Presented to: Dr.

Lakshmi Dodda
Presented by: Nicolas Abdel Nour
 What is hypertension
• Hypertension is defined as an abnormal
elevation in diastolic pressure and/or systolic
pressure.

Isolated Systolic Hypertension: Defined as SBP ≥ 140mmHG and DBP ≤ 90mmHG

60% of hypertensives > 80 years old
 Hemodynamic Basis of Hypertension

Increase in arterial blood pressure is

caused by either:
– an increase in systemic vascular
resistance (SVR)
• determined by the vascular tone (i.e.,
state of constriction) of systemic
resistance vessels
– an increase in cardiac output (CO)
• determined by heart rate and stroke
volume
 Categories of Hypertension
There are two types of high blood pressure.
Primary (essential) hypertension
no identifiable cause of high blood pressure.
This type of high blood pressure, tends to
develop gradually over many years.
Secondary hypertension
tends to appear suddenly and cause higher
blood pressure than does primary
hypertension:
• Kidney problems
• Adrenal gland tumors
• Thyroid problems
• Certain defects in blood vessels you're
born with (congenital)
• Certain medications, such as birth control
pills, cold remedies, decongestants, over-
the-counter pain relievers and some
prescription drugs
• Illegal drugs, such as cocaine and
amphetamines
• Alcohol abuse or chronic alcohol use
• Obstructive sleep apnea
Renal Artery Stenosis
 Chronic Renal Disease

• diabetic nephropathy;
glomerulonephritis etc.
• Damage caused to the nephrons
– Impaired excretion of sodium
→sodium retention and ↑blood
volume → ↑ cardiac output
– May also result in ↑ release of renin
Primary Aldosteronism
 Stress
• Activation of sympathetic
nervous system →
↑norepinephrine in heart and
blood vessels → ↑ cardiac
output and ↑ systemic vascular
resistance
• Adrenal medulla secretes
catecholamines (epinephrine
and norepinephrine)
– ↑ angiotensin II, aldosterone
and vasopressin
– Cardiac and vascular
hypertrophy = sustained ↑
blood pressure
 Sleep Apnea
• Higher incidence of
hypertension
• The mechanism of
hypertension may be related
to sympathetic activation
and hormonal changes
associated with repeated
periods of apnea-induced
hypoxia and hypercapnea,
and from stress associated
with the loss of sleep.
 Hyper- or hypothyroidism
• Excessive thyroid hormone induces
systemic vasoconstriction, an ↑
blood volume, and ↑ cardiac
activity, all of which can lead to
hypertension. 
• Hypothyroidism unclear
– may be related to ↓ tissue
metabolism reducing the release
of vasodilator metabolites,
thereby producing
vasoconstriction and increased
systemic vascular resistance.
 Pheochromocytoma

• ↑↑ catecholamines (both
epinephrine and
norepinephrine)
– This leads to alpha-
adrenoceptor mediated
systemic
vasoconstriction
and beta-
adrenoceptor mediated
cardiac stimulation →
↑↑ arterial pressure.
 Pre-eclampsia
• 3rd trimester of pregnancy
• ↑ blood volume and
tachycardia 
• increase cardiac output
 Aortic coarctation
• Elevated pressures proximal to the
coarctation (i.e., elevated arterial
pressures in the head and arms)

• Reduced systemic blood flow and

reduced renal blood flow → ↑ renin and
an activation of the renin-angiotensin-
aldosterone system → ↑ blood volume
and arterial pressure

• Baroreceptor reflex in blunted due to

structural changes in the walls of vessels
where the baroreceptors are located
– Baroreceptors become desensitized to
chronic elevation in pressure and
become "reset" to the higher pressure
 Risk factors
• Age. The risk of high blood pressure increases as you age. about age
45, high blood pressure is more common in men. Women after age 65.
• Race. High blood pressure is particularly common among blacks
• Family history. High blood pressure tends to run in families.
• Being overweight or obese. The more you weigh the more blood you
need to supply oxygen and nutrients to your tissues. As the volume of
blood circulated through your blood vessels increases, so does the
pressure on your artery walls.
• Not being physically active. People who are inactive tend to have
higher heart rates. The higher your heart rate, the harder your heart
must work with each contraction and the stronger the force on your
arteries. Lack of physical activity also increases the risk of being
overweight.
• Using tobacco. Not only does smoking or chewing tobacco
immediately raise your blood pressure temporarily, but the chemicals in
tobacco can damage the lining of your artery walls. This can cause
your arteries to narrow, increasing your blood pressure. Secondhand
smoke also can increase your blood pressure.
• Too much salt (sodium) in your diet. 
• Too little potassium in your diet. Potassium helps balance the
amount of sodium in your cells. If you don't get enough potassium in
your diet or retain enough potassium, you may accumulate too much
sodium in your blood.
• Drinking too much alcohol.
If you drink alcohol, do so in moderation. For healthy adults, that
means up to one drink a day for women of all ages and men older than
age 65, and up to two drinks a day for men age 65 and younger.
• Certain chronic conditions. Certain chronic conditions also may
increase your risk of high blood pressure, such as kidney disease and
sleep apnea.
• Sometimes pregnancy contributes to high blood pressure, as well.
• Although high blood pressure is most common in adults, children may
be at risk, too. For some children, high blood pressure is caused by
problems with the kidneys or heart. But for a growing number of kids,
poor lifestyle habits, such as an unhealthy diet, obesity and lack of
exercise, contribute to high blood pressure.
 symptoms
• Most people with high blood
pressure have no signs or
symptoms, even if blood
pressure readings reach
dangerously high levels.
• Although a few people with
early-stage high blood pressure
may have dull headaches, dizzy
spells or a few more nosebleeds
than normal, these signs and
symptoms usually don't occur
until high blood pressure has
reached a severe or life-
threatening stage.
 Complications

Uncontrolled high blood pressure can lead to:

• Heart attack or stroke. High blood pressure can
cause hardening and thickening of the arteries
(atherosclerosis), which can lead to a heart attack,
stroke or other complications.
• Aneurysm. Increased blood pressure can cause
your blood vessels to weaken and bulge, forming
an aneurysm. If an aneurysm ruptures, it can be
life-threatening.
• Heart failure. To pump blood against the higher
pressure in your vessels, your heart muscle
thickens. Eventually, the thickened muscle may
have a hard time pumping enough blood to meet
your body's needs, which can lead to heart failure.
• Weakened and narrowed blood vessels in your
kidneys.This can prevent these organs from
functioning normally.
• Thickened, narrowed or torn blood vessels in
the eyes.This can result in vision loss.
• Trouble with memory or understanding. 
 Presentation
and considerations
• It is usually asymptomatic, except accelerated hypertension.
All patients need a full history and physical examination. Look hard for a cause (renal,
endocrine, etc. - as above) in the young, severe hypertensive.
Start by talking to the patient:
• Take a full drug history (non-steroidal anti-inflammatory drugs (NSAIDs), oral contraceptives,
steroids, licorice, sympathomimetics, i.e. cold cures).
• Are they aware of the hypertension? Episodic feelings 'as if about to die' or headaches, or
paroxysmal sweats or palpitations, suggest phaeochromocytoma.
• Consider renal causes: is there a present, past or family history of renal disease? Are the
kidneys palpable? Is there an abdominal or loin bruit (renovascular disease) or delayed or
weak femoral pulses (coarctation).
• Does the patient look Cushingoid or might he or she have Conn's syndrome (tetany, weak
muscles, polyuria, hypokalaemia)?
• Consider contributory factors: obesity, excess alcohol, salt intake and lack of exercise,
environmental stress, and cardiovascular risk factors (smoking, diabetes, cholesterol and
family history) ready for your management plan.
• Assess the degree of end-organ damage or complications of hypertension; previous
cerebrovascular event (CVE), transient ischaemic attack (TIA), dementia or known left
ventricular hypertrophy (LVH)/left ventricular (LV) strain, ischaemic heart disease (IHD),
peripheral vascular disease, renal impairment? Perform ophthalmoscopy; dilate with 1%
tropicamide if there is poor view.
 Screening for hypertension
• Measuring blood pressure
• Use a correctly calibrated and maintained machine (manual or automatic).
• Seated BP is adequate except in elderly or diabetic patients who may have orthostatic
hypotension (standing BP is needed as well - after at least one minute's standing).
If standing systolic blood pressure (SBP) is 20 mm Hg or lower than when seated, review
medication, measure all subsequent blood pressures with the person standing (consider
specialist referral if postural hypotension symptoms persist).
• Remove tight clothing and support the arm with the hand relaxed and the cuff (of appropriate
size:The inflatable part of the blood pressure cuff should cover about 80 percent of the
circumference of your upper arm. The cuff should cover two-thirds of the distance from your
elbow to your shoulder. ) at heart level.
• Initially, measure BP in both arms; if there is a persistent difference of >20 mm Hg between
arms then ensure subsequent blood pressures are taken in the arm with the higher reading.
• Use an automated machine or the following manual method (if the pulse is irregular (e.g. in
atrial fibrillation), always use the manual method):
• Inflate the cuff whilst palpating the brachial artery, until the pulse disappears. This provides an
estimate of systolic pressure.
• Inflate the cuff until 30 mm Hg above systolic pressure, then place a stethoscope over the
brachial artery. Deflate the cuff at 2 mm Hg per second.
• Systolic pressure: the appearance of sustained repetitive tapping sounds (Korotkov I).
Diastolic pressure: usually the disappearance of sounds (Korotkov V). However, in some
individuals (e.g. pregnant women) sounds are present until the zero point. In this case the
muffling of sounds,(Korotkov IV), should be used.
• Record to the nearest 2 mm Hg.
• If initial BP is ≥140/90 mm Hg, take a second or even third reading and record the lowest as
the clinic BP.
 Investigations

• Routine investigation should be limited to:

– Urine dipstick test for protein and blood.
– Serum creatinine and electrolytes and eGFR.
– Fasting blood glucose.
– Fasting serum total and high-density lipoprotein (HDL) cholesterol.
– 12-lead ECG (looking for LVH or signs of IHD).
• Specific investigations for a suspected secondary cause:
– Plasma calcium.
– CXR.
– polysomnograph
– Renal ultrasound.
– Intravenous urogram (IVU).
– Renal arteriography.
– 24-hour urinary vanillylmandelic acid (VMA) x 3.
– Urinary free cortisol.
Treatment
• Primary (essential) Hypertension

• Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium

channel blockers.

• Hypertension with CHF

• Diuretics, ACE inhibitors/ARBs, β-blockers (compensated CHF),

aldosterone antagonists.
.

• Hypertension with diabetes mellitus

• ACE inhibitors/ARBs. Calcium channel blockers, diuretics, β-blockers, α-

blockers.
 β-blockers

Decrease cardiac output and renin

secretion (due to β1-receptor
blockade on JGA cells).

TOXICITY:
Impotence, cardiovascular adverse
Effects (bradycardia, AV block,
CHF), CNS adverse effects
(seizures, sedation, sleep
alterations), dyslipidemia
(metoprolol), and asthmatics/
COPDers (may cause exacerbation)
 Loop diuretics

Furosemide(lasix),torsemide(demadex),
Ethacrinic acid(edecrin)

MECHANISM
Inhibits cotransport system (Na+/K+/2 Cl-) of thick
ascending limb
of loop of Henle. Abolishes hypertonicity of
medulla, preventing concentration of urine.
Stimulates PGE release (vasodilatory effect
on afferent arteriole); inhibited by NSAIDs.Increases
Ca2+ excretion.

TOXICITY :
Ototoxicity, Hypokalemia, Dehydration, Allergy
(sulfa), Nephritis (interstitial), Gout.
 Hydrochlorothiazide
MECHANISM
Thiazide diuretic. Inhibits NaCl reabsorption
in early distal tubule,  diluting capacity of the
nephron.  Decrease Ca2+ excretion.

TOXICITY:
Hypokalemic metabolic alkalosis,
hyponatremia, hyperGlycemia,
hyperLipidemia, hyperUricemia, and
hyperCalcemia. Sulfa allergy.

Commonly used brand names in the United States: Aquatensen

(methyclothiazide), Diucardin (hydroflumethiazide), Diulo (metolazone), Diuril
(chlorothiazide), Enduron (methyclothiazide), Esidrix (hydrochlorothiazide),
Hydro-chlor (hydrochlorothiazide), Hydro-D (hydrochlorothiazide), HydroDIURIL
(hydrochlorothiazide), Hydromox (quinethazone), Hygroton (chlorthalidone),
Metahydrin (trichlormethiazide), Microzide (hydrochlorothiazide), Mykrox
(metolazone), Naqua (trichlormethiazide), Naturetin (bendroflumethiazide),
Oretic (hydrochlorothiazide), Renese (polythiazide), Saluron
(hydroflumethiazide), Thalitone (chlorthalidone), Trichlorex (trichlormethiazide),
Zaroxolyn (metolazone).
 ACE inhibitors

MECHANISM
Inhibit ACE Ž  ,decreases angiotensin II Ž and GFR by
preventing constriction of efferent arterioles.
Levels of renin  increase as a result of loss of feedback
inhibition. Inhibition of ACE also prevents
inactivation of bradykinin, a potent vasodilator.

TOXICITY
Cough, Angioedema (contraindicated in C1
esterase inhibitor deficiency), Teratogen (fetal
renal malformations), increase Creatinine ( decrease GFR),
Hyperkalemia, and Hypotension. Avoid in
bilateral renal artery stenosis, because ACE
inhibitors will further  decrease GFR Žand lead to renal failure.

Angiotensin II receptor blockers (-sartans) have

effects similar to ACE inhibitors but do not increase
 bradykinin Ž  so less risk of cough or angioedema.
 K+-sparing diuretics

Spironolactone(aldactone) and eplerenone (Inspra)

MECHANISM:
aldosterone receptor antagonists in the cortical
collecting tubule.

TOXICITY:
Hyperkalemia (can lead to arrhythmias),
endocrine effects with spironolactone (e.g.,
gynecomastia, antiandrogen effects).
 Renin inhibitors

•  Aliskiren (Tekturna) slows down

the production of renin, an enzyme
produced by your kidneys that
starts a chain of chemical steps that
increases blood pressure.
• Toxicity:
Due to a risk of serious
complications, including stroke,
you shouldn't take aliskiren with
ACE inhibitors or ARBs
 Calcium channel blockers:

MECHANISM:
Block voltage-dependent L-type
calcium channels of cardiac and
smooth muscle, thereby reduce
muscle contractility.
Vascular smooth muscle—amlodipine
= nifedipine > diltiazem >
verapamil.
Heart—verapamil > diltiazem >
amlodipine = nifedipine (verapamil
= ventricle).

TOXICITY:
Cardiac depression, AV block,
peripheral edema, flushing,
dizziness, hyperprolactinemia, and
constipation.
Hydralazine(Apresoline )

MECHANISM:
increase cGMP Ž and lead to smooth muscle relaxation.
Vasodilates arterioles > veins; afterload reduction.

CLINICAL USE:
Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with
methyldopa.Frequently coadministered with a β-blocker to prevent reflex tachycardia.

TOXICITY:
Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea,
headache,angina.
Lupus-like syndrome.

Hypertensive emergency:(≥ 180/120 mmHg)

Commonly used drugs include nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.
Nitroprusside(Nitropress ): Short acting; increase cGMP via direct release of NO
Can cause cyanide toxicity (releases cyanide).

Fenoldopam(Corlopam ): Dopamine D1 receptor agonist—coronary, peripheral, renal, and

splanchnic vasodilation.  decrease BP and increase natriuresis
α-blockers
Nonselective
Phenoxybenzamine (irreversible): Pheochromocytoma (used preoperatively) to
prevent catecholamine (hypertensive) crisis
Toxicity: Orthostatic hypotension, reflex tachycardia

α1 selective (-osin ending)

Prazosin, terazosin,doxazosin, tamsulosin
Urinary symptoms of BPH; hypertension (except tamsulosin)

Toxicity:
1st-dose orthostatic hypotension, dizziness,
headache
 Lifestyle changes to treat high blood pressure

• No matter what medications your doctor prescribes to treat your high blood
pressure, you'll need to make lifestyle changes to lower your blood pressure.
• Your doctor may recommend several lifestyle changes, including:
• Eat healthy foods. 
• Decrease the salt in your diet. A lower sodium level — 1,500 milligrams (mg) a
day — is appropriate for people 51 years of age or older, and individuals of any
age who are African-American or who have hypertension, diabetes or chronic
kidney disease.
• Maintain a healthy weight. 
• Increase physical activity. 
• Limit alcohol.
• Don't smoke. 
• Manage stress. 
• Monitor your blood pressure at home.
• Practice relaxation or slow, deep breathing.
Thank you
 references
• http://www.mayoclinic.org/diseases-
conditions/high-blood-pressure/
• http://www.patient.co.uk/education/hyperte
nsion
• http://en.wikipedia.org/wiki/Hypertension
• FIRST AID USMLE STEP 1 2014