Acute respiratory distress syndrome mechanical ventilation therapy
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Mechanical Ventilation Therapy
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Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed inevitable. The origin of infection, when surgically treatable, must be operated on. When sepsis is diagnosed, appropriate local medical protocols should be enacted.
Commonly used supportive therapy includes particular techniques of mechanical ventilation and pharmacological agents whose effectiveness with respect to the outcome has not yet been proven. It is now debated whether mechanical ventilation is to be considered mere supportive therapy or actual treatment, since it may substantially affect survival.
- Further information: Pressure Regulated Volume Control
The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application. Three parameters are used: PEEP (positive end-expiratory pressure, to maintain maximal recruitment of alveolar units), mean airway pressure (to promote recruitment and predictor of hemodynamic effects) and plateau pressure (best predictor of alveolar overdistention). 
Conventional therapy aimed at tidal volumes (Vt) of 12-15 ml/kg. Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). The ARDS Clinical Network, or ARDSNet, completed a landmark trial that showed improved mortality when ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. Low tidal volumes (Vt) may cause hypercapnia and atelectasis.
Low tidal volume ventilation was the primary independent variable associated with reduced mortality in the NIH-sponsored ARDSnet trial of tidal volume in ARDS. Plateau pressure less than 30 cm H2O was a secondary goal, and subsequent analyses of the data from the ARDSnet trial (as well as other experimental data) demonsrtate that there appears to be NO safe upper limit to plateau pressure; that is, regardless of plateau pressure, patients fare better with low tidal volumes (see Hager et al, American Journal of Respiratory and Critical Care Medicine, 2005).
APRV (Airway Pressure Release Ventilation) and ARDS / ALI
Although a particular ventilation mode has yet to be "proven in clinical trials"* more effective than others in treating patients with ARDS, ever increasing empirical evidence and clinical experience is showing that APRVis the primary mode of choice when ventilating a patient with ARDS or ALI (Acute Lung Injury).
Advantages to APRV ventilation include: decreased airway pressures, decreased minute ventilation, decreased dead-space ventilation, promotion of spontaneous breathing, almost 24 hour a day alveolar recruitment, decreased use of sedation, near elimination of neuromuscular blockade and an often positive effect on cardiac output (due to the negative inflection from the elevated baseline with each spontaneous breath).
A patient with ARDS on average spends 8 to 11 days on a mechanical ventilator; APRV may reduce this time significantly.
- *This would require a side by side study of APRV and the current ARDSNet protocol. There seems to be little political will, within the medical community, to address the need for this study, in spite of the successes seen with APRV.
Positive end-expiratory pressure
Positive end-expiratory pressure (PEEP) must be used in mechanically-ventilated patients in order to contrast the tendency to collapse of affected alveoli.
Ideally, a 'perfect' PEEP would match the increased alveolar surface tension, caused by surfactant deficiency and external pressure (edema), thus restoring a normal time constant in all affected units.
However, because of the cited inherent inhomogeneity, surface tension varies, and so do PEEP requirements for the diseased units. Furthermore, high levels of PEEP may impair venous blood return to the right heart, although the actual impact of PEEP on hemodynamics is still debated.
The 'best PEEP' used to be defined as 'some' cmH2O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed alveoli, and more importantly the overdistention of aerated units, occur throughout the whole inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it is still used by some to define the minimum PEEP to be applied to their patients. Some of the newest ventilators have the ability to automatically plot a pressure-volume curve. The possibility of having an 'instantaneous' tracing trigger might produce renewed interest in this analysis.
PEEP may also be set empirically. Some authors suggest performing a 'recruiting maneuver' (i.e., a short time at a very high continuous positive airway pressure, such as 50 cmH2O (4.9 kPa), to recruit, or open, collapsed unit with a high distending pressure) and then to increase PEEP to a rather high level before restoring previous ventilation. The final PEEP level should be the one just before the drop in PaO2 (or peripheral blood oxygen saturation) during a step-down trial.
PEEP 'stacks up' to Pl during volume-controlled ventilation. At high levels, it may cause significant overdistension of (and injury to) compliant, aerated units, and higher plateau pressures at the same Vt.
Intrinsic positive end-expiratory pressure (Intrinsic PEEP, iPEEP) or auto-PEEP, is not detected during normal ventilation. However, when ventilating at high frequencies, its contribution may be substantial, both in its positive and negative effects. There are 'underground', unproven claims that the Amato and NIH/ARDS Network studies got a positive result because of the high iPEEP levels reached by spontaneously breathing patients in low-volume assist-control ventilation. Whether or not that is true, it is a fact that iPEEP has been measured in very few formal studies on ventilation in ARDS patients, and its entity is largely unknown. Its measurement is recommended in the treatment of ARDS patients, especially when using high-frequency (oscillatory/jet) ventilation.
A compromise between the beneficial and adverse effects of PEEP is, as usual, inevitable.
- Mechanical ventilation is an essential part of the treatment of ARDS. As loss of aeration (and the underlying disease) progress, the work of breathing (WOB) eventually grows to a level incompatible with life.
- Mechanical ventilation is initiated to relieve respiratory muscles of their work, and to protect the usually obtunded patient's airways.
- Mechanical ventilation may constitute a risk factor for the development, or the worsening, of ARDS.
- Aside from the infectious complications arising from invasive ventilation with tracheal intubation, positive-pressure ventilation directly alters lung mechanics during ARDS. The result is higher mortality, when injudicious techniques are used.
- In 1998, Amato et al published a paper showing substantial improvement in the outcome of patients ventilated with lower tidal volumes (Vt) (6 mL·kg-1). This result was confirmed in a 2000 study sponsored by the NIH. Although both these studies were widely criticized for several reasons, and although the authors were not the first to experiment lower-volume ventilation, they shed new light on the relationship between mechanical ventilation and ARDS.
- One opinion is that the forces applied to the lung by the ventilator may work as a lever to induce further damage to lung parenchyma. It appears that shear stress at the interface between collapsed and aerated units may result in the breakdown of aerated units, which inflate asymmetrically due to the 'stickiness' of surrounding flooded alveoli. The fewer such interfaces around an alveolus, the lesser the stress.
- Indeed, even relatively low stress forces may induce signal transduction systems at the cellular level, thus inducing the release of inflammatory mediators.
- This form of stress is thought to be applied by the transpulmonary pressure (gradient) (Pl) generated by the ventilator or, better, its cyclical variations. The better outcome obtained in patients ventilated with lower Vt may be interpreted as a beneficial effect of the lower Pl. transpulmonary pressure, is an indirect function of the Vt setting on the ventilator, and only trial patients with plateau pressures (a surrogate for the actual Pl) were less than 32 cmH2O]] (3.1 kPa had improved survival.
- The way Pl is applied on alveolar surface determines the shear stress to which lung units are exposed. ARDS is characterized by an usually inhomogeneous reduction of the airspace, and thus by a tendency towards higher Pl at the same Vt, and towards higher stress on less diseased units.
- The inhomogeneity of alveoli at different stages of disease is further increased by the gravitational gradient to which they are exposed, and the different perfusion pressures at which blood flows through them. Finally, abdominal pressure exerts an additional pressure on inferoposterior lung segments, favoring compression and collapse of those units.
- The different mechanical properties of alveoli in ARDS may be interpreted as having varying time constants (the product of alveolar compliance × resistance). A long time constant indicates an alveolus which opens slowly during tidal inflation, as a consequence of contrasting pressure around it, or altered water-air interface inside it (loss of surfactant, flooding).
- Slow alveoli are said to be 'kept open' using positive end-expiratory pressure, a feature of modern ventilators which maintains a positive airway pressure throughout the whole respiratory cycle. A higher mean pressure cycle-wide slows the collapse of diseased units, but it has to be weighed against the corresponding elevation in Pl/plateau pressure.
- The prone position also reduces the inhomogeneity in alveolar time constants induced gravity and edema.
- ↑ Malhotra A (2007). "Low-tidal-volume ventilation in the acute respiratory distress syndrome". N Engl J Med 357 (11): 1113-20. PMID 17855672.
- ↑ Irwin RS, Rippe JM (2003). Irwin and Rippe's Intensive Care Medicine, 5th ed., Lippincott Williams & Wilkins. ISBN 0-7817-3548-3.
- ↑ Amato M, Barbas C, Medeiros D, Magaldi R, Schettino G, Lorenzi-Filho G, Kairalla R, Deheinzelin D, Munoz C, Oliveira R, Takagaki T, Carvalho C (1998). "Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome.". N Engl J Med 338 (6): 347-54. PMID 9449727.
- ↑ MacIntyre N (2000). "Mechanical ventilation strategies for lung protection.". Semin Respir Crit Care Med 21 (3): 215-22. PMID 16088734.
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