Pulsus paradoxus.

Abstract

Previous studies from this laboratory (1-3) have shown that the paradoxical pulse of experimental cardiac tamponade is produced by an exaggerated inspiratory decline of left ventricular stroke volume. Most investigators have concentrated on one of three principal mechanisms of this inspiratory decrease of left ventricular stroke output. An early postulate (4) was that because of high intrapericardial pressure throughout the respiratory cycle, extrapericardial venous pressure falls more than atrial pressure during inspiration, thus reducing cardiac filling and stroke volume (5-7). With this mechanism, inspiratory pulmonary venous pooling would be expected to occur. A second major theory proposes that the tense pericardium is further stretched during inspiration by downward movement of the diaphragm and forward motion of the sternum, increasing cardiac compression and reducing filling of the left heart (8, 9). A third concept depends upon persistence of the normal inspiratory increase in right heart filling during cardiac tamponade. This increase in volume of the right heart and great vessels within the taut pericardial sac is believed to raise the intrapericardial pressure and thus hinder left heart filling by raising left atrial pressure (10, 11).With any of the above three mechanisms, an inspiratory decrease of pressure gradient from pulmonary veins to left atrium would be expected and has been consistently reported (4-7). Thus, additional investigation is required to determine the fundamental mechanism responsible for the paradoxical pulse of cardiac tamponade. In our previous paper (2), exaggerated inspiratory decrease of

RETRACTED: Pulsus paradoxus; historical and clinical perspectives

“…The relatively higher negative pressure in the pulmonary circulation compared to the left atrium in patients causes some back flow of blood from the left atrium into the pulmonary veins during inspiration. Therefore, during inspiration the fall in the left ventricular stroke volume is reflected as a fall in the systolic blood pressure [14][15][16]. The converse is true for expiration.…”

“…Several complex mechanisms generate PP in cardiac tamponade [15], the most important of which is an amplified interdependence between the right and left sides of the heart inside a restricted pericardial space. When the contents of the pericardial sac increase, due to accumulation of pericardial fluid or with cardiac dilatation, the effective compliance of all chambers becomes that of the tightly-stretched pericardium [30].…”

Comparação da variação da pressão sistólica e de pulso nas ventilações com pressão e volume controlados: estudo experimental em coelhos

“…Durante a respiração espontânea, a pressão arterial diminui na inspiração enquanto na ventilação com pressão positiva observa-se o seu aumento, ao passo que na expiração ocorre o inverso 11,12 . Estes efeitos observados durante a ventilação mecânica sobre a hemodinâmica, ainda são dependentes do estado cardiovascular inicial, sendo mais exacerbados na presença de hipovolemia 2,13,14 .…”

“…Esta flutuação na pressão arterial sistólica durante a ventilação mecânica ( Fig. 1 e 2) já é conhecida, e tem sido denominada de diferentes formas: VPS, pulso paradoxo reverso e ainda variação na pressão de pulso 2,11,12,14,19,21,30,31 . Até o presente momento, os resultados obtidos ratificam que a VPS e a VPP podem ser empregadas com segurança, como indicadoras da resposta hemodinâmica aos fluidos, em pacientes sob ventilação mecânica 16,17,25,59 .…”

“…7,87 11,3 9,28 8,37 8,87 8,72 7,66 7,28 9,04 14,74 13,01 13,18 Tabela A.14-Medidas descritivas para a variável pressão arterial média (mmHg). M0 M1 M2 M0 M1 M2 M0 M1 M2 M0 M1 M2 1 12,0 12,0 12,0 16,0 16,0 16,0 15,9 14,2 16,4 17,0 17,0 17,0 2 14,8 14,0 14,5 12,0 11,0 13,0 15,4 14,4 16,2 17,0 17,0 14,0 3 15,9 15,7 16,1 14,8 16,3 16,3 18,0 18,4 18,1 17,9 17,8 15,6 4 14,2 15,4 15,3 13,1 14,0 14,3 14,6 15,2 15,9 17,4 17,…”