Oxygenation Notes

7/29/2019 Oxygenation Notes

1/23

OOXXYYGGEENNAATTIIOONN LLEECCTTUURREE

RReessppiirraattoorryy SSyysstteemm......

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

NOCsReview the following:

Respiratory status:Gas ExchangeVentilation

Tissue Perfusion:Pulmonary

Acid-Base Balance

NICs

Acid-Base Management

Gas exchange, Impaired

VVeennttiillaattiioonn aanndd PPeerrffuussiioonn AAllvveeoollaarr DDeeaadd SSppaaccee

+ ventilation


2/23

- perfusion

IInnttrraappuullmmoonnaarryy SShhuunnttiinngg - ventilation + perfusion

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

EEppiiddeemmiioollooggyy

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 control3. may have impaired ventilator drive or arousal mechanisms

Treatment:

1. Surgical / remove obstruction2. CPAP3. Support group

PPrroobblleemmssoofftthheeLLOOWWEERRAAIIRRWWAAYYStatistics:

Decrease number of deaths R/T acute & chronic respiratory infections due toantibiotics

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.


3/23

PPRREEVVEENNTTIIOONN

Education/advocacy for smoke-free environment (The use of tobacco is the #1 risk todeveloping 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

OObbssttrruuccttiivvee && RReessttrriiccttiivveeLLuunngg DDiissoorrddeerrss

RReessttrriiccttiivvee LLuunngg DDiissoorrddeerrssGeneral (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

OObbssttrruuccttiivvee LLuunngg DDiissoorrddeerrssAsthmaCOPD

Acute Bronchitis Chronic Bronchitis Emphysema

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

OObbssttrruuccttiivvee 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)


4/23

OOBBSSTTRRUUCCTTIIVVEECChhaarraacctteerriizzeedd bbyy::

INCREASED TO AIR FLOW

RREESSTTRRIICCTTIIVVEECChhaarraacctteerriizzeedd bbyy::

DDEECCRREEAASSEEDD CCOOMMPPLLIIEENNCCEE OOFF TTHHEE LLUUNNGG OORR CCHHEESSTT WWAALLLL OORR BBOOTTHH

OOBBSSTTRRUUCCTTIIVVEE LLUUNNGG DDIISSOORRDDEERRSSEEMMPPHHYYSSEEMMAA

Loss of elastic recoil secondary to breakdown of lung tissue and enlargement of alveolarspaces - leads to retention of CO2

Emphysema is the most severe form of COPD is characterized by abnormal, permanentenlargement of the air spaces past the terminal bronchioles, resulting in the destruction of thealveolar walls

The affected terminal bronchioles contain mucus plugs and the eventual resulting loss ofelasticity 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 theirmouth to prevent thrush.

1963 - Discovery of deficiency of AAT (Alpha Protease Inhibitor) which is associated withserous and premature development of emphysema. These enzymes (Pancreatic Elastase,Trypsin, Chymotrypsin,Granulocyte Elastase) defend thelungs against destructive processesR/T Neutrophil Elastase whichdestroys 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

AAAATT((aallpphhaa--11--pprrootteeaasseeiinnhhiibbiittoorr)) 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


5/23

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 abnormalelastin destruction does not occur

Permanent destruction of the alveoli Due to irreversible destruction of the protein elastinElastinis important for maintaining the strength of the alveolar walls The loss ofelastinalso 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)

EETTIIOOLLOOGGYY 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 smokingEEPPIIDDEEMMIIOOLLOOGGYY

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

smokingHeredity Environmental irritants/pollution

PPAATTHHOOPPHHYYSSIIOOLLOOGGYYCentrilobular Emphysema((CCLLEE))

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)

PPaannlloobbuullaarr EEmmpphhyysseemmaa ((PPLLEE))

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

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


6/23

Medications and therapies and their effectiveness

AAsssseessssmmeenntt 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

LLAABBFFIINNDDIINNGGSSABGs may be normal due to compensation for the destruction by increased resp rate

Even in the presence of hypoxemia overcompensation may result in respiratoryalkalosis

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

DDIIAAGGNNOOSSTTIICCTTEESSTTSSChest X-Ray -- positive findings indicate increased radiolucency of lungs withdiaphragm 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

IINNTTEERRVVEENNTTIIOONNSS 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


7/23

Falling out of favor in the prior year

PPaattiieennttsswwiitthhCCOOPPDDccaannhheellpptthheemmsseellvveessiinnmmaannyywwaayyss

Stop smoking Avoid work-related exposures to dust & fumes

Avoid air pollution, and curtail physical activity during alertsRefrain 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

AAnnootthheerr NNuurrssiinngg DDiiaaggnnoossiissAltered nutrition: less than body requirements related to dyspnea, sputum

production, or fatigue

IInntteerrvveennttiioonnss::

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)

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

MMoorree NNUURRSSIINNGG DDIIAAGGNNOOSSIISS 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

NNuurrssiinngg DDiiaaggnnoosseess 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

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


8/23

breathing to overcome airway obstructionDisturbed 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

NNuurrssiinngg IInntteerrvveennttiioonnssAirway Management

Administer humidified air or oxygen immediately Regulate fluid intake Monitor respiratory and oxygenation statusAdminister drug therapy (bronchodilators, corticosteroids)Auscultate lung sounds before and after treatments (first time you listen they

sound horrible, have them take deep breaths & then lungs should sound better)

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

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

NNuurrssiinngg IInntteerrvveennttiioonnssRespiratory Monitoring

Rate, rhythm, depth, and effort (overall patterns)

Monitor for increased restlessness, anxiety, and air hungerNote changes in SaO2, ABG values

NNuurrssiinngg IInntteerrvveennttiioonnssAnxiety Reduction

Calming & reassuring attitudes (help w/ fear & anxiety of not beingable to breathe).

Stay with patient

Encourage slow breathing (pursed lips)

NNuurrssiinngg IInntteerrvveennttiioonnss Teaching: Disease Process & Prescribed Medication

Identify level of knowledge (make sure patient understands what is going on, whyyou 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


9/23

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

PPuullmmoonnaarryy FFuunnccttiioonn TTeessttssAArrtteerriiaall BBlloooodd GGaasseess ((AABBGGss))

Arterial 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.

PPllaannnniinngg && IInntteerrvveennttiioonnMMeeddiiccaattiioonnss::

Bronchodilatorsto 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 inhalersAlbuterol(fast acting broncho dialators dont need to be used all the time, pollen)

CorticosteroidsSolu Medrol IV or PO to alleviate acute symptoms by decreasing inflammation (hour glass vial, powderin 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)

Antibioticsto manage respiratory tract infections Mucolytics and expectorantsto thin and aid in removal of mucus Analgesics (nsaid or Tylenol for aches & pain)

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

season Given yearly Cost for people > 65 is paid by Medicare

Recommended for: >50 years old Chronic heart or lung disease HIV (compromised immune system)Anyone living in large groups People who may transmit the flu to high risk groups

Nurses, doctors, and other healthcare workers

YYoouu sshhoouulldd NNOOTT ggeett tthhee fflluu sshhoottss iiff Allergic to eggs Hx of Guillain-Barre Syndrome


10/23

Acute illness or feverSSiiddee eeffffeeccttss 40 years

PPuullmmoonnaarryyEEmmbboolliissmm..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


11/23

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

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

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)

V/Q mismatching

Intrapulmonary shunt

Dead space ventilation Hypotension (from reduced left-heart venous return)


12/23

Right heart failure V-Q lung scan (limited specificity)test will come back saying limited

specificity not really sure if there is a clot.MRI Pulmonary angiographyCXR may show evidence of pulmonary infarct (also limited specificity) Lower extremity venous duplex (DVT requires same tx as PE)like a

Doppler (study of the leg) A negative study does not exclude PE!

MEDICAL INTERVENTIONS:

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

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

NURSING DIAGNOSIS

Impaired gas exchange

Heparin NomogramAnticoagulation form Venous

Thrombosis/Peripheral Vascular DiseaseAdjustment Contingency Table

(25,000 units Heparin/500ml D5W)

PTT Bolus (units) Hold (min) Rate Change Repeat PTTBelow 41 2000 unit 0 min +4ml/hr (200units/hr) 6hrs41-49 1000 units 0 min +2ml/hr (100units/hr) 6hrs50-80 0 0 min NO RATE CHANGE next AM81-89 0 0 min -2ml/hr (100units/hr) 6hrs90-106 0 60 min -4ml/hr (200units/hr) 6hrsAbove 106 0 120 min -4mil/hr (200units/hr) 6hrs

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 surgeryprotamine sulfate is drug given immed reverses heparin.


13/23

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

RReessttrriiccttiivvee LLuunngg DDiissoorrddeerrss 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

PPNNEEUUMMOONNIIAA 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 ofexudate

LLUUNNGG CCAANNCCEERR 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

PPAATTHHOOPPHHYYSSIIOOLLOOGGYY > 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 lymphsystem

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

glands.

SSTTAATTSS,, CCAAUUSSEESS && RRIISSKK FFAACCTTOORRSS
http://ww3.komotv.com/Global/story.asp?S=2314233http://ww3.komotv.com/Global/story.asp?S=2314233http://ww3.komotv.com/Global/story.asp?S=2314233


14/23

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 thatof a nonsmoker

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

DDIIAAGGNNOOSSTTIICC TTEESSTTSS 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

SSTTAATTSS,, CCAAUUSSEESS && RRIISSKK FFAACCTTOORRSS Heredity Preexisting pulmonary diseases

Incidence of lung cancer correlates with the degree of urbanization and populationdensity Second hand smoke exposure Risk of developing lung cancer is directly related to total exposure to cigarette smoke

- Pack Year History

CCLLIINNIICCAALL MMAANNIIFFEESSTTAATTIIOONNSS 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

CCLLIINNIICCAALL MMAANNIIFFEESSTTAATTIIOONNSSLater manifestations: anorexia fatigue weight loss


15/23

hoarseness if mediastinal involvement may have

pericardial effusion cardiac tamponade dysrhythmias

DDIIAAGGNNOOSSTTIICC SSTTUUDDIIEESS Chest X-ray CT scans MRI PET - (position-emission tomography) - measurement of differential metabolic activity in normal and

diseased tissue

DDeeffiinniittiivvee ddiiaaggnnoossiiss ooff lluunngg ccaanncceerr iiss mmaaddee bbyy:: IIddeennttiiffiiccaattiioonn ooffmmaalliiggnnaanntt cceellllss

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

Mediastinoscopy

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

CommitteesTTNNMMstaging system.

T = denotes tumor size. Location, and degree of involvement N = indicates regional lymph node involvementM = represents the presence or absence of distant metastases

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

TTHHEERRAAPPEEUUTTIICC MMAANNAAGGEEMMEENNTTSurgical 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

NNUURRSSIINNGG MMAANNAAGGEEMMEENNTTNursing 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


16/23

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

IImmppaacctt ooff AAsstthhmmaa iinn tthhee UU..SS..

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

HHyyppeerrvveennttiillaattiioonn 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.

SSiiggnnss aanndd SSyymmppttoommss ooff AAsstthhmmaa 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


17/23

Hypoxemia Nasal flaring

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 Hyperirritability or hyperresponsiveness tracheobronchial tree

Bronchoconstriction in response to physical, chemical and pharmacolgicagents

EEaarrllyy PPhhaassee ((3300--6600 mmiinnuutteess)) Triggered by allergen or irritantMAST cell degranulation -- Immune Mediator Release

Bronchial smooth muscle constrictionMucous Secretion Vascular Leakage

LLaattee PPhhaassee ((55--66 hhoouurrss ttoo 22 ddaayyss)) Infiltration (esoinophils and neutrophils) Bronchial hyperreactivity Imflammation

Infiltration with monocytes and lymphocytes

GG gerdAA allergensSS smoking, strong odors


18/23

PP pets & pestsBB beer, wine & deliRR resp.infectionsEE emotional/stress

AA

activities

TT timingHH humidity, cold air or sudden temp change

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

MMAANNAAGGEEMMEENNTT OOFF AASSTTHHMMAAPreventiveMAST Cell stabilizer Long acting beta 2 agonists (serevent) Inhaled corticosteroids EpinephrineTheophylline

Pharmacological TreatmentShort acting beta2-agonists (Bronchodilators)

End inol

TheophyllineAnticholinergic Agents - AtroventCorticosteroids


19/23

Long acting beta2-agonist and corticosteriod combinationCromolynLeukotriene-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, RespbidTheophylline levelToxicity causes the following symptoms: nausea, vomiting,

headache, insomnia, and, in rare cases, disturbances in heartrhythm and convulsions.

Anticholinergic Agents - AtroventActs as a bronchodilator over timeNot for acute attacks

It may be useful for certain older asthma patients who also haveemphysema or chronic bronchitis.

A combination with a beta2-agonist might be helpful for patients who donot initially respond to treatment with a beta2-agonist alone.

CorticosteriodsChronic managementInhaled:

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 corticosteriodcombination


20/23

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 hasantihistamine properties that block asthma triggers such as allergens, cold, orexercise.

Side effects: nasal congestion coughing sneezing wheezing nausea

nosebleeds dry throat.

Leukotriene-antagonistszafirlukast (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 andspasms in the airways of people with asthma.

Used to prevent asthma attacks.Gastrointestinal distress is the most common side effect

RRiisskk ffoorr aalltteerreedd rreessppiirraattoorryy ffuunnccttiioonn rreellaatteedd ttoo eexxcceessssiivvee oorr tthhiicckk sseeccrreettiioonnsssseeccoonnddaarryy ttoo aasstthhmmaa

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

MMeeddiiccaallllyy DDiiaaggnnoossiinngg AAsstthhmmaa Health history & physical exam Pulmonary Function Tests (PFTs)

Spirometry Peak expiratory flow rates (PEFR)

Sputum or blood culture for eosinophils Arterial blood gases (ABGs) & oximetry


21/23

Serum IgE levels: elevated Chest x-ray: hyperinflation during attack Allergy skin testing

MMeeddiiccaallllyy DDiiaaggnnoossiinngg AAsstthhmmaa Pulmonary Function Tests (PFTs)

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

Aid in determining degree of obstruction

MMeeddiiccaallllyy DDiiaaggnnoossiinngg AAsstthhmmaa

Arterial 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, respiratoryacidosis.

AAsstthhmmaa SSeevveerriittyy CCllaassssiiffiiccaattiioonnSStteepp 11:: MMiilldd IInntteerrmmiitttteenntt

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

AAsstthhmmaa SSeevveerriittyy CCllaassssiiffiiccaattiioonnSStteepp 22:: MMiilldd PPeerrssiisstteenntt

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)

AAsstthhmmaa SSeevveerriittyy CCllaassssiiffiiccaattiioonn


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SStteepp 33:: MMooddeerraattee PPeerrssiisstteenntt

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)

AAsstthhmmaa SSeevveerriittyy CCllaassssiiffiiccaattiioonnSStteepp 44:: SSeevveerree PPeerrssiisstteenntt

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)

SSttaattuuss AAsstthhmmaattiiccuuss 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

NNuurrssiinngg DDiiaaggnnoosseess

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 exchangeActivity intolerance r/t fatigue, tightness of chest, shortness of breath Risk for infection r/t ineffective airway clearance and decreased pulmonary

function

PPllaann aanndd IInntteerrvveennttiioonnssSee NIC

Airway Management Respiratory Monitoring


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Allergy ManagementAnxiety Reduction Positioning Vital Sign Monitoring

Per physician order:Albuterol via nebulizer

Oxygen therapy Order ABGs

NNuurrssiinngg DDiiaaggnnoosseess

Anxiety r/t inability to breath effectively, fear of suffocation Ineffective breathing pattern r/t anxietyAnxiety 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 usePlan and Interventions

See NIC:Airway Management Respiratory MonitoringAnxiety Reduction Positioning Vital Sign MonitoringAirway Clearance

Per physician order: 40% oxygenation via Venturi Mask IV Methylprednisolone Start transfer to ICU

NNuurrssiinngg DDxxAAnnxxiieettyy rreellaatteedd ttoo tthhrreeaatt ooff uunnkknnoowwnn ddeeaatthh sseeccoonnddaarryy ttoo sseevveerree aasstthhmmaa aattttaacckk

IInntteerrvveennttiioonnss:: Encourage verbalization of feelings, perceptions, and fears Provide objects that symbolize safeness Identify when level of anxiety changesEExxppeecctteedd OOuuttccoommeess:: Pt will verbalize feelings

Pt will surround him/herself with a safe environment Pt will identify the beginning signs of anxiety

Oxygenation Notes

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