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Positive pressure ventilation: what is the real cost?

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Title: Positive pressure ventilation: what is the real cost?


1
Positive pressure ventilationwhat is the real
cost?
  • Br J Anaesth 2008 101 446-57
  • R4 ???

2
Positive pressure ventilation
  • Copenhagen polio epidemic
  • Reduction in mortality 87 ? 40
  • considerable deviation from the normal
    physiological mechanism of respiration
  • by Mushin in 1st edition of Ventilation of the
    Lungs
  • Pathophysiological price to pay
  • Not all complications are obvious or immediate

3
Oxygenation and ventilation
  • Monitoring of oxygenation
  • Focuses on inspired oxygen concentration,
    arterial blood gases
  • Arterial values of oxygenation not ideal
    parameters
  • Circulation
  • Tissue and cell transport
  • Mitochondrial function between lung and cell
  • In the critically ill
  • Relatively low arterial saturation ? but,
    adequate tissue oxygenation
  • Jeopardous tissue oxygenation ? not related
    directly to lungs
  • Low saturation PaO2 poorly correlate with
    tissue oxygenation
  • Difficult to oxygenate -gt tolerance develops
    rapidly -gt no markers of tissue hypoxia
  • few patients with lung injury die of hypoxemia
  • Reconsider about methods of assessing adequacy of
    oxygenation

4
Breathing, ventilation, and intrathoracic
pressures
  • In spontaneous breathing
  • Inspiration
  • Small negative intrapleural, interstitial,
    alveolar pressures
  • Expiration
  • Intrapleural pr returns atmospheric, but
    remains negative
  • Interstitial alveolar pr atmospheric or
    slightly positive
  • In positive pressure ventilation
  • Inspiration
  • High intrathoracic pr
  • Expiration
  • Return towards atmospheric pressure

5
Ventilation, alveolar ventilation, and recruitment
  • Surfactant
  • Modifies the effects of Laplaces law
  • Small alveoli are easy to inflate less tendency
    to collapse
  • In positive pressure ventilation
  • Individual time constants of lung regions or
    alveoli
  • Airway resistance alveolar compliance
  • Determine the effect of pressure in different
    regions of lung
  • Positive pressure -gt preferentially aerate high
    compliance areas
  • Collapsed alveoli may require high sustained
    pressure

6
Ventilation, alveolar ventilation, and
recruitment - continued
  • Recruitment
  • Opening maintaining open potentially under
    ventilated areas
  • To hence alveolar surface area involved in gas
    exchange
  • Initial sustained high pressure with subsequent
    PEEP at various levels
  • In ARDS
  • Only achieved a mean recruitment of 13
  • High levels of PEEP (15 mmHg) are more effective
  • Both in maintaining alveolar patency improving
    oxygenation
  • Effective in preventing collapse and derecruiment
  • ? Sustained increase in intrathoracic pressure

7
Ventilation, alveolar ventilation, and
recruitment - continued
  • Result of recruitment is unpredictable
  • Increase gas distribution not to abNL areas
  • Over-inflating funcional areas
  • ? potentially impairing their function
  • Recruitment in damaged lungs
  • ? may exacerbate problems

8
Ventilation pressure and stretch
  • Lower peak pressure ventilation
  • Reduce mortality
  • Shear forces occur particularly in initiating
    inflation
  • May cause injury
  • Stress shear forces
  • Cytokine production increased
  • White cell sequestration
  • May predispose to injury infection
  • In recruitment
  • Lowering of the peak pressure
  • Whereas higher PEEP
  • ? maintains alveolar patency reduces the shear
    forces

9
Ventilation and surfactant
  • Distortion of surfactant spread
  • With positive pressure ventilation
  • Forced air ? pressure waveform
  • Wave formation in surfactant layers
  • Altering the uniformity of spread
  • Influences the production function of
    surfactant
  • In lung injury (inflammation)
  • Reduced type II pneumocytes ? reduced surfactant
    production
  • Release protein other materials
  • Affects ability of surfactant to form surface
    structures
  • Membrane permeability changes ? Fluid dilution of
    surfactant
  • Polymerizing fibrin ? Adsorbs surface active
    compounds
  • Role in immune defence of surfactant
  • Influence inflammatory response
  • Substantial role in mucosal immunity
  • ? Vicious cycle to cause further injury

10
Effects on the cardiovascular system
  • In normal breathing
  • In inspiration, assists venous return, pulm
    capillary flow
  • With positive pressure ventilation
  • During inspiration increased intrathoracic
    pressure
  • Decrease venous return, RV output, pulm blood
    flow
  • On expiration intrathoracic pressure returns to
    zero
  • PEEP ? positive pressure continued ? inhibit
    venous return
  • Fluid administration improves venous return
    cardiac output
  • Increase CVP, increase end-capillary pressures in
    lungs other organ
  • Salt water retention
  • Classically d/t increased secretion of
    anti-diuretic hormone
  • More recently, atrial natriuretic peptide
    implicated
  • Correction by IV fluid ? further fluid retention

11
The pulmonary capillary and blood flow
  • Mean capillary pressure 7-10 mmHg
  • Normal breathing
  • Interstitium alveoli pressure lower than
    capillary perfusion pressure
  • Pressure within lung lower than capillary
    pressure
  • In COPD with hyperinflation
  • High intrathoracic pressure on expiration
  • ? increasing capillary resistance
  • Positive pressure ventilation
  • Peak inspiratory pressure limited to 30 mmHg
  • Compress capillary, impede flow
  • In expiration, PEEP of 15 mmHg
  • Prevents recovery of normal flow
  • Inflatable lung region pressure transmitted
  • Damaged or infected lung better perfusion
  • ? impeded capillary flow (ineffective hypoxic
    vasoconstriction)

12
The pulmonary capillary and blood flow -
continued
  • High venous pressure secondary to positive
    pressure ventilation
  • ? interstitial fluid retention
  • Capillary stress failure in extreme exercise
    in racehorses
  • Pulmonary artery pressure, inflation pressure,
    venous pressure high
  • ? damage the integrity of capillary endothelium
  • Probably also seen in humans
  • Compensatory mechanisms ineffective
  • May aggravate ventilation-perfusion mismatch

13
Lymphatics
  • Functions drainage defence
  • Lung lymphatics
  • Within interstitium, thin, single cell conduits
    with valves
  • Inspiration negative pressure ? drain into
    lymphatics
  • Pressure in pph lymphatics max 4 mmHg
  • Hydrostatic gradient between lymphatics central
    veins
  • During inspiration
  • Flow easily impeded by
  • External pressure on lymphatic walls
  • Outflow resistance

14
Lymphatics -continued
  • Positive pressure ventilation
  • During inspiration
  • Push fluid from alveolus to interstitium
    lymphatics
  • May compress thin-walled vessels
  • High CVPs
  • Significant hydrostatic barrier to flow
  • During expiration
  • Allow resumption of flow
  • In PEEP
  • Helps remove fluid from alveoli, but reduction in
    thoracic duct drainage
  • ? fluid retention in interstitium
  • PEEP in injured lung
  • Increases lymph production, but impairs lymph
    flow
  • Impaired drainage
  • ? fluid accumulation in lung pleural spaces
  • ? increased susceptibility to lung infection

15
Organ systemsand positive pressure ventilation
  • Effects on kidney
  • Decreased cardiac output
  • Decrease in GFR
  • Diversion of intra-renal blood flow
  • Effects of PEEP on hepato-splanchnic circulation
  • Venous congestion
  • Reduced portal blood flow
  • Increased hepatic blood volume
  • Reduced hepatosplanchnic lymphatic drainage
  • Sustained increases in CVP lead to
  • Venous congestion
  • Increased end-capillary pressure
  • Altered fluid dynamics within organs
  • Affects lymphatic function
  • Raised intraabdominal pressure
  • Impairs lymphatic drainage
  • High thoracic duct pressure
  • Increases interstitial fluid in liver kidneys

16
Conclusions
  • Ventilation with PEEP
  • Proven, effective modality in anesthesia ICU
  • But, cause physiological derangements
  • Redistribution of alveolar ventilation
  • Altered capillary perfusion
  • Functional changes in surfactant
  • Transcapillary fluid shifts
  • Impaired lymphatic drainage
  • Impeded venous return
  • Prolonged ventilation
  • Lung injury
  • Infection
  • Multi-organ system dysfunction
  • Real cost of ventilation or oxygenation
  • ? higher than realized

17
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20
Conclusions - continued
  • Are there potential alternatives?
  • Tank or cuirasses
  • Generate a negative inspiratory pressure
  • Development of bedside extracorporeal oxygenation
  • Using the heart as the pump
  • Lung assist devices
  • In their infancy
  • For future progress
  • Recognition of physiological derangement
  • Accepting the physical physiological
    constraints
  • In further evolution of positive pressure
    ventilation
  • Technology of positive pressure ventilation
  • Now more than 50 yr old
  • Time to consider alternatives
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