Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease (COPD)

is a group of diseases characterized by the pathological limitation of airflow in the airway that is not fully reversible. COPD is the umbrella term for chronic bronchitis, emphysema and a range of other lung disorders.

Causes
COPD primarily refers to obstruction in the lungs from two chronic lung conditions. Many people with COPD have both: Emphysema. This lung disease causes inflammation within the fragile walls of the alveoli. This can destroy some of the walls and some of the elastic fibers, which allows small airways to collapse when you breathe out. This impairs airflow out of your lungs. Chronic bronchitis. This condition, which is characterized by an ongoing cough, causes inflammation and narrowing of the major and smaller bronchial tubes. Chronic bronchitis also causes increased mucus production, which can block the narrowed tubes. Asthmatic bronchitis also is sometimes classified as COPD, because it obstructs airways and makes it difficult to inhale. Asthmatic bronchitis also known as bronchial asthma is a term used to describe chronic bronchitis accompanied by contractions of the muscle fibers in the lining of the airways (bronchospasm). Cigarette smoke and other irritants (cigar smoke, secondhand smoke, pipe smoke, air pollution and certain occupational fumes)

Pathophysiology

Chronic Bronchitis
Cigarette Smoking RTI Environmental Pollutants Inflammation Bradykinin, Histamine & Prostaglandin Synthesis Capillary Permeability Fluid/Cellular Exudation

Edema of mucuc membrane

Hypersecretion of mucus Persistent Cough

Pathophysiology

Emphysema
Cigarette Smoking Heredity Aging Process Disequilibrium between ELASTASE & ANTIELASTASE Destruction of ELASTIC RECOIL Overdistention of ALVEOLI Retention of CO2

Hypoxia

Respiratory Acidosis

Pathophysiology

Asthma
Allergy (Extrinsic) Inflammation (Intrrinsic) Histamine, Bradykinin, Prostaglandin synthesis Serotonin, Leukotrienes, ECF-A, SRS-A Bronchospasm

Bronchoconstriction
Edema of mucus membranes Hypersecretion of mucus

Narrowing of Airways Work of breathing

Pathophysiology: Asthma
Tends to sit up Restlessness Tachypnea/dyspnea Tachycardia Flaring of alae nasi Diaphoresis Cold clammy skin Wheezing Retractions Pallor- cyanosis Exhaustion

Slow, shallow respiration (hypoventilation)

Retention of CO2 (airtrapping) Hypoxia Respiratory Acidosis

Assessment

Cough Dyspnea Chest Pain Sputum Production Adventitious breath sounds Pursed-lip breathing Tends to assume upright, leaning forward position Alteration in LOC Alteration in skin color (pallor to cyanosis)

Alteration in skin temperature (cold to touch) Alteration in thoracic anatomy (barrel chest) Clubbing of fingers Polycythemia Voice changes Decreased metabolism Weakness Fatigue Anorexia Weight loss

Management

Rest Increase fluid intake Diet: calorie, CHON, CHO O2 Therapy: 1 to 3 lpm Avoid smoking, alcohol, envrionmental pollutants Chest physiotherapy Bronchial hygiene measures (Steam inhalation, Aerosol inhalation, Medimist inhalation)

Management

Pharmacotherapy:
Expectorants (Guaiafenessin)/mucolytic (Mucomyst/Mucosolvan) Antitussives: (Dextrometorphan/Codeine) Bronchodilators: (Aminophylline/Ventolin/Bricanyl/Alupent) Antihistamine: (Benadryl) Steroids Antimicrobials

Respiratory Failure
Submitted by: Shirley M. Aromin RN

is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. is a medical term for inadequate gas exchange by the respiratory system. Respiratory failure can be indicated by observing a drop in blood oxygen level (hypoxemia) and/or a rise in arterial carbon dioxide (hypercapnia) which can be written as (PaO2 < 60 mmHg, PaCO2 > 45 mmHg).

Respiratory Failure

Respiratory failure is divided into type I and type II. Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels. Type II respiratory failure involves low oxygen, with high carbon dioxide. Type I respiratory failure occurs because of damage to lung tissue. This lung damage prevents adequate oxygenation of the blood (hypoxaemia); however, the remaining normal lung is still sufficient to excrete the carbon dioxide being produced by tissue metabolism. This is possible because less functioning lung tissue is required for carbon dioxide excretion than is needed for oxygenation of the blood. Type II respiratory failure is also known as 'ventilatory failure'. It occurs when alveolar ventilation is insufficient to excrete the carbon dioxide being produced. Inadequate ventilation is due to reduced ventilatory effort, or inability to overcome increased resistance to ventilation - it affects the lung as a whole, and thus carbon dioxide accumulates.

Causes
Underlying Problem
Airway obstruction

Causes
Chronic bronchitis, emphysema, bronchiectasis, cystic fibrosis, asthma, bronchiolitis, inhaled particles Obesity, sleep apnea, drug intoxication

Poor breathing

Muscle weakness

Myasthenia gravis, muscular dystrophy, polio, Guillain-Barr syndrome, polymyositis, stroke, amyotrophic lateral sclerosis, spinal cord injury Scoliosis, chest wound, extreme obesity, thoracoplasty Acute respiratory distress syndrome, drug reaction, pulmonary fibrosis, fibrosing alveolitis, widespread tumors, radiation, sarcoidosis, burns

Abnormality of chest wall

Abnormality of lung tissue

Type

I:

Pathophysiology
Pneumonia; TB; Fungal infections; Neardrowning; chemical or smoke inhalation; liquid aspiration Increased pulmonary capillary permeability

Left ventricular heart failure/Pulmonary edema or fluid overload Increased pulmonary capillary pressure

Pumonary congestion & distended pulmonary vessels Peripheral airway resistance decreased lung compliance Fluid collects in the interstitial spaces compressing peripheral airways Alveoli becomes filled with fluid (pulmonary edema); decreased total lung capacity intrapulmonary shunting & HYPOXIA

Pathophysiology: Type I Supresses formation & effectiveness of surfactantsmicroatelectasis- reduced functional residual capacity; Reduced lung compliance

SEVERE HYPOXEMIA

Pathophysiology
Type

II:

Chronic bronchitis; Emphysema; Massive obesity; Severe kyphosis; Asthma low oxygen, with high carbon dioxide. Inability to generate enough alveolar ventilation

Increased PaCO2 & decreased PaO2

Difficulty performing forced expiratory tests retention of Carbon dioxide

Assessment

Tidal volume and vital capacity - these measurements can be taken by simple 'spirometry'. Blood Gas Analysis Pulse Oximetry A complete blood count may indicate anemia, which can contribute to tissue hypoxia, whereas polycythemia may indicate chronic hypoxemic respiratory failure. A chemistry panel may be helpful in the evaluation and management of a patient in respiratory failure. Abnormalities in renal and hepatic function may either provide clues to the etiology of respiratory failure or alert the clinician to complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function.

Measuring serum creatine kinase with fractionation and troponin I helps exclude recent myocardial infarction in a patient with respiratory failure. An elevated creatine kinase with a normal troponin I may indicate myositis, which occasionally can cause respiratory failure. In chronic hypercapnic respiratory failure, serum thyroid-stimulating hormone should be measured to evaluate the possibility of hypothyroidism, a potentially reversible cause of respiratory failure. Imaging Studies: Chest Radiograph and Echocardiography

Management

Endotracheal intubation Management of Fluids and Electrolytes Pharmacotherapy:

Antibiotics help when infections (sepsis) as well as pneumonia are involved in respiratory failure. Bronchodilators, for example, theophylline compounds, sympathomimetic agents (albuterol, metaproterenol, isoproterenol), anticholinergics (ipratropium bromide), and corticosteroids, reverse bronchoconstriction and reduce tissue inflammation. Other drugs, such as digitalis, improve cardiac output, and drugs which increase blood pressure in shock can improve blood flow to the tissues.

Management

Bronchoscopy Intravenous Nutritional Support Chest Physiotherapy X-ray Monitoring Lung Transplantation

Cor Pulmonale
Submitted by: Shirley M. Aromin RN

Cor Pulmonale

In cor pulmonale, hypertrophy and dilatation of the right ventricle develop secondary to a disease affecting the structure or function of the lungs or its vasculature. This condition occurs at the end stage of various chronic disorders of the lungs, pulmonary vessels, chest wall, and respiratory control center. It doesnt occur with disorders stemming from congenital heart disease or those affecting the left side of the heart.

Facts about cor pulmonale

Cor pulmonale causes about 25% of all types of heart failure. About 85% of the patients with cor pulmonale also have COPD and about 25% of patients with bronchial COPD eventually develop cor pulmonale. Its most common in smokers and in middleaged and elderly men; however, the incidence in women is rising.

Risk Factors
Cor pulmonale may result from: Disorders that affect the pulmonary parenchyma Pulmonary diseases that affect the airways (COPD and bronchial asthma) Vascular diseases (vasculitis, pulmonary emboli, or external vascular obstruction resulting from a tumor or aneurysm) Chest wall abnormalities, including such thoracic deformities as kyphoscoliosis and pectus excavatum (funnel chest) Neuromuscular disorders such (muscular dystrophy and poliomyelitis) External factors (Obesity & living at a high altitude)

Three types of disorders are responsible for cor pulmonale: Pulmonary restrictive disorders (fibrosis or obesity) Pulmonary obstructive disorders (bronchitis) Primary vascular disorders (recurrent pulmonary emboli) * Hypoxic constriction of pulmonary blood vessels and obstruction of pulmonary blood flow lead to increased pulmonary resistance, which progresses to cor pulmonale.

Pathophysiology
Pulmonary disorder

Anatomic alterations in the pulmonary blood vessels & functional alterations in the lungs
Increased pulmonary vascular resistance Pulmonary hypertension Right ventricular hypertrophy Heart failure Cor pulmonale

Signs & Symptoms

In early stages: Chronic productive cough Exertional dyspnea Wheezing respirations Fatigue & weakness As cor pulmonale progresses: Dyspnea at rest Tachypnea Othopnea Dependent edema Enlarged, tender liver Hepatojugular reflux Right upper quadrant disconmpfort Tachycardia Decreased cardiac output CXR: reveals characteristic of underlying lung disease

Diagnostic Tests

Pulmonary artery catheterization (inc. R ventricular & pulmonary artery pressures) Echocardiography or Angiography (R ventricular enlargement) CXR (large central pulmonary arteries & R ventricular enlargement) ABG analysis (decreased PaO2) Pulse oximetry (reduced SaO2 level)

ECG [(+) arrythmias & atrial fibrillation during svere hypoxia, prominent P waves & inverted T wave in right precordial leads] Pulmonary function test (shows underlying lung disease) MRI (measures right ventricular mass, wall thickness & ejection fraction) Cardiac catheterization (measures pulmonary vascular pressures) Hematocrit (typically over 50%) Serum hepatic enzyme levels (elevated level of aspartate aminotranferase with hepatic congestion & decreased liver function) Serum bilirubin levels (elevated if liver dysfunction & hepatomegaly are present)

Treatment
Therapy for the patient with cor pulmonale has 3 aims: 1. Reducing hypoxemia & pulmonary vasoconstriction 2. Increasing exercise tolerance 3. Correcting the underlying condition when possible

Treatment
Bed rest Antibiotics for an underlying RTI Potent pulmonary artery vasodilator to treat primary pulmonary HTN (Diazoxide, Nitroprusside or Hydralazine) Continuous administration of low concentrations of oxygen to decrease pulmonary HTN, polycythemia & tachypnea Mechanical ventilation in acute disease Low sodium diet with restricted fluid Phlebotomy to decrease RBC mass & anticoagulation with small doses of heparin to decrease risk of thromboembolism *Tx may vary, depending on the underlying cause. For example, the pt may need a tracheotomy if he has an uper airwy obstruction. He may require corticosteroids if he has vasculitis or an autoimmune disorder.