Page 231 - Cardiac Nursing

xd
6
6
q
q
xd
6
/09
1
1
/29
/29
/09
q
In
p
20
c.
c.
In
20
4-2
10.
10.
a
a
4-2
p
p
p
07
A
A
t
ara
a
a
t
ara
ara
07
7 P
M
M
1:1
1:1
7 P
Pa
g
e 2
e 2
Pa
g
g
0-c
K34
K34
09_
09_
0-c
LWB
LWBK340-c09_ p pp204-210.qxd 6/29/09 11:17 PM Page 207 Aptara Inc.
LWB
C HAPTER 9 / Physiologic Adaptations With Aging 207
70 years. Mitral annular calcification contributes to mitral steno- dependent changes in the electrical system increase the potential
sis, mitral regurgitation, atrial arrhythmias, and heart block. 8 for conduction abnormalities as well as supraventricular and ven-
tricular dysrhythmias.
Cardiac Functional Changes
Vascular System
Changes in ventricular filling (preload) and diastolic function oc-
cur with aging. There is progressive slowing of the early diastolic Structural Changes
9
filling rate coupled with augmented late diastolic filling. Aug- With advancing age, a series of structural changes take place in the
mentation of late diastolic filling results from vigorous atrial con- vascular system. Central arterial vessel diameter tends to increase
traction and is accompanied by atrial enlargement. Despite these and the intimal and medial layers tend to thicken. 12 In the arte-
changes in filling, end-diastolic volume in the sitting or supine rial intima, the endothelial cells become irregular in size and shape
position is not usually reduced in women and is slightly increased with an increase in connective tissue. Calcification and lipid dep-
9
in men. The change in end-diastolic volume from rest to exercise osition also occur. Some scientists argue that intimal media (IM)
increases with age. 10 This refutes the previously held belief that thickening is an early stage of atherosclerosis. IM thickness pre-
LV filling is impaired in the healthy, older heart. dicts the coexistence of silent coronary artery disease in screened
Clinical implications of age-related changes in ventricular fill- subjects. 13 However, IM thickening may be an intrinsic age-
ing include greater dependence on atrial contraction, which is lost related change that provides a foundation for the subsequent de-
with atrial fibrillation and greater sensitivity to hypovolemia. The velopment of atherosclerosis. Similar controversy surrounds age-
14
importance of adequate intravascular volume increases further associated endothelial dysfunction, systemic arterial stiffening,
with tachycardia, which limits filling time. and arterial pulse-pressure widening. Whether age-related changes
There is no change in resting systolic function, heart rate, or or early atherosclerosis, combinations of these processes occur to
9
cardiac output during healthy aging. Maximum heart rate during varying degrees in older people. Age-associated vascular changes
dynamic exercise decreases with age (maximum heart rate 220 – interact with traditional cardiovascular risk factors to produce
age). This age-related decrease in maximum heart rate explains the clinical atherosclerosis.
age-related decrease in maximum cardiac output in healthy peo-
ple. Maximum cardiac output reserve is approximately 3.5-fold in Functional Changes
younger and 2.5-fold in older people. 9
Age-associated increase in IM thickness is accompanied by in-
creased arterial stiffness. Arterial stiffness increases the pulse-wave
Electrical System velocity, transmitting the pulse wave faster than the actual move-
ment of blood. When the pulse wave reaches branch points in the
Controversy and conflicting evidence exists about the effects of
aging on the cardiac electrical system. In the absence of disease or arterial tree, the wave is reflected back toward the heart. At distal
extreme stress on the cardiac function, the electrical system is ad- locations, the reflected waves augment systolic pressure and re-
15
equate for normal conductivity. Limited data support a marked duce diastolic pressure. Data from epidemiological studies indi-
age-associated increase in the prevalence and complexity of ven- cate that increased pulse-wave velocity is seen with age and also in
16,17
9
tricular ectopy at rest and during exercise. Ventricular ectopic the context of atherosclerosis and diabetes.
beats are evident on 24-hour ambulatory electrocardiogram in Age-related changes are also seen in the intravascular environ-
more than 75% of men and women aged greater than 64 years, ment. Increases in fibrinogen and procoagulant factors are seen
11
with a somewhat higher prevalence in men than women. In 2% without countering increases in anticoagulant factors. Under
to 4% of asymptomatic, healthy older adults, 3 to 5 beat salvos of stress, there is increased binding of platelets to the arterial wall and
non-sustained ventricular tachycardia are present; runs of more increased levels of plasminogen activator inhibitor in older people
8,18
than 5 beats are rare. compared to younger people. These changes contribute to the
There appears to be a decrease in the number of pacemaker age-associated increase in acute coronary syndrome.
cells in the sinus node and greater irregularity in their shape. By Elevation of the blood pressure is not a normal age change;
age 75 years, only 10% of original nodal cells remain, although however, it is a change that frequently occurs with the process of
this is compatible with normal pacemaker activity, it also explains aging. Isolated systolic hypertension, in particular, is a distinct
the increased incidence of sick sinus syndrome among older pa- pathologic process and accounts for more than 50% of cases
tients. The number of conducting cells in the atrioventricular of hypertension. It is defined as a systolic pressure greater than
(AV) node and the His bundle decreases in people older than 140 mm Hg and diastolic pressure below 90 mm Hg and is prob-
70 years of age. The decrease in the number of cells in the His ably the result of arterial stiffening and loss of arterial compliance
19
bundle begins after age 40, and after age 50 years in the right bun- that occur with aging. Treatment of systolic hypertension fol-
dle. Fibrosis of the cardiac conduction system is strongly associated lows the same principles as treatment of hypertension in general
with aging. Idiopathic bundle–branch fibrosis is a common cause (see Chapter 35).
of chronic atrioventricular block in people older than 65 years of
age. The atrial and AV nodal refractory periods increase with age. Autonomic Nervous System
It is not clear whether these changes are caused by altered cate- Modulation
cholamine or vagal stimulation with age.
The normal electrocardiogram shows little change with age. Optimal cardiovascular function requires communications be-
There may be small increases in the PR, QRS, and QT intervals, tween the cardiovascular system and autonomic nervous system.
along with a small decrease in the amplitude of the QRS complex. Under stress the sympathetic component of the autonomic nerv-
When challenged by disease or adverse circumstances, the age- ous system prevails, producing arterial vasoconstriction while