critical care medicine
Ventilatory Failure
Treatment of Ventilatory Failure
Treatment of cause Often positive pressure ventilation Treatment of ventilatory failure aims to correct the imbalance between the strength of the respiratory system and its load and varies with etiology. Obvious precipitants (eg, bronchospasm, mucus plugging, foreign bodies) should be corrected if possible. Patients with status asthmaticus should be treated in an intensive care unit by personnel skilled in airway management. (See also Treatment of Acute Asthma Exacerbations .) Noninvasive positive pressure ventilation (NIPPV) can immediately reduce the work of breathing and may forestall endotracheal intubation until drug therapy can take effect. The mask introduction must be done carefully to enhance comfort by perhaps starting with titration of expiratory positive airway pressure (EPAP) alone because one of the major functions of inspiratory positive airway pressure (IPAP) is to increase tidal volume, and, in these patients, end-expiratory lung volume approaches total lung capacity (see also Conventional mechanical ventilation via Tracheal Intubation is indicated for impending respiratory failure as indicated clinically by signs such as obtundation, monosyllabic speech, slumped posture, and shallow breathing. ABG values that reveal worsening hypercapnia are also an indication, although blood gas confirmation is not required and should not replace the physician’s judgment. Oral intubation is preferred over nasal because a larger endotracheal tube, which decreases airway resistance and permits easier suctioning, can be used. Hypotension and Pneumothorax occasionally occur after intubation for status asthmaticus and acute exacerbations of COPD (see also Although it is possible to reduce peak airway pressure by reducing peak flow rate or by changing the flow waveform to a descending profile (ie, so that the flow rate is high at the beginning of the breath and decreased over time), such changes shouldnotbe made. Although high flow rates require a high pressure to overcome the high airway resistance of status asthmaticus, this pressure is dissipated across robust, cartilage-containing airways. Lower flow rates (eg,<60 L/minute) reduce time available for exhalation, thereby increasing the end-expiratory volume (and the resultant intrinsic PEEP) and allowing a greater inspiratory volume during the next breath. Occasionally, patients with high intrinsic PEEP may need to have PEEP increased on the ventilator to facilitate triggering and reduce inspiratory work of breathing. Using low tidal volumes often results in hypercapnia, which is permitted for the greater good of reducing dynamic hyperinflation. An arterial pH>7.15 is generally well tolerated physiologically but often requires large doses of sedatives and opioids. Neuromuscular blockers should be avoided after the peri-intubation period because use of these agents in combination with corticosteroids can cause a severe and occasionally irreversible myopathy, particularly after 24 hours of combined use. Patient agitation should be managed with sedation rather than paralysis, but ideally ventilation can be adjusted to patients’ needs so as to reduce the need for sedation. Most patients with status asthmaticus improve to the point of liberation from mechanical ventilation within 2 to 5 days, although a minority experience protracted severe airflow obstruction. See Liberation from Mechanical Ventilation for a discussion on the general approach. In patients with acute-on-chronic respiratory failure (ACRF) caused by Chronic Obstructive Pulmonary Disease (COPD) , the oxygen cost of breathing is several times that of patients without underlying lung disease. This increased respiratory load occurs in the setting of barely adequate neuromuscular competence, so patients easily become too tired to maintain ventilation. These patients are vulnerable to respiratory failure from seemingly trivial insults, and recovery requires systematic identification and correction of these precipitants (see also Noninvasive positive pressure ventilation (NIPPV) is the preferred initial treatment for many patients with ACRF, resulting in decreased rates of ventilator-associated pneumonia, length of stay, and mortality compared with endotracheal intubation. Perhaps 75% of patients managed with NIPPV do not require endotracheal intubation. Advantages include the ease of application and removal; once initial stabilization has occurred, NIPPV may be stopped temporarily to allow oral intake in selected patients. Trials of unassisted breathing are easily done, and NIPPV can be reapplied as indicated. Settings should be adjusted to the work of breathing as assessed by patient report, respiratory rate and tidal volume, and accessory muscle use. In many patients, EPAP alone may be sufficient, which is beneficial because one of the major functions of inspiratory positive airway pressure is to increase tidal volume, and, in these patients, end-expiratory lung volume approaches total lung capacity (see also Respiratory Mechanics ). Deterioration (and need for endotracheal intubation) is best assessed clinically; ABG measurements may be misleading. Although worsening hypercapnia typically indicates treatment failure, patients differ markedly in tolerance of hypercapnia. Some patients with PaCO2 Conventional mechanical ventilation in ACRF aims to minimize dynamic hyperinflation and counter the adverse effects of Respiratory Mechanics while resting the fatigued respiratory muscles. Initial recommended settings are assist-control (A/C) with a tidal volume of 5 to 7 mL/kg and a respiratory rate of 20 to 24/minute, although some patients need lower initial rates to limit intrinsic PEEP. This intrinsic PEEP represents an inspiratory threshold load that must be overcome by the patient to trigger the ventilator, further increasing the work of breathing and preventing full rest on the ventilator. To counterbalance the effect of intrinsic PEEP, external PEEP should be applied to a level Most patients require full ventilatory support for 24 to 48 hours before spontaneous breathing trials are considered. It has not been determined whether this duration of treatment is needed to rest the respiratory muscles or to allow hyperinflation to diminish, thereby increasing respiratory muscle strength. The patient often sleeps heavily during this time and, in contrast to patients with asthma, typically requires little sedation. Adequate rest is often not achieved unless sufficient attention is paid to ongoing patient effort. This effort may manifest as accessory muscle use, inappropriately low airway pressures at the onset or throughout inspiration, or frequent failures to trigger the ventilator, indicating high intrinsic PEEP, weakness, or both. 