevent joint contractures and muscular atrophy - ROM and positioning - special attention to paralyzed or weak side 1) trochanter roll at the hip to prevent external rotation, 2) hand cones (not rolled washcloths) to prevent hand contractures 3) arm supports with slings and lap boards to prevent shoulder displacement 4) avoidance of pulling the pt by arm to avoid shoulder displacement 5) posterior leg splints, footboards, or high-top tennis shoes to prevent foot-drop 6) hand splints to reduce spasticity Integumentary 1) pressure relief by position changes, special mattresses, or wheelchair cushions o side-backside q 2 hr o positon on weak/paralyzed side for only 30 mins o epidermis and dermis are damaged if redness does not go away for 15 mins o do not massage damage area o pillows under lower extremities 2) good skin hygiene 3) emollients applied to dry skin 4) early mobility Gastrointestinal - most common problem is constipation - may need bowel retraining Urinary - poor bladder control  incontinence - promote normal bladder function and avoid indwelling catheters o long term use is associated with CAUTI - avoid bladder overdistention - bladder retraining program: o adequate fluid intake with most of it given between 7 AM and 7 PM o scheduled toileting q 2 hrs using bedpan, commode, or bathroom while encouraging usual position for urinating o observe for signs of restlessness, which may indicate need for urination o assessment for bladder distention by palpation - ultrasound measures how much urine is in bladder after voiding – incomplete emptying may cause UTI Nutrition - assess for gag reflex before feeding o usually speech therapist or occupational therapist is the one responsible to create exercises to stimulate swallowing - severe impairment may require enteral or parenteral nutrition support - mouth care before feeding helps stimulate sensory awareness and salivation and can facilitate swallowing - remain in high Fowler’s position for feeding and for 30 mins afterward - foods should be easy to swallow and provide enough texture, temperature, and flavor to stimulate swallow reflex - crushed ice can be a stimulant - pureed foods not recommended - thin liquids are difficult to swallow and may promote coughing - avoid milk products - PEG tube if inadequate oral diet or dysphagia persists - promote self-feeding Communication - support psychological needs - assess ability to speak and to understand - use gestures to support verbal cues - collaborate with speech therapist to assess Sensory-Perceptual Alterations - Right side stroke pt o high risk for injury due to mobility difficulties o verbal directions o break task down into simple steps o environmental control o provide nonslip socks o assist or remind pt to dress weak or paralyzed side or shave forgotten side of the face (one-sided neglect) - Left side stroke pt o nonverbal cues and instructions are helpful for comprehension - homonymous hemianopsia (blindness in the same half of each visual field) o initially, arrange environment within pt’s perceptual field o later, let pt learn to compensate - safety measures such as closely observing pt, elevate side rails, lower height of the bed, using video monitors - use eye patch if diplopia - if corneal reflex is absent, observe closely and protect against eye injuries – artificial tears or gel, eye shield at night - ptosis is generally not treated b/c it does not inhibit vision Coping - provide information and emotional support AMBULATORY AND HOME CARE - critical factor in discharge planning is the pt’s level of independence in performing ADLs - prepare pt and caregiver for discharge thru teaching, demonstration and return demonstration, practice, and evaluation of self-care skills - plan follow-up care - identify community resources to provide recreational activities, group support, spiritual assistance, respite care, adult day care, and home assistance based on needs Rehabilitation - goal: maximize pt’s abilities - most pts see maximum benefit in the 1st yr of recovery after a stroke - physical therapy focuses on mobility, progressive ambulation, transfer techniques, and equipment needed for mobility - occupational therapy emphasizes retraining for skills of daily living such as eating, dressing, hygiene, and cooking – occupational therapists are skilled in cognitive and perceptual evaluation and training - speech therapy focuses on speech, communication, cognition, and eating abilities Musculoskeletal function - most pts begin to show signs of spasticity with exaggerated reflexes within 48 hrs after the stroke – denotes progress toward recovery - as improvement continues, small voluntary movements of the hip or shoulder may be accompanied by involuntary movements in the rest of the extremity (synergy) - the final stage of recovery occurs when pt has voluntary control of isolated muscle groups - balance training - assess whether pt autocorrect their posture when sitting on edge of bed - Bobath method – help pt gain control over patterns of spasticity by inhibiting abnormal reflex patterns - constraint-induced movement therapy (CIMT) – encourages pt to use weakened extremity by restricting movement of normal extremity - supportive or assistive equipment Stroke Survivorship & Coping - often exhibit emotional responses inappropriate or atypical for the situation 1) distract pt who suddenly becomes emotional 2) explain to the pt and family that emotional outbursts may occur after a stroke 3) maintain a calm env’t 4) avoid shaming or scolding pt during emotional outbursts Sexual Function - teach about optional positioning of partners, timing for peak energy times, and pt and partner counseling ACUTE RENAL FAILURE - Prerenal causes: - factors that ↓ systemic circulation  ↓ glomerular perfusion and filtration of the kidneys (tubular and glomerular function is preserved) - in prerenal oliguria, there is no damage to the kidney tissue (parenchyma) – different from intrarenal oliguria - oliguria is caused by ↓ circulating blood volume - prerenal conditions can lead to intrarenal disease if renal ischemia is prolonged Intrarenal causes: - include conditions that cause direct damage to the parenchyma, resulting in impaired nephron function - damage usually results from prolonged ischemia, nephrotoxins (e.g. AG antibiotics, contrast media), hgb released from hemolyzed RBCs, or myoglobin released from necrotic muscle cells - nephrotoxins  obstruction of intrarenal structures by crystallizing or by causing damage to the epithelial cells of tubules - hgb and myoglobin can block tubules and cause renal vasoconstriction - Acute tubular necrosis (ATN) – most common intrarenal cause of AKI and is primarily result of ischemia, nephrotoxins, or sepsis o potentially reversible if the basement membrane is not destroyed and the tubular epithelium regenerates o most common cause of AKI for hospitalized pts Postrenal causes: - involve mechanical obstruction in the outflow of urine  urine refluxes into the renal pelvis  impairing kidney function - bilateral ureteral obstruction  hydrohephrosis (kidney dilation), ↑ in hydrostatic pressure, and tubular blockage  progressive decline in kidney function o if relieved w/in 48 hrs of onset, complete recovery is likely o after 12 weeks, recovery is unlikely - prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis MANIFESTATIONS - AKI has a prolonged course when parenchymal is damage - prerenal and postrenal AKI that has not caused intrarenal damage usually resolves quickly with tx of the cause - when pt does not recover from AKI  CKD - RIFLE classification is used to describe the stages of AKI (Table 47-3) - AKI may progress thru phases: o oliguric phase – most common manifestations: ▪ urinary changes • oliguria – reduction in urine output to < 400mL/day – occurs within 1 to 7 days of the injury to kidneys • if cause is ischemia, often occurs within 24 hrs • if nephrotoxic drugs are involved, onset may be delayed for as long as 1 wk • nonoliguria > 400 mL/day – about 50% of pts (makes initial diagnosis difficult) • lasts on average 10 to 14 days but can last months in some casese • the longer the oliguric phase lasts, the poorer the prognosis for complete recovery • changes in urine output generally do not correspond to changes in GFR – however, can be helpful in differentiating etiology of AKI o e.g. anuria is usually seen with UT obstruction, oliguria is commonly seen w/ prerenal etiologies, and nonoliguric AKI is seen w/ interstitial nephritis and ATN • urinalysis may show casts, RBCs, and WBCs o casts are formed from mucoprotein impressions of the necrotic renal tubular epithelial cells, which detach or slough into the tubules • urinalysis may show a specific gravity fixed at around 1.010 and urine osmolality at about 300 mOsm/kg  same sp gravity and osmolality of plasma, thus reflecting tubular damage w/ loss of concentrating ability by the kidney • proteinuria – if kidney failure related to glomerular membrane dysfunction ▪ fluid volume • hypovolemia has the potential to exacerbate all forms of AKI • reversal w/ fluid replacement is often sufficient to tx many forms of AKI • when urine output ↓ fluid retention occurs • severity of sx depends on extent of fluid overload o e.g. distended neck veins w/ bounding pulses if anuria and oliguria o e.g. edema or HTN • fluid overload  HF, pulmonary edema, pericardial and pleural effusions ▪ metabolic acidosis • kidneys cannot synthesize ammonia or excrete acid products of metabolism • bicarb depleted in buffering H+ , defective reabsorption and regeneration of bicarb • Kussmaul respirations (rapid, deep respirations) may develop to compensate by ↑ exhalation of CO2 ▪ sodium balance • damaged tubules cannot conserve sodium  normal or ↓ serum Na • avoid excessive Na intake b/c it can lead to volume expansion, HTN, and HF • uncontrolled hyponatremia or water excess can lead to cerebral edema ▪ potassium excess • kidneys normally excrete 80% to 90% of K – but in AKI, kidney is impaired to excrete K • hyperkalemia is more of a risk if AKI is caused by massive tissue trauma b/c damaged cells release additional K into the EC fluid • bleeding and blood transfusions  cellular destruction  release of more K • acidosis worsens hyperkalemia – H+ ions enter the cells and drive K out • usually asymptomatic • pt may complain of weakness w/ severe hyperkalemia • peaked T waves, wide QRS complex, and ST segment depression on ECG • cardiac muscle is intolerant of acute ↑ in K, so tx is essential! ▪ hematologic disorders • hospital-acquired AKI often occurs in pts w/ multiorgan failure • leukocytosis is often present w/ AKI • most common cause of death in AKI is infection – most common sites are urinary and respiratory systems • CBC w/ eosinophilia suggest an allergic response and possibly interstitial nephritis, polyarteritis nodosa, or atheroemboli ▪ waste product accumulation • ↑ BUN and serum creatinine • ↑ BUN can be caused by dehydration, corticosteroids; or catabolism resulting from infections, fever, severe injury, or GI bleeding • best serum indicator of AKI is creatinine ▪ neurologic disorders • occur when nitrogenous waste products accumulate in brain and other nervous tissue • manifestations can be as mild as fatigue and difficulty concentrating , and then escalate to seizures, stupor, and coma • asterixis (flapping tremor when the wrist is extended ) o Diuretic phase ▪ daily urine output is usually around 1 to 3 L, but may reach 5 L or more ▪ nephrons are still not fully functional though ▪ high urine volume is caused by osmotic diuresis from high urea concentration in glomerular filtrate and inability of tubules to concentrate urine ▪ kidneys have recovered ability to excrete wastes, but not to concentrate urine ▪ hypovolemia and hypotension if massive fluid losses  monitor for hyponatremia, hypokalemia, and dehydration ▪ may last 1 to 3 weeks ▪ near end of this phase, acid-base, electrolyte, and waste product values begin to normalize o Recovery phase ▪ begins when GFR ↑, allowing BUN and serum Cr levels to plateau and then ↓ ▪ kidney function may take up to 12 months to stabilize ▪ some do not recover and progress to end-stage kidney disease ▪ elderly less likely to have complete recovery ▪ some scar tissue remains but no clinically significant loss of function DIAGNOSTIC STUDIES - need thorough hx - prerenal causes – if hx of dehydration, blood loss, or severe heart disease - intrarenal causes – if nephrotoxic drugs or recent hx of blood transfusion or radiologic study using contrast media - postrenal causes – if hx of changes in urinary stream, stones, BPH, or cancer of bladder or prostate - ↑ in serum Cr may not be evident until there is a loss of > 50% of kidney function - urinalysis – urine sediments, osmolality, Na content, Sp gravity - kidney ultrasound – for evaluating possible kidney disease and obstruction - renal scan – assess abnormalities in kidney blood flow, tubular function, and the collecting system - CT scan – identify lesions, masses, obstructions, and vascular anomalies - renal biopsy – best method for confirming intrarenal causes - MRI/MRA with contrast media gadolinium is a no no if pt has kidney failure COLLABORATIVE CARE (Look at Hauck’s outline) Renal Replacement Therapy (RRT) indicated in AKI if: 1) volume overload, resulting in compromised cardiac and/or pulmonary status 2) ↑ serum K 3) metabolic acidosis (serum bicarb < 15 mEq/L) 4) BUN > 120 mg/dL 5) significant change in mental status 6) pericarditis, pericardial effusion, or cardiac tamponade Continuous Renal Replacement Therapy (CRRT) - provided continuously over approx. 24 hrs thru cannulation of an artery and vein or cannulation of 2 veins Hemodialysis - method of choice when rapid changes are required in a short time - more complicated process - requires specialized staff and equipment, vascular access, anticoagulation therapy - rapid fluid shifts during HD may cause hypotension NUTRITION - goal in AKI is to maintain adequate caloric intake – 30 to 35 kcal/kg and 0.8 to 1.0 g of protein/kg of desired body weight - get adequate energy primarily from carbs and fat sources - restrict Na as needed to prevent edema - get 30% to 40% of total calories from fat, or use fat emulsion IV infusions - if pt cannot maintain adequate oral intake, then go for enteral nutrition - if GI tract not functional, go for parenteral nutrition (but may need daily HD or CRRT to remove excess fluid) (concentrated parenteral formulas available as substitute) NURSING INTERVENTIONS - Monitor VS, daily I&O, and fluid & electrolyte balance o 1 kg = 1000 mL of fluid - Assess: o urine for color, sp gravity, glucose, protein, blood, and sediment o general appearance, including skin color, edema, neck vein distention, and bruises o if dialysis, observe access site for inflammation and exudate o mental status, LOC o oral mucosa for dryness and inflammation o lungs for crackles and rhonchi or diminished breath sounds o S3 gallop, murmurs, or pericardial friction rub o dysrhythmias - Caution: o Aggressive diuretic therapy for fluid overload can lead to ↓ in renal blood flow!!! o Some OTC analgesics may worsen kidney function if pt has mild CKD o ACEi can ↓ perfusion pressure and cause hyperkalemia o However ACEi are frequently used to prevent proteinuria and progression of kidney disease, esp in diabetics - Infection is leading cause of death in AKI – infection precautions! - Mouth care to prevent stomatitis, which develops when ammonia (produced by bacterial breakdown of urea) in saliva irritates mucous membranes END STAGE RENAL DISEASE Chronic kidney disease (CKD) - progressive, irreversible loss of kidney function - either presence of kidney damage or GFR < 60 mL/min/1.73m2 for > 3months - last stage of kindey failure = end-stage kidney (renal) disease (ESKD) = GFR < 15 mL/min - RRT is required to maintain life if ESKD - leading causes are DM and HTN - CKD are frequently asymptomatic MANIFESTATIONS (look at Hauck’s outline) - uremia – syndrome in which kidney function declines to the point that sx may develop in multiple body systems - during early stages, no change in urine - as CKD progresses, ↑ difficulty w/ fluid retention and require diuretic therapy - cellular insensitivity to insulin  impaired glucose metabolism  defective carbohydrate metabolism  mild to moderate hyperglycemia and hyperinsulinemia - insulin depends on kidneys for excretion  diabetics may require less insulin  will be able to discontinue insulin prior to dialysis - hyperinsulinemia stimulates hepatic production of triglycerides  ↑ triglycerides - almost all pts with uremia develop dyslipidemia, with ↑ VLDLs, ↑ LDLs, and ↓ HDLs - fatal dysrhythmias if potassium reaches 7 to 8 mEq/L - sodium can be ↑, normal, or low in kidney failure o impaired Na excretion  water retention o large quantities of water retained  dilutional hyponatremia o Na retention  edema, HTN, HF o generally restricted to 2 g/day - hypermagnesemia o is a problem if pt is ingesting additional Mg o manifestations include absence of reflexes, ↓ mental status, cardiac dysrhythmias, hypotension, and respiratory failure - metabolic acidosis - anemia - bleeding tendencies - ↑ susceptibility to infection in advanced CKD, due to changes in leukocyte function and altered immune response and function - CV diseases (dysrhythmias, pericarditis) caused by o HTN, ↑ lipids o vascular calcification, arterial stiffness o left ventricular hypertrophy (LVH) caused by long-standing HTN, ECF volume overload, and anemia - Kussmaul respirations, dyspnea - stomatitis with exudates and ulcerations, a metallic taste in the mouth, and uremic fetor (urinous odor of the breath) - anorexia and N/V if CKD progresses to ESKD and is not treaed with dialysis - weight loss, malnutrition - diabetic gastroparesis if diabetic - Neurologic changes: o depressed CNS  lethargy, apathy, ↓ ability to concentrate, fatigue, irritability, and altered mental ability o seizures and coma may result from rapidly ↑ BUN and hypertensive encephalopathy o restless leg syndrome in stage 5 o peripheral neuropathy o paresthesia o treat with dialysis - CKD mineral and bone disorder (CKD-MBD) o kidney deteriorate  vitamin D is not converted to its active form in kidney  no activated vit D to optimize absorption of Ca from GI tract  ↓ serum Ca level o hypocalcemia  parathyroid gland secretes PTH  stimulates bone demineralization  Ca released from bone  Phosphate is released as well o hyperphosphatemia  ↓ serum Ca o uremic red eye is caused by irritation from Ca deposits in the eye - pruritus is more prevalent in pts receiving dialysis o caused by dry skin, calcium-phosphate deposition in the skin, sensory neuropathy - uremic frost – rare; urea crystallizes on the skin; seen only when BUN > 200 mg/dL - Reproductive changes o infertility and ↓ libido o women: ▪ ↓ estrogen, progesterone, LH, causing anovulation and menstrual changes (usually amenorrhea) ▪ menses and ovulation may return after dialysis o men: ▪ loss of testicular consistency, ↓ testosterone, low sperm counts DIAGNOSTIC STUDIES - first indicator is persistent proteinuria (1+ protein on standard dipstick testing ≥ 2x over 3 mo) - screen for CKD with dipstick evaluation of proteinuria or evaluation for microalbuminuria - ratio > 300 mg albumin per 1 g Cr  CKD - urinalysis – detect RBC, WBC, protein, casts, and glucose - ultrasound – detect obstructions and size of kidneys - kidney biopsy – definitive diagnosis - measure GFR to determine kidney function COLLABORATIVE CARE (refer to Hauck’s outline) - Upon diagnosis of CKD, therapy is aimed at tx CV disease in addition to slowing the progression of kidney disease! - For stages 1 thru 4, focus is on control of HTN, hyperparathyroid disease, anemia, hyperglycemia, dyslipidemia - HTN o target BP = 130/80 for CKD o 125/75 if pt has significant proteinuria o weight loss if obese o therapeutic lifestyle changes e.g. exercise, avoid alcohol, smoking cessation o diet recommendations o antihypertensive drugs ▪ diuretics, CCB, ACEi, ARB ▪ ACEi and ARB for diabetics and those with nondiabetic proteinuria • caution in pts with ESKD b/c they can further ↓ GFR and ↑ serum K - CKD-MBD o limit dietary P 1g/day ▪ restrict P only if pt requires RRT o administer phosphate binders ▪ calcium acetate (PhosLo) ▪ calcium carbonate (Caltrate) ▪ administer with each meal ▪ constipation is a frequent side effect ▪ when Ca levels ↑ or if existing vascular or soft tissue calcifications  change to noncalcium-based phosphate binders, such as lanthanum carbonate (Fosrenol) and sevelamer carbonate (Renvela) o supplement vit D ▪ if serum levels < 30 ng/mL o control secondary hyperparathyroidism ▪ with activated vit D • oral or UV calcitriol (Rocaltrol, Caclijex) • IV paricalcitol (Zemplar) • oral or IV doxercalciferol (Hectorol) ▪ cinacalcet (Sensipar) ▪ if severe hyperparathyroid disease  subtotal or total parathyroidectomy o limit aluminum and Mg preps - Anemia o epoetin alfa (Epogen, Procrit) IV or SC 2 to 3x/week – use lowest dose possible ▪ may exacerbate existing HTN ▪ cause iron deficiency • iron supplementation if plasma ferritin conc < 100 ng/mL • Ca binds to iron – so do not take at the same time as phosphate binders o darbepoetin alfa (Aranesp) weekly or biweekly (longer acting) o significant ↑ of hgb & hct will be seen 2 to 3 weeks later o goal is individualized in order to reduce need for blood transfusions o folic acid 1 mg/day o avoid blood transfusions unless acute blood loss or symptomatic anemia (i.e. dyspnea, excess fatigue, tachycardia, palpitations, chest pain) - Dyslipidemia o statins (HMG-CoA reductase inhibitors) -- ↓ LDL (for pts not yet on dialysis) ▪ simvastatin has a higher rate of myopathy than atorvastatin o fibrates e.g. gemfibrozil (Lopid) -- ↓ triglyceride - Adjust drug doses and frequency based on kidney function!!!! NUTRITION - calorie-protein malnutrition is a potential and serious problem that results from altered metabolism, anemia, proteinuria, anorexia, and N - if stage 1 thru 4, many clinicians just encourage normal protein; avoid high-protein diets - dialysis pt – protein is not routinely restricted - need high protein intake in peritoneal dialysis to compensate for the losses (1.2 g/kg of IBW per day) - water and other fluids are NOT routinely restricted in stages 1 thru 5 who are NOT receiving HD - pts on HD have a more restricted fluid intake than pts on PD - diuretics to reduce fluid retention - fluid intake for HD pt = 600 mL + amt equal to the previous day’s urine output - limit fluid intake so that weight gains are no more than 1 to 3 kg between dialyses (interdialytic weight gain) - restrict Na to 2 to 4 kg/day o 1 g of NaCl (salt) = 400 mg sodium o avoid meats, pickled foods, canned soups and stews, frankfurters, cold cuts, soy sauce, salad dressings, etc - K restriction depends on kidney’s ability to excrete K o restrict K to 2 to 3 g (39 g = 1 mEq) o most salt substitutes contain KCl so AVOID if pt is on K restriction! o PD pts do not usually have K restriction and may need K supplementation - in ESKD, phosphate should be limited to ~ 1 g/day o avoid meat, dairy products o many foods that are high in phosphate are also high in protein – need phosphate binders in this case KIDNEY TRANSPLANT REJECTION Can be prevented by using immunosuppression therapy, performing ABO and HLA matching, and ensuring that the crossmatch is negative Hyperacute Rejection - occurs mins to hrs after transplantation b/c blood vessels are rapidly destroyed - occurs due to preexisting antibodies against the transplanted tissue or organ - no tx, have to remove transplanted organ - occurs rarely Acute Rejection - most commonly manifests in the first 6 months after transplantation - usually mediated by the recipient’s lymphocytes, which have been activated against the donated tissue or organ - can also occur when recipient develops antibodies to the transplanted organ - not uncommon to have at least one rejection episode, esp w/ organs from deceased donors - usually reversible w/ immunosuppressants - all pts require long-term immunosuppressants, strongest doses are given during the first few months Chronic Rejection - occurs over months or yrs and is irreversible - can occur for unknown reasons or from repeated episodes of acute rejection - transplanted organ is infiltrated w/ large #s of T and B cells characteristic of an ongoing, low-grade, immune-mediated injury - results in fibrosis and scarring - in kidney transplants, it manifests as fibrosis and glomerulopathy - no definitive therapy for this type of rejection - tx is primarily supportive PERITONEAL DIALYSIS - excess fluid is removed by ↑ osmolality of the dialysate (osmotic gradient) with the addition of glucose CATHETER PLACEMENT - insert 60 cm catheter thru anterior abd wall - the Dacron cuffs act as anchors and prevent migration of microorganisms down the shaft from the skin - within a few weeks, fibrous tissue grows into the Dacron cuff, holding the catheter in place and preventing bacterial penetration into the peritoneal cavity - catheter placement usually done via surgery - Preparation prior to insertion: o empty bladder and bowel o weigh the pt o signed consent form - after placement, PD may be initiated immediately with low volume exchanges, or delayed for 2 weeks pending healing and sealing of the exit site - once catheter incision site is healed, pt may shower and pat dry - may or may not require dressing changes - showering is preferred over bathing - observe for signs of infection 3 phases: INFLOW - prescribed amount of solution (usually 2 L) is infused thru an established catheter over 10 mins - flow rate may be ↓ if pt has pain - after solution has been infused, inflow clamp is closed before air enters tubing DWELL - diffusion and osmosis occurs - can last from 20 or 30 mins to 8 hrs or more, depending on method DRAIN - takes 15 to 30 mins - may be facilitated by gently massaging abdomen or changing position - cycle starts again with infusion of another 2 L of solution Dialysis solutions - glucose is the most effective osmotic agent to remove fluid o but has been associated w/ high rates of peritoneal glucose absorption leading to problems with hypertriglyceridemia, hyperglycemia, and long-term peritoneal membrane dysfunction - icodextrin - amino acid solutions – primarily for pts requiring nutritional supplementation Peritoneal Dialysis Systems - Automated Peritoneal Dialysis (APD) o allows pts to do dialysis while they sleep o built in alarms and monitors o disconnect in the AM and leave fluid in abdomen during the day o difficult to achieve the required solute and fluid clearance solely with nighttime PD o so one or two daytime manual exchanges may be needed - Continuous ambulatory peritoneal dialysis (CAPD) o done while pt is awake during the day o manual exchange o require aseptic technique COMPLICATIONS OF PD - exit site infection o most commonly caused by Staph Aureus or Staph epidermidis (from skin flora) o redness at site, tenderness, and drainage o treat immediately with antibiotics - peritonitis o usually caused by Staph Aureus or Staph epidermidis o results from contamination or from progression of an exit site or tunnel infection o abdominal pain, cloudy peritoneal effluent with WBC > 100 cells/µL (> 50% neutrophils), or positive gram stain culture in peritoneal effluent o give antibiotics orally, IV, or intraperitoneally o repeated infections cause adhesions in peritoneum - hernias o can develop in predisposed individuals such as multiparous women and older men o in most situations after hernia repair, PD can be resumed after several days - lower back problems o due to ↑ intraabdominal pressure o tx with orthopedic binders and regular strengthening exercises - bleeding o bleeding after initial catheter placement is ok o bloody effluent over several days or new appearance of blood in effluent indicate active intraperitoneal bleeding! o check BP and hct - pulmonary complications o atelectasis, pneumonia, and bronchitis may occur from repeated upward displacement of the diaphragm,  ↓ lung expansion o the longer the dwell time, the greater likelihood for pulm compl o tx with frequent repositioning and deep-breathing exercises, elevate HOB - protein loss o plasma proteins, amino acids, and polypeptides are lost in dialysate fluid HEMODIALYSIS - gradient is created by ↑ pressure in the blood compartment (positive pressure) or ↓ pressure in the dialysate compartment (negative compartment) - ECF moves into the dialysate b/c of the pressure gradient VASCULAR ACCESS (refer to Hauck’s outline) Arteriovenous Fistulas - SC AVF is usually created in the forearm or upper arm with an anastomosis between an artery and a vein (usually cephalic or basilic) - fistula allows arterial blood to flow thru the vein – essential to provide rapid blood flow for HD - arterialized vein takes 6 weeks to mature (large caliber and thicker walls) - AVF should be placed at least 3 months before the need for HD - thrill and bruit are created by arterial blood moving at a high velocity thru vein Arteriovenous Grafts - made of synthetic materials (PTFE, Teflon) and forms a bridge between arterial and venous blood supplies - need 2 to 4 weeks to heal - more likely to become infected than AVFs – may require surgical removal - Risks: o development of distal ischemia (steal syndrome) – numbness or tingling of fingers and poor capillary refill o pain o aneurysm development Never perform BP measurements, insertion of IV lines, and venipuncture in the extremity with vascular access!! – in order to prevent infection and clotting Temporary vascular access - catheterization of internal jugular or femoral vein when immediate vascular access is required - flexible Teflon, silicone rubber, or polyurethane catheter - the catheters usually have a double external lumen – one lumen for blood removal and one for blood return - not recommended to discharge pt due to high rates of infection, dislodgment, and malfunction - long-term cuffed HD catheters o provide temporary access while pt is waiting for fistula placement or as long-term access when other forms of access have failed o exits on upper chest wall and is tunneled SC to the internal or external jugular vein PROCEDURE FOR HD - before beginning tx, complete assessment on fluid status, condition of vascular access, T, and general skin condition - difference between postdialysis weight and present predialysis weight determines ultrafiltration or amt of weight (from fluid) to be removed - while pt is on dialysis, take VS q 30 to 60 mins b/c rapid BP changes may occur - two 14 to 16 gauge needles – one to pull blood from circulation, one to return dialyzed blood - add heparin to blood b/c blood clots when in contact with foreign substance - usually 3 to 4 hrs 3 days/wk - short daily HD, long nocturnal HD, in-center HD, and home HD are available COMPLICATIONS OF HD - hypotension o may precipitate lightheadedness, N/V, seizures, vision changes, and chest pain from cardiac ischemia o tx by ↓ volume of fluid being removed and infusion of 0.9% saline - muscle cramps o associated with hypotension, hypovolemia, high ultrafiltration rate, and low-Na dialysis solution o more frequently seen during 1st month after initiation of dialysis o tx by ↓ ultrafiltration rate and administering fluids (saline, glucose, mannitol) ▪ hypertonic Na is not recommended ▪ hypertonic glucose is preferred - loss of blood o it is essential to rinse back all blood, to closely monitor heparinization and to hold firm but nonocclusive pressure on access sites until risk of bleeding has passed - hepatitis o infection control practices and vaccinations – you know the drill! RADIATION THERAPY CANCER TREATMENT -- Radiation Therapy • One of the oldest nonsurgical methods of cancer treatment • 50% of all cancer patients will receive radiation therapy at some point in their treatment • Radiation is the emission of energy from a source and travels through space or some material • Different types of ionizing radiation are used to treat cancer • Technologic advances • Low-energy beams • Expend energy quickly • Penetrate a short distance • Useful for skin lesions • High-energy beams • Greater depth of penetration • Suitable for optimal dosing of internal targets while sparing skin • radiation to surrounding healthy tissue must be limited to the maximal tolerated dose for that specific tissue • Dosage is expressed by gray (Gy) or centigray (cGy) • 1 centigray = 1 rad • 1 gray = 100 rads • Radiation absorbed dose (rad) • Unit of absorbed dose of radiation • 1 rad = 0.01 joules per kilogram of tissue • Total doses divided into fractions • Typically delivered once a day for 5 days a week for 2 to 8 weeks • Standard fractionation • Number and strength of doses is determined by mitotic rate of target tissue, with rapidly growing tumors being more sensitive • Simulation • A process by which the radiation treatment fields are defined, filmed, and marked out on the skin • The radiation oncologist specifies the dose and volume of area to be treated • Target tumor defined using • Variety of imaging techniques • Physical examination and surgical reports • Marks placed on skin to outline treatment field • Critical normal structures in treatment field are protected • Radiation is used to treat a carefully defined area of the body • Not a primary treatment for systemic disease • May be used by itself, or with chemotherapy or surgery • To treat primary tumors • For palliation of metastatic lesions • rapidly dividing cells exhibit early acute responses to radiation • tissues with slowly proliferating cells manifest later responses to radiation • less responsive tumors result in a slower and perhaps incomplete response e.g. prostate cancer • rapidly proliferating tissues : • bone marrow • lining of GI system • skin, hair, nails • External radiation (teletherapy) • Most common radiation treatment • Patient exposed to radiation from a megavolt machine • Gamma knife technology—Cobalt • Cyclotron—Neutrons or protons • Linear accelerator—Ionizing radiation • worry about the skin the most • Internal radiation (brachytherapy) • Implantation or insertion of radioactive materials into or close to tumor • Minimal exposure to healthy tissue • Commonly used in combination with external radiation as a supplemental boost tx • Patient is emitting radioactivity • Limit amount of time near patients being treated • Organize care – to limit time spent in direct contact w/ pt • Use shielding – if available • Wear film badge to monitor exposure • pts with permanent implants (sources have fairly short half-lives and are weak emitters) the radioactive exposure to the outside and to others is low • may be discharged with minimal precautions • because source is nonpenetrating, small differences in distance are critical • only care that must be delivered near the source, such as checking placement of implant, is performed in close proximity • pts with temporary implants are radioactive only while the source is in place Immobilization Device Linear Accelerator NURSING MANAGEMENT NURSING IMPLICATIONS Common side effects: • BONE MARROW SUPPRESSION • Myelosuppression: most common systemic side effect of chemotherapy can occur w/radiation (local effect) • ↓ in production of cells responsible for providing immunity (leukocytes), carrying oxygen (erythrocytes) and/or those responsible for normal blood clotting (thrombolytic) • typically experience lowest blood counts (nadir) between 7-10 days after initiation of therapy • WBC – affected within 1-2 wks • platelets – affected in 2-3 wks • RBC – affected at than 120 days • Treatment-induced reductions in RBCs and WBCs can result in • Infection • Hemorrhage • Overwhelming fatigue • NEUTROPENIA • more common in pts receiving chemo than radiation • serious risk factor for life threatening infection and sepsis • significant neutropenia will prompt tx delay or modification (i.e. lower dosages) • prevent infection by hand hygiene and other precautions • monitor T routinely – fever due to neutropenia is a medical emergency! • WBC growth factors – are routinely used to reduce the duration of chemo-induced neutropenia • filgrastim (Neupogen), pegfilgrastim (Neulasta) • also a prophylactic measure • THROMBOCYTOPENIA • bone marrow depressed secondary to chemotherapy • malignant infiltration of bone marrow crowds out normal marrow • risk of bleeding is apparent when platelet count falls < 50,000/µL • platelet transfusions when platelet count falls < 20,000/µL • nursing management: • observe for signs of bleeding (e.g. petechiae, ecchymosis) • monitor platelet counts • anemia • common in radiation or chemotherapy • generally a later onset ~3-4 months after tx initiation • for low hgb levels  RBC growth factors: darbepoetin (Aranesp), epoetin (Procrit) • symptomatic anemia  RBC transfusions (however, in general should be avoided) • Fatigue • causes: • anemia • accumulation of toxic substances left in the body after cells are killed • the need for extra energy to repair and heal body tissue damaged by tx • lack of sleep caused by some chemo drugs • Encourage conservation strategies • Rest before activity • Get assistance with activity • Remain active during periods of time patients feel better • e.g. walking programs • maintain exercise and activity within tolerable limits • remain active to improve mood • Maintain nutritional and hydration status • Assess for reversible causes of fatigue • e.g. anemia, hypothyroidism, depression, anxiety, insomnia, dehydration, or infection • Gastrointestinal (GI) effects • GI cells are highly proliferative – replaced q 2-6 days • GI cells injury  N/V/D, mucositis, anorexia • Prophylactic administration of antiemetics • Assess for signs and symptoms of • Alkalosis, dehydration, and I & O • Nonirritating, low-fiber, high-calorie, high-protein diet • Antidiarrheal, antimotility, and antispasmodic medications • Anorexia • peaks at about 4 wks of tx and resolve more quickly than fatigue • Monitor carefully to avoid weight loss • Weigh twice weekly • Recommend small, frequent, high-protein, high-calorie meals • Encourage nutritional supplements • STOMATITIS, mucositis, esophagitis • epithelial cells are destroyed by chemotherapy or radiation tx when located in field (e.g. head and neck, stomach, esophagus) • inflammation and ulceration occur due to rapid cell destruction Nursing management: • assess oral mucosa daily and teach pt to do this • encourage nutritional supplements (e.g. Ensure, Carnation Instant Breakfast) if intake decreasing • be aware that eating, swallowing, and talking may be difficult (may require analgesics) • instruct in diet modification as necessary (avoidance of irritating spicy or acidic foods; selection of moist, bland, and softer foods) • encourage pt to keep oral cavity clean and moist by performing frequent oral rinses with saline or salt and soda solution • encourage pt to use artificial saliva to manage dryness (radiation) • discourage us of irritants such as tobacco and alcohol, hydrogen peroxide • apply topical anesthetics (e.g., viscous lidocaine, oxethazaine) • Skin reactions • Occur in radiation treatment field • Acute or chronic • Develop 1 to 24 hours after treatment • Generally progressive as treatment dose accumulates • mild erythema, hyperpigmentation, hand- foot syndrome, alopecia • generally hair does not grow back until 3- 4 weeks after drugs discontinued • often new hair has different color and texture • erythema is an acute response followed by DRY DESQUAMATION if the rate of cell sloughing is faster than the ability of the new epidermal cells to replace dead cells, • uncomfortable • result in pruritus • need to lubricate • WET DESQUAMATION occurs with exposure of the dermis and weeping of serous fluid • pain • drainage • ↑ risk of infection • keep clean with normal saline compresses or modified Burrow’s solution soaks • protect w/ moisture vapor-permeable dressings or Vaseline petrolatum gauze • skin reactions are particularly evident in areas of skinfolds or where skin is subjected to pressure, such as behind the ear; in gluteal folds; or on perineum, breast, collar line, and bony prominences DRY DESQUAMATION WET DESQUAMATION NURSING MANAGEMENT: • Prevent infection • Facilitate wound healing • Protect irritated skin temperature extremes • Avoid constricting garments, harsh chemicals, and deodorants • Help patients deal with hair loss • the area undergoing radiation therapy may safely be washed with lukewarm water if it is done gently and if care is taken not to injure the skin • avoid lotions, ointments, talcum powder, sunlight • Pulmonary effects • May be progressive and irreversible • Cough, dyspnea, pneumonitis, pulmonary edema • Treatment • Bronchodilators • Expectorants/cough suppressants • Bed rest • Oxygen • Cardiovascular effects • Patients with preexisting coronary artery disease are more vulnerable • Radiation-induced heart disease is more likely in patients given high doses of radiation and doxorubicin • Herceptin is cardiotoxic • Reproductive effects • Inform patient of expected sexual side effects • Use appropriate shielding • Encourage discussion of issues related to sexuality • Refer to counseling if needed • Coping • Assist in planning • Transportation, nutrition, emotional support • Teach symptom management to maintain quality of life • Offer community resources • Tell patient what to expect to decrease anxiety • Encourage discussion of fears • Reassure patient that situation is only temporary • Inform patient of provided supportive care LATE EFFECTS OF RADIATION AND CHEMOTHERAPY • Increased risk for leukemias and other secondary malignancies • Secondary malignancies, other • Multiple myeloma • Non-Hodgkin’s lymphoma • Cancers of the • Bladder, kidney, ureters, osteosarcoma of rib, scapula, clavicle, humerus, sternum, ilium, and pelvis • Fibrosarcomas have been reported several years after radiation therapy • Smoking may significantly increase the risk of secondary malignancies • Secondary malignancies are usually resistant to therapy RADIATION SAFETY - pt with temporary implants are radioactive only while the source is in place - for permanent implants, the sources have fairly short half-lives and are weak emitters so radioactive exposure to the outside and to others is low – may be discharged with minimal precautions - ALARA (as low as reasonably achievable) and time, distance, shielding - organize care to limit the time spent in direct contact with the pt - to minimize anxiety and confusion, tell the pt the reason for time and distance limitations before the procedure - the radiation safety officer will indicate how much time at a specific distance can be spent with the pt – determined by the dose delivered by the implant - since the source is nonpenetrating, small differences in distance are critical - only care that must be delivered near the source, such as checking placement of the implant, is performed in close proximity - use shielding if available - do not deliver care without wearing a film badge indicating cumulative radiation exposure - do not share the film badge, do not wear it anywhere but at work, and return it according to the agency’s protocol BURNS CHF - Abnormal clinical syndrome that involves inadequate pumping or filling of the heart - HF unable to provide sufficient blood to meet oxygen needs of the tissues - Associated with CAD, MI ETIOLOGY AND PATHOPHYSIOLOGY - Primary risk factors: HTN and CAD – will have history of HTN - Other risks: age, DM, smoking, obesity and high cholesterol - Anything that interferes with mechanism that regulates cardiac output - Primary causes: conditions that directly damage the heart (35-1) o CAD and MI o HTN – hypertensive crisis o Rheumatic heart disease o CHD – VSD and such o Pulmonary hypertension o Cardiomyopathy – viral, postpartum, drug abuse o Hyperthyroidism o Valvular disorders – mitral stenosis o Myocarditis - Precipitating causes often increase the workload of the ventricles, resulting in an acute condition that results in decreased cardiac function. o Anemia (decreased oxygen supply increases workload of heart to meet the demand) o Infection (increased oxygen demand) o Thyrotoxicosis (increased heart rate and workload) o Hypothyroidism (increased risk for atherosclerosis) o Dysrhythmias (decreased CO and increased workload) o Bacterial endocarditis (infection increases workload, can also cause valvular disorders) o Pulmonary embolism (increased workload to pump blood into lungs) o Paget’s disease (increased workload secondary to increased vasculature bed) o Nutritional deficiencies (decreased cardiac function increases workload) o Hypervolemia (increased preload increases workload) - Systolic failure – inability of heart to pump blood effectively caused by impaired contractile function, increased afterload, cardiomyopathy, and mechanical abnormalities (valve stuff) - Diastolic failure – inability of ventricles to relax and fill during diastole, referred to as HF with normal ejection fraction – results in decreased CO - Mixed systolic and diastolic failure – seen in disease states such as dilated cardiomyopathy o Low BP, low CO, poor renal perfusion TYPES OF HEART FAILURE LEFT HF – RELATED TO LUNGS - Most common – result of left ventricular dysfunction - Prevents normal, forward blood flow and causes blood to back up in LA and pulmonary veins - Increase pulmonary pressure – fluid leakage into alveoli – pulmonary congestion and edema Right HF – ALL OVER THE BODY - RV fails to contract effectively – blood backs up into RA and venous circulation o JVD, hepatomegaly, splenomgaly, vascular congestion of GI tract, peripheral EDEMA - May result from acute condition: right ventricular infarction or pulmonary embolism or cor pulmonale - Primary cause – LF heart failure CLINICAL MANIFESTATION ACUTE DECOMPENSATED HEART FAILURE ADHF - Inc rea sed in pulmonary venous pressure is caused by failure of LV – BASICALLY WORSENING OF SYMPTOMS - Can manifest PULMONARY EDEMA – life threatening – lung alveoli filled with fluid – most common cause is LHF secondary to CAD o Anxious, pale, cyanotic, cool and clammy, dyspnea SOB, o RR>30, wheezing, accessory muscles used and coughing with frothy, blood tinged sputum o Crackles, rhonchi heard o HR rapid and BP varies depending on severity of HF CHRONIC HEART FAILURE - Fatigue – EARLIEST SIGN of chronic HF – can be from anemia as well from poor nutrition or ACE drugs - Dyspnea – often accompanied by orthopnea – GOTTA ASK HOW MANY PILLOWS PATIENT USE o Paraoxsymal nocturnal dyspnea – patient suddenly want to stand up - Cough – one of first sign – not relieved by pposition change or OTC drugs - Tachycardia – early sign – reduced CO causes SNS activation – can be reduced with Beta blockers - Edema – development of edema or sudden weight gain of 3 lbs in 2 days = ADHF o Not all lower extremity edema result from HF - Nocturia – increased renal blood flow and dieresis when lying down at night - Skin changes – dusky, lower extremity shiny and swollen – can cause brown color overtime - Behavioral changes – restlessness, confusion and decreased attention span or memory - Chest pain - - Weight changes – fluid retention – cardiac cachexia COMPLICATIONS OF HF - Pleural effusion – from increased pressure in pleural capillaries - Dsyrhythmias – enlargement of chambers cause abnormal conduction o Places patient with A-fib at risk for stroke – requires antidsyrhythmic or anticoagulants - Left ventricular thrombus – risk for stroke - Hepatomegaly - Renal failure DIAGNOSTIC STUDIES - Difficult – may mimic other conditions – anemia, lung disease - Endomyocardial biopsy EMB – done on patients with unexplainable onset of HF - ECG, chest x-ray and heart catheterization o PREOP: any allergies to iodine? Keep patient NPO o POSTOP: assess insertion site for bleeding, distal pulses, body aligned for 4 hours - Labs: BNP LEVELS HIGH o Can also be caused by pulmonary embolism, renal failure and acute coronary syndrome COLLABORATIVE CARE ADHF - Need continuous monitoring and assessment – ECG and O2 sat – Vitals and I&O Q1H - If pulmonary artery catheter is placed: evaluate Co and pulmonary artery wedge pressure PAWP o Normal PAWP – 8-12 mmHg – Patient will probably have 30 mmHg - Supply O2: In severe pulmonary edema patient – might need intubation or mechanical ventilation - If hospitalize in telemetry – asses Q4H vitals, pulse oximetry and I&O - If patient is dyspneic – HIGH FOWLER’S POSITION with feet dangling at bed side - Ultrafiltration UF – remove salt and water from patient’s blood – for those who show resistance to diuretics. - Intraaortic balloon pump – increases coronary blood flow to heart muscles and decreases heart workload called counterpulsation - Assess patient for depression and anxiety – they have poor adherence to treatment plans CHRONIC HF - MAIN GOAL: treat underlying causes and contributing factors, maximize CO, reduce symptoms improve ventricular function, improve quality of life, preserve target organ function and improve mortality and morbidity risks - Administer O2 – improve saturation and assist in meeting tissue O2 needs – relieve dyspnea and fatigue - Rest – depends on severity of patient – exercise program such as cardiac rehabilitation offered - NON-PHARM STUFF – biventricular pacing or cardiac resynchronization therapy - Implantable cardioverterdefibrillator ICD to prevent V-tach - Mechanical options – Intraaortic balloon pump or ventricular assist device o IABP – can limit bed rest and increase infection in long term use o VAD – can be permanent known as destination therapy or wait until there is a donor DRUG THERAPY - Diuretics – treatment of volume overload (PRELOAD) o Loop: Furosemide (LASIX) and bumetanide (BUMEX) – can be administered IV and act rapidly in kidneys o Can cause HYPOKALEMIA – leg cramps, weakness, fatigue and constipation ▪ Need food high in potassium – banana, cantaloupe, apricots, prunes, raisin - Vasodilators – reduce circulating blood volume and improve coronary artery circulation o IV Nitroglycerin – reduces preload ▪ When titrating – monitor BP frequently 5-10 minutes to avoid hypotension o Sodium nitroprusside (Nipride)– reduces both preload and afterload ▪ Complications: hypotension, thiocyanate toxicity (after 48 hours) ▪ Assess BP 5-10 mins, must titrate slowly ▪ Headache, nausea, dizziness, dyspnea, blurred vision, sweating, restlessness can occur o Nesiritide (Natrecor) – recombinant form of BNP, arterial and venous dilation ▪ Reduction of PAWP and decrease in systemic BP ▪ Used for short term ADHF – does not require titration ▪ Also monitor BP closely o NITRATE – for chronic HF – smooth muscles of vessel walls, can be used with hydralazine for those who can’t tolerate ACE or ARBS ▪ Don’t mix with Viagra – can cause hypotension o BiDil (hydralazine) – for African Americans – watch for headaches and dizziness - Renin-Angiotensin-Aldosterone System Inhibitors RAAS o ACE inhibitors – primary drug of choice for blocking RAAS in HF patients, increases CO but may decrease BP. ▪ Captopril • Watch for hypotension and hyperkalemia – especially first dose hypotension • Skipping dose or stopping can cause rebound HTN • Angioedema – can develop and life threatening o Angiotensin II receptor blockers – unable to tolerate ACE inhibitors – prevent vasoconstrictor and aldosterone- secreting effects of angiotensin II o Aldosterone Antagonist – block harmful effects of aldosterone on the heart blood vessels. Also potassium sparing diuretics ▪ Spironolactone (Aldactone) • Monitor potassium levels – use with caution with digoxin because potassium educe effects of it. • Avoid bananas, oranges and dry apricots • Male side effect – gynecomastia – male breasts - B-adrenergic Blockers – directly blocks negative effects of SNS – increase HR – reduce effect of renin o Dosage increase every 2 weeks o Adverse: edema, worsening of HF, hypotension, fatigue and bradycardia o Carvedilol (Coreg) ▪ Overdose – bradycardia, hypotension, bronchospasm, cardiogenic shock ▪ Obtain standing BP 1 hour dosing to assess tolerance ▪ Abrupt withdrawal – sweating, palpitations and headaches - Morphine – reduces preload and afterload – treatment of acute coronary syndrome and HF o Relief of dyspnea and anxiety o USE cautiously in ADHF - Positive inotropes – increase myocardial contractibility o B-adrenergic agonist – Dopamine (Intropin) and dobutamine (Dobutrex) ▪ Monitor IV site for extravasation – another word for LEAKAGE – can cause tissue necrosis ▪ High dose may produce ventricular dsyrhythmias o Phosphodiesterase inhibitors – Inamrinone (Inocor) and milrinone (Primacor) ▪ Not recommended as initial treatment for ADHF ▪ Increase myocardial contractibility and peripheral vasodilation ▪ Enhances calcium entry ▪ Watch for: dysrhythmias, thrombocytopenia and hepatotoxicity o Digitalis (Digoxin) – increases force of cardiac contraction, decrease HR ▪ Risk for toxicity – HYPOKALEMIA most common ▪ Other signs: anorexia, N/V, fatigue, headache, depression and visual changes ▪ Late signs: dysrhythmias – bradycardia and AV block ▪ Withold medication until symptoms subside – ANTIDOTE IS IV DIGOXIN IMMUNE FAB (OVINE or DIGIBIND) NUTRITIONAL THERAPY - LOW SODIUM DIET - First – obtain detail diet history – what does patient eat and does he/she dine out a lot o Remember to be culturally sensitive! - Dietary approaches to stop hypertension – DASH diet - Limit 2g of sodium per day – don’t eat anything that’s over 400 mg/serving o AVOID: processed meat, cheese, bread, cereals, canned soups and canned vegetables - Fluid restriction – not commonly prescribed – 2L/day - suggest ice chips, hard candy or ice pops - Weigh-self same time each day – before breakfast - CALL PROVIDER IF – gain 3 lbs over 2 days NURSING MANAGEMENT PLANNING - Decrease in symptoms – SOB, fatigue - Decrease in peripheral edema - Increase in exercise tolerance - Adherence with medical regimen - No complications related to HF HEALTH PROMOTIONS - Teach about HTN or high cholesterol measures to manage BP or with medication, diet and exercise - Encourage to obtain vaccinations against flu and pneumonia ACUTE INTERVENTION - When ADHF – admit to ED, stabilize and manage in ICU - Successful management depends on: o HF is progressive disease and treatment plans are established along with quality of life goals o Symptom management is controlled by patient with self-management tools o Salt and sometimes water must be restricted o Energy must be conserved o Support system essential for treatment plan - Reduction of anxiety – may increase myocardial workload – may use sedatives AMBULATORY AND HOME CARE - Nursing responsibilities o Teach about physiologic changes that have occurred o Helping patient adapt to both physiologic and psycholigc changes o Integrating patient and caregiver in overall care plan - Review sign and symptoms of HF exacerbations - Risk for anxiety and depression – EMPHASIZE they can live life without chronic help problems – take medications for the rest of their lives o Sometimes difficult because they are asymptomatic - Teach drug contraindications o Pulse rate taken 1 full minute - >50 BPM = CAN’T TAKE BETA BLOCKERS or DIGOXIN – call provider to make sure - Give supplemental potassium for people take loop diuretics - Monitor BP frequently - Instruct patient in energy conserving and efficient behavior after evaluation of daily activities has been done o Cardiac rehabilitation - Help patient explore alternative activities they enjoy that causes less stress - Nitroglycerin teaching o Sensitive to light o Should sting when placed under tongue – after 3rd administration within 5 minutes apart – symptoms not resided – CALL 911 - Call 911 also when o Gain of 2 plus lbs/day o Worsening of edema, SOB o Orthopnea o Persistent cough DRUGS USED DURING CARDIAC ARREST O2 THERAPY AND MECHANICAL VENTILATION CENTRAL LINE CARE PACEMAKER - Electrical device used to pace heart when the normal conduction pathway is damaged o Programmable pulse generator – power source – kind of like a battery o One or more conducting leads to myocardium - Pace atrium and one or both ventricles - Demand pacemaker – most common – firing only when HR drops below preset rate o Sensing device inhibits pacemaker when HR adequate o Triggers when no QRS complexes within set time frame - Antitachycardia pacing: delivery of stimulus to ventricle to terminate tachydysrhythmias (VT) - Overdriving pacing: pacing the atrium at rate 200-500 impulses/min to terminate atrial tachycardia PERMANENT PACEMAKER - Total implantation, subcutaneously over pectoral muscle on patient’s non-dominant side - Pacing leads placed transvenously to RA or both ventricles and attached to power source CARDIAC RESYNCHRONIZATION CRT - Resynchronize cardiac cycle by pacing both ventricles – biventricular pacing - Used to treat patients with HF – can be combined with ICD for maximum therapy TEMPORARY PACEMAKER - Has the power source outside the body. Provide a bridge to permanent pacemaker or until dysrhythmias are resolved : Three types: o Tranvenous: lead or leads that are threaded transvenously to RA or RV and attached to external power source o Epicardial: attaching atrial and ventricular pacing lead to epicardium during heart surgery. o Transcutaneous: provide adequate HR and rhythm to patient in emergency situation. ▪ Non-invasive procedure, used until definitive therapy is available ▪ Important to tell patient what to expect before procedure – will have muscle contractions ▪ Provide analgesics or sedatives when its used. MONITORING PATIENTS WITH PACEMAKER - Failure to sense – when pacemaker fails to recognize spontaneous atrial or ventricular activity, and fires inappropriately – CAN LEAD TO VT o Caused by pacer lead damage, battery failure, sensing set too high of dislodgement of electrode - Failure to capture - Electrical charge to myocardium is insufficient to produce atrial or ventricular contraction – LEAD TO BRADYCARDIA or ASYSTOLE o Pacer lead damage, battery failure, electrode dislodgement, charge set too low, or fibrosis at electrode tip - Monitor for complications o Infection and hematoma formation at insertion site o Pneumothorax, failure to sense of capture o Perforation of atrial or ventricular septum by pacing lead o End of life battery power on testing the pacemaker - GIVE IV PROPHYLACTIC BEFORE and AFTER INSERTION – to prevent complications o Chest x-ray to rule out pneumothorax, observe insertion site and continue ECG - Postprocedure o Get out of bed once patient is stable o LIMIT ARM or SHOULDER ACTIVITY – prevent dislodging new implants o Assess insertion site for bleeding or infection – pain or elevated temperature o Teachings – body image concerns and such ▪ Keep incision dry for 4 days after implant ▪ Avoid high electrical generators ▪ NO MRI unless it is approved as safe ▪ Microwaves are OK ▪ Don’t stand near antitheft devices, if you’re gonna steal just say I have pacemaker. ▪ Airplanes are alright ▪ Have pacemaker ID or Medic alert ID CARDIAC RHYTHMS ASSESSMENT OF CARDIAC RHYTHM EVALUATION OF DYSRHYTHMIAS - Electrophysiologic study (EPS) – identify causes of heart blocks, brady and tachy abnormal heart beats, and syncope. o Can also study locate accessory pathways and determine effectiveness of anti-dysrhythmia drugs - Holter monitor – continuously record ECG while performing regular activities - Exercise treadmill used to assess heart too! TYPE OF DYSRHYTHMIAS SINUS BRADYCARDIA - Same as sinus rhythm – less than 60 bpm (OK for athletes) - Occur in response to carotid sinus massage, Valsalva maneuver, hypothermia, increase ICP, vagal stimulation, and certain drugs (Beta blockers, calcium channel blockers) - Common disease: hypothyroidism, increased ICP, hypoglycemia and inferior MI MANIFESTATIONS - Hypotension, pale cool skin, weakness, angina, dizziness or syncope, confusion or SOB ECG CHARACTERISTICS - P wave precedes each QRS complex and is NORMAL shape and duration TREATMENT - Atropine – anticholinergic – FIRST CHOICE – INCREASES HR - Transcutaneous pacing, dopamine (Intropin) or epinephrine (Adrenalin) – if Atropine doesn’t work - Pacemaker may be needed - Stop drugs if its causing bradycardia SINUS TACHYCARDIA - NSR: 110-200 BPM – caused by vagal inhibition or sympathetic stimulation - Associated with physiologic and psychologic stressors (exercise, fever, pain, MI, anxiety or fear) - Drugs can cause increase: epinephrine, norepinephrine, atropine, caffeine, theophylline, hydralazine or pseudo (making meth drug) - NORMAL EVERYTHING – P WAVE, QRS. CLINICAL MANIFESTATION - Dizziness, dyspnea, hypotension, angina (HADD) - Angina in patients with CAD or acute MI TREATMENT - Guided by cause: If pain causing tachycardia, treat that - Vagal maneuver - B-adrenergic blockers: Metaprolol (Lopressor), adenosine (Adenocard) - Calcium channel blockers: diltiazem (Cardizem) - Cardioversion if patient is unstable PREMATURE ATRIAL CONTRACTION - Contraction from ectopic focus in atrium in location other than SA node - Travels across atria by abnormal pathway, ABNORMAL P WAVE o P wave hidden, QRS interval > 0.12 seconds, 60-100 BPM - May be stopped, delayed or conducted normally at AV node - Causes: emotional stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolyte imbalance, disease (COPD or heart diseases) CLINICAL MANIFESTATION - Palpitations or heart skips a beat TREATMENT - Monitor for more serious dysrhythmias - Withhold sources of stimulation – maybe tell that person to stop drinking coffee - B-adrenergic blockers PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA PSVT - Dysrhythmia starting in an ectopic focus anywhere above the bifurcation of Bundle of His - Occurs because of reentrant phenomenon – PAC triggers run of repeated premature beats o Re-excitement of atria when there is one way block o BRIEF ASYSTOLE, ABNORMAL P maybe hidden from T, SHORTENED PR INTERVAL - Associated with overexertion, stress, deep inspiration, stimulants, disease or digitalis toxicity CLINICAL MANIFESTATIONS - HR 150-220 BPM - HR>180 causes decrease in CO and stroke volume - Hypotension, palpitations, dyspnea and angina (PADD) Treatment - Vagal stimulation – Valsalva, carotid massage, and coughing - IV adenosine – DRUG OF CHOICE – short half-life and well tolerated (10 sec) o Injection close to heart as possible o Give IV rapidly and follow with rapid 20 mL NS flush –because of short life o Monitor ECG continuously – ASYSTOLE WILL BE COMMON o Observe for flushing, dizziness, chest pain and palpitations - IV B-adrenergic blockers, calcium channel blockers or Amiodarone can be used - Cardioversion – if other therapy don’t work or patient becomes unstable - Radiofrequency catheter ablation – for WPW syndrome ATRIAL FLUTTER - Atrial tachydysrhythmia by recurring regular, SAWTOOTH shape flutter waves - Rarely occurs in normal heart – associated with disease – CAD, HTN, mitral valve disorders, pulmonary embolism, lung disease or digoxin toxicity - Atrial rate: 200-350 BPM, ventricular rate: 150 BPM, 2:1 conduction ratio - Waves represent atrial depolarization followed by repolarization – PR interval UNMEASURABLE CLINICAL MANIFESTATION - Loss of atrial kick associated with decreased CO – can cause HF - INCREASE RISK OF STROKE – need to give warfarin to prevent thrombus formation TREATMENT - Goal: slow ventricular response by increasing AV block - Drugs: calcium channel blocks, beta blockers or antidysrhythmia drugs - Electrical cardioversion – for unstable patients - Radiofrequency catheter ablation – TREATMENT OF CHOICE ATRIAL FIBRILLATION - Total disorganization of atrial electrical activity – multiple ectopic foci, resulting loss of atrial contraction o Looks like: lots of squiggly line like Arabic writing and then upside down R… - Paroxsymal or persistent – violent outburst or constant - Most common dysrhythmia - Prevalence increases with age and in patients with heart diseases - Atrial: 350-600 BPM, Ventricular: 60-100BPM, PR interval not measurable, QRS complex normal CLINICAL MANIFESTATION - Decreased CO and increased risk of stroke TREATMENT - Goal: Decrease ventricular response, prevent stroke and conversion to normal sinus - Pharmacologic or electrical cardioversion – reduced exercise tolerance with rate control drugs, contraindications to warfarin o Most common antidysrhythmia drugs: AMIODARONE and IBUTILIDE - ANTICOAGULATION – IF A-FIB LONGER THAN 48 HOURS, NEED WARFARIN FOR 3-4 WEEKS, OR IF CARDIOVERSION AND OTHER DRUGS DON’T WORK. >2 DAYS!!!!! o Important to rid clots before electrical cardioversion because of risk of stroke - Radiofrequency ablation as well - Maze procedure – cyroablation – cold therapy to stop formation and conduction of three signals and restore NSR. JUNCTIONAL DYSRHYTHMIA - Dysrhythmias start in area AV node because SA node fails to fire - AV node becomes the pacemaker – retrograde transmission of impulse to atria - Abnormal P wave, normal QRS (R is upside-down) - Associated with disease or drugs – CAD, HF, MI, rheumatic heart disease, digoxin, caffeine… - 40-60 BPM, P wave abnormal or hidden, PR interval <0.12 seconds CLINICAL MANIFESTATIONS - Junction serves as safety mechanism when SA not effective – DO NOT SUPPRESS - If rhythm is rapid – reduction of CO TREATMENT - Atropine – DRUG OF CHOICE - Correct cause – stop the drug causing it – if person is smoking or drinking coffee, ask them to stop? - Cardioversion should NOT be used FIRST-DEGREE AV BLOCK - Every impulse is conducted to ventricles but the time of AV conduction is prolonged - Associated with CAD, rheumatic fever, hyperthyroidism, electrolyte imbalance, vagal stimulation and drugs such as digoxin, beta blockers, calcium channel blockers and flecainide - HR normal and rhythm regular, P wave normal, PR >0.20 seconds, R also upside-down - Asymptomatic - No treatment – just monitor for changes in rhythm for more serious AV blocks SECOND-DEGREE AV BLOCK TYPE I (MOBITZ I, WENCKEBACH) - Gradual lengthening of PR interval – prolonged AV conduction time until atrial impulse in non-conducted and QRS complex is missing - May be from digoxin or beta blockers and diseases - Bradycardia, PROLONGED PR interval and normal QRS width, R wave normal – Looks like 2 fangs - Usually result of ischemia or inferior MI, usually transient and well tolerated - If patient is symptomatic o Atropine or temporary pacemaker if patient have MI - Monitor closely for hypotension, HF or shock SECOND-DEGREE AV BLOCK TYPE II - P wave non-conducted without progressive PR lengthening - More serious – 2:1 or 3:1 ratios P waves to QRS complex – a BUMP and then 2 fangs (P waves) - QRS > 0.12 seconds and R is upside down - Associated with heart rheumatic heart disease, CAD, anterior MI and drug toxicity - Decreased CO – hypotension and ischemia - Treatment: temporary pacemaker or permanent depending if patient becomes symptomatic THIRD-DEGREE AV BLOCK - Complete heart block – one form of AV dissociation in which no impulses from atria are conducted to ventricles - NORMAL P WAVE ALONG WITH PROLONGED QRS COMPLEX AND RATIO 3:1 - Associated with CAD, MY, myocarditis, cardiomyopathy, amyloidosis and scleroderma and drugs - Decrease in CO – lead to syncope, HF or shock - TREATMENT: TRANSCUTANEOUS PACEMAKER UNTIL TEMPORARY TRANVENOUS PACEMAKER CAN BE INSERTED - Drugs to increase HR until pacing starts – atropine, dopamine, epinephrine CHEAT CODE TO REMEMBER THE ORDER: QRS – DOWN, UP, DOWN, UP PREMATURE VENTRICULAR CONTRACTIONS - PVC – contraction coming from an ectopic focus in the ventricles - Wide and distorted in shape compared with a QRS complex coming down the normal conduction pathway. - Ventricular bigeminy – every other beat is a PVC - Ventricular Trigeminy – every 3rd beat is PVC - Couplet – two consecutives PVC - V-tach – 3 or more PVC - R-T – occurs when PVC falls on T wave of preceding beat CLINICAL MANIFESTATIONS - Associated with stimulants, electrolyte imbalances, hypoxia and heart disease - P wave not visible, PR not measurable, prolonged QRS, and large T wave and opposite of QRS - Not harmful with normal heart, but CO reduction, angina and HF in diseased heart - ASSESS APICAL-RADIAL PULSE – might have pulse deficit TREATMENT - Correct cause – hypoxia or electrolyte imbalances - Assess hemodynamic status – see if drug therapy is needed - Beta blockers, procainamide or amiodarone VENTRICULAR TACHYCARDIA - 3 or more PCV – occurs when ectopic focus fire repeatedly and ventricles takes control as pacemaker - Different forms of VT, depending on QRS o Monomorphic – QRS same size, shape and direction o Polymorphic– QRS changes back and force in shape, size and duration ▪ Torsades de points – French for I hate med-surg… o Nonsustained – less than 30 seconds - Development of VT is ominous – LIFE THREATENING – decreased CO or VF – LETHAL! - >30 seconds and sustained CLINICAL MANIFESTATION 54 - Associated with MI, CAD, electrolyte imbalances, long QT syndrome, or drugs - Ventricular rate: 150-250 BPM, P wave buried in QRS and QRS is wide and prolonged - Can be stable or unstable (pulseless) - Sustained VT – decreased in CO – Hypotension, pulmonary edema, cerebral blood flow, cardiopulmonary arrest - Dysthymias must be treated promptly TREATMENT - Treat precipitating causes – hypoxia - VT WITH PULSE treated with antidysrhythmics or cardioversion o Monomorphic – IV procainamide, sotalol or amiodarone o Polymorphic – IV magnesium, isoproterenol, phenytoin (Dilantin) or antitachycardia pacing - Pulseless VT – CPR and RAPID DEFIBRILLATION – FIRST LINE!!! o Vasopressors and antidysrhythmias if defibrillation doesn’t work VENTRICULAR FIBRILLATION - Severe derangement of heart rhythm characterized by ECG by irregular waveforms of varying shapes and amplitudes. Multiple firing of multiple ectopic foci in ventricle – ventricle is QUIVERING, no effective contraction and no CO occurs – LETHAL - Associated with MI, ischemia, diseases and procedures (catheter stimulation of ventricle. - HR NOT MEASUREABLE, RHYTHM IS IRREGULAR AND CHAOTIC, P WAVE INVISIBLE, QRS AND PR NOT MEASURABLE CLINICAL MANIFESTATION - Unresponsive, pulseless and apneic – must treat rapidly or patient might die TREATMENT - IMMEDIATE CPR OR ACLS – DEFIBRILLATION – MOST EFFECTIVE within 2 MINUTES - Epinephrine, vasopressin ASYSTOLE - Total absence of ventricular electrical activity – no ventricular contraction – depolarization does not occur - Patient unresponsive, pulseless and apneic - Might be caused by VF - ALWAYS assess patient with more than one lead – prognosis is extremely poor - Generally patients with end stage HF or prolonged arrest - Treatment: CPR or ACLS measures – then with epinephrine or vasopressin or intubation PULSELESS ELECTRICAL ACTIVITY - PEA organized electricity seen on ECG, but patient NO PULSE - Common after defibrillation - Prognosis is poor unless treated right away H T pneumonic Hypovolemia, Hypoxia, Hydrogen Ion, Hypo/Hyperkalemia, Hypoglycemia, Hypothermia Toxin, Tamponade, Thrombosis, Tension pneumothorax, Trauma Treatment – same as Asystole CARDIOVERSION AND DEFIBRILLATION Defibrillation - tx of choice to end VF and pulseless VT - most effective when the myocardial cells are not anoxic or acidotic - rapid defibrillation (w/in 2 mins) is critical to a successful pt outcome - involves the passage of an electric shock thru the heart to depolarize the cells of the myocardium - goal: following repolarization of myocardial cells will allow the SA node to resume the role of pacemaker - biphasic defibrillators deliver successful shocks at lower energies and with fewer postshock ECG abnormalities than monophasic defribrillators - biphasic defibrillators deliver the first and any successive shocks using 120 to 200 joules - after the first shock, start CPR immediately beginning with chest compressions - manual defibrillators require you to interpret heart rhythms, determine the need for a shock, and deliver a shock - automatic external defibrillator (AED) can detect heart rhythms and advise the user to deliver a shock using hands-free defibrillator pads - General steps for defibrillation 1) CPR should be in progress until the defibrillator is available 2) turn the defibrillator on, select the proper energy level 3) check to see that the synchronizer switch is turned off 4) apply conductive materials (e.g. defibrillator gel pads) to the chest, one to the right of the sternum just below the clavicle and the other to the left of the apex 5) charge the defibrillator using the button on the defibrillator or the paddles 6) position the paddles firmly on the chest wall over the conductive material 7) call and look to see that everyone is “all clear” to ensure that personnel are not touching the pt or the bed at the time of discharge 8) deliver the charge by depressing buttons on both paddles simultaneously R-ON-T PHENOMENON The "R-on-T phenomenon" is the superimposition of an ectopic beat on the T wave of a preceding beat. Early observations suggested that R-on-T was likely to initiate sustained ventricular tachyarrhythmias. More recent experimental and clinical observations suggest that R-on-T is not a critical determinant of primary ventricular fibrillation in acute myocardial infarction; represents few of the initiating beats of paroxysmal ventricular tachycardia; and represents at worst only a small risk in terms of sudden death. Apparently when the capacity for sustained repetitive beating has not been clinically obvious, R-on-T is quite unlikely to result in ventricular tachyarrhythmias, even in the presence of coronary heart disease. However, in the setting of acute myocardial infarction, inability to always identify the precursors of tachyarrhythmias strengthens the argument for prophylactic treatment of patients. CARDIAC PAIN AND PAIN MANAGEMENT ICU/ED- PRIORITIZING, TRIAGE, MASS CASUALTY CHOLECYSTECTOMY PANCREATITIS ESOPHAGEAL VARICES - Tortuous veins at lower end of esophagus englarged and swollen – CAN BLEED EASILY! - May have melena or hematemesis [Show More]

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