oxygenation lecture
DESCRIPTION
OXYGENATION LECTURE. M. Catherine Hough, Ph.D, RN University of North Florida COH - Department of Nursing. 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 - PowerPoint PPT PresentationTRANSCRIPT
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