Page 664 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 54: Acute-on-Chronic Respiratory Failure 483

which 8.1% required a period of respiratory support ; 13.2% of patients 7.24 and P CO 2 77 mm Hg) hospital mortality was 32% and only 5% of the
8
with respiratory failure requiring mechanical ventilation in a recent patients received ICU level care. All-cause 1-year mortality was 55%. 17
survey USA survey of 180,326 hospitalizations had significant comorbid Some patients will return to an acceptable quality of life (QOL), and
pulmonary disease. In surgical ICUs, COPD is an important problem as some even go back to work. In a prospective cohort of 611 ambula-
9
well, since it is one of the more common reasons for a prolonged postop- tory COPD patients, Esteban et al reported that when controlled for
18
erative recovery. An approach to this disease is an essential component COPD disease severity and baseline QOL, number of hospitalizations
of the intensivist’s armamentarium. for AECOPD was an independent predictor of reduced QOL in COPD;
This chapter describes the pathophysiology and management of 7% of patients required three or more admissions and experienced par-
patients with chronic pulmonary disease (most with COPD) who require ticularly marked deterioration in QOL over 5 years of follow-up. In a
intensive care for decompensation of their normally precariously balanced cohort of 1016 patients admitted with a COPD exacerbation and a Pa CO 2
ventilatory state. This acute deterioration superimposed on stable disease >50 mm Hg, 1-year survival was 47%, but only 26% of the patients rated
is termed acute-on-chronic respiratory failure (ACRF). Patients may pres- their QOL as good or better when surveyed at 6 months. 7
ent to the ICU with worsening dyspnea, deteriorating mental status, or Predictors of poor survival include the underlying cause of chronic
respiratory arrest. Especially when there is a preexisting diagnosis of lung respiratory failure and a high BODE index (an integrated assessment of
19
disease, the diagnosis of ACRF can be made easily. However, it is impor- body mass index, airflow obstruction, dyspnea, and exercise capacity), older
tant to remember that not all patients with severe COPD will have been age, 7,15,20 more than three acute exacerbations in 5 years, history of conges-
20
so identified. In many patients with respiratory distress, congestive heart tive heart failure, cor pulmonale, presence of serious comorbid disease,
7
21
failure or pulmonary thromboembolism is considered first; making a cor- lower P O 2 : Fi O 2 ratio, lower serum albumin level, 7,15,22 chronically elevated
7
rect diagnosis of ACRF requires a high index of suspicion. On occasion, P CO 2 20 development of extrapulmonary organ failures, 14,15 and requirement
the disease is even more occult, for example, in a postoperative patient for >72 hours of ventilation. However, these indicators are not sufficiently
21
who fails extubation and then is noted to have hyperinflation on the chest refined to allow accurate prognostication in an individual patient.
radiograph. Since optimal therapy depends on accurate diagnosis, under- As a result, critical care resource utilization and costs are substantial.
lying COPD should be part of the differential diagnosis for most patients Ely and coworkers calculated that respiratory care costs were almost
with dyspnea or inability to sustain unassisted ventilation. twice as much for patients with COPD compared with non-COPD related
A severe acute exacerbation of COPD (AECOPD) is characterized respiratory failure ($2422 [$1157-$6100] vs $1580 [$738-$3322], respec-
by a sustained worsening from the stable state that is acute in onset tively; p = 0.01, $1996), despite similar ICU lengths of stay and mechani-
and requires hospitalization. 10,11 The typical symptoms are dyspnea that cal ventilation days. However, attributable health care costs and resource
23
has been worsening over days, often with increased cough and sputum utilization for ACRF management are influenced strongly by prevailing
production. Physical examination typically demonstrates respiratory care models. In 2008, hospital charges for patients managed for ACRF
distress, accessory muscle use, a prolonged expiratory time, recruitment complicating AECOPD were approximately $35,000 if care with NIV
of expiratory muscles, and wheezing. As discussed below, the absence of alone was successful. However, costs increased to more than $100,000 if
respiratory distress is not necessarily reassuring and when associated invasive MV was required during the hospitalization. Significant efficien-
8
with somnolence is a grave and ominous sign of impending respiratory cies have been reported when noninvasive ventilation is administered in
arrest. The chest radiograph is usually abnormal, reflecting the chronic ward-based settings although outcomes may be less satisfactory. 17
24
lung disease, but only in 15% to 20% of cases reveals an acute finding (eg, Ideally, patients followed in the clinic with known, severe COPD will
pneumonia, pneumothorax, pulmonary infarction, pulmonary edema) be encouraged to discuss with their physicians their wishes regarding
that results in a change of management. Sometimes there are indica- intensive care before acute deterioration. Unfortunately, this is only
12
tors of acute infection, such as purulent sputum, fever, leukocytosis, and occasionally accomplished. It is our approach to fully support patients
25
a new radiographic infiltrate. Typical initial arterial blood gas values on with ACRF who believe their QOL is acceptable and have an apprecia-
of 60 to 70 mm Hg. tion of the burden and potential outcomes of ICU treatment, especially
26
room air show a P O 2 of 35 to 45 mm Hg and a Pa CO 2
Comparison with values obtained when the patient is stable can be useful since most will be managed successfully with noninvasive ventilation,
as many patients have compensated metabolic acidosis with chronically and most of those intubated will eventually be successfully liberated
at baseline. Electrocardiography (ECG) may show signs from the ventilator and survive to hospital discharge. 15,16,27 On the other
elevated Pa CO 2
of right atrial enlargement or right ventricular hypertrophy and strain. hand, when mechanical ventilation seems excessive to the patient or
P-wave amplitude >1.5 mm is universal in patients with AECOPD (but physician, defining the goals of care as the provision of comfort and
not necessarily ACRF), although classical P pulmonale (P-wave amplitude relief from dyspnea and pain is appropriate. We urge clinicians car-
28
in leads II, III, and/or aVF >2.5 mm) is uncommon. Resolution of the ing for COPD patients with compensated respiratory failure to address
exacerbation is associated with an amplitude reduction of approximately advance directives and desire for life-sustaining therapies during routine
0.8 mm. Thus serial ECG may be useful in assessing response to therapy. ambulatory clinic appointments when informed and deliberate decision
13
Although the short-term risk of death is high for ACRF, the prognosis making can be shared by the patient and their loved ones.
8
for patients with ACRF is not uniformly poor, despite severe underly-
ing pulmonary impairment. In a prospective analysis of 250 admissions PATHOPHYSIOLOGY
(180 patients) to an ICU for acute respiratory failure complicating COPD,
hospital mortality was 21% and was strongly associated with the develop- Alveolar ventilation is maintained by the central nervous system, which
ment of extrapulmonary organ failures. However, more recent analyses acts through nerves and the respiratory muscles to drive the respiratory
14
of patients discharged after an episode of ACRF complicating AECOPD pump. The three subsets of ventilatory failure are loss of adequate drive,
in the USA between 1998 and 2008 revealed a bimodal mortality rate. impaired neuromuscular competence, and excessive respiratory load.
Chandra and colleagues reported that while mortality for patients requir- This concept is developed in Figure 54-1. The central nervous system
ing intubation and MV (mechanical ventilation) remained at 22%, the drives the inspiratory muscles via the spinal cord and phrenic and inter-
rate for patients managed exclusively with NIV was closer to 6% in 2008, costal nerves. Inspiratory muscle contraction lowers pleural pressure,
an approximately 50% reduction over the course of a decade. Six-month thereby inflating the lungs. The pressure generated by the inspiratory
8
and 1-year survival following ACRF approximates 40% and 45%, respec- muscles (neuromuscular competence) must be sufficient to overcome
tively. 15,16 These rates may in part be explained by the uniform manage- the elastance of the lungs and chest wall and abdomen (elastic load), as
ment of ACRF patients in ICUs in North America. This is not the case well as the flow resistance of the airways (resistive load). Spontaneous
in other regions. For example, a recent Scottish single center experience ventilation can be sustained only as long as the inspiratory muscles are
reported that among 275 patients treated with NIV (mean baseline pH of able to maintain adequate pressure generation. 29

section04.indd 483 1/23/2015 2:20:05 PM