Hypertension – Ch 33 (Lewis)

Hypertension – High BP – defined as persistent systolic BP >= 140

mm Hg, diastolic BP >90 mm Hg or current use of antihypertensive
medication.
CVD - cardiovascular disease is the number one cause of death in
women in the US.

African American have highest prevalence of hypertension in the world

– they produce less rennin and do not respond as well to angiotension
inhibitors.

Blood pressure – is the force exerted by the blood against the walls
of the blood vessel.
Arterial blood pressure = Cardiac output X Systemic vascular
resistance
Cardiac Output (CO) – is the total blood flow through the systemic or
pulmonary circulation per minute. CO described as the stroke volume
(SV) – amount of blood pumped out of the left ventricle per beat.

Systemic vascular resistance (SVR) – is the force opposing the

movement of blood within the blood vessels. Any change in the radius
of arteries/arterioles creates major change in SVR.

Barorecptors – specialized nerve cells in carotid arteries that

maintain BP stability. It is less responsive in older adults.

When BP drops it stimulates:

SNS – Sympathetic Nervous System – which constrict peripheral
arterioles, increases heart rate (HR), and increased contractility of the
heart. It increases both CO and SVR

When BP increases it stimulates:

Parasympathetic Nervous System (vagus nerve) – vasodilation in
peripheral arterioles, decreases heart rate, decreases force of
contraction of the heart. It decreases CO

Renal System – regulates sodium excretion – an increase in sodium

retention increases in water retention – increasing stroke volume and
cardiac output, increasing BP. It releases from kidneys enzyme renin
that converts angiotensin to ACE- angiotension-converting
enzyme. It also stimulates adrenal cortex to secrete aldosterone –
which causes salt and water retention in the kidneys.
Endocrine System – Stimulation of the SNS results in release of
epinephrine along with a small fraction of norepinephrine by the
adrenal medulla – this increses CO by increasing HR and myocardial
contractility.

Isolated Systolic Hypertension - most common with adults 50 and

older – SBP >=140mm Hg coupled with DBP <90 mm Hg. ISH –
caused by loss of elasticity in large arteries from atherosclerosis.

Pseudohypertension – aka false hypertension can occur with

advanced (often calcified) arteriosclerosis. It is suspected when
arteries feel rigid –only accurate way to measure BP is through use of
an intraarterial catheter.

Etiology – primary and secondary

Primary Hypertension – Without specific underlying cause – 90 –
95% - sodium intake, obesity/weight, diabetes, excessive alcohol have
been identified as factors.

Secondary Hypertension – are a result of other disease 5 – 10 %(ex.

Kidney disease, adrenal gland disease, sleep apnea, medications,
pregnancy)

Pathophysiology for primary hypertension

*Heredity
*Water and Sodium Retention
*Altered Renin-Angiotension Mechanism
*Stress and Increase Sympathetic Nervous System Activity
*Insulin Resistance and Hyperinsulinemia – insulin resistance is a risk
factor for development of hypertension and cardiovascular disease.
*Endothelial Cell Dysfunction

Clinical Manifestations or secondary symptoms are fatigue, reduced

activity tolerance dizziness, palpitations, angina and dyspnea
(shortness of breath).

Most common complications of hypertension are:

Heart (hypertensive heart disease) – CAD (Coronary Artery Disease)
Arterial changes result in stiffened arterial wall and a narrowed
internal lumen and high incidence of CAD, resulting problems of
angina and myocardial infarction (MI).
Brain (cerebrovascular disease)
Peripheral vasculature (peripheral vascular disease)
Kidney (nephrosclerosis) – earliest manifestation of renal dysfunction
is nocturia.
Eyes (retinal damage) – blurring of vision, retinal hemorrhage and loss
of vision.

DASH (Dietary Approaches to Stop Hypertension)

Drug Therapy for hypertension treatment – have two main actions:
1. they decrease the volume of circulating blood
2. they reduce SVR (systemic vascular resistance)

Diuretics – promote sodium and water excretion. Thiazide – type

diuretics are used as initial therapy for most patients with
hypertension.
Adrenergic (SNS) inhibitors – diminishing the SNS effects that
increase BP.
Direct vasodilators – decrease BP by relaxing vascular smooth muscle and
reducing SVR.
Calcium channel blockers – increase sodium excretion and cause
arteriolar vasodilation by preventing the movement of extracellular
calcium into cells.

Angiotensin inhibitors - 2 type

First – angiotension-cconverting enzyme (ACE) inhibitors –
prevent the conversion of angiotensin I to angiotensin II (not allowing
vasoconstriction and sodium and water retention).
Second – A-II receptor blockers (ARBs) – prevents angiotensin II
from binding to its receptors in the walls of the blood vessels.

Side effects of drugs

Thiazide and loop diuretics – hyperuricemia (elevated blood level of
uric acid), hyperglycemia (high blood sugar – usually diabetes
mellitus), and hypokalemia (low blood potassium –major positive ion
found inside of cells)
Ace inhibitors – high levels of bradykinin – which cause caughing…
they may be switched to ARB (angiotensin II receptor blockers)
Adrenergic inibitors - Orthostatic hypotension and sexual
dysfunction.
Vasodilators and angiotensin inhibitors – tachycardia and orthostatic
hypotension.

Resistant Hypertension – is the failure to reach goal BP in patients who

are adhereing to full doses of an appropriate 3 drug therapy regimen that
includes a diuretic.

Auscultatory gap – gap between the first Korotkoff sound and subsequent
beats. Must be careful with older adults.

Hypertensive Crisis – is a severe and abrupt elevation in BP, The rate of

rise of BP is more important than the absolute value in determining the need
for emergency treatment.
Hypertensive urgency – develops over days to weeks, patient’s BP is
severely elevated but there is no clinical evidence of target organ damage.
Hypertensive encephalopathy – sudden rise in BP associated with
headache, nausea, seizures, etc. Encephalopathy are the results of
increased cerebral capillary permeability leading to edema and disruption of
cerebral function.

When treating hypertensive emergencies use:

MAP – mean arterial pressure MAP = (SBP + 2 DBP) / 3
Initial treatment goal is to decrease MAP by no more than 25% within
minutes to 1 hour. If patient is stable target goal for BP is 160/100 to 110
mm Hg over next 2 – 6 hours. Avoid lowering the BP excessively – may
decrease cerebral, coronary or renal perfusion.
IV drugs used for hypertensive emergencies include vasodialators.

Important tables to look at 33-5, 33-11 & 33-12