The lungs are a remarkable feat of engineering. They receive the entire right ventricular cardiac output and they are called upon at birth to function without cessation. The lungs are contained in a space with a volume of approximately 4 L, but they have a surface area for gas exchange that is the size of a tennis court (∼85 m2). This large surface area is comprised of myriads of independently functioning respiratory units. Unlike the heart, but similar to the kidneys, the lungs demonstrate functional unity; that is, each unit is structurally identical and functions just like every other unit. a marathon runner who staggers across the 26-mile finish line in less than 3 hours or someone who swims the English Channel in record time is rarely limited by the amount of oxygen taken up by the lungs. The reason is that gas exchange can increase more than 20-fold to meet the body's energy demands. These examples of human activity not only underscore the functional capacity of the lungs but also illustrate the important role respiration plays in our extraordinary adaptability.
Explain Pip, Palv and Ptp (transpulmonary)
Values after a quiet expiration
Explain static & dynamic lung components..
*The component which only causes change in volume is refered to as static component. E,g. transpulmonary P and compliance determine lung volume only……whereas the parameter that causes air flow is refered to as dynamic component. E.g. alveolar pressure (Palv)The key message in Figure 26-15 is that during inspiration, the negative shift in PIP has two effects. Thebody invests some of the energy represented by %PIP into transiently making PA more negative (dynamiccomponent). The result is that air flows into the lungs, and VL increases. But this investment in PA is onlytransient. Throughout inspiration, the body invests an increasingly greater fraction of its energy in makingPTP more positive (static component). The result is that the body maintains the new, higher VL. By the endof inspiration, the body invests all of the energy represented by %PIP into maintaining VL and none intofurther expansion. The situation is not unlike that faced by Julius Caesar as he, with finite resources,conquered Gaul. At first, he invested all of his resources in expanding his territory at the expense of thefeisty Belgians. But as the conquered territory grew, he was forced to invest an increasingly greater fractionof his resources in maintaining the newly conquered territory. In the end, he necessarily invested all of hisresources into maintaining his territory, and was unable to expand further.
Ptp = Palv – Pip
What would happen if, having inflated the lungs to TLC, we allowed PIP to increase to 0 cm H2O onceagain? Obviously, the VL would decrease. However, the lungs follow a different path during deflation (seeFig. 26-5B, upper blue curve). The difference between the inflation and the deflation paths is known ashysteresis, and it exists because a greater pressure difference is required to open a previously closedairway than to keep an open airway from closing. As an example, the horizontal line in Figure 26-5B showsthat inflating collapsed lungs to FRC requires a PIP of -12 cm H2O, whereas maintaining previously inflatedlungs at FRC requires a PIP of only -5 cm H2O. During normal respiration, the lungs exhibit much lesshysteresis, and the hysteresis loop (see Fig. 26-5B, green loop) lies close to the deflation limb of the blueloop.Green small compliance curves – Dynamic Compliance
*In emphysema, the situation is reversed. The disease process, a common consequence of cigarettesmoking, destroys pulmonary tissue and makes the lungs rather floppy. An important part of the diseaseprocess is the destruction of the extracellular matrix, including elastin, by elastase released frommacrophages Normal mice that are exposed to cigarette smoke develop emphysema rapidly, whereas thedisease does not develop in "smoker" mice lacking the macrophage elastase gene. The same increase inPTP that produces a 500-ml VL increase in normal lungs produces a substantially larger VL increase inlungs with emphysema. In other words, static compliance is much greater (i.e., much less elastic recoil). Because it requires work to inflate the lungs against their elastic recoil, one might think that a littleemphysema might be a good thing. Although it is true that patients with emphysema exert less effort toinflate their lungs, the cigarette smoker pays a terrible price for this small advantage: The destruction ofpulmonary architecture also makes emphysematous airways more prone to collapse during expiration,drastically increasing airway resistance. Hence in emphysema, static compliance increases – since volume is increasing; but dynamic compliance decreases – decreased airflow.
RESPIRATION<br />Dr. Faraz A. Bokhari<br />
If you cant breathe, nothing else matters!<br />(American Lung Association)<br />
Introduction<br />Why respire?<br />Gas exchange<br />Host defense (barrier b/w outside and inside)<br />Metabolism (produces/metabolizes compounds)<br />Gas exchange<br />Pulmonary ventilation<br />Diffusion of O2 and CO2 b/w alveoli and blood<br />Transport of O2 and CO2 in blood and body fluids to & from body's tissue cells<br />Regulation of ventilation <br />
Physiological Anatomy<br />Upper airway<br />All structures from nose to the vocal cords, including sinuses and the larynx<br />Conditioning of inspired air<br />Lower airway<br />Trachea, airways & alveoli<br />
The Airway Tree:Conducting zone<br />Consists of trachea and first 16 generations of airway branches<br />First four generations are subjected to changes in -ve and +ve pressures, & contain a considerable amount of cartilage (to prevent airway collapse)<br />Cartilage present up to lobar and segmental bronchi<br />Disappears in bronchioles<br />Bronchioles are suspended by elastic tissue of lung parenchyma<br />This elasticity keeps them patent<br />Blood supply: Bronchial vessels<br />No gas exchange<br />
The Airway Tree:Respiratory zone<br />Composed of last seven generations <br />Consists of respiratory bronchioles, alveolar ducts and alveoli<br />Blood supply: pulmonary circulation<br />Pulmonary circulation receives all of CO<br />
The Airway Tree:Respiratory zone<br />Adult lungs contain 300 to 500 million alveoli<br />Combined internal surface area: 75 m2<br />Represents one of the largest biological membranes in the body<br />With age number and size increases till adolescence!<br />after adolescence, alveoli only increase in size <br />Smoking induced damage can be reversed in a limited way only!<br />
Physiological Anatomy<br />Lung are covered by the visceralpleura and are encased by the parietal pleura<br />Potential space b/w these 2 layers<br />Layer of fluid allows for smooth gliding of lung as it expands in the chest<br />Pressure within this space is normally kept negative<br />Pneumothorax<br />Hemothorax<br />
Mechanics of Pulmonary Ventilation<br />Lungs can be expanded and contracted in 2 ways: <br />By downward and upward movement of the diaphragm<br />To lengthen or shorten the chest cavity<br />By elevation and depression of the ribs <br />To increase and decrease the anteroposterior diameter of the chest cavity<br />Physical events<br />Pump Handle movement<br />Bucket-handle movement<br />
Pressures Involved in Breathing<br />Barometeric P<br />P exerted by the air we breathe<br />@ sea level: 760 mmHg<br />Dalton’s law:<br />Pb is equal to sum of partial pressures of individual gases<br />Pb = PN+PO2+PH2O+PCO2<br />Changes in respiratory pressures during breathing are often expressed as pressure relative to atmospheric P<br />When relative pressures are used, Pb = zero<br />
Partial pressures and percentages of Respiratory Gases at Sea Level (PB = 760 mm Hg)<br />
Pressures Involved in Breathing<br />Intrapleural Pressure<br />Less than Pb<br />Since the 2 elastic recoils are opposite<br />Pip in fact is intrathoracic pressure<br />In upright subject:<br />Greatest vacuum (least Pip) – lung apex<br />Lowest vacuum (highest Pip) – lung base<br />Average (Resting) value = -5 cm water<br />
Pressures Involved in Breathing<br />Alveolar pressure (Palv)<br />Pressure inside the alveoli<br />Decreases during inspiration<br />Atmospheric air fills in <br />Transpulmonary pressure (Ptp)<br />Distending pressure<br />Ptp = Palv – Pip<br />
Interaction of Pressures Involved in Breathing<br />
Static Vs Dynamic Lung<br />Re-expanding:<br />Cadaver lung<br />Collapsed lung <br /> Pneumothorax!<br />Initially pressure is required to ‘regain’ original lung & chest wall volume (static component)<br />The lung is now expanded<br />In vivo, over and above ‘static P’, more pressure is required to overcome inertia and resistance of tissues (airways) & air molecules (dynamic component)<br />
Static Vs Dynamic Lung<br />Ptp = Palv – Pip<br />Pip = (-Ptp) + Palv<br />Thus, Pip has 2 aspects*:<br />Transpulmonary pressure (Ptp) – Static component<br />Alveolar pressure (Palv) – Dynamic component<br />Compliance (dV/dP) varies<br />Static compliance<br />Change in volume for a given change in Ptp with zero gas flow<br />Dynamic compliance<br />Measurements made by monitoring TD used<br />While intra thoracic pressure (Pip) measured during the instance of zero air flow occurring at the end inspiritory and expiratory levels with each breath<br />
Compliance*<br />Extent to which lungs will expand for each unit increase in Ptp<br />C=dV/dP<br />Stages of compliance:<br />Stage1 [Stable VL): <br />Less volume change for pressure change<br />Surface tension makes it difficult to open an airway<br />Stage2 (airway start opening):<br />Stepwise decreases in PIP beyond -8 - produce dV <br />dV first small, then larger<br />
Compliance<br />Stage3<br />Linear expansion of open airways<br />Stage4<br />Limit of airway inflation<br />Hysteresis<br />Mostly due to surface tension<br />Less due to elastic forces<br />
Compliance Vs Elastance<br />Compliance is a measure of distensibility<br />Elastance is a measure of elastic recoil<br />These both oppose each other!<br />Compliancedecreases as Elastanceincreases:<br />Pulmonary fibrosis (restrictive lung disease)<br />Pulmonary hypertension/congestion<br />Decreased surfactant – increased surface tension (prematurity, artificial ventilation)<br />Complianceincreases as Elastancedecreases<br />Normal ageing (alteration in elastic tissue)<br />Asthma (unknown reason)<br />Emphysema* (obstructive lung disease)<br />
Compliance & Surface Tension<br />ELASTIC FORCES of the lungs:<br />(1) Lung tissue elastic forces<br /> (elastin& collagen fibers)<br />(2) Elastic forces caused by surface tension<br /> (Tension created by fluid-air interface)<br />Lung tissue elastic <br />forces (air-filled lung) I/3<br />of total<br />Surface tension forces - 2/3<br />
Surfactant<br />Surface active agent<br />Greatly reduces surface tension of water<br />Secreted by Type II alveolar epithelial cells<br />Most important components:<br />Dipalmitoylphosphatidylcholine<br />Surfactant apoproteins <br />Calcium ions<br />Premature babies lack surfactant<br />
Lung-Thoracic CageCompliance<br />Thoracic cage has its own compliance!<br />Compliance (lung-cage): 110 ml/cm water<br />Compliance (lung): 200 ml/cm water<br />When the lungs are expanded to high volumes/ compressed to low volumes - checked by chest compliance limitations<br />