Positive pressure ventilation: what is the real cost?

1. Positivepressure ventilation:what is the real cost? Br J Anaesth 2008; 101: 446-57 R4 김용일

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 • Monitoringof 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 -> tolerance develops rapidly -> 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 Laplace’s 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 -> 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 • InARDS • 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 • Damagedor 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 pphlymphatics : 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

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