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![Trans pulmonary pressure (pressure at airway opening
minus pleural pressure) [= Transrespiratory pressure?]
Transpulmonary pressure is the distending force of the
lung
The airway-pressure gauge on a positive-pressure
ventilator displays transrespiratory pressure](https://image.slidesharecdn.com/conv-150326101557-conversion-gate01/75/Conv-ventilation-physi-14-2048.jpg)
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Conv. ventilation physi
- 1. Physiology of positive pressureventilation SAMIR EL ANSARY
- 2. Global Critical Care https://www.facebook.com/groups/1451610115129555/#!/groups/145161011512 9555/ Wellcomein our new group ..... Dr.SAMIR EL ANSARY
- 3. Mechanical ventilation – Supports/ replaces the normal ventilatory pump moving air in & out of the lungs. Primary indications – a.apnea b.Ac. ventilation failure c. Impending ventilation failure d.Severe oxygenation failure
- 4. Goals Manipulate gasexchange ↑ lung vol – FRC, end insp / exp lung inflation Manipulate work of breathing (WOB) Minimize CVS effects
- 5. ARTIFICIAL VENTILATION - Creates atransairway P gradient by ↓ alveolar P to a level below airway opening P - Creates – P around thorax e.g. iron lung chest cuirass / shell - Achieved by applying + P at airway opening producing a transairway P gradient Negative pressure ventilation Positive pressure ventilation
- 6. ventilation without artificialairway -Nasal , face mask adv. 1.Avoid intubation / c/c 2.Preserve natural airway defences 3.Comfort 4.Speech/ swallowing + 5.Less sedation needed 6.Intermittent use Noninvasive Disadv 1.Cooperation 2.Mask discomfort 3.Air leaks 4.Facial ulcers, eye irritation, dry nose 5.Aerophagia 6.Limited P support e.g. BiPAP, CPAP
- 7. Ventilatory support FULL PARTIAL Allenergy provided by ventilator e.g. ACV / full support SIMV ( RR = 12-26 & TV = 8-10 ml/kg) Pt provides a portion of energy needed for effective ventilation e.g. SIMV (RR < 10) Used for weaning WOB total = WOB ventilator (forces gas into lungs)+ WOB patient (msls draw gas into lungs)
- 8. Understanding physiology ofPPV 1) Different P gradients 2) Time constant 3) Airway P ( peak, plateau, mean ) 4) PEEP and Auto PEEP 5) Types of waveforms
- 9.
- 11. Distending pressure oflungs Elastance load Resistance load Distending pressure
- 12. Flow through theairways is generated by Transairway pressure (pressure at the airway opening minus pressure in the lungs). Expansion of the elastic chamber is generated by Transthoracic pressure (pressure in the lungs minus pressure on the body surface).
- 13. Transrespiratory pressure (pressureat the airway opening minus pressure on the body surface) is the sum of these two pressures and is the total pressure required to generate inspiration. Transrespiratory pressure can have two components, one secondary to the ventilator (pvent) and one secondary to the respiratory muscles (Pmusc)
- 14. Trans pulmonary pressure(pressure at airway opening minus pleural pressure) [= Transrespiratory pressure?] Transpulmonary pressure is the distending force of the lung The airway-pressure gauge on a positive-pressure ventilator displays transrespiratory pressure
- 15. Pressure, volume, andflow are functions of time and are called variables. They are all measured relative to their values at end expiration. Elastance and resistance are assumed to remain constant and are called parameters.
- 16. Elastance(measure of stiffness)is the inverse of compliance(measure of stretchiness) An increase in elastance implies that the system is becoming stiffer.
- 17. Mean airway pressurePaw = Transrespiratory pressure Mean alveolar pressure Palv = Transthoracic pressure
- 18. Transpulmonary pressure isthe distending pressure in a spontaneously(negative) breathing patient Transrespiratory pressure is the distending pressure in positive pressure ventilation
- 20. Airway pressures Peak inspP (PIP) • Highest P produced during insp. • PRESISTANCE + P INFLATE ALVEOLI • Dynamic compliance • Barotrauma Plateau P • Observed during end insp pause •P INFLATE ALVEOLI •Static compliance •Effect of flow resistance negated
- 21. Time constant • Definedfor variables that undergo exponential decay • Time for passive inflation / deflation of lung / unit t = compliance X resistance = VT . peak exp flow Normal lung C = 0.1 L/cm H2O R = 1cm H2O/L/s COAD – resistance to exp increases → time constant increases → exp time to be increased lest incomplete exp ( auto PEEP generates). ARDS - inhomogenous time constants
- 22. Why and howto separate dynamic & static components ? • Why – to find cause for altered airway pressures • How – adding end insp pause - no airflow, lung expanded, no expiration
- 23. How -End inspiratoryhold • Pendelluft phenomenon • Visco-elastic properties of lung End-inspiratory pause Ppeak < 50 cm H2O Pplat < 30 cm H2O Ppeak = Pplat + Paw
- 24. At the startof inflation, the airway pressure immediately rises because of the resistance to gas flow (A), and at the end of inspiratory gas flow the airway pressure immediately falls by the same pressure (A) to an inflexion point. Thereafter, the airway pressure more gradually declines to the plateau pressure. The loss of airway pressure after the inflexion (B) is due to gas redistribution (Pendelluft) and the visco- plasto-elastic lung and thorax behaviour
- 25. P2(Pplat) is thestatic pressure of the respiratory system, which in the absence of flow equals the alveolar pressure, which reflects the elastic retraction of the entire respiratory system. The pressure drop from PIP to P1 represents the pressure required to move the inspiratory flow along the airways without alveolar interference, thus representing the pressure dissipated by the flow- dependent resistances(airway resistance).
- 26. The slow post-occlusiondecay from P1 to P2 depends on the viscoelastic properties of the system and on the pendulum-like movement of the air (pendelluft). During the post-inspiratory occlusion period there is a dynamic elastic rearrangement of lung volume, which allows the different pressures in alveoli at different time constants to equalize, and depends on the inhomogeneity of the lung parenchyma.
- 27. The lung regionsthat have a low time constant (ie, rapid zones), where the alveolar pressure rises rapidly, are emptied in the lung regions that have higher time constants (ie, slow zones), where the pressure rises more slowly because of higher resistance or lower compliance
- 28. The static complianceof the respiratory system mirrors the elastic features of the respiratory system, whereas The dynamic compliance also includes the resistive (flow-dependent) component of the airways and the endotracheal tube
- 29. When the inspiratorypause is shorter than 2 seconds, P2 does not always reflect the alveolar pressure. The compliance value thus measured is called quasi- static compliance. In healthy subjects the difference between static compliance and quasi-static compliance is minimal, whereas it is markedly higher in patients who have acute respiratory distress syndrome or chronic obstructive pulmonary disease
- 30. Ppeak < 50cm H2O; Pplat < 35 cm H2O – to avoid barotrauma
- 31. • Pendulum likemovement of air between lung units • Reflects inhomogeneity of lung units • More in ARDS and COPD • Can lead to falsely measured high Pplat if the end- inspiratory occlusion duration is not long enough
- 32.
- 33. Mean airway P(MAP) • average P across total cycle time (TCT) • MAP = 0.5(PIP-PEEP)X Ti/TCT + PEEP • Decreases as spontaneous breaths increase • MAPSIMV < MAPACV • Hemodynamic consequences Factors 1. Mandatory breath modes 2. ↑insp time , ↓ exp time 3. ↑ PEEP 4. ↑ Resistance, ↓compliance 5. Insp flow pattern
- 34. PEEP BENEFITS 1. Restore FRC/ Alveolarrecruitment 2. ↓ shunt fraction 3. ↑Lung compliance 4. ↓WOB 5. ↑PaO2 for given FiO2 DETRIMENTAL EFFECTS 1. Barotrauma 2. ↓ VR/ CO 3. ↑ WOB (if overdistention) 4. ↑ PVR 5. ↑ MAP 6. ↓ Renal / portal bld flow PEEP prevents complete collapse of the alveoli and keep them partially inflated and thus provide protection against the development of shear forces during mechanical inflation
- 35. How much PEEPto apply? Lower inflection point – transition from flat to steep part - ↑compliance - recruitment begins (pt. above closing vol) Upper inflection point – transition from steep to flat part - ↓compliance - over distension
- 36. Set PEEP aboveLIP – Prevent end expiratory airway collapse Set TV so that total P < UIP – prevent overdistention Limitation – lung is inhomogenous - LIP / UIP differ for different lung units
- 37. Auto-PEEP or IntrinsicPEEP • What is Auto-PEEP? – Normally, at end expiration, the lung volume is equal to the FRC – When PEEPi occurs, the lung volume at end expiration is greater then the FRC
- 38. Auto-PEEP or IntrinsicPEEP • Why does hyperinflation occur? – Airflow limitation because of dynamic collapse – No time to expire all the lung volume (high RR or Vt) – Lesions that increase expiratory resistance Function of- Ventilator settings – TV, Exp time Lung func – resistance, compliance
- 39. Auto-PEEP or IntrinsicPEEP • Auto-PEEP is measured in a relaxed pt with an end-expiratory hold maneuver on a mechanical ventilator immediately before the onset of the next breath
- 40. Inadequate expiratory time- Air trapping iPEEP Flow curve FV loop 1. Allow more time for expiration 2. Increase inspiratory flow rate 3. Provide ePEEP
- 41. Disadv 1. Barotrauma /volutrauma 2. ↑WOB a) lung overstretching ↓contractility of diaphragm b) alters effective trigger sensitivity as autoPEEP must be overcome before P falls enough to trigger breath 3. ↑ MAP – CVS side effects 4. May ↑ PVR Minimising Auto PEEP 1. ↓airflow res – secretion management, bronchodilation, large ETT 2. ↓Insp time ( ↑insp flow, sq flow waveform, low TV) 3. ↑ exp time (low resp rate ) 4. Apply PEEP to balance AutoPEEP
- 42. Cardiovascular effects ofPPV Spontaneous ventilation PPV
- 43. Determinants of hemodynamiceffects due to – change in ITP, lung volumes, pericardial P severity – lung compliance, chest wall compliance, rate & type of ventilation, airway resistance
- 44. Low lung compliance– more P spent in lung expansion & less change in ITP less hemodynamic effects (DAMPNING EFFECT OF LUNG) Low chest wall compliance – higher change in ITP needed for effective ventilation more hemodynamic effects
- 45. Effect on CO( preload , afterload ) Decreased PRELOAD 1.compression of intrathoracic veins (↓ CVP, RA filling P) 2.Increased PVR due to compression by alveolar vol (decreased RV preload) 3.Interventricular dependence - ↑ RV vol pushes septum to left & ↓ LV vol & LV output Decreased afterload 1. emptying of thoracic aorta during insp 2. Compression of heart by + P during systole 3. ↓ transmural P across LV during systole
- 46. PPV ↓ preload, ventricular filling ↓afterload , ↑ventricular emptying CO – 1. INCREASE 2. DECREASE 1. Intravascular fluid status 2. Compensation – HR, vasoconstriction 3. Sepsis, 4. PEEP, MAP 5. LV function
- 47. Effect on otherbody systems
- 48. Overview 1. Mode ofventilation – definition 2. Breath – characteristics 3. Breath types 4. Waveforms – pressure- time, volume –time, flow- time 5. Modes - Volume & pressure limited 6. Conventional modes of ventilation 7. Newer modes of ventilation
- 49. What is a‘ mode of ventilation’ ? A ventilator mode is delivery a sequence of breath types & timing of breath
- 50. Breath characteristics A= whatinitiates a breath - TRIGGER B = what controls / limits it – LIMIT C= What ends a breath - CYCLING
- 51. TRIGGER What the ventilator sensesto initiate a breath Patient • Pressure • Flow Machine • Time based Recently – EMG monitoring of phrenic Nerve via esophageal transducer Pressure triggering -1 to -3 cm H2O Flow triggering -1 to -3 L/min
- 52. CONTROL/ LIMIT Variable notallowed to rise above a preset value Does not terminate a breath Pressure Volume Pressure Controlled • Pressure targeted, pressure limited - Ppeak set • Volume Variable Volume Controlled • Volume targeted, volume limited - VT set • Pressure Variable Dual Controlled • volume targeted (guaranteed) and pressure limited
- 53. CYCLING VARIABLE Determines theend of inspiration and the switch to expiration Machine cycling • Time • Pressure • Volume Patient cycling • Flow May be multiple but activated in hierarchy as per preset algorithm
- 54. Breath types Spontaneous Both triggeredand cycled by the patient Control/Mandatory Machine triggered and machine cycled Assisted Patient triggered but machine cycled
- 55. Waveforms 1. Volume -time 2.Flow - time 3. Pressure - time
- 56. a) Volume –time graphs 1. Air leaks 2. Calibrate flow transducers
- 57. b) Flow waveforms 1.Inspiratory flow waveforms
- 58. Sine Square Decelerating • Resembles normal inspiration •More physiological • Maintains constant flow • high flow with ↓ Ti & improved I:E • Flow slows down as alveolar pressure increases • meets high initial flow demand in spont breathing patient - ↓WOB Accelerating • Produces highest PIP as airflow is highest towards end of inflation when alveoli are less compliant Square- volume limited modes Decelerating – pressure limited modes Not used
- 59. Inspiratory and expiratoryflow waveforms
- 60. 2. Expiratory flowwaveform Expiratory flow is not driven by ventilator and is passive Is negative by convention Similar in all modes Determined by Airway resistance & exp time (Te) Use 1.Airtrapping & generation of AutoPEEP 2.Exp flow resistance (↓PEFR + short Te) & response bronchodilators (↑PEFR)
- 61. c) Pressure waveform 1.Spontaneous/ mandatory breaths 2. Patient ventilator synchrony 3. Calculation of compliance & resistance 4. Work done against elastic and resistive forces 5. AutoPEEP ( by adding end exp pause)
- 62. Classification of modesof ventilation Volume controlled Pressure controlled TV & inspiratory flow are preset Airway P is preset Airway P depends on above & lung elastance & compliance TV & insp flow depend on above & lung elastance & compliance
- 64. Volume controlled Pressurecontrolled Trigger - patient / machine Patient / machine Limit Flow Pressure Cycle Volume / time time / flow TV Constant variable Peak P Variable constant Modes ACV, SIMV PCV, PSV
- 65. Volume controlled Pressurecontrolled Advantages 1. Guaranteed TV 2. Less atelectasis 3. TV increases linearly with MV Advantages 1. Limits excessive airway P 2. ↑ MAP by constant insp P – better oxygenation 3. Better gas distribution – high insp flow ↓Ti & ↑Te ,thereby, preventing airtrapping 4. Lower WOB – high initial flow rates meet high initial flow demands 5. Lower PIP – as flow rates higher when lung compliance high i.e early insp. phase Disadvantages 1. Limited flow may not meet patients desired insp flow rate- flow hunger 2. May cause high Paw ( Disadvantages 1. Variable TV ↑TV as compliance ↑ ↓TV as resistance ↑
- 66. Conventional modes ofventilation 1. Control mandatory ventilation (CMV / VCV) 2. Assist Control Mandatory Ventilation (ACMV) 3. Intermittent mandatory ventilation (IMV) 4. Synchronized Intermittent Mandatory Ventilation (SIMV) 5. Pressure controlled ventilation (PCV) 6. Pressure support ventilation (PSV) 7. Continuous positive airway pressure (CPAP)
- 67. 1. Control mandatoryventilation (CMV / VCV) • Breath - MANDATORY • Trigger – TIME • Limit - VOLUME • Cycle – VOL / TIME • Patient has no control over respiration • Requires sedation and paralysis of patient
- 68. 2. Assist ControlMandatory Ventilation (ACMV) • Patient has partial control over his respiration – Better Pt ventilator synchrony • Ventilator rate determined by patient or backup rate (whichever is higher) – risk of respiratory alkalosis if tachypnoea • PASSIVE Pt – acts like CMV • ACTIVE pt – ALL spontaneous breaths assisted to preset volume • Breath – MANDATORY ASSISTED • Trigger – PATIENT TIME • Limit - VOLUME • Cycle – VOLUME / TIME Once patient initiates the breath the ventilator takes over the WOB If he fails to initiate, then the ventilator does the entire WOB
- 69. 3. Intermittent mandatoryventilation (IMV) Breath stacking Spontaneous breath immediately after a controlled breath without allowing time for expiration ( SUPERIMPOSED BREATHS) Basically CMV which allows spontaneous breaths in between Disadvantage In tachypnea can lead to breath stacking - leading to dynamic hyperinflation Not used now – has been replaced by SIMV • Breath – MANDATORY SPONTANEOUS • Trigger – PATIENT VENTILATOR • Limit - VOLUME • Cycle - VOLUME
- 70. 4.Synchronized Intermittent Mandatory Ventilation(SIMV) • Breath – SPONTANEOUS ASSISTED MANDATORY • Trigger – PATIENT TIME • Limit - VOLUME • Cycle – VOLUME/ TIME
- 71. • Basically, ACMVwith spontaneous breaths (which may be pressure supported) allowed in between • Synchronisation window – Time interval from the previous mandatory breath to just prior to the next time triggering, during which ventilator is responsive to patients spontaneous inspiratory effort • Weaning Adv Allows patients to exercise their respiratory muscles in between – avoids atrophy Avoids breath stacking – ‘Synchronisation window’
- 72. 5.Pressure controlled ventilation(PCV) • Breath – MANDATORY • Trigger – TIME • Limit - PRESSURE • Cycle – TIME/ FLOW Rise time Time taken for airway pressure to rise from baseline to maximum
- 73. 6.Pressure support ventilation(PSV) • Breath – SPONTANEOUS • Trigger – PATIENT • Limit - PRESSURE • Cycle – FLOW ( 5-25% OF PIFR) After the trigger, ventilator generates a flow sufficient to raise and then maintain airway pressure at a preset level for the duration of the patient’s spontaneous respiratory effort
- 75. Newer modes ofventilation
- 77. Dual modes ofventilation Devised to overcome the limitations of both V & P controlled modes Dual control within a breath Switches from P to V control during the same breath e.g. VAPS PA Dual control from breath to breath P limit ↑ or ↓ to maintain a clinician set TV ANALOGOUS to a resp therapist who ↑ or ↓ P limit of each breath based on TV delivered in last breath
- 78. Dual control withina breath Combined adv – 1. High & variable initial flow rate of P controlled breath ( thereby - ↑ pt – vent synchrony, ↓WOB, ↓sense of breathlessness) 2. Assured TV & MV as in V controlled breaths Starts as P limited breaths but change over to V limited breath by converting decelerating flow to constant flow if minimum preset TV not delivered
- 79. 1. Breath triggered(pt/ time) – 2. P support level reached quickly – 3. ventilator compares delivered and desired/ set TV 4. Delivered = set TV -------- Breath is FLOW cycled as in P controlled modes 5. Delivered < set TV -------- Changeover from P to V limited ( flow kept constant + Ti ↑) P rises above set P support level till set TV delivered
- 80. Dual control –breath to breath P limited + FLOW cycled Vol support / variable P support P limited + TIME cycled PRVC
- 81. Volume support Allows automaticweaning of P support as compliance alters. OPERATION – C = V P changes during weaning & guides P support level Preset & constant P support dependent on C compliance ↑ - P support ↓ ↓ - P support ↑ By 3 cm H2O / breath Deliver desired TV
- 83. Pressure regulated volumecontrolled (PRVC) • Autoflow / variable P control • Similar to VS except that it is a modification of PCV rather than PSV
- 84. 1. Conventional Vcontrolled mode – very high P would have resulted in an attempt to deliver set TV -------- BAROTRAUMA 2. Conventional P controlled mode – inadequate TV would have been delivered
- 85. Shifts between Psupport (flow cycled)& P control (time cycled) mode with pt efforts Combines VS & PRVC If no efforts : PRVC (time cycled) As spontaneous breathing begins : VS (flow cycled) Automode
- 86. Pitfalls : During theswitch from time-cycled to flow cycled ventilation Mean airway pressure hypoxemia may occur Automode
- 87. Compensates forthe resistance of ETT Facilitates “ electronic weaning “ i.e pt during ATC mimic their breathing pattern as if extubated ( provided upper airway contorl provided) Operation As the flow ↑ / ETT dia ↓, the P support needs to be ↑to ↓WOB ∆P (P support) α (L / r4 ) α flow α WOB Automatic Tube Compensation
- 88. Static condition Single Psupport level can eliminate ETT resistance Dynamic condition Variable flow e.g. tachypnoea & in different phases of resp. P.support needs to be continously altered to eliminate dynamically changing WOB.
- 89. 1. Feed resistivecoef of ETT 2. Feed % compensation desired 3. Measures instantaneous flow Calculates P support proportional to resistance throughout respiratory cycle Limitation Resistive coef changes in vivo ( kinks, temp,molding, secretions) Under/ overcompensation may result.
- 90. Airway pressure releaseventilation (APRV) • High level of CPAP with brief intermittent releases to a lower level Conventional modes – begin at low P & elevate P to accomplish TV APRV – commences at elevated P & releases P to accomplish TV
- 91. Higher plateau P– improves oxygenation Release phase – alveolar ventilation & removal of CO2 Active patient – spontaneous breathing at both P levels Passive patient – complete ventilation by P release
- 92. Settings 1.Phigh (15 –30 cmH2O ) 2.Plow (3-10 cmH2O ) == PEEP 3. F = 8-15 / min 4. Thigh /Tlow = 8:1 to 10:1 If ↑ PaCO2 -↑ Phigh or ↓ Plow - ↑ f If ↓ PaO2 - ↑ Plow or FiO2
- 94. Proportional Assist Ventilation •Targets fixed portion of patient’s work during “spontaneous” breaths • Automatically adjusts flow, volume and pressure needed each breath
- 95. WOB Ventilator measures –elastance & resistance Clinician sets -“Vol. assist %” reduces work of elastance “Flow assist%” reduces work of resistance's Increased patient effort (WOB) causes increased applied pressure (and flow & volume) ELASTANCE (TV) RESISTANCE (Flow)
- 97. Biphasic positive airwaypressure (BiPAP) PCV & a variant of APRV Time cycled alteration between 2 levels of CPAP BiPAP – P support for spontaneous level only at low CPAP level Bi-vent - P support for spontaneous level at both low & high CPAP Spontaneous breathing at both levels Changeover between 2 levels of CPAP synchronized with exp & insp
- 99.
- 100. Advantages 1. Allows unrestrictedspontaneous breathing 2. Continuous weaning without need to change ventilatory mode – universal ventilatory mode 3. Synchronization with pt’s breathing from exp. to insp. P level & vice versa 4. Less sedation needed
- 101. Neurally Adjusted VentilatoryAssist (NAVA)
- 102. Global Critical Care https://www.facebook.com/groups/1451610115129555/#!/groups/145161011512 9555/ Wellcomein our new group ..... Dr.SAMIR EL ANSARY
- 103. GOOD LUCK SAMIR ELANSARY ICU PROFESSOR AIN SHAMS CAIRO [email protected]
Editor's Notes
- #12 Flow through the airways is generated by Transairway pressure (pressure at the airway opening minus pressure in the lungs). Expansion of the elastic chamber is generated by Transthoracic pressure (pressure in the lungs minus pressure on the body surface). Transrespiratory pressure (pressure at the airway opening minus pressure on the body surface) is the sum of these two pressures and is the total pressure required to generate inspiration. Transrespiratory pressure can have two components, one secondary to the ventilator (pvent) and one secondary to the respiratory muscles (Pmusc) Trans pulmonary pressure (pressure at airway opening minus pleural pressure) [= Transrespiratory pressure?] Transpulmonary pressure is the distending force of the lung The airway-pressure gauge on a positive-pressure ventilator displays transrespiratory pressure Pressure, volume, and flow are functions of time and are called variables. They are all measured relative to their values at end expiration. Elastance and resistance are assumed to remain constant and are called parameters.– PPMV 2nd edition 2006 Elastance(measure of stiffness) is the inverse of compliance(measure of stretchiness), and an increase in elastance implies that the system is becoming stiffer. Mean airway pressure Paw = Transrespiratory pressure Mean alveolar pressure Palv = Transthoracic pressure ?transpulmonary pressure is the distending pressure in a spontaneously(negative) breathing patient and transrespiratory pressure is the distending pressure in positive pressure ventilation
- #24 At the start of inflation, the airway pressure immediately rises because of the resistance to gas flow (A), and at the end of inspiratory gas flow the airway pressure immediately falls by the same pressure (A) to an inflexion point. Thereafter, the airway pressure more gradually declines to the plateau pressure. The loss of airway pressure after the inflexion (B) is due to gas redistribution (Pendelluft) and and the visco-plasto-elastic lung and thorax behaviour P2(Pplat) is the static pressure of the respiratory system, which in the absence of flow equals the alveolar pressure, which reflects the elastic retraction of the entire respiratory system. The pressure drop from PIP to P1 represents the pressure required to move the inspiratory flow along the airways without alveolar interference, thus representing the pressure dissipated by the flow-dependent resistances(airway resistance). The slow post-occlusion decay from P1 to P2 depends on the viscoelastic properties of the system and on the pendulum-like movement of the air (pendelluft). During the post-inspiratory occlusion period there is a dynamic elastic rearrangement of lung volume, which allows the different pressures in alveoli at different time constants to equalize, and depends on the inhomogeneity of the lung parenchyma. The lung regions that have a low time constant (ie, rapid zones), where the alveolar pressure rises rapidly, are emptied in the lung regions that have higher time constants (ie, slow zones), where the pressure rises more slowly because of higher resistance or lower compliance The static compliance of the respiratory system mirrors the elastic features of the respiratory system, whereas the dynamic compliance also includes the resistive (flow-dependent) component of the airways and the endotracheal tube When the inspiratory pause is shorter than 2 seconds, P2 does not always reflect the alveolar pressure. The compliance value thus measured is called quasi-static compliance. In healthy subjects the difference between static compliance and quasi-static compliance is minimal, whereas it is markedly higher in patients who have acute respiratory distress syndrome or chronic obstructive pulmonary disease - Lucangelo U; Respir Care 2005;50(1):55–65 Ppeak < 50 cm H2O; Pplat < 35 cm H2O – to avoid barotrauma – ACCP concensus conference – Slutsky AS – Chest 1993
- #41 In most patients with obstructive lung disease, failure to reach zero flow at the end of a relaxed expiration signifies that lung volume is above functional residual capacity and indicates dynamic hyperinflation High inspiratory flow allow short inspiratory time and therefore longer expiratory time for any given respiratory rate . Volume control ventilation is better than pressure control for COAD patients
- #59 The parameter that is manipulated to drive inflation is known as the ‘control’ parameter, while the parameter that is measured to provide feedback to limit or augment the control parameter is described as the ‘target’ or ‘limit’ parameter