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Air Flow and Respiration: Understanding the Mechanics and Factors Involved - Prof. Douglas, Study notes of Biology

The concepts of air flow and respiration, discussing the role of airway resistance, boyle's law, lung volume, and various factors affecting lung compliance. It also covers the processes of inspiration and expiration, as well as the impact of muscle contractions and external pressures on lung function. Additionally, it touches upon conditions that can affect airway resistance and lung compliance, such as asthma and respiratory distress syndrome.

Typology: Study notes

2011/2012

Uploaded on 05/26/2012

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Download Air Flow and Respiration: Understanding the Mechanics and Factors Involved - Prof. Douglas and more Study notes Biology in PDF only on Docsity! 20 April Air Flow Air flow, F = ΔP / R where R is airway resistance F = (Palv – Patm) / R ΔP (aka Prs) is the difference between the pressure of air in the atmosphere and the pressure of air in the alveoli Airflow is always down the air pressure gradient Between breaths: Palv = Patm, F is 0, and there is no airflow Inspiration: Palv < Patm, F is negative, and airflow goes into lungs Expiration: When Palv > Patm, F is positive, and airflow goes out of lungs Figure 13-8 Boyle’s law states that the pressure of a fixed number of gas molecules is inversely proportional to the volume of the container. Boyle’s Law and Air Flow V x P = K (constant) at a constant temperature and constant number of gas molecules. Shows pressure and volume are inversely related. Pressure is number of molecules striking a surface per unit time. When chest wall expands: V of the lungs increase, consequently P must decrease. P in this case is Palv. Air flows into the alveoli (inspiration), because (Palv < Patm). When the chest wall contracts: V of the lungs decrease, and P must increase. Air moves out of the alveoli, because Palv > Patm. Fig 13-10: Resting Table 13-3: Determinants of lung volume Convention: Patm = 0 Between breaths, Pip is negative due to passive elastic recoil of lungs and chest wall Pneumothorax Hole in chest wall and its pleura due to stabbing or chest wall surgery. P ip becomes 0. Ptp = 0 – 0 = 0. No transpulmonary pressure to keep the lungs open and it collapses (atelectasis). The chest wall also expands because its elastic recoil is not opposed. This lung is nonfunctional. Fortunately, there are two independent lungs with separate plurae. Q: How would you re- inflate the lung? Pneumothorax when excess pressure applied during artificial respiration of premature baby: Lungs still fragile. Perforation of lung, causing Pip = 0 Fig 13 – 13 Fig 13 – 12 Inspiration is the result of the expansion of the thoracic cage in response to skeletal muscle contraction The expansion reduces alveolar pressure (Palv) below atmospheric pressure (Patm), so air moves into the lungs Figure 13 – 15 Expiration is the result of reducing the volume of the thoracic cage; in a resting person, this occurs in response to skeletal muscle relaxation The volume reduction increases alveolar pressure (Palv) above atmospheric pressure (Patm), so air moves out of the lungs Muscles: Inspiration Diaphragm – Most important breathing muscle. Phrenic nerve Aps cause diaphragm to contract towards the abdomen. This causes the thorax to expand Transpulmonary pressure distends and opens the airways (critical factor). Pressure increases during inspiration, increasing bronchi radius, thereby reducing resistance. P ip decreases during respiration, radius is reduced, increasing resistance (see figure 13 – 13) Lateral traction: Elastic connective tissue fibers are attached to bronchi at one end and to lung tissue on the other end. Inspiration: lung expands, pulling on the elastic fibers to increase the radius of bronchi. This works together with transpulmonary pressure. Forced expiration: Forced compression of the chest wall, increases P ip, compresses lung tissue, reduces the radius of bronchi and increases resistance. The greater the forced expiration, the greater the resistance. Regulation of Bronchi Radius II Epinephrine relaxes the smooth muscles of the airways (beta-adrenergic receptors). The sympathetic nervous system generally dilates the airways. Epinephrine i.v. to treat severe bronchoconstriction Parasympathetic nervous system: ACh binds muscarinic receptors to cause bronchial constriction and asphyxiation Nerve gas inhibits acetylcholinesterase, increases ACh, and causes severe bronchial constriction and asphyxiation. Leukotrienes: Inflammation increases production of this eicosanoid in the lung, causing bronchoconstriction Histamine: Strong bronchoconstrictor (allergic reaction) Carbon dioxide: Expired CO2 causes bronchodilation Diseases Increasing Airway Resistance I Asthma: Chronic inflammation with release of leukotrienes causing bronchoconstriction. Among many causes: allergens such as pollen, infections, environmental factors (cigarette smoke, pollutants) Treatments Beta-adrenergic agonists (mimic epinephrine) – vasodilates Antagonists of muscarinic cholinergic receptors – block constriction Leukotriene inhibitors - block bronchoconstriction Glucocorticoids - block inflammation
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