Fig. 8.1
Image of nasal continuous positive airway pressure (CPAP) interface. (Care of ResMed)
Fig. 8.2
Oronasal face mask for NPPV. (ResMed)
NPPV commonly employs either volume- or pressure-targeted ventilation. With volume-targeted ventilation, a fixed tidal volume is determined, and the ventilator will generate a pressure to achieve that tidal volume. This will lead to a variable pressure in the airways depending on the compliance and resistance of the respiratory system as well as patient effort. A major disadvantage of this system is that the patient’s potentially varying ventilatory requirements are not taken into account; the patient always receives the same predetermined tidal volume. In addition, if there is a leak, there will be no increase in the flow rate to compensate, which will lower the generated pressure, in turn reducing the delivered tidal volume. Volume-targeted ventilation is frequently utilized as average volume-assured pressure support (AVAPSTM) and intelligent volume-assured pressure support (iVAPSTM).
AVAPSTM was developed to ensure the delivery of targeted tidal volume, using an algorithm that automatically adjusts pressure support to meet the changing patient needs while maintaining the target tidal volume (Fig. 8.3).
Fig. 8.3
Waveform for average volume-assured pressure support (AVAPS™) mode: waveform analysis of the changes in inspiratory positive airway pressure (IPAP) to meet the desired and preset tidal volume. (Courtesy of Philips-Respironics)
iVAPSTM targets minute ventilation, accounting for anatomical dead space, and uses a backup rate to improve patient synchrony and comfort. This system automatically adjusts the level of pressure support to achieve and maintain target minute ventilation (Fig. 8.4). Both devices utilize a pneumotachometer internal to the machine to monitor and adjust their respective algorithms.
Fig. 8.4
Waveform analysis for intelligent volume-assured pressure support (iVAPS™): waveform analysis of the changes in inspiratory positive airway pressure (IPAP) to meet the desired and preset alveolar ventilation. (Courtesy of ResMed)
In pressure-targeted ventilation, the device is set to deliver a predefined positive pressure with variable airflow to maintain a constant airway pressure. Under these circumstances, the volume delivered is not fixed and depends on interactions between the ventilator, the patient’s respiratory system (specifically airway resistance and compliance), and the degree of unintentional leak. While the tidal volume and therefore the minute ventilation are variable under these conditions, it does allow for compensation for leaks. Traditional bi-level positive pressure ventilation (variable positive airway pressure, VPAPTM, or bi-level positive airway pressure, BiPAPTM) utilizes pressure-targeted ventilation using a preset fixed inspiratory and expiratory pressure level.
Some patients with chronic respiratory failure will require tracheotomy and use of home ventilation. Devices compatible with home ventilation via tracheotomy are illustrated in Table 8.1.
Table 8.1
Comparison of different options for home ventilation
Trilogy | Stellar 150 | LTV | |
|---|---|---|---|
Modes of ventilation | PC, VC, bi-level | PC, VC | PC, VC, PS, AC/SIMV |
Portable | Yes | Yes | Yes |
Data download capabilities | Yes | Yes | No |
Supplemental O2 | Yes | Yes | Yes |
Backup rate | Yes | Yes | Yes |
Indications for Noninvasive Positive Pressure Ventilation
It is well established that NPPV is beneficial in the acute care setting, with potential to reduce hospital morbidity, reduce intubation rates, facilitate liberation from mechanical ventilation, and decrease hospital length of stay [11]. Numerous studies, including randomized controlled trials (RCT) using NPPV in acute exacerbations of COPD, have demonstrated effectiveness. Continuous positive airway pressure (CPAP) alone has also been shown to be effective in avoiding intubation in patients with acute pulmonary edema [5]. The utility of NPPV in acute hypoxemic respiratory failure is not as clear and requires further investigation.
NPPV in selected chronic respiratory failure phenotypes has been demonstrated to stabilize ventilation and gas exchange, and improve daytime symptoms. The two major types of chronic hypercapnic respiratory failure we focus on in this chapter are restrictive thoracic/lung disease (neuromuscular disease, kyphoscoliosis, obesity hypoventilation syndrome) and obstructive lung disease (COPD) .
Restrictive Thoracic/Lung Disease
NPPV for restrictive thoracic/lung disease has been successfully utilized for decades. It is well established that the use of NPPV improves gas exchange and symptoms in patients with restrictive lung disease. Bach and Ellis demonstrated improvement in daytime gas exchange and symptoms of hypercapnia including fatigue, daytime hypersomnolence, and morning headaches with NPPV [1, 13]. The seminal paper was published in 1998 by Dr. Simonds and her colleagues [11]. This was an uncontrolled observational study examining the role of NPPV in chronic respiratory failure with survival, gas exchange, and quality of life as the outcomes. All patients had an average arterial pCO2 of approximately 77 mmHg and average arterial pO2 of approximately 56 mmHg breathing ambient air. They were nonambulatory, and therapy was initiated in the hospital for nocturnal use. Arterial pO2 and pCO2 levels improved significantly on NPPV, and these improvements were maintained over time as the patient continued to use NPPV (Fig. 8.5). A favorable impact on survival was observed (Fig. 8.6).
Fig. 8.5
Results of noninvasive ventilation in patients with chronic respiratory failure from neuromuscular disease in 18 patients. There was a decrease in baseline arterial pCO2 levels (pCO2 77 → 40–50 mmHg), while also improving oxygenation (pO2 56 mmHg → 80–90 mmHg) [1]. PaO 2 arterial partial pressure of oxygen, PaCO 2 arterial partial pressure of carbon dioxide
Fig. 8.6
Decline in mortality in 23 patients with chronic respiratory failure from neuromuscular disease using noninvasive positive airway pressure ventilation (NIPPV here). With the use of NIPPV, there is an initial slight decrease in survival (1-year survival 85 %), but then there is a plateau in mortality from year 2 to 5, maintained at 73 % with the use of NIPPV [11]
These observational studies demonstrated the benefits of NPPV in chronic respiratory failure, presumably allowing rest for the respiratory muscles, with improvement in gas exchange, lung compliance, lung volume, and mortality.
Indications and contraindications for NPPV in restrictive lung disease are listed below.
1.
Symptoms: morning headaches, daytime hypersomnolence, dyspnea
2.
Signs: right heart failure or cor pulmonale
3.
Gas exchange/ventilatory abnormalities:
(a)
Daytime arterial pCO2 > 45 mmHg
(b)
Nocturnal oxygen desaturation < 90 % for ≥ 5 min
4.
Other:
(a)
Recovery from acute respiratory failure with persistent CO2 retention
(b)
Multiple hospitalizations for acute respiratory failure
Contraindications
1.
Inability to protect airway: impaired cough or swallowing
2.
Excessive airway secretions
3.
Need for continuous ventilatory assistance
4.
Inability to comprehend therapy
Obstructive Lung Disease
The utility of NPPV therapy in obstructive lung disease is not as clear as in patients with restrictive lung disease. The literature supports the use of NPPV in acute or chronic respiratory failure in patients with obstructive lung disease (mostly COPD) by reducing the need for mechanical ventilation as well as by improving mortality and hospital length of stay. In one RCT, Plant et al. assessed the impact of NPPV in 236 participants with COPD exacerbations and respiratory acidosis (pH 7.25–7.35). NPPV demonstrated a reduced need for intubation (15 vs. 27 %, p = 0.02) and a more rapid improvement in respiratory acidosis [17].
The impact of NPPV in chronic respiratory failure for stable severe COPD has been inconsistent. One of the largest RCTs examining the role of NPPV in chronic respiratory failure for COPD was performed by McEvoy et al. [18]. In this study, 144 patients were assigned to either nocturnal NPPV and long-term oxygen therapy (LTOT) or LTOT alone. Participants on NPPV used a mean inspiratory positive airway pressure (IPAP) of 13 cm H2O and mean expiratory positive airway pressure (EPAP) of 5 cm H2O. Average objective adherence was 4.5 h a night. No difference in arterial pCO2 or forced expiratory volume in 1 s (FEV1) was found between the two groups in 12 months of follow-up (Table 8.2 and Fig. 8.7). The study did identify a minimal survival advantage in participants with NPPV + LTOT over participants with LTOT alone, but this was at the expense of questionnaire-associated poorer general and mental health, and less vigor. Recently, Köhnlein et al. demonstrated a survival advantage of 1 year in patients with stable hypercapnic COPD patients randomized to NPPV versus usual care [19]. The survival benefit was only realized if the participants accepted therapy, and awake arterial pCO2 was decreased by 20 % from baseline.
Table 8.2
Comparison of arterial pCO2 (arterial partial pressure of carbon dioxide, PaCO 2 ) and forced expiratory volume in 1 s (FEV1) levels when treated either with noninvasive ventilation (NIV) and long-term oxygen therapy (LTOT) versus LTOT alone. There was no statistically significant difference in either arterial pCO2 levels or FEV1 after either 6 or 12 months of therapy with NIV therapy when compared to LTOT [18]
Baseline | 6 months | 12 months | ||
|---|---|---|---|---|
PaCO2 (mmHg) | LTOT | 54.2 (52.0–56.4) | 55.1 (52.1–58.1) | 52.2 (49.5–54.9) |
n = 45 | n = 43 | n = 29 | ||
NIV + LTOT | 54.1 (51.7–56.5) | 52.9 (50.5–55.3) | 53.2 (50.6–55.8) | |
n = 54 | n = 44 | n = 43 | ||
FEV1.0 (% pred) | LTOT | 23.9 (21.9–25.9) | 23.4 (21.4–25.4) | 26.3 (24.1–28.5) |
n = 51 | n = 47 | n = 38 | ||
NIV + LTOT | 25.3 (22.3–28.3) | 24.9 (21.7–28.1) | 24.1 (21.1–27.1) | |
n = 58 | n = 56 | n = 47 |
Fig. 8.7
Survival advantage: Use of noninvasive ventilation (NIV) + long-term oxygen therapy (LTOT) showed a minimal survival advantage when compared to LTOT alone [2]
Current indications for NPPV in obstructive lung disease due to COPD are listed below.
Indications [16]
1.
Symptoms: fatigue, hypersomnolence, dyspnea
2.
Gas exchange/ventilatory abnormalities:
(a)
Arterial pCO2> 55 mmHg
(b)
Arterial pCO2 50–54 mmHg AND O2 saturation < 88 % for > 10 % monitoring time
3.
Pharmacologic therapy failure with maximal bronchodilators and steroids
Initiating Therapy
We have discussed the different modes of ventilation, types of NPPV, and the indications for initiating therapy. With the exception of the Köhnlein [19] report, no definite blueprint for success exists, and favorable outcomes depend on multiple variables.
Initiation of NPPV can be initiated in an inpatient or outpatient setting. Patients with restrictive lung disease or neuromuscular disease with chronic respiratory failure and who are followed by pulmonary physicians are likely to be monitored for alveolar hypoventilation (hypercapnia) . These patients are frequently initiated on NPPV as outpatients in the sleep laboratory. This allows both the patient and the technologists, the entire night, to titrate the pressure, work on interface issues while minimizing unintentional mask leak, monitor ventilation with end tidal CO2 or transcutaneous CO2, and maximize patient comfort with the therapy as well as to determine whether treatment is optional for both non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. These patients frequently have evidence of hypercapnic respiratory failure based on an awake arterial blood gas. Titration can be initiated during the daytime in the sleep laboratory, again working with the sleep technologist on making sure the pressure and interface work well with the patient. Patients with neuromuscular disease tend to do very well with NPPV because the etiology of their respiratory failure is due to progressive muscle weakness, and they have relatively normal lungs with normal respiratory system compliance. Improvements in quality of life and symptoms are readily achieved in this setting, which in turn encourages adherence to therapy.
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