Cardiovascular Conditions

Hypertension
Dr. Anmar AL-TAIE

Introduction
 Hypertension (high blood pressure BP) can be defined as a systolic BP ≥140
mmHg and /or diastolic BP ≥ 90mmHg.
 It is an important risk factor for the future development of cardiovascular diseases
(CVD).
 The mean blood pressure is the product of cardiac output and total peripheral
resistance.
 In most hypertensive individuals, cardiac output is not increased, and high blood
pressure arises as a result of increased total peripheral resistance caused by
constriction of small arterioles.

Complications of Hypertension
Epidemiology
 Hypertension is a condition of older individuals.
 Under the age of 75 years old, men are at greater risk than women.
 While diastolic pressure peaks at age 50 years old, systolic pressure continues to
increase with advancing age, making isolated systolic hypertension a common
feature of old age.
 Hypertension is more common in black people of African Caribbean origin, who
are also at particular risk of stroke and renal failure.

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Types of hypertension
1. Essential hypertension: unknown aetiology and may be of genetic factors.
2. Secondary hypertension: 5–10% of cases to some other disease process.

Hypertension Classification
The NICE (2011) guidance classifies hypertension as follows:
 Stage 1 hypertension: Clinic blood pressure is 140/90 mmHg or higher.
 Stage 2 hypertension: Clinic blood pressure is 160/100 mmHg or higher.
 Severe hypertension: Clinic systolic blood pressure is 180 mmHg or higher or
clinic diastolic blood pressure is 110 mmHg or higher.
Contributing factors
 Obesity, excess alcohol or salt intake and lack of exercise.
 Use of drugs, including OTC medications such as cold and flu remedies.
 Smoking, diabetes, and hyperlipidaemia.
Clinical presentation
 Hypertension is an incidental finding when subjects present for screening or with
unrelated conditions.
 Severe cases may present with headache, visual disturbances, or evidence of
target organ damage (stroke, ischemic heart disease or renal failure).

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Malignant (accelerated) hypertension
 It is a medical emergency characterized by greatly elevated BP (>220/120 mmHg)
associated with evidence of ongoing small vessel damage.
 It requires hospital admission and rapid control of BP over 12–24 h towards
normal levels.
 The clinical features are confusion, headache, visual loss, seizures and coma
 It presents on:
1. Fundoscopy as papilledema, hemorrhages and/or exudates.
2. Renal damage as hematuria, proteinuria and impaired renal function.
3. Hypertensive encephalopathy, which is caused by small vessel changes in the
cerebral circulation associated with cerebral edema.
4. Brain imaging (MRI) demonstrates extensive white matter changes.
Evidence of end-organ damage
 Examination of the optic fundi to detect retinal changes.
 ECG to detect left ventricular hypertrophy or subclinical ischemic heart disease.
 Renal function and urinary for microalbuminutria (an indicator of a higher risk of
future end-stage renal disease and overall vascular risk).
Diagnosis of hypertension
 Annual measurement with high normal (130–139 mmHg systolic or 85–89 mmHg
diastolic).
 BP should be measured using a well-maintained sphygmomanometer of validated
accuracy.
 Blood pressure should initially be measured in both arms, and if there is a
difference of more than 20 mmHg sustained after repeat measurement, the arm
with the highest value should be used for subsequent monitoring readings.
 Differences of more than 15 mmHg between arms may indicate risk of underlying
vascular disease and an increased risk of all-cause and cardiovascular (CV)
mortality.
 The subject should be relaxed, and at least at the first presentation, blood pressure
should be measured in both the sitting and the standing positions to identify any
postural changes.

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  An appropriate-sized cuff should be used because one that is too small will result
in an overestimation of the patient’s blood pressure.
 The arm should be supported level with the heart.

Treatment

Target clinic blood pressures in the presence of comorbidities

Non-Pharmacological Approaches
 General health education.
 Weight loss results in reduction in BP of about 2.5/1.5 mmHg/kg
(Diet: fruit, vegetables, and low-fat dairy, fish, low-fat poultry, and whole grains
while minimizing red meat, confectionary and sweetened drinks).
 Reduce salt intake. A daily sodium intake of <100 mmol (i.e., 6 g sodium chloride
or 2.4 g elemental sodium).
 Regular aerobic exercise at least 3 times a week for at least 30 min.
 Alcohol intake should be restricted to two (females) or three (males) units per
day.
 Smoking quitting or reduce cigarette consumption.

A. Pharmacological Approaches
1. Adrenoreceptor antagonists
 They reduce:
1. Cardiac output in the short term and during exercise.

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2. Renin secretion by antagonising β-receptors in the juxtaglomerular apparatus.
 Cardioselective (β1-selectiveblockers are not entirely free of these adverse effects).
 Thiazide + a β-blocker should be avoided, if possible, in diabetes (e.g., obese,
strong family history of diabetes, South Asian origin)
 β-Blockers are suitable for younger hypertensive with coronary heart disease.
 They are effective in suppressing atrial fibrillation.

2. Diuretics
 Their diuretic action is achieved by blockade of distal renal tubular sodium
reabsorption.
 They reduce BP by reducing circulating blood volume.
 The longer term, they reduce total peripheral resistance, suggesting a direct
vasodilator action.
 Most BP lowering effect occurs with very low doses of thiazide diuretics.
 Loop diuretics are no more effective at lowering BP than thiazides.
 They are effective in significant impaired renal function, or the patient is
receiving agents that inhibit the renin–angiotensin system.
 They are a suitable choice if heart failure is present.
 Spironolactone (a potassium sparing diuretic) is not suitable for 1st -line therapy
but important treatment for resistant hypertension and in hyperaldosteronism.
3. Renin-angiotensin-aldosterone antagonists
 ACE inhibitors block the conversion of angiotensin I to angiotensin II.
 ARBs block the action of angiotensin II at the angiotensin II type 21 receptor.
 Since angiotensin II is a vasoconstrictor and stimulates the release of aldosterone,
antagonism results in vasodilation and potassium retention as well as inhibition of
salt and water retention.
 ACE inhibitors also block kininase production and, thus, prevent the breakdown
of bradykinin. This appears to be important in the aetiology of ACE inhibitor
induced cough, which is a troublesome side effect in 10–20% of users.

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 ARBs do not inhibit kininase and are an appropriate choice for patients who are
intolerant of ACE inhibitors because of cough.

4. Calcium channel blockers

 These agents block slow calcium channels in the peripheral blood vessels and/or
the heart.
 The dihydropyridine group work almost exclusively on l-type calcium channels in
the peripheral arterioles and reduce blood pressure by reducing total peripheral
resistance.
 The non-dihydropyridine group, verapamil, and diltiazem, are primarily on the
heart, reducing heart rate and cardiac output.
 Long acting dihydropyridines are preferred because:
1. They are more convenient for patients
2. Avoid the large fluctuations in plasma drug concentrations that may be associated
with adverse effects.
 They are an appropriate choice as add-in therapy for patients inadequately
controlled using other agents.

5. Centrally acting agents

 Methyldopa and moxonidine inhibit sympathetic outflow from the brain, resulting
in a reduction in total peripheral resistance.
 Methyldopa is not widely used because it has pronounced central adverse effects,
including tiredness and depression.
 It is mainly used in pregnancy since it does not cause foetal abnormalities.
 It is also occasionally used in patients with resistant hypertension.
 Moxonidine is a newer agent that blocks central imidazoline and α2-
adrenoceptors found within the medulla oblongata of the brain.

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Drug selection
 Drugs should be chosen based on efficacy, safety, convenience to the patient and
cost.
 Combinations of low doses of antihypertensive drugs are better tolerated than
single drugs taken in high dose.

Summary of Antihypertensive Drug Treatment

Special patient groups
A. Race
 African Caribbean people have reduced plasma renin activity and, as a result,
ACE inhibitors and ARBs are less effective.
 Treatment with diuretic and calcium channel blockers, while β-blockers appear
less effective, at least when used as monotherapy.
B. Elderly
 They have a high prevalence of hypertension, with over 70% having blood
pressures greater than 140/90 mmHg and at high absolute risk of CVD
 They are at risk of drug adverse effects as postural hypotension
 Calcium channel blockers and low-dose thiazide diuretics are safe and effective.
 β-Blockers are less effective.

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C. Diabetes
 Target blood pressure should be less than 135/85 mmHg or less than 130/80
mmHg if there is albuminuria or two or more signs of metabolic syndrome
present.
 The presence of hypertension indicates the presence of diabetic nephropathy.
 ACE inhibition reduce BP and slow the rate of decline in renal function.
 ACE inhibitors should be first-line therapy.
 Thiazides, β-blockers, calcium channel blockers and α-blockers are all suitable as
add-on treatments to ACE inhibitors.
 If further antihypertensive therapy is required, ACEI plus CCB with the addition
of a diuretic if necessary is endorsed.
D. Renal disease
 Good BP control slows the progression of renal dysfunction.
 Treatment is with ACE inhibitors since they reduce:
1. The incidence of end-stage renal failure
2. Reduce 24-h protein loss and should be used in patients with 24-h protein
excretion of >3 g or rapidly progressive renal dysfunction.
 Salt restriction is important in managing hypertension in renal disease.
 Thiazide diuretics are ineffective and loop diuretics should be used when a
diuretic is needed.
E. Stroke
 Hypertension is the most important risk factor for stroke in patients with or
without previous stroke. Using of Perindopril plus indapamide combination
F. Pregnancy
 An increased BP before 20 weeks gestation indicates pre-existing chronic
hypertension.
 Hypertension diagnosed after 20 weeks gestation may indicate gestational
hypertension.
 Patients with elevated BP in pregnancy are at increased risk of pre-eclampsia and
intrauterine growth retardation.
 Frequent checks of BP, urinalysis, and foetal growth.
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 Pre-eclampsia is diagnosed when the BP increases by 30/15 mmHg from
measurements obtained in early pregnancy or if the diastolic blood pressure
exceeds 110 mmHg and proteinuria is present.
 BP should be treated if it exceeds 150–160/100–110 mmHg.
 Methyldopa is the drug of choice.
 Calcium channel blockers, hydralazine and labetalol are also used.
 β-Blockers (atenolol), are used less often as they are associated with intrauterine
growth retardation.
 Diuretics reduce the incidence of pre-eclampsia but decrease maternal blood
volume.
 ACE inhibitors and ARBs are contraindicated, as they are associated with
oligohydramnios, renal failure, and intrauterine death.
G. Oral contraceptives
 Combined oral contraceptives results in an increase of 5/3 mmHg in blood
pressure. Progesterone-only preparations do not cause hypertension.
Ancillary drug treatment
A. Aspirin
 Aspirin reduces CV events for 50 years patients and have either evidence of target
organ damage or a 10-year cardiovascular disease risk of >20%.
 Blood pressure should be controlled (<150/90 mmHg) before aspirin is instituted.
B. Lipid-lowering therapy
 Treatment with statins such as atorvastatin 10 mg is associated with reductions in
coronary heart disease and stroke. Statin, should be prescribed to patients under
80 years of age with a total cholesterol >3.5 mmol/L who either have pre-existing
vascular disease or a 10-year cardiovascular risk of >20%.

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 Summary of Antihypertensive Drugs and Common Therapeutic Problems

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