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**COPD: Description and Significance
- Preventable, treatable disease characterized by Persistent airflow limitation, progressive
- Chronic inflammatory response of airways to noxious particles or gases (usually related to smoking)
- =>Fourth leading cause of death in the United States
- More than 50% die within 10 years of diagnosis
=>Includes: Chronic bronchitis charaterized by inflammation and structural changes (narrowing of airways, increased mucus) along with emphysemia in alveolar structures (desctruction of alveolar air sacs)
**Mechanisms Underlying Airflow Limitation & Measured by spirometry
(COPD percent to confirm?)
Inflammation which leads to Small airway disease (bronchiolitis) AND Parenchymal destruction (Emphysema)
.Airway inflammation leads to airway remodeling leads to narrowing of small airways (and eventually scar tissue formation)
Parenchymal destruction:Airflow limitationLoss of alveolar attachments leads todecreased elastic recoil
- WHICH BOTH LEAD TO AIRFLOW LIMITATION:
- Measured by spirometry: Forced vital capacity of air exhaled during the first second of exhalation (numerator) divided by the total Forced vital capacity (FEV1/FVC).
- <70% CONFIRMS COPD. <80% confirms airway limitaton
- FEV1: Amount of air that they exhale that first second of exhalation (numerator.)
- FVC: Breath in and breath out, the total amount of air blown out (denominator)
presecnce of chronic productive courgh for 3 months in each of 2 consecutive years in a patinent whom other cough factors are ecluded.
abonrmal permanent enlargment of air spaces distal to the termainal bronchioles accompanied by destruction of their walls w/o obvious fibrosis.
COPD: Etiology; Risk factors
Cigarette smokingOccupational and environmental (air pollution)InfectionsGeneticsGrowth & DevelopmentGenderAging
**COPD: Cigarette Smoking
- Clinically significant airway obstruction develops in 15% to 20% of smokers
- 80% to 90% of COPD deaths are related to tobacco smoking
- Approximately 4000 chemicals (more than 60 carcinogens) are inhaled in cigarette smoke
- =>Effects on respiratory tract
- Increased mucus production
- Hyperplasia of mucus glands
- Lost or decreased ciliary activity
- =>Carbon monoxide↓ O2 carrying capacity (nicotine has affinity to oxygen)
- ↑ Heart rate
- Impaired psychomotor performance and judgment
**COPD: Occupational and Environmental s
=>COPD can develop with intense or prolonged exposure toDusts, vapors, irritants, or fumesHigh levels of air pollutionFumes from indoor heating or cooking with fossil fuel
- Recurring Resp tract infections (influenza, strept pneumonia) impair normal defense mechanisms
- Increases risk factor for COPD
- Infections intensify pathologic destruction of lung tissue which limits ability to receive oxygen
- Remodeling causes lung tissue scaring
**COPD: Genetics=>alpha-Antitrypsin (AAT) deficiency (caused in young people who don't smoke); more common in northern european descent.Genetic risk factor for COPDAccounts for <1% to 2% of COPD=> treatable, med that slows progression of COPD is Alpha Protein Inhibitor (but expensive), not a cure.
- =>alpha-Antitrypsin (AAT) deficiency (caused in young people who don't smoke); more common in northern european descent.
- Genetic risk factor for COPD
- Accounts for <1% to 2% of COPD
=> treatable, med that slows progression of COPD is Alpha Protein Inhibitor (but expensive), not a cure.
**COPD: Growth & Development
- -anything that affects the lung during pregnancy
- Frequent childhood diseases Low birth weight correlation and FEV1
- children exposed to second hand smoke.
Unclear but women may be more susceptible to affects of tobacco than men, but prevalence is equalWomen with severe COPD exhibit smaller airway lumens & thicker airway walls
- =>Natural changes in the aging lungs
- Gradual loss of elastic recoil
- Lungs become rounded and smaller
- Loss of alveolar supporting structures (destruction of parenchymal lung tissue and scar tissue formation)
- Decreased number of functional alveoli
- Decreased arterial O2 levels
- Thoracic cage changes from osteoporosis and calcification of costal cartilages (means less lung expansion)
-Chronic inflammation of the airways, lung parenchyma (respiratory bronchioles and alveoli) and pulmonary blood vessels. Defining feature: NOT fully reversibel airflow limitation during forced exhalation, caused by loss of elastic recoinl and airflow obstruction from mucous hypersecretion, edma and bronospasm.
-Processes such as: airflow limitation, air trapping, gas exchange abornalities, muccus hypersecretion
-Main characteristic: inability to expire air (especially in smaller airways, getting trapped in expiration and lack of elastic recoil makes expiration deifficult -> hyperexpansion of lungs.
-Gas exchange abonormalities: Increase CO2 (hypercapnia) along with hypoxemia; V/Q mismatch occurs
-Pulmonary hypertension eventually leads to hypertropy of R ventricle (cor pulmonale) dilation and eventually right sided heart failure.
=> The predominant inflammatory cells in COPD:
- =>Primary process is inflammation: '
- Inhalation of noxious particles
- Mediators released cause damage to lung tissue and they start caussing damaage
- Airways inflamed
- Parenchyma destroyed (structures that support the alveoli)
neutrophils, macrophages, and lymphocytes which attract inflammatory mediatiors (leukotrienes) and result in structural lug changes.
^^ALL LEADING TO COPD where you have:
- COPD: Pathophysiology (schematic)
- -Breath in noxious particles leads to
- 1. Inflammation of central airways: Inflammatory cells (lymphocytes, macrophages, neutrophils) and mediators; release all wbc granulocytes
- 2. Peripheal airway remodeling
- 3. Parenchymal destruction: Imbalance b/w proteinase and antiproteinase
- 4. Pulmonary vasc changes: Thick vessels, infltration of inflammatory cells, collagen deposit and capillary bed destrcuction
Mucus Hypersecretion, cillia dysfunction, airflow limited, hyperinflated lungs, gas exchange abnormalities, pulmonary hypertension and cor pulmonale.
**COPD Clinical Manifestations:
- -Chronic intermmiten cough
- -not being able to take deep breath, air hunger-dyspnea (late stages) with alveoli overdistension and air trapping -> flattened diapgram so breathing through partial inflated lung
- -Fatigue, weight loss (advanced COPD)-Barrel, AP chest
- -Hypoxemia over time (paO2 <60 and SaO2 <88) and hypercapnia (PaCO2 >45)
- -Polycthemia: increased RBC to compensate for lack of O2
**Emphysema & Structural changes
- Abnormal permanent enlargement of the air space distal to the terminal bronchioles ( alveoli permanently enlarged) AND Destruction of bronchioles without obvious fibrosis
- -Only 10% of patients have pure emphysema, usually coexists with chronic bronchitis
- => Structural changes:
- Hyperinflation of alveoli
- Destruction of alveolar walls
- Destruction of alveolar capillary walls
- Narrowed & tortuous small airways
- Loss of lung elasticity
- Decreased pulmonary capillary bed leading to pulmonary resistance and right sided heart failure (Cor Pulmonale)
- -Impaired gas exchange result from destruction in overdistended alveoli walls, increases dead space in lungs so that air goes in BUT NO GAS EXCHANGE! In a V/Q perfusion scan, there's ventillation (air goes in) w/o perfusion (no exchange)
- -THIS LEADS TO HYPOXEMIA: Oxygen staying in blood w/o tissues
- note: Hypoxia: o2 in tissues.
**Emphysema: Two types disease process
- =>Centrilobular (central part of lobule)
- Dilation and destruction of respiratory bronchioles and pulmonary capillary bed
- Prominent in upper lobes;
- --Distal overdistension (broccoli)
- =>Panlobular (destruction of whole lobule)
- Affects respiratory bronchioles, alveolar ducts, and alveolar sacs
- Prominent in lower lobes-
- central expansion.
**Emphysema Clinical Manifestations:
Dyspnea on exertion, during ADL’s, and rest
Minimal coughing with no to minimal sputum
Alveoli over-distended leading to air trapping (increased chest circumferences=> barrel chest), flattened diaphragm, and increased chest circumference
More of a chest breather, rely on intercostals and accesory muscles rather than diapgragm (normal)
-Usually underweight due to hypermetabolic symptoms, body trying hard to keep up /:
Early hypoxemia with activity but late hypercapnia (increased CO2 in blood) usually not prevalent till the later stages.
Tend to be underweight due to hypermetabolism 2° to increased work of breathing.
**Chronic Bronchitis: Defn & Struc Chanegs
- =>Definition: Presence of chronic productive cough for 3 or more months in each of 2 successive years
- Other causes of chronic cough are excluded: like viral infections, etc.
- -Increased, frequent, productivecough in winter time, exacerbated in winter months
- -frequent resp infections usuallly occur since you have decreased ability to fight infections
- -increased airway resistance: harder to get air into lungs (bluish, cyanotic due to decreased Oxygen in blood)
- -Increased RBC to compensation for decreased level of Oxygen in blood But STILL NOT PERFUSING WELL ENOUGH.
- =>Structural changes:
- Hyperplasia of mucus secreting glands in trachea & bronchi
- Increase in goblet cells
- Disappearance of cilia
- Chronic inflammatory changes & narrowing of small airways
- Altered function of alveolar macrophages prevalent in INCREASED bronchial infections
**Chronic Bronchitis: Clinical Manifestations:
Frequent productive cough: Presence of cough and sputum production for at least 3 months in each of 2 consecutive years; Especially during the winter. (damp air triggers, in winter months, cigarette smoking)
Bronchospasm (difficulty breathing) at end of paroxysms of cough
Frequent respiratory infections: Due to alteration of alveolar macrophages.
Late dyspnea (difficulty breathing after cough) as well as Hypoxemia and hypercapnia
Bluish-red color: Polycythemia as a response to chronic hypoxemia
Normal weight to heavyset (if more on bronchitis side vs. Emphysema
- =>Supporting structures of lungs are destroyed
- Air goes in easily but remains in the lungs
- Bronchioles tend to collapse (air trapping with overdistended alveoli)
- Alveoli over-distended leading to air trapping, flattened diaphragm, and increased chest circumference (barrel chest)
=>Pulmonary vascular changes Blood vessels thicken from all macrophages and wbc's going into wall. Surface area for diffusion of O2 decreases
**Pathological Changes in COPD
- Mucous hypersecretion
- Ciliary dysfunction
- Airflow limitation
- Pulmonary hyperinflation
- Gas exchange abnormalities
- Pulmonary hypertension
- Dysfunction of peripheral & respiratory muscles
**COPD: CO2 Retention
Normally, high CO2 levels stimulate drive to breathe.Patients that receive excessive supplemental O2 can develop CO2 retention. But why? Reasons are debatable.
1) Reduction in hypoxic drive (carbon dioxide narcosis)- When CO2 levels are chronically elevated, the resp center becomes less sensitive to CO2 as a stimulant to breathe. Decreased O2 becomes drive to breathe. Thus, supplemental O2 can suppress drive.COPD: CO2 Retention
2) Both O2 and CO2 bind to Hgb molecules. Administering supplemental O2 can push CO2 from the Hgb and into the blood causing Co2 levels to rise in the blood.
3) In COPD the relationship between air exchange within lungs and blood flow within lungs (V/Q mismatch) result in reduced removal of CO2.
**COPD: Physical Examination findings r)
- Prolonged expiratory phase: body trying to get rid of CO2
- Decreased breath sounds
- ↑ Anterior-posterior diameter
- Bluish-red color of skin: Polycythemia (Increased RBCs) and cyanosis (fingertips, lips, generally a red colo
**Stages of COPD: FEV1 (Forced Expiratory Volume)
- =>Stage 1 (Mild)
- FEV1 >80%
- Treatment: Reduce risk factors. PRN rescue bronchodilators
- =>Stage 2 (Moderate)
- -something <70 that confirms COPD
- FEV1 50-80%;
- Treatment: Same as Stage 1, with need of additional PRN bronchodilator and start of pulmonary rehab
- =>Stage 3 (Severe)
- FEV1 30-50%:
- Treatment: Same as Stage 2 with additional corticosteroid inhaler if repeated exacerbations
- =>Stage 4 (Very Severe)
- FEV1 <30% OR <50% + chronic respiratory failure
- Treatment: Same as Stage 3 with need for long term O2 and possibility of surgery
- Cor pulmonale
- Acute exacerbations of COPD
- Acute respiratory failure
- Peptic ulcer disease (due to corticosteroid use)
=>Hypertrophy of right side of heart
- -Results from pulmonary hypertension due to constriction of pulmonary vessels in response to alveolar hypxia, with acidosis.
- -Chronic alveolar hypoxia stimulates vascular remoedling, and erythropoesis and polycythemia which increases pulm vas resistance and develop pulmonary HTN.
- -Pulm HTN increases workload on R ventricle to push blood into lungs.
- -Dyspnea is the most common symtom of Cor Pulmonale; lung sounds normal or crackles
- -BNP (B type Natriurtetic peptide) may diagnose hear failure elevated.
- -treatment: low flow long term Oxygen therapy, Diuretics. SABA for the breathless or short acting bronchodilators
that results from pulmonary hypertension (back up of fluid into heart and then into lungs) THIS is Late manifestation of chronic pulmonary heart disease which Eventually causes right-sided heart failure
- Distended neck veins
- Hepatomegaly with upper quadrant tenderness (vesssels in liver is congested and backed up with blood, upper quad tenderness)
- Ascites (due to liver full of blood)
- Epigastric distress
**Pathophysiology of Cor Pulmonale
COPD which leads to hypoxia in tissues -> Polycythemia and Hyperviscosity -> Pulm hypertension (blood is too thick)
Hypoxia-> vasoconstriction -> Vascular resistance (makes o2 harder to exchange) -> Pulm Hypertension
Reduction of pulm vascular bed (destruction of lung supporting structure)
Acidosis & Hypercapnia-> pulmm vaoconstriction and resistance.
PULMONARY RESISTANCE LEADS TO R VENT HYPERTROPHY --> COR PULMONALE --> RIGHT SIDED HEART FAILURE!!
**Acute Exacerbations of COPD
- Signaled by change in usual condition: Dyspnea, Cough, Sputum
- Associated with poorer outcomes
- Primary causes: Tracheobronchial infection and Air pollution
- Teach pt. to report any changes in baseline
**Acute Respiratory Failure
- =>Caused by
- Cor pulmonale
- Discontinuing bronchodilator or corticosteroid medication (stopped using meds)
- Overuse of sedatives, benzodiazepines, and opioids (decreases respiratory rates)
- Surgery or severe, painful illness involving chest or abdomen (not expanding chest enough due to pain)
Medications: cardioselctive beta adrenergic blockers (atenolol, metoprolol) can be safetly used.
**Peptic Ulcer Disease
Increased incidence with COPD patients who chronically retain CO2Commonly in duodenum and painless (they don't know until blood in stool shows up)From chronic use of bronchodilators and corticosteroids
COPD patients more susceptible to S pneumonia and H influenza (give pneumonia vaccines at age 65! get it every FIVE years)
**Depression & Anxiety
Depression may be four times more likely for COPD patients
- =>Anxiety complications
- Respiratory compromise
- Diagnosis confirmed by pulmonary function tests
- Chest x-rays: Hyperinflation
- Reduced FEV/FVC ratio (the lower the fev, the sicker the patient)
- Increased residual volume (air trapping)
- Decreased O2sat with ambulation (drop with activity)
- =>History and physical examination
- ABG typical findings
- Low PaO2↑ PaCO2 (resp acidotic)
- ↓ pH
- ↑ Bicarbonate level found in late stages COPD (body attempting to compensate for acidosis b/c bicarb is a base.)
=>ECG can determine presence of right-sided heart failure
Assess and monitor the diseaseReduce risk factors=>Manage stable COPD (multidisciplinary team)Pharmacologic therapyOxygen therapySurgical managementPulmonary rehabilitationManage exacerbations
**COPD: Pharmacologic Therapy
- Relaxes smooth muscle in the airway
- Improves ventilation of the lungs
- ↓ Dyspnea and ↑ in FEV1
- Inhaled route is preferred
- => Commonly used bronchodilators
- Β2-Adrenergic agonists
**Inhaled corticosteroid therapy
Used for moderate-to-severe casesNot for long-term use
**COPD: Oxygen Therapy
- =>O2 therapy is used to
- Reduce work of breathing
- Maintain PaO2
- Reduce workload on heart
- =>Long-term O2 therapy improves
- Exercise capacity
- Cognitive performance
- Sleep in hypoxemic patients
Used because O2 has a drying effect on the mucosaSupplied by nebulizers, vapotherm, and bubble-through humidifiers
- =>O2 delivery systems are high or low flow'
- Low flow is most common
- Low flow is mixed with room air, and delivery is less precise than high flow
- =>Complications of oxygen therapy
- CO2 narcosis: High tolerance for CO2 develops in COPD pts, so their drive to breathe is "hypoxemia". So provide lowest level of oxygen.
- O2 toxicity: Results from prlonged level of oxygen resulting in severe inflamm response b/c oxygen radicals and damage to alveolar capillary membranes result in pulm edema, suuntinng blood and hypoxemia --> ARDs.
- Absorption atelectasis
- Infection: heated nebulizers present highest risk: supports bacterial growth (pseudomonas aeruginosa)
- =>Chronic O2 therapy at home
- Improves: Prognosis, Mental acuity, Exercise intolerance
- Reduces: Hematocrit & Pulmonary hypertension
- Periodic re-evaluations are necessary to determine duration of use
When high concentrations of oxygen are iven, nitrogen is washed out of the alveli and replaced with oxygen. If airway obstruction occur, the oxygen is absorbed into the bloodstream and the alveoli collapse. This process is called absoption atelectasis.
**COPD: Surgical Therapy
=>Lung transplantationSingle lung—most common due to donor shortagesProlongs lifeImproves functional capacityEnhances quality of life if they're strong enough to survive surgery.
=>COPD: Pulmonary Rehabilitation
Note: using accessory muscles results in fatiuee
- Respiratory therapy
- Breathing retraining:
- -Pursed lip breathing: to prolong exhalation and thereby prevent bronchiolar collapse and air trapping
- -Diaphragmatic breathing: cocuses on using diaphragm instead of accessory muscles of the chest: achieve max inhalation and slow the respiratory rate.
- Effective coughing: Huff coughing
- Flutter mucus clearance device: A.k.a. Acapella
- Aerosol nebulization therapy
- =>Chest physiotherapy
- Postural drainage
- -Indicated for:
- Excessive, difficult-to-clear bronchial secretions
- Retained secretions in artificial airway
- Lobular atelectasis from mucous plug
Hands in a cup-like position to create an air pocketAir-cushion impact facilitates movement of thick mucus- NOTE: No percussion overKidneys Sternum Spinal cordBony prominencesTender or painful area
- Facilitates movement of secretions to larger airways
- Mild vibration tolerated better than percussion
- -Flutter mucus clearance device: Produces vibration in lungs to loosen mucus for expectoration, Handheld device
- -High-frequency chest compression: Inflatable vest that vibrates the chest, Works on all lobes, More effective than CPT
- =>Postural drainage
- Gravity assists in bronchial drainageTechniques are individualized according to patient’s pulmonary condition and response to initial treatment
**COPD: Pulmonary Rehabilitation- Breathing Styles
- =>Breathing retraining
- Decreases dyspnea, improves oxygenation, and slows respiratory rate
=>Pursed-lip breathing: Prolongs exhalation and prevents bronchiolar collapse and air trapping
- =>Effective coughing:
- Main goals
- Conserves energy
- Reduces fatigue
- Facilitates removal of secretions
**COPD: Nutritional Therapy
- => Weight loss and malnutrition are common
- Pressure on diaphragm from a full stomach causes dyspnea
- Difficulty breathing while eating leads to inadequate consumption
- =>To decrease dyspnea and conserve energy
- Rest at least 30 minutes before eating
- Use bronchodilator
- Prepare foods in advance
- => Diet:
- High-calorie, high-protein diet is recommended
- Fluids (intake of 3 L/day) should be taken between meals (limit liq during meal time)
- Eat 5 to 6 small meals to avoid bloating and early satiety
- =>Avoid Foods that require a great deal of chewing (exhausting..)
- Exercises and treatments 1 hour before and after eating
- Gas-forming foods
Nursing management & Patient Education
Smoking cessationBreathing exercisesInspiratory muscle trainingActivity pacing/Self-care activitiesPhysical conditioningO2 therapyNutritional therapyCoping measures
A "pink puffer"
is a person where emphysema is the primary underlying pathology. As you recall, emphysema results from destruction of the airways distal to the terminal bronchiole--which also includes the gradual destruction of the pulmonary capillary bed and thus decreased inability to oxygenate the blood. So, not only is there less surface area for gas exchange, there is also less vascular bed for gas exchange--but less ventilation-perfusion mismatch than blue bloaters. The body then has to compensate by hyperventilation (the "puffer" part). Their arterial blood gases (ABGs) actually are relatively normal because of this compensatory hyperventilation. Eventually, because of the low cardiac output, people afflicted with this disease develop muscle wasting and weight loss. They actually have less hypoxemia (compared to blue bloaters) and appear to have a "pink" complexion and hence "pink puffer". Some of the pink appearance may also be due to the work (use of neck and chest muscles) these folks put into just drawing a breath.
A "blue bloater"
is a person where the primary underlying lung pathology is chronic bronchitis. Just a reminder, chronic bronchitis is caused by excessive mucus production with airway obstruction resulting from hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi. Unlike emphysema, the pulmonary capillary bed is undamaged. Instead, the body responds to the increased obstruction by decreasing ventilation and increasing cardiac output. There is a dreadful ventilation to perfusion mismatch leading to hypoxemia and polycythemia. In addition, they also have increased carbon dioxide retention (hypercapnia). Because of increasing obstruction, their residual lung volume gradually increases (the "bloating" part). They are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces--the "blue" part.