2. Systemic and local blood pressure must be tightly
regulated.
Although hypertension is a common health problem, it
typically remains asymptomatic until late in its course.
3. Hypertension contributes to the pathogenesis of
coronary heart disease and cerebrovascular
accidents, cause cardiac hypertrophy and heart
failure (hypertensive heart disease), aortic
dissection, and renal failure.
4. The mechanisms of hypertension in the vast
majority of people remain unknown; referred to as
"essential hypertension".
5. A sustained diastolic pressure greater than 90 mm
Hg, or a sustained systolic pressure in excess of
140 mm Hg, constitutes hypertension; systolic
blood pressure is more important than diastolic
blood pressure in determining cardiovascular risk.
6. Accurate Blood Pressure Measurement
The equipment should be regularly inspected and validated.
The operator should be trained and regularly retrained.
The patient must be properly prepared and positioned and
seated quietly for at least 5 minutes in a chair.
The auscultatory method should be used.
Caffeine, exercise, and smoking should be avoided for at
least 30 minutes before BP measurement.
An appropriately sized cuff should be used.
7. 25% of individuals in the general population are
hypertensive.
The prevalence and vulnerability to complications
increase with age.
They are also higher in African .
8. Worldwide prevalence estimates for HTN may be as
much as 1 billion.
7.1 million deaths per year may be attributable to
hypertension.
9. Regulation of Blood Pressure
Blood pressure is a complex trait involving the
interaction of multiple genetic and environmental
factors that influence two hemodynamic variables:
cardiac output
peripheral vascular resistance
10. Cardiac output is affected by blood volume which
is strongly dependent on sodium concentrations.
Peripheral resistance is regulated predominantly
at the level of the arterioles and is influenced by
neural and hormonal inputs.
11. Normal vascular tone reflects an interplay
between circulating factors that induce
vasoconstriction (e.g., angiotensin II and
catecholamines) and vasodilation (e.g., kinins,
prostaglandins, and nitric oxide)
12. Resistance vessels also exhibit autoregulation.
Other local factors such as pH and hypoxia,
neural interactions (α- and β-adrenergic systems),
are also involved.
13. The kidneys (primarily) and adrenals (secondarily)
are central players in blood pressure regulation;
they interact with each other to modify vessel tone
and blood volume, as follows;
renin-angiotensin - aldosterone system
prostaglandins and nitric oxide
14. Atrial natriuretic peptide, secreted by heart atria in
response to volume expansion (e.g., in heart
failure) inhibits sodium reabsorption in distal
tubules and causes global vasodilation.
15. Pathogenesis of Hypertension
Ninety percent to 95% of hypertension is
idiopathic (essential hypertension), which is
compatible with long life.
Most of the remainder of "benign hypertension" is
secondary hypertension.
16. Classification
Essential vs secondary HT
Benign vs malignant HT
• Essential HT
90 - 95% of cases.
Pathogenetic mechanisms multifactorial and poorly
understood.
• Secondary HT
5 - 10% of cases.
Hypertension due to a recognisable disease.
17. About 5% of hypertensive persons show a rapidly
rising blood pressure that if untreated leads to
death within 1 or 2 years.
Termed accelerated or malignant hypertension.
18. The clinical syndrome is characterized by;
severe hypertension (diastolic pressure over
120mmHg)
renal failure
retinal hemorrhages and exudates, with or
without papilledema.
19. Benign HT
- moderate increase in blood pressure.
- long clinical course.
- little clinical effects in early stages.
Malignant HT
- diastolic pressure > 130 mm Hg
- severe impact on cardiovascular system,
kidneys and central nervous system.
20. Malignant HT:
- May arise in previously normotensive individuals,
but
more commonly as a complication of benign HT.
- Relatively uncommon (1-5% of hypertensive
patients).
- Aggressive treatment is required.
21. Hypertensive Urgencies
Severe elevated BP in the upper range of
stage II hypertension.
Without progressive end-organ dysfunction.
Examples: Highly elevated BP without severe
headache, shortness of breath or chest pain.
Usually due to under-controlled HTN
22. Hypertensive Emergencies
Severely elevated BP (>180/120mmHg).
With progressive target organ dysfunction.
Require emergent lowering of BP.
Examples: Severely elevated BP with:
Hypertensive encephalopathy
Acute left ventricular failure with pulmonary edema
Acute MI or unstable angina pectoris
Dissecting aortic aneurysm
28. Secondary HTN-Clues in Medical
History
Onset: at age < 30 yrs ( Fibromuscular dysplasia) or
> 55 (athelosclerotic renal artery stenosis), sudden
onset (thrombus or cholesterol embolism).
Severity: Grade II, unresponsive to treatment.
Episodic, headache and chest pain/palpitation
(pheochromocytoma, thyroid dysfunction).
Morbid obesity with history of snoring and daytime
sleepiness (sleep disorders)
29. Secondary HTN-clues on Exam
Pallor, edema, other signs of renal disease.
Abdominal bruit especially with a diastolic
component (renovascular)
Truncal obesity, purple striae, buffalo hump
(hypercortisolism)
31. Essential Hypertension
Both increased blood volume and increased
peripheral resistance contribute to the increased
pressure.
Essential hypertension results from an interplay
of multiple genetic and environmental factors
affecting cardiac output and/or peripheral
resistance.
32. Essential hypertension is associated with:
- peripheral vascular resistance
(pathogenesis poorly understood)
- Sodium and water retention
blood volume, cardiac output
33. Genetic variants in the renin-angiotensin system
may contribute to the known racial differences in
blood pressure regulation.
Environmental factors; stress, obesity, smoking,
physical inactivity, and heavy consumption of salt
34. Vascular Pathology in Hypertension
Hyaline Arteriolosclerosis. consists of a
homogeneous pink hyaline thickening of the walls
of arterioles with loss of underlying structural
detail and with narrowing of the lumen
35. Hyperplastic Arteriolosclerosis; associated with
"onion-skin," concentric, laminated thickening of
the walls of arterioles with luminal narrowing.
Characteristic of (but not limited to) malignant
hypertension.
In malignant hypertension, these hyperplastic
changes are accompanied by fibrinoid necrosis.
38. Cardiovascular
Heart
- Increased workload on left ventricle
Left ventricular hypertrophy
left ventricular failure.
- Greater thickness of left ventricle
decreased perfusion and ischaemia of
subendocardial region of myocardium.
40. Arteries
- Accelerated atherogenesis.
- risk of developing aortic dissecting aneurism.
Arterioles: Arteriolosclerosis
- Benign HT:
Deposition of eosinophilic (‘hyaline’) material in vessel
walls due to influx of plasma proteins.
- Malignant HT:
Thickening of intima.
Necrosis of vessel walls ('fibrinoid' necrosis) and
formation of micro-aneurisms (of Bouchard) in brain.
41. CNS
- Rupture of micro-aneurisms of small penetrating
arteries Intracerebral haemorrhage.
- Risk of cerebral infarction due to atherosclerosis
of circle of Willis.
- Acute malignant HT: ‘Hypertensive encephalopathy’
due to cerebral oedema (headache, nausea and vomiting,
visual disturbances, seizures and disturbances of
consciousness).
43. The Eyes
Retinopathy, retinal hemorrhages and
impaired vision.
Vitreous hemorrhage, retinal detachment
Neuropathy of the nerves leading to
extraoccular muscle paralysis and dysfunction
44. Patient Evaluation Objectives
(1) To assess lifestyle and identify other
cardiovascular risk factors or concomitant disorders
that may affect prognosis and guide treatment
(2) To reveal identifiable causes of high BP
(3) To assess the presence or absence of target
organ damage and CVD
45. Cardiovascular Risk factors
Hypertension
Cigarette smoking
Obesity (body mass index ≥30 kg/m2)
Physical inactivity
Dyslipidemia
Diabetes mellitus
Microalbuminuria or estimated GFR <60 mL/min
Age (older than 55 for men, 65 for women)
Family history of premature cardiovascular disease (men
under age 55 or women under age 65)