Ma. Perhonen et al., Deterioration of left ventricular chamber performance after bed rest - "Cardiovascular deconditioning" or hypovolemia?, CIRCULATION, 103(14), 2001, pp. 1851-1857
Citations number
31
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Orthostatic intolerance after bed rest is characterized by hypov
olemia and an excessive reduction in stroke volume (SV) in the upright posi
tion. We studied whether the reduction in SV is due to a specific adaptatio
n of the heart to head-down tilt bed rest (HDTBR) or acute hypovolemia alon
e.
Methods and Results-We constructed left ventricular (LV) pressure-volume cu
rves from pulmonary capillary wedge pressure and LV end-diastolic volume an
d Starling curves from pulmonary capillary wedge pressure and SV during low
er body negative pressure and saline loading in 7 men (25 +/-2 years) befor
e and after 2 weeks of -6 degrees HDTBR and after the acute administration
of intravenous furosemide, Both HDTBR and hypovolemia led to a similar redu
ction in plasma volume. However, baseline LV end-diastolic volume decreased
by 20 +/-4% after HDTBR and by 7 +/-2% after hypovolemia (interaction P<0.
001). Moreover, SV was reduced more and the Starling curve was steeper duri
ng orthostatic stress after HDTBR than after hypovolemia, The pressure-volu
me curve showed a leftward shift and the equilibrium volume of the left ven
tricle was decreased after HDTBR; however, after hypovolemia alone, the cur
ve was identical, with no change in equilibrium volume. Lower body negative
pressure tolerance was reduced after both conditions; it decreased by 27<p
lus/minus>7% (P<0.05) after HDTBR and by 18<plus/minus>8% (P<0.05) after hy
povolemia.
Conclusions-Chronic HDTBR leads to ventricular remodeling, which is not see
n with equivalent degrees of acute hypovolemia. This remodeling leads to a
greater decrease in SV during orthostatic stress after bed rest than hypovo
lemia alone, potentially contributing to orthostatic intolerance.