Respiration detailed notes for third year PDF

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SU 1: Pulmonary ventilation Muscles that cause lung expansion and contraction. Lungs can be expanded and contracted in 2 ways: 1. Downward and upward movement of the diaphragm to lengthen and shorten the chest cavity. 2. Elevation and depression of the ribs to increase and decrease diameter of the chest. Inspiration muscles 1. External intercostals. 2. Sternocleidomastoid. 3. Anterior serrati. 4. Scaleni.  diaphragm.

Expiration muscles 1. Abdominal recti. 2. Internal intercostals  diaphragm.

1) Pleural Pressure – Pip. → Pressure of fluid in space between lung pleura and chest wall. → - Pressure. → Beginning of inspiration = -5mmHg to -7.5mmHg. → - Pressure formed causes  in lung volume. 2) Alveolar pressure - Palv → Pressure in alveoli. → During inspiration = -1. During expiration = +1 → To cause an inward flow af air during inspiration the alveoli pressure must fall below Atmospheric pressure. 3) Transpulmonary pressure. – Ptp = Palv-Pip → Difference between pleura and alveolar pressure. → It measures elastic force in the lungs. During Inspiration: 1. Lung volume  due to constriction of the intercostal muscles + diaphragm. 2. Diaphragm moves . 3. Downward movement of diaphragm increases interpulmonary volume. 4.  Interpulmonary volume =  Interpulmonary pressure. • Interpulmonary pressure is 1mmHg below atmospheric pressure. • Interpulmonary pressure = 759mmHg. • Atmospheric pressure = 760mmHg. 5. O2 will flow into lung from high pressure to low pressure. During expiration 1. Lung volume  due to intercostal muscles and diaphragm that relax. 2. Diaphragm moves . 3.  Interpulmonary volume =  Interpulmonary pressure. → Interpulmonary pressure is 1mmHg above atmospheric pressure. → Interpulmonary pressure = 761mmHg. • Atmospheric pressure = 760mmHg. 4. Air moves out of lungs. Alicia Kotze 28411544 pg. 1

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Pressure of air that cause movement of air in and out the lungs.

Ventilation and lung mechanisms.

Steps of respiration

Ventilation: Exchange of air between the atmosphere and alveoli by bulk flow. Bulk flow: Important: • Pressures are given relative to atm pressure (Patm =760mmHg) at sea level. → It  in proportion to an  in altitude. Example: Palv between breaths = 0mmHg – It’s the same as Patm at any given altitude. F = 0; Palv – Patm = 0; Palv = Patm. Inspiration = Patm < Palv Expiration = Patm > Palv

→  in volume of container =  the pressure of the gas. →  in volume of container =  the pressure of the gas.

Alicia Kotze 28411544 pg. 2

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How change in lung dimension causes a change in alveolar pressure: Boyle’s Law

Inspiration 1. Activation of phrenic nerve causes diaphragm to contract. 2. Diaphragm moves . 3. Intercostal muscles contract = They move upward and outward. 4. Thoracic size . 5. Thoracic wall moves farther away from lung surface. 6. Intrapleural pressure becomes sub atmospheric. 7. Intrapleural pressure. 8. Transpulmonary pressure . 9. Transpulmonary pressure is greater than the elastic recoil exerted by the lungs. 10. Lungs expand. 11. Enlargement of lungs causes  size of alveoli. 12. Boyle’s Law = Pressure within alveoli  to less than atmospheric. 13. Palv < Patm. 14. This pressure difference causes bulk flow of air from atmosphere into alveoli. Expiration 1. At end of inspiration motor neurons to the diaphragm and inspiratory intercostal muscles decrease firing and muscles relax. 2. Diaphragm and chest wall are no longer actively pulled out. 3. They start to recoil inward. 4. Interpleural pressure becomes less atmospheric. 5. Transpulmonary pressure decreases. 6. The Transpulmonary pressure acting to expand the lungs is now smaller than the elastic recoil exerted by the more expanded lungs 7. Lungs passively recoil to their original dimension. 8. Lungs become smaller. 9. Air in alveoli become compressed by Boyles law. 10. Alveolar pressure greater than atmospheric pressure. 11. Palv > Patm. 12. Air flows from alveoli into the atmosphere. Which respiratory pressures play a role to provide for the inflow and outflow of air? - Atmospheric pressure - Alveolar pressure

Alicia Kotze 28411544 pg. 3

Lung Compliance: → The extent to which the lungs will expand for each unit increase in transpulmonary pressure. Factors that affect lung compliance: 1. Elasticity of the lung tissue. 2. Surface tension. – Forces of H2O molecules in alveoli surface. •

 In lung compliance = Lung increases in size. o Type II alveoli cells secrete Surfactants. =  Surface tension of H2O.

Surfactants Effect on surface tension: →  Surface tension of H2O molecules. → Thus  lung compliance. – easer for the lungs to expand. → Deep breathing increases surfactant production because type II cells stretch and release surfactant. After thoracic/abdominal surgery operation = Important to take deep breaths to  surfactants. Importance of surfactant on different sizes of the alveoli: - Surfactant  effect on smaller alveoli. - Reduces surface tension of small alveoli below that of larger alveoli - Stabilizes alveoli.

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Work during inspiration to provide pulmonary ventilation: 1. Compliance force • Expands the lung against the lung + chest elastic forces. 2. Tissue resistance • Overcomes the viscosity of the lung + chest wall structures. 3. Airway resistance • Moves air into the lungs. Airway resistance pathology: Asthma: → Airway smooth muscles contact strongly. → Chronic inflammation of the airways. This causes an increase in airway resistance. Medication for asthma include: - Anti-inflammatory drugs to reduce inflammation. - Bronchodilator drugs to overcome acute smooth muscle contractions.

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Chronic bronchitis: → Excessive mucus production in the bronchi. • Mucus causes obstruction in the airways. • And thickening of the inflamed airways. Emphysema: → Destruction of the alveolar membrane. → This increases lung compliance. Cigarette smoke plays a big role -  Airway resistance. -  Diffusion. -  Ventilation. Pulmonary Volumes and capacities VC = ERV + TV + IRV. IC = TV + IRV. FRC = RV + ERV. TLC = RV + VC.

Obstructive lung disease (See SU4) → Increased airway resistance. →  FEV → Normal VC →  Ventilation. → Expiration is hard. Restrictive lung disease (See SU4) → Normal airway resistance. → Impaired respiratory movement because of abnormalities in the lung tissue. → Normal FEV. →  VC. →  Lung volume. → Inspiration is hard. Ventilation 1. Alveolar ventilation. • Tempo at which new air fills the lungs. 2. Minute ventilation. • Total ventilation per minute. • Min ventilation = TV + Respiratory rate.

Alveolar dead space. • No blood flow to alveoli. • Air in alveoli not used for gas exchange.

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Dead space → Air that does not reach the gas exchange area.

Anatomical dead space. • 150ml Of atmospheric air that enters the system never reaches the alveoli – it just moves in and out of the airways. • These airways = Anatomical dead space. Physiological dead space. • Alveolar dead space + Anatomical dead space = Physiological dead space. • This is wasted ventilation = Air that is inspired does not take part in gas exchange. Effects of Anatomical dead space on alveolar ventilation. Anatomical dead space = Volume of the conducting airways. Of the 500ml tidal volume breath: - 350ml enters the airway involved in gas exchange. - 150ml remains in the conducting airways and does not take part in gas exchange. Nervous and local control of the bronchiolar Musculature. 1. Sympathetic Dilation of the Bronchioles. • Sympathetic control is weak. – Only a few fibers penetrate the lung. • Bronchial tree – Exposed to epinephrine and nor epinephrine. o Released into the blood by sympathetic stimulation. • This causes dilation. Alicia Kotze 28411544 pg. 6

2. Parasympathetic constriction. • Vagus nerve penetrate the lung parenchyma. • Secretes acetylcholine – Causes mild constriction of the bronchioles. Parasympathetic nerves can also be activated by reflexes In the lungs - Like irritation of the epithelial membrane - Caused by dust, smoke and infections. Asthma – Causes constriction. → Parasympathetic stimulation worsens it. → Drugs are given to block the effects of acetylcholine such as atropine. Atropine – Drug used to treat dogs when they are poisoned.

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SU 2: Gas exchange in the lungs Partial pressure: Rate of diffusion of gas is directly proportional to the pressure caused by the gas alone. Sum of partial pressure = Atmospheric pressure = 760mmHg. Factors that determine partial pressure: 1. Concentration. 2. Solubility coefficient. 3. Attraction of molecules. 4. Henry’s Law → If Partial pressure is higher in one area than another = Net diffusion from high pressure area to low pressure area. Example: • If partial pressure is greater in the gas phase in the alveoli (True of O2) than more molecules will diffuse into the blood. • If partial pressure of gas is greater in the dissolved state in blood (True for CO 2) diffusion will occur towards the gas phase in alveoli.

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Partial pressure of CO2 and O2 in various places of the body.

Vapor pressure of H2O. • Atmospheric air is breathed into respiratory passages (Non-humidified air) • H2O vaporizes from surfaces. • Air gets humidified. • At normal body temperature vapor pressure = 47mmHg. • When gas mixture becomes fully humidified the partial pressure of the H2O vapor in the gas mixture = 47mmHg. REMEMBER: Partial pressure of Vapor pressure at body temperature = 47mmHg. Quantifying the Net rate of Diffusion on fluids. Factors that affect the rate of gas diffusion in a fluid: 1. Solubility of the gas in fluid. 2. Cross-sectional area of fluid. 3. Distance through which the gas must diffuse. 4. Molecular weight of gas. 5. Temperature of fluid. Alicia Kotze 28411544 pg. 8

Compositions of Alveolar air and Atmospheric air are different. • Alveolar are does not have same concentration of gases as atmospheric air. Reasons: 1. Alveolar air is only partially replaced by atmospheric air with each breath. 2. O2 is constantly being absorbed into the pulmonary blood from alveolar air. 3. CO2 is constantly diffusing pulmonary blood into the alveoli. 4. Dry atmospheric air that enters the respiratory passages is humidified even before it reaches the alveoli. Humidification of air in the respiratory passages. • Partial pressure of water vapor is 47mmHg = Also Partial pressure of water vapor in alveoli air. • Because total pressure in the alveoli cannot rise to more than atmospheric pressure(760mmHg) the water vapor dilutes all the other gasses in the inspired air. Alveolar air is slowly renewed by atmospheric air. Importance of slow replacement of Alveolar air: • Prevents sudden changes in [gas] in blood. • Prevents excessive increase and decrease in: o Tissue oxygenation. o Tissue [CO2]. o Tissue pH. Partial pressure of gasses as they enter and leave the lungs at sea level.

[O2] and Partial pressure in the Alveoli. • • • •

O2 is continually being absorbed from the alveoli into the blood of the lungs. New O2 is continually being breathed u=into the alveoli from the atmosphere. O2 rapidly absorbed in the blood = Lower [] in alveoli. New O2 breathed into the alveoli = Higher [] in alveoli.

O2 in alveoli and its partial pressure is controlled by: 1. Rate of absorption of O2 into the blood. 2. Rate new O2 entering the lungs.

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Effect of alveolar ventilation and absorption of O2 on the alveolar partial pressure of O2. – PO2. • •

One curve represents O2 absorption at a rate of 250ml/min. Another curve represents a rate of 1000ml/min.

Affect 1 shown in curves: Point A: Red curve. • Normal ventilatory rate of 4.2L/min and an O2 consumption/absorption of 250ml/min. Blue curve: • Shows O2 absorption rate during moderate exercise. • 1000ml of O2 is being absorbed each min. How to maintain alveolar PO2 at normal value of 104mmHg during moderate exercise? → The rate of alveolar ventilation must increase four-fold to keep normal PO2.

Effect of alveolar ventilation and release of CO2 on alveolar PCO2. •

CO2 formed by the body than carried in the blood to the alveoli and is removed from the alveoli by ventilation.

Affect 1 shown in curves: Point A: Red curve: • Normal ventilatory rate of CO2 excretion 200ml/min. • Normal rate of alveolar ventilation is 4.2L/min.

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Affect 2 shown in curves: • Extreme  in alveolar ventilation can never increase alveolar PO2 above 149mmHg as long as the person is breathing normal atmospheric air at sea level. – 149mmHg is the max PO2 in humidified air at this pressure. • If person breathes gases that have partial pressures of O2 higher than 149mmHg the alveolar OO2 can approach these high pressures at high rates of ventilation.

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Blue curve: • Ventilatory rate of CO2 excretion od 800ml/min. Affect 2 shown in curves: • Alveolar PCO2  directly in proportion to rate of CO2 excretion – When 800ml of CO2 are excreted per min. Affect 3 shown in curves: • PCO2  in inverse proportion to alveolar ventilation.

Alicia Kotze 28411544 pg. 10

Diffusion of gases through the respiratory membrane Layers of the respiratory membrane: 1. Surfactant -  surface tension. 2. Alveolar epithelium. 3. Alveolar Basement membrane. 4. Interstitial space between alveolar epithelium and capillary membrane. 5. Capillary basement membrane. 6. Capillary endothelial. → RBC membrane touches capillary wall so that O2 and CO2 don’t pass through a lot of plasma as they diffuse between the alveolus and RBC. =  Rapidity of diffusion. Factors that affect the rate of gas diffusion through the respiratory membrane. 1. Thickness of membrane: a. If the membrane is thick the respiratory gasses must then diffuse not only through the membrane but also through the fluid. b. Fibrosis → Can  thickness in some parts of the respiratory membrane. c. Increased thickness will interfere with normal gas exchange. 2. Surface area of the respiratory membrane: a. Big surface area = More diffusion. b. Emphysema = Causes destruction of alveolar walls. =  Area of respiratory membrane. 3. Diffusion coefficient: a. This depends on the gas solubility in the membrane and inversely the square root of gas molecules weight. 4. Pressure difference: a. This is the difference between the partial pressure of the gas in the alveoli and the partial pressure of the gas in the pulmonary capillary blood. b. If partial pressure is greater in the gas phase in the alveoli (True of O 2) than more molecules will diffuse into the blood. c. If partial pressure of gas is greater in the dissolved state in blood (True for CO2) diffusion will occur towards the gas phase in alveoli. Diffusion capacity of Respiratory membrane. Volume of a gas that will diffuse through the membrane each minute for a partial pressure difference of 1mmHg. Diffusion capacity of O2: • Diffusion capacity of O2 under normal conditions = 21ml/min/mm. Diffusion capacity of O2 during exercise: • Pulmonary blood flow. • Alveolar ventilation • O2 Diffusion capacity. Increase is caused by: 1. Opening of many dormant pulmonary capillaries and extra dilation of already open capillaries – increases surface area of blood in which O2 can diffuse into. 2.  Ventilation – perfusion ratio. During exercise =  Alveolar ventilation = Greater diffusion capacity = Oxygenation of blood. Diffusion capacity of CO2: • PCO2 in blood not far different from PCO2 in alveoli. • Diffusion capacity of CO2 is 20 times more than O2.

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Ventilation – Perfusion Ratio – Va/Q ratio. Va/Q = 0 (Shunt) → No ventilation. – Air in the alveolus comes to equilibrium with blood O2 and CO2. → Normal blood flow. → PO2 = 40 mmHg. → PCO2 = 45 mmHg. Va/Q = 1 (Normal) → Optimal O2 and CO2 exchange. → PO2 = 104 mmHg. → PCO2 = 40 mmHg. Va/Q =  (Dead space) → No capillary blood flow to carry O2 away and bring CO2 to the alveoli. → Alveolar air becomes = to the humidified air. → Air that is inspired loses no O2 to the blood and gains no CO2 from the blood. → PO2 = 149 mmHg. → PCO2 = 0 mmHg.

Physiological dead space: • Enough ventilation. • Alveolar blood flow is low. • There is more O2 available in alveoli than can be transported away by flowing blood. • Ventilation of these alveoli is wasted. • Ventilation of anatomical dead space is also wasted. • Sum of these 2 types of wasted ventilation = Physiological dead space. Abnormalities of the Va/Q ratio: Abnormal Va/Q in the upper and lower normal lung. Upper Lung: • Blood flow and ventilation are lower in upper lung than lower lung. • Blood flow is greater than Ventilation. • Va/Q in top lung. • This causes a moderate degree of Physiological dead space. Lower lung: • Ventilation is greater than Blood flow. • Va/Q in lower lung. • Fraction of blood does not become oxygenated = Physiological shunt. Alicia Kotze 28411544 pg. 12

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Physiological Shunt: • Inadequate ventilation to provide the O2 needed to fully oxygenate blood flowing through the alveoli capillaries. • Certain amount of venous blood passing through the pulmonary capillaries does not become oxygenated. = Shunted blood. • Total amount of shunted blood per minute = Physiological shunt. • The greater the physiological shunt the greater the amount of blood that fails to be oxygenated as it passes through the lungs.

During exercise: → Blood flow to upper lung . → This  Physiological dead space. →  Effectiveness of gas exchange. Abnormal Va/Q in Chronic obstructive lung disease. People who smoke → Develop bronchial obstructions. → Obstructions become so severe - alveolar trapping develops. → This leads to emphysema. → Emphysema causes alveolar walls to be destroyed. 2 Abnormalities occur in smokers: 1. Bronchioles are obstructed. a. Alveoli beyond obstructions are unventilated → Va/Q = 0 b. Causes Physiological shunt. 2. Alveolar walls become destroyed. a. There is still ventilation – Most ventilation is wasted because of inadequate blood flow to transport gasses. → Va/Q =  b. Causes Physiological dead space. Thus, in chronic obstructive lung disease some areas of the lung exhibit Physiological shunt and other areas Physiological dead space. Local Homeostatic responses in the lungs They Maximize the efficiency of gas exchange.

Net adaptive effects of vasoconstriction and bronchoconstriction are to: 1. Supply less blood flow to poorly ventilated areas – Thus, diverting blood flow to well-ventilated areas. 2. Redirect air away from diseased/damaged alveoli towards healthy alveoli. ______________________________________________________________________________

Alicia Kotze 28411544 pg. 13

SU 3: Transport of O2 and CO2 in blood and tissue.

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Oxygen Transport of O2 from the lungs to the body tissue: • O2 diffuses from alveoli to pulmonary capillary blood = PO2 in alveoli is greater than PO2 in capillary blood. • O2 diffuses from capillary blood into surrounding tissue = PO2 in capillary blood is greater than PO2 in tissue. • O2 is metabolized in tissue and form CO2. • Intracellular PCO2 . • CO2 diffuses into capillary blood. • Blood flows to the lungs. • CO2 diffuses from blood into alveoli = PCO2 in in capillary blood is greater than in alveoli. • CO2 is expired. Diffusion of O2 from alveoli to the pulmonary capillary blood. • • • • • • •

Blood moves from tissue into capillaries. Large amount of O2 was removed from this blood as it passed through the peripheral tissue. PO2 of venous blood entering the pulmonary capillaries at the arterial end = 40 mmHg. The venous blood travels through the capillary into the alveoli. PO2 in alveoli = 104 mmHg. In the alveoli O2 diffuses into b...