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CA (620,000)
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Lecture

BIOC33H3 Lecture Notes - Biofeedback, Lipid Profile, Mean Arterial Pressure


Department
Biological Sciences
Course Code
BIOC33H3
Professor
Stephen Reid

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Chapter 33: Hypertension
Hypertension, or high blood pressure (BP), is defined as a persistent systolic blood
pressure (SBP) greater than or equal to 140 mm Hg, diastolic blood pressure (DBP)
greater than or equal to 90 mm Hg, or current use of antihypertensive medication. There
is a direct relationship between hypertension and cardiovascular disease (CVD).
Contributing factors to the development of hypertension include cardiovascular risk
factors combined with socioeconomic conditions and ethnic differences.
Hypertension is generally an asymptomatic condition. Individuals who remain
undiagnosed and untreated for hypertension present the greatest challenge and
opportunity for health care providers.
REGULATION OF BLOOD PRESSURE
BP is the force exerted by the blood against the walls of the blood vessel. It must be
adequate to maintain tissue perfusion during activity and rest.
Regulation of BP involves nervous, cardiovascular, endothelial, renal, and endocrine
functions.
o Sympathetic nervous system (SNS) activation increases heart rate (HR) and
cardiac contractility, produces widespread vasoconstriction in the peripheral
arterioles, and promotes the release of renin from the kidneys.
o Baroreceptors, located in the carotid artery and the arch of the aorta, sense
changes in BP. When BP is increased, these receptors send inhibitory impulses to
the sympathetic vasomotor center in the brainstem resulting in decreased HR,
decreased force of contraction, and vasodilation in peripheral arterioles.
o A decrease in BP leads to activation of the SNS resulting in constriction of the
peripheral arterioles, increased HR, and increased contractility of the heart.
o In the presence of long-standing hypertension, the baroreceptors become adjusted
to elevated levels of BP and recognize this level as “normal.”
o Norepinephrine (NE), released from SNS nerve endings, activates receptors
located in the sinoatrial node, myocardium, and vascular smooth muscle.
o Vascular endothelium produces vasoactive substances and growth factors.
Nitric oxide, an endothelium-derived relaxing factor (EDRF), helps
maintain low arterial tone at rest, inhibits growth of the smooth muscle
layer, and inhibits platelet aggregation.
Endothelin (ET), produced by the endothelial cells, is an extremely potent
vasoconstrictor.
o Kidneys contribute to BP regulation by controlling sodium excretion and
extracellular fluid (ECF) volume.
Sodium retention results in water retention, which causes an increased
ECF volume. This increases the venous return to the heart, increasing the
stroke volume, which elevates the BP through an increase in CO.
o Endocrine system:
The adrenal medulla releases epinephrine in response to SNS stimulation.

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Epinephrine activates 2-adrenergic receptors causing vasodilation. In
peripheral arterioles with only 1-adrenergic receptors (skin and kidneys),
epinephrine causes vasoconstriction.
The adrenal cortex is stimulated by A-II to release aldosterone.
Aldosterone stimulates the kidneys to retain sodium and water. This
increases BP by increasing CO.
ADH is released from the posterior pituitary gland in response to an
increased blood sodium and osmolarity level. ADH increases the ECF
volume by promoting the reabsorption of water in the distal and collecting
tubules of the kidneys resulting in an increase in blood volume and BP.
CLASSIFICATION OF HYPERTENSION
Hypertension is classified as follows:
o Prehypertension: BP 120 to 139 / 80 to 89 mm Hg
o Hypertension, Stage 1: BP 140 to 159 / 90 to 99 mm Hg
o Hypertension, Stage 2: systolic BP greater than or equal to 160 or diastolic BP
greater than or equal to 100 mm Hg.
Subtypes of hypertension:
o Isolated systolic hypertension (ISH): average SBP greater than or equal to 140
mm Hg coupled with an average DBP less than 90 mm Hg. ISH is more common
in older adults. Control of ISH decreases the incidence of stroke, heart failure,
cardiovascular mortality, and total mortality.
o Pseudohypertension (false hypertension) occurs with advanced arteriosclerosis.
Pseudohypertension is suspected if arteries feel rigid or when few retinal or
cardiac signs are found relative to the pressures obtained by cuff.
ETIOLOGY OF HYPERTENSION
Primary (essential or idiopathic) hypertension: elevated BP without an identified
cause; accounts for 90% to 95% of all cases of hypertension.
Secondary hypertension: elevated BP with a specific cause; accounts for 5% to 10% of
hypertension in adults.
PATHOPHYSIOLOGY OF PRIMARY HYPERTENSION
The hemodynamic hallmark of hypertension is persistently increased SVR.
Water and sodium retention:
o A high-sodium intake may activate a number of pressor mechanisms and cause
water retention.
Altered renin-angiotensin mechanism:
o High plasma renin activity (PRA) results in the increased conversion of
angiotensinogen to angiotensin I causing arteriolar constriction, vascular
hypertrophy, and aldosterone secretion.

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Stress and increased SNS activity:
o Arterial pressure is influenced by factors such as anger, fear, and pain.
o Physiologic responses to stress, which are normally protective, may persist to a
pathologic degree, resulting in prolonged increase in SNS activity.
o Increased SNS stimulation produces increased vasoconstriction, increased HR,
and increased renin release.
Insulin resistance and hyperinsulinemia:
o Abnormalities of glucose, insulin, and lipoprotein metabolism are common in
primary hypertension.
o High insulin concentration in the blood stimulates SNS activity and impairs nitric
oxidemediated vasodilation.
o Additional pressor effects of insulin include vascular hypertrophy and increased
renal sodium reabsorption.
Endothelial cell dysfunction:
o Some hypertensive people have a reduced vasodilator response to nitric oxide.
o Endothelin produces pronounced and prolonged vasoconstriction.
CLINICAL MANIFESTATIONS OF HYPERTENSION
Often called the “silent killer” because it is frequently asymptomatic until it becomes
severe and target organ disease occurs.
Target organ diseases occur in the heart (hypertensive heart disease), brain
(cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney
(nephrosclerosis), and eyes (retinal damage).
Hypertension is a major risk factor for coronary artery disease (CAD).
Sustained high BP increases the cardiac workload and produces left ventricular
hypertrophy (LVH). Progressive LVH, especially in association with CAD, is associated
with the development of heart failure.
Hypertension is a major risk factor for cerebral atherosclerosis and stroke.
Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels,
leading to the development of peripheral vascular disease, aortic aneurysm, and aortic
dissection.
Intermittent claudication (ischemic muscle pain precipitated by activity and relieved with
rest) is a classic symptom of peripheral vascular disease involving the arteries.
Hypertension is one of the leading causes of end-stage renal disease, especially among
African Americans. The earliest manifestation of renal dysfunction is usually nocturia.
The retina provides important information about the severity and duration of
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