Summary

These lecture notes cover various aspects of ventilation, including the introduction, mechanics, and pressure differences involved in the process. It details the roles of respiratory muscles, lung and thorax compliance, and resistance in the ventilation process. The notes also discuss the concepts of transrespiratory pressure, transalveolar pressure, and transthoracic pressure.

Full Transcript

Egan Chapter 11 Ventilation Introduction to Ventilation ◦ The primary function of the lungs are to supply the body with oxygen (O2) and remove the waste, carbon dioxide (CO2).  In order to perform these functions, the lungs must be adequately ventilated....

Egan Chapter 11 Ventilation Introduction to Ventilation ◦ The primary function of the lungs are to supply the body with oxygen (O2) and remove the waste, carbon dioxide (CO2).  In order to perform these functions, the lungs must be adequately ventilated. 2 Introduction to Ventilation  Ventilation is the process of moving gas (usually air) in and out of the lungs  Ventilation is to be distinguished from respiration, which refers to the physiologic processes of oxygen use at the cellular level.  In health  Ventilation is regulated to meet the body’s needs under a wide range of conditions  In disease  When the process of ventilation is impaired it can create more work for the patient to breathe in attempt to ventilate Copyright © 2017 Elsevier Inc. All Rights Reserved. 3 Mechanics of Ventilation  Ventilation is cyclic: inspiration and expiration  Tidal volume (VT): gas moved per phase Volume measured during either inspiration or expiration  Facilitates removal of CO , replenishes O 2 2  To ventilate, the respiratory muscles have to generate changes in a pressure gradient so that gas will flow in and out of the lungs.  Lung and thorax compliance and resistance have an affect on ventilation  The load respiratory muscles overcome to produce ventilation  Healthy lungs at rest, inspiratory load is minimal, while expiration is passive Copyright © 2017 Elsevier Inc. All Rights Reserved. 4 Pressure Differences During Breathing  Gases move due to pressure gradients  Produced by thoracic expansion/contraction  Due to elastic properties of airways, alveoli, and chest wall  Transrespiratory pressure (PTR)  Everything that exists between pressure measured at airway opening (PAO) and pressure measured at body surface (PBS)  PTR = PAO – PBS Equation follows direction of flow PAO is higher than PBS  Components of transrespiratory pressure include: Airway, lungs, and chest wall  This gradient causes gas flow in and out of lungs Copyright © 2017 Elsevier Inc. All Rights Reserved. 5 Pressure Gradients (Pressure Differences)  Gas or liquid will move from areas of high pressure to areas of low pressure  In pulmonary physiology, pressure difference called “pressure gradient”  Gases move “down” its pressure gradient From high-pressure area to low-pressure area Pressure Differences During Breathing (Cont.)  Transairway pressure (PTAW)  PTAW = PAO– PA  Whatever exists between pressure measured at airway opening and pressure measured in alveoli of lungs  Transalveolar pressure (PTA)  PTA = PA– Ppl  Whatever exists between pressure measured in model alveolus and pressure measured in pleural space (Ppl).  Transchestwall pressure (PTCW)  Chest wall exists between pressure measured in pleural space and pressure on body surface  PTCW = Ppl – PBS Copyright © 2017 Elsevier Inc. All Rights Reserved. 7 Pressure Differences During Breathing (Cont.)  Transpulmonary pressure difference (PTP) – Maintains alveolar inflation  Pulmonary system (airways and alveolar region), defined: PTP = PAO – Ppl Pressures must be measured to derive mechanical properties of pulmonary system  Under either static or dynamic (breathing) conditions (static – no flow, dynamic – air flow) Copyright © 2017 Elsevier Inc. All Rights Reserved. 8 Pressure Differences During Breathing (Cont.)  Transthoracic pressure difference (PTT)  PTT = PA – PBS  Causes gas to flow into and out of alveoli during breathing  Beginning of inspiration in spontaneous breathing subject, PA is subatmospheric compared to PAO Causes air to flow into alveoli  Beginning of exhalation is opposite PA is higher than PAO Causing air to flow out of airway Copyright © 2017 Elsevier Inc. All Rights Reserved. 9 Pressure Differences During Breathing (Cont.)  Inspiration begins  When muscular effort expands the thorax  Thoracic expansion causes a decrease in Ppl Causes positive change on expiratory PTP and PTA, which induces flow into lungs  Inspiratory flow is proportional to (+) change in transairway pressure difference The higher the change in PTA, the higher the flow  Ppl continues to decrease until the end of inspiration  Alveolar filling slows when alveolar pressure approaches equilibrium with the atmosphere and inspiratory flow decreases to zero Copyright © 2017 Elsevier Inc. All Rights Reserved. 10 Pressure Differences During Breathing (Cont.)  Beginning of expiration  Thoracic recoil causes Ppl to start to rise  Thus, transpulmonary pressure difference starts to decrease  PTP is decreasing; opposite of inspiration So flow is in opposite (negative) direction Driving force for expiratory flow is energy stored in combined elastances of lungs and chest wall  Pleural pressures: always negative (subatmospheric) during normal inspiration and exhalation  During forced inspiration (big downward movement of diaphragm), pleural pressure can drop up to –50 cm H2O Copyright © 2017 Elsevier Inc. All Rights Reserved. 11 In this picture the Pao is 10 due to positive pressure ventilation. The pleural pressure is 0 yet the patient still has a 500 Vt (same volume as spontaneous breathing patient but achieved differently) Copyright © 2017 Elsevier Inc. All Rights Reserved. 12 Spontaneous versus Positive Pressure Breathing  Two important points to remember are ◦ (1) both SB and PPV accomplish inspiration by increasing PL, the pressure distending the lungs, and ◦ (2) because PPV raises the Ppl, it tends to compress the veins that bring blood back to the heart, ultimately impeding cardiac output. Spontaneous breathing has the opposite effect because inspiration lowers Ppl further, augmenting venous blood return to the heart. Beachey, Will. Respiratory Care Anatomy and Physiology: Foundations for Clinical Practice, 3rd Edition. Mosby, 2013. VitalBook file. 13 INHALATION  https://youtu.be/NB1aCBId6qA  When we inhale in we expand our thoracic cavity and expand the lungs to take in more volume which decreases pleural pressure (Boyle’s Law)  Increasing thoracic volume causes fewer collisions between gas molecules and between gas molecules and the thorax. The lower number of collisions decreases the pressure exerted by the gas, which reduces PA below PB so air flows into the lungs until PA again equals PB at end inspiration.  To look at it another way: this increases the transpulmonary pressure gradient which maintains alveolar inflation. Transpulmonary Pressure Gradient PTP = Alveolar pressure PA – pleural pressure PPL)  This causes the alveolar pressure to fall below the airway opening pressure and this pressure gradient causes air to flow into the lungs 14 INHALATION  Inhalation stops when alveolar pressure equals the airway opening pressure.  The higher the pressure gradient the higher the flow.  https://youtu.be/lr5dDmTASos 15 Balloon Model of Ventilation A. Inspiration caused by downward movement of rubber sheet (diaphragm)  Atmospheric pressure is greater than pressure in side of balloon When we pull down in the diaphragm it increases the size of the thoracic cavity and increases volume which in turn causes the pleural pressure to decrease. Because the lung is elastic, the decrease in pleural pressure gets transmitted to inside the alveoli which in turn causes the intra-alveolar pressure to decrease This creates a pressure gradient to between the intra-alveoli pressure and atmospheric pressure Because atmospheric pressure is higher than intralveolar pressure then gas will move from higher pressure to lower pressure Copyright © 2017 Elsevier Inc. All Rights Reserved. 17 Balloon Model of Ventilation B. End-inspiration (equilibrium point, no gas flow). Gas flows until equillibrium  Atmospheric pressure is equal to pressure inside balloon To Summarize The atmospheric pressure is more positive and as muscles contract it increases space in the thoracic cavity and per Boyle’s Law the decrease in pressure will increase the volume. It does this because expanding the lungs causes gas molecules to have more room to move around. When there is more room to move around there is less pressure. Less pressure = more volume. Then as gas flows until alveolar pressure equals the atmospheric pressure. 19 EXHALATION Once air enters the lungs, how does air get out of the lungs?  The lung is stretched during inspiration, so when the inspiratory muscles relax, the lung recoils to compress the alveolar gas volume.  Exhalation should normally be passive  This causes alveolar pressure to be higher than atmospheric pressure which will then cause air to flow from the higher pressure to the lower pressure 20 EXHALATION  Specifically, when the diaphragm relaxes, its elasticity causes it to return to its dome shape, decreasing the vertical dimension of the thoracic cavity.  Again, the lung is stretched during inspiration, so when the inspiratory muscles relax, the lung recoils to compress the alveolar gas volume. 21 Balloon Model of Ventilation C. Expiration caused by elastic recoil of diaphragm upward movement  Pressure inside balloon is greater than atmospheric pressure On exhalation, diaphragm relaxes and moves upward causing size of the thoracic cavity to decrease which decreases the volume This causes pleural pressure to increase Because lungs are elastic the increase in the pleural pressure is transmitted to the alveoli which causes the intra-alveolar pressure to increase Now the intra-alveolar pressure is higher than atmospheric the gas will flow from higher pressure to lower pressure Copyright © 2017 Elsevier Inc. All Rights Reserved. 23 Balloon Model of Ventilation D. End-expiration (equilibrium point, no gas flow)  Atmospheric pressure is equal to pressure inside balloon To Summarize Exhalation On exhalation, diaphragm relaxes and moves upward causing size of the thoracic cavity to decrease which decreases the volume This causes pleural pressure to increase Because lungs are elastic the increase in the pleural pressure is transmitted to the alveoli which causes the intra-alveolar pressure to increase Now the intra-alveolar pressure is higher than atmospheric the gas will flow from higher pressure to lower pressure 25 Which of the following statements about alveolar pressure (Palv) during normal quiet breathing is true? A. It is positive during inspiration and negative during expiration B. It is the same as intrapleural pressure C. It is negative during inspiration and positive during expiration D. It always remains less than atmospheric pressure Copyright © 2017 Elsevier Inc. All Rights Reserved. 26 What happens during normal inspiration? 1. The Ppl increases further below atmospheric 2. Transpulmonary pressure gradient widens 3. Palv drops below that at the airway opening A. 1 and 2 only B. 2 and 3 only C. 1 only Copyright © 2017 Elsevier Inc. All Rights Reserved. 27 During expiration, why does gas flow out from the lungs to the atmosphere? A. Palv is less than at the airway opening B. Palv is the same as at the airway opening C. Palv is greater than at the airway opening D. Airway pressure is greater than Palv Copyright © 2017 Elsevier Inc. All Rights Reserved. 28 Break into assigned groups and take turns teaching and explaining the process of of inhalation and exhalation discussing the atmospheric and subatmospheric pressures Some students will be called at random to explain to the class 29 Why is this important? Newborn infant showing intercostal and subcostal retractions  The muscles of inspiration contract forcefully in an effort to generate a greater negative intrapleural and intra-alveolar pressure to draw in more air.  Inspiratory retractions overlying the chest wall are a direct result of increased negative intra-pleural pressure (Used with permission from the author: T. Des Jardins, WindMist LLC) Where else will these concepts apply?. An RT called to assist in care of 22-year-old male motorcycle crash victim who presents in emergency room with numerous abrasions, lacerations, and very serious chest injury (multiple broken ribs over right anterior chest)  In this case, RT must be aware of how the following items profoundly affect patient’s ability to breathe when chest wall is unstable: ◦ Negative intrapleural pressure ◦ Transpulmonary pressure ◦ Transthoracic pressure Flail Chest  Right-sided flail chest  http://youtu.be/mJ_FYwUqzsM When this patient inhales the transpulmonary (PAO-Ppl) and transthoracic (PA-PB)pressure gradients cause his lung to sink in. This is called flail chest This causes the patient’s inspiratory volume to decrease When he exhales, the pressure gradients cause the broken ribs to bulge outward This causes some of the air from the unaffected lung to move into the affected lung – directly under the broken rib rather than be exhaled out Putting the patient on the positive pressure ventilator eliminates the negative intrapleural pressures changes during inspiration. So this stops the adverse effects of transpulmonary and(Used with permission from the author: T. Des Jardins, WindMist LLC) transthoracic pressure gradients during inspiration. Figure 2-12. Forces Opposing Lung Inflation  Lungs have tendency to recoil inward, while chest wall has tendency to move outwards  Those opposing forces keep lung at its resting volumes (FRC) Functional Residual Capacity  Opposition to lung inflation can be put into either  elastic forces: tissues of the lungs, thorax, and abdomen, along with surface tension in the alveoli  frictional forces: resistance caused by gas flow through the airways (natural and artificial), and tissues moved during breathing Copyright © 2017 Elsevier Inc. All Rights Reserved. 33 Forces Opposing Lung Inflation  Elastic opposition to ventilation  Elastic and collagen fibers provide resistance to lung stretch.  Application of air pressure into lungs causes stretch.  Greater pressure causes greater stretch until it just can’t stretch anymore.  Deflation is passive recoil and less force is required to maintain same volume. 34 Forces Opposing Lung Inflation (Cont.)  Elastic opposition to ventilation  During deflation, lung volume at any given pressure is slightly greater than during inflation.  Difference between inflation and deflation curves is hysteresis Copyright © 2017 Elsevier Inc. All Rights Reserved. 35 Surface Tension Forces  Hysteresis partly caused by surface tension  Surface tension opposes lung inflation  Hysteresis tells the clinician if something other than simple elastic tissue forces are present  Lung recoil occurs due to tissue elasticity and surface tension  Pulmonary surfactant reduces lung surface tension  Produced in alveolar type II pneumocytes  Surfactant stabilizes alveoli by preventing collapse  When surface area decreases, ability of pulmonary surfactant to lower surface tension increases  Read mini clini on page 230 Copyright © 2017 Elsevier Inc. All Rights Reserved. 36 Hooke’s Law  Elastance is the natural ability of matter to responds directly to force and return to it’s original shape (like a rubber band)  In respiratory, inflation stretches tissue. The elastic properties of the lungs and chest wall oppose inflation so to increase the volume, pressure must be applied.  In pulmonary physiology, elastance is defined as change in pressure per change in volume Hooke’s Law Applying one unit of force the elastic body will stretch one unit length Same applies with 2 or 3 units of force If it keeps stretching it can’t stretch any further Figure 2-15. Hooke’s Law  When applied to the lungs, volume is substituted for length, and pressure is substituted for force.  Volume varies directly with pressure until the elastic limit of the lung unit is reached. At this point little or no volume occurs. If the pressure continues to rise, the lung unit will rupture.  Hooke’s Law helps explain why hazards such as pneumothorax (resulting from the rupture of alveolar sacs) can occur with the increased pressure of mechanical ventilation. Hooke’s Law Lung Compliance  Compliance is a measure of the lung's ability to stretch and expand  CL defined as change in volume (ΔV) per unit of change in pressure (ΔP) difference across structure or CL = ΔV L (normal 0.2 L/cm H2O) ΔP cm H2O  Pulmonary pathology alters CL  Emphysema , obstructive lung disease, increases CL (loss elastic tissue, lungs more distensible) Large changes in volume for small pressure changes (see next slide)  Fibrosis, restrictive lung disease, decreases C (↑ elastic tissue) L Smaller volume change for any change in pressure Stiffer lungs, usually with reduced volume (see next slide) Copyright © 2017 Elsevier Inc. All Rights Reserved. 41 Lung Compliance (Cont.) Copyright © 2017 Elsevier Inc. All Rights Reserved. 42 Compliance  Increase compliance caused by loss of elastic fibers (like in emphysema).  The lungs are more stretched out so that a normal transpulmonary pressure gradient results in a larger lung volume  Hyperinflation is used to describe an abnormally increased lung volume  Decrease in compliance may be caused by pulmonary fibrosis which affects the connective tissue making them stiff so they are unable to take in more volume Copyright © 2017 Elsevier Inc. All Rights Reserved. 43 Relationship Between Chest Wall and Lung  Lungs and chest wall recoil in opposite directions  Compliance in both is ~0.2 L/cm H2O  Each oppose other, resulting in system compliance of ~0.1 L/cm H2O  FRC (Functional Residual Capacity) established at resting lung level where tendency of chest wall to expand equals that of lungs to collapse Occurs at ~40% TLC (total lung capacity) Copyright © 2017 Elsevier Inc. All Rights Reserved. 44 Chest Wall Ankylosing spondylitis Severe kyphoscoliosis Frictional Resistance to  Ventilation Friction opposition occurs only when the system is in motion.  Tissue viscous resistance  Impeded motion caused by tissue displacement (lungs, rib cage, diaphragm, abdominal organs)  Obesity fibrosis, ascites can also increase impedance  Accounts for approx. 20% of total resistance 46 Frictional Resistance to Ventilation  Airway resistance (~80% of of the frictional resistance to ventilation)  Basically, when gas is trying to flow into the airways but it is being impeded, we call that airway resistance.  Gas flow causes frictional resistance, hence part of the reason we would give heliox (mini clinic page 234) Airway radius exponential effect (r4) on resistance Artificial airway size or bronchospasm  Resistance is highest at nose (50% of total resistance) falls to ~20% of total resistance at small airways  Resistance in nonventilated patient is measured in a pulmonary function laboratory Copyright © 2017 Elsevier Inc. All Rights Reserved. 47 Factors that affect resistance  Laminar flow requires less driving pressure than turbulent flow.  Driving pressure is the difference between inspiratory and expiratory pressure, could also be the difference between PEEP and plateau pressures (Mech Vent class) Copyright © 2017 Elsevier Inc. All Rights Reserved. 48 Airway Resistance  Reducing the radius of a tube by half requires a 16-fold increase in pressure to maintain a constant flow.  Larger driving pressures may be needed  Driving pressure is the difference in pressure from point A to point B  Coffee stirrer or straw? Which one would you like to breathe through and why?  When we use smaller endotracheal tubes it increases WOB for the patients because of the reduced radius.  Refer to rule of thumb on page 234 49  During inspiration the stretch of surrounding lung tissue and widening of the transpulmonary pressure gradient increases the diameter of the airways  This increase with increasing lung volumes decreases airway resistance  As lung volume decreases toward residual volume, airway diameters also decrease and airway resistance dramatically increases  This explains why wheezing is most often heard during exhalation. Copyright © 2017 Elsevier Inc. All Rights Reserved. 50 Rule of Thumb page 236  Patients who have emphysema can directly influence the EPP in their airways to reduce airway collapse and closure  Airway collapse may occur in patients who have emphysema because the normal support structure for small airways has been destroyed.  By exhaling through “pursed lips”, a patient with emphysema change the pressure at the airway opening.  The gentle back pressure created counters the tendency for small airways to collapse by moving EPP toward the larger airways Copyright © 2017 Elsevier Inc. All Rights Reserved. 51 Work of Breathing (WOB)  Respiratory muscles perform work.  Inhalation is active  Exhalation is passive  Forced exhalation requires work.  Pulmonary disease can dramatically increase WOB.  Restrictive disease work is greater due to elastic tissue recoil.  Obstructive disease work is greater due to increased Raw. 52 Pathology’s Affect on WOB A, Normal B, Restrictive disease: slope of the volume-pressure curve is less, showing increased elastic work C, Obstructive disease: Frictional resistance increases dramatically, noted as bulging inspired and expired curves Copyright © 2017 Elsevier Inc. All Rights Reserved. 53  Patient’s with stiff lungs will breathe faster because of the increased elastic WOB.  This pattern of breathing minimizes the mechanical work of distending the lungs but at the expense of more energy to increase the RR  Patient’s with airway obstruction will take on a different pattern to reduce frictional WOB.  These patients may breathe more slowly using pursed lip breathing on exhalation to minimize airway resistance Copyright © 2017 Elsevier Inc. All Rights Reserved. 54 Metabolic Impact of Increased WOB  Respiratory muscles consume O2 to perform work  The rate of O2 consumption (VO2) reflects energy requirements, and can indirectly measure WOB  O2 cost of breathing (OCB) is indirect measurement of WOB  Normal OCB 30% Limits exercise tolerance Impacts ability to wean from mechanical ventilation  In shock, intubation and mechanical ventilation may be indicated to decrease excess oxygen consumption of respiratory muscles  Preserves oxygen delivery for vital organs Copyright © 2017 Elsevier Inc. All Rights Reserved. 55 WOB  Patients who already have muscle weakness are at higher risk for muscle fatigue.  Things like: electrolyte imbalance, shock, sepsis, or disease that causes muscle weakness also play a role in WOB  VT decreases, RR increases, muscle fatigue, gas exchange does not function well 56 Distribution of Ventilation  In upright lung ventilation and perfusion.. (V/Q) are matched best at bases ( called the dependent area).  Ventilation – air movement in & out of lungs  Perfusion – Circulation of blood through tissues 57 Distribution of Ventilation  In healthy lungs, neither ventilation () or perfusion () are distributed evenly  Result: uneven ventilation to perfusion ratio  / ratio of 0.8  In upright lung, ventilation and perfusion (/) are matched best at bases (dependent area)  Apical alveoli are larger but harder to ventilate compared to those at bases  Gravity pulls more blood to bases  In local disease, place good lung down for better / matching. (example is lobar pneumonia) Copyright © 2017 Elsevier Inc. All Rights Reserved. 58 59 Factors Affecting Distribution of Ventilation  Because of varying transpulmonary pressure gradients  Alveoli at the apexes have larger resting volumes than the bases  Because of these larger volumes, the apexes will expand less during inspiration than alveoli at bases  Alveoli at the bases expand more than the alveoli at the apexes  Therefore in an upright patient the base of the lungs will receive approximately 4 times as much ventilation! Without ventilation there is no oxygenation Copyright © 2017 Elsevier Inc. All Rights Reserved. 60 When your patient is in distress sit the patient upright if it is safe to do so Copyright © 2017 Elsevier Inc. All Rights Reserved. 61 Time Constants  Time (in seconds) necessary to inflate a particular lung region to approximately 60% of its potential filling capacity  Lung regions that have either increased Raw or increased CL require more time to inflate  Alveoli said to have long time constant  Lung regions that have either decreased Raw or decreased CL require less time to inflate  Alveoli said to have short time constant Factors Affecting Distribution of Ventilation (Cont.)  Lung unit has long time constant (TC) if CL and Raw is high  Lung unit has short time TC if CL and Raw is low  Effects of unequal lung TCs are different for different ventilator modes Copyright © 2017 Elsevier Inc. All Rights Reserved. 63 Efficiency of Ventilation  To be EFFECTIVE ventilation the body must meet the needs for O2 uptake and CO2 removal.  To be EFFICIENT, ventilation should consume little O2 and produce maximum amount of CO2  Healthy lungs waste some gas due to  Anatomic deadspace of conducting airways  Alveoli that are ventilated but have little or no perfusion (alveolar deadspace) 64. Minute and Alveolar Ventilation  Ventilation = expressed in liters per minute of fresh gas entering the lungs  Total volume moved in and out per minute = Minute ventilation (E)  Normal E = 5-10 L/min  E= fB  VT  6 L/min = 12 breaths/min  0.5 L (500 mL) E driven by CO2 production (metabolic rate) and subject size Copyright © 2017 Elsevier Inc. All Rights Reserved. 65 Dead Space Ventilation  Alveolar dead space (VDalv)  Volume of gas ventilating unperfused alveoli  Alveoli receive gas, but no perfusion or: have ventilation exceeding perfusion (high / ratios) excess ventilation, more than necessary to arterialize alveolar blood is wasted ventilation Copyright © 2017 Elsevier Inc. All Rights Reserved. 66 Dead Space Ventilation (Cont.)  Usually related to defects in pulmonary circulation  e.g., pulmonary embolism Blocks portion of pulmonary circulation  Apical alveoli have minimal or no perfusion in normal upright subject at rest, contributing to dead space Copyright © 2017 Elsevier Inc. All Rights Reserved. 67 Dead Space Ventilation (Cont.) Copyright © 2017 Elsevier Inc. All Rights Reserved. 68 69

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