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CHAPTER 49: Management of the Ventilated Patient 425

VENTILATOR-INDUCED LUNG INJURY withdrawing ventilation or PEEP can challenge the circulation, espe-
cially in those with severe left ventricular dysfunction, impeding libera-
When the lungs of patients with the acute respiratory distress syn- tion from the ventilator. 16
drome (ARDS) are distended excessively, through high tidal volumes
or high positive end-expiratory pressure (PEEP), injury follows. Local
pulmonary inflammation ensues, including areas of previously healthy CHOOSING A VENTILATOR MODE
lung, and systemic inflammation is seen, potentially causing distant
8
organ failures. Increasing evidence suggests that ventilated patients with Technological innovations have provided a plethora of modes by which
normal lungs (having central nervous system failure, eg, or undergoing a patient can be mechanically ventilated. These have been developed
surgery) may also be at risk when large (12 mL/kg) tidal volumes are with the hope of improving gas exchange, patient comfort, or speed of
used (see Chap. 51). In light of these findings, tidal volume should return to spontaneous ventilation. Aside from minor subtleties, how-
9,10
probably be limited also in these patients as discussed more fully below. ever, nearly all modes allow full rest of the patient, on the one hand, or
substantial exercise, on the other, while providing a suitable foundation
for maintaining gas exchange and protecting the lung. Thus, in the great
VENTILATOR-INDUCED DIAPHRAGM DYSFUNCTION majority of patients, choice of mode is merely a matter of patient or phy-
Like skeletal muscles, the diaphragm suffers atrophy and contractile sician preference. Noninvasive ventilation should be considered before
dysfunction during critical illness and mechanical ventilation, termed intubation and ventilation in many patients who are hemodynamically
VIDD. 11,12 This occurs acutely, worsens progressively, and is associated stable and do not require an artificial airway, especially those with acute-
with prolonged ventilation and risk of death. Muscle protein synthesis on-chronic respiratory failure, postoperative respiratory failure, and
13
is inhibited and multiple pathways of self-destruction are up-regulated. cardiogenic pulmonary edema. Management of the patient ventilated
14
Also like in peripheral muscle, active contraction (ie, active breathing) noninvasively is discussed thoroughly in Chap. 44.
can effectively modify the degree of catabolism, helping to maintain Choosing a ventilatory mode and settings appropriate for each
contractile function. This has potentially important implications for individual patient depends not only on the physician’s goals (rest vs
selection of mode, adjustment of settings based on patient-ventilator exercise; lung protection; limitation of autoPEEP; gas exchange), but
interaction, role for sedation and SBTs, and endpoints for ventilator also on knowledge of the mechanical properties of the patient’s respira-
settings. For example, these findings regarding VIDD suggest that the tory system. Determining respiratory system mechanics is an integral
ventilator should generally be set so as to encourage patient triggering, part of ventilator management and a routine component of examina-
rather than passivity (unless profound shock or hypoxemia prevents tion of the critically ill patient, discussed fully in Chap. 48 (Ventilator
this). Further, adjusting ventilator settings to achieve a modest degree Waveforms). The intensivist can combine clinical information, chest
of patient effort should perhaps override alternative strategies, such radiography, lung ultrasound, and respiratory system mechanical prop-
as those based on standard protocols or relying on arterial blood gas erties to categorize the patient into one of four prototypes: (1) normal
analysis. It is also interesting to speculate to what degree daily sedative gas exchange and mechanics; (2) significant airflow obstruction (as in
interruption, spontaneous breathing trials, and noninvasive ventilation status asthmaticus or acute exacerbations of COPD); (3) ARDS; and
exert their beneficial effects through reductions in VIDD. (4) restriction of lung or chest wall. Appropriate initial ventilator settings
and subsequent adjustments for each of these four states are discussed
CARDIOPULMONARY INTERACTIONS later in this chapter.
If full rest of the respiratory muscles is desired, it is incumbent on the
Cardiopulmonary interactions describe the complex, and mutually physician to ensure that this is indeed achieved. Although some patients
important, relationships between respiration (and mechanical venti- are fully passive while being ventilated (those with deep sedation,
lation) and the circulation, largely because these systems are deeply some forms of coma, metabolic alkalosis, sleep-disordered breathing),
intertwined within the thorax. Circulatory abnormalities and treatments most patients will make active respiratory efforts, even on volume
have implications for lung function. At the same time, lung injury, venti- assist-control ventilation (VACV), at times performing extraordinary
17
lation, and PEEP can support or cripple the circulation. amounts of work. Unintended patient effort can be difficult to rec-
Mechanical ventilation affects the circulation through cyclic changes ognize but, aside from obvious patient effort, may be signaled by an
in the pleural pressure (Ppl), direct effects on the pulmonary circulation inspiratory fall in intrathoracic pressure (as noted on a central venous
and right ventricular afterload, and indirect consequences of altered gas or pulmonary artery pressure tracings or with an esophageal balloon),
exchange and work of breathing. In contrast to spontaneous breathing by triggering of the ventilator, or by a careful analysis of real-time
when the Ppl falls during inspiration, mechanical ventilation tends to flow and pressure waveforms, discussed more fully in Chap. 48. When
make Ppl rise. Following institution of or changes in mechanical ventila- there is evidence of unwanted patient effort, ventilator adjustments,
tion, the increment in Ppl relates to patient effort (both inspiratory and psychological measures, pharmacologic sedation, and therapeutic
expiratory), tidal volume, chest wall compliance, and the magnitude of paralysis can be useful. Ventilator strategies to reduce the patient’s
any alveolar recruitment. Higher tidal volumes and a stiffer chest wall work of breathing include increasing the minute ventilation to reduce
produce greater changes in Ppl and accordingly greater effects on the Pa CO 2 (although this may run counter to other goals of ventilation,
circulation. PEEP has a similar impact, except that the degree of Ppl especially in patients with ARDS or severe obstruction), increasing
augmentation depends on the magnitude of PEEP, the lung and chest the inspiratory flow rate, and changing the mode to pressure-targeted
wall compliances, and whether lung is recruited or not: more recruit- ventilation, as in pressure-support ventilation (PSV) mode or pressure
ment causes a greater change in Ppl. The dominant circulatory impact assist-control ventilation (PACV).
of ventilation tends to be mediated through changes in Ppl (since this For most patients, however, some degree of triggering and work are
largely determines the juxtacardiac pressure), most notably by reduc- desired because this is likely to reduce the degree of VIDD as described
ing right ventricular preload. Impaired right heart filling accounts for above. If some work of breathing on the patient’s part is desired, this can
much of the hemodynamic depression of positive pressure ventilation be achieved through any of the existing ventilatory modes. The amount
and PEEP, although right ventricular afterload plays a role in some, of work done may be highly variable, however, and depends on the spe-
especially those with severe ARDS. Modes of ventilation that preserve cific mode, the settings chosen within each mode, and the interaction
15
spontaneous breathing dampen the rise in average pleural pressure and between the patient and the ventilator. A recurring question during the
may be associated with less circulatory depression. time when a patient can carry some of the work of breathing is, “Can
Ventilation can support the circulation, too, by raising left ventricular this patient breathe without ventilatory assistance?” This issue is more
preload, reducing afterload, and easing the work of breathing. Similarly, fully developed in Chap. 60, Liberation From Mechanical Ventilation.

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