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(Circulation. 1998;97:292.)
© 1998 American Heart Association, Inc.

Correspondence

Inhaled NO and Pulmonary Vasodilation

Bernard G. Krohn, MD

Good Samaritan Hospital, Los Angeles, Calif

To the Editor:

Hare et al¹ concluded that inhaled nitric oxide (NO) caused selective pulmonary vasodilation in patients receiving left ventricular assist device support and that this accounted for the increase in mean left atrial pressure, which they considered a beneficial hemodynamic effect.

The evidence for pulmonary vasodilation was that pulmonary vascular resistance (PVR) decreased. However, pulmonary vasodilation (an observable quantity) and decreased PVR (a calculated quantity) are not synonymous, and either can exist in the absence of the other: PVR (dynes · s · cm^-5)=80x(Mean Pulmonary Artery Pressure-Mean Left Atrial Pressure)/Cardiac Output.²

In their patients whose mean pulmonary artery pressure (in mm Hg) and cardiac output (in liters per minute) were fixed, NO increased left atrial pressure (LAP), decreasing PVR in the above equation. The authors, previously observing patients without left ventricular assist devices, reported that NO increased left atrial pressure and left ventricular filling pressure while it decreased stroke volume index, a negative inotropic effect.³ In the present study, the increased left atrial pressure also resulted from increased left ventricular filling pressure. The above standard equation for PVR omits Poiseuille's factor for the radius of the tubes and calculates decreased PVR independent of the radius of blood vessels.

In other patients, assisted by left ventricular assist devices as NO was inhaled, left ventricular assist device output was increased, thereby increasing the denominator to give a lower calculated PVR, again without invoking vasodilation.

What prevents NO from dilating pulmonary blood vessels in patients who have severe heart failure . . . [Full Text of this Article]

Joshua M. Hare, MD

Division of Cardiology, Johns Hopkins University, Baltimore, Md