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RESPIRATORY SYSTEM

This article explores the functional anatomy and physiology of the respiratory system, including the role of the lungs, lung mechanics, and control of breathing. Topics covered include the structure of the lungs, mechanics of inspiration and expiration, control of breathing, and the importance of maintaining a healthy respiratory system.

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RESPIRATORY SYSTEM

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  1. RESPIRATORY SYSTEM

  2. FUNCTIONAL ANATOMY AND PHYSIOLOGY • Lungs occupy upper two thirds bony thorax • Inspiration involves downward contraction of diaphragm outward & upward movement of the ribs at costovertebral joints caused by external intercostal muscles

  3. Expiration is passive due to elastic recoil of lungs

  4. Lung mechanics • Healthy alveolar walls contain a fine network of elastin and collagen fibres • The volume of the lungs at the end of breath out is called the functional residual capacity (FRC)

  5. At this volume the inward elastic recoil of the lungs (resulting from elastin fibres and the surface tension in the alveoli) is balanced by the resistance of the chest wall to inward distortion, causing negative pressure in the pleural space

  6. Elastin fibres allow the lungs to be easily distended but collagen fibres restrict expansion • So in health, the maximum inspiratory volume is limited by the lung (rather than chest wall)

  7. Elastin fibres in the alveolar walls maintains small airway patency by radial traction on the airway walls • During normal breathing, small airways narrow during expiration because of surrounding high alveolar pressure, but are prevented from collapsing by radial traction

  8. So the volume that can be exhaled is thus limited purely by capacity of expiratory muscles to distort chest wall inwards. • In emphysema loss of alveolar walls, leaves the small airways unsupported and their collapse on expiration causes air trapping and high end expiratory volume

  9. Control of breathing • Respiratory motor neurons in the medulla are the origin of the respiratory cycle • Their activity is modulated by multiple external inputs in health and in disease • Central chemoreceptors in the ventrolateral medulla sense the pH of the cerebrospinal fluid (CSF) and are indirectly stimulated by a rise in arterialPCO2

  10. The carotid bodies sense hypoxaemia & are activated by arterial PO2 values below 8KPa(60mmHg). • Cortical(volitional) and limbic(emotional) influences can override the automatic control of breathing

  11. The lungs are designed for gaseous exchange (oxygen uptake and carbon dioxide elimination) through the process of ventilation and molecular diffusion • To maintain health, purified air must be presented to the alveolar epithelial surface to aerate pulmonary capillary blood

  12. Ambient air, which contains environmental debris, microbes, and possibly solubilized toxins must be cleaned • Cleaning is done by system of host defenses that usually removes these contaminants

  13. Mechanically (by sneezing, rhinorrhea, coughing, and mucociliary clearance) • Innate (natural) immunity or adaptive (acquired) immunity • This immunity is compromised by systemic illness or the side effects of other medical therapy

  14. Although the respiratory tract is a unit of branching tubes leading to the air exchange–alveolar surface, it functionally has distinct anatomic segments • Naso-oropharynx or upper airways • Conducting airways (larynx, trachea, and bronchi that branch to terminal bronchioles) • Respiratory bronchioles, alveolar ducts and alveoli

  15. Vascular and neural structures are integral to each segment • Lymphatic channels begin at the level of respiratory bronchioles and flow upward into the hilar nods

  16. The airways and their accompanying blood supply develop from the foregut and primitive esophagus • The conducting airway system has approximately 14 generations of branches, which are extended by another 10 branches within the acinar airways, finally ending as alveolar sacs

  17. Later developments in the foetus initiate progressive thinning of the mucosal epithelial layer in distal bronchi and then the respiratory bronchioles to a single cell surface

  18. Because this mucosal surface that lines the airways down to the respiratory bronchioles is in breath-to-breath contact with the external environment, mechanisms to clean inspired air are dispersed along the entire tract

  19. Deglutition and respiration are coordinated exquisitely by the epiglottis and laryngeal musculature to direct fluids and food into the esophagus and air into the subglottic trachea • Control is not perfect, aspiration can occur in normal persons during sleep causing cough and asthma

  20. The surface of the nasal mucosa is similar to that in the lower conducting airways with respect to ciliary function and immunologic components • Mucociliary clearance declines with age, causing more frequent occurrence of respiratory infections in the elderly

  21. The conducting airways begin with the trachea, 10 cm in length • At the carina, it divides into two major bronchi, and then multiple smaller bronchial branches • Branching reduces resistance to airflow and reduces the speed of air as it prepares to enter the acinar ducts and alveolar sacs

  22. Here any 0.5- to 3-μm particulates settle out if present by the slower movement the air • The thickness of the mucosal surface attenuates as the pseudostratified cell layer flattens to become a single cell layer in the terminal bronchioles

  23. Here the less protected surface may become more vulnerable to injury from inhaled toxins and microbes producing chronic inflammation (bronchiolitis)

  24. The respiratory bronchioles, which are positioned between the distal conducting airways and the alveolized air exchange surface, functionally separate the upper and lower respiratory tracts

  25. This segment is a bottleneck for airflow and a last surface to capture small particles and microbial or antigenic debris before the alveolar space as the immune responses can be initiated here

  26. The respiratory bronchioles can be the site of airway obstruction • Inflammation typical of bronchiolitisobliterans, chronic graft rejection after lung transplantation and lung involvement by collagen vascular diseases

  27. In this transition segment, several changes occur • Single-layer cuboidal epithelial surface further differentiates into alveolar type I cells that cover the alveolar lining surface & type II cells(pneumocytes)

  28. Type II pneumocytes produce surfactant that reduces surface tension and counteracts tendency of alvevoli to collapse under surface tension

  29. Pulmonary brush cells with microvilli are dense in this area and may be involved with chemosensing or trapping of inhaled particles and pollutants as well as with regulation of fluid and solute absorption

  30. Surface host defenses change from mucociliary clearance to macrophage phagocytes, inflammatory cells (neutrophils or eosinophils), and opsonins • Finally, the changeover is made from the bronchial arterial blood supply for the conducting airways to the pulmonary artery–pulmonary capillary blood

  31. The air exchange compartment, or the alveolar space, is composed of about 480 million alveoli supported by a fibrous scaffolding and intertwined with a meshwork of pulmonary artery capillaries that permit air-blood contact(distance is < 0.4 micron)

  32. VENTILATION & PERFUSION • Gravity determines the distribution of ventilation and blood flow in the lungs • Most ventilation and perfusion goes to dependent zones • Locally, hypoxia constricts pulmonary arterioles and airway CO2 dilates bronchi

  33. Diseases which impair ventilation locally result in desaturated and CO2-laden blood entering the pulmonary veins, causing arterial hypoxaemia

  34. Increased ventilation of remaining normal lung units increase CO2 excretion, correcting arterial CO2 to normal, but cannot augment oxygen uptake or correct hypoxaemia, because maximal oxygen uptake in these normal lung units is limited by the capacity of haemoglobin

  35. The resulting pattern of blood gas abnormality is hypoxia with normocapnia, which is termed 'type I respiratory failure

  36. Hypoxia with hypercapnia is termed type II respiratory failure • It is seen if there is severe generalised ventilation-perfusion mismatch (insufficient normal lung to correct CO2) or a disease which reduces total ventilation

  37. Ventilation is reduced by diseases of the lung or chest wall & also diseases affecting any part of the neuromuscular mechanism of ventilation like, • brain injury • narcotic poisoning • polyneuropathies • myopathies

  38. The pulmonary circulation in health operates at low pressure (approximately 24/9 mmHg), and can accommodate large increases in flow (e.g. during exercise) without much rise in pressure

  39. Pulmonary hypertension may result when pulmonary vessels are destroyed by emphysema, obstructed by thrombus or involved in interstitial inflammation or fibrosis

  40. INVESTIGATIONS • A detailed history, thorough examination and basic haematological and biochemical tests usually suggest the likely diagnosis

  41. Chest X-RAY • Performed on the majority of patients • A postero-anterior (PA) film provides information on the lung fields, heart, mediastinum, vascular structures and the thoracic cage

  42. Lateral film, is requested if pathology is suspected behind the heart shadow or deep in the diaphragmatic sulci • Increased shadowing may represent accumulation of fluid, lobar collapse or consolidation

  43. Consolidation does not change the position of the mediastinum • Presence of an air bronchogram means that proximal bronchi are patent • Collapse (implying obstruction of the proximal bronchus) is accompanied by loss of volume and displacement of the mediastinum towards the affected side

  44. Ring shadows (diseased bronchi seen end-on), tramline shadows (diseased bronchi side-on) or tubular shadows (bronchi filled with secretions) suggests bronchiectasis • Pleural fluid is suggested by a shadow which, in the erect patient, ascends towards the axilla

  45. Right middle lobe pneumonia

  46. Right pneumothorax

  47. Right upper lobe collapse

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