Chapter 4: Management of Patients with Chronic Pulmonary Disease

Pathophysiology of Chronic Obstructive Pulmonary Disease

Symptomatic during the middle adult years

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Airflow limitation is progressive

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associated with the lungs' abnormal inflammatory response to noxious particles or gases

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Chronic inflammation/body's attempt to repair

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Injury-repair process (repeat)

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Scar tissue formation

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Narrowing occurs

Trachea and bronchi

increased number of goblet cells, enlarged submucosal glands resulting to hypersecretion of mucus (during COPD)

Bronchioles

inflammation--thickening-narrowing (during COPD)

Alveoli

decrease in elastic recoil (during COPD)

Chronic Bronchitis

- presence of cough and sputum production for at least 3 months in each of two consecutive years

- most likely to occur during the winter (exacerbation)

Alveoli

- (in Chronic Bronchitis) damaged and fibrosed, resulting in altered function of the alveolar macrophages (destroys foreign particles- bacteria)

- as a result, patient becomes more susceptible to respiratory infection

Pathophysiology of Chronic Bronchitis

- Inflammation

- Increased number of mucous glands

- Excess mucus causing chronic cough

Causes of Chronic Bronchitis

- smoking

- chemical exposure

- air pollution

Mechanism of Chronic Bronchitis

damages the airways typically produces cough due to its effects on the mucus producing cells in the linings of the airways

Blue bloaters

- blue (cyanotic) and obese

- classic appearance of px with chronic bronchitis

Emphysema

- -mpaired oxygen and carbon dioxide exchange results from destruction of the walls of overdistended alveoli

- abnormal distention of the airspaces beyond the terminal bronchioles and destruction of the walls of the alveoli

Pathophysiology of Emphysema

Alveolar walls destroyed (infection)

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increase in dead space

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impaired oxygen diffusion

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hypoxemia

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CO2 elimination impaired

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hypercapnia (increased carbon dioxide tension in arterial blood)

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Respiratory Acidosis

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alveolar walls continue to break down

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Pulmonary capillary bed is reduced in size

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Resistance to pulmonary blood flow

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Right ventricle--higher blood pressure in pulmonary artery

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Right sided heart failure--long term high BP in pulmo artery

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back up of blood in the venous system

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Edema, distended neck veins, pain in the liver

Panlobular and Centrilobular

2 main types of emphysema

Pathophysiology of Panlobular Emphysema

Hyperinflated (hyperexpanded) chest, dyspnea on exertion, weight loss

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Instead of being an involuntary passive act, expiration becomes active and requires muscular effort

Panlobular Emphysema

hyperinflation in alveoli

Centrilobular Emphysema

hyperinflation is in spaces before the alveoli

air trapping

hallmark sign of airway diseases which causes uild up of CO2

active expiration

a compensatory mechanism to expel extra CO2 and air trapped in the alveoli

Causes of Emphysema

- smoking (active or passive)

- chemical exposure

- air pollution

- genetics

alpha 1 antitrypsin deficiency

- genetic cause of emphysema and COPD

- an enzyme inhibitor that normally counteracts the destruction of lung tissue by certain other enzymes

Diagnosis of Emphysema

- Pathological: permanent enlargement and damage to air spaces

- hyperinflated lungs with flattened diaphragm (x-ray)

Mechanism of Emphysema

- damages the alveoli

- air sacs loses their elasticity, swell and some even burst

Pink Puffers

- no cyanosis, pursed lip breathing

- barrel chest

- classic appearance of px with emphysema

Causes of Chronic Obstructive Pulmonary Disease

- Exposure to tobacco smoke (80-90% of cases)

- secondhand smoke

- increased age

- occupational exposure

- indoor and outdoor air pollution

- genetic abnormalities

3 primary symptoms of COPD

1. Chronic cough (may be intermittent and unproductive)

2. Sputum production

3. dyspnea (may occur as disease progresses)

often worsen over time

Tripod position

- Typical posture of a person with chronic obstructive pulmonary disease—primarily emphysema.

- tends to lean forward and uses the accessory muscles of respiration to breathe, forcing the shoulder girdle upward and causing the supraclavicular fossae to retract on inspiration.

Diagnostics Tests for COPD

- Spirometry

- ABG

- CXR

Grade I COPD

Severity: Mild

Pulmonary Function:

- FEV1/FVC

Grade II COPD

Severity: Moderate

Pulmonary Function:

- FEV1/FVC

Grade III COPD

Severity: Severe

Pulmonary Function:

- FEV1/FVC

Grade IV COPD

Severity: Moderate

Pulmonary Function:

- FEV1/FVC

Management for COPD

- reduce risk and symptoms

- smoking cessation

- Nicotine replacements: (gum, inhaler, nasal spray, transdermal patch, sublingual tablet, or lozenge)

- Varenicline

Varenicline

a nicotinic acetylcholine receptor partial agonist, may assist in smoking cessation

O2 therapy for COPD

- 1-2 LPM via nasal cannula

- 24% via venturi mask at 2-3 LPM

- should be aiming for an SaO2 of 88-92%

SaO2

oxygen saturation of arterial blood

SpO2

oxygen saturation detected by pulse oximeter

high levels of O2 in COPD

DO NOT administer O2 in high levels

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Retention of CO2

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High levels of O2

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Suppresses CO2 chemoreceptors

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V/Q imbalance

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Hypercapnic state

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Respiratory drive depression

Pharmacologic Therapy for COPD

- Bronchodilators

- Beta 2-Adrenergic Agonists

- Muscarinic antagonists (anticholinergics)

- Inhaled corticosteroids (ICS)

Bronchodilators

relieve bronchospasm by improving expiratory flow through widening of the airways and promoting lung emptying with each breath

Beta 2-Adrenergic Agonists

- (SABAs) short-acting beta-2-adrenergic agonists

- (LABAs) long-acting beta-2 adrenergic agonists

(SABAs) short-acting beta-2-adrenergic agonists

- Albuterol

- Levalbuterol

- Terbutaline

(LABAs) long-acting beta-2 adrenergic agonists

- Salmeterol

- Formoterol

- Arformoterol

Muscarinic antagonists (anticholinergics)

- (SAMAs) short acting muscarinic antagonist

- (LAMAs) long acting muscarinic antagonist

(SAMAs) short acting muscarinic antagonist

Ipratropium bromide

(LAMAs) long acting muscarinic antagonist

Tiotropium bromide

Inhaled corticosteroids (ICS)

- improves the symptoms of COPD but they do not slow the decline in lung function

- NO to long term use: can cause muscle weakness, decrease ability to function, and respiratory failure

- Budesonide

- Fluticasone

Combination Therapy

- ICS + LABA, LABA +LAMA

- to avoid the use of multiple devices

Exacerbation of COPD

an event in the natural course of the disease characterized by acute changes (worsening) in the patient's respiratory symptoms beyond the normal day-to- day variations

Surgical Management for COPD

- Bullectomy

- Lobectomy

Bullectomy

surgical option for select patients with bullous emphysema.

Lung Volume Reduction Surgery/Lobectomy

- involves the removal of a portion of the diseased lung parenchyma

- This type of surgery does not cure the disease but may improve health status, exercise tolerance, and the patient's overall quality of life

Pulmonary Rehabilitation

- primary goals: to reduce symptoms, improve quality of life, and increase physical and emotional participation in everyday activities

- includes assessment, education smoking cessation, physical reconditioning, nutritional counseling, skills training, and psychological support

Pulmonary Rehabilitation

- Patients are taught methods to alleviate symptoms

- Breathing exercises, as well as retraining and exercise programs, are used to improve functional status

Diaphragmatic Breathing

Goal: to use and strengthen the diaphragm during breathing

Pursed-Lip Breathing

Goal: to prolong exhalation and increase airway pressure during expiration, thus reducing the amount of trapped air and the amount of airway resistance