HYPERTENSION

Hypertension is persistently high arterial blood pressure, the force exerted per unit area on the
walls of arteries. The systolic blood pressure (SBP), the upper reading in a blood pressure
measurement, is the force exerted on the walls of blood vessels as the heart contracts and
pushes blood out of its chambers. The lower reading, known as diastolic blood pressure
(DBP), measures the force as the heart relaxes between contractions.
Blood pressure is measured in millimetres (mm) of mercury (Hg). Adult blood pressure is
considered normal at 120/80 mm Hg.
Pathophysiology:
Blood pressure is a function of cardiac output multiplied by peripheral resistance (the
resistance in the blood vessels to the flow of blood). Thus the diameter of the blood vessel
markedly affects blood flow. When the diameter is decreased (as in atherosclerosis)
resistance and blood pressure increase. Conversely, when the diameter is increased (as with
vasodilator drug therapy), resistance decreases and blood pressure is lowered. Many systems
maintain homeostatic control of blood pressure. The major regulators are the sympathetic
nervous system (SNS) for short-term control and the kidney for long-term control. In
response to a fall in blood pressure, the SNS secretes norepinephrine, a vasoconstrictor,
which acts on small arteries and arterioles to increase peripheral resistance and raise blood
pressure. Conditions that result in overstimulation of the SNS (i.e., certain adrenal disorders
or sleep apnea) result in increased blood pressure. The kidney regulates blood pressure by
controlling the extracellular fluid volume and secreting renin, which activates the renin-
angiotensin system (RAS). Abnormal blood pressure is usually multifactorial. In most cases
of hypertension, peripheral resistance increases. This resistance forces the left ventricle of the
heart to increase its effort in pumping blood through the system. With time, left ventricular
hypertrophy (LVH) and eventually heart failure can develop.
Common genetic variants of the RAS gene, including angiotensin-converting enzyme (ACE)
and angiotensinogen, have shown relationships with hypertension. An increased production
of these proteins may increase production of angiotensin II, the primary mediator of the RAS,
thus increasing blood pressure. Angiotensin II may also trigger low-grade inflammation
within the blood vessel wall, a condition that predisposes to hypertension. Hypertension often
occurs with other risk factors for CVD, including visceral (intra-abdominal) obesity, insulin
resistance, high triglycerides, and low HDL cholesterol levels. The coexistence of three or
more of these risk factors leads to metabolic syndrome. Accumulation of visceral fat
synthesizes increased amounts of angiotensinogen, which activates the RAS and increases
blood pressure. Also, angiotensin II, the primary mediator of the RAS, promotes the
development of large dysfunctional adipocytes, which produce increased amounts of leptin
and reduced quantities of adiponectin. Higher levels of leptin and lower amounts of
circulating adiponectin activate the SNS, a key component of the hypertensive response.
Major complications of hypertension includes:
 Hardened arteries
 Cardiovascular disease
 Angina
  Heart attack
 Left ventricular hypertrophy
 Heart failure/ Left-side heart failure
 Stroke
 Cerebrovascular disease
 Cerebral haemorrhage
 Eye complications
 Retinal damage
 Impaired vision
 Kidney disease
 Kidney failure/ End-stage renal disease
 Death

Etiology:
 Genetic factors: Currently it is believed that there is polygenic inheritance and when
environmental factors are not healthy, hypertension is precipitated.
 Body weight and height: Hypertension increases with increase in the weight and
height. Hence those who are obese have higher blood pressure values. Increase in
BMI increases hypertension
 Age: Increases steeply with age. Now scientists have found shifts in BP. It is found in
adolescents and the young as well.
 Gender: Rise is greater in men than women but after menopause, the difference
decreases.
 Factors that may increase reabsorption by sodium can cause hypertension.
 Changes in rennin-angiotensin: Aldosterone system and excretion of adrenocorticoids
and prolactin may affect blood pressure.
 Hyperinsulinemia of obese may influence blood pressure susceptibility through renal
sodium reabsorption and transport.
 Dietary factors: Excess calories, fats especially saturated fat and cholesterol in large
quantities can increase blood pressure. Refined carbohydrates (sugars) could have an
effect but studies in humans are inconclusive. High fibre intakes are beneficial
(soluble fibre). Possible role of chloride, low potassium (K) and high sodium diets is a
suspect. Less calcium and magnesium in diet could cause hypertension.
 Modern lifestyle: Sedentary life devoid of exercise, stress, smoking, tobacco intake,
alcohol are pointing towards increases in blood pressure.
 ATHEROSCLEROSIS
Atherosclerosis is an arterial lesion characterized by patchy thickening of the intima
(innermost coal of artery) comprising of fat and layers of collagen like fibres. This is a slow
or progressive disease, degenerative in nature affecting small and large arteries and weaken
them leading to proliferation. This leads to problems in smooth flow of blood. These deposits
are referred to as plaque. The plaque reduces the size of the lumen of the artery and
consequently, the amount of blood flow. The reduced blood flow causes an inadequate
nutrient and oxygen supply and water removal from the tissues, leading to a condition
referred to as ischemia. These condition causes pain in the chest which is referred to as
angina pectoris and it radiates down the left arm. When the lumen narrows so much so that a
blood clot occurs in a coronary artery and blood flow is cut off, a heart attack can result. The
dead tissue that results is called an infarct. The heart muscle that receives the blood is the
myocardium. Thus, such an attack is referred to as an acute myocardial infarction (MI).
Atherosclerosis is thus categorized as a continuum of as fatty streaks, intermediate lesions,
fibrous plaques and complicated lesions. There are 5 phases to atherosclerosis:
 Phase I: Asymptomaticphase, consists of fatly streaks which are non-obstructive, lipid
filled cells.
 Phase 2: Consists of plaque with high lipid content and prone to rupture usually the
type of lipid is LDLc.
 Phase 3: Acute complicated phase with rupture and non-occlusive thrombus.
 Phase 4: Acute complicated lesions with occlusive thrombus, which are associated I
with angina/myocardial infarction and even sudden death.
 Phase 5: Fibrotic or occlusive lesion. Large thrombi call cause serious acute defects.

Pathophysiology:
Atherosclerosisinvolves the accumulation of plaque within the walls ofthe arteries. It starts
with injury to the endothelial cells with anassociated inflammatory response involving
phagocytes andmonocytes. Once in the tissue, monocytes evolve into macrophagesthat ingest
oxidized cholesterol and become foam cellsand then fatty streaks in these vessels.
Intracellular micro calcificationoccurs, forming deposits within the vascular smoothmuscle
cells of the surrounding muscular layer. A protective fibrin layer (atheroma) forms between
the fattydeposits and the artery lining. Atheroma produce enzymes thatcause the artery to
enlarge over time, thus compensating forthe narrowing caused by the plaque. This
“remodelling” of theshape and size of the blood vessel may result in an aneurysm.
Atheroma can rupture or break off, forming a thrombus(blood clot), where they attract blood
platelets and activate theclotting system in the body. This response can result in a
blockageand restricted blood flow.Only high-risk or vulnerable plaque forms thrombi.
Vulnerableplaque are lesions with a thin fibrous cap, few smooth musclecells, many
macrophages (inflammatory cells), and a large lipidcore. Arterial changes begin in infancy
and progressasymptomatically throughout adulthood.The clinical outcome of impaired
arterial function arisingfrom atherosclerosis depends on the location of the impairment.In the
coronary arteries atherosclerosis can cause angina (chestpain), MI, and sudden death; in the
cerebral arteries it causesstrokes and transient ischemic attacks; and in the
peripheralcirculation it causes intermittent claudication, limb ischemia(inadequate blood
supply), and gangrene. Thusatherosclerosis is the underlying cause of many forms of
CVD.Dyslipidaemia refers to a blood lipid profile that increases therisk of developing
atherosclerosis. Three important biochemicalmeasurements in ASCVD include lipoproteins,
total cholesterol,and triglycerides. Cholesterol is delivered into cell walls bylow-density
lipoprotein (LDL), especially smaller particles. Toattract and stimulate the macrophages, the
cholesterol must bereleased from the LDL particles and oxidized, a key step in theongoing
inflammatory process. Additionally, macrophages mustmove excess cholesterol quickly into
high-density lipoprotein(HDL) particles to avoid becoming foam cells and dying.
Thetypical dyslipidaemia condition is one in which LDL levels areelevated (hyperlipidaemia)
and HDL levels are low.

ANGINA PECTORIS
Angina pectoris is a type of IHD characterized by paroxysmal and usually recurrent attacks of
substernal or precordial chest discomfort, described as constricting, crushing, squeezing,
choking, or knifelike pain. The pain may radiate down the left arm or to the left jaw (called as
referred pain).
The cause is usually insufficient coronary blood flow. The insufficient flow results in a
decreased oxygen supply to meet an increased myocardial demand for oxygen in response to
physical exertion or emotional stress
1. Physical Exertion: Isometric exercise of the arms (e.g., raking, lifting heavy objects, snow
shovelling) can cause exertion angina
2. Temperature Extremes: Blood vessels constrict in response to a cold stimulus. Blood
vessels dilate and blood pools in the skin in response to a hot stimulus.
3. Strong Emotions: Stimulate the sympathetic nervous system, activating the stress response.
4. Consumption of Heavy Meal: During the digestive process, blood is diverted to the GI
system, reducing blood flow in the coronary arteries.
5. Tobacco Use, Environmental Tobacco Smoke: Nicotine stimulates catecholamine release,
causing vasoconstriction
6. Sexual Activity: Increases the cardiac workload and sympathetic stimulation.
7. Stimulants (e.g., cocaine, amphetamines): Increase HR and subsequent myocardial oxygen
demand
Angina pectoris is not a disease. It is a symptom of coronary artery disease. Ischemia results
from a lack of oxygen and blood flow to the heart muscle.
Angina pectoris is due to inadequate perfusion and is caused by transient (15 seconds to 15
minutes) myocardial ischemia that falls short of inducing the cellular necrosis that defines
infarction i.e. duration and severity is not sufficient for infarction
There are three types of angina pectoris:
Stable Angina/ Typical Angina:
 It is the most common form of angina. It is caused by atherosclerotic disease with
usually ≥70% to 75% narrowing of lumen. This reduction (due to ≥ 70% stenosis) of
blood flow in coronary vessels makes the heart vulnerable, so whenever there is
increased demand, e.g. physical activity, emotional excitement, or any other cause of
increased cardiac workload, there is angina pain.
 The chest pain is episodic and associated with exertion or some other form of stress.
Is usually relieved by rest (thereby decreasing demand) or with a strong vasodilator
like nitro-glycerine.
Unstable or Crescendo Angina:
 It is an unstable and progressive condition.
 Pain occurs with progressively increasing frequency, and is precipitated with
progressively less exertion, even at rest, and tends to be of more prolonged duration.
 It is induced by disruption or rupture of an atheroma plaque with superimposed partial
thrombosis. Unstable angina is often the precursor of subsequent acute MI. Thus also
called as preinfarction angina.
Prinzmetal’s Variant Angina:
 Is an uncommon pattern of episodic angina that occurs at rest and is due to coronary
artery spasm. Prinzmetal angina generally responds promptly to vasodilators, such as
nitro-glycerine and calcium channel blockers. Not related to atherosclerotic disease.
The etiology is not clear.

Myocardial infraction
Myo means muscle, “Cardiac” heart, infarction means “death of tissues due to lack of blood
supply”It is also called heart attack. It occurs when coronary arteries become blocked and the
part of myocardial muscles become dead due to prolonged lack of oxygen supply to the
muscle cells.
Coronary artery cannot supply enough blood to the heart in response to the demand due to
CAD
 Within 10 seconds myocardial cells experience ischemia
 Ischemic cells cannot get enough oxygen or glucose
 Ischemic myocardial cells may have decreased electrical & muscular function
 Cells convert to anaerobic metabolism.
 Cells produce lactic acid as waste
 Pain develops from lactic acid accumulation
 Pt feels anginal symptoms until receiving demand increase oxygen requirements of
myocardial cells
Pathophysiology:
We all know that heart attack i.e. myocardial infarction is not the beginning but a last stage
representing acute clinical manifestation of CHD. Several clinical trials and autopsy studies
have indicated that the process of developing atherosclerotic lesions can begin as early as
during infancy and that it may take several decades for the lesions to develop into fatty
streaks and fibrous plaques that ultimately cause stenosis. (Complete blockage) of the
arteries. Diffuse intimal thickening during infancy which is considered to be a normal
physiological and not a pathological process can result in the initialization of early clinical
manifestations which may appear in the smooth muscle cell layer between the endothelium
and the internal elastic lamina. These lesions may progress and develop into fatty streaks to
reach their maximum extent in the aortas over a period of two decades among individuals
having elevated cholesterol and/or triglyceride levels. There is also focal proliferatio11 of
smooth muscle cells which are termed as gelatinous lesions because they have a low lipid but
high water content. Some of these lesions may become large and develop a greyish opaque
centre while remaining soft and translucent around the edges. These are referred to as the
transitional lesions. These lesions at times develop a fibrous cap with atheromatous lipids in
the centre and are known as fibrous plaques. Such fibrous plaques may coalesce together
resulting in blockage of the arteries and hence reduced flow of blood to the tissues. The
irritating presence of plaques may cause injury to the intima of the arteries which may result
in thrombosis. Myocardial infarction/cerebral stroke is the ultimate result of stenosis in the
arteries.
The risk factors of myocardial infarction are divided in two groups.
Non-modifiable:
 Increasing age.
 Male sex.
 Family history of HTN, DM, IHD
 Genetic abnormalities.
Modifiable:
 Dietary habit.
 Physical Inactivity.
 Obesity
 Alcohol and Smoking.
 Hypertension.
 Diabetes mellitus.
 Hypercholesterolemia.

Symptoms:
 Chest pain occurs suddenly, severe immobilizing chest pain that not relieved by rest,
position change, and medications.
 Increased jugular venous distention
  BP may be elevated because of sympathetic stimulation or decreased BP because of
decreased contractility, development if cariogenic shock
 Decrease pulse rate
 ST- segment and T-wave changes, ECG may show tachycardia, bradycardia, or
dysrhythmias.
 Increased jugular venous distention and ST- segment and t-wave changes in ECG
 Shortness of breath (SOB)
 Dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion.
 Pulmonary edema
 Nausea and vomiting
 Genitourinary or oliguria: Decreased urinary output may indicate cariogenic Shock
 Skin: Cool, clammy, diaphoretic, and pale appearance on skin.
 Neurologic symptoms: Anxiety, restlessness, and light headiness
 Psychological: Fear with feeling of impending doom or patient may deny that
anything is wrong.
Complications:
 Dysrhythmias (the most common complications after an MI in 80% of MI cases).
 Acute pulmonary edema
 Heart failure
 Cariogenic shock
 Papillary muscle dysfunction
 Pericarditis and cardiac tamponed