Page 673 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

492 PART 4: Pulmonary Disorders

to tidal volume. In addition, a minute ventilation higher than 10 L/min
TABLE 54-3 Important Predictors of Treatment Success or Failure in Acute
Respiratory Failure Complicating COPD often is employed, particularly during the first few minutes of manual-
assisted ventilation. Finally, as the work of breathing is assumed by the
Predictors for Treatment Success Predictors for Treatment Failure ventilator, V ˙ CO 2 drops by as much as 20%. All of these factors join to dra-
> 45 mm Hg pH < 7.25 matically lower the patient’s Pa CO 2 once assisted ventilation begins. Since
pH 7.25-7.35, Pa CO 2 preexisting compensatory metabolic alkalosis is the rule, life-threatening
GCS >14 GCS < 11 alkalemia (pH >7.7) can easily be achieved. This scenario can be avoided
APACHE-II score < 29 APACHE-II score >29 by simply aiming for a more reasonable minute ventilation, approximat-
Respiratory rate 24-30/min Significant comorbidities ing the patient’s own pattern of breathing. Typical initial ventilator set-
Response to NIV within 1-2 h Respiratory rate >30/min tings are described below. There is no need to attempt to normalize pH,
https://kat.cr/user/tahir99/
Training/experience of the team with NIV Additional pneumonia a maneuver that merely serves to waste the bicarbonate that has been so
vigorously conserved during the evolution of respiratory failure.
Standardized NIV protocol Severe mask leakage We generally recommend head-up intubation with a wide-diameter
Patient-ventilator asynchrony endotracheal tube, not laryngeal mask. Depolarizing muscle relaxants
Ineffective triggering should be avoided and if necessary, short-acting nondepolarizing agents
Agitation or intolerance such as rocuronium or cisatracurium should be considered.
Encephalopathy Initial Ventilator Settings We generally initiate ventilation using the assist-
control mode, since one of the goals in this phase is to rest the loaded
Inability to clear secretions respiratory muscles (see Chap. 49). We implement a modified “lung-
GCS (Glasgow coma scale score). protective” ventilation strategy appreciating that this approach has not
Adapted with permission from Budweiser S, Jorres RA, Pfeifer M. Treatment of respiratory failure in COPD. been prospectively validated in ACRF patients. Tidal volumes of about
Int J Chron Obstruc Pulmon Dis. 2008;3(4):605-618. 5 to 7 mL/kg are used (about 350-500 mL) with a respiratory rate of
20 to 24 per minute to emulate basal breathing patterns and minimize
improvement is occurring or not; the degree of dyspnea over time is patient-ventilator dyssynchrony. Once stabilized, avoiding alkalemia is
a useful guide to the likelihood of success without intubation. Most as important as at the time of intubation. Hypocapnia worsens bron-
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patients with ACRF are tachypneic, reflecting their excessive drive. A choconstriciton, impedes respiratory drive in patients with chronic
rate that remains above 35 to 40 per minute, or a rate that continues respiratory acidosis, enhances renal bicarbonate wasting, and adversely
to rise despite therapy and NIV, is predictive of respiratory failure. affects cardiovascular function. Post hypercapnic alkalosis was identified
Deterioration of mentation commonly precedes respiratory arrest even in 20% of 84 patients mechanically ventilated for ACRF and was inde-
is adequate. Patients become confused, less able to converse, pendently associated with prolonged ventilation and ICU length of stay.
when SP O 2
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then poorly rousable. Thoracoabdominal paradox and respiratory alter- We recognize and tolerate “therapeutic” or permissive hypercapnea as
nans are rarely seen and are probably not useful signs. a potentially salutary consequence of lower V t and tolerate pH values as
low as 7.20 in the absence of hemodynamic instability. This approach
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Phase 2: Late ACRF Requiring Intubation: This phase consists of the has not been systematically studied in ACRF, but observations in acute
immediate periintubation management and the first few days of respiratory failure where hypercarbia and modest levels of respiratory
mechanical ventilation. In many respects, treatment initiated in the acidosis are tolerated suggest an association with improved outcomes 170
pre-intubation phase (bronchodilator and corticosteroid administra- As discussed above, PEEPi presents an inspiratory threshold load
tion, in particular) is continued, but several additional concerns become to the patient with ACRF. The patient must generate enough force to
relevant. Care consists of stabilizing the patient on the ventilator, counterbalance PEEPi before the breathing effort results in any inspira-
ensuring rest of the patient and respiratory muscles, improving neu- tory flow and before it can trigger the ventilator. We assiduously and
romuscular competence, reducing load, providing prophylaxis against frequently monitor for the presence of PEEPi in the ventilated ACRF
complications while optimizing definitive therapy for any precipitant patients by clinical examination of the subxiphoid epigastrium par-
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such as infection. Optimal treatment at this time is likely to facilitate titioning lung mechanics to detect increases in Pplat, end-expiratory
timely and prompt liberation from mechanical ventilation. occlusion technique and inspection of the terminal expiratory phase
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Periintubation Risks There are two common pitfalls in the immediate post- of the ventilator flow wave form for persistent expiratory flow at
intubation period: life-threatening alkalosis and hypotension. Both are the initiation of the subsequent breath (Chap. 48). This difficulty
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related to overzealous ventilation, and both are avoidable by taking the cannot be sidestepped by lowering the triggering sensitivity on the
patient’s own ventilatory pattern prior to intubation into consideration. ventilator or by using flow triggering. Applying external PEEP, roughly
Hypotension is a consequence of escalating PEEPi following intubation. equal to the PEEPi, does reduce the work of breathing (and trigger-
The degree of dynamic hyperinflation is proportional to V ˙ e. PEEPi ing) by a significant amount, as depicted in Figure 54-1. 102,175 In some
has the same deleterious consequences on venous return as externally patients, externally applied PEEP causes additional hyperinflation,
applied PEEP and can cause serious hypoperfusion. This can be par- with detrimental hemodynamic effects and a potentially increased risk
ticularly prominent in patients with ineffective circulating volumes of barotrauma. 176,177 However, most patients with ACRF demonstrate
(“preload”) and concomitant right heart dysfunction when vasodilatory flow limitation, so that external PEEP (in amounts up to about 85% of
and sympatholytic sedatives are used for intubation. The key to avoid- the PEEPi) has no significant impact on the expiratory flow-volume
ing this pitfall is to prevent excessive ventilation, particularly during relationship, lung volume, or hemodynamics. 178,179 Strategies to shorten
bag-valve-mask preoxygenation before intubation attempts. When ventilator inflation time (T ) are not generally helpful unless inspiratory
I
hypotension occurs, the circulation can usually be promptly restored by flow is inordinately low, although PEEPi can be reduced modestly. 180
simply ceasing ventilation for 30 seconds, then reinstituting ventilation Several newer pressure-cycled modes of ventilation have been assessed
along with measures to reduce PEEPi and restore circulating volume. It in ACRF. 181-183 Taken together these represent only minor advances in
is also our practice in patients without decompensated left heart failure terms of patient synchrony, comfort, and outcomes. Current iterations
to administer a fluid bolus immediately prior to sedation for intubation. of closed-loop computer algorithms for targeting stable minute ventila-
Most patients with ACRF have a minute ventilation of 10 L/min or tion settings (adaptive support ventilation, ASV), however, may apply
less and breathe at tidal volumes of about 300 mL with a rapid shallow excessively high V t in COPD patients with ACRF. For these reasons
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breathing pattern. Physicians commonly choose ventilator settings with we continue to select volume-cycled assist control as the initial mode for
60
a higher tidal volume and a correspondingly lower ratio of dead space the majority of patients.

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