Interfaces, Mask Leaks, Patient-Ventilator Interaction, and Respiratory Failure
Interfaces
Patient interfaces (mask types) for NIV include nasal prongs, full facial mask, or most commonly, an oronasal mask.31 For successful delivery of positive pressure, there must be an adequate fit or seal with minimal air leak to establish a ventilator circuit. Even though there is no perfect interface, patient comfort and treatment efficacy should be balanced. The interface chosen should minimize skin damage, maximize seal, and optimize patient-ventilator interface. The interfaces have straps that are used to secure the mask in place and balance the tension and stress on the skin to ensure a good seal and to avoid excess focal pressure that may result in complications such as skin breakdown, necrosis, or discomfort. Multiple interfaces and mask types have been evaluated in different acute-care situations, and it is important the clinician be familiar with the various options available for NIV interface and delivery.
Mask Leaks
Unintentional leaks are an unavoidable reality with NIV use. The ventilators designed for NIV typically use a single-limb circuit with an intentional leak port close to the patient. This port provides resistance and, as the ventilator produces airflow, it can subsequently generate pressure. Because this leak port is incorporated into the interface, it is important to utilize the same manufacturer of the ventilator and interface to avoid interface-ventilator mismatch.32
In some cases, unintentional leaks have been linked to asynchrony leading to increased work of breathing, ineffective delivery of breaths, and missed triggering events.33 The goal of any chosen interface is the lowest measurable unintentional leak rate as higher values demonstrate significant variability (and inaccuracy) of measured tidal volumes (VT).34 Overtightening the mask should be avoided since it can compromise both patient comfort and increase the chance of skin necrosis or breakdown.
Patient-Ventilator Interaction
The importance of the patient-ventilator interaction and the development of synchrony between the two cannot be overstated. After initial application, the patient should be closely monitored as he or she begins to work with the ventilator. This is especially important in BiPAP.
Optimal patient-ventilator synchrony can be difficult to achieve, especially in the NIV-naïve patient with critical respiratory distress. Of note, approximately 20% to 30% of patients with ARD cannot be managed by NIV,11 and asynchrony, though difficult to quantify in the acute-care setting, may contribute to this number.
Respiratory Failure
Acute respiratory failure is caused by a change in the patient’s baseline gas exchange, resulting in an inability to provide sufficient levels of O2 or to ventilate adequately. The etiologies of ARF are characterized into four types.
Type I. Also referred to as hypoxemic respiratory failure, type I is the most common and is characterized by an arterial oxygen tension (PaO2) of less than 60 mm Hg, with either normal or low levels of arterial CO2 that is not responsive to supplemental O2.
Type II. This type of respiratory failure is characterized by alveolar hypoventilation, with a PaCO2 level greater than 45 mm Hg, although hypoxemia may also be present due to concomitant loss of central nervous system drive.
Type III. Failure primarily occurs in the perioperative setting where the functional residual capacity is reduced in combination with increasing atelectasis.
Type IV. Type IV ARF is secondary to circulatory failure and resolves when shock is corrected.35,36
Regardless of the respiratory failure etiology, the patient is at risk of further deterioration and the need for endotracheal intubation.
Physiologic effects of NIV
Once the interface is secured, NIV has several important effects on both the cardiac and pulmonary systems. For this discussion, intrathoracic pressure (PIT) is considered synonymous with mean airway pressure (Paw).
Noninvasive ventilation improves airflow, lung volumes, and subsequent VT while overcoming pulmonary atelectasis. The increase in lung volume is directly proportional to an increase in Paw. This effect is only seen after overcoming airway resistance and chest wall and lung compliance. There is also an improvement in alveolar recruitment and redistribution of pulmonary blood flow37 with decreased work of breathing.
With the increase in PIT, there is decreased venous return to the right heart and a resulting decrease in cardiac preload.38 In the setting of acute cardiogenic pulmonary edema (ACPE), this effect is highly favorable. However, in the volume-depleted or hemodynamically unstable patient, this may result in a drop in cardiac output and hypotension. The “normal” heart is more sensitive to preload, and the application of positive pressure can cause a significant decrease in cardiac output. Cardiac afterload is reduced through multiple mechanisms, including directly from a decreased left-ventricular (LV) preload and also from a decrease in the LV transmural pressure (referred to as PTM).