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Mechanics of respiration Surfactant. Lecture 12 Thursday, February 8, 2007 Refs. Medical Physiology Chapters 25 and 26, Moore & Agur, Moore and Dalley, Ganong. External Respiration. External respiration The process of transporting oxygen from the atmosphere to the mitochondria .
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Mechanics of respirationSurfactant Lecture 12 Thursday, February 8, 2007 Refs. Medical Physiology Chapters 25 and 26, Moore & Agur, Moore and Dalley, Ganong
External Respiration • External respiration • The process of transporting oxygen from the atmosphere to the mitochondria . • The process of transporting CO2 from the mitochondria to the atmosphere. • Transportation of gasses requires diffusion across barriers. • Diffusion depends on a gradient. • Convection (mixing on one or both sides of the barrier) increases sharpness of gradient at surface of barrier.
Overview of mechanics of respiration • Basic system: a gas exchange organ (lungs) and a pump (chest) to move air in and out • Inspiration- moving air in -active process Enlarging the rib cage increases negative pressure in pleural space. • As pressure inside lung becomes more negative air moves in. • Expiration- movement of air out - at rest is mainly a passive process due to recoil.
Changes in size of rib cage M&D fig.1.8Inspiration: chest cavity becomes wider and longer.
Muscles involved in inspiration • At rest: • External intercostals elevate ribs. • Diaphragm (75% of change in volume) • Either alone can maintain adequate ventilation • With increased effort: • Subcostal muscles • Levator costarum • Serratus posterior superior • Neck muscles-scalenes and sternocleidomastoid
Muscles involved in expiration • At rest: • No expiratory muscles contract • Contraction of inspiratory muscles acts as a brake to slow expiration. • With increased effort: • Internal intercostals depress ribs. • Transverse thoracic • Serratus posterior inferior • Abdominal muscles push diaphragm up.
Additional muscles involved in respiration • Laryngeal muscles • Abductor muscles contract during inspiration opening the glottis. • Bronchial muscles • Bronchi dilate during inspiration (sympathetic) and constrict during expiration (parasympathetic) • Other mediators such as Substance P, adenosine, and peptidoleukotrienes cause bronchoconstriction. • Chemical irritants and cold air cause bronchoconstriction. • VIP (vasoactive intestinal peptide)causes bronchodilation.
Why do the lungs expand with the chest wall? • Surface tension. • There is a small amount of fluid between the visceral pleural and parietal pleura. • The two pleurae can slide against each other but do not pull apart similar to 2 plates of glass with water between them • If a large amount of air or fluid enters the pleural cavity, the lungs collapse. • Pneumothorax, hydrothorax, hemothorax
Negative pressure in pleural space and attraction of pleural surfaces keep lungs expanded M&A 2
Intrapleural and intrapulmonary pressures • Intrapleural pressure is less than atmospheric pressure ~-2.5 mm Hg • As chest expands, the pressure becomes more negative ~-6 mm Hg. • As the lungs are pulled into a more expanded position, the intrapulmonary pressure decreases to ~-1.2 mm Hg and air flows in. • When inspiration stops, the recoil increases intrapulmonary pressure and air flows out.
Graphs of intrapleural (middle) and intrapulmonary (top) pressures Ganong fig. 34-6
Lung Volumes and Capacities • Tidal volume (TV): The volume of air that moves with each breath at rest. Inspiratory volume =expiratory volume. • Inspiratory reserve volume (IRV): The volume of air inspired with maximum respiratory effort above TV. • Inspiratory capacity (IC): IRV + TV • Expiratory reserve volume (ERV): The volume expelled by maximum expiratory effort greater than the passive expiration. • Vital capacity (VC): TV + IRV + ERV
Lung volume definitions cont. • Residual volume (RV): The volume left in lungs after maximal expiratory effort. After the first breath the lungs will always contain some air. • Dead space: The space occupied by gas that does not exchange with pulmonary capillaries. • Functional residual capacity (FRC): ERV + RV • Total lung capacity (TLC): IRV + TV + ERV + RV • or VC + RV or IC + FRC
Typical volumes in liters Men Women IRV 3.3 1.9 TV 0.5 0.5 ERV 1.0 0.7 RV 1.2 1.1 Total 6.0 4.2 VC 4.8 3.1
Lung compliance • A measure of the ease of expansion of the lung • Compliance = change in volume/change in pressure. • Normal value is 0.2 L/ cm H2O. • The pressure volume curve is curvilinear and shows hysteresis. • The curves are different for inflation and deflation with air. • High compliance means lung has high distensibility. • Low compliance implies stiffness.
Lung disease changes compliance Pulmonary congestion and interstitial pulmonary fibrosis shift the curve down and to the right. • Emphysema shifts the curve up and left
Without surfactant, surface tension would make smaller alveoli collapse into larger ones. MP 26-7E
Surfactant • The hysteresis in the inflation-deflation pressure volume curves is primarily due to surface tension. • It takes more pressure to open a closed airway • Both the elastic recoil of the lung and surface tension tend to collapse the alveoli. • Surfactant lowers the surface tension. • Main component of surfactant (>60%) is dipalmitoylphosphatidylcholine made by type II pneumocytes in lamellar bodies.
Surfactant causes a braking action as the alveolus inflates MP 26-10
Surfactant deficiency • Without adequate surfactant areas of alveoli collapse (atelectasis). • Immature lungs do not have enough surfactant -cause of infant respiratory distress syndrome IRDS
Ventilation • Respiratory ventilation or minute volume • Volume expired x breaths per min • At rest: tidal volume (500 ml) x 12/min = 6 L • Alveolar ventilation is lower than minute volume due to anatomic dead space (150 ml) • (500-150) x 12/min = 4.2 L • Maximal voluntary ventilation • Largest volume that can be moved into and out of the lungs in 1 min by voluntary effort. • Normal: 125-170 L/m
Measurements of pulmonary function • Vital capacity is measured as the largest volume that can be expired after maximal inspiratory effort. • FEV1 is the fraction of vital capacity expired during the first second of forced expiration Example: in asthma VC can be normal but FEV1 is reduced because of bronchial constriction