Respiratory System Anatomy and Physiology PDF

Section 1- Anatomy Upper respiratory tract Nose and nasal cavity Paranasal sinuses Pharynx Larynx Lower respiratory tract Trachea Bronchi and smaller bronchioles Lungs and alveoli  Anatomy Upper respiratory tract...

Section 1- Anatomy Upper respiratory tract Nose and nasal cavity Paranasal sinuses Pharynx Larynx Lower respiratory tract Trachea Bronchi and smaller bronchioles Lungs and alveoli  Anatomy Upper respiratory tract Nose and nasal cavity Provides airway for respiration Moistens and warms air Filters inhaled air Contains olfactory receptors Involved in speech  Anatomy Upper respiratory tract Paranasal sinuses Air containing cavities in the skull Lined with mucous membrane Possible functions: Decreases weight of skull Increases resonance of voice Buffer against facial trauma LINK Insulates sensitive structures from rapid temperature fluctuations Humidifies and heats air Immunological defense  Anatomy Upper respiratory tract Pharynx The upper part of the throat Nasopharynx Simply an air passageway Closes while swallowing Contains nasopharyngeal and tubal tonsil Oropharynx Food and air passageway Epiglottis closes during inspiration to prevent aspiration Contains palatine and lingual tonsils Laryngopharynx LINK Connects throat to esophagus Extends to branching of respiratory (laryngeal) and digestive (esophageal) pathways  Anatomy Upper respiratory tract Larynx Connects the laryngopharynx to the trachea Contains vocal folds Thyroid gland sits on the outside of the larynx Main function is protective Aids in coughing and other reflexes Prevents food / fluid from entering lungs  Anatomy Lower respiratory tract Bronchi and smaller bronchioles Primary bronchi Secondary bronchi Tertiary bronchi Terminal → respiratory bronchioles Contains mucus and cilia to remove contaminants Can constrict or dilate to modify airflow Link  Anatomy Lower respiratory tract Lungs Right lung contains three lobes; left has two Oblique and horizontal fissures present Covered by visceral pleura Ribs and diaphragm covered by parietal pleura Space between lungs and ribs = pleural cavity LINK  Anatomy Lower respiratory tract Alveoli Millions present on respiratory bronchioles Consists of: Type I cells (squamous epithelium) Type II cells (cuboidal epithelium) Contain lamellar bodies → surfactant secretion LINK Alveolar macrophages The janitor of the alveoli and bronchioles  Anatomy Lower respiratory tract Alveoli Capillaries surround the alveoli (respiratory or alveolar-capillary membrane) to facilitate gas exchange CO2 is diffused out of blood and into the alveoli for exhalation O2 is diffused out of the alveoli and into the blood LINK Alveolar type I cell → alveolar basement membrane → capillary basement membrane → capillary endothelial cells How would the respiratory membrane be affected in chronic bronchitis or emphysema?  Anatomy Lower respiratory tract Alveoli Must expand and contract to facilitate gas exchange Compliance and Elasticity governs how well the lungs/alveoli can inflate and deflate What would be the consequence of poor compliance? Poor elasticity?  Anatomy Lung blood supply Two pathways of blood supply 1) Pulmonary vessels Responsible for gas exchange Deoxygenated blood arrives through pulmonary artery from the right ventricle Arrives at respiratory membrane and becomes oxygenated Pulmonary veins return oxygenated blood to left atrium 2) Bronchial vessels Come from systemic circulation Oxygenates the lung tissue itself LINK  Anatomy The conducting system includes all sites involved in conducting air into the lungs Nose → nasal cavity → pharynx → larynx → trachea → bronchi → bronchiole → terminal bronchioles The respiratory zone (or lung parenchyma) consists of where gas exchange occurs Respiratory bronchioles Alveolar ducts Alveolar sacs Alveoli  Respiration Cells continually use O2 and release CO2 Respiration is the exchange of gases between the atmosphere, blood and cells. Includes: Pulmonary ventilation External respiration Internal respiration  Respiration Pulmonary ventilation Inspiration Air is pulled into the lungs when alveolar pressure < atmospheric pressure Air is pushed out of the lungs when alveolar pressure > atmospheric pressure Pressure is controlled by contraction or relaxation of the diaphragm External intercostal muscles also aid in expanding or contracting thorax Forced inhalation additionally involves accessory muscles of inspiration  Respiration Pulmonary ventilation Inspiration Quiet inspiration An active process representing normal breathing Involves diaphragm and intercostal muscles Forced inspiration Used in times of extra need Sternocleidomastoids, scalenes, pectoralis minor used LINK  Respiration Pulmonary ventilation Expiration Quiet expiration A passive process Diaphragm relaxes and raises upwards Forced expiration Uses obliques and intercostals to contract inwards to help force air out Activated when air movement out of the lungs impeded LINK  Respiration External Respiration Exchange of gases between blood and external environment CO2 removed, O2 gained Occurs via diffusion Occurs at the alveoli – capillary membrane Normal partial pressure oxygen (paO2) gradient: Alveolar space = 100 mmHg Deoxygenated blood = 40 mmHg Normal partial pressure carbon dioxide (paCO2) gradient: Alveolar space = 40mmHg Deoxygenated blood = 45 mmHg  Respiration External Respiration Ventilation and Perfusion Matching Exchange of gas and blood supply must be balanced for proper external respiration Must be enough air in the alveoli, bloodflow in the capillaries, and hemoglobin to carry the oxygen Can compensate for minor imbalances via bronchoconstriction or vasoconstriction of the pulmonary arteries Example: asthma attack Ventilation – perfusion (V/Q) mismatch can occur in severe lung disease Ventilation (L/min) and blood flow (L/min) are not at an optimal ratio (0.8)  Respiration External Respiration Ventilation and Perfusion Matching Causes of V/Q mismatch V/Q=0 → V/Q=∞ → Any mismatch leads to hypoxemia  Respiration Internal Respiration Exchange of gases between blood and cells Oxygen carried by hemoglobin to systemic circulation Reaches capillaries of various tissues Oxygen diffuses into cells; CO2 diffuses into blood Oxygen then used cellular respiration  Type 1 Respiratory Failure Type 1 respiratory failure is the inability of lungs to perform adequate gas exchange Potential causes: Lung disorder (asthma, COPD) Pneumonia Pulmonary- edema, fibrosis, embolism, hypertension Leads to hypoxemia Oxygen saturation falls 7.0. eg., HCO3 PaCO2: Pressure or tension exerted by dissolved CO2 gas in blood PaO2: Indicates the level of oxygenation of arterial blood Metabolic – refers to a disorder from an alteration in HCO3 - influenced by the kidneys Respiratory – refers to a disorder from an alteration in CO2 - influenced by the lungs  Acid-base Balance Compensation may occur Body attempts to keep pH in normal range Respiratory compensation: lungs can modulate how much CO2 is retained or excreted Metabolic compensation: Kidneys can modulate how much HCO3 is retained or excreted Acute vs. chronic compensation determines risk  Lung Function Testing Two main tests Spirometry A spirometer objectively assesses an individual’s pulmonary performance Measures how much air you can move in and out of lungs Peak-flow meter Utilized in people with asthma Used by an individual to compare current results to personal best  Lung Function Testing Spirometry will measure several indices of lung function Lung volumes: Tidal Volume Inspiratory Reserve Volume Expiratory Reserve Volume Residual Volume Lung capacity: Total Lung Capacity Functional Residual Capacity Vital Capacity Airflow measures Forced expiratory volume in 1 second (FEV1) Forced vital capacity (FVC) FEV1 / FVC ratio  Lung Function Testing FEV1 / FVC ratio details Helps differentiate between restrictive and obstructive lung disease Obstructive = low FEV1/FVC, normal FVC Restrictive = normal FEV1/FVC ratio, but low FVC  Lung Function Testing Spirometry to determine reversibility of airway obstruction Test repeated 10-15m after inhaling a bronchodilator If FEV1 increases, obstruction is present  Effect of Fitness and Aging on Respiratory System Proper respiration requires and strong cardiovascular system Exercise causes blood flow to increase and more O2 to be consumed As fitness improves: Lungs can accommodate higher volumes of air Increased diffusion of respiratory gases Strengthens cilia and diaphragm Strengthens other muscles of inspiration / expiration VO2 max increases  Effect of Fitness and Aging on Respiratory System People who smoke have poor exercise tolerance for many reasons: Nicotine causes bronchoconstriction Lung fibrosis Excess mucous secretion Inhibited cilia Destruction of elastic fibers  Effect of Fitness and Aging on Respiratory System Age-related impact on lung function: Respiratory tissues and chest wall becomes more rigid Weak respiratory muscles Vital capacity gradually decreases Macrophages activity decreases Cilia less active  Introduction Asthma is a chronic inflammatory disorder characterized by: Paroxysmal or persistent symptoms Dyspnea, wheezing, cough, chest tightness, sputum production Airway hyper-responsiveness to a variety of stimuli  Epidemiology Over 3 million Canadians are currently living with asthma, with Canada having one of the highest rates in the world Childhood asthma is the #1 chronic condition in Canada in children Most diagnosed by age 5 15% of children between 4 & 11 8.5% > age 12 Leading cause of ER hospitalizations of children 6 out of 10 people with asthma do not have control of their condition  Etiology and Risk Factors Genetic Predisposition Hygiene Hypothesis Atopic vs non-atopic Gender Maternal factors Perinatal factors Factors during childhood Factors during adulthood  Etiology and Risk Factors Genetic Predisposition Many genes involved that influence asthma: Development of asthma → pre-disposing to atopy Severity of condition → airway hyper-responsiveness Response to therapy  Etiology and Risk Factors Environmental factors Hygiene Hypothesis Limited exposure to normal environmental stimuli may cause the allergic immunologic system to develop more than the system to fight infections Children who are at lower risk for developing asthma: Are exposed to high levels of bacteria or endotoxin Have older siblings Have early enrollment into child care Experience exposure to cats and dogs in early life In those with exposure to fewer antibiotics  Etiology and Risk Factors Atopic vs non-atopic Allergic responses can result in asthma The greater an individual’s sensitization, the higher the likelihood of asthma High levels of Immunoglobulin E (IgE) found Exposure to high levels of allergens increases likelihood of asthma House dust mite Indoor fungi Cockroach allergen Indoor animals* Farm animals  Etiology and Risk Factors Sex Childhood asthma has a greater prevalence in males Equal from age 20 – 40 Age 40: Females > males  Etiology and Risk Factors Maternal factors Increasing maternal age → lower risk of asthma Diet during pregnancy Vitamin D High omega-6 vs. low omega-3 Maternal asthma control Prenatal exposure to maternal smoking Certain medication use (acetaminophen, antibiotics, acid-suppressors)  Etiology and Risk Factors Perinatal factors Pre-eclampsia Prematurity Mode of delivery – caesarean? Breastfeeding Vitamin D supplementation  Etiology and Risk Factors Factors during childhood =Viral infections predictive of asthma later in life Respiratory syncytial virus (RSV) Human rhinovirus (HRV) Medication use in infancy Acetaminophen Ibuprofen Antibiotics Air pollution Tobacco smoke exposure Obesity  Etiology and Risk Factors Factors during adulthood Obesity Tobacco smoke (first and second-hand) Occupational exposures Rhinitis  Etiology and Risk Factors Asthma triggers Irritants Respiratory tract infections Weather Stress Hormonal fluctuations Gastro-esophageal reflux disease Medication (ASA / NSAIDs, beta-blockers) Sulfites  Pathophysiology Hallmarks of asthma pathology: bronchial hyper-reactivity bronchial inflammation Airway obstruction (bronchoconstriction, mucous plugs) LINK  Pathophysiology Physiology of bronchial hyper-reactivity Begins with sensitization to an allergen Allergen exposure → production of specific IgE antibodies IgE production regulated by Th2 cells Th2 over-expressed in sensitized individuals → activated by dendritic cells IgE antibodies then bind to mast cells Subsequent exposure to allergen → binds to IgE antibody on mast cell → release of mediators Various mediators released: Histamine Leukotrienes Cytokines Tumor necrosis factor-alpha (TNF-a)  Pathophysiology Physiology of bronchoconstriction Allergen induced bronchoconstriction: Mast-cell mediators bind to smooth muscle, causing bronchoconstriction Non-allergen induced: Irritants Exercise Cold air NSAIDs or ASA Stress Occurs through three mechanisms Spasmodic state → from the parasympathetic nervous system releasing acetylcholine Inflammation of bronchi Excessive mucous production  Pathophysiology Physiology of bronchial inflammation Early phase reaction Occurs within several minutes of inhalation of allergen Mast cells release mediators → histamine and leukotrienes acts quickly Leads to bronchospasm and constriction Late phase reaction Occurs within hours Cytokines and TNF-a recruit inflammatory cells Continued bronchospasm and constriction Inflammation builds Hyper-responsiveness increases Continued inflammation eventually leads to airway remodeling  Pathophysiology Physiology of airway remodeling Remodeling is irreversible! Increases airflow limitations and exacerbation of previous processes Pathologic changes: Vascular dilation Edema Subepithelial fibrosis Epithelial damage Inflammatory cell infiltration Smooth muscle hypertrophy Mucous gland hypertrophy Sub-basement membrane thickening  Clinical Presentation Intermittent episodes of wheezing, cough and dyspnea Chest tightness and chronic cough in some Symptoms often worse at night or upon waking Presence of repeatable triggers Possible signs of atopy Wheezing video  Clinical Presentation Lung function testing results FEV1/FVC +12%) Sensitive to bronchoprovocation testing  Prognosis and Complications Complications Asthma exacerbation – status asthmaticus Episode of worsening asthma symptoms, lung function, and hyper- responsiveness Most common in those with underutilized anti-inflammatory therapy Feedback loop: inflammation → increased bronchial hyper-responsiveness → increased infiltration of allergic and inflammatory mediators → bronchoconstriction and obstruction (air-trapping) → inflammation… Can progress without treatment and become life-threatening Most common reason for hospitalizations in asthmatics 5-10% of cases require ventilator support and ICU admission 0.5-3% mortality rate  Prognosis and Complications Complications Asthma exacerbation – status asthmaticus Unresponsive to bronchodilator treatment alone Must be intensively treated promptly – predict what would be used in an emergency situation If treatment is delayed: Cardiac arrest Respiratory failure Hypoxemia Pneumothorax Asthma attack video  Prognosis and Complications Complications Airway remodeling Fatigue Underperformance at work / school Inability to exercise Frequent hospitalizations Pneumonia and influenza GERD Sleep apnea  Introduction A chronic respiratory condition characterized by: Persistent symptoms Airflow limitation and narrowing airways Chronic inflammation Mucociliary dysfunction Mix of Obstructive bronchiolitis (chronic bronchitis) and Emphysema  Epidemiology Affects approximately 5% of Canadians >35 years old 85% of COPD deaths mainly caused by continued smoking or exposure 4th leading cause of death in Canada; only chronic illness with increasing mortality 3rd leading cause of death world-wide  Etiology and Risk Factors Exposure to particles Cigarette smoking most prominent cause General air quality and pollution Airway responsiveness Higher responsiveness increases COPD risk Genetic polymorphisms Matrix Metalloproteinases (MMPs) excess Alpha-1 antitrypsin deficiency Old Age  Pathophysiology Emphysema Refers to airway collapse due to loss of lung recoil caused by alveolar wall destruction Caused by an imbalance between proteolysis and anti-proteolysis in the lungs Elastase is the main enzyme responsible for proteolysis in the lungs Produced by neutrophils and macrophages Irreversibly inhibited by alpha-1-anitrypsin MMP also involved LINK Leads to: Air trapping Impaired gas diffusion Lung hyperinflation  Pathophysiology Chronic Bronchitis Chronic inflammation of the bronchioles leads to several changes Increased oxidative stress and inflammatory mediators Increase in goblet cells → mucous hypersecretion Hyperplasia of submucosal mucous glands Ciliary dysfunction Fibrosis and thickening of bronchiole walls Edema and smooth muscle contraction All of the above lead to narrowing of small airways and obstruction  Clinical Presentation Presentation depends on pathology: emphysema, chronic bronchitis, or mixed Emphysema – “pink puffer” Chronic bronchitis – “blue bloater” Shortness of breath Shortness of breath Barrel chest Chronic productive cough Enlarged lungs Excessive mucous production Weight loss Wheezing Pink skin Pulmonary hypertension (due to Accessory muscle use alveolar hypoxia shunting blood to Pursed lip breathing healthy alveoli) Hypoxemia/co2 Weight gain Peripheral edema Cyanosis Hypoxemia Hypercapnia (resp acidosis) Right-sided heart-failure Fluid retention These represent the extremes! Mixed type presentation is more likely  Prognosis and Complications Prognosis COPD is progressive; cannot halt decline of lung function and FEV1 Depends on severity of disease, management of comorbidities, level of fitness Predictors of mortality Low FEV1 and rate of decline Continued smoking Low BMI (