OXYGENATION LECTUREOXYGENATION LECTURE

Respiratory System...Respiratory System...Structure & Function

Lower Respiratory Tract…

Alveolar ducts Alveoli - FUNCTIONAL UNIT OF THE LUNG– ~300,000,000 ALVEOLI IN THE LUNG– Total Volume of ~ 2500 ml– Surface area for gas exchange that is about the size of a tennis court– SURFACTANT

NURSING DIAGNOSIS (definition and defining characteristics:

Ineffective airway clearance

Gas Exchange, ImpairedNOCs

Review the following: Respiratory status: Gas Exchange Ventilation

Tissue Perfusion: Pulmonary

Acid-Base Balance

NICs

Acid-Base Management

Gas exchange, Impaired

Ventilation and PerfusionVentilation and Perfusion Alveolar Dead SpaceAlveolar Dead Space + ventilation

- perfusion Intrapulmonary ShuntingIntrapulmonary Shunting - ventilation + perfusion

OBSTRUCTIVE SLEEP APNEAOBSTRUCTIVE SLEEP APNEA Periodic apneic or hypopneic episodes during sleep associated with Upper airway obstruction due to pharyngeal collapse, leading to Awakening and resulting restoration of airway patency Sleep recurs almost immediately and the cycle repeats itself, often hundreds of times each night

EpidemiologyEpidemiology Prevalence estimated at 4% male; 2% female (NEJM 328:1230, 1993) May be as much as 40-50% of hypertensive Pts 90% of pts with nocturnal angina (Lancet 4/29/95)

Incidence greatest age 40-60

Highly underdiagnosed, perhaps due to the gradual onset of s/s More 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 sleep

2. influences on palatal muscle control3. may have impaired ventilator drive or arousal mechanisms

Treatment: 1. Surgical / remove obstruction2. CPAP3. Support group

Problems of the LOWER AIRWAYProblems of the LOWER AIRWAYStatistics: Decrease number of deaths R/T acute & chronic respiratory infections due to antibiotics Increase in TB over last ten years, especially the last 5years due to AIDS/HIV More people living with COPD (>17 million) ^ incidence of lung cancer, especially among women ^ number of teenagers starting to smoke Pneumonia is the leading cause of death by infectious disease in the U.S.

PREVENTIONPREVENTION Education/advocacy for smoke-free environment (The use of tobacco is the #1 risk to developing COPD and lung cancer

Most people start smoking in high school

Nicotine addiction results in withdrawal symptoms

Smoking is tied to ETOH (alcohol) consumption and lower achievement

Advertising targets fantasies and insecurities of teens and young adults

Obstructive & Restrictive Obstructive & Restrictive Lung DisordersLung Disorders

Restrictive Lung DisordersRestrictive Lung Disorders General (extrapulmonary) head injuries, tumors, OD (overdose) Neuromuscular (extrapulmonary) GB (guillian barre), ALS, MD, Polio Chest Wall (intrapulmonary/extrapulmonary) trauma Pleural Disorders (intrapulmonary) pleural effusion, pleurisy Parenchmal (parenchmal) atelectasis, pneumonia, TB, pulmonary fibrosisObstructive Lung DisordersObstructive Lung Disorders Asthma COPD Acute Bronchitis Chronic Bronchitis Emphysema

Characteristics of Lung DisordersCharacteristics of Lung DisordersRestrictiveRestrictive Reduced Vital Capacity Reduced Total Lung Capacity Normal or reduced Functional Residual Capacity Cause difficulty with inspiration

ObstructiveObstructive Decreased resistance to airflow Normal or decreased Vital Capacity Increased Total Lung Capacity Increased Functional Residual Capacity Increased Residual Volume

We will not be tested on normal pulmonary function(total lung capacity is total amount we can get in. vital capacity is a normal breath)

OBSTRUCTIVEOBSTRUCTIVECharacterized by:Characterized by:

INCREASED TO AIR FLOW

RESTRICTIVERESTRICTIVECharacterized by:Characterized by:

DECREASED COMPLIENCE OF THE LUNG OR CHEST WALL OR BOTHDECREASED COMPLIENCE OF THE LUNG OR CHEST WALL OR BOTH

OBSTRUCTIVE LUNG DISORDERSOBSTRUCTIVE LUNG DISORDERSEMPHYSEMAEMPHYSEMA

Loss of elastic recoil secondary to breakdown of lung tissue and enlargement of alveolar spaces - leads to retention of CO2 Emphysema 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 AAT (alpha-1-protease inhibitor)(alpha-1-protease inhibitor) Familial emphysema have a hereditary deficiency of AAT Number of Americans with this genetic deficiency small (~70,000) 1 in 3,000 newborns have a genetic deficiency of AAT 1 to 3 percent of all cases of emphysema are due to AAT deficiency

Critical that these people not smoke The 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, and AAT which inhibits elastase.

In normal individuals, there is enough AAT to protect elastin so that abnormal elastin destruction does not occur

Permanent destruction of the alveoli Due to irreversible destruction of the protein elastin Elastin is important for maintaining the strength of the alveolar walls The loss of elastin also causes collapse or narrowing of the bronchioles End result of above sequence limits airflow out of the lungs. (air is trapped… purse lipped breathing helps to expire a little more)

ETIOLOGYETIOLOGY Precise 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 smoking

EPIDEMIOLOGYEPIDEMIOLOGY Symptoms usually occur in the fifth or sixth decade of life Typical patient is male over the age of 55 with a history of tobacco smoking Heredity Environmental irritants/pollution

PATHOPHYSIOLOGYPATHOPHYSIOLOGYCentrilobular Emphysema (CLE)(CLE)

Distention and damage of the respiratory bronchioles Uneven disease distribution throughout the lung Usually more severe in the upper portions More common than Panlobular emphysema (PLE)

Panlobular Emphysema (PLE)Panlobular Emphysema (PLE)

More uniform enlargement and destruction of the alveoli in the pulmonary acinus More diffuse and is more severe in the lower lungs

ASSESSMENTASSESSMENTS&SSubjective Hx and onset of symptoms (how old were you when you started to cough? Smoking Hx (how many years? Pack year history?) Family Hx Past or present exposure to environmental irritants (working around coal mines or shipyards) Activity intolerance, fatigue Anorexia, weight loss Symptoms of hypoxemia - restlessness, confusion

Medications and therapies and their effectiveness

AssessmentAssessment......Objective Increased airway resistance Decreased Expiratory Force Mild hypoxemia (pick up w/ O2 sat monitor) Barrel Chest Increased AP diameter Increased Accessory Muscles

ABG’s show compensation (pH is normalizing & CO2 will start to drop) Increased respiratory rate Dyspnea Decreased breath sounds Late inspiratory crackles Decreased O2 saturation

LAB FINDINGSLAB FINDINGS ABG’s may be normal due to compensation for the destruction by increased resp rate

Even in the presence of hypoxemia overcompensation may result in respiratory alkalosis

PO2 normal or slightly low at rest, but drops with activity CBC usually normal

DIAGNOSTIC TESTSDIAGNOSTIC TESTS Chest X-Ray -- positive findings indicate increased radiolucency of lungs with diaphragm in low position AAT assay to check for deficiency Pulmonary functions tests -- Increased residual volume, functional residual capacity, total lung capacity Diffusing capacity is reduced because of tissue destruction Decreased Forced Expiratory Volume Vital Capacity may be normal or slightly reduced until late state of disease

INTERVENTIONSINTERVENTIONS Bronchodilators may provide relief from symptoms but will not cure the disease Antibiotics if there is an infectious process occurring Steroids during acute exacerbation's (get them weaned off as soon as possible) Low flow oxygen (1-2 liters) Breathing exercises Respiratory therapy & CPT (chest physiotherapy) Lung reduction surgery Performed only on pts with severe emphysema

Avg. hospital LOS ~ 2 weeks Require pre and post op extended pulmonary rehab Falling out of favor in the prior year

Patients with COPD can help Patients with COPD can help themselves in many waysthemselves in many ways

Stop smoking Avoid work-related exposures to dust & fumes Avoid air pollution, and curtail physical activity during alerts Refrain from contact with people that have URI… (upper respiratory infection) Get pneumonia vaccination and yearly influenza shots Avoid excessive heat, cold and high altitudes Drink fluids (to help thin the secretions) Maintain good nutrition – high protein Consider allergy shots

Another Nursing DiagnosisAnother Nursing DiagnosisAltered nutrition: less than body requirements related to dyspnea, sputum

production, or fatigueInterventions:Interventions: Explain importance of consuming adequate amounts of nutrients Provide a pleasant, relaxed atmosphere for eating (small meals several times a day, wear oxygen

while eating)

Expected Outcomes:Expected Outcomes: Pt will verbalize & understand importance of adequate nutrition Pt will use a comfortable environment for meals Pt will eat slower and smaller meals

More NURSING DIAGNOSISMore NURSING DIAGNOSIS Ineffective airway clearance Altered Gas Exchange Breathing pattern, Ineffective Activity Intolerance Infection: Actual or Potential Risk for Nutrition: Less than Body Requirement Fear Anxiety Knowledge Deficit

Nursing DiagnosesNursing Diagnoses Ineffective 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 restlessness Ineffective therapeutic regimen management r/t lack of information about COPD and its treatment

Nursing DiagnosesNursing Diagnoses

Activity intolerance r/t fatigue, energy shift to meet muscle needs for breathing to overcome airway obstruction Disturbed body image r/t decreased participation in physical activities Impaired home maintenance r/t deficient knowledge regarding control of environmental triggers Ineffective coping r/t personal vulnerability to situational crisis

Nursing InterventionsNursing Interventions Airway Management Administer humidified air or oxygen immediately Regulate fluid intake Monitor respiratory and oxygenation status Administer 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 expansion Deep 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 InterventionsNursing Interventions Respiratory Monitoring Rate, rhythm, depth, and effort (overall patterns) Monitor for increased restlessness, anxiety, and air hunger Note changes in SaO2, ABG values

Nursing InterventionsNursing Interventions Anxiety Reduction Calming & reassuring attitudes (help w/ fear & anxiety of not being able to breathe). Stay with patient Encourage slow breathing (pursed lips)

Nursing InterventionsNursing Interventions Teaching: Disease Process & Prescribed Medication Identify 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 medication Include family and significant others

Pulmonary Function TestsPulmonary Function TestsArterial Blood Gases (ABGs)Arterial Blood Gases (ABGs)

Arterial Blood Gases (ABGs) Determines how much oxygen is available to perfuse peripheral tissues Normal values: pH: 7.35 - 7.45 PaCO2: 35 - 45 PaO2: 80 - 100 HCO3: 22 - 26 SaO2: 95 - 100 Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory acidosis.

Planning & InterventionPlanning & InterventionMedicationsMedications::

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 infections Mucolytics and expectorants – to thin and aid in removal of mucus Analgesics (nsaid or Tylenol for aches & pain)

Flu ShotsFlu Shots Given early October to mid November (however can be given any time during the flu season Given yearly Cost for people > 65 is paid by Medicare

Recommended for: >50 years old Chronic heart or lung disease HIV (compromised immune system) Anyone living in large groups People who may transmit the flu to high risk groups Nurses, doctors, and other healthcare workers You should NOT get the flu shots if You should NOT get the flu shots if

Allergic to eggs Hx of Guillain-Barre Syndrome Acute illness or feverSide effectsSide effects <1 out of 3 develop site soreness Rare to have fever, aches Recent 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 EMBOLISMPULMONARY 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 INTERVENTIONS Embolectomy (if it is large enough)

NURSING DIAGNOSIS Impaired gas exchange

Pulmonary Embolism….Pulmonary Embolism….Risk factors for PERisk factors for PE

Recent 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….Pulmonary Embolism….Predisposing factors & Precipitating Conditions that make some higher risk for

developing DVT/PE Prolonged immobility or paralysis Injury to vascular endothelium Hypercoagulability CVP catheter (central venous pressure catheter) History CV disease Cancer Trauma

Pregnancy & estrogen use

Virchow’s TriadThree primary factors that predispose to venous thrombosis: Venous stasis Injury to vascular endothelium Hypercoagulability

Typical clinical featuresTypical clinical featuresS&S Tachypnea Dyspnea, sudden onset or worsening of chronic dyspnea Tachycardia Pleuritic chest pain or chest pain that is nonretrosternal and nonpleuritic Syncope Cough Feeling of impending doom Hemoptysis Arterial oxygen saturation < 92% on room air Low-grade fever (occasionally) Hemoptysis Hypoxemia Pleural friction rub Clinical evidence of DVT Sudden hypertension

Prophylaxis for DVT Mechanical intervention to decrease venous status

Early ambulation or change position q2h Compression stockings (or Ted stockings) Intermittent pneumatic compression stockings

Pharmacologic agents Low molecular wt. Heparin Low dose unit Heparin Warfarin Low dose ASA (81 mg enteric coated baby aspirin)

Hypoxemia in PE caused by V/Q mismatching

Intrapulmonary shunt

Dead space ventilationClinical features of severe PE:Clinical features of severe PE:

Hypotension (from reduced left-heart venous return)

Right heart failure

Dignostic Evaluation to ConfirmDignostic Evaluation to Confirm PEPE

V-Q lung scan (limited specificity) – test will come back saying “limited specificity”… not really sure if there is a clot. MRI Pulmonary angiography CXR 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:

Anticoagulation Low molecular wt. Heparin (lovenox) Low dose unit Heparin Warfarin

SURGICAL INTERVENTIONS Embolectomy GFF (green field filter)… looks like an umbrella, goes in the vein to trap the clot)

NURSING DIAGNOSIS Impaired 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 min NO 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 Filter

Restrictive Lung DisordersRestrictive Lung Disorders General head injuries, tumors, OD Neuromuscular GB, ALS, MD, Polio Chest Wall Trauma Pickwickian syndrome

Pleural Disorders pleural effusion, pleurisy, pneumothorax Parenchmal atelectasis, pneumonia, TB, pulmonary fibrosis, ARDS

PNEUMONIAPNEUMONIA Acute 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 exudate

LUNG CANCERLUNG CANCER Primary 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 cancer 5-year survival rate is 13% Found most frequently in person 40-75 years of age

PATHOPHYSIOLOGYPATHOPHYSIOLOGY > 90% of lung cancer originate from the epithelium of the bronchus (bronchogenic) Primary lung cancers are often categorized into histologic types Mets occurs primarily by direct extension and via the blood circualtion and the lymph system

Common sites for mets are the liver, brain, bones, scalene lymph nodes, and adrenal glands.

STATS, CAUSES & RISK FACTORSSTATS, CAUSES & RISK FACTORS Smoking is responsible for ~ 80-90% of all lung cancers

~ 1 out of every 10 heavy smokers develop lung cancer

The 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 nonsmoker

Inhaled carcinogens - such as asbestos, nickel, iron, air pollutants, etc. increase the risk of lung cancer

DIAGNOSTIC TESTSDIAGNOSTIC TESTS Chest X-Ray: Shows increased bronchovascular markings Pulmonary functioning tests: Decreased forced expriatory volume and vital capacity, and increased residual volume Arterial Blood Gas (ABG) studies respiratory acidosis, hypercapnia, Hypoxia Complete Blood Count Elevated Hbg and Hct (polycythemia) Elevated WBC Pulse Oximetry Pt. usually hypoxic Sputum C&S: neutrophils and bronchial epithelial cells present

STATS, CAUSES & RISK FACTORSSTATS, CAUSES & RISK FACTORS Heredity Preexisting pulmonary diseases Incidence of lung cancer correlates with the degree of urbanization and population density Second hand smoke exposure Risk of developing lung cancer is directly related to total exposure to cigarette smoke - Pack Year History

CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS General nonspecific & appear late in the disease process Dependent on the type of lung cancer Often there is extensive mets before symptoms become apparent Persistent cough (may or may not be productive) Chest Pain

DyspneaCLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

Later manifestations: anorexia fatigue weight loss hoarseness if mediastinal involvement may have pericardial effusion cardiac tamponade dysrhythmias

DIAGNOSTIC STUDIESDIAGNOSTIC STUDIES Chest X-ray CT scans MRI PET - (position-emission tomography) - measurement of differential metabolic activity in normal and diseased tissue

Definitive diagnosis of lung cancer is made by:Definitive diagnosis of lung cancer is made by: Identification of Identification of malignant cellsmalignant cells

Radionuclide scans (liver, bone, brain …) Pulmonary angiography and lung scans Mediastinoscopy

Staging of TumorsStaging of Tumors Staging of nonsmall cell lung cancer (NSCLC) is performed according to the American Joint Committee’s TNM TNM staging system.

T = denotes tumor size. Location, and degree of involvement

N = indicates regional lymph node involvement

M = represents the presence or absence of distant metastases

Staging of small cell lung cancer (SCLC) not useful because the cancer has usually metastasized by the time the Dx has been made.

THERAPEUTIC MANAGEMENTTHERAPEUTIC MANAGEMENT Surgical resection - decision is dependent on type and location of tumor Lobectomy pneumonectomy Radiation therapy Curative approach with resectable tumor but poor surgical risk Adjuvant with other approaches Palliative to reduce symptoms Chemotherapy Used as adjuvant Laser surgery

NURSING MANAGEMENTNURSING MANAGEMENTNursing Diagnosis Ineffective airway clearance R/T increased tracheobronchial secretions Anxiety R/T lack of knowledge of diagnosis or unknown prognosis and Rx Ineffective breathing pattern R/T decreased lung capacity

Planning - Overall goals are that the pt with lung cancer will have: effective breathing patterns adequate airway clearance adequate oxygenation of tissues minimal to no pain realistic attitude toward Rx and prognosis

ASTHMAASTHMAImpact of Asthma in the U.S.Impact 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/year

– NCHS 1998 CDC asthma surveillance

Affects 24,700,000 individual in U.S Increased 60% over the prior 10 years ~ 2 million ED visits/year Mortality has doubled since 1978 African-Americans: death rate is 2 to 5 times that of Caucasian death rate Account for ~ 20 million lost work days/year Annual health care costs ~ 12.7 billion $

American Lung Association Fact Sheet 2002

HyperventilationHyperventilation Airway 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 AsthmaSigns and Symptoms of Asthma Abrupt or gradual onset Inspiratory and/or expiratory wheezing Shortness of breath Non-productive cough leading to thick, stringy mucus during attack

Position: High Fowlers, tripod Percussion: Hyperresonance Prolonged expiration Tachycardia Tachypnea Use of accessory muscles Dyspnea Chest tightness Hypoxemia Nasal flaring

Asthma …Asthma …The high morbidity/mortality rate is due to: inaccurate assessment of disease increased allergens/irritants in the environment delay in seeking medical help inadequate medical Rx limited access to health care non adherence with prescribed therapy

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

Hyperirritability or hyperresponsiveness tracheobronchial tree

Bronchoconstriction in response to physical, chemical and pharmacolgic agents

PHASES OF ASTHMAPHASES OF ASTHMAEarly Phase (30-60 minutes)Early Phase (30-60 minutes) Triggered by allergen or irritant MAST cell degranulation -- Immune Mediator Release Bronchial smooth muscle constriction Mucous Secretion Vascular Leakage

Late Phase (5-6 hours to 2 days)Late Phase (5-6 hours to 2 days) Infiltration (esoinophils and neutrophils) Bronchial hyperreactivity Imflammation

Infiltration with monocytes and lymphocytes

ASTHMA TRIGGERSASTHMA TRIGGERS GG gerd AA allergens SS smoking, strong odors PP pets & pests BB beer, wine & deli RR resp. infections EE emotional/stress AA activities TT timing HH humidity, cold air or sudden temp change

Clinical PresentationClinical Presentation Abrupt or gradual onset Wheezing – inspiratory &/or expiratory Nasal flaring Dyspnea/SOB Anxiety Tachypnea Tachycardia

Percussion: Hyperresonance Use of accessory muscles Sitting upright or forward (tripod) Hypoxemia Prolonged expiration Cough – nonproductive leading to thick, stringy mucus during attack

MANAGEMENT OF ASTHMAMANAGEMENT OF ASTHMAPreventive MAST Cell stabilizer Long acting beta 2 agonists (serevent) Inhaled corticosteroids Epinephrine Theophylline

Pharmacological Treatment Short acting beta2-agonists (Bronchodilators) End in –ol Theophylline Anticholinergic Agents - Atrovent Corticosteroids Long acting beta2-agonist and corticosteriod combination Cromolyn Leukotriene-antagonists

Short acting beta2-agonists Albuterol, Levalbuterol (Xoponex) Side effects: Anxiety. Tremor. Restlessness. Headache. Patients may experience fast and irregular heartbeats. Interaction with beta blockers

Theophylline Theo-Dur, Theolair, Slo-Phyllin, Slo-bid, Constant-T, Respbid Theophylline level Toxicity causes the following symptoms: nausea, vomiting, headache, insomnia, and, in rare cases, disturbances in heart rhythm and convulsions.

Anticholinergic Agents - Atrovent Acts as a bronchodilator over time Not for acute attacks It 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.

Corticosteriods Chronic 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 combination

Long-acting beta2-agonists, including salmeterol (Serevent) and formoterol (Foradil) Used for prevention of asthma attack Formoterol 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.Cromolyn

Cromolyn 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 congestion coughing sneezing wheezing nausea nosebleeds dry 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 Risk for altered respiratory function related to excessive or thick secretions secondary to asthmasecondary to asthma

Interventions:Interventions: Regulate fluid intake to thin secretions Administer bronchodilators as appropriate Encourage slow, deep breathing; turning and coughingExpected Outcomes:Expected Outcomes: Pt will consume 2-3 L of fluid per day Pt will use brondhodilators when short of breath Pt will practice breathing exercises

Medically Diagnosing AsthmaMedically Diagnosing Asthma Health history & physical exam Pulmonary Function Tests (PFTs) Spirometry Peak expiratory flow rates (PEFR) Sputum or blood culture for eosinophils Arterial blood gases (ABGs) & oximetry Serum IgE levels: elevated Chest x-ray: hyperinflation during attack Allergy skin testing

Medically Diagnosing AsthmaMedically Diagnosing Asthma Pulmonary Function Tests (PFTs)

Reveals a low expiratory flow rate, forced expiratory volume, and forced vital capacity with functional residual capacity and total lung capacity

Aid in determining degree of obstruction

Medically Diagnosing AsthmaMedically Diagnosing Asthma

Arterial Blood Gases (ABGs) Determines how much oxygen is available to perfuse peripheral tissues Normal values: pH: 7.35 - 7.45 PaCO2: 35 - 45 PaO2: 80 - 100 HCO3: 22 - 26 SaO2: 95 - 100 Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory acidosis.

Asthma Severity ClassificationAsthma Severity Classification Step 1: Mild IntermittentStep 1: Mild Intermittent

S/S < 2x week Nocturnal s/s < 2x month PEFR < 20% variability Exacerbations brief with variable intensity No daily medication needed

Asthma Severity ClassificationAsthma Severity Classification Step 2: Mild PersistentStep 2: Mild Persistent

S/S > 2x week, but < 1x daily Nocturnal s/s > 2x month PEFR 20% - 30% variability Exacerbations may or may not affect ADLs One medication daily (low-dose corticosteroid or slow release theophylline)

Asthma Severity ClassificationAsthma Severity Classification Step 3: Moderate PersistentStep 3: Moderate Persistent

S/S daily Nocturnal s/s > 1x week PEFR > 30% variability Exacerbations 2x daily Exacerbations affect ADLs One or two daily medications (med-dose corticosteroid &/or inhaled bronchodilator)

Asthma Severity ClassificationAsthma Severity Classification Step 4: Severe PersistentStep 4: Severe Persistent

S/S continuous Nocturnal s/s frequent PEFR > 30% variability Exacerbations frequent Exacerbations affect and limit ADLs Two daily medications (high-dose corticosteroid & inhaled bronchodilator)

Status AsthmaticusStatus Asthmaticus Is the most severe form of asthma A severe life-threatening complication of an asthma attack Persistent status of acute asthma exacerbation that does not respond to usual treatments Hypoxemia worsens Expiratory rate and volume further decrease May lead to respiratory failure Repeated attacks may cause irreversible emphysema Buildup of CO2 acidosis BP Airways narrow further making it very difficult to move air in and out of the lungs Requires intubation and ventilator support

Nursing DiagnosesNursing Diagnoses

Anxiety r/t inability to breath effectively, fear of suffocation

Ineffective breathing pattern r/t airway obstruction/resistance Inadequate tissue perfusion r/t impaired gas exchange Activity intolerance r/t fatigue, tightness of chest, shortness of breath Risk for infection r/t ineffective airway clearance and decreased pulmonary function

Plan and InterventionsPlan and Interventions See NIC Airway Management Respiratory Monitoring Allergy Management Anxiety Reduction Positioning Vital Sign Monitoring Per physician order: Albuterol via nebulizer Oxygen therapy Order ABG’s

Nursing DiagnosesNursing Diagnoses

Anxiety r/t inability to breath effectively, fear of suffocation Ineffective breathing pattern r/t anxiety Anxiety r/t medication side effect Impaired gas exchange r/t inflammation of airways, ventilation-perfusion imbalance Ineffective airway clearance r/t excessive mucus production Inadequate tissue perfusion r/t impaired gas exchange Impaired spontaneous ventilation r/t asthma Risk for decreased cardiac output r/t dysrhythmias associated with respiratory acidosis Risk for infection r/t potential corticosteroid use

Plan and Interventions See NIC: Airway Management Respiratory Monitoring Anxiety Reduction Positioning Vital Sign Monitoring Airway Clearance Per physician order: 40% oxygenation via Venturi Mask IV Methylprednisolone Start transfer to ICU

Nursing DxNursing DxAnxiety related to threat of unknown death secondary to severe asthma attackAnxiety related to threat of unknown death secondary to severe asthma attack

Interventions:Interventions: Encourage verbalization of feelings, perceptions, and fears Provide objects that symbolize safeness Identify when level of anxiety changes

Expected Outcomes:Expected Outcomes: Pt will verbalize feelings Pt will surround him/herself with a safe environment Pt will identify the beginning signs of anxiety