Page 827 - Cardiac Nursing

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C HAPTER 35 / Hypertension 803
DISPLAY 35-2 Cardiovascular Risk Factors Changes in the Vascular Endothelium. The vascular en-
dothelium is the largest organ in the body. 50 Vascular endothelial
cells are extremely active and play a critical role in regulation of
Major Risk Factors
blood vessel tone and cellular activity in the vascular wall. En-
Hypertension dothelial cells modulate blood vessel tone by secreting a variety of
Cigarette smoking dilator and constrictor substances. In addition to their effect on
2
Obesity (body mass index 30 kg/m ) vascular tone, these substances and other factors produced by the
Physical inactivity
Dyslipidemia endothelium, may also modify platelet aggregation, thrombo-
Diabetes mellitus genicity of the blood, vascular inflammation, and oxidative stress
Microalbuminuria or estimated GFR 60 mL/min and, over the long term, influence cell migration and proliferation
Age (older than 55 years for men and 65 years for women) with subsequent development and progression of atherosclerosis
Family history of premature cardiovascular disease (men and its complications. 50
younger than 55 years or women younger than 65 years) Impaired endothelial vasodilation has been identified in persons
with HTN and even in the normotensive children of hypertensive
Target Organ Damage parents. 51,52 However, it is not yet clear whether endothelial dys-
Heart function is a precursor of HTN or a sequel. Improved understand-
• Left ventricular hypertrophy ing of the molecular basis for endothelial dysfunction in HTN may
• Angina or prior myocardial infarction provide a pathway to developing new therapies to reduce the impact
• Prior coronary revascularization of HTN. Other factors that cause endothelial dysfunction include
• Heart failure aging, hyperlipidemia, insulin resistance/diabetes, tobacco use,
Brain physical inactivity, and hyperhomocysteinemia. 50
• Stroke or transient ischemic attack
• Chronic kidney disease Atherosclerosis. Atherosclerosis is a complex degenerative
Peripheral arterial disease condition that is characterized by endothelial dysfunction and lipid
Retinopathy
accumulation in the endothelium and media, followed by wall thick-
ening and outward remodeling, and later by luminal encroachment,
GFR, glomerular filtration rate. thrombosis, and occlusion. 53 Atherosclerosis manifests as coronary
From Chobanian, A. V., Bakris, G. L., Black, H. R., et al. (2003). The Seventh Report
of the Joint National Committee on Prevention, Detection, Evaluation, and Treat- heart disease, cerebrovascular, and peripheral arterial disease and is a
ment of High Blood Pressure: The JNC 7 report. JAMA, 289(19), 2560–2572. major worldwide source of morbidity and mortality. Atherosclerotic
(Erratum in JAMA, 2003, 290[2], 197.)
plaque formation involves the interaction of genetic predisposition
and environmental risk factors with diffuse vascular injury. Many of
these factors are also involved in the pathogenesis of HTN. HTN
Evaluation of hypertensive patients has three objectives: (1) to as-
sess lifestyle and identify other cardiovascular risk factors or con- promotes or accelerates all phases of the development of atheroscle-
53
comitant disorders that may affect prognosis and guide treatment rotic lesions, from plaque formation to rupture.
(Display 35-2); (2) to reveal identifiable causes of high BP (Display Heart. Parallel structural and functional changes in the large
35-1); and (3) to assess the presence or absence of TOD and CVD arteries (stiffness), cardiac mass (hypertrophy), and myocardial re-
7
(Display 35-2). Morbidity and mortality associated with HTN are laxation and filling (diastolic dysfunction) occur at an accelerated
predominately the consequence of damage to a selected set of organs, rate with chronic HTN. The pressure overload associated with
known as “TOD,” which include the blood vessels, heart, brain, kid- HTN promotes left ventricular hypertrophy (LVH) that leads to
neys, and eyes. Evidence of TOD is a serious prognostic indicator in left ventricular dysfunction and heart failure. HTN also promotes
a person with HTN. Mechanisms of TOD are described below. vascular endothelial and renal dysfunction that directly impacts the
progression of heart failure, which in turn affects vascular en-
Vascular Changes Associated With HTN dothelial and renal dysfunction. Hypertensive individuals have a
54
HTN can influence the endothelium, vascular smooth muscle, ex- two- to four-fold increased risk of coronary heart disease and heart
tracellular matrix, and connective tissue of the arteries. Alterations failure and those individuals with prehypertension have a 1.6- to
of vascular structure that occur during chronic HTN may be re- 2.5-fold increased risk of CVD, both compared with those who are
ferred to as remodeling or hypertrophy. 47 Eutrophic inward re- normotensive. 55,56 Aggressive HTN control can prevent the devel-
modeling, or “remodeling,” refers to a decrease in lumen diameter opment of LVH and lead to regression of LVH. However, it re-
without a change in the thickness of the arterial wall or the char- mains controversial whether there are differential drug effects on
acteristic of the material within the vessel wall. In contrast, hy- reversing LVH related to HTN.
pertrophic inward remodeling, or “hypertrophy,” is defined as a
decrease in lumen diameter associated with an increase in wall Kidney. HTN is both a cause and consequence of chronic
thickness and vessel wall material. In either case, narrowing of the kidney disease (CKD). The incidence and prevalence of CKD and
vessel lumen is associated with increased vascular resistance. 48 end-stage renal disease, presumed to be secondary to primary
Some of the factors that contribute to the hypertrophy and re- HTN, have increased considerably over the past two decades and
modeling processes appear to be different. Mechanisms of hyper- are particularly high among African Americans. HTN causes re-
57
trophy may include increased arterial pulse pressure, sympathetic nal damage through multiple mechanisms. One mechanism is is-
nerve activity, angiotensin II, genetic factors, endothelin-1, nitric chemia with glomerular hypoperfusion causing glomerulosclerosis
oxide, and oxidative stress. 47,49 Mechanisms of remodeling may and subsequently tubulointerstitial fibrosis. Other mechanisms of
include intravascular pressure, angiotensin II, genetic factors, en- injury, such as endothelial dysfunction, cholesterol oxidation, cig-
dothelin-1, 3 integrins. 47 arette smoking, and proteinuria, act in concert with high systemic