Page 675 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

494 PART 4: Pulmonary Disorders

(see Chap. 39). Noninvasive leg studies have been challenged in this load/strength imbalance. However, the poor individual performance
setting as well. characteristics of these maneuvers make them unreliable for pre-
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The intimate epidemiological associations between chronic pulmo- dicting sustained spontaneous breathing and successful liberation.
nary diseases and cardiovascular diseases (including coronary artery However, by daily integrating respiratory parameters of load/strength
disease, cardiomyopathy, stroke, and arrhythmias) make these conditions balance with other validated parameters, such as f/V ratio, readi-
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frequent and often challenging co-conspirators in the evolution and pro- ness for a SBT can be determined. Additionally, the impact of thera-
gression of ACRF. Arrhythmias are common in the setting of respiratory peutic maneuvers can be assessed by serially evaluating respiratory
failure. Fortunately, they are rarely a serious problem, but they can serve parameters. For example, while PEEPi remains at 10 cm H O, there is
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to distract the physician from more important issues, may limit the dose little point in trying to make the patient breathe. Indeed, in such a cir-
of bronchodilator drugs, and sometimes are significant in themselves. cumstance, efforts should be directed to attempting to reduce the work of
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The most common rhythms are sinus tachycardia, atrial fibrillation, breathing. On the other hand, when PEEPi has resolved and strength is
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atrial flutter, multifocal atrial tachycardia, and ventricular premature adequate (usually when the NIF >30 cm H O), mechanical ventilation
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beats. β -agonists, macrolides, and electrolyte disturbances can cause is no longer necessary and the patient should be able to tolerate at least
.
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transmural dispersion of repolarization abnormalities such as Qt prolon- 30 minutes of spontaneous, minimally assisted breathing.
gation, T-wave alternans, and P-wave dispersion as precursors to serious Failure to liberate from mechanical ventilation can be caused
arrhythmias. It can be difficult to judge the contributions of hypoxemia, by myocardial ischemia or acute left ventricular failure. Coronary
cor pulmonale, metabolic derangements, underlying coronary artery dis- artery disease, left and right ventricular dysfunction and failure are
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ease, and drug toxicity to arrhythmogenesis. Treatment should focus on all common in patients with ACRF, particularly those with COPD.
rectifying the underlying respiratory failure, since doing so usually has a The additional myocardial wall stress and oxygen demand of respira-
beneficial impact on arrhythmias. Hypoxemia and electrolyte abnormali- tory muscles during a SBT can precipitate ischemia and acute left-
ties should be corrected as a first priority. Monitoring should be initiated, ventricular failure. 209
and, if arrhythmias continue despite correction of apparent exacerbating Congestive heart failure may be occult. Diligent efforts to diagnose
factors, myocardial ischemia should be excluded. Atrial fibrillation can and manage myocardial ischemic burden and manage LV failure are
be controlled with a calcium channel blocker or digoxin (see Chap. 36). essential in order to achieve successful liberation. An elevation of
β-blockers should generally be avoided for fear of worsening lung func- N-terminal pro-brain natriuretic peptide (NT-proBNP ) ≥184.7 pg/mL
tion, although short-acting, selective drugs have occasionally been used after a 2-hour SBT has a sensitivity of 88% and specificity of 91% for
with success. Multifocal atrial tachycardia often responds to verapamil, intercurrent cardiac ischemia and/or cardiogenic pulmonary edema as
sometimes with restoration of sinus rhythm, and there appears to be a an etiology of recurrent SBT failure in patients with ACRF but no his-
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role for parenteral magnesium as well (see Chap. 36). tory of active cardiac disease. 210
While β1-selective receptor antagonists appear safe in patients with
Phase 3: Liberation From the Ventilator: The fundamental principle that stable COPD, it remains unclear if the cardiovascular benefits of initi-
guides management in this phase is that successful liberation from the ating these drugs in patients with ACRF outweigh the adverse effects
ventilator requires that the premorbid, compensated relationship between on bronchial hyperreactivity. Similarly it is unknown if β-blockade is
neuromuscular competence and load be reestablished. Therefore, a effective cardioprotection against the deleterious effect of β -receptor
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strategy for successfully discontinuing mechanical ventilation empha- agonists used in these patients. The use of positive inotrope infusions
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sizes increasing the strength and decreasing the load, while avoiding during SBT has been proposed in failure-to-liberate patients with severe
sedatives that may impair drive. We use a nurse/ respiratory therapist- LV systolic dysfunction but has not been associated with meaningful
led protocol that emphasizes daily testing of readiness for spontaneous improvements in likelihood of liberation. 211
breathing, targeted sedation strategies with daily sedation withdrawal, As highlighted above, respiratory alkalosis as a consequence of over-
formal spontaneous breathing trials (SBT), and triggers for liberation enthusiastic ventilation is a major concern and diligent efforts should be
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including early extubation to NIV as discussed below and reviewed in made to avoid. Similarly, metabolic alkalosis as a consequence of chronic
further detail in Chap. 60. This approach has been demonstrated to be renal bicarbonate reabsorption and regeneration can prolong the tran-
particularly effective in achieving successful ventilator liberation. 199,200 sition to unassisted breathing. Efforts to pharmacologically manage
However, similar results may be achieved in well-staffed, well-organized alkalosis in ACRF either with respiratory stimulants (doxapram,
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closed-management ICUs where decisions to liberate are directed by medroxyprogesterone, aminophylline) or by inducing a metabolic
expert intensivists. Therapy may be highly focused, such as repleting acidosis with acetazolamide, are, however, ineffective in abbreviating
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inorganic phosphate, relieving a pneumothorax, addressing neuro- ventilator dependence and should be avoided.
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psychiatric components including delirium, or managing right heart When discontinuation of mechanical ventilation is imminent, it is
syndrome. More often, a broad assault on many potential precipitants, useful to anticipate the respiratory pattern that the patient will soon
namely bronchospasm, infection, electrolyte derangement, and fatigue, assume. We have been impressed that patients ventilated at supraphysi-
is used. When load has been reduced and neuromuscular competence ologic tidal volumes, such as 800 to 1000 mL, experience respiratory
promoted, the patient will be able to breathe free of assistance. On the distress and agitation when they resume their usual pattern of 30 breaths
other hand, if a compensated balance of strength and load cannot be per minute at a V of 300 mL. By choosing a pattern of mechanical
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restored, attempts at spontaneous breathing will be futile. A corollary ventilation that more closely approximates spontaneous respiration
principle is that the specifics of ventilator management, such as the mode (eg, A/C mode, V of 420 mL, rate of 20 per minute), the transition from
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chosen or the device used, are less important. 202,203 Only the patient’s the ventilator is smoothed.
improving physiology determines the ability to maintain ventilation as For patients that fail to reestablish load/strength balance within 72 hours
determined by the patient’s ability to tolerate short periods of unassisted of initiating therapy, there is a significant prospect of prolonged
breathing (SBT). This point has been confirmed by recent trials of wean- mechanical ventilation, tracheostomy, and complications that increase
ing methods, which have shown that frequent T-piece trials are superior morbidity and mortality. A significant shift in approach involves elec-
to MV (and, variably, pressure-support as well), probably because they tive extubation to NIV for patients who consistently fail SBTs after
more readily demonstrate to the physician that the ventilator is no longer 48 to 72 hours (the second “bookend” in the therapeutic library of
necessary. 200,203-205 This issue is more fully elaborated in Chap. 60. therapy for ACRF). In a randomized controlled trial of extubation
Respiratory parameters (negative inspiratory force [NIF], peak pres- to NIV versus continued intubation and ventilation in 50 ACRF
sure [Ppk], plateau pressure [Pplat], PEEPi) have historically been patients failing a T-piece trial at 24 to 36 hours of initial ventilation
used to evaluate the progress of the patient and resolution of the via an endotracheal tube, NIV reduced the period of mechanical

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