The effects of positive pressure on the ventricles are opposite in the normal heart, with a decrease in both right and LV preload, increased right ventricular afterload and decreased LV afterload,39,40 as well as an overall decrease in cardiac chamber size that is directly proportional to the level of PPV.41 For the decompensated CHF patient, this can produce an increase in cardiac output simply by shifting the patient to a more favorable (leftward) position on the Frank-Starling curve.42-44
Troubleshooting
Once NIV is initiated, it is imperative, at least initially, to remain at bedside to monitor progress and improvement. Even though NIV is beneficial in the acute setting, it should always be viewed as a temporary bridging measure. With improvement, NIV may be discontinued, but in cases of failure, it is necessary to proceed with endotracheal intubation.
As the patient synchronizes with the ventilator, changes should be seen rather quickly, including improvement in the work of breathing, a restoration of mental status (if significant hypercapnia is present), and improved oxygenation. In the patient with severe uncontrolled hypertension and resulting flash pulmonary edema, the reduction in preload and afterload should contribute to a decrease in systolic BP (in addition to medical therapy). There should be a low threshold for obtaining an initial arterial blood gas (or a venous sample coupled with end-tidal CO2 data) as it may be helpful to guide therapy.
Noninvasive ventilation is similar to mechanical ventilation in that the clinician should not view it is as a static therapy, but rather as a dynamic process. For application of NIV in the acute setting, it should be recognized that the patient’s physiology is deranged (albeit transiently); as physiology eventually returns to preexisting levels, changes in NIV-pressure levels (or modes) are therefore necessary. Moreover, initial starting pressures may not be adequate to either overcome deficits in oxygenation, ventilation, or provide significant preload/afterload reduction. Knowledge of which parameters or values to adjust contribute to increased patient comfort, patient safety, improved cardiopulmonary dynamics, and a faster restoration of ventilatory status. In essence, the EP at the bedside should always ask himself or herself “what am I trying to fix?”
When the patient begins to develop synchrony with the ventilator, improvement and stabilization in the measured VT should be observed. The goal of delivered VT should be 6 to 10 mg/kg of ideal body weight. An increase in the IPAP value will improve the VT and decrease the work of breathing, and it should be the first value increased to reduce PaCO2. The use of EPAP will help to reduce intrinsic positive-end expiratory pressure and atelectasis and reduce upper airway obstruction. Increasing EPAP will improve oxygenation. Table 3 lists the common starting values for both modes of NIV and provides troubleshooting suggestions.
To date, no clinical trials have addressed the optimal initiation strategy or application settings for NIV. It should be understood, however, that the initial settings will typically be lower pressures to ensure patient comfort and development of familiarity with the device and interaction. For BiPAP, it is common to start with settings of 10/5 (IPAP/EPAP), and then titrate up (not exceeding 25 cm H2O) and maintaining minimum pressure support of 4 to 5 cm H2O. For CPAP, initial settings of 5 to 10 cm H2O are reasonable. Increased pressures can lead to patient discomfort, unintentional leak, and the development of patient-ventilator associated asynchrony.12 The goal is to balance therapeutic effect(s) with patient comfort. Higher pressures, even though they may be optimal, must be balanced with patient comfort as long as it is physiologically acceptable.
With increasing support, there may be an increase in mask leak; despite this, increasing levels of pressure or volume ventilation have been shown to increase minute ventilation (referred to as VE).45 In cases such as acute pulmonary edema or significant hypercapnia, initial higher-pressure settings may only be necessary for a brief time to reverse the pathology present and restore normal ventilation and hemodynamics. After the initial application, IPAP, EPAP, and FiO2 all may require titration.
Patients who fail to show improvement (either clinically or based on ventilatory parameters) or those with persistent mental status abnormalities, agitation, excessive secretions, or ventilator asynchrony after 1 hour of NIV are at high risk for NIV failure.46,47
Interpreting the Literature
Sizeable and sometimes conflicting literature exists on the subject of NIV. Despite a lack of clear and consistently reproducible benefit in morbidity, NIV use continues to increase. There are multiple factors that make interpretation of the results difficult and at times seemingly contradictory. Careful examination of the literature therefore must be undertaken before applying NIV to daily practice. Inconsistency of therapy type delivered, NIV pressure settings, pressure adjustments, patient monitoring, differing mask types, ventilator designs, endpoints, patient populations and the influence of cotreatments can all influence outcomes and potential benefit. To further complicate the data, unmeasured factors such as patient tolerance, interface fit, mask leak, and patient-ventilator asynchrony may be grouped as “NIV failure.”