Page 670 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 54: Acute-on-Chronic Respiratory Failure 489

A risk of NIV that is not often discussed is its potential to lull the 100% oxygen, which caused a rise in the mean P O 2 to 225 mm Hg, while
physician-nurse-respiratory therapist team into a sense of comfort the mean P CO 2 plateaued at 88 mm Hg. V ˙ e fell by a small amount, and
while the patient continues to worsen. Time spent trying NIV will, in drive remained supranormal. In 12 intubated patients recovering from
these patients, potentially lead to a later, more urgent intubation in a ACRF, an increase in Fi O 2 to 0.7 from a baseline of 0.3 to 0.4 resulted in a
more exhausted patient with significantly greater tissue hypoxia. This significant increase in Pa O 2 but no significant change in Pa CO 2 , dead space,
very real concern was corroborated by Chandra et al who reported or respiratory drive measured by the P method. 111
0.1
an alarming increase in the frequency and mortality rates for ACRF Three further studies have confirmed that worsened respiratory aci-
patients requiring invasive MV after a trial of NIV—presumably because dosis is modest and manageable in ACRF patients receiving O therapy
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NIV was ineffective. Over the decade from 1998 to 2008 in the USA, titrated to SP O 2 of 90%. 117-119 Our point is not to claim that hypoxic drive
approximately 5% of patients with AECOPD required transition to MV in patients with ACRF does not exist—it clearly does —but to empha-
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from NIV. However, mortality for this group increased progressively at size that oxygen must nevertheless be given. High concentrations of
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a time when mortality for NIV alone patients was decreasing. By 2008, inspired oxygen are not usually necessary in ACRF, unless pneumonia
patients transitions to MV had a 61% higher odds of death compared or pulmonary edema is present, since hypoxemia is due largely to secre-
with patients initiated on MV (95% CI 24%-109%) and startling 677% tion related V ˙ /Q ˙ mismatching, not to shunt. Nevertheless, we believe
greater odds of death compared with patients treated with NIV alone that the risks of oxygen therapy have been greatly overstated, often
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(95% CI 475%-948%). 8 leading physicians to withhold a potentially lifesaving therapy. The goal
Avoiding intubation and conventional mechanical ventilation nearly of oxygen therapy is to maintain SP O 2 >90% (range 88%-92%) and Pa O 2
always depends on discerning the cause of ACRF and reversing it. >60 mm Hg. This goal can usually be attained with a face mask at 30%
10
Thus, while NIV is initiated, each of the potential causes enumerated in to 35% or a nasal cannula at 3 to 5 L/min. A rise in P CO 2 is likely, but that
Figure 54-2 should be reviewed in light of the clinical presentation. On in itself is of little importance. Patients may progress to respiratory failure
occasion, impending respiratory failure can be averted by a specific inter- despite oxygen therapy, but not because of it. For this reason, careful
vention targeted to one precipitant, such as rib fracture (intercostal nerve serial assessments by the ICU team of physician-nurse-respiratory
block) or pulmonary edema (diuresis, afterload reduction). More often, therapist are essential.
several contributors are identified, such as worsened bronchospasm, elec- By contrast, there is emerging evidence that hyperoxemia in AECOPD
trolyte derangement and infection. Thus treatment must be broad based. patients, particularly in the pre-hospital period, is strongly associated
Since NIV is intermittently but variably interrupted for patient com- with worse outcomes. In a randomized study of high-flow versus titrated
fort and nutritional intake, the approach to weaning and liberation from oxygen therapy, Austin and coworkers determined that mortality was
NIV has not been prospectively evaluated and requires an individualized reduced by 78% for patients with confirmed COPD (relative risk 0.22,
but consistent approach. Weaning to liberation can be initiated if the 95% CI 0.05-0.91; p = 0.04) in association with less frequent respiratory
patient feels symptomatically improved, pH is >7.35 and stable, there acidosis or hypercapnia. While this observation has not been corrobo-
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is progress toward resolution of underlying precipitants and respiratory rated, it is our practice to avoid hyperoxia but to carefully titrate Fi O 2 to
rate during spontaneous breathing has normalized following the first achieve SP O 2 of 88% to 92%.
24 hours or longer. We find that initially reducing IPAP levels by 10% to Pharmacotherapy Bronchodilators are an essential part of the early manage-
20% over 12 hours while retaining EPAP at 7 to 10 cm H O is an effec- ment of these patients. While much of the airflow obstruction of COPD
2
tive first step. Many patients with significant PEEPi experience increased is irreversible, most patients have some reversible component. 123,124 In
work of breathing if EPAP is reduced too rapidly. We provide periods stable COPD, combinations of a β-agonist and ipratropium have been
of 30 to 60 minutes of spontaneous breathing with supplemental nasal demonstrated to be superior to either drug alone. However in a meta-
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cannula oxygen alternating with NIV for 3 to 4 hours. Periods of spon- analysis of four randomized studies, combination therapy for acute
taneous breathing are progressively prolonged over 1 to 2 days until the exacerbations of COPD does not result in greater short-term broncho-
patient is tolerating 4 to 6 hours off NIV. In up to a third of patients, the dilation compared with either albuterol or ipratropium alone. Despite
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initial efforts to liberate can be unsuccessful. If rapid shallow breathing, these data, current practice continues to support combination therapy
pursed-lip breathing, or tachycardia recurs, our approach is to defer liber- if airflow obstruction persists despite maximal doses of β-agonists or if
ation efforts for a further 8 to 12 hours and continue NIV or make a deci- treatment-limiting tachycardia is experienced. Respiratory stimulants
sion to advance to intubation (see below). Guideline recommendations would be predicted not to work in this setting, since drive is already
suggest continuing NIV for 16 hours on day 2, 12 hours on day 3 includ- supranormal. Indeed, doxapram and similar drugs are now rarely used
ing 6 to 8 hours overnight use, and discontinuing NIV on day 4, unless since their toxicity is substantial and their efficacy minimal, 127,128 partic-
continuation is clinically indicated. 89,109 Our preference is to provide ularly when compared with NIV. We believe there is no role for these
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NIV at night for the first 2 to 3 nights after the patient is weaned.
drugs. Similarly there is no evidence to support routine use of mucolytic
agents or chest percussion.
Oxygen Supplemental oxygen administration is a cornerstone of treatment.
110
Despite this a pervasive myth that patients with ACRF rely on hypoxic β-Agonists Inhaled, β -selective agents (albuterol, bitolterol, terbutaline,
2
drive to breathe persists. Physicians are often hesitant to supply oxygen, metaproterenol) should be given by metered-dose inhaler (MDI), unless
fearing that patients will stop breathing, necessitating intubation. Since patient distress makes that impractical, since these routes seem to
usually be equally efficacious in nonventilated patients. Administration may be
12
these patients are typically hypoxemic on presentation (P O 2
about 30-40 mm Hg), failure to supply adequate oxygen is a potentially facilitated by the use of a chamber device. Higher doses than usual
devastating treatment error. Unrelieved hypoxemia in the face of acide- can be given, such as 4 to 10 (or more) puffs every 20 to 60 minutes,
mia, fatiguing respiratory muscles, and an often failing right ventricle although there is no clear benefit from frequent doses and tachycardia
risks arrhythmia, myocardial infarction, cerebral injury, renal failure, or atrial fibrillation can be particularly concerning in the elderly. A
and respiratory arrest. handheld nebulizer (0.5 mL albuterol or 0.3 mL metaproterenol mixed
Studies of patients with COPD have shown convincingly that V ˙ e is main- with 2.5 mL saline solution) may be useful in patients who cannot use
tained despite treatment with even 100% oxygen, 111-113 and that there is a an MDI reliably, but otherwise this route confers no additional effi-
retained augmentation of respiratory drive in response to hypercarbia. cacy. Nebulized albuterol 2.5 mg is as efficacious as 5 mg administered
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typically rises, but this effect is attributed 4 hourly in terms of outcomes including length of hospital stay or recov-
When oxygen is given, the P CO 2
largely to worsened matching of ventilation and perfusion and the ery of lung function. Levoisomeric albuterol provides no significant
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Haldane effect, not to hypoventilation. In one series, patients with ACRF overall benefits compared with racemic albuterol when administered by
of 65. They were then placed on nebulization for AECOPD. Parenteral agents (eg, epinephrine 0.3 mL
116
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had a mean initial P O 2 of 38 and P CO 2

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