Spontaneous and controlled ventilation: superficially similar, inherently different.
Work of breathing
With healthy lungs and normally coordinated respiratory muscles, the energy expended to accomplish ventilation under resting conditions is remarkably small--in the range of 1-2 percent of the body's total oxygen consumption. Assuming exhalation occurs by passive elastic recoil, the two primary components of the absolute power requirement for inspiration are the average pressure developed across the lungs and chest wall per liter of ventilation and the minute ventilation demand. The inspiratory pressure need per unit of ventilation is influenced by the resistance and compliance of the lungs and chest wall, as well as by gas trapping, if present. For a lung with a specified set of mechanical properties, the oxygen consumed per unit time during spontaneous ventilation increases as an exponential function of minute ventilation. The steepness of this relationship as well as the magnitude of the energy expenditure rise as the resistance of the airways increases, due to progressive air trapping. A second important consideration is that respiratory pump efficiency degrades as the respiratory muscles are disadvantaged by hyperinflation. Finally, activation of the expiratory muscles occurs as minute ventilation increases. It should be clear, therefore, that reducing minute ventilation demand is a key therapeutic intervention for the patient in acute respiratory distress due to ARDS or acutely exacerbated airflow obstruction.
Relieving the respiratory workload by positive pressure ventilation can make a major contribution to meeting oxygen demand, and thereby taking strain off of a taxed heart, reducing oxygen extraction and increasing mixed venous and arterial blood saturations. A considerable portion of the literature that addresses heart-lung interactions explores the hemodynamic consequences of initiating positive pressure ventilation. The negativity of average pleural pressure increases in parallel with minute ventilation and the impedance of the lungs through which air flows. Apart from the associated reduction in the work of breathing, using positive pressure causes a marked upward shift in the pleural pressure that surrounds the heart and central blood vessels. Depending on the contractile vigor and the loading conditions of the ventricles, this rise in pleural pressure may impede venous return and compromise preload, or improve the function of the failing heart. The topic is too complex to delve into here, but a quick synopsis is that the increase in pleural pressure may improve RV function by reducing the wall tension of the overstretched right ventricle as well as relieve pressure on the shared septum between the right and left ventricular chambers, improving both left sided filling and afterload. Such effects may not be noticed if the heart is healthy and able to easily compensate for changing loading conditions, but may be dramatic for a compromised heart whose adaptive capacity is limited and whose circulating intravascular volume is reduced. The widespread use of beta blocking drugs and diuretics accentuates the impact of converting to positive pressure ventilation--or vice versa with opposite effects when ventilation is discontinued.
Physiological observations made over the past four decades have shown consistently that the distribution of the tidal breath changes both with the intensity of breathing effort and with the conversion to positive pressure ventilation. At low levels of ventilation, the accessory muscles are relatively silent, whereas the diaphragm assumes the majority of the breathing workload. This activity skews ventilation toward the peri-diaphragmatic regions, where perfusion tends to be richest. As minute ventilation rises, however, the accessory muscles of inspiration contribute increasingly and active exhalation begins. Distributions of regional distention and ventilation change, therefore, with ventilatory demand. Lung inflation with positive pressure will favor the most flexible zones of the coupled lung and chest wall, which under passive conditions are located ventrally. Much has been made of the strong advantage of the spontaneous pattern of breathing for gas exchanging efficiency. While generally true, ample caution is indicated.. First, at high levels of spontaneous ventilatory effort, contractions of the expiratory muscles drive the respiratory system below its resting functional residual capacity, encouraging lung collapse that impairs gas exchanging efficiency. Indeed, imposing controlled ventilation may be associated with improved oxygenation due to increased FRC, reduced shunt, and better match-up between oxygen delivery and consumption.
Furthermore, ventilation perfusion matching influenced not only by the ventilation gradient we have been discussing, but also by the adaptability of the blood vessels to redistribute flow according to the composition of alveolar gas. Thus, the potentially adverse impact of positive pressure ventilation on V/Q matching may be minimal in a healthy lung. The existence of lung pathology--which is often disproportionate in the peridiaphragmatic zones--may interfere with this compensation and offset any advantage relating to a favorable ventilation gradient. In practice, one cannot confidently predict the direction of the alteration in gas exchange that will occur when the ventilation pattern is controlled. Spontaneous breathing is often--but not always--better.
Distribution of Lung Liquids
It stands to reason that the central blood vessels would be better filled during spontaneous ventilation, motivated by the lower intrathoracic pressure, more favorable conditions for venous return, and higher vascular distending pressures. When the microvessels are leaky, this tendency for vascular congestion may translate into a greater tendency for pulmonary edema, especially if cardiac output is high. Controlled ventilation generally reduces cardiac output as well as the trans-vascular filling pressures.
There is another important reason that controlling ventilation may reduce lung water--one that is infrequently appreciated. It is interstitial pressure that surrounds the microvessels, and this unmeasured pressure is usually assumed equivalent to the pleural pressure. If one considers what the interstitial pressure is during negative and positive pressure ventilation, the inescapable conclusion is that for the same lung volume, it must be higher under controlled conditions, even when end expiratory alveolar pressure is the same or PEEP is not used. An example may drive home the point: Suppose the trans-lung (trans-pulmonary) pressure--the difference between alveolar and pleural pressures--were the same during inflation by negative and by positive pressure. (This would mean that the lung has the same dimensions.). Further, suppose that the chest wall and lung have similar compliance and that a targeted end-inspiratory trans-pulmonary pressure (of 15 cmH2O, say) is accomplished using the respiratory muscles alone or passively by positive pressure alone. Assuming the former, the intrapleural pressure would be minus 15 cm H2O, whereas during passive inflation it would be positive 15 cmH2O (and the plateau would be 30 cmH2O). Because interstitial pressure is believed to be similar to intrapleural pressure, the peak difference in interstitial pressure that occurs when converting from spontaneous breathing to positive pressure ventilation would be 30 cmH2O! The average difference in interstitial pressure over the entire tidal cycle would be considerably less, of course, because passive expiratory interstitial pressures are not affected by the means by which the lung is inflated. Nonetheless, assuming that average microvascular capillary pressures (intra-luminal pressures) remained similar, the implication for edema formation is obvious--less fluid should form under positive pressure conditions, even if PEEP and cardiac output were the same.
The point of making this comparison between spontaneous and positive pressure ventilation is that important differences exist between them which may inflict harm or confer benefit, depending on the clinical circumstances we confront.. With strong physiologic grounding, the clinical caregiver can utilize knowledge of these differences to improve the welfare of the patients whose care we are committed to improve.
Dr. Marini, Professor of Medicine at the Univ. of Minnesota, is a clinician-scientist whose investigative work has concentrated in the cardiopulmonary physiology and management of acute respiratory failure.
by John Marini MD
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|Title Annotation:||MECHANICAL VENTILATION|
|Publication:||FOCUS: Journal for Respiratory Care & Sleep Medicine|
|Date:||May 1, 2010|
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