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  • 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.

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  • RESPIRATION
    Dr. Faraz A. Bokhari
  • If you cant breathe, nothing else matters!
    (American Lung Association)
  • Introduction
    Why respire?
    Gas exchange
    Host defense (barrier b/w outside and inside)
    Metabolism (produces/metabolizes compounds)
    Gas exchange
    Pulmonary ventilation
    Diffusion of O2 and CO2 b/w alveoli and blood
    Transport of O2 and CO2 in blood and body fluids to & from body's tissue cells
    Regulation of ventilation
  • Physiological Anatomy
    Upper airway
    All structures from nose to the vocal cords, including sinuses and the larynx
    Conditioning of inspired air
    Lower airway
    Trachea, airways & alveoli
  • The Airway Tree:Conducting zone
    Consists of trachea and first 16 generations of airway branches
    First four generations are subjected to changes in -ve and +ve pressures, & contain a considerable amount of cartilage (to prevent airway collapse)
    Cartilage present up to lobar and segmental bronchi
    Disappears in bronchioles
    Bronchioles are suspended by elastic tissue of lung parenchyma
    This elasticity keeps them patent
    Blood supply: Bronchial vessels
    No gas exchange
  • The Airway Tree:Respiratory zone
    Composed of last seven generations
    Consists of respiratory bronchioles, alveolar ducts and alveoli
    Blood supply: pulmonary circulation
    Pulmonary circulation receives all of CO
  • The Airway Tree:Respiratory zone
    Adult lungs contain 300 to 500 million alveoli
    Combined internal surface area: 75 m2
    Represents one of the largest biological membranes in the body
    With age number and size increases till adolescence!
    after adolescence, alveoli only increase in size
    Smoking induced damage can be reversed in a limited way only!
  • Physiological Anatomy
    Lung are covered by the visceralpleura and are encased by the parietal pleura
    Potential space b/w these 2 layers
    Layer of fluid allows for smooth gliding of lung as it expands in the chest
    Pressure within this space is normally kept negative
    Pneumothorax
    Hemothorax
  • Lung-Chest Wall Interaction
  • Mechanics of Pulmonary Ventilation
    Lungs can be expanded and contracted in 2 ways:
    By downward and upward movement of the diaphragm
    To lengthen or shorten the chest cavity
    By elevation and depression of the ribs
    To increase and decrease the anteroposterior diameter of the chest cavity
    Physical events
    Pump Handle movement
    Bucket-handle movement
  • Pump Handle – AP Diameter
  • Bucket Handle – Lateral Expansion
  • Muscles of Respiration
    INSPIRATION
    Principal
    Diaphram (domes descend – increase longitudinal aspect)
    External intercostals (elevate ribs – increase AP aspect)
    Accessory
    Sternocleidomastoid muscles (lift upward on the sternum)
    Scaleni (lift the first two ribs)
    EXPIRATION
    Quiet breathing
    Passive recoil of lungs
    Active breathing
    Internal intercostals (depress ribs)
    Abdominal recti (depress lower ribs, compress abdominal contents)
    External/internal oblique
  • Inspiratory Sequence – General Concept
  • Quiet Inspiratory Sequence -General Concept
  • Quiet Expiratory Sequence -General Concept
  • Pressures Involved in Breathing
    Barometric pressure (Pb)
    Intrapleural pressure (Pip)
    Alveolar pressure (Palv)
    Transpulmonary pressure (Ptp)
  • Pressures Involved in Breathing
    Barometeric P
    P exerted by the air we breathe
    @ sea level: 760 mmHg
    Dalton’s law:
    Pb is equal to sum of partial pressures of individual gases
    Pb = PN+PO2+PH2O+PCO2
    Changes in respiratory pressures during breathing are often expressed as pressure relative to atmospheric P
    When relative pressures are used, Pb = zero
  • Partial pressures and percentages of Respiratory Gases at Sea Level (PB = 760 mm Hg)
  • Pressures Involved in Breathing
    Intrapleural Pressure
    Less than Pb
    Since the 2 elastic recoils are opposite
    Pip in fact is intrathoracic pressure
    In upright subject:
    Greatest vacuum (least Pip) – lung apex
    Lowest vacuum (highest Pip) – lung base
    Average (Resting) value = -5 cm water
  • Pressures Involved in Breathing
    Alveolar pressure (Palv)
    Pressure inside the alveoli
    Decreases during inspiration
    Atmospheric air fills in
    Transpulmonary pressure (Ptp)
    Distending pressure
    Ptp = Palv – Pip
  • Interaction of Pressures Involved in Breathing
  • Pneumothorax
  • Static Vs Dynamic Lung
    Re-expanding:
    Cadaver lung
    Collapsed lung
    Pneumothorax!
    Initially pressure is required to ‘regain’ original lung & chest wall volume (static component)
    The lung is now expanded
    In vivo, over and above ‘static P’, more pressure is required to overcome inertia and resistance of tissues (airways) & air molecules (dynamic component)
  • Static Vs Dynamic Lung
    Ptp = Palv – Pip
    Pip = (-Ptp) + Palv
    Thus, Pip has 2 aspects*:
    Transpulmonary pressure (Ptp) – Static component
    Alveolar pressure (Palv) – Dynamic component
    Compliance (dV/dP) varies
    Static compliance
    Change in volume for a given change in Ptp with zero gas flow
    Dynamic compliance
    Measurements made by monitoring TD used
    While intra thoracic pressure (Pip) measured during the instance of zero air flow occurring at the end inspiritory and expiratory levels with each breath
  • Compliance*
    Extent to which lungs will expand for each unit increase in Ptp
    C=dV/dP
    Stages of compliance:
    Stage1 [Stable VL):
    Less volume change for pressure change
    Surface tension makes it difficult to open an airway
    Stage2 (airway start opening):
    Stepwise decreases in PIP beyond -8 - produce dV
    dV first small, then larger
  • Compliance
    Stage3
    Linear expansion of open airways
    Stage4
    Limit of airway inflation
    Hysteresis
    Mostly due to surface tension
    Less due to elastic forces
  • Compliance Vs Elastance
    Compliance is a measure of distensibility
    Elastance is a measure of elastic recoil
    These both oppose each other!
    Compliancedecreases as Elastanceincreases:
    Pulmonary fibrosis (restrictive lung disease)
    Pulmonary hypertension/congestion
    Decreased surfactant – increased surface tension (prematurity, artificial ventilation)
    Complianceincreases as Elastancedecreases
    Normal ageing (alteration in elastic tissue)
    Asthma (unknown reason)
    Emphysema* (obstructive lung disease)
  • Compliance - Emphysema
  • Compliance & Surface Tension
    ELASTIC FORCES of the lungs:
    (1) Lung tissue elastic forces
    (elastin& collagen fibers)
    (2) Elastic forces caused by surface tension
    (Tension created by fluid-air interface)
    Lung tissue elastic
    forces (air-filled lung) I/3
    of total
    Surface tension forces - 2/3
  • Surfactant
    Surface active agent
    Greatly reduces surface tension of water
    Secreted by Type II alveolar epithelial cells
    Most important components:
    Dipalmitoylphosphatidylcholine
    Surfactant apoproteins
    Calcium ions
    Premature babies lack surfactant
  • Lung-Thoracic CageCompliance
    Thoracic cage has its own compliance!
    Compliance (lung-cage): 110 ml/cm water
    Compliance (lung): 200 ml/cm water
    When the lungs are expanded to high volumes/ compressed to low volumes - checked by chest compliance limitations