.

HYPERTENSION
Sustained high blood pressure is known as hypertension. Blood pressure 140/90, at least
two readings on separate occasion is considered hypertension.

Key points

Based on office BP, the global prevalence of hypertension was estimated to

be 1.13 billion in 2015.

The majority of subjects ( >95 %) have essential (primary)

hypertension

In about 5% of cases, cause of hypertension can be discovered

Secondary hypertension is more likely and investigations should be

performed to rule out secondary causes

In over 90% of cases no specific cause is found and the hypertension is known as
essential.Predisposing factors include:

• Genetic factors: children of hypertensive patients are more prone to develop

hypertension.
• Obesity, lack of exercise
• Heavy alcohol intake
• Excessive salt intake
• Cigarette smoking
• Polycythemia
• NSAIDs increase blood pressure about 5mmHg
• Low potassium intake
• Sympathetic over activity
Hypertension may be secondary. Symptomatic or secondary hypertension is not an independent
disease, and is accompanied by another disease.

There are several causes of secondary hypertension:

 renal disease(diabetic nephropathy, renovascular disease, glomerulonephritis,

vasculitides, chronic pyelonephritis, polycystic kidneys)
 endocrine disease – Cushing syndrome, Conn syndrome, phaeochromocytoma,
acromegaly glucocorticoid-remediable hypertension, hyperparathyroidism
 oral contraceptive pill
 eclampsia
 coarctation of the aorta
Pathophysiology
In its early stages hypertension is thought to be characterised by increased cardiac output with
normal peripheral resistance. As hypertension progresses peripheral resistance increases and
cardiac output returns to normal.

Classification
Table 5.1 Blood pressure (BP) classification

Category SBP (mmHg) DBP (mmHg)

Optimal BP <120 <80
Normal BP <130 <85
High–normal BP 130-139 85-89
Grade 1 hypertension 140-159 90-99
Grade 2 hypertension 160-179 100-109
Grade 3 hypertension >180 110>

Clinical presentations
Hypertension is usually asymptomatic, although a patient will occasionally complain of
headache. Visual disturbance occur in severe or accelerated hypertension.

It can be clinical signs of an underlying cause (radiofemoral delay or weak femoral pulses, renal
enlargement or bruit, or cushingoid features) and evidence of end-organ damage (heart failure,
retinopathy, aortic aneurysm, carotid or femoral bruit) should be sought.

Ten year cardiovascular risk categories (Systematic COronary Risk Evaluation system)
People with any of the following:
Very high Documented CVD, either clinical or unequivocal on imaging.
risk • Clinical CVD includes acute myocardial infarction, acute coronary
syndrome, coronary or other arterial revascularization, stroke, TIA, aortic
aneurysm, and PAD
• Unequivocal documented CVD on imaging includes significant plaque (i.e.
>_50% stenosis) on angiography or ultrasound; it does not include increase in
carotid intima-media thickness
• Diabetes mellitus with target organ damage, e.g. proteinuria or a with a
major risk factor such as grade 3 hypertension or hypercholesterolaemia
• Severe CKD (eGFR _10%).
High risk People with any of the following:
• Marked elevation of a single risk factor, particularly cholesterol >8 mmol/L
(>310 mg/dL), e.g. familial hypercholesterolaemia or grade 3 hypertension (BP
>_180/110 mmHg)
• Most other people with diabetes mellitus (except some young people with type
1 diabetes mellitus and without major risk factors, who may be at moderate-
risk)

Hypertensive LVH

Moderate CKD eGFR 30-59 mL/min/1.73 m2 )

A calculated 10 year SCORE of 5-10%

Moderate People with:
risk • A calculated 10 year SCORE of >1 to< 5%
Grade 2 hypertension
• Many middle-aged people belong to this category
Low risk People with:
• A calculated 10 year SCORE of <1%
BP = blood pressure; CKD = chronic kidney disease; CVD = cardiovascular disease; eGFR =
estimated glomerular filtration rate; LVH = left ventricular hypertrophy; TIA = transient
ischaemic attack; PAD = peripheral artery disease; SCORE = Systematic Coronary Risk
Evaluation.

Examination
The blood pressure ismeasured at rest. If high (systolic > 140 mmHg, diastolic > 90 mmHg),
check in both arms, and unless very severe recheck on at least three separate occasions before
considering treatment. For exclude secondary hypertension requires following examination:

 Observe the face for evidence of Cushing syndrome – usually caused by corticosteroid
administration.
 Examine for aortic coarctation – feel both radials and measure blood pressure in both
arms. Look for radial–femoral delay, weak femoral pulses, bruits of the coarctation and
scapular anastomoses which may produce visible pulsations.
 Listen for an epigastric or paraumbilical bruit of renal artery stenosis.

Investigation

• ECG
 • fasting glucose
• full lipid profile (total, HDL and LDL cholesterol and triglycerides)
• urea and electrolytes (U&E)
• urinalysis for blood and protein.

If secondary hypertension is suspected: urinary cortisol, plasma renin-aldosterone levels,

renal ultrasound, magnetic resonance angiography (MRA) of renal arteries, MAG3 renogram,
and 24-hour urinary catecholamines or vanillyl mandelic acid (VMA).

Severe hypertension
Malignant hypertension is diagnosed when severe hypertension (systolic blood pressure (SBP)
> 200 mmHg ±diastolic blood pressure (DBP) > 130 mmHg) with papilloedema.

Treatment
Management of patients with high blood pleasure requires lifestyle changes and pharmacologic
therapy.

Lifestyle changes including:

 Eating a heart-healthy diet with less salt

 Getting regular physical activity
 Maintaining a healthy weight or losing weight if you're overweight or obese
 Limiting the amount of alcohol you drink

Drug class:

Diuretics Thiazides
Hydrochlorothiazide 6.25–50 mg (1–2), Chlorthalidone 25–50 mg (1);Contraindications:
Diabetes, dyslipidemia, hyperuricemia, gout, hypokalemia
Loop diuretics
Furosemide 40–80 mg (2–3), Ethacrynic acid 50–100 mg (2–3);
Contraindications: Diabetes, dyslipidemia, hyperuricemia, gout, hypokalemia.
Aldosterone antagonists K+ retaining
Spironolactone 25–100 mg (1–2), Eplerenone50–100 mg (1–2), Amiloride5–10 mg (1–2)
Triamterene50–100 mg (1–2);
Contraindications: Renal failure, hyperkalemia

Beta blockers
Cardioselective: Atenolol 25–100 mg (1); Metoprolol 25–100 mg (1–2);
Nonselective:Propranolol 40–160 mg (2), Propranolol LA 60–180 (1);
Combined alpha/ beta: Labetalol 200–800 mg (2), Carvedilol, 12.5–50 mg (2);
Contraindications: Asthma, 2nd-3rd-degree heart block, sick-sinus syndrome.

Alpha antagonists
Selective: Prazosin 2–20 mg (2–3), Doxazosin 1–16 mg (1), Terazosin 1–10 mg (1–2);
Nonselective:Phenoxybenzamine 20–120 mg (2–3);
Sympatholytics Central
Clonidine 0.1–0.6 mg (2), Clonidine patch0.1–0.3 mg (1/week), Methyldopa250–1000 mg (2)
Reserpine0.05–0.25 mg (1), Guanfacine 0.5–2 mg (1);
ACE inhibitors
Captopril 25–200 mg (2), Lisinopril10–40 mg (1), Ramipril 2.5–20 mg (1–2);
Contraindications: Acute renal failure, bilateral renal artery stenosis, pregnancy, hyperkalemia

Angiotensin II antagonists
Losartan25–100 mg (1–2), Valsartan 80–320 mg (1), Candesartan 2–32 mg (1–2);
Contraindications:Renal failure, bilateral renal artery stenosis, pregnancy, hyperkalemia

Renin inhibitors
Aliskiren 150–300 mg (1);Contraindications: Pregnancy.
Calcium antagonists
Dihydropyridines: Nifedipine (long-acting)30–60 mg (1);
Nondihydropyridines:Verapamil (long-acting)120–360 mg (1–2); Diltiazem (long-acting)180-
420 mg (1);Contraindications:2nd- or 3rd-degree heart block
Direct vasodilators
Hydralazine 25–100 mg (2), Minoxidil 2.5–80 mg (1–2). Contraindications: Severe coronary
artery disease.

Diuretics Low-dose thiazide diuretics often areused as first-line agents alone or in

combination withother antihypertensive drugs. Thiazides inhibit the Na+Cl− pump in the
distal convoluted tubule and hencincrease sodium excretion. In the long term, they also
may act as vasodilators. Loop diuretics is the Na+-K+-2Cl− co transporter in the thick
ascending limb of the loop of Henle.Loop diuretics generally are reserved for hypertensive
patients with reduced glomerular filtration rates.

Blockers of the renin-angiotensin systemACEIs decrease the production of angiotensin II

increase bradykinin levels, and reduce sympathetic nervous system activity.ARBs provide
selective blockade of AT1 receptors, and the effect of angiotensin II on unblocked AT2
receptors may augment their hypotensive effect. Both classes of agents are effective
antihypertensive agents that may be used as monotherapy or in combination with
diuretics, calcium antagonistsand alpha blocking agents.

Aldosterone antagonists Spironolactone isa nonselective aldosterone antagonist that may

be used alone or in combination with a thiazide diuretic.

Beta Blockersβ-Adrenergic receptor blocker lower blood pressure by decreasing cardiac

output, due to a reduction of heart rate and contractility. Other proposed mechanisms by which
beta blockers lower blood pressure include a central nervous system effect and inhibition of
renin release. Beta blockers are particularly effective in hypertensive patients with tachycardia.

Adrenergic Blockers
Postsynaptic, selectiveα-adrenoreceptor antagonists lower blood pressure bydecreasing
peripheral vascular resistance. They are effective antihypertensive agents used either as
monotherapyor in combination with other agents. They are also effective in treating lower
urinary tract symptoms in men with prostatic hypertrophy.

Sympatholytic agents
Centrally acting α2 sympathetic agonists decrease peripheral resistance byinhibiting
sympathetic outflow. They may be particularly useful in patients with autonomic neuropathy.

Calcium channel blockers

Calcium antagonists reduce vascular resistance through L-channelblockade, which reduces
intracellular calcium andblunts vasoconstriction. This is a heterogeneous group of agents that
includes drugs in the following threeclasses: phenylalkylamines (verapamil),
benzothiazepines (diltiazem), and 1,4-dihydropyridines (nifedipinelike).

2. CORONARY ARTERY DISEASE (CAD)

Atherosclerosis
Atherosclerosis is a disease of the large and medium-sized arteries. The term
atherosclerosis is derived from Latin and means gruel-like (‘athero’) hardening
(‘sclerosis’) of the arteries.
Causes of atherosclerosis progressive build up of fatty plaques within the arterial wall,
which finally results in a significant reduction of the vessel lumen, impairing blood flow to
the distal tissues.
Alteration of normal endothelial cell function may allow deposition of macrophages, which form
foam cells and provoke proliferation of smooth-muscle cells and connective tissue. Cholesterol
crystals and other lipids accumulate at the base of plaques, which are covered by a fibrous cap.
Plaque activation and rupture leads to thrombosis and myocardial ischemia(acute coronary
syndrome).
Myocardial ischaemia is normally caused by atherosclerosis, but cardiac pain is also produced
by:
. aortic dissection
. paroxysmal tachycardias
. severe anaemia, cardiomyopathy, coronary artery
embolism and vasculitis – all rare causes.

Pathophysiology
The atherogenic process is characterized by:
• dysfunction of the endothelial lining of the vessel
• inflammation of the vascular wall
• build up of lipids, cholesterol, and inflammatory cells in the vessel wall
• accumulation of cellular debris within the intima and subintimal layers of the vessel.

Endothelial dysfunction
The initiating trigger of this disease process appears to be injury of arterial endothelial cells
from exposure to stimuli including:
• tobacco toxins
• oxidized low-density lipoprotein (LDL)
• advanced glycation end-products
• elevated homocysteine
• infectious agents.

Risk Factors for Atherosclerosis

Genetic abnormalities
Family history
Male gender
Increasing Age
Hardened (trans)unsaturated fat intake
High carbohydrate intake
Postmenopausal estrogen deficiency
Physical Inactivity
Obesity
C-reactive protein
Diabetes
Cigarette smoking
Hypertension
• Inflammation
• Hyperhomocystinemia
• Metabolic syndrome
• Lipoprotein
• Factors affecting hemostasis
• Stressful lifestyle

Screening and diagnosis

Stress Test
Coronary Angiography
Electro- cardiogram
Other test:
•Blood tests: used to evaluate kidney and thyroid function as well as to check cholesterol levels
and the presence of anemia.
•Chest X-ray: shows the size of the heart and whether there is fluid build up around the heart
and lungs.
•Echocardiogram: shows a graphic outline of the heart’s movement
•Ejection fraction (EF): determines how well the heart pumps with each beat.

Treatment

•Lifestyle changes
•Medications
•Angiography and stenting
•Bypass surgery

Dyslipidemia

Disorder of Lipid & Lipoprotein Metabolism, important modifiable risk factor for CAD

A common form of Dyslipidemia is characterized three lipid abnormalities: elevated

triglycerides, elevated LDL and reduced HDL cholesterol.

Causes
Primary:  Genetic Disorders
Secondary: diabetes, nephrotic syndrome, hypothyroidism, drug – induced, hypertension.
Physiology of lipids
Chylomicrons transport fats from the intestinal mucosa to the liver and In the liver, the
chylomicrons release triglycerides and some cholesterol and become low-density lipoproteins
(LDL). LDL then carries fat and cholesterol to the body’s cells. High-density lipoproteins (HDL)
carry fat and cholesterol back to the liver for excretion. When oxidized LDL cholesterol gets
high, atheroma formation in the walls of arteries occurs, which causes atherosclerosis. HDL
cholesterol is able to go and remove cholesterol from the atheroma.

Table …Goal of lipids

LDL HDL Total Serum triglycerides

cholesterol
<100-optimal <40 low <200 < 150 normal
desirable
100-129 near >60 high 200-239 150-199 borderline
optimal borderline
130-159 borderline >240 high 200-499 high
160-189 high >500 very high
>190 very high

Treatment of Hyperlipidemia

Exercise
Low-cholesterol diet
Lifestyle modification

3.ANGINA PECTORIS

The diagnosis of angina based on the clinical history. The chest pain or discomfort can be
typical and atypical. Typical chest pain is central/retrostenal and may radiate to the jaw and
arms and relieved (usually within minutes) with rest or glyceryl trinitrate. Occasionally, it
disappears with continued exertion (‘walking through the pain’). Typical angina has all three
features, atypical angina two out of the three, and non-anginal chest pain one or less of
these features.
Chest pain can range from mild ache to a most severe pain that provokes sweating and fear,
may be associated breathlessness.
Angina pectoris refers to the pain caused by myocardial ischaemia. Ischaemia is usually
caused by coronary stenosis due to atheroma but may be caused by tachycardia, anaemia,
aortic stenosis, LVH of other aetiologies, syndrome X (chest pain with normal coronary
arteries), and coronary artery spasm (Prinzmetal).

Table /// Canadian cardiovascular society

functional classification of angina
Class I No angina with ordinary activity. Angina with strenuous activity.
ClassII angina during ordinary activity e.g. walking up hills, walking rapidly upstairs,
with mild limitation activities
Class III angina with low levels of activity e.g. walking 5-100 yards on the flat, walking
one the flight of stairs with marked restriction activities
Class IV Angina at rest or with any level of exercise

Angina is often classified according to its temporal pattern and its relation to exertion because
this loosely reflects prognosis.

Stable angina
Angina is stable when it is not a new symptom and when there is no change in the
frequency or severity of attacks.

Unstable angina
Unstableangina refers to angina of recent onset (<24 h) or a deterioration in previous stable
angina with symptoms frequently occurring at rest, i.e. acutecoronary syndrome.

Refractory angina
Refractory angina refers to patients with severe coronary disease in whom
revascularization is not possible and angina is not controlled by medical therapy.
Variant (Prinzmetal’s)
Variant (Prinzmetal’s) angina refers to an angina that occurs without provocation,
usually at rest, as a result of coronary artery spasm. It occurs more frequently in
women.

Cardiac syndrome X
Cardiac syndrome X refers to those patients with a good history of angina, a positive
exercise test and angiographically normal coronary arteries.

Physical examination
There are usually no abnormal findings in angina, although occasionally a fourth heart sound
may be heard.
 • Measure the pulse rate. This may be slowed by inferior ischaemia due to
atrioventricular (AV) node ischaemia. A resting tachycardia, if present, usually
represents activation of the sympathetic nervous system but may be due to an arrhythmia
precipitated by ischaemia.
• BP measurement is essential to look for evidence of hypertension (predisposing to
atheroma), or hypotension (may reflect cardiac dysfunction or over-medication).
• Precordial examination should include palpation for LVH, cardiac enlargement, or
dyskinesis, and auscultation for added heart sounds (heart failure or acute ischaemia),
aortic stenosis or mitral regurgitation (due to papillary muscle dysfunction).
• Examine for signs of heart failure by listening for fine, late-inspiratory crepitations
at the lung bases, and looking for dependent pitting oedema (typically bilateral ankle
±leg oedema, but sacral oedema may be the only manifestation if the patient has been
recumbent for some time).
• Look for evidence of peripheral vascular disease by palpating for aortic aneurysm,
feeling the carotid and limb pulses, listening for carotid, renal or femoral artery
bruits, and assessing tissue integrity and capillary refill of the legs and feet.
Diagnosis and investigations for angina
Patients presenting with chest pain should have a 12-lead ECG performed to exclude
an acute coronary syndrome. In many patients the ECG is normal between attacks although
evidence of old myocardial infarction (e.g. pathological Q waves), left ventricular
hypertrophy or left bundle branch block may be present. During an attack, transient ST
depression, T wave inversion or other changes of the shape of the T wave may appear.
The diagnosis of stable angina can be made on clinical assessment alone OR by clinical
assessment combined with anatomical (cardiac catheterization or CT coronary angiography)
or functional imaging (SPECT, stress-echocardiography, stress-magnetic resonance imaging).

Differential diagnosis
The differential diagnosis of anginal chest pain is wide and includes:
• other upper GI problem (gastritis, peptic ulcer, pancreatitis, cholecystitis)
• pericarditis
• aortic dissection
• mitral valve prolapse
• coronary emboli (LV mural thrombus, atrial myxoma)
• anxiety and hyperventilation
• musculoskeletal chest wall pain
• cervical or thoracic root pain
• pneumothorax, pneumonia, or pulmonary embolus
• oesophageal problem (inflammation/spasm)

Management
Lifestyle :Stop smoking. Encourage daily aerobic exercise within limits of exercise capacity.
Look at occupational needs and advise adjustment if symptom level not compatible. Advise
healthy diet, collaborating with dieticians if required.
Patients should be informed as to the nature of their condition and reassured that the
prognosis is good (annual mortality <2%). Underlying problems, such as anemia or
hyperthyroidism, should be treated. Management of coexistent conditions, such as diabetes
and hypertension, should be optimized.
Antiplatelet:Aspirin (75 mg/24 h) In all cases unless active peptic ulcer disease or bleeding
diathesis. Those with past peptic ulcer disease may take a gastroprotective agent such asa H 2
antagonist or proton pump inhibitor. Side effects – gastrointestinal bleeding.
Indicated if treating other condition, e.g. hypertension, heart failure, chronic kidney disease.

Antianginals :B-blockers: 1st line (e.g.atenolol 25–100 mg od or metoprolol 25–50 mg tds).

Start on suspicion of IHD. Inhibit beta-adrenoceptors, reduce heart rate and BP, reduce
myocardial oxygen consumption. Side-effects – fatigue, peripheral vasoconstriction (cold
peripheries), erectile dysfunction,
Bronchospasm.
Calcium antagonists :(e.g. amlodipine5–10 mg od or diltiazem MR 90–180 mg bd) if B-
blocker contraindicated. Inhibit calcium channels in myocardium, cardiac conductive tissue and
vascular smooth muscle.
Diltiazem and verapamil – contraindicated in severe bradycardia, left ventricular failure with
pulmonary congestion, second- or third-degree AV block.
Side-effects – constipation (verapamil), ankle oedema (amlodipine, diltiazem), reflex
tachycardia (amlodipine)
Vasodilator - Nitrates: (e.g. GTN spray) Used for control of breakthrough angina. Long-acting
nitrates (e.g. isosorbide mononitrate MR 60–120 mg od) are a useful addition to B-blockers for
prevention of attacks. Prophylaxis and treatment of angina – rapid onset Repeat after 5 min if
symptomatic.
Side-effects – headache and flushing. Contraindicated with phosphodiesterase type-5 inhibitors
Statins : Reduce mortality by approximately one-third in all risk groups. However, the
underlying risk of events must be taken into account when considering starting the drug because
absolute risk reduction in young patients with low-risk IHD may be very small, with a possible
harm of myositis, hepatic failure, and reduced compliance with other medications.