Mark D. Tasch, M.D.
Clinical Associate Professor, Department of Anesthesia
Indiana University School of Medicine
1120 South Drive, FH #204
Indianapolis, IN 46202-5115
Mark_Tasch@anesthesia.iupui.edu
With advancing age, the autonomic nervous system (ANS), heart
and blood vessels become less capable of maintaining hemodynamic
stability. While aging is, of course, a heterogeneous process
both within and among individuals, some aspects are characteristic
of the elderly cohort. Typical developments include a diminution
in the tonic influence of the parasympathetic nervous system
(PNS), a decline in the responsiveness of b -receptors and a
progressive replacement of supple, functional cardiac and vascular
tissue by stiff, fibrotic material.
With advancing age, increasing arterial rigidity tends to elevate
the systemic vascular resistance (SVR). Increased sympathetic
nervous system (SNS) activity may also contribute to the increase
in SVR, although this age-related change is controversial in
its magnitude and importance. Hypertension in the elderly is
characterized by a disproportionate increase in systolic pressure.
In consequence, the left ventricle (LV) must work harder to
eject blood into a more rigid aorta. This chronic strain eventually
causes the LV to become hypertrophied. Also controversial is
the degree to which aging is associated with decreases in cardiac
output (CO) and stroke volume (SV) at rest. Decreases of upwards
of 5 percent per decade have been described, but other studies
show very little change with age. Part of the disparity may
revolve around the cardiovascular health of the subjects studied
and the fact that the decrease in metabolic demand with age
can be expected to reduce cardiac output requirements.
Veins are also subject to progressive stiffening with age.
The decreased compliance of the capacitance system reduces its
ability to "buffer" changes in intravascular volume. Thus, aging
can exaggerate the hypotension that results from blood loss,
as well as from the peripheral pooling of blood with general
or conduction anesthesia.
Increased stiffness of the (hypertrophied) elderly cardiac
ventricle impairs diastolic filling and could cause a reduction
in end-diastolic volume. The elderly heart may have an increased
end-diastolic pressure that can overcome the stiffened ventricle,
but the proof of this assertion is weak except in those elderly
patients with severe diastolic dysfunction. In such cases, the
elevated left ventricular filling pressures are reflected into
the left atrium and the pulmonary vasculature and can lead to
pulmonary congestion. Clinically important diastolic dysfunction
likely involves poor ventricular relaxation in early diastole
as well as the natural ventricular tissue stiffening from aging
and hypertrophy. In less affected elderly individuals, ventricular
filling may be preserved without excessive increases in atrial
pressure via the atrial kick to enhance late diastolic filling.
Loss of the sinus rhythm, a common event during general anesthesia,
may well depress cardiac output and arterial pressure more markedly
in the elderly than it would in a normal younger patient.
In healthy young adults, the baseline autonomic tone is dominated
by the parasympathetic branch. With advancing age, tonic parasympathetic
outflow declines, while overall sympathetic neural activity
increases. However, elderly subjects generally manifest a reduced
responsiveness to b -adrenergic stimulation. Although resting
heart rates do not change much with age, the maximal attainable
heart rate, stroke volume, ejection fraction, cardiac output
and oxygen delivery (DO2) are all reduced in healthy older adults.
The administration of b -adrenergic agonists elicits lesser
inotropic and chronotropic responses in the elderly, while b
-blocking drugs retain their effectiveness. (In contrast, the
vascular responses to exogenous a -adrenergic agonists do not
appear to be much affected by age, although experimental results
are not all in agreement.)
As aging impairs both the diastolic filling and the chronotropic
and inotropic responsiveness of the heart, the ability of the
older patient to cope with perioperative stress is predictably
impaired. Increased metabolic demands, such as those imposed
by sepsis or postoperative shivering, may not be met when the
maximal CO and DO2 are limited by aging. While young adults
can compensate for blood loss (exacerbated by anesthetic-induced
vasodilation) with increases in heart rate and ejection fraction,
the elderly cannot so readily maintain their cardiac output
and are more dependent upon vasoconstriction to sustain adequate
arterial pressures.
The maintenance of hemodynamic homeostasis largely depends
upon the baroreceptor reflex. Baroreceptors in the aortic arch
and carotid sinus are actually stretch receptors; a decrease
in distention of these receptors results in augmented SNS activity
and inhibition of PNS outflow. Arterial stiffening may reduce
the ability of the baroreceptors to transduce changes in pressure,
diminishing the magnitude of the baroreflex. Both aging and
hypertension are associated with increased arterial rigidity.
It is therefore not surprising that, in general, both advancing
age and chronic hypertension, alone or together, are associated
with impairment of baroreflex responsiveness. This impairment
likely contributes to the increased susceptibility of older
adults to orthostatic hypotension, a problem that is exacerbated
by the common administration of diuretic and other medications,
such as those used to treat hypertension, depression and Parkinsonism.
The aging of cardiac and vascular tissues, the decline of b
-adrenergic and baroreceptor responsiveness and common pharmacologic
regimens thus combine to render the elderly patient less capable
of defending his or her CO and BP against the usual perioperative
challenges. In addition, atherosclerosis may convert a moderate
degree of hypotension into an intolerable reduction in cardiac,
cerebral or renal blood flow. Although different individuals
age in different ways and degrees, we can expect our older patients
to require greater vigilance and more active interventions to
guide them safely through surgery and anesthesia.
Bibliography:
Rooke GA, Robinson BJ. Cardiovascular and autonomic nervous
system aging. Problems in Anesthesia. 1997; 9(4):482-497.
Tasch MD, Stoelting RK. Autonomic nervous system. In: McLeskey
CH, ed. Geriatric Anesthesiology. Baltimore: Williams
& Wilkins; 1997:57-70.