[The influence of therapy (sympathomimetic amines versus vasodilators) in the indexes of ejection fraction derived from an analysis of Doppler aortic flow].
OBJECTIVE
To assess the influence of inotropic IV therapy--dobutamine and/or dopamine--versus vasodilator therapy--nitroprusside, captopril or hydralazine--in aortic flow ejection phase indexes obtained by pulsed Doppler echocardiography.


METHODS
In 17 patients admitted to the ICU (11 males, 62 +/- 14 years, 9 with ischemic cardiomyopathy and 8 with dilated cardiomyopathy, all in sinus rhythm), with congestive heart failure, and submitted to tailored therapy, 53 serial pulsed Doppler and hemodynamic evaluations were made as the therapy changed the hemodynamic and clinical status. Considering serial consecutive evaluations, a hemodynamic improvement was obtained only with inotropics in 13 (group A), and with vasodilators in only 15 (group B). The following ejection phase indexes were calculated from Doppler registers: average acceleration (AvAc) and ejection force (EFor), calculated according to the formula: Efor = 1.06 x Aortic Orifice Area x AvAc x Acceleration Velocity Time Integral.


RESULTS
Arterial blood pressure increased in gr A (76.2 +/- 14.1 to 81.4 +/- 14.8 mm Hg, p < 0.05) and decreased in gr B (85.1 +/- 12.6 to 76.2 +/- 9.7 mm Hg (p < 0.05). In both groups there was a significant (p < 0.05) increase in cardiac output (CO)-from 3.9 +/- 1.1 to 4.9 +/- 1.4 L/min in group A, and from 3.9 +/- 1.2 to 4.4 +/- 1.2 L/min in group B. CO increased 18.7% in group A and 13.8% in group B (NS). There was a decrease in pulmonary capillary wedge pressure (PCWP) from 19.5 +/- 6.0 to 15.1 +/- 5.8 mm Hg in group A (p < 0.05), and from (16.9 +/- 5.7 to 12.1 +/- 4.6 mm Hg in group B (p < 0.05). PCWP decreased 19.7% in group A and 27.8% in group B (NS). Systemic vascular resistance (SVR) changed from 18.2 +/- 7.0 to 16.2 +/- 7.1 Wood U in group A (p < 0.05), and from 22.3 +/- 9.3 to 17.7 +/- 5.7 Wood U in group B (p < 0.05). In group A, AvAc increased-from 1347 +/- 611 cm.s-2 (p < 0.05), as did Efor-from 15.4 +/- 10.7 to 20.2 +/- 11.0 g.cm,s-2 (p < 0.05), whereas in group B there was no significant change in either AvAc-from 1337 +/- 284 to 1277 +/- 256 cm.s-2, or Efor-from 22.7 +/- 17.0 to 23.8 +/- 15.0 g.cm.s-2.


CONCLUSIONS
Vasodilator therapy, although inducing hemodynamic changes similar to inotropics, does not alter the ejection phase indexes. Therefore, AvAc and Efor, in spite of being calculated from the aortic flow, are independent of the changes in PCWP and SVR and seem to reflect changes in inotropism in the clinical setting.
Serviço de Cardiologia, Hospital de Santa Marta., Lisboa.
S
S
Martins
L
L
do Rosário
R M
RM
Soares
A
A
Sequeira
M J
MJ
Sousa
L
L
Sousa
M
M
Oliveira
R
R
Ferreira
L
L
Branco
L
L
Ferreira
S
S
Ramos
A M
AM
Antunes
D002216:Captopril / Q000627:therapeutic use; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy* / Q000503:physiopathology; D004280:Dobutamine / Q000627:therapeutic use; D004298:Dopamine / Q000627:therapeutic use; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D006830:Hydralazine / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D009599:Nitroprusside / Q000627:therapeutic use; D011669:Pulmonary Wedge Pressure; D013318:Stroke Volume / Q000187:drug effects*; D013566:Sympathomimetics / Q000627:therapeutic use*; D014655:Vascular Resistance; D014665:Vasodilator Agents / Q000627:therapeutic use*
D013566:Sympathomimetics; D014665:Vasodilator Agents; D009599:Nitroprusside; D006830:Hydralazine; D004280:Dobutamine; D002216:Captopril; D004298:Dopamine