Respiratory System Lecture Notes PDF

# Lecture #1 Respiratory System ## Respiration * External respiration refers to the exchange of oxygen & CO₂ between the external environment & the cells of the body. * Exchange between air & lungs * Alveoli, where gas exchange occurs. * Exchange between lungs & blood * Goes from...

# Lecture #1 Respiratory System ## Respiration * External respiration refers to the exchange of oxygen & CO₂ between the external environment & the cells of the body. * Exchange between air & lungs * Alveoli, where gas exchange occurs. * Exchange between lungs & blood * Goes from heart to lungs. * Pulmonary circulation. * Systemic circulation is lungs to heart to body (good blood). * Transport in blood * O₂ transported from lungs to tissues. * CO₂ transported from tissues to lungs. * Mainly in the circulatory system. * Exchange between blood & cells * Deliver O₂ where it needs to go (tissues cells). * Cellular respiration - happens in cells & makes CO₂ as waste. * Considered as internal respiration. ## How Respiratory & Conducting Systems Differ **Respiratory** * In the alveoli or the part above the alveoli which is called bronchioles. * Alveoli have blood vessels running past them where gas exchange occurs. * Here there is very thin epithelia lining the alveoli so gas can exchange easier. **Conducting** * Move air to get down to the alveoli. * More complex epithelium as you go up the more cilia & on the bronchi & epithelium. * Goblet cells make the mucous. * More in the conducting system. * Conducting system warms air as it moves down. * Cilliated cells - bigger airways have more. * The trachea is the biggest airway & divides into 2 main branches (bronchi), which enter the R & L lungs. * The bronchi continue to branch into narrower, shorter, numerous airways known as bronchioles where gas exchange occurs. * Clustered at the end are the alveoli where gas exchange occurs between air & blood. * The trachea & larger bronchi are fairly rigid tubes encircled by cartilaginous rings that help the airways resist compression from collapsing. * Smaller bronchioles contain smooth muscle to hold them open, but their walls are thin. ## What Happens in the Conducting Airways * **Mucuscailliary Escalation** - Tries to get anything in your lungs you don't want there to get out. * Cilia very important cause they move & push stuff along with it. * They all move in one direction. * Very important in the conducting airway. * **The Airways in Cross Section** * Conducting Airway * More involuntary. * Bronchioles are adjustable - If muscles relax up to a certain point - this is bronchodilation (this refers only to bronchioles) - they can only adjust due to less cartilage & muscle. * Bronchoconstriction - smooth muscle contracts. * It squeezes the whole tube making it more narrow. It affects how much air gets to the alveoli ## Closer Look at Alveoli * Capillaries are very small. * Blood vessels cover the alveoli. * **Alveolar Cells** - Lining the alveolus is flat cells that are important for gas exchange. These are known as Type 1 Alveolar cells. * Type 2 Alveolar cells are not used in gas exchange. * They don't need to be skinny because they are not long/skinny. * These cells make protein/fat known as surfactant which is important for breaking the surface tension in the alveolus. * Type 1 cells have fluid which can get in the way of gas exchange so surfactant fluid helps break up the surface tension of this. ## Arrangement of Thoracic * Thorax (chest wall) * Thoracic Cavity (Space Inside Thorax) * The lungs themselves cannot expand/contract on their own. Instead, they rely on the surrounding muscles to generate movement during breathing. ## Inspiration (Breathing In) * Diaphragm is the main muscle involved. * When it contracts, it moves downward & increases the size of the thoracic cavity, which allows lungs to expand. * This also stretches the lungs & increases the space inside the thoracic cavity, enabling air to flow in. * **Types of Inspiration:** * Quiet (passive breathing). Only the diaphragm contracts. No additional muscles are involved. * Active (Forced Breathing) - during activities like exercise (accessory muscles) assist in expanding the thoracic cavity further. * **Accessory muscles of inspiration:** * -Scalenes & sternocleidomastoid help lift the ribs (upper) & sternum further ↑ chest cavity volume. * These muscles are active only during forced or active inspirations. * External intercostal muscles: located between the ribs. They contract to help expand the chest cavity. ## Expiration (Breathing Out) * **Passive Expiration** - During quiet breathing, the diaphragm simply relaxes & returns to its original shape, allowing the thoracic cavity to decrease in volume & air flow out. * **Active (Forced) Expiration** -during activities like intense exercise, other muscles assist including: * Abdominal muscles - Help squeeze aid out of the lungs by compressing the chest cavity during activities like intense exercise. * Internal intercostal muscles - Pulls the ribs downward & inward, reducing thoracic cavity volume. * These muscles are only active during forced expiration. ## Volume Changes * **Inspiration** * ↑ Thoracic cavity volume, allowing the lungs to expand & air to flow in. * During active inspiration, the ↑ in volume is much greater. * **Expiration** * ↓ Thoracic cavity volume, forcing air out of the lungs. * In active expiration, the ↓ in volume is more significant due to additional muscle involvement. ## Arrangement of Lungs in Pleural Sacs * **Pleural Sacs** - Each lung is enclosed in its own pleural sac, which is a double layered membrane. * Parietal Pleura - outer layer, attached to the thoracic wall. * Visceral Pleura - inner layer, directly covering the lung. * Between these layers is the pleural cavity which is filled with pleural fluid/Intrapleural fluid. * This fluid reduces friction between the layers during breathing. * It also helps create a bond between the lung & the thoracic wall preventing the lungs from collapsing. * **Importance of the pleural cavity & fluid:** If pleura is damaged or punctured, air/fluid can enter the pleural cavity, disrupting the pressure balance & potentially causing the lung to collapse. ## Mechanics of Breathing: Roles of Alveolar & Pleural Pressure * When volume changes, pressure changes in the opposite direction. * **Inspiration:** * Lung volume ↑ & Pressure ↓. * Lower pressure inside the lungs allows air to flow in. * **Expiration** * Lung volume ↓ & Pressure ↑. * Higher pressure inside the lungs pushes air out. ## Atmospheric & Alveolar Pressure * **Atmospheric Pressure** - The pressure outside the body. Air pressure is 760mmHg on an average day. * **Alveolar Pressure (PA)** - Pressure inside the alveoli (air sacs in the lungs). * Can change during breathing. * At rest, the alveolar pressure & atmospheric pressure are equal & it is 0. * During inspiration, alveolar pressure is lower (-) than atmospheric pressure * During expiration, alveolar pressure is higher (+) than atmospheric pressure. ## Pleural Pressure * **Pleural Pressure** - Pressure between pleural membranes. * Always negative & never positive. * Never ever higher or lower than atmospheric pressure. * If pleural pressure becomes 0/positive, the chest wall & lung detaches from the chest wall. ## Elasticity & Recoil of Lung * Lungs have natural recoil, meaning they return to their original shape after stretching. * **Importance of lung - thorace cavity connection:** Pleural connection is vital for lung expansion. Laxing this connection causes the lungs to collapse, as they cannot expand on their own. ## Pneumothorax & Pleural Pressure * Normal intrapleural pressure is naturally always negative relative to atmospheric pressure, unless there's an issue such as a pneumothorax (collapsed lung). * **Spontaneous Pneumothorax** - This can occur due to respiratory diseases that cause damage or, in rare cases, extreme physical exertion (ex high impact sports). * Small tears may heal on their own; however, larger tears often require surgical intervention. * **Traumatic Pneumothorax** * Caused by trauma, such as a puncture to the chest cavity that breaches the chest wall. * When the chest cavity is punctured, the seperation of the pleural membranes conses the lungs to collapse. * This resulb in the lungs no longer being attached to the chest wall. * Lungs shrivel like a deflated balloon. * Pleural pressure rises to 0 (equal to atmospheric pressure). * Affected lung becomes non-functional because air can no longer enter it. ## Law of Laplace + Alveolar Stability * Alveoli vary in size, with some smaller & others larger. * Each alveolus has a thin fluid layer surrounding it, primarily composed of water. This fluid layer is subject to surface tension due to water molecules, creating a natural tendency to stick together. * **Small Alveoli** - Water molecules are closer together, making them more prone to collapsing inward. * **Large Alveoli** - Water molecules are farther apart, reducing the risk of collapse. ## Role of Surfactants * Surfactants produced by Alveolar Type 2 cells, disrupt water molecules cohesion, reducing surface tension. * In small alveoli, surfactants are more concentrated. * In large alveoli, surfactants are less concentrated, as the risk of collapse is lower. * Without surfactants, small alveoli would collapse due to surface tension. ## Respiratory Cycle 1. **Just before inhalation (after exhalation)** - Alveolar pressure is 0 (equal to atmospheric pressure). Pleural pressure remains negative due to the separation of membranes. * As the separation ↑, the pressure becomes more negative. * No muscle contraction occurs at this stage. 2. **Inspiration Onset** - Inspiratory muscles contract, ↑ lung & volume. * Alveolar pressure drops (becomes negative) creating a pressure gradient that draws air into the lungs. * Pleural pressure becomes more negative as the chest wall expands. 3. **End Inspiration** - Air continues to flow into the lungs briefly after muscle contraction stops. Alveolar pressure returns to 0 as pressure gradient equalizes. * At this point, lung volume is at its maximum & pleural pressure is at its most negative. * No muscles contracting. 4. **Expiration Onset** - The diaphragm relaxes, ↓ lung & alveolar volume. * Alveolar pressure rises above atmospheric pressure (becomes positive), pushing air out. * Pleural pressure returns to baseline (-5) then back to -5. * A minus means air goes in & a plus means air flows out. * The cycle repeats with one inhalation & one exhalation, comprising a single respiratory cycle. ## Rate of Airflow * Rate of airflow correlates with alveolar pressure changes (graph). * During rapid alveolar pressure changes (ex inspiration onset) airflow is fast. * At 0 alveolar pressure, airflow slows as the pressure gradient diminishes. ## Volume of Air Movement * Lung volume during inspiration & during expiration. At the end of expiration, no air remains in motion. ## How do we move gas in the body * Time for gas transport & exchange. * Exchange of air in the alveoli between the lung and blood. * O₂ rich and CO₂ poor. * Exchange is between blood & tissues. * O₂ poor and CO₂ high. * Gases largely diffuse due to the difference in partial pressure. * Remember that there are a lot of things that influence diffusion across a membrane (notes). ## Factors Affecting Diffusion * Surface area (larger SA = faster diffusion.) * Thickness of the membrane (thinner = faster diffusion) * Partial pressure gradients (greater differences = faster diffusion). ## Air is a Mixture of Gases * Total atmospheric pressure is the sum of the partial pressures of individual gases. * Patm = 760 mmHg. * Poz = Patm X % of gas. * Air is always 21% O₂ so Poz = 100 mmHg. ## Why Does Air Change With Altitude? * Air is always 21% O₂ so why does oxygen content change with elevation (notes)? * At higher altitudes, atmospheric pressure decreases. Lower pressures reduce the partial pressure of O₂, making it harder for the body to take in O₂. * Mount Everest's atmospheric pressure can drop to 250mmHg, normal is 760 mmHg ## These are some numbers to know * **Left side: Pulmonary Circulation** - Blood flows from the heart to the lungs & back to the heart. * Goal is removing CO₂ & replenishing O₂. * **Inspiration** - Air enters lungs containing high O₂ & low CO₂. * High O₂ allows O₂ to diffuse into the blood, while low CO₂ enables the removal of CO₂ from the blood. * **Pulmonary blood flow:** * Deoxygenated blood when blood low in O₂ & travels to the lungs for exchange. * Oxygenated blood when blood high in O₂ leaves the lung. ## Pulmonary Exchange * **Before Exchange** - Blood is containing low O₂ (40) & high CO₂ (46). * **After Exchange** - Blood is high in O₂ (100) & ​low in CO₂ (40). ## Ideas Impact of activity * When active, your cells produce more CO₂ due to ↑ cellular respiration. * **Right side: Systemic Circulation** - Blood flows from the heart to the tissues & back. * Good blood is delivered to tissues while poor blood returns to the heart. ## Gas Exchange * O₂ is 100 before but drops below 40 & can go as low as 20 with high activity. * CO₂ is 40 before & increases above 46. * CO₂ is then transported to the lungs to be exhaled. * **Venous blood:** Referred to as used up blood & found in veins. * **Arterial blood:** Referred to as good blood. ## How is O₂ Transported * Plasma carries tiny % of O₂ (2%). * Most O₂ binds to Hb (on RBCs). * Reversible reaction so can be bound or O₂ just alone. * **Oxyhemoglobin** is O₂ that is bound. ## Hemoglobin * 4 globular proteins, each with heme group. * Each heme group has an iron. * Each iron carries one O₂. * **Conformational changes & affinity** (notes). * **Structure:** * Made of 4 globular proteins, each with 3-dimensional structure. ## Affinity * Easier for the first O₂ to bind to Hb. * After O₂ binds, the structure changes, ↑ affinity for subsequent O₂ molecules. * Binding of the 2nd & 3rd O₂ is easier, but the 4th O₂ is harder to bind. ## Carbon Monoxide * Competes with O₂ & binds more tightly to Hb than O₂. * It blocks O₂ binding. * If high CO, then need hospital & high O₂ to reverse binding. ## CO₂, H+ & O₂ * All have separate binding sites & don't compete with each other. * Can have conformational change & binding difficult. ## O₂ Saturation Curves * **Y-axis:** % of Hb saturated with O₂. * **X-axis:** Partial pressure of O₂ (PO₂). * **Key Points:** * PO₂ = 100mmHg (lungs), hemoglobin saturation is 100%. * PO₂ = 40 mmHg (tissues), saturation is 75%. * During exercise, PO₂ in tissues drops to 20, & Hb saturation decreased to 30% facilitating O₂ delivery to tissues. ## Anemia * Despite fewer RBCs/less hemoglobin, anemia appears normal on the saturation curve. * However, total O₂ content is lower. ## Oxygen Saturation (Dissociation) Curve * Curve shows the relationship between O₂ levels & hemoglobin saturation. * Binding changes with each additional O₂ molecule, so the saturation curve of Hb is not linear. ## Notes * 1st O₂ is hard to bind, but subsequent bindings are easier. * Release of O₂ occurs in tissues where PO₂ is lower. ## Plateau Phase * At high PO₂, Hb is nearly fully saturated (97-100%). * This phase ensures a safety margin for O₂ supply even when PO₂ drops slightly. * Nearly all 4 Fe on all Hb are bound to O₂ - this ensures O₂ delivery to tissues that need it most, especially during exercise. * Look at Graph ## How can Someone with Anemia Have 100% Saturation but Poor O₂ Content? * Anemia affects the total O₂ carrying capacity of the blood but not the oxygen saturation of Hb. * **Oxygen Saturation** - refers to the % of Hb that is bound to O₂. Even in anemia, the Hb present in RBCs can still become fully saturated with O₂ when exposed to normal levels of O₂ in the lungs (PO₂ around 100). Thus, the saturation curve looks normal. * **Reduced Hb levels** - In anemia, the total amount of Hb is reduced because there are fewer RBCs or less Hb in each RBC. While the Hb present is fully saturated, there is less of it available to transport O₂ to tissues. ## Thoracic O₂ Content * O₂ content is the total amount of O₂ in the blood, which depends on both: * The Hb concentration. * The O₂ saturation level. * If Hb levels are low, the total O₂ content will be reduced, even if Hb is 100% saturated. Even with normal O₂ saturation, tissues recieve less O₂, leading to symptoms like fatigue, weakness & shortness of breath. ## O₂ Binding to Hb * Hb picks up O₂ in the lungs to transport it to tissues where it's needed. * Importance of balance: * If O₂ stays bound too tightly, it won't be delivered to tissues. * We want to store it, but we don't want it to irreversibly bind it, because we need it in free form to diffuse into the tissues. ## Normal Curve (Red line) * **Alveoli (lungs):** PO₂ = 100, Hb is 100% saturated. * **Normal resting cells:** PO₂ = 40, Hb is 75% saturated. * **Exercising cells:** PO₂ = 20, more O₂ is released to meet higher demand. ## Curve Shifts * **Curve shifts** indicate a ↑ or ↓ in the affinity of Hb for O₂, making it easier or harder to release O₂ to tissues. * **R Shift:** Indicates a ↑ in Hb's affinity for O₂, making it easier to release O₂ to tissues. O₂ is more likely to bind. * **L Shift:** Indicates a ↓ in Hb's affinity for O₂, making it harder to release O₂ to tissues & more likely to bind. * Less common but occurs in certain conditions. ## Cause of Curve Shifts * **Right Shift** (easier release of O₂) * **Exercise:** Tissues need more O₂. * **↑ PCO₂:** Higher CO₂ levels move the curve to the right, making O₂ more available for tissues. * **↑ Temp:** Heat from active muscles. * **↑ Acidity:** More CO₂ in the blood makes it more acidic (produces H+ ions). Higher acidity reduces Hb affinity for O₂. * **2,3 Bisphosphoglycerate (BPG):** By product of metabolism, sometimes called diphosphoglycerate. ↑ during intense activity as muscles work harder & metabolize more - O₂ can be unloaded off to tissues.