Pathophysiology of obstructive and restrictive lung disease

Learning Outcomes At the end of the lecture, student should be able to: Explain the pathophysiology of obstructive lung disease and restrictive lung disease Compare the pathophysiology of obstructive lung disease and of restrictive lung disease Differentiate and compare the pulmonary function test patterns in obstructive versus restrictive disease Describe the effects of obstructive and restrictive lung disease on arterial blood oxygenation.

Obstructive pulmonary disease Lung disease that makes it hard to breathe. Increased airway resistance (flow) first symptoms can be so mild that people mistakenly think that "getting old." tends to get worse over a period, but catching it early, along with good care, can help many people stay active and may slow the disease

Obstructive pulmonary disease Characterized by airway obstruction that is worse with expiration. More force is required to expire a given volume of air, or emptying of lungs is slowed, or both. Examples are - emphysema, asthma, chronic bronchitis, cystic fibrosis

Emphysema damages the tiny air sacs in the lungs, air sacs can't expand and contract properly. Alveoli enlarge which trap stale air. Very few capillaries great trouble exhaling.

Chronic Bronchitis Its calling card is a nagging cough with plenty of mucus . swollen wall of small airways, constant oozing of mucus, and scarring. Trapped mucus block airflow and become a breeding ground for germs..

Asthma Bronchiolar constriction, mucus hypersecretion, inflammatory swelling

Common Symptoms Inside the lungs, clogging of the airways and damage the tiny, balloon-like sacs (alveoli) Shortness of breath in everyday activities Wheezing Chest tightness Constant coughing Producing a lot of mucus (sputum) Feeling tired Frequent colds or flu

Advanced Symptoms make it difficult to walk, cook, clean house, or even bathe. Coughing up excess mucus and feeling short of breath may worsen. Swollen legs or feet from fluid buildup Weight loss Less muscle strength and endurance A headache in the morning Blue or grey lips or fingernails (due to low oxygen levels)

Pathophysiology-Multifactorial Fundamental physiologic problem is increased resistance to airflow as a result of caliber reduction of conducting airways. This increased resistance can be caused by (1) obstruction within the lumen due to increased secretions (as seen in asthma and chronic bronchitis) (2) Airway wall thickening and airway narrowing can result from the inflammation seen in both asthma and chronic bronchitis (3) loss of surrounding supporting structure, with expiratory airway collapse resulting from the destruction of lung elastic tissue.

Pathophysiology-Multifactorial Airway inflammation , hypertrophy of mucus secreting cells, increased goblet cells in bronchioles and finally decreased ciliary cells and their activity leading to- an accelerated loss of elasticity of lung tissue. Due to the loss of pulmonary elastic recoil the alveoli are more prone to collapse thus leading to emphysema in almost all cases. decrease in the space available for gas exchange. Increased secretions in the lower respiratory tract unable to move out due to low ciliated cells activity.

Pathophysiology-Multifactorial Peptide neurotransmitters may also play a role. The proinflammatory neuropeptide substance P , released from unmyelinated afferent fibers in the airways and induce smooth muscle contraction and mediate release of secretions from mast cells. interruption of its action by Vasoactive intestinal peptide (VIP) due to its cleavage, can promote bronchoconstriction.

Restrictive diseases Restrictive diseases are those in which inhalation is never fully complete leading to difficulty in inspiration. Decreased compliance (volumes) Examples are pulmonary fibrosis, sarcoidosis, asbestosis, silicosis

Restrictive Lung Disease Characterized by reduced lung volume, either because of an alteration in lung parenchyma or reduced lung volume because of a disease of the pleura, chest wall, or neuromuscular apparatus In physiological terms, restrictive lung diseases are characterized by reduced total lung capacity (TLC), vital capacity, or resting lung volume. Accompanying characteristics are preserved airflow and normal airway resistance, which are measured as the FRC.

Cystic fibrosis Cystic fibrosis is an inherited disease of the mucus and sweat glands. It affects mostly lungs, pancreas, liver, intestines, sinuses and sex organs. CF causes mucus to be thick and sticky. The mucus clogs the lungs, causing breathing problems and making it easy for bacteria to grow. can lead to problems such as repeated lung infections and lung damage.

Pathophysiology Disorders leading to reduction or restriction of lung volumes are divided into 2 groups based on anatomical structures. intrinsic lung diseases or diseases of the lung parenchyma Extrinsic lung diseases such as diseases of any of these structures chest wall, pleura, and respiratory muscles

Pathophysiology- intrinsic inflammation or scarring of the lung tissue (interstitial lung disease) or result in filling of the air spaces with exudates and debris (pneumonitis). characterized according to etiological factors. They include idiopathic fibrotic diseases, connective-tissue diseases, drug-induced lung disease, and primary diseases of the lungs (including sarcoidosis).

Idiopathic Pulmonary Fibrosis lungs becomes thick and stiff, or scarred, over time Causes; Cigarette smoking Viral infections, influenza A virus, hepatitis C virus, HIV, and herpes virus.

Sarcoidosis the lungs have gross pathology and there is inflammation within the alveoli (lower inset). Several other organs may be involved, as seen in a shoulder image of a patient with sarcoidosis (upper inset).

Pathophysiology-Extrinsic Diseases of any of these structures chest wall, pleura, and respiratory muscles being component of the respiratory pump, result in lung restriction, impaired ventilatory function, and respiratory failure the total compliance by the respiratory system is reduced, and, hence, lung volumes are reduced. e.g, non-muscular diseases of the chest wall, neuromuscular disorders

Comparison of the pulmonary function test patterns in obstructive versus restrictive disease

Spirometery in normal and obstructive lung disease

Normal Restrictive Lung disease

Obstructive disease Restrictive disease In Obstructive pulmonary disease, FEV 1 reduction disproportionate compared to the FVC key to diagnosing obstructive lung dysfunction Restrictive lung disease is characterized by a reduction in FVC with a normal or elevated FEV1/FVC ratio. Distinguish from obstructive disease

Restrictive disease Obstructive disease Functional residual capacity and residual volume of the lung increased because of the difficulty in expiring air from the lungs greatly reduced maximum expiratory rate Reduction in FRC and other lung volumes because of pathology in lungs, pleura, or the structures of the thoracic cage. Obesity may reduce chest wall compliance

Comparison of the pathophysiology of obstructive lung disease and of restrictive lung disease

Restrictive disease Obstructive disease Anatomy affected - airways Breathing difficulty - expiration Pathophysiology -↑airway resistance Pulmonary functions- ↓airway flow rates Anatomy affected – lung tissue or thorax Breathing difficulty - inspiration Pathophysiology -↓lung, or thoracic, compliance Pulmonary functions- ↓lung volumes,or capacities

Restrictive disease Obstructive disease alveoli is expanding but it is unable to deflate or slowly. lung volumes increase in obstructive diseases, People with obstructive lung disease have shortness of breath due to difficulty exhaling all the air from the lungs. Because of damage to the lungs or narrowing of the airways inside the lungs, exhaled air comes out more slowly than normal. . Alveoli deflates but is unable to inflate properly due to either lung scarring, fibrosis, or extra-parenchymal problems. lung volumes greatly decreased in restrictive cases. most often results from a condition causing stiffness in the lungs themselves. In other cases, stiffness of the chest wall, weak muscles, or damaged nerves may cause the restriction in lung expansion.

Restrictive disease Obstructive disease At the end of a full exhalation, an abnormally high amount of air may still linger in the lungs. Obstructive lung disease makes it harder to breathe, especially during increased activity or exertion As the rate of breathing increases, there is less time to breathe all the air out before the next inhalation People with restrictive lung disease cannot fully fill their lungs with air. Their lungs are restricted from fully expanding

Restrictive disease Obstructive disease Diameter of the tube (airways) The smaller the diameter, the less flow varies to the 4th power e.g. A change in diameter of 2 causes a 16 fold change in resistance Airway diameter increases during inhalation and decreases during exhalation Compliance essentially means the volume change for any given pressure Compliance measures the distensibility of the lung tissue of the lung tissue “Good” lung compliance means that the lungs expand easily Stiff lungs usually have lower volumes

Arterial Blood Oxygenation in Obstructive disease

Arterial Blood Oxygenation in Obstructive disease

Arterial Blood Oxygenation in Obstructive disease Low oxygen (hypoxaemia) and/or high carbon dioxide Ventilation-perfusion mismatching accounts for essentially all of the reduction in PaO2 that occurs in COPD A blood sample taken from a vein may show a high blood count (reactive polycythemia), a reaction to long-term hypoxemia. An elevation of arterial level of carbon dioxide (PaCO2) is not expected until the FEV1 is less than 25% of predicted and even then may not occur. Non-uniform ventilation and ventilation-perfusion mismatching are characteristic of COPD, reflecting the heterogeneous nature of the disease process within the airways and lung parenchyma.

Arterial Blood Oxygenation in Restrictive disease Decreased Arterial PO2 and PCO2 is normal or low as a consequence of increased ventilation under the stimuli of hypoxia Hypoxemia is commonly seen, results from an increased physiologic dead space and relatively fixed minute ventilation leading to an increase in both high and low / mismatching areas. Hypercapnia is a grave sign, implying an inability to maintain adequate alveolar ventilation as a result of excess work of breathing Only in the later stages of disease, when the increased lung elastic recoil and work of breathing prevent appropriate ventilation, does the PaCO2 rise above normal.