Left Atrial Function
The left atrium serves three major roles that exert a profound
effect on LV filling and overall cardiovascular performance. The left atrium is
a contractile chamber that actively empties immediately before the onset of LV systole
and establishes final LV end-diastolic volume.[157]
[158]
The left atrium is a reservoir that stores
pulmonary venous return during LV contraction and isovolumic relaxation after the
closure and before the opening of the mitral valve.[159]
The left atrium also is a conduit that empties its contents into the left ventricle
down a pressure gradient after the mitral valve opens[160]
and continues to transfer pulmonary venous blood flow passively during LV diastasis.
These contraction, reservoir, and conduit functions of the left atrium mechanically
facilitate the transition between the almost continuous flow through the pulmonary
venous circulation and the intermittent filling of the left ventricle.[161]
Advances in the understanding of left atrial (LA) mechanical function have been
reviewed elsewhere.[162]
The negative inotropic effects of halothane and methoxyflurane
were initially described by Paradise and colleagues[163]
[164]
[165]
in rat
atrial myocardium in vitro. Volatile anesthetics also depress the contractile function
of atrial myocardium obtained from guinea pigs,[166]
rabbits,[81]
and humans.[167]
[168]
[169]
These
actions have been attributed to reductions in transsarcolemmal Ca2+
influx
through voltage-dependent Ca2+
channels and decreases in Ca2+
availability from the SR,[81]
mechanisms that are
similar to those responsible for anesthetic-induced depression of LV myocardium.
[170]
The negative inotropic effects of volatile
agents in the intact left atrium were quantified using pressure-volume analysis ( Fig.
7-13
).[171]
Desflurane, sevoflurane,
and isoflurane reduced LA contractility (i.e., Ees
) by approximately 50%
at an end-tidal concentration of 1.2 MAC ( Fig.
7-14
). The magnitude of this effect in LA myocardium was similar to the
degree of LV contractile depression produced by these agents as quantified with LV
end-systolic pressure-volume relationships.[41]
Desflurane, sevoflurane, and isoflurane also impaired LA and LV relaxation to similar
degrees. These data indicate that volatile anesthetics produce equivalent alterations
in contractility and relaxation in LA myocardium compared with LV myocardium.[171]
The magnitude of reductions in LA inotropic and lusitropic states produced by the
volatile anesthetics was also similar in the intact left atrium, supporting the results
obtained in isolated human atrial myocardium.[169]
Desflurane, sevoflurane, and isoflurane altered LA passive mechanical
behavior.[171]
LA reservoir function (i.e., V loop
area and reservoir volume) was maintained
Figure 7-13
Continuous left ventricular (LV) pressure, rate of increase
of LV pressure (LV dP/dt), aortic pressure, left atrial (LA) pressure, LA short-
and long-axis dimensions, and LA volume wave forms and corresponding LA pressure-volume
diagrams resulting from intravenous administration of phenylephrine (200 µg)
were observed in a typical experiment. The LA maximum elastance (solid
circles) and end-reservoir pressure and volume (solid
squares) for each pressure-volume diagram were used to obtain the slopes
(Ees
and Eer
) and extrapolated volume intercepts of the LA
end-systolic and end-reservoir pressure-volume relationships to quantify myocardial
contractility and dynamic chamber stiffness, respectively. (Adapted from
Gare M, Schwabe DA, Hettrick DA, et al: Desflurane, sevoflurane, and isoflurane
affect left atrial active and passive mechanical properties and impair left atrial-left
ventricular coupling in vivo: Analysis using pressure-volume relations. Anesthesiology
95:689–698, 2001.)
during the administration of anesthetic concentrations less than 1.0 MAC ( Fig.
7-15
). This preservation of reservoir function contributed to the relative
maintenance of LV stroke volume[41]
by compensating
for decreases in LV filling associated with a reduced contribution of LA contraction.
The volatile anesthetics also reduced dynamic LA chamber stiffness, an action that
most likely contributed to the preservation of reservoir function because the delays
in LA relaxation and declines in LV systolic function that also occurred would be
expected to decrease reservoir function.[172]
However,
LA reservoir function was reduced during administration of higher concentrations
of the volatile anesthetics because further impairment of LA relaxation and LV contractility
occurred. Decreases in the ratio of LA stroke work to total pressure-volume diagram
area and the increases in the ratio of LA conduit to total reservoir volume were
also produced by desflurane, sevoflurane, and isoflurane. These data indicated that
the LA contribution to LV filling becomes less active and more passive during the
administration of the volatile agents.
Desflurane, sevoflurane, and isoflurane decreased the ratio of
LA to LV elastance (Ees
/ELV
), consistent with impaired mechanical
matching between these chambers (see Fig.
7-14
). Volatile anesthetics have been shown to produce LV diastolic dysfunction
by delaying LV isovolumic relaxation and impairing early LV filling in association
with direct negative inotropic effects.[1]
The
attenuation of transfer of kinetic energy from the left atrium to the left ventricle
probably resulted from the combination of LA contractile depression and LV systolic
and diastolic dysfunction. Volatile anesthetic-induced abnormalities in LA-LV matching
were greater than analogous impairment of LV-arterial coupling evaluated using a
similar series elastic chamber model in a previous investigation[41]
because these agents produced beneficial alterations in the determinants of LV afterload
[143]
[144]
that
partially compensated for simultaneous depression of LV myocardial contractility.
Figure 7-14
Histograms depicting the slope (Ees
, top
panel) of the left atrial (LA) end-systolic pressure-volume relationship,
LA relaxation (RLA
, middle panel), and
the slope (Eer
, bottom panel) of the LA
end-reservoir pressure-volume relationship (i.e., dynamic chamber stiffness) under
baseline conditions (Control) and during the administration of 0.6, 0.9, and 1.2
minimum alveolar concentrations (MACs) of desflurane (black
bars), sevoflurane (red bars), or isoflurane
(gray bars). *, Significantly (P
< .05) different from the control; †, significantly (P
< .05) different from 0.6 MAC. (Adapted from Gare M, Schwabe DA, Hettrick
DA, et al: Desflurane, sevoflurane, and isoflurane affect left atrial active and
passive mechanical properties and impair left atrial-left ventricular coupling in
vivo: Analysis using pressure-volume relations. Anesthesiology 95:689–698,
2001.)
