OXYGENATION LECTURE

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 Gas

airway clearance

Exchange, Impaired

NOCs
Review the following:
Respiratory

status:

Gas Exchange Ventilation

Tissue

Perfusion: Balance

Pulmonary
Acid-Base

NICs
Acid-Base

Management

Gas

exchange, Impaired

Ventilation and Perfusion

Alveolar Dead Space

+ ventilation

- perfusion - ventilation + perfusion

Intrapulmonary Shunting

OBSTRUCTIVE 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

Epidemiology
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 10years

There 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 control 3. may have impaired ventilator drive or arousal mechanisms Treatment: 1. Surgical / remove obstruction 2. CPAP 3. Support group

Problems of the LOWER AIRWAY

Statistics: 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.

 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

PREVENTION

Obstructive & Restrictive Lung Disorders

Restrictive 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 fibrosis

Obstructive Lung Disorders Asthma COPD

Acute Bronchitis Chronic Bronchitis Emphysema

Characteristics of Lung Disorders Restrictive

Reduced Vital Capacity Reduced Total Lung Capacity Normal or reduced Functional Residual Capacity Cause difficulty with inspiration

Obstructive
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)

OBSTRUCTIVE
Characterized by:
INCREASED TO AIR FLOW

RESTRICTIVE
Characterized by:
DECREASED COMPLIENCE OF THE LUNG OR CHEST WALL OR BOTH

OBSTRUCTIVE LUNG DISORDERS

EMPHYSEMA
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 exhaling

Use 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 doesnt 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, dont get second hand smoke

AAT (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)

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 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

ETIOLOGY

EPIDEMIOLOGY

PATHOPHYSIOLOGY
Centrilobular Emphysema (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)

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

ASSESSMENT
S&S Subjective
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

Assessment...
Objective
Increased airway resistance Decreased Expiratory Force Mild hypoxemia (pick up w/ O2 sat monitor) Barrel Chest Increased AP diameter Increased Accessory Muscles ABGs show compensation (pH is normalizing & CO2 will start to drop) Increased respiratory rate Dyspnea Decreased breath sounds Late inspiratory crackles Decreased O2 saturation

ABGs 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 Chest X-Ray -- positive findings indicate increased radiolucency of lungs with diaphragm in low position AAT assay to check for deficiency Pulmonary functions tests -

LAB FINDINGS

DIAGNOSTIC 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

INTERVENTIONS
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 themselves 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 Diagnosis

Altered nutrition: less than body requirements related to dyspnea, sputum production, or fatigue
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: 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 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

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 Activity intolerance r/t fatigue, energy shift to meet muscle needs for

Nursing Diagnoses

Nursing Diagnoses

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

Airway Management

Nursing Interventions

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) Positioning for chest expansion Deep breathing, hold for 2 seconds, and cough 2-3 times

Cough Enhancement

These interventions will help them to maintain their airway. Often the secretions are worse in the morning

Respiratory Monitoring

Nursing Interventions
hunger

Rate, rhythm, depth, and effort (overall patterns) Monitor for increased restlessness, anxiety, and air Note changes in SaO2, ABG values

Anxiety Reduction
Calming

Nursing Interventions

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

Teaching: Disease Process & Prescribed Medication

Nursing Interventions

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 patients ability to self-administer medications Instruct patient on purpose, action, dosage, and duration of each medication Include family and significant others

Pulmonary Function Tests

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 & Intervention

Medications:
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 dont 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 Analgesics (nsaid or Tylenol for aches & pain)
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

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:

Flu Shots

>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 Allergic to eggs Hx of Guillain-Barre Syndrome

 Acute illness or fever Side effects <1 out of 3 develop site soreness Rare to have fever, aches Recent research shows that flu shots do not increase asthma attacks NOTE: flu vaccine is made from a virus that is no longer active NO one can catch the flu from flu shot.

PULMONARY EMBOLISM
MEDICAL INTERVENTIONS
Anticoagulants (prevents a clot from forming, coumadin & heparin) Thrombolytic therapy (break up a present clot, TPA, streptokinase & eurokinase) PE usually comes from legs

SURGICAL INTERVENTIONS
Embolectomy (if it is large enough)

NURSING DIAGNOSIS
Impaired gas exchange

Pulmonary Embolism.
Risk 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.
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

Virchows Triad

Three primary factors that predispose to venous thrombosis: Venous stasis Injury to vascular endothelium Hypercoagulability

Typical clinical features

S&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 ventilation

Clinical features of severe PE:

Hypotension (from reduced left-heart venous return)

 Right heart failure

Dignostic Evaluation to Confirm PE

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 Nomogram
Anticoagulation form Venous Thrombosis/Peripheral Vascular Disease

Adjustment Contingency Table

(25,000 units Heparin/500ml D5W) PTT Bolus (units) Hold (min) Rate Change Repeat PTT
6hrs 6hrs next AM 6hrs 6hrs 6hrs

Below 41 2000 unit 41-49 1000 units 50-80 0 81-89 0 90-106 0 Above 106 0

0 min +4ml/hr (200units/hr) 0 min +2ml/hr (100units/hr) 0 min NO RATE CHANGE 0 min -2ml/hr (100units/hr) 60 min -4ml/hr (200units/hr) 120 min -4mil/hr (200units/hr)

PTT = 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 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

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

PNEUMONIA

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 > 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.

LUNG CANCER

PATHOPHYSIOLOGY

STATS, 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

Chest X-Ray:

DIAGNOSTIC TESTS

Shows increased bronchovascular markings Decreased forced expriatory volume and vital capacity, and increased residual volume

Pulmonary functioning tests: Arterial Blood Gas (ABG) studies

respiratory acidosis, hypercapnia, Hypoxia Elevated Hbg and Hct (polycythemia) Elevated WBC Pt. usually hypoxic
neutrophils and bronchial epithelial cells present

Complete Blood Count Pulse Oximetry Sputum C&S:

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

STATS, CAUSES & RISK FACTORS

CLINICAL 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 Dyspnea

CLINICAL MANIFESTATIONS Later manifestations:

anorexia fatigue weight loss

 hoarseness if mediastinal involvement may have

pericardial effusion cardiac tamponade dysrhythmias

DIAGNOSTIC 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: Identification of malignant cells

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

Staging of nonsmall cell lung cancer (NSCLC) is performed according to the American Joint Committees

Staging of Tumors

TNM staging system.

T= N= M=

denotes tumor size. Location, and degree of involvement indicates regional lymph node involvement 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.

Surgical resection - decision is dependent on type and location of tumor

THERAPEUTIC MANAGEMENT

Lobectomy pneumonectomy Curative approach with resectable tumor but poor surgical risk Adjuvant with other approaches Palliative to reduce symptoms Used as adjuvant

Radiation therapy

Chemotherapy Laser surgery

NURSING MANAGEMENT
Nursing 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

ASTHMA
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

Airway walls are thickened with inflammatory exudates which enhances bronchospasms and reduces expiratory flow.

Hyperventilation

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 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
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

PATHOPHYSIOLOGY
Hyperirritability or hyperresponsiveness tracheobronchial tree Bronchoconstriction in response to physical, chemical and pharmacolgic agents

PHASES OF ASTHMA
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) Infiltration (esoinophils and neutrophils) Bronchial hyperreactivity Imflammation Infiltration with monocytes and lymphocytes

ASTHMA TRIGGERS
G gerd A allergens S smoking, strong odors

P B R E A T H

pets & pests beer, wine & deli resp. infections emotional/stress activities timing humidity, cold air or sudden

temp change

Clinical 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 ASTHMA
Preventive 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 secondary to asthma
Interventions: Regulate fluid intake to thin secretions Administer bronchodilators as appropriate Encourage slow, deep breathing; turning and coughing 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

Health history & physical exam Pulmonary Function Tests (PFTs)

Medically Diagnosing Asthma

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 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 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 Classification Step 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 Classification Step 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 Classification

 Step 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 Classification Step 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 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 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

See NIC

Plan and Interventions

Airway Management Respiratory Monitoring

Allergy Management Anxiety Reduction Positioning Vital Sign Monitoring Albuterol via nebulizer Oxygen therapy Order ABGs

Per physician order:

Nursing 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 40% oxygenation via Venturi Mask IV Methylprednisolone Start transfer to ICU

Per physician order:

Nursing Dx
Anxiety related to threat of unknown death secondary to severe asthma attack
Interventions: Encourage verbalization of feelings, perceptions, and fears Provide objects that symbolize safeness Identify when level of anxiety changes Expected Outcomes: Pt will verbalize feelings Pt will surround him/herself with a safe environment Pt will identify the beginning signs of anxiety