POSITIVE AIRWAY PRESSURE THERAPY
Positive airway pressure therapy can be used in patients who are breathing spontaneously as well as those who are mechanically ventilated. The princi-pal indication for positive airway pressure therapy is a decrease in FRC resulting in absolute or relative hypoxemia. By increasing transpulmonary distend-ing pressure, positive airway pressure therapy can increase FRC, improve (increase) lung compliance, and reverse ventilation/perfusion mismatching.Improvement in the latter parameter will show as a decrease in venous admixture and an improvement in arterial O 2 tension.
Application of positive pressure during expiration as an adjunct to a mechanically delivered breath is referred to as PEEP. The ventilator’s PEEP valve provides a pressure threshold that allows expiratory flow to occur only when airway pressure exceeds the selected PEEP level.
Application of a positive-pressure threshold dur-ing both inspiration and expiration with sponta-neous breathing is referred to as CPAP. Constant levels of pressure can be attained only if a high-flow (inspiratory) gas source is provided. When the patient does not have an artificial airway, tightly fitting full-face masks, nasal masks, nasal “pillows” (ADAM circuit), or nasal prongs (neonatal) can be used. Because of the risks of gastric distention and regurgitation, CPAP masks should be used only on patients with intact airway reflexes and with CPAP levels less than 15 cm H2O (less than lower esophageal sphincter pressure in normal persons). Expiratory pressures above 15 cm H2O require an artificial airway.
The distinction between PEEP and CPAP is often blurred in the clinical setting because patients may breathe with a combination of mechanical and spon-taneous breaths. Therefore, the two terms are often used interchangeably. In the strictest sense, “pure” PEEP is provided as a ventilator-cycled breath. In contrast, a “pure” CPAP system provides only sufficient continuous or “on-demand” gas flows (60–90 L/min) to prevent inspiratory airway pres-sure from falling perceptibly below the expiratory level during spontaneous breaths (Figure 57–5). Some ventilators with demand valve–based CPAP systems may not be adequately responsive and result in increased inspiratory work of breathing.
This situation can be corrected by adding low levels of (inspiratory) PSV if in a volume-targeted mode or changing to a pressure-targeted mode. In clini-cal practice, controlled ventilation, PSV, and CPAP/ PEEP support can be delivered by most modern ICU ventilators. Manufacturers have also developed specific devices to deliver bilevel inspiratory posi-tive airway pressure (IPAP) with expiratory positive airway pressure (EPAP) in either a spontaneous or time-cycled fashion. The term bilevel positive air-way pressure (BiPAP) has become a commonly usedphrase, adding to the confusion of airway pressure terminology.
The major effect of PEEP and CPAP on the lungs is to increase FRC. In patients withdecreased lung volume, appropriate levels of either PEEP or CPAP will increase FRC and tidal ven-tilation above closing capacity, will improve lung compliance, and will correct ventilation/perfusion abnormalities. The resulting decrease in intrapul-monary shunting improves arterial oxygenation. The principal mechanism of action for both PEEP and CPAP appears to be expansion of partially col-lapsed alveoli. Recruitment (reexpansion) of col-lapsed alveoli occurs at PEEP or CPAP levels above the inflection point, defined as the pressure level on
a pressure–volume curve at which collapsed alveoli are recruited (open); with small changes in pressure there are large changes in volume (Figure 57–6). Although neither PEEP nor CPAP decreases total extravascular lung water, studies suggest that they do redistribute extravascular lung water from the interstitial space between alveoli and endothelial cells toward peribronchial and perihilar areas. Both effects can potentially improve arterial oxygenation.
Excessive PEEP or CPAP, however, can overdis-tend alveoli (and bronchi), increasing dead space ventilation and reducing lung compliance; both effects can significantly increase the work of breath-ing. By compressing alveolar capillaries, overdisten-tion of normal alveoli can also increase pulmonary vascular resistance and right ventricular afterload.
A higher incidence of pulmonary barotrauma is observed with excessive PEEP or CPAP, particularly at levels greater than 20 cm H 2O. Disrup-tion of alveoli allows air to track interstitially along bronchi into the mediastinum (pneumomediasti-num). From the mediastinum, air can then rupture into the pleural space (pneumothorax) or the peri-cardium (pneumopericardium) or can dissect along tissue planes subcutaneously (subcutaneous emphy-sema) or into the abdomen (pneumoperitoneum or pneumoretroperitoneum). A bronchopleural fistula is the result of failure of an air leak to seal (close). Although barotrauma must be considered in any discussion of CPAP and PEEP, in fact, it may be more clearly associated with higher peak inspira-tory pressures that result with increasing level of PEEP or CPAP. Other factors that may increase the risk of barotrauma include underlying lung disease, stacking of breaths (from too frequent breaths or too short expiratory times) so that intrinsic PEEP (dynamic hyperinflation or autoPEEP) develops, large VT (>10–15 mL/kg), and younger age.
Nonpulmonary adverse effects are primarily cir-culatory and are related to transmission of the ele-vated airway pressure to the contents of the chest. Fortunately, transmission is directly related to lung compliance; thus, patients with decreased lung com-pliance (most patients requiring PEEP) are least affected.
Progressive reductions in cardiac output are often seen as mean airway pressure and, second-arily, mean intrathoracic pressure rise. The principal mechanism appears to be intrathoracic pressure– related inhibition of return of venous blood to the heart. Other mechanisms may include leftward displacement of the interventricular septum (inter-fering with left ventricular filling) because of the increase in pulmonary vascular resistance (increased right ventricular afterload) from overdistention of alveoli, leading to an increase in right ventricular volume. Left ventricular compliance may therefore be reduced; when this occurs, to achieve the same cardiac output may require a higher filling pressure. An increase in intravascular volume will usually at least partially offset the effects of CPAP and PEEP on cardiac output. Circulatory depression is most often associated with end-expiratory pressures greater than 15 cm H2O.
PEEP-induced elevations in central venous pressure and reductions in cardiac output decrease both renal and hepatic blood flow. Circulating levels of antidiuretic hormone and angiotensin are usually elevated. Urinary output, glomerular filtration, and free water clearance decrease. Increased end-expiratory pressures, because they impede blood drainage from the brain and blood return to the heart, may increase intracranial pressure in patients whose ventricular compliance is decreased. Therefore, in patients on mechanical ventilation for acute lung injury and who have evi-dence of increased intracranial pressure, the level of PEEP must be carefully chosen to balance oxygen-ation requirements against potential adverse effects on intracranial pressure.
The goal of positive-pressure therapy is to increase oxygen delivery to tissues, while avoiding the adverse sequelae of excessively increased (>0.5) FIO2. The latter is best accomplished with an adequate car-diac output and hemoglobin concentration. Ideally, mixed venous oxygen tensions or the arteriovenous oxygen content difference should be followed. The salutary effect of PEEP (or CPAP) on arterial oxygen tension must be balanced against any detrimental effect on cardiac output. Volume infusion or inotro-pic support may be necessary and should be guided by hemodynamic measurements.
At optimal PEEP the beneficial effects of PEEP exceed any detrimental risks. Practically, PEEP is usually added in increments of 3–5 cm H2O until the desired therapeutic end point is reached. The most commonly suggested end point is an arte-rial oxygen saturation of hemoglobin of greater than 88–90% on a nontoxic inspired oxygen con-centration (≤50%). Many clinicians favor reducing the inspired oxygen concentration to 50% or less because of the potentially adverse effect of greater oxygen concentrations on the lung. Alternatively, PEEP may be titrated to the mixed venous artery oxygen saturation (SVO2> 50–60%). Monitoring lung compliance and dead space has also been suggested.
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