Lecture 5: Disorders of the Respiratory System PDF

Lecture-5: Disorders of the Respiratory System PATH200/310 1  Outlines ❑ Components of the respiratory system ❑ Respiration Process, Compliance And Lung Volume ❑ The disease process of selected respiratory diso...

Lecture-5: Disorders of the Respiratory System PATH200/310 1  Outlines ❑ Components of the respiratory system ❑ Respiration Process, Compliance And Lung Volume ❑ The disease process of selected respiratory disorders (causes, manifestations, and pathophysiology of selected respiratory disorders: ✓ Asthma ✓ Chronic obstructive pulmonary disease (COPD) ✓ Pleural effusion ✓ Bronchiectasis ✓ Atelectasis ✓ Pneumonia ✓ Tuberculosis ✓ Respiratory failure 2  Learning objectives: By the end of this lecture, each student will be able to : ❑ Identify the common function of the respiratory system. ❑ State the difference between the conducting and the respiratory airways. ❑ Describe the causes, manifestations, and treatment of selected respiratory disorders: ✓ Asthma ✓ Chronic obstructive pulmonary disease (COPD) ✓ Pleural effusion ✓ Bronchiectasis ✓ Atelectasis ✓ Pneumonia ✓ Tuberculosis ✓ Respiratory failure ❑ Explain the disease process of selected respiratory disorders 3  INTRODUCTION The respiratory system’s major function is gas exchange, in which air enters the body on inhalation; travels throughout the respiratory passages exchanging oxygen for carbon dioxide at the tissue level; and expels carbon dioxide on exhalation. The upper airway The lower airway The alveoli are the chief units of gas exchange. PATH200/SPRING 21-22/NSG DEPT/MACHS 4  Components of The Respiratory System ❑ Ventilation The movement of air between the atmosphere and the respiratory portion of the lungs ❑ Perfusion The flow of blood through the lungs ❑ Diffusion The transfer of gases between the air-filled spaces(alveoli ) in the lungs and the blood in the pulmonary capillaries PATH200/SPRING 21-22/NSG DEPT/MACHS 5  Composition of The Alveolar Structures ❑ Type I Alveolar Cells Flat squamous epithelial cells across which gas exchange takes place ❑ Type II Alveolar Cells Produce surfactant, a lipoprotein substance that decreases the surface tension in the alveoli and allows for greater ease of lung inflation ❑ The pleural cavity The pleural cavity is a potential space between the parietal and visceral pleura. It contains a small volume of serous fluid, which acts as a lubricant PATH200/SPRING 21-22/NSG DEPT/MACHS 6  RESPIRATION ▪ The process of gas exchange between atmospheric air and the blood at the alveoli, and between the blood cells and the cells of the body. ▪ Oxygen diffuses from the air into the blood at the alveoli to be transported to the cells of the body. ▪ Carbon dioxide diffuses from the blood into the air at the alveoli to be removed form the body. ◼ Ventilation: The movement of air in and out of the airways. The thoracic cavity is an airtight chamber. The floor of this chamber is the diaphragm. ◼ Inspiration: contraction of the diaphragm (movement of this chamber floor downward) and contraction of the external intercostal muscles increases the space in this chamber. Lowered intrathoracic pressure causes air to enter through the airways and inflate the lungs. PATH200/SPRING 21-22/NSG DEPT/MACHS 7  RESPIRATION Image result for human ventilation ◼ Expiration: with relaxation, the diaphragm moves up and intrathoracic pressure increases. This increased pressure pushes air out of the lungs. Expiration requires the elastic recoil of the lungs. ◼ Inspiration normally is 1/3rd of the respiratory cycle and expiration is 2/3rds. 8  COMPLIANCE Image result for RESPIRATORY Compliance ◼ Measure of the ease with which lungs and thorax expand.(The distensibility of the lungs) ◼ The greater the compliance, the easier it is for a change in pressure to cause expansion ◼ A lower-than-normal compliance means the lungs and thorax are harder to expand PATH200/SPRING 21-22/NSG DEPT/MACHS 9  LUNG VOLUMES ❑ Tidal volume (TV)- 500ml The volume of air inhaled and exhaled with each breath ❑ Inspiratory reserve volume (IRV) - 3000ml The maximum volume of air that can be inhaled after a normal inhalation ❑ Expiratory reserve volume (ERV)- 1100ml The maximum volume of air that can be exhaled forcibly after a normal exhalation ❑ Residual volume (RV)- 1200ml The volume of air remaining n the lungs after a maximum exhalation 10  VENTILATION PERFUSION (V/Q RATIO) Ventilation is the movement of air in and out of the lungs. Air must reach the alveoli to be available for gas exchange. Perfusion is the filling of the pulmonary capillaries with blood. Adequate gas exchange depends upon an adequate V/Q ratio, a match of ventilation and perfusion. Ventilation and perfusion imbalance causes shunting of blood, resulting in hypoxia (low cellular oxygen level). 11 VENTILATION PERFUSION (V/Q RATIO) 12  VENTILATION PERFUSION (V/Q RATIO) Normal ratio 1:1 ventilation matches perfusion 1. Low ventilation-perfusion ratio( Shunts) When perfusion exceeds ventilation Blood bypasses the alveoli without gas exchange occurring. This is seen with obstruction of the distal airway ✓ Pneumonia ✓ Atelectasis ✓ Tumor ✓ Mucus plug. 13  VENTILATION PERFUSION (V/Q RATIO) 2. High Ventilation–Perfusion Ratio (Dead Space) When ventilation exceeds perfusion, the alveoli do not have an adequate blood supply for gas exchange. This is seen in the following disorders: ✓ Pulmonary emboli ✓ pulmonary infarction ✓ cardiogenic shock. 3. The absence of ventilation and perfusion (Silent Unit) This is seen in the following disorders ✓ Pneumothorax ✓ Severe acute respiratory distress syndrome 14  ASTHMA Asthma is a chronic inflammatory airway disorder characterized by airflow obstruction and airway hyperresponsiveness to multiple stimuli. This is caused by bronchospasm, edema of the airway mucosa, and increased mucus production with plugging and airway remodeling. Asthma may result from sensitivity to extrinsic or intrinsic allergens. Extrinsic(atopic): it results from specific external allergens e.g dust and pollen. Asthma begins in childhood. Intrinsic(non-atopic): it results from internal non-allergenic factors e.g infection Mixed Asthma: this is the combination of extrinsic and intrinsic asthma 15  ASTHMA: Causes Extrinsic allergens Intrinsic allergens ✓ Animal dander ✓ Anxiety ✓ Food additives containing ✓ Coughing or laughing sulfites ✓ House dust or mold ✓ Emotional stress ✓ Feather pillows ✓ Endocrine changes ✓ Pollen ✓ Fatigue ✓ Genetic factors ✓ Humidity variations ✓ Irritants ✓ Temperature variations PATH200/SPRING 21-22/NSG DEPT/MACHS 16 ASTHMA - PATHOPHYSIOLOGY 17 ASTHMA - PATHOPHYSIOLOGY 18  ASTHMA Clinical Findings: Sudden dyspnea, wheezing, and tightness in the chest Coughing that produces thick, clear, or yellow sputum Tachypnea, tachycardia Profuse perspiration Hyperresonant lung fields Diminished breath sounds. Asthma that occurs with cyanosis, confusion, and lethargy indicates the onset of life-threatening status asthmaticus and respiratory failure. TREATMENT Bronchodilators, Corticosteroids, Mast cell stabilizers, Leukotriene modifiers 19 https://www.youtube.com/watch?v=4aK76DoxKGk 20  CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Chronic obstructive pulmonary disease (COPD) refers to chronic bronchitis and emphysema, a pair of two commonly co- existing diseases of the lungs in which the airways become narrowed. This leads to limiting airflow to and from the lungs causing shortness of breath. 21  CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) CAUSES: 1)Smoking 2) Occupational exposures- exposure to workplace dust found in coal mining, gold mining, and the cotton textile industry 3) Air pollution 4) sudden airway constriction in response to inhaled irritants, 5) Genetics-Alpha 1-antitrypsin deficiency is a genetic condition where the body does not make enough of a protein, alpha 1-antitrypsin. This protects the lungs from damage caused by inflammatory responses to tobacco smoke. Types of Chronic Obstructive Pulmonary Disease ⮚ Emphysema ⮚ Chronic Bronchitis 22  EMPHYSEMA ◼ The enlargement of the airspaces in emphysema results in hyperinflation of the lungs and increased total lung capacity. ◼ Results from the breakdown of elastin by enzymes, called proteases, which digest proteins ◼ Proteases, especially elastase, are released from neutrophils, alveolar macrophages, and other inflammatory cells. ◼ Causes: smoking and alpha1-antitrypsin deficiency ◼ Barrel chest 23  CHRONIC BRONCHITIS Airway obstruction is caused by inflammation of the major and small airways. Cigarette smoking is the major causal factor. Airway lumen occluded by secretions and narrowed by a thickened wall leads to airflow obstruction and COPD copious sputum expectoration upon arising from sleep 24 25  CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) ❑ CLINICAL MANIFESTATIONS ❑ TREATMENT ✔ Chronic cough ✔ Bronchodilators to alleviate ✔ Sputum production bronchospasms ✔ Wheezing ✔ Effective coughing to remove secretions ✔ Chest tightness ✔ Postural drainage to help mobilize secretions ✔ Dyspnoea on exertion ✔ Chest physiotherapy to mobilize secretions ✔ Wt.loss ✔ Antibiotics to allow treatment of respiratory ✔ Respiratory infections tract infections ✔ Barrel chest- chronic hyperinflation ✔ Smoking cessation leads to loss of lung elasticity. ✔ Increased fluid intake to thin mucus 26 https://www.youtube.com/watch?v=2nBPqSiLg5E 27  PLEURAL EFFUSION Pleural effusion, a collection of fluid in the pleural space Mainly due to heart failure, TB, pneumonia, pulmonary infections and pulmonary embolism A form of a restrictive lung disease. Clinical manifestation: Decreased or absent breath sounds, stabbing pain during respiratory movement, decreased fremitus, a dull, flat sound when percussed, acute respiratory distress, and tracheal deviation. PATH200/SPRING 21-22/NSG DEPT/MACHS 28  BRONCHIECTASIS Bronchiectasis: is a chronic, irreversible Clinical Manifestations dilation of the bronchi and bronchioles. ✓ Chronic cough Causes: ✓ The production of purulent sputum in copious amounts. ✓ Airway obstruction ✓ Many patients with this disease ✓ Diffuse airway injury have hemoptysis. ✓ Pulmonary infections ✓ Clubbing of the fingers ✓ Genetic disorders ✓ The patient usually has repeated ✓ Idiopathic causes episodes of pulmonary infection. 29 BRONCHIECTASIS PATHOPHYSIOLOGY 30  RESPIRATORY INFECTIONS- PNEUMONIA An inflammation of the lung parenchyma that is caused by a microbial agent. ▪ Inflammatory process resulting in edema of the parenchymal lung tissue ▪ Extravasation of fluid into the alveoli causing hypoxemia ▪ Primarily affects terminal gas-exchanging portions of the lung 31  RESPIRATORY INFECTIONS- PNEUMONIA Types ❑ Community-acquired pneumonia: Occurs either in the community setting or within the first 48 hours of hospitalization ❑ Hospital-acquired pneumonia: The onset of pneumonia symptoms more than 48 hours after admission to the hospital. ❑ Pneumonia in immunocompromised host ❑ Aspiration pneumonia: pulmonary consequences resulting from the entry of endogenous or exogenous substances into the lower airway. Clinical Manifestation - Fever - Dyspnea - Cough, Sputum Production - Tachycardia - Tachypnea - X-ray abnormalities Treatment: Antibiotics 32  ATELECTASIS ▪ Closure or collapse of alveoli is often described in relation to x-ray findings and clinical signs and symptoms. ▪ Occurs frequently in the postoperative patients ▪ Immobilized patients who have a shallow, monotonous breathing pattern. ▪ Excess secretions or mucus plugs may also cause obstruction of airflow and result in atelectasis in an area of the lung. ▪ Risk factors: patients with impaired cough mechanisms (eg, postoperative, musculoskeletal or neurologic disorders) or in debilitated, bedridden patients. ▪ Excessive pressure on the lung tissue, which restricts normal lung expansion on inspiration. Eg: Fluid accumulating within the pleural space (Pleural effusion)Air in the pleural space (pneumothorax)Blood in the pleural space (hemothorax). 33  Pathophysiology of Atelectasis Reduced alveolar ventilation or any type of blockage that impedes the passage of air to and from the alveoli The trapped alveolar air becomes absorbed into the bloodstream, but outside air cannot replace the absorbed air because of the blockage Isolated portion of the lung becomes airless and the alveoli collapse Atelectasis 34  ATELECTASIS CLINICAL MANIFESTATIONS Onset is insidious. Cough, sputum production, and low-grade fever. The fever that accompanies atelectasis is due to infection or inflammation distal to the obstructed airway. Dyspnea, tachycardia, Tachypnea, pleural pain, and central cyanosis (a bluish skin) Anxious. Prevention: Frequent turning Early ambulation Encourage appropriate deep breathing and coughing to mobilize secretions and prevent them from accumulating. 35  Pulmonary Tuberculosis o M. tuberculosis is a nonmotile, nonsporulating, acid-fast rod that secretes niacin; when the bacillus reaches a susceptible site, it multiplies freely o Highly communicable disease caused by Mycobacterium tuberculosis o Because M. tuberculosis is an aerobic bacterium, it primarily affects the pulmonary system, especially the upper lobes, where the oxygen content is highest, but also affects other areas of the body, such as the brain, intestines, peritoneum, kidney, joints, and liver. 36  Pulmonary Tuberculosis Risk Factors for Tuberculosis ✓ Child younger than 5 years of age ✓ Drinking unpasteurized milk if the cow is infected with bovine tuberculosis ✓ Homeless individuals or those from a lower socioeconomic group, minority group, or refugee group ✓ Individuals in constant, frequent contact with an untreated or undiagnosed individual ✓ Individuals living in crowded areas, such as long-term care facilities, prisons, and mental health facilities ✓ Older client ✓ Individuals with malnutrition, infection, immune dysfunction, or human immunodeficiency virus infection; or immunosuppressed as a result of medication therapy ✓ Individuals who abuse alcohol or are intravenous drug users 37 Transmission Pulmonary Tuberculosis ✓ Via the airborne route by droplet infection. ✓ When infected individual coughs, laughs, sneezes, or sings, droplet nuclei containing tuberculosis bacteria enter the air and may be inhaled by others. ✓ Identification of those in close contact with the infected individual is important so that they can be tested and treated as necessary. ✓ When contacts have been identified, these persons are assessed with a tuberculin skin test and chest x-rays to determine infection with tuberculosis. ✓ After the infected individual has received tuberculosis medication for 2 to 3 weeks, the risk of transmission is reduced greatly. 38  Pulmonary Tuberculosis Pathophysiology of TB: Droplets enter the lungs, and the bacteria form a tubercle lesion. The body’s defense systems encapsulate the tubercle, leaving a scar. If encapsulation does not occur, bacteria may enter the lymph system, travel to the lymph nodes, and cause an inflammatory response termed granulomatous inflammation. Primary lesions form; the primary lesions may become dormant but can be reactivated and become a secondary infection when re-exposed to the bacterium. In an active phase, tuberculosis can cause necrosis and cavitation in the lesions, leading to rupture, the spread of necrotic tissue, and damage to various body parts. 39 40  Acute Respiratory Failure, Respiratory failure: can be viewed as a failure in gas exchange due to either heart or lung failure, or both. It is not a specific disease but can occur in the course of a number of conditions that impair ventilation, compromise the matching of ventilation and perfusion, or impair gas diffusion. Acute respiratory failure may occur in previously healthy people as the result of acute disease or trauma involving the respiratory system, or it may develop in the course of a chronic neuromuscular or lung disease. 41  Acute Respiratory Failure, Respiratory failure is a condition in which the respiratory system fails in one or both of its gas exchange functions The function of the respiratory system can be said to consist of two aspects: Gas exchange (movement of and across the alveolar-capillary membrane) Ventilation (movement of gases into and out of the alveoli due the action of the respiratory muscles, respiratory center in the CNS, and the pathways that connect the centers in the CNS With the respiratory muscles). Respiratory failure is commonly divided into two types: 1) Hypoxemic respiratory failure due to failure of the ga exchange function of the lung. 2) Hypercapnic/hypoxemic respiratory failure due to ventilatory failure" The classification should not be viewed as rigid since lung disorders that cause impaired gas exchange can be complicated by ventilatory failure. In addition, ventilatory failure can be accompanied by lung disorders that impair gas diffusion. 42 43  Acute Respiratory Failure, Treatment ❑ The failure consists of specific therapy directed toward the underlying disease, ❑ Respiratory supportive care directed toward maintenance of adequate gas exchange, and general supportive care. ❑ A number of treatment modalities are available, including the establishment of an airway and the use of anti-inflammatory bronchodilators, mucolytics, and antibiotics for respiratory infections. ❑ The main therapeutic goal in acute hypoxemic respiratory failure is to ensure adequate oxygenation of vital organs, which is generally accomplished by mechanical ventilation 44  References: ▪ NORRIS, T. (2019). Porth’s Pathophysiology Concepts of Altered Health States. 10th ed. Wolters Kluwer ▪ Ian Peate, (2021) Fundamentals of applied pathophysiology: an essential guide for nursing & healthcare students. 4th ed. ▪ Hoboken, NJ : Wiley-Blackwell Dignle, M., Mulvihill, M., Zelman, M. & Tompary, E. (2011). Introductory pathophysiology for nursing & healthcare professionals. |Pearson ▪ Nair, M., & Peate, I. (2015). Pathophysiology for nurses at a glance (nursing and healthcare). Publisher: West Sussex, England: John Wiley & Sons, Inc PATH200/MACHS 45