As these procedures become more common, the RCP will have a greater impact on related outcomes.
Recent advances in cardiac surgery for congenital defects in the neonate have demonstrated the need for the selection of appropriate ventilator strategies in the operating room (as well as later, in the ICU). The latest generation of mechanical ventilators gives the clinician the ability to use ventilator settings that optimize gas exchange and improve the weaning process for these patients. Inspired gases are also available for the selective alteration of pulmonary vascular resistance (PVR). To maximize the effects of these inspired gases on the pulmonary vasculature, appropriate ventilator settings and strategies are needed. As surgical procedures for neonates with congenital cardiac disease become more complex, the RCP must have a complete understanding of cardiopulmonary physiology and must know how to use new ventilatory technology for these patients.
Physiology of the First Breath
Clinical knowledge of the first breath of life assists the clinician in understanding the gas exchange and pulmonary perfusion changes that occur in the neonatal cardiopulmonary system. This information will provide the framework for selecting an appropriate ventilator strategy for these patients. During fetal circulation, the amount of blood flow to the lungs is approximately 3.5 percent of total cardiac output; the remaining flow shunts to the left atrium via the foramen ovale. Within moments of the first breath, the infant moves from fetal to transitional circulation. Perfusion and oxygenation of the lungs begin immediately. As oxygenation increases, the pulmonary vasculature responds with vasodilatation and a corresponding decrease in PVR.
As the PVR decreases and pulmonary perfusion increases, blood flow reverses through the foramen in response to the need for increased intravascular volume. Over the next few days, as right ventricular compliance decreases following the PVR decrease, right ventricular atrial pressure decreases below left atrial pressure and the foramen ovale closes.
As these changes occur in the foramen ovale, simultaneous alterations affect the ductus arteriosus, which is sensitive to oxygen and responds with vasoconstriction and, ultimately, closure. In premature infants, failure of the ductus to close may lead to respiratory distress (related to excessive pulmonary perfusion, leading to pulmonary edema and hypoxia). The use of intravenous indomethacin may promote rapid closure of the ductus arteriosus. For some children born with specific congenital cardiac defects, however, closure of the ductus would lead to death due to insufficient systemic or pulmonary perfusion. For these patients, administration of prostaglandin will promote dilation of the ductus and maintain adequate blood flow.
During positive-pressure ventilation (PPV), an increase in PVR may lead to dilation of the right ventricle and decreased pulmonary perfusion. This elevation in PVR may also cause shunting of the desaturated blood through the foramen ovale, promoting significant hypoxemia. This pattern is similar to that of the fetal circulation and may be attributable to the parameters chosen for mechanical ventilation.
Inspiratory flow pattern is important and must be included in the development of a ventilator strategy intended to minimize the effects of PPV on circulation. A decelerating flow pattern will minimize changes in PVR and their effects on pulmonary perfusion and right ventricular function.1 Figure 1, page 34, shows the interface of the gas exchange unit and the pulmonary vasculature.
As inspired gas enters the region of the respiratory bronchiole, the pattern of the inspiratory flow generated by the ventilator will increase shear forces along the lateral walls of the bronchiole. These increases may trigger vasoconstriction and an associated increase in PVR. A decelerating flow pattern improves gas exchange by maintaining the interface of convection and diffusion in order to optimize dead space ventilation.2
The mean airway pressure should also be adjusted to a level that prevents blood from being shunted through the foramen ovale.
Setting ventilation parameters in a way that minimizes the effects of mechanical ventilation on the circulation is an important aspect of selecting a ventilation strategy. Capnography and dead space measurements are noninvasive, breath-by-breath assessments of ventilation and circulation that can assist the clinician in selecting appropriate ventilator settings for children who have congenital cardiac disease.3
The same information is useful when mechanical ventilation is being used in newborn infants, particularly in ensuring that mean airway pressure does not adversely affect blood flow; this could produce shunting through the foramen ovale or ductus arteriosus. If blood is shunted through the foramen ovale in response to an increase in mean airway pressure, pulmonary perfusion will decrease immediately and dead space will increase accordingly. This will change the shape of the capnogram. Figure 2 shows a normal capnogram and the three phases of expired carbon dioxide.
If there is shunting through the foramen ovale, the slope of phase III of the capnogram will flatten and the alveolar plateau will be absent.4 In this situation, the clinician can adjust the ventilator settings to optimize gas exchange while maintaining appropriate pulmonary blood flow. Carbon dioxide elimination responds to the efficiency of ventilator resetting and is a useful monitor for infants after cardiac surgery.5
Figure 3, page 36, illustrates the modified Blalock-Taussig shunt, a surgical procedure performed to improve pulmonary blood flow. A Gore-Texr graft inserted between the subclavian artery and the pulmonary artery improves pulmonary perfusion, but is extremely sensitive to changes in intrathoracic pressure. Excessive mean airway pressures may prevent blood flow through the graft and decrease pulmonary perfusion. Capnography and dead space monitoring can help the clinician select appropriate levels of ventilator support for gas exchange while maintaining adequate pulmonary blood flow.
Ventilation After Bypass
Patients undergoing cardiac surgery for congenital conditions who require cardiopulmonary bypass (CPB) are ventilated using continuous positive airway pressure during the surgical procedure. The lungs are subject to microatelectasis during CPB, and exhibit various physiologic responses to this procedure. Surfactant washout, interstitial edema, and associated lung water accumulation all promote a decrease in static lung compliance. In particular, neutrophil activation and activation of the complement cascade cause the release of substances that are direct causes of pulmonary vasoconstriction. These physiologic responses increase PVR and lead to hypoxia. Selecting the correct ventilator settings at this time is crucial to improving gas exchange (so that the pulmonary vasculature will stabilize, minimizing pulmonary vasoconstriction and related pulmonary hypertension).
Monitoring dead space during the initial stages of weaning from CPB will aid the anesthesiologist in adjusting the ventilator for the desired gas exchange and will document any deleterious effects of the chosen ventilator settings on pulmonary blood flow.6 Lung mechanics surveillance is also useful in determining a ventilator strategy following chest-wall closure. Dynamic lung compliance decreases upon closure of the chest wall, and an increase in ventilator pressure settings may be necessary. Measurements collected at the end of the surgical procedure and during closure of the chest wall will assist clinicians in the postoperative management of the patient in the ICU.
Pulmonary Vasculature Control
The combined use of particular ventilator settings and inspired gases that alter the pulmonary vasculature permits the clinician to manipulate the PVR as needed to improve pulmonary perfusion, as well as to achieve adequate gas exchange.
Treatment of pulmonary hypertension may require the acid-base balance to remain in the alkalotic range, in conjunction with inspired nitric oxide treatment. A ventilator workstation uses low flow rates for the administration of the gas, and the level of nitric oxide is easy to adjust. The primary limitations of nitric oxide therapy are the production of nitrogen dioxide and (when nitric oxide levels rise above 5 ppm) increased levels of methemoglobin. Nitrogen dioxide can be maintained at levels below 1 ppm by setting the working pressure in such a way that, at the peak of inspiration, the pressure value decreases by 5 cm H2O. The workstation, interfaced with a central ventilator monitor, documents and trends breath-by-breath data for 24 hours. This documentation, used to assess the efficiency of ventilator settings and associated strategies, provides information for patient databases as well as for educational purposes.
Appropriate ventilator settings and strategies are important to the efficient delivery of nitric oxide to the gas exchange units in the lungs.7 At Valley Children’s Hospital, Fresno, Calif, the initial ventilator settings used are:
- pressure control,
- an inspiratory to expiratory ratio of 1:1,
- a positive inspiratory pressure of
28 cm H2O,
- a respiratory rate of 26 breaths per minute,
- a positive end-expiratory pressure of
6 cm H2O,
- a fraction of inspired oxygen of 0.6, and,
- nitric oxide provision at 10 ppm.
The clinician then adjusts these ventilator parameters to achieve optimal gas exchange, pulmonary perfusion (assessed using capnography and dead space measurement), and lung compliance. Patients undergoing surgical correction of lesions associated with single-ventricle defects (such as hypoplastic left heart syndrome) may develop pulmonary hyperperfusion and require an increase in PVR to improve systemic blood flow. Treatment for these patients is the opposite of that for patients with pulmonary hypertension: the blood must remain acidotic through hypoxic ventilation or the addition of carbon dioxide. Nitrogen or carbon dioxide could replace the nitric oxide used to treat pulmonary hyperperfusion. Adjustments to the flow of the selected inspired gas are necessary to maintain the desired level of hypoxia or hypercarbia. Measurements of dead space and lung mechanics will guide the clinician in setting and resetting the ventilator and in titrating the inspired gases to obtain the desired results on cardiopulmonary function. Attention to arterial and mixed venous blood gas levels is essential during the titration of gases in order to prevent dangerous disturbances in acid-base balance and systemic perfusion. The use of noninvasive monitors, however, will decrease the need for frequent sampling for blood gas analysis. Decreasing the need for frequent sampling is very important in the newborn to minimize blood loss.
Weaning an infant from mechanical ventilation following cardiac surgery requires a multidisciplinary approach, so the entire ICU staff should be involved in developing a weaning strategy.
This approach addresses the special needs of infants, includes a plan for sedation that involves a team concept, and has, as goals, early extubation and ICU discharge. To improve the weaning process, newer-
generation mechanical ventilators are used to provide alternative modes; this allows ventilation to be fine-tuned to meet a patient’s specific needs. The use of pressure- and volume-supported ventilation improves the weaning process for the newborn, compared to the traditional intermittent mandatory ventilation mode.8 Ventilators that incorporate these modes and permit patient-initiated flow triggering decrease the work of breathing and adjust the peak inspiratory pressure as the patient’s cardiopulmonary status improves.
As surgical repair of congenital cardiac disease continues to improve, the RCP will assume greater responsibility for the treatment of these children and will have a direct impact on related outcomes.
David H. Walker, MA, RRT, RCP, is chief technology officer, Valley Children’s Hospital, Fresno, Calif. Andrew J. Parry, MD, is assistant professor, pediatric cardiac surgery, University of California San Francisco, and attending pediatric cardiac surgeon, Valley Children’s Hospital.
1. Sternberg R, Sahebjami H. Hemodynamic and oxygen transport characteristics of common ventilatory modes. Chest. 1994;105:1798-1804.
2. Fletcher R, Niklason L, Derefeldt B. Gas exchange during controlled ventilation in children with normal and abnormal pulmonary circulation. Anesth Analg. 1986; 3:155-163.
3. Fletcher R. Relationship between alveolar dead space and arterial oxygenation in children with congenital cardiac disease. Br J Anaesth. 1989;62:168-176.
4. Taskar V, John J, Larson A, Wetterberg T, Jonson B. Dynamics of carbon dioxide elimination following ventilator resetting. Chest. 1995;108:196-202.
5. Fletcher R. The Single Breath Test for Carbon Dioxide [thesis]. Lund, Sweden: University of Lund; 1980.
6. Arnold JH, Thompson JE, Benjamin PK. Respiratory dead space measurements in neonates during extracorporeal membrane oxygenation. Crit Care Med. 1993;21:1895-1900.
7. Putensen C, Rasanen J, Lopez F, Downs JB. Continuous positive airway pressure modulates effect of inhaled nitric oxide on the ventilation-perfusion distributions in canine lung injury. Chest. 1994;106:1563-1569.
8. Pitotrowski A, Sobala W, Kawczynski B. Patient-initiated, pressure-regulated, volume-controlled ventilation compared with intermittent mandatory ventilation in neonates: a prospective, randomized study. Intensive Care Med. 1997;23:975-981.