copd lecture notes

, , COPD: CPT 1COPD: CPT 1

UTECH UTECH Dr E. Watson PharmD.Dr E. Watson PharmD.

Learning ObjectivesLearning Objectives: : upon upon completion of this lecture, the student should completion of this lecture, the student should

be able tobe able to Define the two major forms of chronic Define the two major forms of chronic

obstructive COPD.obstructive COPD. Be familiar with The Global initiative Be familiar with The Global initiative

for Chronic Obstructive Lung Disease for Chronic Obstructive Lung Disease (GOLD) definition of COPD. (GOLD) definition of COPD.

Ref: http://www.goldcopd.org.Ref: http://www.goldcopd.org. List the risk factors associated with List the risk factors associated with

COPD.COPD. Describe the pathophysiology of Describe the pathophysiology of

COPD. COPD.

Learning Objectives Cont’d.Learning Objectives Cont’d.

Describe the signs and symptoms of Describe the signs and symptoms of COPD.COPD.

Differentiate between chronic Differentiate between chronic bronchitis and emphysema.bronchitis and emphysema.

Describe the non-pharmacologic Describe the non-pharmacologic and pharmacologic management of and pharmacologic management of COPD.COPD.

To identify the role of the To identify the role of the pharmacist in the management of pharmacist in the management of COPD.COPD.

Key PointsKey Points

COPD is a preventable and treatable COPD is a preventable and treatable disease with significant extra-disease with significant extra-pulmonary effects that may contribute pulmonary effects that may contribute to severity in individual patients. to severity in individual patients.

The airflow limitation is generally not The airflow limitation is generally not reversible and is progressive.reversible and is progressive.

The most common risk factor The most common risk factor worldwide is cigarette smoking. worldwide is cigarette smoking. Smoking cessation is to be offered to Smoking cessation is to be offered to all patients still smoking.all patients still smoking.

Key Points cont’d.Key Points cont’d.

Consider a diagnosis of COPD for Consider a diagnosis of COPD for any patient with dyspnea, chronic any patient with dyspnea, chronic cough and exposure to risk cough and exposure to risk factors. Confirm with spirometry.factors. Confirm with spirometry.

Four components to the Four components to the management; assess and monitor, management; assess and monitor, reduce risk factors, manage stable reduce risk factors, manage stable COPD and manage exacerbations.COPD and manage exacerbations.

Key Points cont’d.Key Points cont’d.

Pharmacotherapy aims at prevention Pharmacotherapy aims at prevention and control of symptoms, reduce and control of symptoms, reduce frequency and severity of frequency and severity of exacerbations, improve QOL and exacerbations, improve QOL and improve exercise tolerance.improve exercise tolerance.

Patient education is an important Patient education is an important part of therapy. Thus the pharmacist part of therapy. Thus the pharmacist is integral to the management. is integral to the management.

COPD is often associated with COPD is often associated with exacerbation of symptoms.exacerbation of symptoms.

Definition: National Heart, Lung Definition: National Heart, Lung and Blood institute (NHLBI) and and Blood institute (NHLBI) and

WHOWHO

COPD is a group of chronic respiratory COPD is a group of chronic respiratory disorders that lead to progressive disorders that lead to progressive tissue degeneration and obstruction tissue degeneration and obstruction in the airways and lungs that is not in the airways and lungs that is not fully reversible.fully reversible.

They are debilitating conditions that They are debilitating conditions that affect the individual’s ability to work affect the individual’s ability to work and function independently.and function independently.

These include; These include; Chronic bronchitisChronic bronchitis, , asthmatic bronchitis and asthmatic bronchitis and emphysemaemphysema. . May coexist. COPD may coexist with May coexist. COPD may coexist with asthma.asthma.

Definition: GOLDDefinition: GOLD

COPD is a preventable and treatable disease COPD is a preventable and treatable disease with significant extra-pulmonary effects that with significant extra-pulmonary effects that may contribute to severity in individual may contribute to severity in individual patients. Its pulmonary component is patients. Its pulmonary component is characterized by airflow limitation that is characterized by airflow limitation that is non-reversible. The airflow resistance is non-reversible. The airflow resistance is normally progressive and is associated with normally progressive and is associated with an abnormal inflammatory response of the an abnormal inflammatory response of the lung to noxious particles or gas.lung to noxious particles or gas.

The GOLD definition does not use the term The GOLD definition does not use the term bronchitis or emphysema and excludes bronchitis or emphysema and excludes asthma (reversible air flow limitation) asthma (reversible air flow limitation)

Chronic BronchitisChronic Bronchitis

Recurrent excessive mucus secretion Recurrent excessive mucus secretion into the bronchial tree resulting in into the bronchial tree resulting in airway obstruction due to edema and airway obstruction due to edema and bronchial inflammation.bronchial inflammation.

Patient has a cough producing more Patient has a cough producing more than 30ml of sputum in 24hrs for at than 30ml of sputum in 24hrs for at least 3 months of the year, for 2 least 3 months of the year, for 2 consecutive years.consecutive years.

Sputum is thick and obstructs airflow. Sputum is thick and obstructs airflow.

EmphysemaEmphysema

A condition of the lung A condition of the lung characterized by abnormal, characterized by abnormal, permanent enlargement of the permanent enlargement of the airspaces distal to the terminal airspaces distal to the terminal bronchioles, accompanied by bronchioles, accompanied by destruction of their walls and destruction of their walls and without any obvious fibrosis. without any obvious fibrosis. There is a lack of uniformity in There is a lack of uniformity in airspace enlargement, resulting in airspace enlargement, resulting in loss of alveolar surface areas.loss of alveolar surface areas.

EmphysemaEmphysema

It causes destruction of the It causes destruction of the alveolar walls and capillaries by alveolar walls and capillaries by increased lung enzymatic increased lung enzymatic activity.activity.

May include; centricinar, May include; centricinar, panacinar and distal acinar.panacinar and distal acinar.

Chronic AsthmaChronic Asthma

Characterized by recurrent, Characterized by recurrent, (intermittent) reversible (intermittent) reversible bronchspasms. bronchspasms.

Reversibility may be spontaneous Reversibility may be spontaneous or after drugs therapy. or after drugs therapy.

Airway inflammation and hyper-Airway inflammation and hyper-responsiveness to a variety of responsiveness to a variety of stimuli are important stimuli are important components of asthma.components of asthma.

Risk factors: MajorRisk factors: Major

Worldwide cigarette smoking is the Worldwide cigarette smoking is the most common encountered risk.most common encountered risk.

The best documented genetic risk The best documented genetic risk factor is a severe alpha 1 trypsin factor is a severe alpha 1 trypsin deficiency.deficiency.

Occupational hazards and indoor Occupational hazards and indoor pollution (biogas burning).pollution (biogas burning).

Age.Age. Male gender.Male gender. Existing impaired lung function.Existing impaired lung function.

Risk factors: MinorRisk factors: Minor

Air pollution.Air pollution. Alcohol.Alcohol. Race.Race. Nutritional status.Nutritional status. Family history.Family history. Bronchial reactivity.Bronchial reactivity.

Pathophysiology; Chronic Pathophysiology; Chronic BronchitisBronchitis

Inhalation of noxious particles and gases Inhalation of noxious particles and gases stimulates the activation of neutrophils, stimulates the activation of neutrophils, macrophages and CD8+ lymphocytes which macrophages and CD8+ lymphocytes which release a variety of chemical mediators, release a variety of chemical mediators, including tumor necrosis factor alpha(TNFa), including tumor necrosis factor alpha(TNFa), interleukin-8 (IL8), and leukotriene B4 interleukin-8 (IL8), and leukotriene B4 (LTB4).(LTB4).

respiratory tissue inflammation results in respiratory tissue inflammation results in vasodilation, congestion, mucosal edema vasodilation, congestion, mucosal edema and globlet cells hypertrophy. These events and globlet cells hypertrophy. These events trigger globlet cell production of excessive trigger globlet cell production of excessive amount of mucus.amount of mucus.


Changes in tissues include increased Changes in tissues include increased smooth muscle cartilage atrophy, smooth muscle cartilage atrophy, infiltration of neutrophils and other infiltration of neutrophils and other cells and impairment of the cilia.cells and impairment of the cilia.

Normally sterile airways become Normally sterile airways become colonized with strep. Pneumoniae, H. colonized with strep. Pneumoniae, H. influenza, RSV, Moraxella catarrhalis influenza, RSV, Moraxella catarrhalis and mycoplasma species, Recurrent and mycoplasma species, Recurrent infections (viral and bacterial) reduce infections (viral and bacterial) reduce ciliary and phagocytic activity, ciliary and phagocytic activity, increase mucus accumulation, increase mucus accumulation, weaken the body’s defenses and weaken the body’s defenses and further destroy small bronchioles.further destroy small bronchioles.


The airway degenerate and overall The airway degenerate and overall gas exchange is impaired, causing gas exchange is impaired, causing exertional dypnea.exertional dypnea.

Hypoxemia results in increasing Hypoxemia results in increasing PaC02. If this is sustained, the brain’s PaC02. If this is sustained, the brain’s respiratory control center and central respiratory control center and central chemoreceptor are desensitized and chemoreceptor are desensitized and compensatory action to correct compensatory action to correct hypoxemia does not occur.hypoxemia does not occur.

Pathophysiology; Pathophysiology; EmphysemaEmphysema

anatomical changes of airways anatomical changes of airways because of the loss of tissue because of the loss of tissue elasticity.elasticity.

Inflammation and excessive mucus Inflammation and excessive mucus secretion cause airway trapping in the secretion cause airway trapping in the alveoli. This contributes to alveoli. This contributes to breakdown of the bronchioles, breakdown of the bronchioles, alveolar walls and connective tissue.alveolar walls and connective tissue.

Clusters of alveoli merge and the Clusters of alveoli merge and the number of alveoli diminishes, leading number of alveoli diminishes, leading to increased space available for air to increased space available for air trapping.trapping.

Pathophysiology; Pathophysiology; EmphysemaEmphysema

Destruction of airway walls Destruction of airway walls causes collapse of small airways causes collapse of small airways on exhalation and disruption of on exhalation and disruption of pulmonary capillary bed.pulmonary capillary bed.

Hypercapnea and respiratory Hypercapnea and respiratory acidosis are uncommon in acidosis are uncommon in emphysema because breathing emphysema because breathing imbalance is compensated for by imbalance is compensated for by increased in respiratory rate increased in respiratory rate

Clinical assessmentClinical assessment

Chronic bronchitis typically has an Chronic bronchitis typically has an insidious onset after age 45insidious onset after age 45

Emphysema usually seen in the 50’s Emphysema usually seen in the 50’s Chronic productive cough is the Chronic productive cough is the

hallmark of chronic bronchitis.hallmark of chronic bronchitis. Dyspnea, lung infiltration, increased Dyspnea, lung infiltration, increased

respiratory effort, altered breathing respiratory effort, altered breathing patterns, abnormal breath sounds patterns, abnormal breath sounds including wheezing and diminished including wheezing and diminished breath sounds.breath sounds.

Progressive and incomplete airflow Progressive and incomplete airflow obstruction. obstruction.

Laboratory Test.Laboratory Test.

chest X-raychest X-ray PFT ( assess pre and post PFT ( assess pre and post

bronchidilators) – decreased FEV1 and bronchidilators) – decreased FEV1 and FVCFVC

ABG – hypoxemia, hypercarbia and ABG – hypoxemia, hypercarbia and acidemiaacidemia

Hct/Hgb – erythrocytosisHct/Hgb – erythrocytosis ECG-RVHECG-RVH CulturesCultures

Classification of COPD by Classification of COPD by severity.severity.

StageStage Lung FunctionLung FunctionStage 1: Mild COPD Stage 1: Mild COPD FEV1/FVC < 70%FEV1/FVC < 70%

FEV1 FEV1 >> 80% 80% predicated predicated

Stage 2: Moderate Stage 2: Moderate

COPDCOPD FEV1/FVC < 50 - 70%FEV1/FVC < 50 - 70%

FEV1 < 80% FEV1 < 80% predicated predicated

Stage 3 Severe Stage 3 Severe COPD COPD

FEV1/FVC < 30 - 70%FEV1/FVC < 30 - 70%

FEV1 < 50% of pred.FEV1 < 50% of pred.

Stage 4: Very Severe Stage 4: Very Severe

COPDCOPD FEV1/FVC < 70%FEV1/FVC < 70%

FEV1 FEV1 < 3< 30% 0% predicated or FEV1 is predicated or FEV1 is < 50% predicated and < 50% predicated and respiratory failure respiratory failure

Differentiating Differentiating CharacteristicsCharacteristics

Chronic Chronic BronchitisBronchitis

EmphysemaEmphysema

Overweight (blue Overweight (blue

bloater)bloater) Thin (pink puffer)Thin (pink puffer)

Mild DyspneaMild Dyspnea Severe DyspneaSevere Dyspnea Copious SputumCopious Sputum Scanty SputumScanty Sputum Frequent InfectionsFrequent Infections Less frequent InfectionsLess frequent Infections HypoxemiaHypoxemia Hypoxemia uncommonHypoxemia uncommon Barrel chestBarrel chest Flattened DiaphragmFlattened Diaphragm Cor pulmonaleCor pulmonale Diffusion capacity Diffusion capacity

decreaseddecreased

Factors Determining Factors Determining Severity of Chronic COPD. Severity of Chronic COPD.

Severity of symptomsSeverity of symptoms Severity of airway limitationSeverity of airway limitation Frequency and severity of Frequency and severity of

exacerbationsexacerbations Presence of complications of COPDPresence of complications of COPD Presence of respiratory insufficiencyPresence of respiratory insufficiency ComorbidityComorbidity General health statusGeneral health status Number of medications needed to Number of medications needed to

manage the diseasemanage the disease

Components of COPD Components of COPD Management.Management.

Assess and monitor diseaseAssess and monitor disease Reduce risk factorsReduce risk factors Manage stable COPDManage stable COPD

-Education-Education

-Non-pharmacologic-Non-pharmacologic

-Pharmacologic-Pharmacologic Manage exacerbationManage exacerbation

Goals of TherapyGoals of Therapy

induce bronchodilationinduce bronchodilation facilitate expectorationfacilitate expectoration limit the impact of the disease on limit the impact of the disease on

daily activitiesdaily activities prevent complicationsprevent complications smoking cession and avoidance smoking cession and avoidance

of irritantsof irritants

Goals of TherapyGoals of Therapy

control life threatening disease control life threatening disease exacerbationsexacerbations

prevent complicationsprevent complications teach patients about disease and teach patients about disease and

the use of medications and the use of medications and improve therapeutic complianceimprove therapeutic compliance

Non-Pharmacological Non-Pharmacological Management. (NPT)Management. (NPT)

Discontinue smokingDiscontinue smoking Chest PhysiologyChest Physiology Breathing exercisesBreathing exercises RehabilitationRehabilitation Preventative measures.Preventative measures.

Discontinue SmokingDiscontinue Smoking

most effective strategy to reduce most effective strategy to reduce the risk of developing COPD and the risk of developing COPD and affect the long-term rate of affect the long-term rate of decline in FEV1. decline in FEV1.

Group therapyGroup therapy Drugs (Chantrix; varenicline), Drugs (Chantrix; varenicline),

nicotine replacement.nicotine replacement. HypnosisHypnosis

Chest PhysiologyChest Physiology

Postural drainagePostural drainage Chest percussion and vibrationChest percussion and vibration Use if > 30 cc sputum/dayUse if > 30 cc sputum/day

Breathing ExercisesBreathing Exercises

Inspire slowly and expire through Inspire slowly and expire through pursed lipspursed lips

Inspiratory muscle trainingInspiratory muscle training Breathing retrainingBreathing retraining

RehabilitationRehabilitation

Exercise reconditioning – increase Exercise reconditioning – increase endurance, exercise tolerance, endurance, exercise tolerance, maximal oxygen consumption maximal oxygen consumption

Energy conservationEnergy conservation Nutrition Nutrition Psychosocial management – Psychosocial management –

anxiety, depression and problems anxiety, depression and problems with cognitive perceptual and with cognitive perceptual and motor activity; financial and motor activity; financial and social resourcessocial resources

Preventative MeasuresPreventative Measures

Vaccines – annual influenza vaccine. Vaccines – annual influenza vaccine. Protection rate is 60-80 %Protection rate is 60-80 %

Pneumococcal vaccine – recommended Pneumococcal vaccine – recommended for patients with COPD, revaccination for patients with COPD, revaccination for patients>65 years if vaccination is for patients>65 years if vaccination is >5 years>5 years

Amantadine – efficacy is 50-90% Amantadine – efficacy is 50-90% 100mg bid for ages 100mg bid for ages <<65mg. 65mg. 100mg/day for ages > 65 years. Useful 100mg/day for ages > 65 years. Useful in non-immunized but exposed in non-immunized but exposed patients patients

Pharmacological Pharmacological Management of COPDManagement of COPD

OxygenOxygen AnticholinergicsAnticholinergics Short acting Beta Agonists (SABA)Short acting Beta Agonists (SABA) Long Acting Beta Agonist (LABA)Long Acting Beta Agonist (LABA) Combination therapy (CT)Combination therapy (CT) TheophyllineTheophylline Oral SteroidsOral Steroids Inhaled steroids (IC)Inhaled steroids (IC) AntibioticsAntibiotics

Oxygen TherapyOxygen Therapy

Administration of oxygen has Administration of oxygen has been shown to increase survival been shown to increase survival and improve QOL.and improve QOL.

Oxygen can reverse hypoxemia, Oxygen can reverse hypoxemia, increase body weight, ameliorate increase body weight, ameliorate right heart failure and improve right heart failure and improve exercise tolerance.exercise tolerance.

Oxygen TherapyOxygen Therapy

Oxygen is needed for:Oxygen is needed for: Pt with PaO2 is < 55mmHg or Sa02 < Pt with PaO2 is < 55mmHg or Sa02 <

88%88% Pt with cor pulmonale or CHF (PaO2 is Pt with cor pulmonale or CHF (PaO2 is

< 55mmHg or Sa02 < 89%)< 55mmHg or Sa02 < 89%) FEV1/FVC<70%; FEV1 <30% or FEV1/FVC<70%; FEV1 <30% or

presence of chronic respiratory failure presence of chronic respiratory failure or right heart failure.or right heart failure.

Specific situations: lung disease e.g. Specific situations: lung disease e.g. sleep apnea with nocturnal symptoms sleep apnea with nocturnal symptoms not corrected by continuous positive not corrected by continuous positive airway pressureairway pressure

Anticholinergics Anticholinergics (e.g. Ipratropium Bromide, (e.g. Ipratropium Bromide, Atropine, Glycopyrrolate, Tiotropium Atropine, Glycopyrrolate, Tiotropium

bromidebromide

Considered 1st line bronchodilators in Considered 1st line bronchodilators in the treatment of COPDthe treatment of COPD

COPD patients are very responsiveness COPD patients are very responsiveness to anticholinergics.to anticholinergics.

Studies have shown equivalent and in Studies have shown equivalent and in some cases more effective than beta some cases more effective than beta agonists in patients with chronic agonists in patients with chronic bronchitis and emphysema.bronchitis and emphysema.

Generally safe with less cardiovascular Generally safe with less cardiovascular S/Es than high doses of beta agonistsS/Es than high doses of beta agonists

MOAMOA

Ipratropium and atropine produce Ipratropium and atropine produce bronchodilation by competitively bronchodilation by competitively inhibiting cholinergic responses. They inhibiting cholinergic responses. They inhibit cyclic guanosine inhibit cyclic guanosine monophosphate leading to relaxation monophosphate leading to relaxation of bronchial smooth muscles of bronchial smooth muscles

Ipratropium also reduces sputum Ipratropium also reduces sputum volume without altering viscosityvolume without altering viscosity

Onset of action is 15mins (vs 5 mins Onset of action is 15mins (vs 5 mins for SABB ; peaks in 60-90 mins, has 6 for SABB ; peaks in 60-90 mins, has 6 hrs duration.hrs duration.

MOAMOA

Tiotropium is a long acting agent that Tiotropium is a long acting agent that protects against bronchoconstriction for protects against bronchoconstriction for >24hours.>24hours.

Onset is 30 mins; peak is 3 hours.Onset is 30 mins; peak is 3 hours. It blocks M1, M2 & M3 receptors but It blocks M1, M2 & M3 receptors but

dissociates quickly from M2 which may dissociates quickly from M2 which may be responsible for rebound be responsible for rebound bronchoconstriction through the release bronchoconstriction through the release of acethylcholine. Ipatropium in contrast of acethylcholine. Ipatropium in contrast binds to M3 over a prolonged period.binds to M3 over a prolonged period.

It is delivered in a handihaler, a single It is delivered in a handihaler, a single load dry-powdered, breath activated load dry-powdered, breath activated device device

DosingDosing

Ipratropium MDI – 2 inhalations (40 Ipratropium MDI – 2 inhalations (40 mcg) qid. May be increased to 6 mcg) qid. May be increased to 6 inhalations qid daily. Use spacer with inhalations qid daily. Use spacer with closed mouth technique.closed mouth technique.

Ipratropium Solution – 500mcg/2.5ml Ipratropium Solution – 500mcg/2.5ml or more via nebulizer qidor more via nebulizer qid

Tiotropium; the recommended dose is Tiotropium; the recommended dose is the inhalation of the contents of one the inhalation of the contents of one capsule once daily capsule once daily

using the handihaler. using the handihaler. It is well tolerated with dry mouth the It is well tolerated with dry mouth the

most common side effect.most common side effect.

Short acting Beta Agonist Short acting Beta Agonist (salbutamol, albuterol (salbutamol, albuterol

Symptomatic benefits, but not as Symptomatic benefits, but not as marked as obtained in asthmamarked as obtained in asthma

Reserved for prn useReserved for prn use Inhaled agents preferredInhaled agents preferred Can be used to assess/monitor Can be used to assess/monitor

patient’s current therapypatient’s current therapy Use to determine reversibility on Use to determine reversibility on

spirometryspirometry S/Es generally seen with high doses S/Es generally seen with high doses

(include palpitation, shakiness (include palpitation, shakiness

MOA / DOSEMOA / DOSE

cause bronchodilation of cause bronchodilation of bronchial smooth muscles. May bronchial smooth muscles. May increase mucociliary clearance increase mucociliary clearance by stimulating ciliary activityby stimulating ciliary activity

Dose: MDI 2-4 puffs q 20 mins for Dose: MDI 2-4 puffs q 20 mins for up to 4 hours, then every 4 hours up to 4 hours, then every 4 hours as needed.as needed.

Nebulization; 2.5mg Nebulization; 2.5mg diluted to a total of 3ml, 3-4 diluted to a total of 3ml, 3-4 times/day over 5-15 minutes.times/day over 5-15 minutes.

Long Acting Beta Agonist; Long Acting Beta Agonist; (salmeterol, formeterol)(salmeterol, formeterol)

approved for use in COPD since approved for use in COPD since 19971997

have positive effect on QOL (one have positive effect on QOL (one inhalation bid dosing)inhalation bid dosing)

used as an add-on therapy where used as an add-on therapy where combination bronchodilator combination bronchodilator therapy is not adequate, patients therapy is not adequate, patients with night time symptoms or with night time symptoms or patients with difficulty complying.patients with difficulty complying.

Slow onset of action and expensiveSlow onset of action and expensive

Combination Therapy Combination Therapy ((Ipatropium/Albuterol)Ipatropium/Albuterol)

The combination ofan inhaled The combination ofan inhaled anticholinergic &beta 2 agonist often is anticholinergic &beta 2 agonist often is used as the disease progresses and used as the disease progresses and symptoms worsen over time.symptoms worsen over time.

Combination of bronchodilators with Combination of bronchodilators with different MOA allows lowest effective different MOA allows lowest effective doses to be used and reduces side doses to be used and reduces side effects. effects.

Superior to either albuterol or Superior to either albuterol or Ipratropium alone.Ipratropium alone.

more convenient but harder to adjust more convenient but harder to adjust therapy.therapy.

TheophyllineTheophylline

2nd or 3rd line therapy2nd or 3rd line therapy potential action include: potential action include: bronchodilationbronchodilation increase mucocillary clearanceincrease mucocillary clearance increase respiratory drive (effective increase respiratory drive (effective

short term)short term) improved cardiovascular function – improved cardiovascular function –

increase RVEF and LVEFincrease RVEF and LVEF increase diaphragmatic contractilityincrease diaphragmatic contractility improve exercise capacityimprove exercise capacity

DosingDosing

Acceptable plasma concentration is 8 Acceptable plasma concentration is 8 - 12 mcg/ml and maximized if - 12 mcg/ml and maximized if necessary up to 20mcg/mlnecessary up to 20mcg/ml

Determine plasma concentration prior Determine plasma concentration prior to dosingto dosing

LD 3mg/kg aminophylline if prior LD 3mg/kg aminophylline if prior theophylline within last 24 hrs and 6 theophylline within last 24 hrs and 6 mg/kg if none, given over 30minsmg/kg if none, given over 30mins

Maintenance infusion of 0.4 mg/kg/hrMaintenance infusion of 0.4 mg/kg/hr Precautions: multiple S/Es, altered Precautions: multiple S/Es, altered

metabolism (smokers, CHF, elderly, metabolism (smokers, CHF, elderly, liver disease), a lot of drug liver disease), a lot of drug interactions.interactions.

Oral SteroidsOral Steroids

Only about 10% of patients benefit from Only about 10% of patients benefit from oral steroids and there is high risk of oral steroids and there is high risk of dependence and side effectsdependence and side effects

Can be used long –term if an objective Can be used long –term if an objective benefit is seen after adequate trial – benefit is seen after adequate trial – Prednisone 30mg qd x 2 weeks or morePrednisone 30mg qd x 2 weeks or more

Some studies show that 50% of patients Some studies show that 50% of patients responding to oral steroids will respond responding to oral steroids will respond to inhaled steroids.to inhaled steroids.

IV Methylprednisolone 50-100 mg q6-8h IV Methylprednisolone 50-100 mg q6-8h can be used in acute exacerbations. can be used in acute exacerbations. Taper as rapidly as possibleTaper as rapidly as possible

Inhaled steroidsInhaled steroids

appropriate for symptomatic appropriate for symptomatic COPD patients with FEV1 < 50% COPD patients with FEV1 < 50% predicted (stage 3 and stage 4) predicted (stage 3 and stage 4) and repeated exacerbationsand repeated exacerbations

treatment has been shown to treatment has been shown to reduce frequency of reduce frequency of exacerbations and improve exacerbations and improve health status.health status.

AntibioticsAntibiotics

indicated if purulent sputum, indicated if purulent sputum, infiltrates on chest x-ray or infiltrates on chest x-ray or positive gram stain (usually positive gram stain (usually pneumococcus or H. influenza)pneumococcus or H. influenza)

should be initiated within 24 should be initiated within 24 hours of symptomshours of symptoms

goal of therapy is to shorten the goal of therapy is to shorten the duration of exacerbations and duration of exacerbations and prevent deteriorationprevent deterioration

AntibioticsAntibiotics

Empirically treat for H. influenza Empirically treat for H. influenza (59%), S pneumoniae (17%) and (59%), S pneumoniae (17%) and M Catarrhalis (12%)M Catarrhalis (12%)

Alternatives: Amoxicillin, Alternatives: Amoxicillin, Cephalosporins or TMX/SMX or Cephalosporins or TMX/SMX or AmpicillinAmpicillin

Macrolides are also good but Macrolides are also good but more expensivemore expensive

Treat for 7-10 daysTreat for 7-10 days

Summary of Therapy by Summary of Therapy by Stage.Stage.

Measure of Drug EffectsMeasure of Drug Effects

Physiologic outcomesPhysiologic outcomes FT – airflow, gas exchange (ABG), FT – airflow, gas exchange (ABG),

diffusiondiffusion Respiratory work – minute ventilation, Respiratory work – minute ventilation,

spirometry.spirometry. Symptomatic Outcomes – patient or Symptomatic Outcomes – patient or

physician assessmentphysician assessment DyspneaDyspnea Functional OutcomesFunctional Outcomes exercise toleranceexercise tolerance work capacity – oxygen consumptionwork capacity – oxygen consumption 12 minutes walking test12 minutes walking test

Measure of Drug EffectsMeasure of Drug Effects

HospitalizationHospitalization Other ConsiderationsOther Considerations

stability of disease and stability of disease and response to therapy.response to therapy.

airflow changes are not airflow changes are not always closely correlated with always closely correlated with exercise capacity.exercise capacity.

Monitoring for EfficacyMonitoring for Efficacy

Parameter Parameter Range Range FrequencyFrequency

FEV1FEV1 Stable/ slowed Baseline and q2mths

declinedecline

Sputum Sputum Decreased/Decreased/ ContinuousContinuous

Production NoneProduction None

Dyspnea Decreased ContinuousDyspnea Decreased Continuous

Exacerbations Decreased ContinuousExacerbations Decreased Continuous

Monitoring for ToxicityMonitoring for Toxicity

ParameterParameter RangeRange FrequencyFrequency

FEV1FEV1 increasing increasing Baseline and Baseline and after 2after 2 months months

FEV1/FVC decreasing Baseline & after 2 months FEV1/FVC decreasing Baseline & after 2 months

Role of the Pharmacist in Role of the Pharmacist in the management of COPD.the management of COPD.

Pharmacist have a tremendous Pharmacist have a tremendous opportunity to identify patients at risk opportunity to identify patients at risk for COPD and to recommend for for COPD and to recommend for referral and assessment. referral and assessment.

Active promotion of activities aimed at Active promotion of activities aimed at smoking cessation is by far the most smoking cessation is by far the most significant step a pharmacist can take.significant step a pharmacist can take.

Patient education aimed at slowing the Patient education aimed at slowing the progress of the disease and improving progress of the disease and improving compliance.compliance.

Role of the Pharmacist in Role of the Pharmacist in the management of COPD.the management of COPD.

Too promote pharmacist/ patient Too promote pharmacist/ patient interaction to empower the interaction to empower the patient and improve patient self-patient and improve patient self-management.management.

Assess and make Assess and make recommendation for drug recommendation for drug therapy based on most current therapy based on most current guidelines and literature.guidelines and literature.

Complications of COPDComplications of COPD

Pulmonary HypertensionPulmonary Hypertension Acute Respiratory FailureAcute Respiratory Failure InfectionsInfections Polycethemia.Polycethemia.

Take Home Points/ Take Home Points/ Summary.Summary.

COPD is a preventable disease that can COPD is a preventable disease that can be managed to reduce exacerbations be managed to reduce exacerbations and improve QOL for patients.and improve QOL for patients.

It is a progressive generally irreversible It is a progressive generally irreversible inflammatory lung disease.inflammatory lung disease.

It includes chronic bronchitis, It includes chronic bronchitis, emphysemia and less significantly, emphysemia and less significantly, chronic asthma. chronic asthma.

Smoking is the major risk factor Smoking is the major risk factor worldwide.worldwide.


COPD is staged according to lung COPD is staged according to lung function. A definitive diagnosed is function. A definitive diagnosed is made by spirometry. Hallmark is made by spirometry. Hallmark is FEV1/FVC ratio<70%.FEV1/FVC ratio<70%.

A major goal of therapy is symptom A major goal of therapy is symptom improvement and a reduction in the improvement and a reduction in the rate of FEV1 decline.rate of FEV1 decline.

Mild COPD maybe treated with NPT + Mild COPD maybe treated with NPT + SABA.SABA.

Moderate COPD add LABA and/or CT.Moderate COPD add LABA and/or CT.


Severe COPD add IC if repeated Severe COPD add IC if repeated exacerbations.exacerbations.

Oral steroids show little benefit and Oral steroids show little benefit and increases toxicity. Chronic use should increases toxicity. Chronic use should be avoided.be avoided.

Long term Oxygen therapy is given in Long term Oxygen therapy is given in cases of acute respiratory failure.cases of acute respiratory failure.

The Pharmacist has an important role The Pharmacist has an important role in the management of COPD; to in the management of COPD; to educate, to prevent exacerbations, educate, to prevent exacerbations, hospitalization, development of hospitalization, development of respiratory failure and death. respiratory failure and death.

ReferencesReferences

1.1. Talbert, Robert L.Talbert, Robert L. Ischemic Heart Disease Ischemic Heart Disease In: Di Piro JT, Talbert RL, Yee In: Di Piro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pharmacotherapy: A Pathophysiologic Approach. Pathophysiologic Approach. 6th ed. NY: McGraw Hill; 2005: 271-277.6th ed. NY: McGraw Hill; 2005: 271-277.

2.2. Budeus M, Hennersdorf M, Perings S, et al. Amiodarone prophylaxis for Budeus M, Hennersdorf M, Perings S, et al. Amiodarone prophylaxis for atrial fibrillation of high-risk patients after coronary bypass grafting: a atrial fibrillation of high-risk patients after coronary bypass grafting: a prospective, double-blinded, placebo-controlled, randomized study. prospective, double-blinded, placebo-controlled, randomized study. Eur Eur Heart JHeart J. 2006 Jul;27(13):1584-91.. 2006 Jul;27(13):1584-91.

3.3. Kerstein J, Soodan A, Qamar M, et al. Giving IV and oral amiodarone Kerstein J, Soodan A, Qamar M, et al. Giving IV and oral amiodarone perioperatively for the prevention of postoperative atrial fibrillation in perioperatively for the prevention of postoperative atrial fibrillation in patients undergoing coronary artery bypass surgery: the GAP study. patients undergoing coronary artery bypass surgery: the GAP study. ChestChest. 2004 Sep;126(3):662-4.. 2004 Sep;126(3):662-4.

4.4. Leavitt BJ, Ross CS, Spence B, et al. Long-term survival of patients with Leavitt BJ, Ross CS, Spence B, et al. Long-term survival of patients with chronic obstructive pulmonary disease undergoing coronary artery chronic obstructive pulmonary disease undergoing coronary artery bypass surgery. bypass surgery. CirculationCirculation. 2006 Jul 4;114(1 Suppl):I430-4. . 2006 Jul 4;114(1 Suppl):I430-4.

5.5. ACC/AHA/ESC Practice Guidelines Circulation. 2006;114:700-752ACC/AHA/ESC Practice Guidelines Circulation. 2006;114:700-752

6.6. Respiratory Care Web ED Accessed at: Respiratory Care Web ED Accessed at: classes.kumc.edu/cahe/respcared/cybercas/cabg2/stevobj.html classes.kumc.edu/cahe/respcared/cybercas/cabg2/stevobj.html

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