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Uremia- a major indicated of CKD, azotemia, increased BUN, n/v, h/a, dizziness GFR should be >60 CKD= GFR less than 60 for 3 months+ ESRD= GFR <15mL/min . leading causes DM and HTN o Uremia; syndrome in which kidney function declines to the point that symptoms develop in multiple body systems. Often occurs when GFR <10mL/min Proteinuria is usually first indication of kidney damage (dipstick) o Urinalysis can detect RBC, WBC, protein, casts, glucose o Ultrasound to exclude obstruction and note size o GFR is preferred over serum creatinine Normal Labs, BUN: 6-20, Creatinine .6-1.2 Drugs for concern with impaired renal function: digoxin, diabetic agents, antibiotics, opiods
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o o o
TABLE 47-2
Prerenal causes are factors external to the kidneys (e.g., hypovolemia) that reduce renal blood flow and lead to decreased glomerular perfusion and filtration. (DECREASED FLUID VOLUME, DECREASED CO, DECREASED PVR, DECREASED RENAL BLOOD FLOW) o Intrarenal causes include conditions that cause direct damage to the renal tissue, resulting in impaired nephron function. Acute tubular necrosis accounts for most cases of intrarenal failure. ( drugs, aminoglycosides, chemical exposure, allergies, infections, NSAIDS, ACE o Postrenal causes involve mechanical obstruction of urinary outflow. Common causes are benign prostatic hyperplasia, prostate cancer, calculi, trauma, and extrarenal tumors.
How would you treat hyperkalemia: TEMPORARY: o Insulin IV and Sodium Bicarb drive potassium into the cell, but it will come back out later. Insulin give with glucose to prevent hypoglycemia o For long term:
Kayexelate- osmotic diarrhea. Administered by mouth or retention enema. When resin is in the bowel, K+ is exchanged for NA+. It removed 1 mEQ of k+ per gram of drug. Mixed with water and sorbitol
Dialysis, brings to normal values within 30 min- 2 hour. MOST EFFECTIVE therapy for K+ removal) Also: calcium gluocnate IV- raises threshold for dysrhtmias
Diabetic: ACE/ARB but use with caition in ESRD because can lower GFR and raise K+
WHAT would be prescribed for anemia related to CKD? Anemia- decreased production of erythropoietin, exogenous EPO is used in the treatment o Epoetin alfa (EPOGEN, PROCRIT)---iv or subq 2-3x/week Target hemoglobin between 10 and 12 g/dL Regular HBG monitoring Dont give exogenous EPO if high BP Iron supplement: folic acid dialazble (in notes I have prokrit subq?) Iron may darken stool
Hemodialysis
Less protein loss, lowers serum triglycerides, rapid fluid/toxin removal Strict dietary/fluid restrictions, risk for HYPOTENSION
COMPLICATIONS OF HD(1187)
Hypotension- from rapid fluid removal , decreased CO and SVR. Drop in bp may precipitate lightheadedness, n/v, seizures, vision changes, chest pain . treat by decreasing volume of fluid being removed, AND INFUSE .9 %SALINE(100-300mL) hold bp drugs before HD if frequent hypotension Muscle cramps- common, reduce ultrafiltration rate, infuse hypertonic saline or normal saline bolus Blood loss: make sure to rinse back all blood, monitor heparinization to avoid excess anticoagulation, and hold firm but nonocclusive pressure on access sites until bleeding had passed Hepatitis : C most common Sepsis : usually from infection of vascular access sites . monitor for signs: fever, hypotension, elevated WBC. make sure to use
Abdominal pain: usually common , from low pH of dialysate solution, or from tip of catheter, so can change its position, or decrease infusion rate Outflow problems: when outflow is <80% of inflow immediately after cath placement, may be caused by a kink or migration of cat hut of pelvic region. Sometimes caused by a full colon, so evacuate the bowel to solve problem Hernias: more likely in predisposed people, like older men and multiparous women. After hernina repair, can continue PD after several days using small dialysate volumes and keeping PT supine Low back problems Bleeding: slight bleeding normal after first few changes. Bloody effluent over several days or new appearance of blood in effluent can indicate active intraperitoneal bleeding. SO CHECK BP AND Hematocrit. Pulmonary complications: atelectasis, pneumonia, bronchitis may occur from repeated upward displacement of the diaphragm, resulting in decreased lung expansion . long dwell time, more likely for pulm. Problems. FREQUENT BREATHING + REPOSITIONING can help , and elevate bed Protein loss. may lose as much as 5-15 g/day. Maintain adequate protein intake Hyperinsulemia from absorbed dialysate glucose (100150g/day) leads to increased insulin secretion , which can stimulate hepatic production of triglycerides
(disequilibrium syndrome) rare.. shift of fluid into brain : n/v, confusion, restlessness, h/a, twitching, seizures nurse should slow or stop dialysis and infuse hypertonic saline solution, albumin, or mannitol to draw fluid from brain cells.
During dialysis, nurse should: take vs every 30-60 minutes, daily weights, patency of av fistula/graft, strict I&OS, monitoring labs , peripheral pulses HD ACCESS pg 1184, know nursing implications of pt with graft or fistula Fistula: arterial blood flow thru vein, best overall patency and least complications, but surgery more time, complicated GRAFT: synthetic, hear bruit, feel thrill..more likely to clot than a fistula . complications: steel syndrome(from distal ischemia), aneurisms, infections
WHEN DOES PATIENT NEED DIALYSIS?? When GFR is less than 15ml/min _______________________________________________________________________ _______________
RESPIRATORY
Page 513 Table 26-10 Know the diagnostics we discussed in class Ct scan- check if allergic to iodine/shellfish, be sure pt is well hydrated before and after V/Q- assesses ventilation and perfusion in lungs. Ventilation without perfusion = pulmonary embolus. Patient inhales a radioactive gas with outlines the alveoli Page 513 Table 26-8 focus on inspection and auscultation What lung sounds will you hear with the COPD patient or the patient with asthma? Wheezes musical, continuous, high pitches. Caused by bronchospasm airway obstruction, tumor Ronchi, crackles- COPD
Pneumonia(ch 28) Know types of pneumonia, causes, treatment and nursing care. Know the same for COPD, asthma
Gram negative are not normal in resp tract Causes: 1)aspiration of normal flora from nasopharynx, 2)inhalation of microorganisms present in the air (ex. Mycoplasma pneumoniae) and fungal pneumonias, and 3)hematogenous spread from from a primary infection elsewhere in the body (example: s aureus) CAP, HAP, and ventilatorAP- (occurs more than 48 hrs after endotracheal intubation)
Health care associated pneumonia (HCAP)- a new onset pneumonia in a PT who 1)was hospitalized in an acute care hospital for 2 days or longer within 90 days of the infection; 2) resides in a long-term care facility, 3) receives IV antibiotic therapy, chemo, or wound care within past 30 days of current infection, or 4) attended a hospital or hemodialysis clinic Most common cause of CAP= STREP. PNEUMONIAE
Pneumocystis jiroveci (PCP) rarely causes pneumonia in healthy ppl but is most common cause in ppl with HIV . must first rule out viral and bacteria PA Cytomegalovirus (CMV) a cause of viral PNA in the immunocompromised PT, particularly in transplant recipients. Use antivirals Pneumococcal PA may have rust colored sputum Manifestations in elderly- confusion or stupor may be only finding (related to hypoxemia) Physical assessment findings: pulmonary consolidation, such as bronchial breath sounds, crackles dullness on percussion, and increased fremitus (S pneumoniae, H. Influenza) Vital PA: variable, chills, fever, dry/nonproductive cough, extrapulmonary symptoms Some complications o Empyema- pus exudate accumulation in pleural cavity (occurs in <5%)- need antibiotic therapy and drainage by chest tube DIAGNOSTIC STUDIES o Chest xray (determine if viral or bacterial and can show presence of pleural effusion) Lobar/segmental consolidation = bacterial (usually S. pneumoniae or Klevsiealla) Diffuse pulmonary infiltrates = viral infection (legionella, or pathogenic fungi) Cavitary shadows = presence of a necrotizing infection with a destruction of lung tissue commonly caused by S. Aureus, a gram bacteria, and M. Tubercolusis. o Do sputum specimen before beginning IV antibiotic therapy (but dont delay antibiotics if a specimen cannot be obtained) o ABGs to assess for hypoxemia (= PaO2 <80%), hypercapnia (paCO2>48 mmHg), and acidosis o Blood cultures are done for patients who are seriously ill o Leukocytosis common with bacterial PA (wbc is usually >15,000 with presence of bands(immature neutrophils)
Patient responds to drug therapy within 1 to 2 days: see decreased temp, improved breathing, and reduced chest pain
NURSING CARE o Hydration important! , fluid intake is individualized if PT has HF, if pt cant maintain oral intake, IV administration of fluids and electroyles becomes necessary o Weight loss usually occurs with PA, so maintain adequate nutritional intake, SMALL, FREQUENT meals are easier for dyspneic patients to tolerate o Health promotion: hygiene, AVOID CIG SMOKE, adequate rest, exercise, vaccines o In hospital, ID patients at risk and take preventative measures (minimize risk of aspiration, side lying position or upright in unconscious pts), turn and reposition at least q 2 hrs, ambulation, reduce VAP o With NG tubes, elevate HOB 30-40 and monitor gastric residual volumes
Assess for gag reflex in patients who have had analgesics in throat o STRICT ASEPTIC TECHNIQUE o Incentive spirometry, chest PT, monitor 02 sats, lung sounds, turn cough deep breathing
ACH 29 ASTHMA
**wheezing, cough, dyspnea, chest tightness after exposure to a precipitating factor or trigger, expiration may be prolonged hyperventilation: hypoxemic, decreased PaCO2 and increased pH (resp alkolosis) pt works harder to breath, Co2 normalizes as patient tires, then increases to produce resp acidosis, which is an ominous sign signifying resp failure ***drugs that may precipitate asthma: NSAIDS, ACE, beta blockers GERD may trigger asthma Acute attack of asthma: signs of hypoxemia (restlessness, anxiety) increased pulse (120+) and BP, difficulty speaking in complete sentences; RR may increase to 30+ breaths/min with use of accessory muscles. HYPERRESONANT lung sounds, also WHEEZES Acute attackpeak flow is 40% of personal best or less than 150mL SILENT CHEST IS OMINOUS SIGN INDICATING SEVERE OBSTRUCTION AND IMPENDING RESP FAILURE classified as mild intermittent, mild persistent, moderate persistent, or severe persistent, based upon current impairment of the patient and their risk for exacerbations. Pulmonary function tests: pt should hold bronchodilator meds for 6 to 12 ours before the test. A pos response to bronchodilator is an increase of more than 200 mL and an increase of more than 12% between preadmin and postamin values ^^serum oesinophil and serum IgE = suggest atopy (allergic tendency), during an acute attack, bedside spirometry may be used to monitor obstruction cbc, electrolytes, sputum specimen can help rule out bacterial infection (but most asthma exacerbations are viral)
In life threatening asthma- these are given IV and tapered rapidly (methylprensidosne IVC given every 4-6 hours, then pt is started on oral glucocorticoids)length of oral gluco= 10 days. Inhaled gluco added when pt is still in hospital . 02 is given, ABG monitoring, iv fluids, sodium bicarbonate for acidosis. Dont do chest pt. epinephrine if SABA not available Fluid intake of 2-3 L/day, adequate rest Wheezing gets louder when resp status is improving Important during an acute attack to relieve patients panic. Firm calm voice, stay with them, pursed lip breathing Health promotion: avoid cig smoke, pet dander, irritants (cold air, aspirin, food, cats, indoor air pollution) o Use of special dust covers on mattresses or pillows, washing bedclothes in hot water or cooler water may with detergent and bleach, avoidance of furred animals, cockroach remains Table 29-2 page 592(CLASSIFICATIONS OF ASTHMA SEVERITY) Table 29-3; (COMPARISON OF ASTHMA AND COPD) Table 29-7 drug therapy. Know those we reviewed in class
DRUGS: SABAs gold standard and most effective (albuterol Inhaled corticosteroids most effective to combat inflammation (fluticasone) Rescue plan: 2-4 puffs of albuterol every 20 mins 3 times to gain rapid control of symptoms
Severe exacerbations: KEEP 02>90%, CONTINUOUS MONITORING, IF PEFR can be obtained, if less than 200L/Min= severe obstruction. Give SABA (and maybe ipratropoum(atrovent)) . nebulized SABAS are continued for several days Corticosteroids 1-2 weeks before max therapeutic effects seen, but some in 24 hours. FIXED schedule dosing o Side effects: easy bruising, accelerated bone loss , local side effects from inhalation: oropharyngal candidasis, hoarseness, dry cough. THESE CAN BE REDUCED BY USING A SPACER with the MDI or by gargling w/ water or mouthwash after each use o Single dose in morning, alternative day dosing o Women, especially postmenopausal, should take calcium and vitamin C supplements + regular weight bearing exercise LEUKOTRIENE modifiers: inhibit leuktrienes with are potent bronchoconstrictors, o ORAL ADMINISTRATION prophylaxis and maintenance therapy o some cause airway edema and inflammation. Not for acute therapy, o bronchodilator and anti-inflammatory o can be used as add on therapy to reduce the doses of ICS ANTICHOLINERGICS: (ipapratropium (ATROVENT)) = block parasympathetic nervous systems bronchoconstricting influence o NEBULIZER, MDI o IPAPTROPRIUM + ALBUTEROL = DUONEB o Less effective than b2 agonists o Used for quick relief in pts unable to tolerate SABAS, or in severe asthma exacerbtion, often nebulized with SABA o Slower onset of action than b2 agonists , peaking at 30 mins to 1 hour, lasting up to 4-6 hrs. common side effect: dry mouth o Vision side effects? Blurred vision if sprayed in eyes B2 ADRONERGIC AGONISTS (ALBUTEROL) o Dont inhibit late phase response o May produce tremors, anxiety, tachycardia, palpitations, nausea o Overuse may cause rebound bronchospams o Shouldnt be used alone for persistent asthma o LABA: SALMETEROL(SEREVENT) .
Effective for 12 hours. Added to daily dose of ICS for long-term control of moderate to severe persistent (Fluticasone/Salmeterol..[advair] NEVER USED AS MONOTHERAPY, shouldnt be used for acute symptoms or from relief of bronchospasm ONCE every 12 hours
HOW TO USE MDI (FIG 29-7) ----May use with spacer 1)Take off cap and shake inhaler 2) breath out all the way 3)hold it the right way 4)as you start breathing in slowly through your mouth, press down on inhaler one timekeep breathing in slowly, as deeply as you 5) hold breath as you count to 10 slowly. Wait 1 min between puffs only for inhaled quick relief medicine (b2 agonists) Rinse mouthpiece and cap in warm water , let dry overnight (clean at least 2 x/week) Dont put canister in water or shake it to see if its empty, you should know how many puffs each canister has and know when to replace it (write the date)
Subjective----past health history (allergies, previous asthma attacks?, triggers? GERD?, exposure?) MEDications: adherence? Inhaler technique? How much SABA use per week? Meds that may precipitate an attack? Aspirin, NSAIDS, BB) Functional health pattern o Health perception health managementfamily history of allergies or asthma, recent URI or sinus infection? o Activity-exercise : fatigue?dyspnea, cough, sputum? Chest tightnesssitting upright to breathe? o Sleep-rest: awakened because of coughing or breathing difficulties? o coping-stress tolerance Objective: general: restlessness, upright or forward leaning body position, confusion..diaphoresis, cyanosis, eczema..nasal discharge,,,polyps, muscosal swelling, wheezing/crackles, diminished/absent breath sounds, rhonchi on ausclatation, hyper resonance on percussion , sputum (thick, white, tenacious) tachypnea and hyperventilation, prolonged expirations.tachycardia, pulsus paradoxus, JVD, HTN or hypotension o Diagnostic findings: decreased 02sat,^^serum oesinophil and serum IgE = suggest atopy (allergic tendency), +skin test for allergens, chest xray showing hyperinflation with attacks, abnormal PFT showing decreased flow rates that improvement between attacks and with bronchodilators Can show when airways are narrowing Stand up, deep breath in, blow out as fast and hard as possible, write down best number out of 3 Personal best peak flow: highest # you can achieve over a 2-week period when asthma is
under good control . to find PEF: o Take peak flow readings at least 2x a day for 2-3 weeks, when you wake up in late afternoon or early evening, 15-20 mins after taking inhaled SABA, and as instructed by health care provider peak flow green zone 80-100%, remain on meds peak flow yellow zone 50-80% personal best . Indicates caution. If continue in yellow zone, take SABA and ask doctor about changing or increasing meds peak flow red zone SABA RIGHT AWAY 50% or less of personal best, indicates serious problemTAKE
ASTHMA NURSING CARE PLAN 29-1 (pg 605) o ineffective airway clearance. Blah blahwarm fluids may help
STAY with PT, encourage slow breathing using pursed lips for prolonged expiration, position comfortably o Deficient knowledge. Teach about IDing and avoiding triggers , PEFT for self management, inhalers, recognize signs and symptoms of impending attack ___________________________________________________________________________________________________________ __________
Chronic bronchitis is the presence of chronic productive cough for 3 months in each of 2 consecutive years in a patient in whom other causes of chronic cough have been excluded. Emphysema is an abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis Classification (0-5)at risk, mild, moderate, severe, very severe 28-24 pg 626 . Past health history and meds important Functional health patterns: o Health perception: smoking? o Nutritional./metabolic: anorexia, wt loss or gain o Activity/exercisedyspnea? SOB? Walk up stairs? Cough, sputum? Orthopnea? o Elimination, sleep rest, coping/stress tolerance o Cognitive/perceptual: headache, chest or abdominal soreness Objective: skin, wheezing, ronchi, crackles, hyperresonant or dull chest sounds on
percussion, jvd, right-sides s3, (cor pulmonale), edema (esp. in feet), ascites, hepatomegaly (cor pulmonale),,, muscle atrophy, increase AP diameter (barrel chest) Pg 620- CO2 Narcosis o Normally CO2 accumulation is the major stimulant of the resp center and causes us to breath. Over time some COPD pts develop a tolerance for high Co2 levels (so resp center loses its sensitivity to the elevated Co2 levels) these peoples drive to breath, then, is hypoxemia. So there are concerns regarding the dangers of administering O2 to COPD patients and reducing their drive to breath. Start low flow 02 until ABGs can be obtained . Before 02 therapy, assess mental status and vital signs (IN SIMPLER TERMS, GIVING TOO MUCH 02 MAY SHUT DOWN THEIR DRIVE TO BREATH, and they retain too much co2) SO PROVIDE 02 AT LOWEST EFFECTIVE DOSE YALL