To the Editor:—

Rivenes et al.  1have presented evidence that sevoflurane and isoflurane preserve forward output in patients with congenital heart disease. Their conclusion that cardiac output is maintained with little change in contractility with sevoflurane and isoflurane is not accurate. The data in their table 4 indicate that systemic vascular resistance decreases with both agents, whereas cardiac output and preload (left ventricular end-diastolic volume) are unchanged. This result is obtained only if contractility decreases. I used the data in table 4 of Rivenes et al.  1to estimate end-systolic elastance (Ees) 2for the isoflurane cases using a computer model 3modified to simulate the characteristics of pediatric hearts. Input variables were heart rate, systemic vascular resistance, and left ventricular end-diastolic volume. The Ees required to generate the ejection fraction (mean value) from table 4 of Rivenes et al.  1for each isoflurane case and the resulting mean arterial pressure and cardiac index are shown in table 1below.

Table 1. End-systolic Elastance as a Function of Isoflurane Concentration: Model Predictions

The mean arterial pressure (MAP) values in table 1are greater than the mean values reported in table 4 of Rivenes et al.  1but are within the mean plus 2 SDs. Although cardiac index (CI) is virtually unchanged, contractility (Ees) decreases 16 and 31% at 1 and 1.5 minimum alveolar concentration (MAC), respectively, for isoflurane. Similar results are obtained for sevoflurane. For patients in whom there is sufficient contractile reserve, this degree of depression may not be clinically significant. However, there are patients with marginal reserves for whom any loss of contractile function may be problematic.

SVRI = systemic vascular resistance index; LVEDVI = left ventricular end-diastolic volume index; Ees = end-systolic elastance; EF = ejection fraction.

* LVEDVI in table 4 of Rivenes et al.  1is echocardiographically measured. LVEDVI × HR × EF should equal CI but is only 70% of measured CI. The LVEDVI here is the actual value. SVI = LVEDVI × EF from table 1is identical to the SVI values for the isoflurane group in Rivenes et al.  1 

Table 1. End-systolic Elastance as a Function of Isoflurane Concentration: Model Predictions
Table 1. End-systolic Elastance as a Function of Isoflurane Concentration: Model Predictions

References

1.
Rivenes SM, Lewin MB, Stayer SA, Bent ST, Schoenig HM, McKenzie ED, Fraser CD, Andropolous DB: Cardiovascular effects of sevoflurane, isoflurane, halothane and fentanyl–midazolam in children with congenital heart disease. A nesthesiology 2001; 94: 223–9
2.
Suga H, Sagawa K, Kostiuk DP: Controls of ventricular contractility assessed by pressure-volume ratio, Emax. Cardiovasc Res 1976; 95: 582–92
3.
Stern RH, Rasmussen H: Left ventricular ejection: Model solution by collocation, an approximate analytical method. Comput Biol Med 1996; 26: 255–61