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- =>Chronic disorder of airways characterized by
- Persistent and variable airway inflammation
- Reversible airway obstruction
- Bronchial hyperresponsiveness (hyperrreactivity) and airway edema
- Wheezing, chest tightness, shortness of breath, and cough
- Unpredictable and variable clinical course
- Associated with significant economic cost, morbidity, and decreased productivity
- =>Affects 25 million Americans
- 18 million adults (1 in 12)
- 7 million children (1 in 11)
- =>The following groups are more likely to have asthma
- People who live in the Northeast/Midwest
- African Americans and Puerto Ricans
- People of lower SES
=>African-Americans most likely to be hospitalized, greatest mortality rate
**Risk Factors and Triggers
- Immune response/hygiene hypothesis
- Exercise: can bring it on, dry cold air makes it worse.
- Air pollutants
- Occupational exposure
- Respiratory infectionsNose/ Sinus problems
- Drug/ Food allergies (asthma=allergic rxn)
- GERD (stomach contents coming up into mouth, going into lungs, irritates the airway -> asthmatic rxn)
**Pathophysiology: Early Phase
Allergen stimulates the release of IgE antibodies (wants to get substance out of the lung) that then link with mast cells (wbcs with granules that contain histamine, cytokines and release this.. causing inflammation. And that's what causes the allergy, not the allergen itself, but the body's reaction to the allergen.)
Mast cell degranulation releases common inflammatory mediators
Vasodilation and cellular infiltration (easier capillary permeability for neutrophils, lymphocytes, and eosinophils)
Inflammatory process results in causing Vascular congestion and edema (pulmonary)
- Thick, tenacious mucusBronchial muscle spasm and constriction (airway clamps down on itself)Bronchial hyperresponsiveness
- => early phase occurs 30-60 mins after that intial exposure to that allergen.
- => if you control the symptoms in the early phase, it'll progress to the late phase, which happens around the same time as the earlly phaase. But you don't see effects until 4-10 hours after exposure. More severe, can last up to 24 hours. Not all people experience it.
ongoing asthmatic attack that they can't get control over.
**Pathophysiology: Late Phase
Initial attack causes infiltration of eosinophils and neutrophils which release EVEN MORE inflammatory mediators (cytokines, histamines, leukotrienes, Prostaglandins); occurs in 50% of asthma pts.
-Parasympathetic NS (autonomic) increased release of acetylcholine (due to allergens) causing increased smooth muscle contraction and mucous secretions leading to bronconstriction.
-chronic inflammation may lbead to structual bronchial wall changes (remodeling), smooth muscle hypertrophy, and angiogenesis (new blood vessels)
-decreased perfusion and ventillation and increased alveolar gas pressure
-> hypoxemic early on with decreased pa CO2 iand increaed pH (respiratory alkalosis) causing lungs to work harder so that CO2 normalizes when patient tires AND THEN INCREASESTO PRODUCE RESPIRATORY ACIDOSIS (MEANING RESP FAILURE)
Self-sustaining cycle of inflammation
Corticosteroids required to treat this phase THIS IS WHEN YOU NEED IT to stop inflammation process.
- =>Chronic inflammation that isn't controlled, can lead toStructural changes known as remodeling (scar tissues, less compliance-doesn't expand as much as the lungs should)
- -Pulmonary fibrosis: scar tissues in the lungs, and lungs don't expan, not a lot they can do about it.
Progressive limitation of airflow obstruction mimics COPD
Allergens activate the B lymphocytes, then plasma cells activated and release IGE antibodies and attach to the mast cells (wbc that release granules that degranulate and push histamine and inflammatory mediatoers all over the body)
- -Antigens attach to antibodies-goes into tissues of lungs-> inflammation and airway constriction symptoms.
- Know what medications treat asthma!
-triggers: exercise, stress can bring out asthma exacerbations
Wheezing (usually on expiration), cough, dyspnea, chest tightness after exposure to irritant
Prolonged expiration (instead of normal 1:2, it's 1:3 at least, as bronchioles constrict during expiration, causing air longer to exit)
S&S of hypoxia: Restlessness, anxiety, tachypnea, increased HR/BP
Tripod positioning (hunched over on bedside table, and using gravity to release pressure of their chest so that get more air into lungs, "I can't get a deep breath")
-episodes occur typically at middle of night and early morning (4-6 am); coinsides with cortisol release (stress hormone
**Severe Acute Attack .
- Any attack can progress to life-threatening
- Wheezing is actually a good sign (means SOME aire is going through)
- Clinical manifestations include: Increased HR/RR/BP, pulse paradoxus, severe anxiety, accessory muscle use, diminished or absent breath sounds, “silent chest”
- -tachypnea: >30 RR
- -HR: >120
- -Peak flow: <40% or less than 150 L/Min (as personal best)
- -Neck vein distension, accesory muscle used
- -Pts too dyspneic to talk, drowsy/confused,
- -Silent chest: Severely diminished breath sounds = OMINOUS SIGN (OBSTRUCTION)
- Status Asthmaticus: life threatening attack that doesn't respond to normal treatment. May end up on ventillators
- Comprehensive H&P:
- -Identify triggers and precipitating factors
- -Family history
- Pulmonary Function Tests
- Allergy Testing
- CXR: usually shows hyperinflation
- Oximetry, ABGs, CBC (high eosiophils suggestive of atoopy), Sputum analysis (especially during acute attacks, rules out bacterial infections)
**Classification & Control
-with severity & control. FIrst determine severity then detrmine how well controlled. All pts regardsless of their classification can suffer severe asthma attacks.
- Intermittent: mild disease, exposed to pollen then asthma, but not a chronic thing
- - <2 days a week (symptoms), no interference with normal activity. Normal lung function.
- Mild persistent: >2 days week but not daily, minor limitaotion
- Moderate persistent: Dialy, Daily SABA use, some limitation, FEV: 60-80 (forced Expiratory Vol)
- Severe persistent: Continuous, often-nightime awakening, SABA several times a day, FEV <60%
- =>Control Well
- -controlled: take meds and everything's fine. <2 day/wk symptom, no SABA use.
- Not well-controlled: >2 days week, some limitation, >2 day use of Saba
- Very poorly controlled: Symptoms through the day, >4 days week, severeal times a day
**Stepwise Treatment Regimen
SABA PRN-Short acting Beta 2 Agonist (rescue inhaler)
low dose ICS-Inhaled corticosteroids
LABA (long acting Beta 2 Agonist) or Low dose ICS
LABA and MEDIUM dose ICS
LABA and HIGH dose ICS
Step 5 plus oral corticosteroid (omalizumab-anti IgE-decreases circulating free igE levels and prevents attaching tomast cells)
- -SABA is for symptom relief, not prevention of EIB (excercise induced bronchospaspm)
-Step down if asthma is well controlled for at least 3 months, step up if needed.
**Intermittent and Persistent Asthma:
-Patients in ALL classifications o asthma require a short term rescue/reliever medication. THe most efffective ones are SABA (short acting veta adrenergic agonsist--Albuterol).
-Patients with persistent asthma should also be on a long-term or controll medication. Inhaled Corticosteroids (Fluicasosne/Dlovent) are the most effect to treat inflamation)
**Severe and Life-Threatening ASthma Exacerbations
First line is SABA in 3 treatments, 30 mins apart.
IF no response, then oral systemic Cortiosteroids for severe, and IV for life-threathening Q4-6 hours which MUST be tapered off -> oral corticos at home. ICS usually added in hospital (high dose to prevent asthma relapse)
- -Life threatenging: adjunct IV magnesium with very low FEV or peak flow <40%.
- -If not, heliox (helium and oxygen)- low density to improve brochodilation effect of albuterol.
- -supplmental O2 by nasal prongs
- -Metabolic rate increase so IV fluids given for opitmal hyddration
- -Sodium Bicarbonate for metabolic or respiratory acidosis in mech ventilated pt b/c effective bronchodilation ob Beta adrenergic agonists is not possible if pt has extreme acidosis.
=> Short Acting Beta 2 Agonists
=> Long Acting Beta 2 Agonists
- =>Short Acting Beta2 Agonists
- Relieve acute bronchospasm; rescue inhaler for all steps. especailly after exercise, they do not inhibit the late phase response of asthma or have anti-inflammatory effects.
- -not used for long term control or for persisten asthma.
- Monotherapy only for Step 1, usually Albuterol
- Caution with cardiac patients (because it increase HR!)
- Ex: Atrovent/Ipratoripium
- =>Long Acting Beta2 Agonists
- Not for acute relief (Doesn't decreease inflammation, so shouldn't be used by itself, but also use short acting or combined ICS)
- -effective for 12 hours; added to ICS for long term control of moderate to severe persistent asthma (step 3 or higher)
- Should not be used as monotherapy, always with ICS.
- Often combined with an ICS
- Salmeterol and formoterol (symbicort-combines LABA with ICS)
- Exact MOA (mech of action)unknown; bronchodilator with mild antinflammatory effects Alternative treatment for step2
- SE, drug interactions make drug undesirable
- Serum drug monitoring
: Se of n/v tachcardia, arrythmias, avoid caffeine!
Block Parasympetheic NS influence (block the bronchosconstricting effect); leffss effective thatn beta 2's, used in quick relief in those pts unable to tolerate SABA. Often nebulized with SABA in severe asthma exacervation
- -onset: 30-1 hr
- -poorly absorbed so little SE's.
- Less effective than beta2 agonists
- Systemic SE uncommon
(Atrovent) often nebulized with albuterol
=> IV & SE's
Anti-inflammatory effects; reduce bronchial hyperresponsiveness, block the late phase response inhibit multiple inflammatory mediators (eospinols, tlympocytes and mast)
Most effective in improving asthma control but must be used short term
ICS first line therapy for step 2-6 (Fluticasone budesonide/Pulmicort)
- Little systemic SE, may not see effects until 2 weeks, rinse mouth
- Fluticasone, budesonide
- Short course therapy Systemic SE so avoid it long term
- Prednisone, prednisolone
- May be used with acute asthma and tapered rapidly (can't stop abruptly)
- -SE;s: High HR, bone pain, osteoporotics (for longterm, give calcium and Vit D), Hyperglycemia, impaired immune system, high WBCs on pts, increased risk of infection (immunosupp), thin skin, acne, hypokalemia!! Spiked appetite (weight gain-be careful)
-essential for control, but don't halt progression of disease, just get rid of symptoms.
- For control only (block inflammatory mediators), used in step 2 and help to reduce dosage of ICS in later steps. Usually well tolerated. Leukotrienes are inflammatory mediators and potent bronchoconstrictors
- PO only
- -monitor Liver enzymes, may interfer with warfarin/coumadin and theophylline.
- -not indicated for use in the reversal of bronchospasm in acute asthma attacks.
- =>Leukotriene Receptor Blockers
- Zafirlukast (Accolate), montelukast (Singulair); SE: HA, dizziness, N/V, fatigue
- =>Leukotriene Inhibitor
- Zileuton (Zyflo); Increased liver enzymes, dyspepsia, HA
Mast cell stabilizers
Prevent mast cells from releasing inflammatory mediators (stops the granules, stops more at the source)SE: cough, runny nose, throat irritationCromolyn Sodium MDI (Metered dose inhaler), HHN (hand held nebulizer)
Monoclonal antibodies (Xolair)
Decrease circulating free IgE level
For severe asthma that's NOT controlled with ICS
: Injection site rxn (bruising, redness, warmth, pain) , malignancy, infection
- =>Antibiotics: if a person gets secodnary bacterial infection, then:
- fluroquinolones (Levoquin), macrolides (azitromax or zpack), tetracylciline(doxycycline), cephalosporin (keflex, cephalexin), penicllin (hemoxicllin or augmentin)
- -know drugs and how they work!
never used as monotherapy, combined withh ICS
- Metered Dose Inhalers (MDIs)
- Dry powder Inhalers (DPI)
Aerosolizes medication to deliver into lungs by making a mist.
Must make a visible mist
Powered by air compressor or O2
Inhalation through mouthpiece (HHN) or mask
usually combination of : Albuterol/Atrovent, given by RT in hospitals.
-disadvantage: potetntial for bacterial growth (should use vinegar-water solutions)
- Sit uprightPatient is to breathe with slow, deep breaths through mouth and hold a few seconds at the end of inspiration Coughing exercises may be encouraged to mobilize secretions after a treatment
- Rinse mouth AFTER use; know how to clean the equipmentAssess patient before and after treatment and evaluate patient response
Metered Dose Inhaler (MDI)-
- like regular inhaler; requires coordination with inhalation
- Handheld pressurized inhalation device that delivers measured dose with each activation
- Examples- ICS, SABA, combo ICS/LABA, mast cell stabilizers
- -Shake well, sloiw inspiration, spacer with corticosteroids, use water to clean
- Use spacer: push medication into spaces and when pt is ready, they will inhale (helps with coordination, hold breath for 10 seconds. Spacer slows delivery so more time to reach lungs.)
- Rinse mouth after
- Know when to replace canister
- Clean as needed
- Avoid overuse
Dry Powder Inhaler (DPI) & Education
- Dry, powdered medication inhaler that is breath activated (symbiocort)
- -little capsule put in contain, poke holes in it, and then breathe in the powerer
- Easier to use than MDIs
- -Don't shake before use, Need rapid inspiration ( medicine delivered only by the pts inspiratory effort, so low FEV may not be able to get full mediceine), no spacer allowed, avoid moisture in cleaning
- Examples- ICS, LABA (Spiriva), combo (Advair, Symbicort)
- => Education
- Avoid humidity
- Monitor external counter, like advair diskus-purple one (tells you how many does you have left)
- Rinse mouth after
**Collaborative Care: Acute Intervention
- Assess respiratory status: Peak flow, lung auscultation, VS, oximetry, ABGs
- Oxygen therapy: Maintain SpO2 > 90%
- Nebulized bronchodilators
- IV, PO steroids
- Fluids: Maintain adequate hydration
- High Fowlers
- Quiet, calm environment
- Monitor CXR, sputum
Ineffective Airway Clearance r/t bronchospasm, excessive mucous production AEB cough, tenacious sputum, fatigue
Anxiety (mild, moderate, or severe) r/t feelings of suffocation AEB SOB, difficulty breathing
Ineffective therapeutic regimen of ?, RT Lack of exposure?, lack of resources?
Impaired gas exchange RT (same as ineffective airway clearance), AEB (ABG’s, H/H, SaO2, decreased capillary refill)Knowledge deficit of MDI, RT lack of exposure? lack of resources?
**Patient Education: Peak Flow Monitoring
- Used for patients after an exacerbation and daily with patients with moderate-to-severe persistent
- Can help pt identify triggers, navigate asthma management plan, and know when to seek care
- => Peak flow numbers categorized into zones
- Green; 80% best, good control
- Yellow: 50-80% best, caution, SABA needed
- Red: <50% best, SABA needed, seek care
=>Used with asthma action plan
**Peak Flow Meter
- Using a Peak Flow Meter: how they monitor disease process at home. The peak flow meter may tell you if there is narrowing in the airway befoer asthma symptoms.
- -measure in L/Min
- -portable hand held device, blow into it hard and fast, moves meter to tell you what lung capacity
- different colors: Green (80%), Yellow (50-80), red (<50%, that's when you need more meds and care)
- -helps pt self manage their illness, they should determine their personal best first and that's used as their baseline
- -must do it 2xday for 2-3 weeks, when they first wake up then early in evening, and after SABDilator used.
- Then physican can make changes.
- severe asthma can decrease to less than 150, positive response to Short Acting bronchodilator is greater than 250 L/min.
- =>Environmental Trigger Control:
- Avoid smoke, other allergensAvoid outdoors/activity when pollution level is highAvoid nonselective beta-blockersAvoid URIs
=>Medication Administration: viral URIS are the most common cause of an acute attack
=>Uses, administration techniques, SE, storage, cleaningdx
risk factors:young boys
atopy: the genetic predisposition to develop an allergic (immunoglobulin E -mediated) response to common allergens.
-Respiratory Tract Infections (Viral) are the major precipitatin factor of an acute asthma attack.
-"Asthma triad" nasal polyps, asthma and sensitivy to aspirin and NSAIDs-> wheezing w/in 2 hours.
-Beta Adrenergic Blockers (PO-Metoprolol/Troprol) may tirgger bronospasms
-ACE (angiotensin Converting Enzymes-Lisinopril) may produce cough.
-GERD reflux trigger bronchosconstription and aspiration; Beta two agonists relax lower esophageal sphincter causing reflux and possible aspiration into lungs)
-Emotions: lead to hyperventilationand hypocapnia-> airway narrowing.
-Exercise Induced asthma occurs after; prnouced during cold, dry air. Ex: swimming in indoor heated pool is less likely to cause asthma than downhill skkiing.
Hyperventillation during exercise may cause airway obstruction due to changes in airway mucosa, with either coolin or rewarming of air and capillary leaking in the airway wall.
goal in asthma care is to maximize the pts ability to safely manage acute asthma exacervations using an asthma action plan.
-Take 2-4 puffs of SABA Q20mins three times as a rescute plan
-keep pt calm and teach pursed lip breathing
Bronchioles; Constriction & Dilation
Bronchioles: Muscular elastic structures responding (contraction/dilation) of smooth muscles
-Bronchodilation: Relaxation of smooth muscles to allow Increased diameter and Increased airflow
-Bronchoconstriction: Narrowing of airway
**BOTH CONTROLLED BY AUTONOMIC NERVOUS SYSTEM**
Sympathetic Branch of the Autonomic Nervous System
Activates Beta 2 Adrenergic receptors in lungs leading to BronchoDILATION (by relaxing smooth muscles)
**Beta Adrenergic AGONISTS**
Beta Adrenergic Agonists
Drugs that activate Beta 2 Receptors in the lungs. Works on the sympathetic branch.
Beta 2 agonists: acute attacks (rescue inhales)
- Causes constriction (by contraction of bronchial smooth muscles)
- -anticholnergic drugs
Block the contraction (by working on the parasympathetic) in order to promote brochodilation.
Ex: Atrovent (Ipatroprium), Combivent and Spiriva.
Bronchodilator (unknown mechanism of action) but chemically related to caffeine.
Ex: aniophyllium. Check drug levels (Therapeutic levels)
Antiinflammatory (dampens activation of inflammatory mediators while increasing activation of anti-inflammatory mediators.
Also sensitize bronchial smooth muscle to be more receptive to beta agonist stimulation.
Reduce Hyper-Responsiveness to allergens.
Ex: Prenisolone, solumedrol
Interfers with synthesis or block actionof Leukotriene inflammatory mediators that produce bronchoconstriction, airway edema, and inflammation (stop it more at the source!)
Mast Cell Stabilizers
Inhibit igE mediated release of inflammation mediators from mast cells and suppress other inflammatory cells like eosinophils.
Stabilizes granulytes so they don't release the cells in the first place.
monoclonal antibodies to igE
Monoclonal antibodies to IgE decrease circulating circulating free igE levels. Prevents igE from attaching to mast cells and preventing release of inflammatory mediators (leukotrienes, histamines, cytokines, and bradykines)