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Chapter 27 Structure and Function of the Respiratory System

Chapter 27 Structure and Function of the Respiratory System. Function of the lung. Gas exchange Protection against infection by alveolar macrophages Surfactant secretion: allow expansion of alveoli with air. The respiratory acinus. Cartilage is present to level of proximal bronchioles

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Chapter 27 Structure and Function of the Respiratory System

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  1. Chapter 27Structure and Function of the Respiratory System

  2. Function of the lung • Gas exchange • Protection against infection by alveolar macrophages • Surfactant secretion: allow expansion of alveoli with air

  3. The respiratory acinus • Cartilage is present to level of proximal bronchioles • Beyond terminal bronchiole gas exchange occurs • The distal airspaces are kept open by elastic tension in alveolar walls

  4. Dead Space • Area where gas exchange cannot occur • Includes most of airway volume • Anatomical dead space (=150 ml) • Airways • Physiological dead space • = anatomical + non functional alveoli • Calculated using a pure O2 inspiration and measuring nitrogen in expired air (fig 37-7) • % area X Ve

  5. Alveolar Volume • Alveolar volume (2150 ml) = FRC (2300 ml)- dead space (150 ml) • At the end of a normal expiration most of the FRC is at the level of the alveoli • Slow turnover of alveolar air (6-7 breaths) • Rate of alveolar ventilation • Va = RR (Vt-Vd)

  6. Types of Shunts • Anatomic shunt • Blood moves from the venous to the arterial side of the circulation without moving through the lungs • Physiologic shunt • Mismatching of ventilation and perfusion with the lung • Results in insufficient ventilation to provide the oxygen needed to oxygenate the blood flowing through the alveolar capillaries

  7. Matching Ventilation and Perfusion • Required for exchange of gases between the air in the alveoli and the blood in pulmonary capillaries • Two factors interfere with the process: • Dead air space and shunt • The blood oxygen level reflects the mixing of blood from alveolar dead space and physiologic shunting areas as it moves into the pulmonary veins.

  8. Effect of pH on ventilation • Normal level of HCO3- = 24 mEq/L • Metabolic acidosis (HCO3- < 24) will + ventilation • Metabolic alkalosis (HCO3- >24) will – ventilation • Kidney regulates HCO3- • Normal level of CO2 = 40 mmHg • Respiratory acidosis (CO2 > 40) will + ventilation • Respiratory alkalosis (CO2 < 40) will – ventilation • Lung regulates CO2

  9. Normal Lung Tissue

  10. Static Lung Volumes • Tidal Volume (500ml) • amount of air moved in or out each breath • Inspiratory Reserve Volume (3000ml) • maximum vol. one can inspire above normal inspiration • Expiratory Reserve Volume (1100ml) • maximum vol. one can expire below normal expiration • Residual Volume (1200 ml) • volume of air left in the lungs after maximum expiratory effort

  11. Static Lung Capacities • Functional residual capacity (RV+ERV) • vol. of air left in the lungs after a normal expir., balance point of lung recoil & chest wall forces • Inspiratory capacity (TV+IRV) • max. vol. one can inspire during an insp effort • Vital capacity (IRV+TV+ERV) • max. vol. one can exchange in a resp. cycle = max exhaled volume • Total lung capacity (IRV+TV+ERV+RV) • the air in the lungs at full inflation

  12. Ventilation-Perfusion Defects • Alveoli that are ventilated but not perfused is ventilatory “dead space” • Alveoli that are perfused but not ventilated leads to “shunting” of non-oxygenated blood from pulmonary to systemic circulation ( a mechanism of cyanosis)

  13. ANS influence on pulmonary vascular smooth muscle • SNS + will cause a mild vasoconstriction • 3 Hz to 30 Hz pulmonary arterial BP about 30% • Mediated by alpha receptors • With alpha blockage response abolished and at 30 Hz. vasodilatation observed as beta receptors are unmasked • Parasympathetic + will cause a mild vasodilatation • (major constrictor effect on pulmonary vascular smooth muscle is low alveolar O2)

  14. Patterns of Breathing • Eupnea • normal breathing (12-17 B/min, 500-600 ml/B) • Hyperpnea •  pulmonary ventilation matching  metabolic demand • Hyperventilation ( CO2) •  pulmonary ventilation > metabolic demand • Hypoventilation ( CO2) •  pulmonary ventilation < metabolic demand • Hypoperfusion •  blood flow to alveoli< metabolic demand

  15. Patterns of breathing (cont.) • Tachypnea •  frequency of respiratory rate • Apnea • Absense of breathing. e.g. Sleep apnea • Dyspnea • Difficult or labored breathing • Orthopnea • Dyspnea when recumbent, relieved when upright. e.g. congestive heart failure, asthma, lung failure

  16. Chapter 28 Respiratory Tract Infections, Neoplasms, and Childhood Disorders

  17. General Signs and Symptoms of Respiratory Disease • Hypoxia : Decreased levels of oxygen in the tissues • Hypoxemia : Decreased levels of oxygen in arterial blood • Hypercapnia : Increased levels of CO2 in the blood • Hypocapnia : Decreased levels of CO2 in the blood • Cyanosis : Bluish discoloration of skin and mucous membranes due to poor oxygenation of the blood • Hemoptysis : Blood in the sputum

  18. General Signs and Symptoms of Respiratory Disease • Cough • Productive cough = raising fluid to the pharynx • Expectoration = spitting • Non-productive cough or hacking • Dyspnea • Shortness of breath • Airway obstruction • Decreased compliance • Cyanosis • Large quantities of unoxygenated blood

  19. Areas Involved in Respiratory Tract Infections • Upper respiratory tract • Nose, oropharynx, and larynx • Lower respiratory tract • Bronchi, bronchioles, and lungs

  20. Upper respiratory tract Infections The common cold The most common viral pathogens for the “common cold” are rhinovirus, parainfluenza virus, respiratory syncytial virus, adenovirus and coronavirus. • These viruses tend to have seasonal variations in their peak incidence. • They gain entry to the body through the nasal mucosa and the surfaces of the eye. They are readily spread from person to person via respiratory secretions. • Manifestations of the common cold include: • Rhinitis:Inflammation of the nasal mucosa • Sinusitis:Inflammation of the sinus mucosa • Pharyngitis:Inflammation of the pharynx and throat • Headache • Nasal discharge and congestion

  21. Upper respiratory tract Infections Influenza • Influenza is a viral infection that can affect the upper or lower respiratory tract. • Three distinct forms of influenza virus have been identified: A, B and C, of these three variants, type A is the most common and causes the most serious illness. • The influenza virus is a highly transmissible respiratory pathogen. • Because the organism has a high tendency for genetic mutation, new variants of the virus are constantly arising in different places around the world. Serious pandemics (spread of infection across a large region) of influenza are seen every 8 to 10 years as a result of this genetic mutation .

  22. Upper respiratory tract Infections Influenza • Symptoms of influenza infection: • Headache • Fever, chills • Muscle aches • Nasal discharge • Unproductive cough • Sore throat • Influenza infection can cause marked inflammation of the respiratory epithelium leading to acute tissue damage and a loss of ciliated cells that protect the respiratory passages from other organisms. • As a result, influenza infection may lead to co-infection of the respiratory passages with bacteria. • It is also possible for the influenza virus to infect the tissues of the lung itself to cause a viral pneumonia.

  23. Upper respiratory tract Infections Treatment of influenza: Bed rest, fluids, warmth Antiviral drugs Influenza vaccine : Provides protection against certain A and B influenza strains that are expected to be prevalent in a certain year. The vaccine must be updated and administered yearly to be effective but will not be effective against influenza strains not included in the vaccine. The influenza vaccine is particularly indicated in elderly people, in individuals weakened by other disease and in health-care workers Influenza

  24. Upper respiratory tract Infections Influenza Drugs for Treating Influenza: • Amantidine • Used orally or by aerosol administration • Effective only against type A influenza • Inhibits viral fusion, assembly and release from the infected host cell • Neuraminidase inhibitors (Zanamavir, Oseltamivir) • New drugs that can be used by inhalation (Zanamavir) or orally (Oseltamivir) • Effective against both type A and B influenza • Inhibits the activity of viral neuraminidase enzyme that is necessary for spread of the influenza virus

  25. Types of Influenza Vaccinations • Trivalent inactivated influenza vaccine (TIIV) • Developed in the 1940s • Administered by injection • Live, attenuated influenza vaccine (LAIV) • Approved for use in 2003 • Administered intranasally

  26. Lower respiratory tract Infections Pneumonia • Pneumonia is a condition that involves inflammation of lower lung structures such as the alveoli or interstitial spaces. • It may be caused by bacteria or viruses such as pneumocystiscarinii. • The prevalence and severity of pneumonia have been heightened in recent years due to the emergence of HIV as well as antibiotic resistance. • Pneumonia may be classified according to the pathogen that is responsible for the infection. • There tend to be distinct organisms that cause pneumonia in the hospital setting vs. the community setting.

  27. Lower respiratory tract Infections Pneumonia • Pathology: • Alveolar • Bronchopneumonia (Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus) • Lobar (Streptococcus pneumoniae) • Interstitial (Influenza virus, Mycoplasmapneumoniae) • Pathogenesis: • Inhalation of air droplets • Aspiration of infected secretions or objects • Hematogenous spread - causing infections away from the original site

  28. Bronchopneumonia vs. Lobar Pneumonia Bronchopneumonia • Acute Inflammation in the walls of the bronchioles Lobar Pneumonia • Lobar pneumonia is a form of pneumonia that affects a large and continuous area of the lobe of a lung

  29. Bronchopneumonia Suppurative (pus) inflammation of lung tissue caused by Staph, Strep, Pneumo & H. influenza Usually bilateral Lower lobes common, but can occur anywhere Complications: Abscess Empyema (is a collection of pus in the space between the lung and the inner surface of the chest wall (pleural space). Dissemination

  30. Bronchopneumonia

  31. Bronchopneumonia

  32. Bronchopneumonia

  33. Bronchopneumonia:

  34. Bronchopneumonia

  35. Lower respiratory tract Infections Pneumonia Individuals Most at Risk for Pneumonia • Elderly • Those with viral infection • Chronically ill • AIDS or immunosuppressed patients • Smokers • Patients with chronic respiratory disease e.g. bronchial asthma.

  36. Potential Pathogens • Typical • Streptococcus pneumoniae • Hemophilusinfluenzae • Mycobacterium catarrhalis • Klebsiellapneumoniae • Atypical • Chlamydiapneumoniae • Legionellapneumophila • Mycoplasmapneumoniae.

  37. Lobar Pneumonia Fibrinosuppurativeconsolidation – whole lobe Rare due to antibiotic treatment. ~95% - Strep pneumoniae The course runs in four stages: Congestion. Red Hepatization – Looks like the liver Gray Hepatizaiton Resolution Lower respiratory tract Infections Pneumonia

  38. Lower respiratory tract Infections Pneumonia • Red hepatisation: (consolidation) describes lung tissue with confluent acute exudation, containing neutrophils and red cells, giving a red, firm, liver-like gross appearance. • Grey hepatisation: follows, as the red cells disintegrate and the remaining fibrinosuppurativeexudate persists, giving a grey-brown appearance. • Resolution: is the favourable final stage in which consolidated exudate undergoes enzymatic and cellular degradation and clearance; normal structure is restored.

  39. Lobar pneumonia: whole lobe(s) involved grey hepatization Lobar pneumonia

  40. Red Hepatisation

  41. Red Hepatisation

  42. Lobar Pneumonia – Gray hep…

  43. Lower respiratory tract Infections Pneumonia A second classification scheme for pneumonia is based on the specific structures of the lung that the organisms infect and includes typical and atypical pneumonia. Typical pneumonia • Usually bacterial in origin. • Organisms replicate in the spaces of the alveoli. Manifestations: • Inflammation and fluid accumulation are seen in the alveoli. • White cell infiltration and exudation can been seen on chest radiographs. • High fever, chest pain, chills, and malaise are present. • Purulent sputum is present. • Some degree of hypoxemia is present.

  44. Lower respiratory tract Infections Pneumonia Atypical pneumonia • Usually viral in origin. • Organisms replicate in the spaces around the alveoli. Manifestations: • Milder symptoms than typical pneumonia. • Lack of white cell infiltration in alveoli. • Lack of fluid accumulation in the alveoli. • Not usually evident on radiographs. • May make the patient susceptible to bacterial pneumonia.

  45. Lower respiratory tract Infections Pneumonia Treatment of pneumonia: • Antibiotics if bacterial in origin. The health-care provider should consider the possibility that antibiotic-resistant organisms are present. • Oxygen therapy for hypoxemia. • A vaccine for pneumococcal pneumonia is currently available and highly effective. This vaccine should be considered in high-risk individuals.

  46. Lower respiratory tract Infections Abscess • An abscess is a complication of severe pneumonia, most typically from virulent organisms such as S. aureus. • Abscesses are complications of aspiration, where they appear more frequently in the right posterior lung.

  47. Lung Abscess: Focal suppuration with necrosis of lung tissue Organisms commonly cultured: Staphylococci Streptococci Gram-negative Anaerobes Frequent mixed infections Mechanism: Aspiration Post pneumonic Septic embolism Neoplasms Productive Cough, Fever. Clubbing Complications:Systemic spread, septicemia.

  48. Clubbing

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