Hostedvoipinfo.net



OXYGENATION LECTURERespiratory System...Structure & FunctionLower Respiratory Tract…Alveolar ductsAlveoli - FUNCTIONAL UNIT OF THE LUNG~300,000,000 ALVEOLI IN THE LUNGTotal Volume of ~ 2500 mlSurface area for gas exchange that is about the size of a tennis courtSURFACTANTNURSING DIAGNOSIS (definition and defining characteristics:Ineffective airway clearanceGas Exchange, ImpairedNOCsReview the following:Respiratory status:Gas ExchangeVentilationTissue Perfusion:PulmonaryAcid-Base BalanceNICsAcid-Base ManagementGas exchange, ImpairedVentilation and PerfusionAlveolar Dead Space+ ventilation- perfusionIntrapulmonary Shunting- ventilation+ perfusionOBSTRUCTIVE SLEEP APNEAPeriodic apneic or hypopneic episodes during sleep associated with Upper airway obstruction due to pharyngeal collapse, leading to Awakening and resulting restoration of airway patencySleep recurs almost immediately and the cycle repeats itself, often hundreds of times each night EpidemiologyPrevalence estimated at 4% male; 2% female (NEJM 328:1230, 1993) May be as much as 40-50% of hypertensive Pts90% of pts with nocturnal angina (Lancet 4/29/95) Incidence greatest age 40-60Highly underdiagnosed, perhaps due to the gradual onset of s/sMore underdiagnosed in women than men.Mean duration of s/s before dx in one series of women was 10yearsThere is normall a moderate degree of hypoventilation during sleep resulting from partial phyarngeal collapse and resulting increase in upper airway resistance. Structural factors: can possibly be a structural abnormality. There is a larger role of women that have structural abnormalities that cause SA. Functional factors: 1. Altered sleep2. influences on palatal muscle control3. may have impaired ventilator drive or arousal mechanismsTreatment: Surgical / remove obstructionCPAPSupport groupProblems of the LOWER AIRWAYStatistics:Decrease number of deaths R/T acute & chronic respiratory infections due to antibioticsIncrease in TB over last ten years, especially the last 5years due to AIDS/HIVMore people living with COPD (>17 million)^ incidence of lung cancer, especially among women^ number of teenagers starting to smokePneumonia is the leading cause of death by infectious disease in the U.S.PREVENTIONEducation/advocacy for smoke-free environment (The use of tobacco is the #1 risk to developing COPD and lung cancerMost people start smoking in high schoolNicotine addiction results in withdrawal symptomsSmoking is tied to ETOH (alcohol) consumption and lower achievementAdvertising targets fantasies and insecurities of teens and young adultsObstructive & Restrictive Lung DisordersRestrictive Lung DisordersGeneral (extrapulmonary)head injuries, tumors, OD (overdose)Neuromuscular (extrapulmonary)GB (guillian barre), ALS, MD, Polio Chest Wall (intrapulmonary/extrapulmonary)traumaPleural Disorders (intrapulmonary)pleural effusion, pleurisyParenchmal (parenchmal)atelectasis, pneumonia, TB, pulmonary fibrosisObstructive Lung DisordersAsthmaCOPDAcute BronchitisChronic BronchitisEmphysemaCharacteristics of Lung DisordersRestrictiveReduced Vital CapacityReduced Total Lung CapacityNormal or reduced Functional Residual CapacityCause difficulty with inspirationObstructiveDecreased resistance to airflowNormal or decreased Vital CapacityIncreased Total Lung CapacityIncreased Functional Residual CapacityIncreased Residual VolumeWe will not be tested on normal pulmonary function(total lung capacity is total amount we can get in. vital capacity is a normal breath)OBSTRUCTIVECharacterized by: INCREASED TO AIR FLOWRESTRICTIVECharacterized by:DECREASED COMPLIENCE OF THE LUNG OR CHEST WALL OR BOTHOBSTRUCTIVE LUNG DISORDERSEMPHYSEMALoss of elastic recoil secondary to breakdown of lung tissue and enlargement of alveolar spaces - leads to retention of CO2Emphysema is the most severe form of COPD is characterized by abnormal, permanent enlargement of the air spaces past the terminal bronchioles, resulting in the destruction of the alveolar walls The affected terminal bronchioles contain mucus plugs and the eventual resulting loss of elasticity of the lung parenchyma resulting in difficulty in exhalingUse tripod or pursed lip breathing to get them to increase the breath. We might see: barrel chest, hyperresonance, clubbing. Spacer on an inhaler helps to prevent person who doesn’t lose any of the medication. Have patient inhale & hold it in… try to hold it as long as they can. Then they need to rinse their mouth to prevent thrush. 1963 - Discovery of deficiency of AAT (Alpha Protease Inhibitor) which is associated with serous and premature development of emphysema. These enzymes (Pancreatic Elastase, Trypsin, Chymotrypsin, Granulocyte Elastase) defend the lungs against destructive processes R/T Neutrophil Elastase which destroys tissue. Bullous Emphysema is the result (cavernous)If a patient has been diagnosed w/ AAT they really need to not smoke, don’t get second hand smoke…AAT (alpha-1-protease inhibitor)Familial emphysema have a hereditary deficiency of AATNumber of Americans with this genetic deficiency small (~70,000)1 in 3,000 newborns have a genetic deficiency of AAT1 to 3 percent of all cases of emphysema are due to AAT deficiencyCritical that these people not smokeThe destruction of elastin that occurs in emphysema is believed to result from an imbalance between two proteins in the lung:An enzyme called elastase which breaks down elastin, andAAT which inhibits elastase.In normal individuals, there is enough AAT to protect elastin so that abnormal elastin destruction does not occurPermanent destruction of the alveoliDue to irreversible destruction of the protein elastinElastin is important for maintaining the strength of the alveolar wallsThe loss of elastin also causes collapse or narrowing of the bronchiolesEnd result of above sequence limits airflow out of the lungs. (air is trapped… purse lipped breathing helps to expire a little more)ETIOLOGYPrecise cause is unknown, but thought to involve destruction of the connective tissue of the lung by protease's that may be facilitated by the effects of cigarette smokingEPIDEMIOLOGYSymptoms usually occur in the fifth or sixth decade of lifeTypical patient is male over the age of 55 with a history of tobacco smokingHeredityEnvironmental irritants/pollutionPATHOPHYSIOLOGYCentrilobular Emphysema (CLE)Distention and damage of the respiratory bronchiolesUneven disease distribution throughout the lungUsually more severe in the upper portionsMore common than Panlobular emphysema (PLE)Panlobular Emphysema (PLE)More uniform enlargement and destruction of the alveoli in the pulmonary acinusMore diffuse and is more severe in the lower lungsASSESSMENTS&SSubjectiveHx and onset of symptoms (how old were you when you started to cough? Smoking Hx (how many years? Pack year history?)Family HxPast or present exposure to environmental irritants (working around coal mines or shipyards) Activity intolerance, fatigueAnorexia, weight lossSymptoms of hypoxemia - restlessness, confusionMedications and therapies and their effectivenessAssessment...ObjectiveIncreased airway resistanceDecreased Expiratory ForceMild hypoxemia (pick up w/ O2 sat monitor) Barrel ChestIncreased AP diameterIncreased Accessory MusclesABG’s show compensation (pH is normalizing & CO2 will start to drop)Increased respiratory rateDyspneaDecreased breath soundsLate inspiratory cracklesDecreased O2 saturationLAB FINDINGSABG’s may be normal due to compensation for the destruction by increased resp rateEven in the presence of hypoxemia overcompensation may result in respiratory alkalosisPO2 normal or slightly low at rest, but drops with activityCBC usually normalDIAGNOSTIC TESTSChest X-Ray -- positive findings indicate increased radiolucency of lungs with diaphragm in low positionAAT assay to check for deficiencyPulmonary functions tests --Increased residual volume, functional residual capacity, total lung capacityDiffusing capacity is reduced because of tissue destructionDecreased Forced Expiratory VolumeVital Capacity may be normal or slightly reduced until late state of diseaseINTERVENTIONSBronchodilators may provide relief from symptoms but will not cure the disease Antibiotics if there is an infectious process occurringSteroids during acute exacerbation's (get them weaned off as soon as possible)Low flow oxygen (1-2 liters)Breathing exercisesRespiratory therapy & CPT (chest physiotherapy)Lung reduction surgeryPerformed only on pts with severe emphysemaAvg. hospital LOS ~ 2 weeksRequire pre and post op extended pulmonary rehabFalling out of favor in the prior yearPatients with COPD can help themselves in many waysStop smokingAvoid work-related exposures to dust & fumesAvoid air pollution, and curtail physical activity during alertsRefrain from contact with people that have URI… (upper respiratory infection)Get pneumonia vaccination and yearly influenza shotsAvoid excessive heat, cold and high altitudesDrink fluids (to help thin the secretions) Maintain good nutrition – high proteinConsider allergy shotsAnother Nursing DiagnosisAltered nutrition: less than body requirements related to dyspnea, sputum production, or fatigueInterventions:Explain importance of consuming adequate amounts of nutrientsProvide a pleasant, relaxed atmosphere for eating (small meals several times a day, wear oxygen while eating) Expected Outcomes:Pt will verbalize & understand importance of adequate nutritionPt will use a comfortable environment for mealsPt will eat slower and smaller mealsMore NURSING DIAGNOSISIneffective airway clearanceAltered Gas Exchange Breathing pattern, Ineffective Activity IntoleranceInfection: Actual or PotentialRisk for Nutrition: Less than Body RequirementFear AnxietyKnowledge DeficitNursing DiagnosesIneffective airway clearance r/t bronchospasm, ineffective cough, excessive mucus production, Anxiety r/t difficulty breathing, perceived or actual loss of control, and fear of suffocation and restlessnessIneffective therapeutic regimen management r/t lack of information about COPD and its treatmentNursing DiagnosesActivity intolerance r/t fatigue, energy shift to meet muscle needs for breathing to overcome airway obstructionDisturbed body image r/t decreased participation in physical activitiesImpaired home maintenance r/t deficient knowledge regarding control of environmental triggersIneffective coping r/t personal vulnerability to situational crisisNursing InterventionsAirway ManagementAdminister humidified air or oxygen immediatelyRegulate fluid intakeMonitor respiratory and oxygenation statusAdminister drug therapy (bronchodilators, corticosteroids)Auscultate lung sounds before and after treatments (first time you listen they sound horrible, have them take deep breaths & then lungs should sound better) Cough Enhancement Positioning for chest expansionDeep breathing, hold for 2 seconds, and cough 2-3 times These interventions will help them to maintain their airway. Often the secretions are worse in the morning…Nursing InterventionsRespiratory MonitoringRate, rhythm, depth, and effort (overall patterns)Monitor for increased restlessness, anxiety, and air hungerNote changes in SaO2, ABG valuesNursing InterventionsAnxiety ReductionCalming & reassuring attitudes (help w/ fear & anxiety of not being able to breathe). Stay with patientEncourage slow breathing (pursed lips)Nursing InterventionsTeaching: Disease Process & Prescribed MedicationIdentify level of knowledge (make sure patient understands what is going on, why you are giving the meds, we need to determine their level of understanding) Instruct on measure to prevent/minimize side effects of treatment (how to properly do a nebulizer treatment, etc…)Evaluate patient’s ability to self-administer medications Instruct patient on purpose, action, dosage, and duration of each medicationInclude family and significant othersPulmonary Function TestsArterial Blood Gases (ABGs)Arterial Blood Gases (ABGs)Determines how much oxygen is available to perfuse peripheral tissuesNormal values:pH: 7.35 - 7.45PaCO2: 35 - 45PaO2: 80 - 100HCO3: 22 - 26SaO2: 95 - 100Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory acidosis.Planning & InterventionMedications:Bronchodilators – to relax smooth muscles in the airways and reduce congestion Xanthine Compounds – Theophylline to reduce mucosal edema and smooth muscle spasms – also strengthens contractility of the diaphragm (can come in tablet… another form can be given IV)Sympathetic Agents: PO, Inhalation (Albuterol, Terbutaline)Rescue inhalers – Albuterol… (fast acting broncho dialators… don’t need to be used all the time, pollen)Corticosteroids – Solu Medrol – IV or PO to alleviate acute symptoms by decreasing inflammation (hour glass vial, powder in the top, you take the metal cap off, push on the rubber plunger… pushes the powder through into the fluid in the bottom & then give a direct IV push. Will start on IV in an acute situation, eventually wean them & get on a PO med) Antibiotics – to manage respiratory tract infectionsMucolytics and expectorants – to thin and aid in removal of mucusAnalgesics (nsaid or Tylenol for aches & pain)Flu ShotsGiven early October to mid November (however can be given any time during the flu seasonGiven yearlyCost for people > 65 is paid by Medicare Recommended for:>50 years oldChronic heart or lung diseaseHIV (compromised immune system) Anyone living in large groupsPeople who may transmit the flu to high risk groups Nurses, doctors, and other healthcare workers You should NOT get the flu shots if Allergic to eggs Hx of Guillain-Barre Syndrome Acute illness or feverSide effects<1 out of 3 develop site sorenessRare to have fever, achesRecent research shows that flu shots do not increase asthma attacksNOTE: flu vaccine is made from a virus that is no longer active – NO one can catch the flu from flu shot. PULMONARY EMBOLISMMEDICAL INTERVENTIONS Anticoagulants (prevents a clot from forming, coumadin & heparin)Thrombolytic therapy (break up a present clot, TPA, streptokinase & eurokinase)PE usually comes from legsSURGICAL INTERVENTIONSEmbolectomy (if it is large enough)NURSING DIAGNOSISImpaired gas exchangePulmonary Embolism….Risk factors for PERecent surgery Recent fx of a lower extremity, especially with immobilization Immobilization, particularly complete bedrest or LE (lower extremity) paralysis Previous DVT or PE Family history of DVT or PE Cancer Obesity Cardiovascular disease Postpartum period Sub therapeutic heparin dose Age > 40 years Pulmonary Embolism….Predisposing factors & Precipitating Conditions that make some higher risk for developing DVT/PE Prolonged immobility or paralysisInjury to vascular endotheliumHypercoagulabilityCVP catheter (central venous pressure catheter) HistoryCV diseaseCancerTraumaPregnancy & estrogen use Virchow’s TriadThree primary factors that predispose to venous thrombosis:Venous stasisInjury to vascular endotheliumHypercoagulability Typical clinical featuresS&STachypnea Dyspnea, sudden onset or worsening of chronic dyspnea Tachycardia Pleuritic chest pain or chest pain that is nonretrosternal and nonpleuritic Syncope CoughFeeling of impending doomHemoptysisArterial oxygen saturation < 92% on room air Low-grade fever (occasionally) HemoptysisHypoxemia Pleural friction rub Clinical evidence of DVT Sudden hypertensionProphylaxis for DVTMechanical intervention to decrease venous statusEarly ambulation or change position q2hCompression stockings (or Ted stockings)Intermittent pneumatic compression stockingsPharmacologic agentsLow molecular wt. Heparin Low dose unit HeparinWarfarinLow dose ASA (81 mg enteric coated baby aspirin)Hypoxemia in PE caused byV/Q mismatchingIntrapulmonary shuntDead space ventilationClinical features of severe PE:Hypotension (from reduced left-heart venous return) Right heart failure Dignostic Evaluation to Confirm PEV-Q lung scan (limited specificity) – test will come back saying “limited specificity”… not really sure if there is a clot. MRIPulmonary angiographyCXR may show evidence of pulmonary infarct (also limited specificity) Lower extremity venous duplex (DVT requires same tx as PE) –like a Doppler (study of the leg) A negative study does not exclude PE! MEDICAL INTERVENTIONS:AnticoagulationLow molecular wt. Heparin (lovenox)Low dose unit HeparinWarfarinSURGICAL INTERVENTIONSEmbolectomyGFF (green field filter)… looks like an umbrella, goes in the vein to trap the clot) NURSING DIAGNOSISImpaired gas exchange…Heparin NomogramAnticoagulation form Venous Thrombosis/Peripheral Vascular DiseaseAdjustment Contingency Table(25,000 units Heparin/500ml D5W) PTT Bolus (units) Hold (min) Rate Change Repeat PTTBelow 41 2000 unit 0 min +4ml/hr (200units/hr) 6hrs41-49 1000 units 0 min +2ml/hr (100units/hr) 6hrs50-80 0 0 minNO RATE CHANGE next AM81-89 0 0 min-2ml/hr (100units/hr) 6hrs90-106 0 60 min-4ml/hr (200units/hr)6hrsAbove 106 0 120 min-4mil/hr (200units/hr) 6hrsPTT = partial thrombosin time? Usually check every 6 hours w/ another PTT. Heparin works very quickly while Coumadin works over a period of days. PTINR is to test Coumadin. PTINR w/ Coumadin will be 2.5 to 3.5. Med to reverse heparin… PTT comes back at 118, physician want to take pt to surgery protamine sulfate is drug given… immed reverses heparin.Vitamin K will immediately reverse Coumadin. Those patients on Coumadin has to know not to eat green leafy veggies… too much vitamin K will reverse the effects of Coumadin. Greenfield FilterRestrictive Lung DisordersGeneralhead injuries, tumors, ODNeuromuscularGB, ALS, MD, PolioChest WallTraumaPickwickian syndromePleural Disorderspleural effusion, pleurisy, pneumothoraxParenchmal atelectasis, pneumonia, TB, pulmonary fibrosis, ARDSPNEUMONIAAcute infection of lung tissue resulting from inhalation or transport via bloodstream of infectious agents, noxious fumes, or radiation therapy. An acute inflammation of the lung parenchyma associated with the production of exudateLUNG CANCERPrimary lung cancer is the leading cause of death in men and women who have malignant disease in the U.S.Mortality rate increasing - in 1994 there were 153,000 deaths from lung cancer5-year survival rate is 13%Found most frequently in person 40-75 years of agePATHOPHYSIOLOGY> 90% of lung cancer originate from the epithelium of the bronchus (bronchogenic)Primary lung cancers are often categorized into histologic typesMets occurs primarily by direct extension and via the blood circualtion and the lymph systemCommon sites for mets are the liver, brain, bones, scalene lymph nodes, and adrenal glands.STATS, CAUSES & RISK FACTORSSmoking is responsible for ~ 80-90% of all lung cancers~ 1 out of every 10 heavy smokers develop lung cancerThe risk of cancer gradually decreases when smoking ceases and continues to decline - estimates are that it takes ~ 15 years for the risk of lung cancer of former smokers to equal that of a nonsmokerInhaled carcinogens - such as asbestos, nickel, iron, air pollutants, etc. increase the risk of lung cancerDIAGNOSTIC TESTSChest X-Ray: Shows increased bronchovascular markingsPulmonary functioning tests:Decreased forced expriatory volume and vital capacity, and increased residual volumeArterial Blood Gas (ABG) studiesrespiratory acidosis, hypercapnia, Hypoxia Complete Blood CountElevated Hbg and Hct (polycythemia)Elevated WBCPulse OximetryPt. usually hypoxicSputum C&S: neutrophils and bronchial epithelial cells presentSTATS, CAUSES & RISK FACTORSHeredityPreexisting pulmonary diseasesIncidence of lung cancer correlates with the degree of urbanization and population densitySecond hand smoke exposureRisk of developing lung cancer is directly related to total exposure to cigarette smoke - Pack Year History CLINICAL MANIFESTATIONSGeneral nonspecific & appear late in the disease processDependent on the type of lung cancerOften there is extensive mets before symptoms become apparentPersistent cough (may or may not be productive)Chest PainDyspneaCLINICAL MANIFESTATIONSLater manifestations: anorexia fatigueweight losshoarsenessif mediastinal involvement may havepericardial effusioncardiac tamponadedysrhythmiasDIAGNOSTIC STUDIESChest X-rayCT scansMRIPET - (position-emission tomography) - measurement of differential metabolic activity in normal and diseased tissueDefinitive diagnosis of lung cancer is made by: Identification of malignant cellsRadionuclide scans (liver, bone, brain …)Pulmonary angiography and lung scansMediastinoscopy Staging of TumorsStaging of nonsmall cell lung cancer (NSCLC) is performed according to the American Joint Committee’s TNM staging system.T=denotes tumor size. Location, and degree of involvementN=indicates regional lymph node involvementM=represents the presence or absence of distant metastasesStaging of small cell lung cancer (SCLC) not useful because the cancer has usually metastasized by the time the Dx has been made.THERAPEUTIC MANAGEMENTSurgical resection - decision is dependent on type and location of tumorLobectomypneumonectomyRadiation therapyCurative approach with resectable tumor but poor surgical riskAdjuvant with other approachesPalliative to reduce symptomsChemotherapyUsed as adjuvant Laser surgeryNURSING MANAGEMENTNursing DiagnosisIneffective airway clearance R/T increased tracheobronchial secretionsAnxiety R/T lack of knowledge of diagnosis or unknown prognosis and RxIneffective breathing pattern R/T decreased lung capacityPlanning - Overall goals are that the pt with lung cancer will have:effective breathing patternsadequate airway clearanceadequate oxygenation of tissuesminimal to no painrealistic attitude toward Rx and prognosisASTHMAImpact of Asthma in the U.S.Affects 17,000,000 individuals in U.S.> 20 million outpatient visits/year> 1.6 million ED visits/year> 500,000 hospitalizations/year> 20 million lost work days/year> 10 million lost school days/yearNCHS 1998 CDC asthma surveillanceAffects 24,700,000 individual in U.SIncreased 60% over the prior 10 years~ 2 million ED visits/yearMortality has doubled since 1978African-Americans: death rate is 2 to 5 times that of Caucasian death rateAccount for ~ 20 million lost work days/yearAnnual health care costs ~ 12.7 billion $American Lung Association Fact Sheet 2002HyperventilationAirway walls are thickened with inflammatory exudates which enhances bronchospasms and reduces expiratory flow.Results in increased work of breathing and hyperinflation away from the obstruction.Air trapping inside the lungs causes the individual to hyperventilate.Signs and Symptoms of AsthmaAbrupt or gradual onsetInspiratory and/or expiratory wheezingShortness of breathNon-productive cough leading to thick, stringy mucus during attackPosition: High Fowlers, tripodPercussion: HyperresonanceProlonged expirationTachycardiaTachypneaUse of accessory musclesDyspneaChest tightnessHypoxemiaNasal flaringAsthma …The high morbidity/mortality rate is due to:inaccurate assessment of diseaseincreased allergens/irritants in the environmentdelay in seeking medical helpinadequate medical Rxlimited access to health carenon adherence with prescribed therapyPATHOPHYSIOLOGYHyperirritability or hyperresponsiveness tracheobronchial treeBronchoconstriction in response to physical, chemical and pharmacolgic agentsPHASES OF ASTHMAEarly Phase (30-60 minutes)Triggered by allergen or irritantMAST cell degranulation -- Immune Mediator ReleaseBronchial smooth muscle constrictionMucous SecretionVascular LeakageLate Phase (5-6 hours to 2 days)Infiltration (esoinophils and neutrophils)Bronchial hyperreactivityImflammationInfiltration with monocytes and lymphocytesASTHMA TRIGGERSGgerdAallergensSsmoking, strong odors Ppets & pestsBbeer, wine & deliRresp. infectionsEemotional/stressAactivitiesTtimingHhumidity, cold air or sudden temp changeClinical PresentationAbrupt or gradual onsetWheezing – inspiratory &/or expiratory Nasal flaringDyspnea/SOBAnxietyTachypneaTachycardiaPercussion: HyperresonanceUse of accessory musclesSitting upright or forward (tripod)HypoxemiaProlonged expirationCough – nonproductive leading to thick, stringy mucus during attackMANAGEMENT OF ASTHMAPreventiveMAST Cell stabilizer Long acting beta 2 agonists (serevent)Inhaled corticosteroidsEpinephrineTheophyllinePharmacological TreatmentShort acting beta2-agonists (Bronchodilators) End in –olTheophyllineAnticholinergic Agents - AtroventCorticosteroidsLong acting beta2-agonist and corticosteriod combinationCromolyn Leukotriene-antagonistsShort acting beta2-agonistsAlbuterol, Levalbuterol (Xoponex)Side effects: Anxiety.Tremor.Restlessness.Headache.Patients may experience fast and irregular heartbeats. Interaction with beta blockersTheophyllineTheo-Dur, Theolair, Slo-Phyllin, Slo-bid, Constant-T, Respbid Theophylline levelToxicity causes the following symptoms: nausea, vomiting, headache, insomnia, and, in rare cases, disturbances in heart rhythm and convulsions. Anticholinergic Agents - AtroventActs as a bronchodilator over timeNot for acute attacksIt may be useful for certain older asthma patients who also have emphysema or chronic bronchitis. A combination with a beta2-agonist might be helpful for patients who do not initially respond to treatment with a beta2-agonist alone. CorticosteriodsChronic management Inhaled:The most recent generation of inhaled steroids include:fluticasone (Flovent), budesonide (Pulmicort), triamcinolone (Azmacort and others), and flunisolide (AeroBid) Oral – last to be used & first to be removed. Used as maintenance in severe cases. prednisone, prednisolone, methylprednisolone, and hydrocortisone.Long acting beta2-agonist and corticosteriod combinationLong-acting beta2-agonists, including salmeterol (Serevent) and formoterol (Foradil)Used for prevention of asthma attackFormoterol has a much faster action than salmeterol and may achieve better control of nighttime asthma. Advair is a single device that contains a combination of both drugs.CromolynCromolyn sodium (Intal) serves as both an anti-inflammatory drug and has antihistamine properties that block asthma triggers such as allergens, cold, or exercise. Side effects: nasal congestioncoughingsneezingwheezingnauseanosebleedsdry throat. Leukotriene-antagonists zafirlukast (Accolate), montelukast (Singulair), zileuton (Ziflo), and pranlukast (Ultair, Onon) Oral medications that block leukotrienes, powerful immune system factors that, in excess, produce a battery of damaging chemicals that can cause inflammation and spasms in the airways of people with asthma.Used to prevent asthma attacks.Gastrointestinal distress is the most common side effect Risk for altered respiratory function related to excessive or thick secretions secondary to asthmaInterventions:Regulate fluid intake to thin secretionsAdminister bronchodilators as appropriateEncourage slow, deep breathing; turning and coughingExpected Outcomes:Pt will consume 2-3 L of fluid per dayPt will use brondhodilators when short of breathPt will practice breathing exercisesMedically Diagnosing AsthmaHealth history & physical examPulmonary Function Tests (PFTs)SpirometryPeak expiratory flow rates (PEFR)Sputum or blood culture for eosinophilsArterial blood gases (ABGs) & oximetrySerum IgE levels: elevatedChest x-ray: hyperinflation during attackAllergy skin testingMedically Diagnosing AsthmaPulmonary Function Tests (PFTs)Reveals a low expiratory flow rate, forced expiratory volume, and forced vital capacity with functional residual capacity and total lung capacityAid in determining degree of obstructionMedically Diagnosing AsthmaArterial Blood Gases (ABGs)Determines how much oxygen is available to perfuse peripheral tissuesNormal values:pH: 7.35 - 7.45PaCO2: 35 - 45PaO2: 80 - 100HCO3: 22 - 26SaO2: 95 - 100Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory acidosis.Asthma Severity ClassificationStep 1: Mild IntermittentS/S < 2x weekNocturnal s/s < 2x month PEFR < 20% variabilityExacerbations brief with variable intensity No daily medication neededAsthma Severity ClassificationStep 2: Mild PersistentS/S > 2x week, but < 1x dailyNocturnal s/s > 2x month PEFR 20% - 30% variabilityExacerbations may or may not affect ADLs One medication daily (low-dose corticosteroid or slow release theophylline) Asthma Severity ClassificationStep 3: Moderate PersistentS/S dailyNocturnal s/s > 1x week PEFR > 30% variabilityExacerbations 2x dailyExacerbations affect ADLs One or two daily medications (med-dose corticosteroid &/or inhaled bronchodilator)Asthma Severity ClassificationStep 4: Severe PersistentS/S continuousNocturnal s/s frequent PEFR > 30% variabilityExacerbations frequentExacerbations affect and limit ADLsTwo daily medications (high-dose corticosteroid & inhaled bronchodilator)Status AsthmaticusIs the most severe form of asthmaA severe life-threatening complication of an asthma attackPersistent status of acute asthma exacerbation that does not respond to usual treatmentsHypoxemia worsensExpiratory rate and volume further decreaseMay lead to respiratory failureRepeated attacks may cause irreversible emphysemaBuildup of CO2 acidosis BPAirways narrow further making it very difficult to move air in and out of the lungsRequires intubation and ventilator supportNursing DiagnosesAnxiety r/t inability to breath effectively, fear of suffocationIneffective breathing pattern r/t airway obstruction/resistanceInadequate tissue perfusion r/t impaired gas exchangeActivity intolerance r/t fatigue, tightness of chest, shortness of breathRisk for infection r/t ineffective airway clearance and decreased pulmonary functionPlan and InterventionsSee NICAirway Management Respiratory MonitoringAllergy ManagementAnxiety Reduction Positioning Vital Sign Monitoring Per physician order:Albuterol via nebulizerOxygen therapyOrder ABG’sNursing DiagnosesAnxiety r/t inability to breath effectively, fear of suffocationIneffective breathing pattern r/t anxietyAnxiety r/t medication side effectImpaired gas exchange r/t inflammation of airways, ventilation-perfusion imbalanceIneffective airway clearance r/t excessive mucus production Inadequate tissue perfusion r/t impaired gas exchangeImpaired spontaneous ventilation r/t asthma Risk for decreased cardiac output r/t dysrhythmias associated with respiratory acidosisRisk for infection r/t potential corticosteroid usePlan and InterventionsSee NIC:Airway Management Respiratory Monitoring Anxiety Reduction Positioning Vital Sign Monitoring Airway Clearance Per physician order:40% oxygenation via Venturi MaskIVMethylprednisoloneStart transfer to ICUNursing DxAnxiety related to threat of unknown death secondary to severe asthma attackInterventions:Encourage verbalization of feelings, perceptions, and fearsProvide objects that symbolize safenessIdentify when level of anxiety changesExpected Outcomes:Pt will verbalize feelingsPt will surround him/herself with a safe environmentPt will identify the beginning signs of anxiety ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download