J Thorac Cardiovasc Surg 1999;117:195-196
© 1999 Mosby, Inc.
Effect of inhaled nitric oxide on left ventricular and pulmonary vascular function
Reply to the Editor:
We appreciate Dr Krohn's interest in our study and the opportunity to address his comments regarding our assessment of myocardial function and the limitations associated with calculation of pulmonary vascular resistance. We respectfully disagree with Dr Krohn's assertion that our conclusions contradict our evidence. As mentioned in our article, previous reports of pulmonary edema and left atrial pressure elevation after administration of inhaled nitric oxide (iNO) in patients with myocardial dysfunction raised concerns about potential myocardial depressant effects of this agent. Our study was undertaken specifically to assess the effects of this pulmonary vasodilator on myocardial systolic and diastolic function. Because clinical hemodynamic parameters such as cardiac output and left ventricular end-diastolic pressure (LVEDP) are influenced by a number of factors (including preload, afterload, contractility, heart rate, and diastolic compliance) in a complex fashion, these parameters cannot be individually used to accurately assess myocardial contractility or diastolic compliance unless all other factors (ie, preload, afterload, and heart rate) are accounted for. Therefore we assessed systolic function by 2 well-accepted load-independent measures of contractility, the preload-recruitable stroke work relationship (PRSWR) and the end-systolic pressure-volume relationship (ESPVR). We assessed diastolic function by the end-diastolic pressure-volume relation (EDPVR). Our data demonstrated clearly that despite slight increases in LVEDP, contractility and diastolic function as assessed by these measures was not altered by administration of iNO. Dr Krohn cites statistically insignificant decreases in cardiac output and increases in left ventricular volume from Table I of our article as "evidence for deterioration of myocardial contractility and diastolic dysfunction," but he ignores increases in mean arterial pressure and systemic vascular resistance and decreases in central venous pressure and heart rate, listed in the same table, all of which are consistent with a decrease in cardiac output in the absence of reduced contractility.
With respect to Dr Krohn's comments regarding the limitations associated with the application of the widely used standard pulmonary vascular resistance (PVR) equation, we are in agreement that this method of PVR calculation is imperfect for the reasons he has enumerated. However, Dr Krohn seems to confuse PVR (affected by pulmonary vascular properties) with right ventricular afterload (affected additionally by left atrial pressure, LAP). Pulmonary vasodilation may reduce PVR while raising LAP, thus leaving PAP and right ventricular afterload relatively unchanged.1 This ought not be viewed as misleading; rather it is simply a natural consequence of the right and left sides of the hearts being connected in series. Furthermore, inasmuch as previous clinical and experimental work have already well established the pulmonary vasodilatory effects of iNO, this was not the focus of our experiment. Rather, since clinically and experimentally observed increases in LAP may be due to a decrease in PVR and/or alterations in ventricular function, we sought to establish whether iNO affects left ventricular systolic or diastolic properties, as described above. We found that the increase in LAP was not due to depression of ventricular function, but was simply a consequence of pulmonary vasodilation.
Michael Argenziano, MD
Marc L. Dickstein, MD
Departments of Surgery and Anesthesiology
Milstein Hospital Building
Room 7-435
177 Fort Washington Ave
New York, NY 10032
12/8/93302
References
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Dickstein ML, Burkhoff D. A theoretic analysis of the effect of pulmonary vasodilation on pulmonary venous pressure: implications for inhaled nitric oxide therapy. J Heart Lung Transplant 1996;15:715-21. [Medline]
