MECHANICS OF BREATHING

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Transcription:

MECHANICS OF BREATHING

NORMAL BREATHING

How Do We Breath? Inspiration is normally active Expiration is normally passive.

Muscles of Respiration Inspiratory muscles Diaphragm. External intercostals. Accessory muscles. Include sternomastoids, scalene muscles, and alae nasi. Expiratory muscles Abdominal muscles. Internal intercostals.

Figure 1: Respiratory Pressures Q62

Important Respiratory Pressure Differences. Airway pressure gradient: P M - P ALV. Transpulmonary pressure: P TP = P ALV - P Pl Transchest wall pressure: P TC = P Pl - P bs Transmural respiratory system pressure: P RS = P ALV - P bs

Balance of Static Forces Increase to Inflate Increase with Inflation +

Three Ways to Inflate the Lungs Increase alveolar pressure Positive pressure respirators. Decrease body surface pressure Iron lungs Activate inspiratory muscles Normal way to breath.

Inflation Dynamics Transmural pressure must overcome: Elastic recoil forces Airway resistance to flow.

MECHANICS OF BREATHING Part 2

ELASTIC CHARACTERISTICS OF THE LUNG

Inflation Hysteresis Hysteresis

Compliance P in Volume V o P V P out Transmural Pressure

Lung Compliance vs. Volume P V Stiff P V Compliant C= V P

Two Major Forces affect Lung Compliance Tissue elastic forces Surface tension forces.

Air vs. Saline Inflation More Compliant Saline Inflation Less Compliant Air Inflation

Surface Tension. T At every gas-liquid interface surface tension develops. Surface Tension is a liquid property LaPlace s Law: T P 1 r 1 P 2 r 2 T P = r 2 = P P r 2 1 1 2 2 = 2 T r If r1 > r 2 Then, P2 > P1 Result: Small Bubble Collapses

Surface Tension. T At every gas-liquid interface surface tension develops. Surface Tension is a liquid property LaPlace s Law: T P 1 r 1 P 2 r 2 T P = r 2 = P P r 2 1 1 2 2 = 2 T r If r1 > r 2 Then, P2 > P1 Result: Small Bubble Collapses

Surfactant Secreted by Type II alveolar cells Dipalmitoyl phosphatidyl choline Lines alveoli Unique surface tension properties: Average surface tension low. Surface tension varies with area: Surface tension rises as area gets bigger Surface tension falls as area gets smaller.

Figure 4: Surfactant

Physiological Importance of Surfactant Increases lung compliance (less stiff) Promotes alveolar stability and prevents alveolar collapse Promotes dry alveoli: Alveolar collapse tends to suck fluid from pulmonary capillaries Stabilizing alveoli prevents fluid transudation by preventing collapse.

Infant Respiratory Disease Syndrome (IRDS) Surfactant starts late in fetal life Total gestation: 39 wks Surfactant: 23 wks 32-36 wks Infants with immature surfactant (IRDS) Stiff, fluid-filled lungs Atelectatic areas (alveolar collapse) Collapsed alveoli are poorly ventilated Effective right to left shunt (Admixture) [lecithin]/[sphingomyelin] ratio Gestational Maturity

Dependent Lung Q63 Dependent Lung the lung in the lowest part of the gravitational field base when in the upright position dorsal portion when supine.

Gravity and Lung Inflation PTP = 0 ( 10) = + 10 cmh20 P PL = -10 cm H 2 O P 1 PALV = 0 P PL = -2.5 cm H 2 O P 2 P = 0 ( 2.5) = + 2. 5 cmh 0 TP 2

Figure 5: Regional Compliance Differences During Inflation V Stiff Compliant V

Regional Lung Volume vs. Regional Lung Ventilation In the upright posture: Relative lung volume is greater at the apex Lung is less compliant (stiffer) at the apex Regional lung ventilation is greatest at the base

Time Constants for Emptying Important regional inhomogeneities: regional differences in airway resistances regional differences in elastic characteristics High resistance and high compliance cause slow emptying. R C Time Constant RC P ALV

Specific Compliance Specific Compliance = Compliance FRC Normalization allows comparison of tissue elastic characteristics Question: How would compliance differ in a child and an adult, both with normal lungs?

INTERACTIONS BETWEEN LUNGS AND CHEST WALL

General Principle The lungs and chest wall operate in series Lung and chestwall compliances add reciprocally: 1 C 1 = + C 1 C Total Chestwall Lung

MECHANICS OF BREATHING Part 3

Figure 6: Chest Wall Mechanics

Chest Wall Mechanics Summary Negative P TT : Found at RV and FRC. Normal tidal breathing in this condition chest wall below its unstressed volume chest tends to spring out Unstressed Volume: 65% of TLC No net recoil Postive P TT : Above 65% of TLC volumes above 65% TLC Chest tends to collapse (spring in).

Figure 7: Lung Mechanics

Lung Mechanics Summary Q64 Always above unstressed volume (minimal volume = 10% TLC). P TP is positive from RV to TLC Lungs always tends to collapse.

Figure 8: Combined Mechanics Q65

Combined Mechanics Summary Functional residual capacity Respiratory system unstressed volume Chest and lung recoil equal and opposite Pneumothorax Uncouples lungs and chestwall Lungs and chest wall move to their unstressed volume lungs always recoil inward chest wall springs outward below 65% TLC chest wall springs inward above 65% TLC

Lung Compliance in Disease Diseases increasing compliance: natural aging emphysema. Diseases decreasing compliance (stiffer lung): pulmonary fibrosis edema (e.g. rheumatic heart disease)

Chestwall Compliance in Disease Actually less compliant (stiffer): chest wall deformation (eg. kyphoscoliosis) Functionally less compliant (stiffer): (Abdominal cavity changes) displacement of the diaphragm (eg. pregnancy) ascites

AIRWAY RESISTANCE

Resistive Forces and Breathing Quiet breathing -- Air flow laminar Resistance -- Poiseuille s Law Pressure gradient proportional to flow. High airflow (e.g. exercise) turbulence and eddy flow Extra pressure gradient proportional to flow rate squared

Distribution of Airway Resistance Major portion larger airways specifically medium size bronchi Small airways (< 2 mm) Only 20% of total airway resistance Resistance increases may foretell coming problems FEF 25-75 supposedly sensitive

Airway Resistance --Smooth Muscle Bronchoconstrictors Vagal tone Histamine Bronchoconstrictors Beta agonists Bronchodilation Anti-cholinergics Q66

Airways and V/Q Matching P A CO 2 Bronchodilation Find high P A CO 2 in poorly ventilated regions These airways tend to dilate. Promotes homogeneous ventilation

Homeostatic Summary Low V/ Q units Alveolar hypoxia Alveolar hypercapnia Homeostasis Alveolar hypercapnia tends to raise ventilation Alveolar hypoxemia tends to lower blood flow Result: V/ Q tends back towards normal

Airway Resistance -- Minimized by High Elastic Recoil Radial traction normally holds bronchi open Airway Low elastic recoil forces causes less radial traction and higher airway resistances: Lower lung volumes Chronic obstructive disease (eg. Emphysema)

Maximum Forced Expiration Peak Flow TLC Volume time RV Effort Independent Limb Peak Flow Flow TLC Volume RV

Summary of Forced Expiration Peak flow occurs early Envelope of effort-independence: Flow depends only on elastic recoil. Flow falls as expiration continues Envelope is eventually joined independent of: Starting volume Initial effort.

Figure 10: Flow Limitation and EPP P alv = P pl +P el P EPP =P pl Ppl P el

Mechanism of Flow Limitation Summary Force expiration: P PL is positive outside the airways. Equal pressure point (EPP). Point at which P airway falls just enough to equal P PL Bronchi collapse Flow proportional to: P ALV - P EPP

Effort Independence of Flow-Volume Envelope Q67 Increased effort Similar increases in P ALV and P EPP. Pressure difference unchanged Therefore, Flow unchanged.

Figure 11: Flow Limitation at Various Lung Volumes High Lung Volume Medium Lung Volume Low Lung Volume

Flow Limitation in COPD (Emphysema) Normal Lung Medium Volume Emphysematous Lung Medium Volume

Forced Inspiration: is Effort-Dependent P PL is Negative Airways are held open.

Clinical Flow-Volume Loops Obstruction

Reference http://www.ursa.kcom.edu/department/slidesets/summer/mechbreathing/ PPMechBreathing.ppt