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Chapter 13 – Respiratory Physiology ReviewDalton’s Law – partial pressures Partial pressure: The pressure exerted by an individual gas in a mixture. > P(partial) = P(total) x [fractional gas concentration]Dalton's Law: the total pressure of a mixture of gases equals the sum of partial pressures of the different gases in the mixture. -Gas flows from high to low pressure along a pressure gradient.-This can be seen when we look at partial pressures of inhaled air versus air in the alveolar sacs, and why oxygen (PO2) goes INTO the alveoli from: tracheal 160-> bronchial 150-> alveolar 100 mmHg, and why carbon dioxide (PCO2) goes OUT of the alveoli from: alveolar 40-> bronchial 0-> tracheal 0 mmHg.-Gas exchange occurs between alveoli and atmospheric air (and between alveolar tissue and capillary tissue) via Simple Diffusion.1-In dry inspired air: PO2 = 160 mmHg and PCO2 = 0 mmHg 2-In humidified air in the trachea/bronchi (H2O @ 37o C): PO2 = 150(bronchi)-160(trachea)mmHg & PCO2 = 0 mmHg 3-Partial pressures of O2 and CO2 in inspired air (air in alveolar sacs): PO2 = 100 mmHg and PCO2 = 40 mmHg4-In Pulmonary arterial blood (deoxygenated): PO2 = 40 mmHg and PCO2 = 46 mmHg5-In Pulmonary venous blood (oxygenated): PO2 = 100 mmHg and PCO2 = 40 mmHgFick’s Law – diffusion of gasesFick’s Law: the net rate of gas-exchange (diffusion) across a membrane is: -proportional to the differences in partial pressure of that gas on either side of that membrane (takes “driving force” and “diffusion coefficient” into consideration) -proportional to the surface area of that membrane available for gas-exchange diffusion -inversely proportional to thickness of that membrane (very thin @ the blood-air-barrier, 0.3-0.7 ?m)*Diffusion Coefficient (D): a constant proportion of a substance that is under molar fluctuation, based on the rate of diffusion of the substance and the concentration gradient (the driving force) of that substance across the given membrane. Means that the higher the Diffusion Coefficient the faster that substance diffuses.Lung Diffusing Capacity (DL)-Is a combined measure of the diffusion coefficient, membrane surface area, and membrane thickness BUT also measures the time needed for O2 to bind Hemoglobin proteins in erythrocytes.-Is used in testing lung functionality and ability to transfer gas into and out of the blood stream (patient blows out as long as they can until the Residual Lung volume is left, then inhale a gas mixture containing small amounts of CO (carbon monoxide) and hold their breath for 10 seconds to allow CO to diffuse. By exhaling into an apparatus after, the change in CO concentration between the initial test gas and exhaled air can be used to determine the Diffusion Capacity of the lungs, since its only limiting factor is the diffusion process. -DL is affected differently by various conditions: >Emphysema: alveolar tissue damage and cell death decreases the surface area available for gas exchange, which decreases diffusing capacity (DL) >Fibrosis: increased fiber production in connective tissue (in this case collagen and elastic fibers) causes the tissue membrane to increase in thickness which decreases diffusing capacity (DL) >Pulmonary Edema: accumulation of fluid in lung tissue causes cell membranes to thicken in order to hold that fluid without rupturing, which decreases diffusing capacity (DL) >Anemia: Decreased Hemoglobin (Hb) content in Erythrocytes decreases the amount of O2 carried by each erythrocyte, which decreases diffusing capacity (DL) as the erythrocytes reach O2 saturation faster with less net [O2] diffusing. >Exercise: capillaries dilate and increase perfusion potential of blood by increasing surface area available for gas exchange, which increases diffusing capacity (DL)Perfusion-limited and Diffusion-limited Gas ExchangePerfusion-limited: If the partial pressures of the diffusing gas reach equilibrium across the alveoli and the pulmonary capillary then the blood becomes “saturated” with that gas and cannot accept any more. This also removes the partial pressure gradient, so instead of moving from high to low partial pressures, the gas diffuses in and out in equal amounts (meaning no net diffusion of O2). To re-set the gradient, blood flow circulates saturated blood out and fresh unsaturated blood in. Diffusion-limited: the diffusion rate and capacity of gases is decreased as a result of a pathological condition that affects one of the three diffusion-dependent factors: -Since gas is exchanged via Simple Diffusion, it will move down its concentration gradient -Surface area of the cell (Pneumocyte Type I) in the alveolar wall, greater surface area = increased diffusion rate/capacity. -The thickness of the membrane(s), thinner membrane = increased diffusion rate, the blood-air-barrier is about 0.3?m-0.7?m (0.5?m on average) >pathologies that limit diffusion: fibrosis and emphysema mainly, but asthma, anemia, and pulmonary edema do as well. >Exercise can INCREASE diffusionAlveoli: singular sac that groups together in multitudes to make up alveolar sac; contain collagen and elastic (elastin) fibers to facilitate expansion, macrophages, and Type I & II alveolar cells called “Pneumocytes” -Pneumocyte Type I: cells lining the alveoli, they cover the alveolar sac surface and make up the surface area for gas-exchange; are simple squamous epithelial cells with tight junctions to make up alveolar tissue, this tissue helps control the humidity of the internal environment of the alveolus (and therefore the partial pressure of the gasses) -Pneumocyte Type II: bigger cells than Type I; they are cuboidal cells meaning they create secretions, most notably Surfactant (which is composed of cholesterol, proteins and a phospholipid: dipalmitoyl phosphatidylcholine or “DPPC”), a fluid secretion that covers and lubricates the alveoli, which inhibits alveoli collapse and decreases the surface tension of the tissue so that they stay open/“inflated”. >Surfactant is more useful in smaller alveoli than in medium or large alveoli, since smaller alveoli have a smaller diameter and less structural components to support the thin, hollow sac.Surface tension of alveoli: the collapsing pressure of alveoli is caused by attractive forces between molecules of liquid lubricating the inside of the alveoli, which is proportional to the surface tension of that alveoli and inversely proportional to that alveoli’s radius. Smaller alveoli have less collagen and elastic fibers supporting their walls than medium and large alveoli do, so they are more susceptible to collapse and have higher collapsing pressure. Surfactant secretions disrupt attractive forces between molecules of alveolar liquids and inhibits collapse, especially in smaller alveoli. Respiratory Physiology-Lung Volumes- Tidal Volume (TV): 0.5L, volume of air inhaled or exhaled normally, during basal respirationInspiratory Reserve Volume (IRV): 3L, volume of air in a deep inhalation that exceeds Tidal Volume inhalation. Used in Sympathetic “Fight or Flight” via β2 receptor excitation by Norepinephrine to relax smooth muscle which dilates bronchi and increases respiration. Also used during exercise, activity, meditation, gasping, etc.Expiratory Reserve Volume (ERV): 1.2L, volume of air in a deep exhalation that exceeds Tidal Volume exhalation. Used during sighing, exercise and activity, meditation, coughing, etc.Residual Volume (RV): 1.2L, volume of air that remains in the lungs and alveolar sacs after Maximal Expiration (reaching near the full 1.2L volume of ERV). This volume cannot be measure via Spirometry, and therefore any combination volume measurement including RV cannot be measured in its entirety using a Spirometer.Dead Space (VD): volumes of gas within the Respiratory System that is not active in gas exchange >Anatomic Dead Space: ~150mL, air volume contained in the conducting portions of the Respiratory System at all times (includes nasal cavity, trachea, 1o, 2o, & 3o bronchi, and bronchioles). Air moves but doesn’t participate in gas exchange. >Physiologic Dead Space: ~1/3 of Tidal Volume, total air volume of the lungs that is not participating in gas exchange, including Anatomic Dead Space and alveoli saturated with gas but not perfusing in (no gas exchange. The volume of air in the saturated alveoli is normally negligible so Physiologic Dead Space should be roughly equal to Anatomic Dead Space in value, UNLESS the patient suffers from a respiratory condition in which ventilation (volume inhaled/exhaled per minute) or perfusion (ability of gas to move down its partial pressure gradient) is negatively impacted.-Ventilation Rates-Minute Ventilation: the volume of gas inhaled and exhaled from the lungs per minute; used diagnostically; includes a measurement of the concentration of carbon dioxide in the blood due to the inverse relationship between [CO2] and minute ventilation: -low [CO2] = high minute ventilation -high [CO2] = low minute ventilationequation: Minute Ventilation = (Tidal Volume) x (# of Breaths per minute)*Basically, if you are respiring more times per minute you will have lower [CO2] in your blood because you are exhaling it at a faster frequency than if you were respiring slowly/less times per minute.Alveolar Ventilation: the volume of O2 gas that enters the alveoli from the lungs and the volume of CO2 that leaves the alveoli from the venous blood per breath, meaning this measurement focuses on the gas exchange occurring between the alveoli and the environment of the lungs rather than between the alveoli and the blood. Focuses on the volume of fresh air entering the lungs and volume of exhaled air leaving the lungs per minute (volume of inhale vs. exhale should be roughly equal, so exhalation volume is only implied in the measurement and not included separately from inhalation volume)-Lung Capacities-Inspiratory Capacity (IC): IC = TV(inhale) + IRV = ~3.5Lthe total volume of air that can be inhaled following a normal quiet exhale of Tidal VolumeFunctional Residual Capacity (FRC): FRC = ERV + RV = ~2.4Lthe total volume of air left in the lungs following a normal quiet exhale of Tidal Volume*includes RV, so this cannot be entirely measured by a SpirometerVital Capacity(VC)/Forced Vital Capacity(FVC): VC/FVC = TV + IRV + ERV = ~4.7Lthe total volume of air that can forcefully be exhaled following a maximal inhalation*does NOT include RV, can be measured with a SpirometerTotal Lung Capacity (TLC): TLC = TV + IRV + ERV + RV = ~5.9Lthe total volume of all 4 volumetric measurements, represents the volume of air in the lungs following a maximal inhalation.*includes RV, so this cannot be entirely measured by a SpirometerForced Expiratory Volume (FEV1): FEV1 = FVC x 0.8 or FEV1÷FVC = 0.8the volume of air a patient is capable of forcibly exhalating within 1 second, “in the first second of a forced maximal exhalation”; FEV1 volume is normally 80% of the patient’s FVC volume. >In patients with Obstructive Respiratory Diseases: FEV1 decreases more than FVC, so the FEV1÷FVC ratio decreases (<0.8). Diseases include Asthma, COPD (bronchitis and emphysema). >In patients with Restrictive Respiratory Diseases: FEV1 decreases less than FVC, so the FEV1÷FVC ratio increases (>0.8). Diseases include Fibrosis, Pulmonary Edema.*Obstructive & Restrictive Respiratory Diseases both reduce FEV1 & FVC but in different ways.Breathing MechanicsInspiration: >Diaphragm: used in all respiration, main muscle in normal breathing; a wide muscle that marks the separation between the Thoracic cavity and the Abdominal cavity. Upon inhalation the thoracic diaphragm contracts and moves down to increase the space in the thoracic cavity for the lungs to expand in. Upon exhalation the thoracic diaphragm relaxes and expands, moving upward to decrease the space in the thoracic cavity to help expulsion of air (passive exhalation). -innervated by the Phrenic nerve (cervical spinal nerve roots C3, C4, C5) >External Intercostal muscles: used in forced inhalation (exercise, “fight or flight”); are the outermost layer of rib muscles; work alongside additional muscles such as Sternocleidomastoid, Pectoralis Major/Minor, Scalene and Subcostal muscles.Expiration: (specifically: forced exhalation due to activity, coughing or disease) >Abdominal muscles: such as External & Internal Oblique muscles and Transversus Abdominus muscle; upon contraction it compresses the abdominal cavity, pushing internal organs and diaphragm upwards, which compresses the thoracic cavity and lungs to expel air. >Internal Intercostal muscles: muscles between each pair of ribs, contract to pull the ribs down and in to compress the thoracic cavity and lungs to expel air.Breathing CycleWithin a breathing cycle intrapleural pressure is negative @ -3 cm H2O before inhalation because of opposing forces: the lungs are trying to collapse, and the chest wall is trying to expand, in addition alveolar pressure is roughly equal to atmospheric pressure (~760 mmHg). During inhalation the diaphragm contracts/thoracic cavity expands and intrapleural pressure decreases to -6 cm H2O because of the increase in air volume in the lungs and the elasticity of the lungs that allows their expansion; alveolar pressure decreases (<760 mmHg). In normal expiration intrapleural pressure returns to -3 cm H2O, alveolar pressure rises slightly above atmospheric pressure (>760mmHg); and the cycle repeats.Nervous System Control of BreathingMedullary Respiratory Center in the Brain Stem: Afferent Sensory information from Chemoreceptors, Lung Stretch Receptors, Irritation Receptors, Juxtacapillary Receptors, and Joint/Tendon/Muscle Receptors is relayed to the Medulla Oblongata by CN X (Vagus) and CN IX (Glossopharyngeal) cranial nerves. The Efferent response information leaves the Medulla Oblongata and is relayed to the Thoracic Diaphragm by the Phrenic nerve (C3-C5). Apneustic Center in the Brain Stem: Lower Pons, stimulates Apneusis (abnormal gasping with pauses before incomplete exhale) and inhalation.Pneumotaxic Center in the Brain Stem: Upper Pons, inhibits involuntary inhalation (giving us the ability to hold our breath, swim underwater, etc) and controls inhalation volume and breathing rate.Oxygen and Carbon Dioxide in the Blood -Dissolved O2: (see Henry’s Law below) for a given PO2, [O2] in the blood is directly proportional to the solubility of O2 in blood. -Bound O2: 4 molecules of O2 are bound to one Hemoglobin (Hb), -O2 is NOT found Chemically modified in the blood, it is ONLY found in Dissolved and Hb-bound forms.-Dissolved CO2: (see Henry’s Law below), low amounts of free dissolved CO2 are found in the blood-Bound CO2: low amounts of CO2 are bound by Hemoglobin and Plasma proteins in the blood-Chemically Modified CO2: the majority (80-90%) of CO2 is found as Bicarbonate (HCO3-) in the bloodHenry’s Law-this law deals with gas exchange that occurs between the alveolar sac and the pulmonary capillaries.Henry’s Law: the amount of a gas that dissolves in a liquid (blood) is directly proportional to the gas’ partial pressure when in equilibrium with that liquid (@ constant temperature), meaning that if two gases have the same partial pressure: >more soluble gases will have a higher concentration of molecules dissolved in the blood >less soluble gases will have a lower concentration of molecules dissolved in the blood*this is pretty much saying that the solubility of a gas when dissolving into the blood (and its ability to reach equilibrium along a gradient) depends on the partial pressure of the gas. -the partial pressure (and concentration) gradient that gas moves along is between its gaseous form (in the alveolus) and its dissolved form (in the blood): >PO2 = 100 mmHg in alveolar air and PO2 = 40 mmHg in the pulmonary artery (deoxygenated blood), so O2 will want to dissolve into the deoxygenated blood. >The opposite occurs with CO2, where PCO2 = 46 mmHg in pulmonary artery (deoxygenated blood) and PCO2 = 40 mmHg in alveolar air, so it will want to diffuse out of blood and into the alveolus in its gas form.*N2 nitrogen gas (~78% of the air we breathe) is only ever carried in its dissolved form and is never bound by Hemoglobin (Hb), and never consumed as we are not a “nitrogen-fixing” species. Nitrogen in its gaseous N2 form is chemically useless to us and stays in the blood as-is. Ultimately it is exhaled in the same amounts it was inhaled in without ever undergoing chemical modifications.Airflow/Airway ResistanceAirflow (Q): defined by/directly proportional to the difference in atmospheric pressure (in units of mL/minute or L/minute) between the oral-nasal cavity and the alveoli (which decreases as the air moves internally)-Airflow is also inversely proportional to Airway Resistance (R), meaning as one increases the other decreases (the opposite is also true). Airway Resistance (R): resistance in the bronchi to air flow upon inhalation/exhalation (in units of “cm H2O/L/second”), most common in medium-sized bronchi. Some neurological factors include: -Parasympathetic stimulation: contraction of bronchial smooth muscle increases airway resistance >irritation, inflammation, anaphylaxis (in allergic reactions and in asthma) all increase airway resistance, which decreases airflow as the airway constricts.-Sympathetic stimulation: stimulation of β2 receptor by Norepinephrine or an Agonist (such as Isoproterenol/Isoprenaline or Albuterol [more specific to β2]) dilates the bronchial smooth muscles to decrease airway resistance, which increases airflow as the airway opens up.-Lung volume: low volume of air in lungs = increased airway resistance, while high volume of air in lungs = decreased airway resistance (due to more turbulent inhale/exhale needed to increase lung volume)-Density/Viscosity of gas in air: >Directly proportional to air flow resistance (if one increases so does the other, opposite is true) >keep in mind that gas density is affected by atmospheric pressure (directly proportional) as well. ................
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