oxygenation lecture

OXYGENATION LECTURE

M. Catherine Hough, Ph.D, RNUniversity of North Florida

COH - Department of Nursing

Respiratory System...

Structure & Function

Lower Respiratory Tract…

Alveolar ductsAlveoli - 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, Impaired

Review the following:Respiratory status:

Gas ExchangeVentilation

Tissue Perfusion:Pulmonary

Acid-Base Balance

NOCs

NICs

Acid-Base Management

Gas exchange, Impaired

Ventilation and Perfusion

Alveolar Dead Space + ventilation - perfusion

Intrapulmonary Shunting - ventilation + perfusion

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

EpidemiologyPrevalence 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

Pathogenesis There is normally a moderate degree of hypoventilation during

sleep resulting from partial pharyngeal collapse and resulting increase in upper airway resistance.

1. This is due to decreased activity of the "upper airway dilator musculature" during sleep.

2. Occasional apneic or hypopneic episodes are normal, esp. in elderly.

3. Prolonged and repetitive apneic/hypopneic episodes are not normal.

Structural factors In most OSA patients, there are no evident structural abnormalities. Most experts, however, believe that subtle underlying structural factors are involved:

a. Narrower upper airway (OSA patients have narrower upper airways on average,

but there' much overlap) b. More "collapsible" airways (+/- evidence for this)

In rare instances, clear structural abnormalities are found

1. nasal obstructing lesions 2. Deviated nasal septum 3. chronic rhinitis 4. masses of the soft palate 5. large T & A's Structural abnormalities may play a larger role in

women

6. 48% of women with OSA in one series had abnormalities of the hard palate

7. >70% with mild OSA 8. In one series of women with OSA, most weren't overweight,

but BMI was correlated with severity (freq. of apneic/hypopneic episodes)

Structural factors …

Functional factors

1. OSA pts may have altered sleep 2. Influences on palatal muscle control, e.g. the reflexes which

normally keep palate open during inspiration 3. May have impaired ventilatory drive or arousal mechanisms

(Sources: Disease-a-month, 4/94; Lancet 344:653, 1994; 344: 656, 1994; Ann. Int. Med. 122: 493, 1995)

TREATMENT1. Surgical - Remove obstruction

2. Mechanical - Nasal CPAP

3. Support Groups

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/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.

PREVENTION

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 consumption and lower achievement

Advertising targets fantasies and insecurities of teens and young adults

Obstructive & Restrictive Lung Disorders

Restrictive Lung Disorders

General head injuries, tumors,

OD Neuromuscular

GB, ALS, MD, Polio Chest Wall

trauma Pleural Disorders

pleural effusion, pleurisy Parenchmal

atelectasis, pneumonia, TB, pulmonary fibrosis

Obstructive Lung Disorders

AsthmaCOPD

Acute Bronchitis Chronic Bronchitis Emphysema

Intr

apul

mon

ary

Extr

apul

mon

ary

Also referred to as Chronic

Airflow Limitation (C

AL)

Characteristics of Lung Disorders

RestrictiveReduced Vital CapacityReduced Total Lung

CapacityNormal or reduced

Functional Residual Capacity

Cause difficulty with inspiration

ObstructiveDecreased resistance

to airflowNormal or decreased

Vital Capacity Increased Total Lung

Capacity Increased Functional

Residual Capacity Increased Residual

Volume

OBSTRUCTIVECharacterized by:

INCREASED TO AIR FLOW

RESTRICTIVECharacterized 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

Emphysema …

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

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 AAT1 to 3 percent of all cases of emphysema are due to

AAT deficiencyCritical that these people not smoke

Healthy Lung Emphysema Lung

The destruction of elastin that occurs in emphysema is believed to result from an imbalance between two proteins in the lung:

1. An enzyme called elastase which breaks down elastin, and

2. 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 alveoliDue 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.

ETIOLOGY

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

EPIDEMIOLOGY

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

HeredityEnvironmental irritants/pollution

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&SSubjective Hx and onset of symptoms Smoking Hx Family Hx Past or present exposure to environmental irritants Activity intolerance, fatigue Anorexia, weight loss Symptoms of hypoxemia - restlessness, confusion Medications and therapies and their effectiveness

Assessment...Objective Increased airway

resistanceDecreased Expiratory

ForceMild hypoxemiaBarrel Chest Increased AP diameter Increased Accessory

Muscles

ABG’s show compensation

Increased respiratory rate

DyspneaDecreased breath

soundsLate inspiratory

cracklesDecreased O2

saturation

LAB FINDINGSABG’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 TESTS

Chest X-Ray -- positive findings indicate increased radiolucency of lungs with diaphragm in low position

AAT assay to check for deficiencyPulmonary 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

INTERVENTIONSBronchodilators may provide relief from symptoms

but will not improve Antibiotics if there is an infectious process occurringSteroids during acute exacerbation'sLow flow oxygen (1-2 liters)Breathing exercisesRespiratory therapy & CPTLung 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 smokingAvoid work-related

exposures to dust & fumes

Avoid air pollution, and curtail physical activity during alerts

Refrain from contact with people that have URI…

Get pneumonia vaccination and yearly influenza shots

Avoid excessive heat, cold and high altitudes

Drink fluidsMaintain good nutrition –

high proteinConsider allergy shots

Another Nursing Diagnosis

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

Interventions:1. Explain importance of consuming adequate amounts of nutrients2. Provide a pleasant, relaxed atmosphere for eating

Expected Outcomes:3. Pt will verbalize & understand importance of adequate nutrition4. Pt will use a comfortable environment for meals5. Pat will eat slower and smaller meals

More NURSING DIAGNOSIS Ineffective airway clearanceAltered Gas Exchange Breathing pattern,

Ineffective Activity Intolerance Infection: Actual or PotentialRisk for Nutrition: Less than Body RequirementFearAnxietyKnowledge Deficit

Nursing 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 restlessness

Ineffective therapeutic regimen management r/t lack of information about COPD and its treatment

Nursing DiagnosesActivity 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 InterventionsAirway Management

Administer humidified air or oxygen immediatelyRegulate fluid intakeMonitor respiratory and oxygenation statusAdminister drug therapy (bronchodilators,

corticosteroids)Auscultate lung sounds before and after treatments

Cough Enhancement Positioning for chest expansionDeep breathing, hold for 2 seconds, and cough 2-3

times

Nursing Interventions

Respiratory MonitoringRate, rhythm, depth, and effort (overall

patterns)Monitor for increased restlessness, anxiety,

and air hungerNote changes in SaO2, ABG values

Nursing Interventions

Anxiety ReductionCalming & reassuring attitudesStay with patientEncourage slow breathing (pursed lips)

Nursing InterventionsTeaching: Disease Process & Prescribed

Medication Identify level of knowledge Instruct on measure to prevent/minimize side effects

of treatment 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 Tests

Asthma Bronchitis Emphysema Forced expiratory volume Vital capacity

Expiratory flow rates

Vital capacity

Residual volume

Total lung capacity WNL

Expiratory flow rates

Total lung capacity

Residual volume

Vital capacity normal or slightly reduced

Arterial 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 - 100

Hypoxemia 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

Sympathetic Agents: PO, Inhalation (Albuterol, Terbutaline) Rescue inhalers – Albuterol…

Corticosteroids – Solu Medrol – IV or PO to alleviate acute symptoms by decreasing inflammation

Antibiotics – to manage respiratory tract infections Mucolytics and expectorants – to thin and aid in removal of mucus Analgesics

Treatment

Flu Shots

Given early October to mid November (however can be given any time during the flu season

Given yearlyCost for people > 65 is

paid by Medicare

Recommended for: >50 years old Chronic heart or lung

disease HIV Anyone living in large

groups People who may transmit

the flu to high risk groups Nurses, doctors, and other

healthcare workers

Treatment

Flu Shots…

You should NOT get the flu shots if

Allergic to eggs Hx of Guillain-Barre

SyndromeAcute illness or

fever

Side effects<1 out of 3 develop site

sorenessRare to have fever, achesRecent 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 a flu shot

Treatment

PULMONARY EMBOLISM

MEDICAL INTERVENTIONSAnticoagulantsThrombolytic therapy

SURGICAL INTERVENTIONSEmbolectomy

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 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

1. Prolonged immobility or paralysis2. Injury to vascular endothelium3. Hypercoagulability4. CVP catheter5. History6. CV disease7. Cancer8. Trauma9. Pregnancy & estrogen use

Virchow’s Triad

Three primary factors that predispose to venous thrombosis:

Venous stasis Injury to vascular endothelium Hypercoagulability

Typical 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 Intermittent pneumatic compression stockings

Pharmacologic agents Low molecular wt. Heparin Low dose unit Heparin Warfarin Low dose ASA

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) MRIPulmonary angiographyCXR may show evidence of pulmonary infarct Lower extremity venous duplex (DVT requires

same tx as PE)A negative study does not exclude PE!

MEDICAL INTERVENTIONS:Anticoagulation

Low molecular wt. HeparinLow dose unit HeparinWarfarin

SURGICAL INTERVENTIONSEmbolectomyGFF

NURSING DIAGNOSIS Impaired gas exchange…

Treatment

Heparin NomogramAnticoagulation form Venous

Thrombosis/Peripheral Vascular Disease

Adjustment Contingency Table(25,000 units Heparin/500ml D5W)

PTT Bolus (units) Hold (min) Rate Change Repeat PTT

Below 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) 6hrs

Greenfield Filter

Venacava

RESTRICTIVE LUNG DISORDERS

Restrictive Lung Disorders

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

Extr

apul

mon

ary

Intr

apul

mna

ry

PNEUMONIA

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 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

PATHOPHYSIOLOGY

> 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

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

DIAGNOSTIC 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 FACTORS

HeredityPreexisting pulmonary diseases Incidence 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 MANIFESTATIONS

General nonspecific & appear late in the disease process

Dependent on the type of lung cancerOften there is extensive mets before symptoms

become apparentPersistent cough (may or may not be productive)Chest PainDyspnea

CLINICAL MANIFESTATIONS

Later manifestations: anorexia fatigueweight losshoarseness 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 Tumors Staging 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 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 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

Treatment

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

Treatment

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

http://www.shirinwadia.com/asthma1.htm

http://www.asthma.ca/adults/about/whatIsAsthma.php

http://www.asthma.ca/adults/about/whatIsAsthma.php

Hyperventilation

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.

http://www.kodomo.co.jp/asthma/ex/x-ray/

Signs and Symptoms of Asthma

Abrupt or gradual onset Inspiratory and/or

expiratory wheezingShortness of breathNon-productive cough

leading to thick, stringy mucus during attack

Position: High Fowlers, tripod

Percussion: Hyperresonance

Prolonged expirationTachycardiaTachypneaUse of accessory

musclesDyspneaChest tightnessHypoxemiaNasal flaring

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

PATHOPHYSIOLOGY

Hyperirritability or hyperresponsiveness tracheobronchial tree

Bronchoconstriction in response to physical, chemical and pharmacolgic agents

PHASES OF ASTHMAEarly Phase (30-60 minutes)Triggered by allergen or irritantMAST cell degranulation -- Immune Mediator

ReleaseBronchial smooth muscle constrictionMucous SecretionVascular Leakage

PHASES…

Late Phase (5-6 hours to 2 days)Infiltration (esoinophils and neutrophils)Bronchial hyperreactivityImflammationInfiltration with monocytes and lymphocytes

ASTHMA TRIGGERSG gerdA allergensS smoking, strong

odors P pets & pests

B beer, wine & deli

R resp. infections

E emotional/stress

A activitiesT timingH humidity,

cold air or sudden temp change

Clinical Presentation

Abrupt or gradual onsetWheezing – inspiratory

&/or expiratory Nasal flaringDyspnea/SOBAnxietyTachypneaTachycardia

Percussion: Hyperresonance

Use of accessory muscles

Sitting upright or forward (tripod)

HypoxemiaProlonged expirationCough – nonproductive

leading to thick, stringy mucus during attack

MANAGEMENT OF ASTHMA

PreventiveMAST Cell stabilizer Long acting beta 2 agonists (serevent)Inhaled corticosteroidsEpinephrineTheophylline

Treatment

Pharmacological TreatmentShort acting beta2-agonists

(Bronchodilators) End in –ol

TheophyllineAnticholinergic Agents - AtroventCorticosteroidsLong acting beta2-agonist and

corticosteriod combinationCromolyn Leukotriene-antagonists

Short acting beta2-agonistsAlbuterol, Levalbuterol (Xoponex)Side effects:

Anxiety.Tremor.Restlessness.Headache.Patients may experience fast and irregular

heartbeats. Interaction with beta blockers

TheophyllineTheo-Dur, Theolair, Slo-Phyllin, Slo-bid,

Constant-T, Respbid Theophylline levelToxicity causes the following symptoms:

nausea vomiting headache Insomnia in rare cases disturbances in heart rhythm and

convulsions.

Anticholinergic Agents - Atrovent

Acts 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 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.

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 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:1. Regulate fluid intake to thin secretions2. Administer bronchodilators as appropriate3. Encourage slow, deep breathing; turning and coughingExpected Outcomes:4. Pt will consume 2-3 L of fluid per day5. Pt will use brondhodilators when short of breath6. Pt will practice breathing exercises

Nursing Dx

Medically Diagnosing Asthma

Health history & physical examPulmonary Function Tests (PFTs)

Spirometry Peak expiratory flow rates (PEFR)

Sputum or blood culture for eosinophilsArterial blood gases (ABGs) & oximetrySerum IgE levels: elevatedChest x-ray: hyperinflation during attackAllergy skin testing

Medically Diagnosing Asthma

Pulmonary Function Tests (PFTs)

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

2. Aid in determining degree of obstruction

Medically Diagnosing AsthmaArterial Blood Gases (ABGs)

Determines how much oxygen is available to perfuse peripheral tissues

Normal values:pH: 7.35 - 7.45PaCO2: 35 - 45PaO2: 80 - 100HCO3: 22 - 26SaO2: 95 - 100

Hypoxemia occurs with early respiratory alkalosis, or in severe cases, respiratory acidosis.

Asthma Severity Classification

Step 1: Mild Intermittent

S/S < 2x weekNocturnal s/s < 2x month PEFR < 20% variabilityExacerbations brief with variable intensity No daily medication needed

Asthma Severity Classification

Step 2: Mild Persistent

S/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 Classification

Step 3: Moderate Persistent

S/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 Classification

Step 4: Severe Persistent

S/S continuousNocturnal s/s frequent PEFR > 30% variabilityExacerbations frequentExacerbations affect and limit ADLsTwo 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 DiagnosesAnxiety r/t inability to breath effectively, fear of

suffocation Ineffective breathing pattern r/t airway

obstruction/resistance Inadequate 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 function

Plan and InterventionsSee 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 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 DxAnxiety related to threat of unknown death secondary

to severe asthma attack

Interventions:1. Encourage verbalization of feelings, perceptions, and fears2. Provide objects that symbolize safeness3. Identify when level of anxiety changesExpected Outcomes:4. Pt will verbalize feelings5. Pt will surround him/herself with a safe environment6. Pt will identify the beginning signs of anxiety