Page 104 - Cardiac Nursing

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80 PA R T I / Anatomy and Physiology
induced vasoconstriction and vasodilation (decreased vascular re- neuronal uptake of norepinephrine, capillary permeability, and
sistance), diuresis and natriuresis. 140,142 width of the junctional cleft can also affect the level of plasma nor-
A deficient KKS (decreased levels of hK1 and kininogen defi- epinephrine. The width of the junctional cleft is particularly impor-
ciency and altered B 1 and B 2 genotypes) plays a role in the patho- tant in the pulmonary vasculature, where spillover is predominantly
genesis of hypertension through altered sodium excretion. 140,143 the result of the wide junctional clefts and not of a high rate of sym-
Bradykinin, which is released during ischemia, may also play a pathetic nervous system activation or norepinephrine release. 153–155
cardioprotective role in myocardial infarction and heart failure.
After a myocardial infarction, ACE inhibition decreases cardiac
dilation and failure by decreasing angiotensin II, but also by pre- ARTERIAL BLOOD PRESSURE
venting the breakdown of kinins. Possible mechanisms for the
KKS effect include increasing coronary blood flow and the pro- Systolic and diastolic blood pressures describe the high and low
motion of angiogenesis and cardiac regeneration, which decrease values of pressure fluctuations around the mean of the arterial
the infarct size and inhibit ventricular remodeling. 140,143,144 The pressure wave. The mean arterial pressure (MAP) in the ascending
beneficial effects of the KKS suggest the possible role for pharma- aorta depends on the cardiac output and SVR:
cological treatment of hypertension, postmyocardial infarction, and
heart failure. 140,145 However, kinins may contribute the adverse MAP CO SVR
side effects (e.g., increased microvascular permeability, cough, and whereas arterial distensibility and left ventricular stroke volume
angioedema) associated with ACE inhibitors. 146 determine the amplitude and contour of the pressure wave. 156
The peak systolic pressure is determined by the volume and ve-
Interaction Between the KKS, RAAS, locity of left ventricular ejection (i.e., the larger the SV, the larger
and Natriuretic Hormones the pulse pressure at any given distensibility), peripheral arterial
resistance, the distensibility of the arterial wall, the viscosity of
The KKS, RAAS, and the natriuretic hormones interact via the blood, and the end-diastolic volume in the arterial blood. 157 Dur-
actions of ACE and neuropeptidase (NEP) (see Fig. 3-7). ACE ing diastole, arterial pressure decreases until the next ventricular
stimulates the conversion of angiotensin I to angiotensin II and contraction, so the minimal diastolic pressure is determined by
degrades kinins. NEP is involved in the metabolism of ANP, BNP, factors that affect the magnitude and rate of the diastolic pressure
CNP, bradykinin, endothelin-1, and angiotensin II and also stim- drop including blood viscosity, arterial distensibility, peripheral
ulates the formation of angiotensin (1–7) from angiotensin I. An- resistance, and the length of the cardiac cycle. Central blood pres-
giotensin (1–7) has vasodilatory and antiproliferative effects that sure measurements (aorta and carotid), which reflect both the an-
inhibit ACE and also counteract the actions of angiotensin II. 147 tegrade pressure and the reflected pressure, may be different from
Angiotensin (1–7) also enhances the effects of bradykinin. peripheral blood pressure measurements (see Chapter 21). 158
Kallikrein, which is the enzyme involved in the formation of During systole, the elastic walls of the aorta and large arteries
bradykinin, may also stimulate the conversion of prorenin to stretch as more blood enters than runs off into the periphery.
renin. 148,149 Renin subsequently causes the conversion of an- Thus, a portion of the stroke volume is stored in the relatively dis-
giotensinogen to angiotensin I. Exploitation of the physiological tensible aorta during systole. During diastole, there is passive elas-
interactions between these three systems may be useful in the tic recoil of the arterial walls, causing continued, but decreasing,
treatment of heart failure and hypertension. For example, ACE in- ejection of blood out of the aorta and into the peripheral arteries.
hibition exerts its antihypertensive effects by decreasing an- The elastic recoil transforms pulsatile flow into more continuous
giotensin II, increasing angiotensin (1–7) levels and potentiating flow in the smaller vessels and explains why the blood pressure
the effects of bradykinin by increasing its level and through direct does not drop to zero during periods of no flow (e.g., diastole).
effect on the B 2 -receptor. 146,147 Triple vasopeptidase inhibitors, Pulse pressure is the difference between the systolic and diastolic
which inhibit NEP as well as ACE and endothelin-1-converting pressures. The aortic pulse pressure is directly proportional to left
enzyme may offer a multimodal approach to the management of ventricular stroke volume and inversely related to arterial compliance,
cardiovascular disease. 146 However, side effects may limit the util- with changes in stroke volume responsible for most acute changes.
ity of some of these medications. For example, omapatrilat (an Pulse pressure Stroke volume/arterial compliance
ACE/NEP inhibitor), which decreased the risk of death and hos-
pitalization in chronic heart failure compared to ACE inhibition A normal pulse pressure at the brachial artery is approximately
alone, 150 was removed from development because of an increased 40 mm Hg. A higher pulse pressure may reflect where the pressure
incidence of angioedema, 151 possibly due to increased bradykinin is measured in the body (increased pulse pressure in the periphery).
or increased endothelin-1-induced nitric oxide production. 146 Ejection velocity also affects the pulse pressure, whereas the SVR
does not affect the pulse pressure as it affects both systolic and
Norepinephrine Spillover diastolic pressures.
Approximately 80% of the norepinephrine secreted at the neuroef-
fector junction is either taken-up by sympathetic neurons (neuronal HEART RATE
reuptake) or broken-down by the enzymes monoamine oxidase or
catechol-O-methyl transferase. The remaining 20% may spill into Control of Heart Rate
the systemic circulation. The spillover is usually proportional to the
increase in sympathetic nervous system activation; thus, the plasma The intrinsic heart rate at rest, without any neurohumoral influ-
norepinephrine level can be used as an approximate indicator of ence, is approximately 100 to 120 beats per minute. The heart
SNS activity. 152 Factors such as the nerve-firing rate, blood flow, rate in the intact, resting person reflects a balance between the