TYPES OF HYPERTENSION

PRIMARY HYPERTENSION : Between 90 and 95% of all cases of

hypertension are primary hypertension, a persistently elevated blood
pressure that cannot be attributed to any identifiable cause.

SECONDARY HYPERTENSION :The remaining 5–10% of cases are

secondary hypertension, which has an identifiable underlying cause.
 RISK FACTORS
NON MODIFIABLE RISK FACTORS

1. Family history: High blood pressure often runs in families.If your parents or other close
blood relatives have high blood pressure, there’s an increased chance that you’ll get it,
too.

2. Age: Blood pressure tends to increase with age. Our blood vessels naturally thicken and
stiffen over time. These changes increase the risk for high blood pressure.
However, the risk of high blood pressure is increasing for children and teens, possibly
because more children and teens are living with overweight or obesity.

3. Gender: Men are more likely than women to develop high blood pressure throughout
middle age. But in older adults, women are more likely than men to develop high blood
pressure. Women who have high blood pressure during pregnancy are more likely to have
high blood pressure later in life.
4. Race or ethnicity: High blood pressure is more common in African American and Hispanic
adults than in white or Asian adults. Compared with other racial or ethnic groups, African
Americans tend to have higher average blood pressure numbers and get high blood pressure
earlier in life. It also tends to be more severe, and some medications are less effective in
treating high blood pressure in them.

5. Medicines
Some prescription and over-the-counter medicines can make it more difficult for your body to
control your blood pressure. Antidepressants, decongestants (medicines to relieve a stuffy
nose), hormonal birth control pills, and non-steroidal anti-inflammatory drugs (NSAIDs) such
as aspirin or ibuprofen can all raise your blood pressure.

6. Chronic kidney disease (CKD): High blood pressure may occur as a result of kidney disease.
And, having high BP may also cause further kidney damage.
7. Several disorders cause secondary hypertension:

• Obstruction of renal blood flow or disorders that damage renal tissue may cause the kidneys
to release excessive amounts of renin into the blood. The resulting high level of angiotensin II
causes vasoconstriction, thus increasing systemic vascular resistance.

• Hypersecretion of aldosterone—resulting, for instance, from a tumor of the adrenal cortex—

stimulates excess reabsorption of salt and water by the kidneys, which increases the volume of
body fluids.

• Hypersecretion of epinephrine and norepinephrine may occur by a pheochromocytoma , a

tumor of the adrenal medulla. Epinephrine and norepinephrine increase heart rate and
contractility and increase systemic vascular resistance.
Modifiable risk factors
•Lack of physical activity: Not getting enough physical activity as part of your lifestyle increases
your risk of getting high blood pressure. Physical activity is great for your heart and circulatory
system in general.

•An unhealthy diet, especially one high in sodium: A diet that is too high in salt consumption, as
well as calories, saturated and trans fat and sugar, carries an additional risk of high blood
pressure.

•Being overweight or obese: Carrying too much weight puts an extra strain on your heart and
circulatory system that can cause serious health problems. It also increases your risk of
cardiovascular disease, diabetes and high blood pressure.

•Drinking too much alcohol: Regular, heavy use of alcohol can cause many health problems,
including heart failure, stroke and an irregular heartbeat (arrhythmia). It can cause your blood
pressure to increase dramatically and can also increase your risk of cancer, obesity, alcoholism,
suicide and accidents.
•Sleep apnea: Obstructive sleep apnea may increase risk of developing high blood.

•High cholesterol: More than half of people with high BP also have high cholesterol.

•Diabetes: Most people with diabetes also develop high blood pressure.

•Smoking and tobacco use: Using tobacco can cause your blood pressure to temporarily
increase and can contribute to damaged arteries.

•Stress: Stress may contribute to increased blood pressure. Also, too much stress can encourage
behaviors that increase blood pressure, such as poor diet, physical inactivity, and using tobacco
or drinking alcohol more than usual.
COMPLICATIONS OF
HYERTENSION
 Complications related to Brain
• Acute severe hypertension above a mean arterial pressure of approximately 150mmHg
exceeds the brain's autoregulatory capacity and results in increased cerebral blood flow
leading to Hypertensive Encephalopathy.

• Chronic hypertension predisposes to:

cerebral vasculature atherosclerosis
 luminal narrowing
 endothelial dysfunction
impaired arterial relaxation
decreased ability to augment cerebral blood flow at low blood pressures

• The pathologic effects of hypertension increase stroke risk by three- to fivefold.

• Hypertension is a risk factor for cognitive impairment and dementia involves having slightly more troubles with
memory, language or thinking than other adults your age have through multifactorial mechanisms including:
 Vascular compromise
 Cerebral small vessel disease
 White matter disease (leukoaraiosis)
 Cerebral microbleeds
 Cerebral atrophy
 Amyloid plaque deposition
 Neurofibrillary tangles

• Blood Brain Barrier Dysfunction: Chronic inflammation, compromises the BBB, which in turn allows for
molecules to leak into the CNS. This then activates astrocytes and microglia, causing an immune response
within the brain. Neuroinflammation can reach regulatory centers of blood pressure such as
the paraventricular nucleus (PVN), leading to sustained elevation of blood pressure.
• Hypertension and Alzheimer's disease

Although there are no direct correlations with hypertension and its association with Alzheimer's
disease, chronic hypertension is associated with
• White Matter Lesions
• Lacunar Infarcts
• Neurotic Plaques
• Neurofibrillary Tangles

ALL PATHOLOGICAL FEATURES OF AD.

 Complications related to Heart
 Also called as Hypertensive Heart.

 Hypertension increases the workload on the heart inducing structural and functional changes
in the myocardium.

 It refers to a constellation of changes in the left ventricle, left atrium, and coronary arteries as
a result of chronic blood pressure elevation.
Hypertensive heart disease may involve:

1. Left ventricular hypertrophy (LVH)/ Enlarged left heart. High blood pressure forces the heart to work
harder to pump blood to the rest of the body. This causes the lower left heart chamber, called the left
ventricle, to thicken and to enlarge. A thickened and enlarged left ventricle raises the risk of heart attack
and heart failure. It also increases the risk of death when the heart suddenly stops beating, called
sudden cardiac death.

2. Heart failure. Heart failure is a progressive clinical syndrome characterized by reduced ability of the
heart to pump blood to meet the body's metabolic demand. High blood pressure strains the heart. Over
time, this can cause the heart muscle to weaken or become stiff and not work as well as it should. The
overwhelmed heart slowly starts to fail.
3. Cardiac arrhythmias

 Most common among these is Afib (atrial fibrillation).

 AFib is an irregular and very rapid heart rhythm associated with increased risk for blood
clots in the heart, stroke, and heart failure
  During normal heart conduction, electrical signals from the sinoatrial node travel through the atria
to the atrioventricular node, passes through the ventricles causing them to contract.

 In AFib, the electrical signals conduct in a chaotic manner firing from multiple locations leading to
faster and irregular heartbeats and characterized by lack of a P-wave and irregular QRS complexes
on an ECG.

4. CORONARY ARTERY DISEASE

• Coronary artery disease in hypertensive heart disease is accelerated by chronic elevation of blood
pressure that induces endothelial dysfunction and exacerbates atherosclerotic processes.

• LVH exacerbates coronary artery disease by promoting myocardial ischemia mediated by a increased
myocardial oxygen demand.

• Blood pressure disturbances and irregularities and cardiac remodeling associated with hypertensive
heart disease increase the risk of coronary artery disease and related complications such as
myocardial infarction, angina, heart failure and Afib.
5. Myocardial remodeling (MR)

Myocardial remodeling (MR) in HHD includes changes in the size, shape, and structure of the heart
cavities, as well as in the biochemical, electrophysiological, and functional properties of the myocardium.
Chronically elevated blood pressure negatively impacts the normal geometry and function of both the
ventricles and atria—primarily the left ventricle (LV) and left atrium (LA), which simultaneously increase in
size as the initial adaptation to a deteriorating function. Consequently, there is a variety of interrelated
alterations between cardiomyocytes, the interstitial space, and the coronary microvasculature.

6. Myocardial and Vascular Fibrosis

Myocardial fibrosis (MF) is considered one of the key features of hypertensive MR. Myocardial stiffness,
which is thought to be a fundamental characteristic of hypertensive maladaption, is associated with
fibrosis, altered contractile and relaxation properties, and changes in cardiac cellularity.

7. Neurohumoral Disorder

Interacting neural, hormonal, and metabolic mechanisms act locally and systemically to regulate
cardiovascular function. Sustained elevation of blood pressure leads to neurohumoral disorders.
Complications related to eye
Hypertensive retinopathy has the following phases:

(a) Vasoconstrictive Phase

• The local autoregulatory mechanisms come into play.
• In the early stages, funduscopy identifies arteriolar constriction, with a decrease in the ratio
of the width of the retinal arterioles to the retinal venules.

(b) Sclerotic Phase

Persistent increase in BP causes:
• Permanent arterial narrowing
• Arteriovenous (AV) crossing changes/ AV nicking: AV crossing changes occur when a
thickened arteriole crosses over a venule and subsequently compresses it as the vessels
share a common adventitious sheath. The compression of the vein with bulging on either
side of the crossing.
• Accentuation of light reflex (silver and copper wiring): Silver wiring or copper wiring is where the
walls of the arterioles become thickened and sclerosed and reflect more light on examination.
(c) Exudative Phase
Seen in patients with severely increased BP:
• Characterized by the disruption of the blood-brain barrier and leakage of blood and plasma into the
vessel wall disrupting the autoregulatory mechanisms
• Retinal signs occur such as retinal hemorrhage (flame-shaped and dot blot): Retinal haemorrhages are
caused by damaged vessels rupturing and releasing blood in the retina. Dot and blot haemorrhages
occur deeper, in the inner nuclear layer or outer plexiform layer. Flame haemorrhages occur in the
nerve fiber layer.
• Hard exudate formation: Hard exudates are caused by damaged vessels leaking lipids onto the retina.
• Necrosis of smooth muscle cells and retinal ischemia (cotton-wool spots). Hard exudates are caused by
damaged vessels leaking lipids onto the retina.

(d) Malignant Hypertension/ Optic Neuropathy

Severe intracranial hypertension leads to optic nerve ischemia and edema (papilledema).

optic disk swelling, which appears as blurring and elevation of disk

margins. The image also shows a characteristic star-shaped macular lesion
caused by leaking retinal vessels.
Also, fibrinoid necrosis of choroidal arterioles occurs leading to segmental infarction of choriocapillaries.

This gives rise to:

•Elschnig's spots: Where the overlying retinal pigment epithelium (RPE) appears yellow
•Siegrist's streak: RPE hyperplasia over choroidal infarcts
•Neurosensory RPE detachments
These signs are termed as choroidopathy.
Complications related to Kidney
Over time, uncontrolled high blood pressure can cause arteries around the kidneys to narrow,
weaken or harden. These damaged arteries are not able to deliver enough blood to the kidney
tissue.

•Damaged kidney arteries don't filter blood well. Kidneys have small, finger-like nephrons that
filter your blood. Each nephron receives its blood supply through tiny hair-like capillaries, the
smallest of all blood vessels. When the arteries become damaged, the nephrons don't receive
the essential oxygen and nutrients. Then the kidneys lose their ability to filter blood and regulate
the fluid, hormones, acids and salts in the body.

•Damaged kidneys fail to regulate blood pressure. Healthy kidneys respond to a hormone called
aldosterone which is produced in the adrenal glands, to help the body regulate blood pressure.
Kidney damage and uncontrolled high blood pressure contribute to a negative spiral. As more
arteries become blocked and stop functioning, the kidneys eventually fail.
HYERTENSION MANAGEMENT
 Lifestyle Management of Hypertension
First-line lifestyle-related measures in the management of high blood pressure:

1. Weight management:
• Weight loss to achieve a BMI <25 kg/m2.
• In most studies, individuals who are overweight or obese can anticipate losing 1 mm Hg both
systolic and diastolic blood pressure for every 2 lb of weight loss.
• The mechanism of blood pressure lowering resulting from weight loss may represent a
decrease in blood volume, an initial diuresis, or reduction in systemic vascular resistance.

2. Regular physical activity: A minimum of 30 min of moderate intensity aerobic exercise ≥ 5

days/week.
 Exercise-induced reduction in peripheral vascular resistance
 Improved vascular endothelial function and arterial elasticity/compliance
 Reduction in peripheral vascular resistance
• Exercise training-induced improvement in insulin sensitivity, which has been associated with
increased renal sodium excretion.
• In addition, exercise training-induced vascular adaptations also include an increase in skeletal
muscle precapillary and capillary vessel numbers (i.e., angiogenesis), and adaptations in
vascular structure including vascular remodeling (arteriogenesis) resulting in a larger conduit
artery lumen diameter, which further contributes to reduced vascular resistance.
3. Proper nutrition and diet: This diet includes combination of sodium intake reduction;
increased intake of potassium, calcium, and magnesium; and moderation of alcohol consumption
have been shown to very effective and is strongly supported by evidence from randomized,
controlled trials and is called as DASH (Dietary approaches to Systolic Hypertension] type eating
plan including, but not limited to:
• Fruits and vegetables
• Fiber rich whole grains
• Moderate in fat-free and low-fat dairy products, and low in saturated and total fat
• Sodium: <1500 mg/day
4. Cessation of cigarette smoking

5. Moderation of alcohol: If consuming alcohol, limiting consumption to no more than two

drinks (2 oz) per day for men and no more than one drink per day for women.

These measures have been shown to reduce systolic blood pressure levels (2–20 mm Hg) and
potentiate antihypertensive drug therapy.

Target Blood pressure levels should be <140/90 or <130/80 mm Hg in the presence of diabetes,
chronic kidney disease, or CVD, with the initial goal to lower the systolic blood pressure.
PHARMACOLOGICAL MANAGEMENT
OF HYPERTENSION
• It is recommended that all patients with Stage 2 hypertension initiate pharmacological
treatment in conjunction with lifestyle change whereas those with uncomplicated Stage 1
hypertension should initiate lifestyle change for a trial of 6–12 months prior to initiation of
pharmacotherapy.

• Numerous different types of antihypertensive drugs are available including thiazide and
potassium-sparing diuretics, β-adrenergic blockers, α-adrenergic blockers, ACE inhibitors, AR
blockers, calcium channel inhibitors, centrally acting drugs, and direct acting vasodilators.

• A thiazide diuretic is usually prescribed as the initial drug choice for patients with Stage 1
hypertension, whereas a two-drug combination is usually the initial prescription for patients
with Stage 2 hypertension (e.g., a thiazide diuretic along with an ACE inhibitor or AR blocker,
or β-adrenergic blocking agent, or calcium channel inhibitor).

• Generally, multiple antihypertensive drugs are required to achieve the therapeutic target
level; it is therefore imperative that the prescribing clinician pay particular attention to
contraindications, drug interactions, and comorbidities when selecting antihypertensive drug
therapy.
 MODE OF ACTION
• Diuretics are medicines that help reduce fluid buildup in the body. They are sometimes called
water pills. Most diuretics help the kidneys remove salt and water through the urine.

• Beta-adrenergic blocking agents. The medicines block the effects of the hormone epinephrine,
also known as adrenaline. Beta blockers cause the heart to beat more slowly and with less
force.

• Alpha blockers are a type of blood pressure medicine. Alpha blockers lower blood pressure by
keeping a hormone called norepinephrine from tightening the muscles in the walls of smaller
arteries and veins. As a result, the blood vessels remain open and relaxed. This improves
blood flow and lowers blood pressure.

• Angiotensin-converting enzyme (ACE) inhibitors are medicines that help relax the veins and
arteries to lower blood pressure. ACE inhibitors prevent an enzyme in the body from making
angiotensin 2, a substance that narrows blood vessels.
• Angiotensin receptor blockers (ARBs), also known as angiotensin II receptor antagonists,
are used to treat high blood pressure.

• Calcium channel blockers are medicines used to lower blood pressure. They stop calcium
from entering the cells of the heart and arteries. Calcium causes the heart and arteries to
squeeze more strongly. By blocking calcium, calcium channel blockers allow blood vessels to
relax and open.
Planning of Hypertension Management