It has been suggested that the pulmonary arterial end-diastolic pressure (EDP) may accurately reflect the level of left ventricular EDP, and therefore be useful in the continuous monitoring of left ventricular EDP in acutely ill patients. Accordingly, pulmonary arterial pressure was recorded simultaneously with left ventricular pressure in 24 patients with normal left ventricular function and in 26 patients with left ventricular myocardial disease and elevated EDP (range 13 to 38 mm Hg; average 22 mm Hg). In patients with normal left ventricular function, the EDPs in the left ventricle and pulmonary artery were equal (range 5 to 12 mm Hg; average 8 mm Hg; maximum difference ± 4 mm Hg). In contrast, in 20 of the patients with impaired left ventricular function, left ventricular EDP was consistently higher than pulmonary arterial EDP, exceeding the pulmonary arterial EDP by 2 to 21 mm Hg (average 8 mm Hg); in 12 of these 20 patients, the pulmonary arterial EDP was 12 mm Hg or less, the upper limit of normal for left ventricular EDP. The left ventricular diastolic pressure prior to atrial contraction correlated more closely with pulmonary arterial EDP. In six patients in whom increases in systemic arterial pressure were induced by methoxamine, and in two patients in whom spontaneous increases in systemic arterial pressure occurred, left ventricular EDP increased by 2 to 11 mm Hg (average 6 mm Hg); pulmonary arterial EDP remained unchanged or increased only slightly (less than 3 mm Hg) in six of the patients, and increased by 4 and 5 mm Hg in the two remaining patients. During increases in heart rate induced by atrial pacing, left ventricular EDP declined in 12 of 14 patients, while pulmonary arterial EDP increased, resulting in a consistent disparity in these pressures (average 11 mm Hg) at heart rates in excess of 124 beats/min. These data indicate that pulmonary arterial EDP does not provide an accurate estimate of left ventricular EDP in patients with chronic left ventricular disease, and in addition it often fails to reflect acute alterations in left ventricular EDP.

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