Respiratory System Notes 2024 PDF

Respiratory System Chapters 17 & 18 The material from chapter 17 is covered in today’s lecture. External Respiration vs Cellular Respiration Most cells rely primarily on cellular respiration for generating the ATP they need for carryi...

Respiratory System Chapters 17 & 18 The material from chapter 17 is covered in today’s lecture. External Respiration vs Cellular Respiration Most cells rely primarily on cellular respiration for generating the ATP they need for carrying out cell processes. Cellular respiration converts energy in bonds of nutrient molecules to energy in bonds of ATP. Requires O2 and produces CO2 Blood high in O2 External respiration is the exchange of gases Blood (specifically O2 and CO2 ) between the high in CO2 atmosphere and the cells of the body. External respiration is how the cells of the body get the O2 they need and how they get rid of their CO2 Pulmonary Circulation: delivers blood high in CO2 to the lungs from the tissues and returns blood high in O2 to the heart that pumps it to the tissues. Right ventricle → pulmonary trunk → lungs → pulmonary veins → left atrium  Respiratory System Functions: Exchange of gases between the atmosphere and the blood. – Cells need O2 for cellular respiration to generate the ATP they need. – Cells produces CO2 as a waste product of cell respiration that must be removed from the body. Homeostatic regulation of body fluid pH Protection from inhaled pathogens and irritating substances. Vocalization. Respiration can be divided into 4 processes: 1. Ventilation: exchange of air between the lungs and environment Two phases: Inhalation (Inspiration): Movement of air into the lungs. Exhalation (Expiration): Movement of air out of the lungs.  Respiration can be divided into 4 processes: 2. Exchange of gases between the air in the lungs and the blood. Occurs across the alveolar-lung capillary interface. 3. Transport of Gases (CO2 & O2) by the blood between the lungs and the capillary beds in the tissues of the body. 4. Exchange of gases (O2 & CO2) between the blood and the tissues. Occurs across the walls of the capillaries in the tissues.  Anatomy of the Respiratory System Respiratory system consists of: Conducting System (airways) Alveoli (interface between air and blood) Bones and Muscles of thorax  Anatomy of the Respiratory System: Airways The airways connect the air in the environment to the gas exchange surface in the lungs. The airways can be divided into the upper respiratory tract and the lower respiratory tract. Secondary bronchi Tertiary bronchi Bronchioles Cardiac alveoli notch  Anatomy of the Respiratory System: Airways Elastic fibers in the walls of the alveoli allow them to expand during inhalation and recoil during exhalation. The walls of the alveoli are surrounded by capillaries. All gas exchange between the blood and the air occurs across the alveolar-capillary interface.  Anatomy of the Respiratory System: Alveolar structure The walls of the alveoli consist of mostly of squamous epithelial cells (Type I alveolar cells) as do the walls of the capillaries. This provides a thin surface area across which gas exchange can occur. The total gas exchange surface area provided by alveoli in both lungs is equal to the surface area of a tennis court. Type II alveolar cells secrete a lipoprotein that acts as a surfactant (more later). Gas exchange  Anatomy of the Respiratory System: Airways In addition to being passageways for conducting air, the airways serve three functions: 1) Warm air being inhaled and remove heat from air being exhaled. - Helps in maintaining a constant body temperature. 2) Humidify air being inhaled and dehumidify the air being exhaled. - Helps prevent dehydration of the body. 3) Filter pathogens and dust particles from inhaled air, preventing them from reaching the gas exchange surface area in the alveoli. Anatomy of the Respiratory System: Airways To carry out the function of filtering pathogens out of inhaled air, the airways (except the alveoli) are lined by a specialized ciliated epithelium called respiratory epithelium (see picture below). The goblet cells of the respiratory epithelium secrete mucous into the airways that traps dust particles and pathogens and prevents them from reaching the alveoli. The mucus layer floats on a watery saline layer that is also secreted by the epithelium. Anatomy of the Respiratory System: Airways The cilia of the respiratory epithelium in the lung airways, trachea, and larynx push the mucus up and out through the larynx into the lower pharynx. The cilia of the respiratory epithelium lining the nasal cavity push the mucus back towards the upper pharynx. Most of this mucus is swallowed into the stomach where stomach acid kills the pathogens and dissolves dust particles. The mucus also contains antibodies that bind and disable pathogens. Infections and other irritations of the airways increases mucus production and may result in clogging airways. Coughing serves to loosen the mucus and clear the clogged airways.  Anatomy of the Respiratory System: Airways Cystic fibrosis is a genetic disease in which there is a loss of saline secretion. As a result the cilia of the respiratory epithelium can’t move the mucus as effectively and the mucus and trapped pathogens accumulate in the lungs. This predisposes people with this disease to recurring lung infections.  Anatomy of the Respiratory System The lungs are contained within a double walled membrane called the pleural sac. Outer wall of the pleural sac lines the inside of the thoracic wall and the inner wall of the pleural sac lines the surface of the lungs. The space between the outer and inner walls of the pleural sac is called the pleural space. The pleural space is filled by a small layer of fluid called the pleural fluid. AKA: Intrapleural space Lung Lung Walls of Heart Pleural sac  Anatomy of the Respiratory System The pleural fluid allows the surfaces of the lungs and thoracic wall to slide across each other as the lungs inflate and deflate during breathing. The pleural fluid also forms a fluid attachment between the outer wall of the lung and the thoracic wall. This fluid attachment keeps the lungs always partially inflated making it easier to expand the lungs during inhalation.  Anatomy of the Respiratory System: Muscles Used for Lung Ventilation Muscles of expiration are not Help the active during external normal quiet intercostals breathing! lift the rib cage Pulls rib cage down & in Expands rib cage up and out Squeeze abdominal contents up Expands chest into thoracic cavity cavity downward  The Universal Gas Laws The universal gas laws are the rules that govern the movement of gases, like O2 and CO2. To understand how the respiratory system works, you must know these laws. The three laws in the table below govern the movement of gases into and out the lungs.  The First Gas Law: Dalton’s Law According to the first gas law (Dalton’s Law): The total pressure of a mixture of gases is equal to the sum of the individual pressures of the gases in the mixture. This can be expressed by the formula: Ptotal = P1+P2+P3+…Pn Where P1 = the pressure of gas 1. This is referred to as the partial pressure of gas 1, etc. The earth’s atmosphere is a mixture of gases. The gases in the atmosphere include: N2 (78%), O2 (21%), CO2 (0.03%), other gases contribute 0.9%. So, most of the atmosphere is not oxygen!  The First Gas Law: Dalton’s Law Normal average atmospheric pressure at sea level is equal to 760 mmHg The partial pressure of a gas in a mixture can be calculated using the formula Pgas = Patm  % of gas in atmosphere So according to Dalton’s Law, Patm = PN2 + PO2 + PCO2 + Pother = 760 mmHg Given 78% 21% 0.03% 0.9% Pgas 593mmHg 160mmHg 0.25mmHg 6.77mmHg Water Dilutes the gases in the mixture  The Second Gas Law The second gas law states that a gas, whether individual or in a mixture, will flow from regions were it is in higher pressure to regions were it is in lower pressure. So, it follows: - That air flow occurs only when there’s a pressure gradient. - To move air into and out of the lungs there has to be a changing pressure gradient between the atmosphere and the air in the lungs. ->To move air in the pressure inside the lungs has to be lower than atmospheric pressure. ->To move air out the pressure inside the lungs has to be higher than atmospheric pressure. ->Expansion and contraction of the thorax during breathing creates pressure differences that moves air in and out of the lungs. In a mixture of gases, an individual gas will also move down its pressure gradient. Ex. PO2 PO2 Important when we discuss alveoli-blood and blood-cell gas exchange.  The Third Gas Law: Boyle’s Law Boyle’s Law states that if the volume of a container of gas changes, the pressure of the gas in the container will change in the opposite manner. Decrea se volume Increas e pressu re  Lung ventilation: Summary of the Principles of Airflow A gas will flow from regions were it is in higher pressure to regions were it is in lower pressure. Air moves into and out of the lungs as a result of a changing pressure gradient. Resistance to flow in the airways follows the same principles as blood flow. – radius of the airways determines resistance to airflow. R a 1/r4, so r R airflow through the airways.  Lung ventilation A single respiratory cycle consists of an inspiration during which air moves into the lungs, followed by expiration during which air moves out of the lungs. During lung ventilation, airflow (AF) through the airways is directly proportional to the pressure difference between the inside of the lungs and the atmosphere, and is inversely proportional to the resistance to airflow in the airways. This can be expressed by the formula: AFa P/R Where  P = pressure difference R = Resistance to airflow Lung Ventilation According to the 2nd Gas Law, to move air into the lungs during inspiration, the air pressure inside the lungs has to be lower than atmospheric pressure. And, to move air out of the lungs during expiration, the air pressure inside the lungs has to be greater than atmospheric pressure.  Lung Ventilation: Pressure Changes during Quiet Breathing The movement of air during lung ventilation results from a changing pressure gradient. The pressures shown below are relative to atmospheric pressure. Pleural pressure changes are caused by volume changes in the pleural space due to thoracic pleural membrane movement. Tidal There is always about 1 liter of air in the lungs, volume even when you fully exhale. This volume of air that is can’t be exhaled is called the Residual volume. Lung Ventilation: Inspiration During normal, quiet breathing the active part of lung ventilation (i.e. the part requiring muscle contraction) is the inspiratory phase. The primary muscles involved in inspiration are the diaphragm and the external intercostals. These muscles are assisted by the scalene and the sternocleidomastoids.  Lung Ventilation: Inspiration When the diaphragm contracts, it pulls downward, and the external intercostals, scalenes and sternocliedomastoids lift the ribs up and out. The actions of these muscles serve to expand the volume of the thoracic cavity Because the lungs have a fluid attachment to the walls of the thoracic cavity via the pleura fluid, as the thoracic cavity expands, the lungs expand Diaphragm Pulls down when it contracts Lung Ventilation: Inspiration As the thoracic cavity and lungs expand, their volume increases. According to Boyle’s law, as the volume of the lungs increases the pressure inside the lungs decreases. When the air pressure in the lungs drops below atmospheric pressure, a pressure gradient is created. P atmosphere > P lungs Lung Ventilation: Inspiration According to the 2nd gas law, when the pressure inside the lungs drops below atmospheric pressure, air will move down the pressure gradient from the atmosphere into the lungs. Lung Ventilation: Expiration During normal, quiet breathing the movement of air out of the lungs is a passive process (i.e. does not require muscle contraction). When the inspiratory muscles relax and recoil back to their original positions the volume of the thoracic cavity returns to its original volume. Lung tissue have elastance that allows it to recoil to its original shape and volume. Lung Ventilation: Expiration According to Boyle’s law, as the lungs return to their original volume the air pressure inside the lungs increases. When the air pressure inside the lungs rises above atmospheric, a pressure gradient is created. Patm < Plungs According to the 2nd gas law, when the pressure inside the lungs rises above atmospheric pressure, air will move down the pressure gradient from the lungs to the atmosphere. Lung Ventilation During Heavy Breathing Sternocleidomastoid and scalene muscles increase their contraction to help in expanding the volume of the thoracic cavity and the lungs beyond what occurs during normal inspiration. This creates a greater pressure gradient that moves more air into the lungs than during normal quiet breathing. Lung Ventilation During Heavy Breathing Also, expiration becomes active (involves muscles). The internal intercostals and abdominal muscles become involved in expiration. Contraction of the internal intercostals pull rib cage down and in. Contraction of the abdominal muscles squeezes the abdominal cavity, pushing the abdominal contents upward. Both serve to squeeze down on chest cavity and lungs, creating a greater pressure gradient that pushes more air out of the lungs. The Work Effort Required to Breathe During normal quiet breathing, expansion of the lungs resulting in inhalation requires muscle contraction, i.e. it requires work effort. The work effort to expand the lungs depends on two factors: The compliance of the lung tissue. The resistance of the airways to air flow. The Work Effort Required to Breathe: Compliance Compliance is the capacity of the lung tissues to stretch. Normal lung tissue stretches easily so it has high compliance. Nevertheless, it requires work to expand the thoracic cavity and stretch the lungs during breathing. However, normally this work effort is minimal. The Work Effort Required to Breathe Diseases that affect compliance are called Restrictive lung diseases (RLD): In RLDs the lung tissue becomes stiff and so compliance is reduced. 2 common causes of RLDs: 1. Build up of scar tissue in the lungs due to exposure to airborne environmental agents (fibrotic disease): Cigarette smoke Asbestos Other chemicals Scar tissue doesn’t stretch as easily as normal lung tissue and so it takes greater work effort to stretch the lungs during inhalation.  The Work Effort Required to Breathe 2. Inadequate production of surfactant (lipoproteins) that normally mix with the fluid coating on the inner surface of the alveoli. The inner surface of the alveoli have to be kept wet to allow gas exchange between the air in the alveoli and the blood in the capillaries. The attraction between the water molecules in this fluid create surface tension that resists expansion. Some of the work of breathing is spent to overcome this surface tension. Normally, lipoproteins, secreted by the Type II alveloar cells, mix with the fluid layer lining the alveoli reducing the attraction between the water molecules and so reducing the surface tension. Substances that reduce surface tension are called surfactants. The reduction in surface tension reduces the work required to stretch of the alveoli during inhalation. If there is inadequate production of these surfactant lipoproteins, then surface tension in the alveoli will be increased and greater work effort will be required to inhale.  In adequate production of surfactant lipoproteins are the cause of Newborn Respiratory Distress Syndrome (NRDS) Synthesis of surfactant lipoproteins doesn’t reach adequate levels until about the 7th months after conception. The lungs of babies born before the 7th month of development don’t have enough surfactant to overcome the surface tension in their alveoli. As a result the lungs of these premature newborns have decreased compliance, and considerably more work effort is required for these premies to inhale. Also, the inadequate levels of surfactant lipoproteins leads to collapse of their alveoli with each exhalation. Reinflation of these collapsed alveoli contributes to the increased work effort during inhalation. If left untreated these premies die from exhaustion and decreased gas exchange. Treatment involves artificial surfactant and forced ventilation to keep alveoli from collapsing. The Work Effort Required to Breathe: Resistance to Airflow through the Airways Just like resistance to blood flow in the blood vessels, resistance to air flow in the airways is determined primarily by the radius of the airways. This relationship can be represented by the formula: R α 1/pr4 Also, just like blood flow in the circulatory system, airflow (AF) through the airways is directly proportional to the radius of the airways to the fourth power. This can be represented by the formula: AF α r4 The majority of the resistance to airflow occurs in the trachea and bronchi. This resistance is fixed (i.e. it does not vary) because the radius of these airways is fixed. This source of resistance to airflow has to be overcome to move air into the lungs. The Work Effort Required to Breathe: Resistance to Airflow through the Airways The main site of variable resistance to airflow occurs in the bronchioles (the smallest airways). The walls of the bronchioles consist of a layer of smooth muscle around a layer of respiratory epithelium. The smooth muscle in the wall of the bronchiole determines the radius of the bronchiole, similar to the way the smooth muscle in the wall of an arteriole determines the radius of the arteriole. The Work Effort Required to Breathe: Resistance to Airflow through the Airways Contraction of the bronchiole smooth muscle leads to a DECREASED bronchiole radius and BRONCHOCONSTRICTION. Relaxation of the bronchiole smooth muscle leads to INCREASED bronchiole radius and BRONCHODILATION.  The Work Effort Required to Breathe: Resistance to Airflow through the Airways 3 Main factors influence the smooth muscle of the bronchioles: 1. Level of CO2 in exhaled air. 2. Histamine from surrounding tissues 3. ANS innervation of the bronchiole smooth muscle. Of these factors, CO2 levels in the exhaled air is normally the most important. The Work Effort Required to Breathe: Resistance to Airflow through the Airways and CO2 Increased CO2 levels in the exhaled air causes bronchodilation. This increases air flow Allows the lungs to get rid of excess CO2 from the body more readily. Decreased CO2 levels in the exhaled air causes bronchoconstriction. This decreases air flow Prevents excess loss of CO2 from the body. CO2 is critical for maintaining normal blood pH.  The Work Effort Required to Breathe: Resistance to Airflow through the Airways and Histamine Histamine is released by mast cells in the lung tissues in response to tissue irritation or damage. Common cause of irritation of lung tissue is inhalation of an allergen (allergy causing agent). Histamine binds to histamine receptors on the bronchiole smooth muscle, causing bronchoconstriction. GOAL: Reduced inhalation of the offending allergen. However, this bronchoconstriction increases resistance to air flow, making it more difficult to breathe. Histamine blockers may be given as an inhalant to block the binding of histamine to the histamine receptors during an allergic reaction to reduce bronchoconstriction making it easier to breathe. The Work Effort Required to Breathe: Resistance to Airflow through the Airways and the Autonomic Innervation of Bronchiole Smooth Muscle The bronchiole smooth muscle is innervated by the parasympathetic subdivision of the ANS: This innervation uses ACh as its neurotransmitter. The Ach binds to muscarinic receptors on the bronchiole smooth muscle. Activation of these receptors causes the smooth muscle of the bronchioles to contract. So, an increase in parasympathetic activity causes BRONCHOCONSTRICTION, a decrease in parasympathetic activity causes BRONCHODILATION. There is no sympathetic innervation of the bronchiole smooth muscle! The Work Effort Required to Breathe: Resistance to Airflow through the Airways and Epinephrine The smooth muscle of the bronchioles also has β2 receptors on it. Activation of these β2 receptors causes relaxation of the bronchiole smooth muscle, and so bronchodilation. These receptors are activated by epinephrine released from the adrenal glands. Lung Ventilation and the Fight or Flight Response Goals of the respiratory system during fight or flight: To rid the body of excess CO2 produced by active skeletal muscles and cardiac muscles during the Fight Or Flight response. Supply increased O2 to the blood to meet the increased needs of the active tissues (skeletal and heart muscle).  Lung Ventilation and the Fight or Flight Response Remember, during the fight or flight response there is an increase in sympathetic activity and a decrease in parasympathetic activity, and release of epinephrine from the adrenal glands. The decreased parasympathetic activity and the epinephrine from the adrenal glands both cause bronchodilation, which results in a decrease resistance to air flow. This makes it easier to move air into/out of the lungs. Facilitates gas exchange between body and environment. Lung Ventilation and Allergic Reactions The release of histamine in response to lung tissue irritation due to an allergen causes bronchoconstriction, increasing resistance to airflow and making it more difficult to breathe. The presence of β2 receptors on the smooth muscle of the bronchioles is the reason epinephrine is administered in cases of severe respiratory distress during an allergic reaction. The administered epinephrine activates β2 receptors on the bronchiole smooth muscle causing bronchodilation. This decreases resistance in the bronchioles and results in increased air flow, making it easier to breathe.  Ventilation Efficiency Ventilation efficiency expresses the effectiveness of the respiratory system in moving air into and out of the lungs. Remember, in the CV system, CO expresses the effectiveness of the heart in pumping: Recall, CO = HR X SV This same concept can be applied to lung ventilation. Ventilation Efficiency: Total Pulmonary Ventilation (TPV) Ventilation efficiency is expressed in terms of Total Pulmonary Ventilation (TPV). TPV is defined as the volume of air moved into or out of the lungs per unit time. TPV can be calculated using the formula: TPV = Ventilation Rate X Tidal Volume = VR (brths/min) x VT (ml of air inhaled or exhaled/brth)  Ventilation Efficiency: TPV VT = Tidal Volume Tidal Volume is the amount of air moved into or out of the lungs during a single breath during normal quiet breathing. Normal adult VT = 500ml Normal adult ventilation rate (VR) = 12-18 breaths per minute. So, if TPV = VR X VT using the slowest normal VR gives a TPV of: 12brths/min X 500ml/brth = 6000ml/min Ventilation Efficiency: TPV So, what this says is that at the slowest normal ventilation rate, 6000ml of air is moved into or out of lungs each minute (TPV = 6000ml/min). Not all of the inhaled air is used in gas exchange. Some of it is used to fill the airways, and so it is not involved in gas exchange with the blood. This is called the “Dead Air” (normally about150ml out of the 500ml of the VT). So, only about 350ml of the 500ml brought into the lungs during a normal quiet breath actually reaches the alveoli and is involved in gas exchange. Ventilation Efficiency: Total pulmonary ventilation vs alveolar ventilation Because only about 350ml of the 500ml brought into the lungs reaches the alveoli and is involved in gas exchange per breath, a more accurate measure of the efficiency of lung ventilation is to calculate the volume of air that actually reaches the alveoli per minute. The volume of air reaching the alveoli per minute is termed the alveolar minute ventilation, or just alveolar ventalition (AV). Alveolar ventilation is calculated using the formula: AV = Vent. Rate X (VT – 150ml) Ventilation Efficiency: Alveolar Ventilation Using the slowest normal breathing rate (12brths/min) to calculate the AV: AV = 12brths/min X (500ml – 150ml) = 4200ml/min of air reaches the alveoli per minute at slowest normal ventilation rate.  Ventilation Efficiency There are two ways to change AV: 1. Increase or decrease VR Increase VR increased AV Decrease VR decreased AV 2. Increase or decrease depth of breathing Increase depth of breathing increased AV Decrease depth of breathing decreased AV More on this in a minute… Alveolar Gas Exchange The primary function of the lungs is the exchange of O2 and CO2 between the air in the alveoli and the blood in the lung capillaries. The primary determinant of the exchange of O2 and CO2 between the alveolar air and capillary blood is the partial pressures of these gases in the alveolar air and in the capillary blood, i.e. the pressure gradients for each gas. The PO2 and PCO2 in the alveolar air is determined by the AV. Alveolar Gas Exchange This graph shows the relationship between the PO2 and PCO2 in the alveolar air and the AV. Normal lowest AV is 4.2L/min. At this AV the PO2 in the alveolar air is 100mmHg, and the PCO2 is 40mmHg. Increasing AV will increase the alveolar PO2 and PCO2 up to an AV of 8L/min. At this AV the PO2 is 120mmHg and the PCO2 is 20mmHg. An AV of 8L/min is achieved at 22brths/min. Above this breathing rate the PO2 and PCO2 don’t change.