Relationship between arterial and peripheral venous lactate levels.

of our patients and found MIS in only the 2 patients reported in our article. ' Neither patient had evidence of myocardial ischemia in proximity to use of the bilevel PAP system; in fact, their problems occurred days after use of the system. In reference to the Hipona study, the preliminary data may reflect a rapid increase in myocardial perfusion, rather than an increase in myocardial ischemia. In CHF, the blood flow to the distended left ventricular (LV) wall is compromised. LV wall tensions are elevated as the result of increased peripheral vascular resistance, decreased (CO), and a distended end-diastolic volume. As Hipona et al. note, the introduction of the bilevel PAP system creates an increase in airway pressure and an increase in intrathoracic pressure. This increase in intrathoracic pressure is transmitted to all intrathoracic structures, including the left ventricle. This additional pressure around the ventricles assists in LV emptying and the movement of blood into the extrathoracic aorta. ' This effect produces a reduction in LV wall tension while increasing the CO. The net result of this effect is exactly what Hipona et al. suggest, a reduction in LV end-diastolic volume. The decrease in LV enddiastolic volume and wall tension may produce a rapid increase in LV myocardial blood flow. A sudden return of blood to compromised areas of the LV wall should produce a washout of myocardial proteins, including CK-MB isoenzymes, which may have leaked from ischemic myocytes. Dramatic reversal of pulmonary edema symptoms have been observed within seconds of institution of the bilevel PAP system, indicating the extremely rapid onset of these cardiovascular effects. Measurement of cardiac enzymes following such a washout would likely demonstrate a transient positive peak. Treatments that do not produce such a rapid resolution of CHF produce a slower resumption of LV blood flow and, hence, a Lower, broader pattern of enzyme leakage. If MI is defined only by the height of a CK or CK-MB value, then the bilevel PAP system might appear to produce an MI in some patients for whom other treatment modalities would not. The clinical data reported for these patients seem to support this explanation. In both Dr. Hipona et al.'s study and our own, the patients' CHFs improved dramatically and endotracheal intubation was averted. If the bilevel PAP system were in fact increasing myocardial ischemia, these patients' CHFs would be expected to worsen rather than improve. It is unlikely that a treatment that increased myocardial cell death would produce an improvement in CO. Other indicators of myocardial ischemia such as ECG findings, complaints of chest pain, or subjective deterioration also should be present in the bilevel PAP system group if it truly produced myocardial ischemia. In terms of the pressures used in the noninvasive pressure support systems, we now routinely use inspiratory positive airway pressures (IPAPs) of 1418 cm H 2 0 with expiratory positive airway pressures (EPAPs) of 1015 cm H 2 0 for our CHF patients. Anecdotal reports from other clinicians using these systems note that EPAPs or CPAPs of 15-20 cm H20 are well tolerated in these patients. In conclusion, our continued clinical experience with this system has convinced us of its efficacy and safety. We have experienced no problem in using this device in the face of coronary artery disease and have begun releasing carefully defined patient groups from the ED following bilevel PAP system treatment for CHF. We do not believe that isolated elevations in CK-MB levels in the face of improvement in all other clinical parameters is indicative of bilevel PAP system-induced MI. Isolated CK-MB elevations most likely represent a washout effect associated with a rapid change in global myocardial perfusion. Based on experience to date. we believe that bilevel ventilation remains a first-line therapy for the management of acute cardiogenic CHF.