GENERAL INTERNAL MEDICINE HOUR

HYPERTENSION
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EDUCATIONAL AIMS
To define Hypertension and briefly discuss its mechanisms
To enumerate the pathological consequences of hypertension
To review the approach in patients with hypertension
To present the management for patients with hypertension
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HYPERTENSION
Level of blood pressure at which the institution of therapy reduces blood pressure–related
morbidity and mortality
Clinical criteria for defining hypertension
Average of two or more seated blood pressure readings during each of two or more
outpatient visits.
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HYPERTENSION

One classification recommends blood pressure criteria for defining normal blood
pressure, prehypertension, hypertension (stages I and II), and isolated systolic
hypertension.
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HYPERTENSION
One of the leading cause of burden of disease
Affects more than one billion individuals
Estimated 9.4 billion deaths per year
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HYPERTENSION
Doubles the risks of Cardiovascular Diseases
Coronary Heart Disease (CHD)
Congestive Heart Failure
Ischemic and Hemorrhagic Stroke
Renal Failure
Peripheral Artery Disease
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MECHANISMS OF HYPERTENSION
STROKE
VOLUME
CARDIAC
OUTPUT
HEART RATE

ARTERIAL
PRESSURE

VASCULAR
STRUCTURE
PERIPHERAL
RESISTANCE
VASCULAR
FUNCTION
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MECHANISMS OF HYPERTENSION

INTRAVASCULAR VOLUME
Sodium - primary determinant of the extra cellular fluid volume
Sodium Chloride Intake > Kidney’s Sodium Excretion > Vascular volume expansion >
Increase Cardiac Output
Blood Flow Autoregulation
Increase Arterial Pressure > Increased Resistance
Blood Flow = pressure across the vascular bed/vascular resistance
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MECHANISMS OF HYPERTENSION

INTRAVASCULAR VOLUME
The initial elevation of blood pressure vascular volume expansion = increase of cardiac
output, peripheral resistance increases and cardiac output reverts toward normal.
Salt activates neural, endocrine and paracrine and vascular mechanisms increase arterial
pressure.
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MECHANISMS OF HYPERTENSION

AUTONOMIC NERVOUS SYSTEM

Adrenergic reflexes modulate blood pressure (short term)
Adrenergic Function + Hormonal and Volume-Related factors (long term)
Cardiovascular Regulators:
Norepinephrine
Epinephrine
Dopamine
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MECHANISMS OF HYPERTENSION

RENIN-ANGIOTENSIN-ALDOSTERONE
Contributes to the regulation of arterial
pressure primarily via vasoconstrictor
properties of angiotensin II and the sodium
retaining properties of aldosterone.
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MECHANISMS OF HYPERTENSION

RENIN-ANGIOTENSIN-ALDOSTERONE
Contributes to the regulation of arterial pressure primarily via vasoconstrictor properties
of angiotensin II and the sodium retaining properties of aldosterone.
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MECHANISMS OF HYPERTENSION

VASCULAR MECHANISMS
Vascular radius and compliance of resistance arteries are important determinants of
arterial pressure.
Resistance flow varies inversely with the fourth power of the radius, and consequently,
small decreases in lumen size significantly increase resistance.
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MECHANISMS OF HYPERTENSION

IMMUNE MECHANISMS, INFLAMMATION, AND OXIDATIVE STRESS

Inflammation and alterations of the immune response have been implicated in the
pathogenesis of vascular injury and hypertension
Increased circulating levels of autoantibodies
Innate and adaptive immunity activation - Hypertension and aortic stiffness
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PATHOLOGICAL CONSEQUENCES OF HYPERTENSION

HEART
Heart Disease is the most common cause of death in hypertensive patients.
Hypertensive Heart Disease- Left ventricular hypertrophy, CHF, atherosclerotic coronary
artery disease and microvascular disease and cardiac arrythmias
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PATHOLOGICAL CONSEQUENCES OF HYPERTENSION

BRAIN
Elevated blood pressure is the strongest risk factor for stroke, the second most frequent
cause of death in the world
Accounts for 5 million deaths each year, with an additional 15 million persons having
nonfatal strokes and incidence rises progressively with increasing blood pressure levels,
particularly systolic blood pressure in individuals aged >65 years.
Treatment of hypertension decreases the incidence of both ischemic and hemorrhagic
strokes.
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PATHOLOGICAL CONSEQUENCES OF HYPERTENSION

KIDNEY
Both a target and a cause of hypertension
Primary renal disease - most common etiology of secondary hypertension
hypertension is a risk factor for renal injury and ESRD
Kidney-related hypertension mechanisms
diminished capacity to excrete sodium
excessive renin secretion in relation to volume status
sympathetic nervous system overactivity
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PATHOLOGICAL CONSEQUENCES OF HYPERTENSION

PERIPHERAL ARTERIES

Target organ for atherosclerotic disease secondary to longstanding elevated blood

pressure.
Vascular disease is a major contributor to stroke, heart disease, and renal failure.
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APPROACH TO THE PATIENT

HISTORY AND PHYSICAL EXAMINATION

Initial assessment should include a complete history

and physical examination

confirm a diagnosis of hypertension

screen for other cardiovascular disease risk factors

screen for secondary causes of hypertension

identify cardiovascular consequences of

hypertension and other comorbidities

assess blood pressure–related lifestyles

determine the potential for intervention

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APPROACH TO THE PATIENT

LABORATORY TESTING

Recommended laboratory tests in the initial evaluation of hypertensive patients.

Repeat measurements of may be obtained after the introduction of a new antihypertensive agent and then
annually or more frequently if clinically indicated.
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MANAGEMENT

LIFESTYLE INTERVENTIONS
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MANAGEMENT

PHARMACOLOGIC THERAPY
Lowering SBP by 10–12 mmHg and DBP by 5–6 mmHg confers relative risk reductions
of 35–40% for stroke and 12–16% for CHD within 5 years of the initiation of treatment.
The risk of heart failure is reduced by >50%; although the benefit of blood pressure
lowering on progression of renal failure is less apparent.
Hypertension control is the single most effective intervention for slowing the rate of
progression of hypertension-related kidney disease.
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MANAGEMENT

PHARMACOLOGIC THERAPY
Selection of antihypertensive agents and combinations of agents should be
individualized.
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PHARMACOLOGICAL THERAPY

DIURETICS

Thiazides inhibit the Na+/Cl– pump in the distal convoluted tubule and hence
increase sodium excretion. In the long term, also may act as vasodilators
Loop diuretics- main pharmacologic target is the Na+-K+-2Cl– cotransporter in the
thick ascending limb of the loop of Henle.
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PHARMACOLOGICAL THERAPY

DIURETICS

Aldosterone Antagonists - Spironolactone is a nonselective aldosterone antagonist that

may be used alone or in combination with a thiazide diuretic.
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PHARMACOLOGICAL THERAPY

BLOCKERS OF THE RENIN–ANGIOTENSIN SYSTEM

ACEIs decrease the production of angiotensin II, increase bradykinin levels, and reduce
sympathetic nervous system activity.
ARBs provide selective blockade of AT1 receptors, and the effect of angiotensin II on
unblocked AT2 receptors may augment their hypotensive effect.
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PHARMACOLOGICAL THERAPY

BETA-BLOCKERS
β-Adrenergic receptor blockers lower blood pressure by decreasing cardiac output
owing to a reduction of heart rate and contractility.
Other proposed mechanisms by which beta blockers lower blood pressure include a
central nervous system effect and inhibition of renin release.
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PHARMACOLOGICAL THERAPY

ALPHA-ADRENERGIC BLOCKERS
Postsynaptic, selective α-adrenoreceptor antagonists lower blood pressure by decreasing
peripheral vascular resistance.
They are effective antihypertensive agents used either as monotherapy or in combination
with other agents.
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PHARMACOLOGICAL THERAPY

SYMPATHOLYTIC AGENTS
Centrally acting α2 sympathetic agonists decrease peripheral resistance by inhibiting
sympathetic outflow.
Particularly useful in patients with autonomic neuropathy who have wide variations in
blood pressure due to baroreceptor denervation.
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PHARMACOLOGICAL THERAPY

CALCIUM CHANNEL BLOCKERS

Calcium antagonists reduce vascular resistance through L-channel blockade, which
reduces intracellular calcium and blunts vasoconstriction.
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PHARMACOLOGICAL THERAPY

DIRECT VASODILATORS
Decrease peripheral resistance and concomitantly activate mechanisms that defend
arterial pressure, notably the sympathetic nervous system, the renin- angiotensin-
aldosterone system, and sodium retention.
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