KIMS PARAMEDIC INSTITUTE

HYPERTENSION
Hypertension is a chronic medical condition that arises when the blood pressure is
abnormally high (greater than 140 mm of Hg systolic and 90 mm of Hg diastolic).
Hypertension occurs when the body’s smaller blood vessels (the arterioles) narrow, causing
the blood to exert excessive pressure against the vessel walls and forcing the heart to work
harder to maintain the pressure. Although the heart and blood vessels can tolerate increased
blood pressure for months and even years, eventually the heart may enlarge (a condition
called hypertrophy) and be weakened to the point of failure.
Hypertension risk factors include obesity, drinking too much alcohol, smoking and family
history. Blood pressure is actually a measure of two pressures, the systolic and the diastolic.
The systolic pressure is the force that blood exerts on the artery walls as the heart contracts to
pump the blood to the peripheral organs and tissues. The diastolic pressure is residual
pressure exerted on the arteries as the heart relaxes between beats. A diagnosis of
hypertension is made when blood pressure reaches or exceeds 140/90 mmHg (read as “140
over 90 millimetres of mercury”).
Types of Hypertension
There are two major types of hypertension and four less frequently found types.

1. Primary (Essential) Hypertension: About 95% of people with high blood

Pressure has essential hypertension or primary hypertension. This condition has no
identifiable medical cause. Elevated blood pressure usually begins to appear between
age 30 and 50, but can begin at older ages. Usually people with essential hypertension have no
symptoms, but may experience frequent headaches, tiredness, dizziness, or nose bleeds.
Although the cause is unknown, contributing factors for essential hypertension may be obesity,
smoking, alcohol, diet and inheritance.

2. Secondary Hypertension: About 5%-10% of people with high blood pressure have secondary
hypertension. This condition has definite cause; the most common cause of secondary
hypertension is an abnormality in the arteries supplying blood to the kidneys. Other causes
include airway obstruction during sleep, diseases and tumors of the adrenal glands, hormone
abnormalities , thyroid disease, and too much salt or alcohol in the diet. Drugs can cause
secondary hypertension, including OTC medications such as ibuprofen and pseudoephedrine.
Pathophysiology
Hypertension causes three major circulatory abnormalities: increased
arteriolar resistance, increased large artery stiffness, and early or premature reflection
of arterial pulse waves. Increased resistance and vessel stiffness in younger hypertensive
patients result from structural changes, including thinning and fracturing of elastin, increased
collagen deposition, and increased wall thickness. These changes manifest primarily as a
greater rise in systolic pressure greater than diastolic pressure. In elderly, an increased arterial
stiffness is the greater factor and may contribute to isolated systolic hypertension, in which
systolic pressure is elevated but diastolic pressure is normal or low. Patients with isolated
systolic hypertension are at substantially increased risk for stroke, coronary heart disease, and
congestive heart failure. Pulse wave reflection refers to the backward rebound of some of the
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cardiac output as it encounters the resistance of the arteries. When arteries are normally
compliant, this reflected flow occurs during diastole and assists with filling of the coronary
arteries. In hypertension, however, reflection occurs prematurely, during systole, contributing to
vascular overload in the aortic arch and in the coronary carotid and renal arteries.
Secondary hypertension accounts for approximately 5-10% of all cases of hypertension, with
the remaining being primary hypertension. Secondary hypertension has an identifiable cause
whereas primary hypertension has no known cause (i.e. idiopathic).
There are many known conditions that can cause secondary hypertension. Regardless of the
cause, arterial pressure becomes elevated either due to an increase in cardiac output, an
increase in systemic vascular resistance, or both. When cardiac output is elevated, it is
generally due to either increased neurohumoral activation of the heart or increased blood.
Increased systemic vascular resistance is most commonly caused, at least initially, by
increased sympathetic activation or by the effects of circulating vasoconstrictors (e.g.,
angiotensin II). Anatomic considerations, such as narrowing of the aorta (e.g.,
coarctation) or chronic changes in vascular structure (e.g., vascular hypertrophy) can also
cause or contribute to increased systemic vascular resistance. Renal artery disease can
because of narrowing of the vessel lumen (stenosis). The reduced lumen
diameter decreases the pressure at the afferent arteriole in the kidney and reduces
renal perfusion. This stimulates renin release by the kidney, which increases circulating
angiotensin II and aldosterone. These hormones increase blood volume by enhancing renal
reabsorption of sodium and water. Increased angiotensin II also causes systemic
vasoconstriction and enhances sympathetic activity. Chronic elevation of angiotensin II
promotes cardiac and vascular hypertrophy. The net effect of these renal mechanisms is an
increase in blood volume that augments cardiac output. Therefore, hypertension caused by
renal artery stenosis results from both an increase in systemic vascular resistance and an
increase in cardiac output.
Symptoms
High blood pressure usually causes no symptoms and high blood pressure often is labelled “the
silent killer”. People who have high blood pressure typically do not know it until their blood
pressure is measured.
Sometimes people with markedly elevated blood pressure may develop:
• Headache
• Dizziness
• Blurred vision
• Nausea and vomiting, and
• Chest pain and shortness of breath.
People often do not seek medical care until they have symptoms arising from the
organ damage caused by chronic (ongoing, long-term) high blood pressure. The
following types of organ damage are commonly seen in chronic high blood pressure:
• Heart attack.
• Heart failure.
• Stroke or transient ischemic attack (TIA).
• Kidney failure.
• Eye damage with progressive vision loss.
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• Peripheral arterial disease causing leg pain with walking (claudication).
• Outpouchings of the aorta, called Aneurysms.
About 1% of people with high blood pressure do not seek medical care until the high blood
pressure is very severe, a condition known as malignant hypertension.
• In malignant hypertension, the diastolic blood pressure (the lower number) often exceeds 140
mm Hg.
• Malignant hypertension may be associated with headache,lightheadedness, nausea, vomiting,
and stroke-like symptoms.
• Malignant hypertension requires emergency intervention and lowering of blood pressure to
prevent brain hemorrhage or stroke.
It is of extreme importance to realize that high blood pressure can be unrecognized for years,
causing no symptoms but causing progressive damage to the heart, other organs, and blood
vessels.
Treatment
Central acting agents
MOA: These prevent the brain from signaling the nervous system to increase heart rate and
narrow blood vessels.
Examples : Clonidine and methyldopa

Calcium Channel Blockers

MOA: These vasodilates the blood vessels and slow heart rate by blocking calcium channel
Examples :Amlodipine, Felodipine, Nicardipine, Nifedipine, Diltiazem verapamil

Drugs acts on RAA system

MOA: Vasodilation of blood vessels.
Decreases release of renin.
Antagonise the angiotensin II receptor.
Examples :Captopril, Enalapril Aliskiren Losartan, Telmisartan

Antiadrenergic drugs
MOA: Vasodilation of blood vessels Reduce conduction of nerve impulses to blood vessels.
Examples :Atenolol, Metoprolol Doxazosin, Phentolamine Carvedilol, Labetalol

Aldosterone Receptor Antagonists

MOA: Block aldosterone that can lead to salt and fluid retention, which can contribute to high
blood pressure.
Examples :Eplerenone, Spironolactone

Diuretics
MOA: Eliminate sodium and water, reducing blood volume.
Examples : Ethacrynic acid, Furosemide hydrochlorothiazide and chlorothiazide.