Page 61 - Cardiac Nursing

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CHAPTER 1 / Cardiac Anatomy and Physiology 37

highest in this region; yet systolic compression is also greatest Blood flow through collateral vessels may contribute signifi-
here, which in part explains why this area has an increased inci- cantly to myocardial perfusion. Patients with similar coronary oc-
dence of infarction. In transmural infarctions (i.e., ones that in- clusions have smaller areas of infarction when collateral develop-
volve the full thickness of the left ventricular wall), the area of in- ment has occurred. Patients with abundant and well-developed
volvement is typically greater on the subendocardial surface than collaterals sometime have a totally occluded coronary artery but
on the subepicardial surface. Another factor contributing to this no evidence of infarction. Blood flow through collateral vessels
infarction pattern is the coronary artery distribution. Because ar- may be insufficient to meet increased demand, such as during ex-
teries enter the myocardium on the epicardial surface and plunge ercise, and is insufficient to prevent necrosis in most cases.
inward through the wall, the most easily compromised distal seg-
ments of the coronary arteries perfuse the endocardium. Clinical Implications
The coronary arteries are innervated by -sympathetic and
parasympathetic fibers. The direct effects of neural outflow are the It is important to analyze the effect of altered clinical states on the
same in the coronary bed as in other systemic beds; -adrenergic myocardial oxygen need. It is useful to consider the Laplace rela-
stimulation (or norepinephrine) constricts arteries and parasym- tion when evaluating oxygen demand in clinical states. For exam-
pathetic (vagal) stimulation dilates them. Pharmacologic doses of ple, hypertrophy of ventricular muscle results in an increase in the
the -adrenergic drug isoproterenol dilate the coronary artery thickness of the ventricular wall. This is advantageous in that wall
bed. Often, however, the direct effect of neural outflow on the tension is lower for the same left ventricular cavity size (same end-
coronary bed is masked because the autonomic nervous system diastolic volume); hence, oxygen consumption is decreased. How-
also affects myocardial metabolism and contractility, and the ef- ever, development of hypertrophy is a double-edged sword. At the
fect of these latter factors predominates. same time that wall tension is decreased, the mass of tissue re-
Local metabolic conditions are the predominant determinants quiring oxygen is increased; the net result may well be a greater
of coronary perfusion. Increased metabolism or hypoxia leads to oxygen demand by the heart. Furthermore, because hypertrophy
vasodilation and increased myocardial blood flow. The mecha- tends to increase the size of the muscle cells without increasing the
nism that mediates this effect is unknown. tissue capillarity, diffusional distances are increased. The supply of
With atherosclerosis, significant resistance can develop in the oxygen to the interior of the fiber may be significantly impaired.
coronary arteries. Lesions that occupy more than two thirds of the With cardiac dilation, left ventricular radius is increased. A larger
vessel’s cross-sectional area may impinge on flow at rest. Such le- end-diastolic volume is associated with higher end-diastolic pressure
sions can prevent the increases in flow necessary when myocardial and increased pressure generation during systole. The Laplace rela-
oxygen demand increases. tionship predicts that both factors lead to increased intramyocardial
wall tension. Stretching of the heart wall is associated with decreased
Collateral Circulation wall thickness, further increasing intramyocardial wall tension.
Collateral arteries are interarterial vessels that can connect two
branches of a single coronary artery or connect branches of the
right coronary artery with branches of the left. In the human THE CARDIAC CYCLE
heart, collaterals are found through the full thickness of the my-
ocardium, with the highest density near the endocardial surface. Every ventricular contraction that propels blood to the body or
Although they are present at birth, collaterals do not become the lungs is the result of the sequential activation of the cardiac
functionally significant unless the myocardium experiences hy- chambers through the coordinated functioning of electrical and
poxic or ischemic insult. Before transformation, the collateral ar- mechanical factors. This section describes the changing cardiac
teries are very narrow. They are devoid of smooth muscle and pressures and volumes that coincide with the time sequence of
therefore are unable to respond to pharmacologic or metabolic va- cardiac events. An understanding of normal or abnormal cardiac
soactive substances. After being stimulated to develop, the collat- functioning depends on familiarity with the cardiac cycle, which
eral tracts increase in diameter and develop a smooth muscle layer is represented graphically in Figure 1-38.
until, ultimately, the vessels are histologically similar to arterioles. For the sake of simplicity, this description of events occurring
When fully developed, these vessels are able to vasodilate when ni- during the cardiac cycle begins with events in the left heart. Figure
trates are administered and may autoregulate. 51 The time course 1-38 should be referred to frequently to obtain an understanding
from ischemic insult until significant enlargement is seen may be of what is occurring concurrently with respect to electrical activ-
as short as 9 days. 62 ity; atrial, ventricular, and aortic pressures; atrial and ventricular
Three conditions are correlated with collateral development: volumes; valvular activity; and heart sounds.
coronary artery disease, chronic myocardial hypoxia, and myocar- Some general points about pressure and timing are useful to re-
dial hypertrophy. In coronary artery disease, the collateral diame- member. Blood flows from the chamber with greater pressure to
ter increases in proportion to the severity of coronary artery nar- the chamber with lower pressure. When valves are open between
rowing. Functionally significant increases in collateral structure two chambers, pressures in both chambers change until they are
are seen with a 75% or greater reduction in the luminal diameter approximately equal. When valves between two chambers are
of a major vessel. Chronic hypoxic myocardium is seen in patients closed, the pressures in the chambers change relatively independ-
with anemia, cyanotic heart disease, and chronic obstructive pul- ently of each other.
monary disease. 63 There is also an increase in collateral diameter Ventricular systole and diastole divide the cardiac cycle into
in hypertrophied hearts. 64 Attempts to stimulate development of two major phases. The cardiac cycle can be further subdivided
51
collaterals with exercise programs have not been successful. Col- into several separate periods during systole and diastole. Because
laterals frequently disappear after successful aortocoronary bypass the cardiac cycle is continuous, the description of these periods
grafting. 65 can begin at any point.