Hypertension is a major global health issue, contributing to millions of deaths and increasing the risk of cardiovascular diseases. The condition can be classified into essential and secondary hypertension, with various genetic, environmental, and lifestyle factors influencing its development. Effective management includes lifestyle changes and pharmacotherapy, while complications may affect multiple organs, necessitating careful monitoring and treatment.

1. HYPERTENSION
Dr. Samee M Adnan
MD Resident (Phase A), Neurology
CMCH

2. FACTS & FIGURES
 HTN is one of the leading causes of the global
burden of disease. (WHO identified)
 Approximately 9.4 million deaths (13 –15% of the
total) and > 1 billion disability-adjusted life years
worldwide.
 Doubles the risk of cardiovascular diseases
 Often is associated with additional cardiovascular
disease risk factors.
 Antihypertensive therapy clearly reduces the risks
of cardiovascular and renal disease
 But large segments of the hypertensive population
are either untreated or inadequately treated.

3. FACTORS INFLUENCING BLOOD
PRESSURE

4. DEFINITION
Hypertension is a
level of blood
pressure which
places an
individual at
increased risk of
cardiovascular
events and,
when treated,
results in more
benefit than
harm.

5. CLASSIFICATION
 Essential hypertension is a heterogeneous genetic
and environmental condition. It accounts almost for
80-95% of cases.
 Secondary hypertension implies increased BP is
secondary to an underlying disorder and accounts
for 5-20% of cases.

6. MECHANISM OF HTN
Intravascular Volume
 Sodium is predominantly an extracellular ion -
primary determinant of the extracellular fluid
volume
 When NaCl intake exceeds the capacity of the
kidney to excrete sodium, vascular volume initially
expands and cardiac output increases.
 In individuals with an impaired capacity to excrete
sodium, greater increases on arterial pressure is
needed to achieve natriuresis & sodium balance.

7. CONT.
Autonomic Nervous System
 Adrenergic reflexes - short term.
 Adrenergic function, in concert with hormonal and
volume related factors- long-term regulation.
 Chronic activation may have a role in the genesis of
long-term increase in BP in those with a genetic
predisposition.
 SNS activation causes:
 increase in stroke volume (via beta 1 receptors).
 increase in heart rate (via beta 1 receptors).
 increase in systemic vascular resistance (via alpha 1
receptors).
 Activation of the RAS (via beta 1 receptor-mediated renin
release)

8. CONT.
Renin-Angiotensin-
Aldosterone
Renin release is mediated
by:
 Decreased afferent
arteriolar (i.e. renal
perfusion) pressure of
any cause.
 Sympathetic nervous
system activation
(through beta 1
receptors).
 Decreased Na+ delivery
to the distal tubule
(sensed by the macula
densa).

9. CONT.
Actions of angiotensin II
 Arteriolar vasoconstriction (and venular constriction
to a lesser extent).
 Efferent renal arteriolar vasoconstriction.
 Aldosterone secretion.
 Adrenaline (epinephrine) release.
 Smooth muscle hypertrophy.
 Increased reabsorption of sodium in PCT.
 Inhibits renin release (negative feedback loop).
 Renal mesangial cell growth and matrix expansion.
 Myocardial growth and matrix expansion.
 Stimulates thirst and ADH release.

10. CONT.
Vasucular mechanism
 Structural, mechanical, or functional changes may
reduce the lumen diameter of small arteries and
arterioles .
 Hypertrophic (increased cell size, and increased
deposition of intercellular matrix) or eutrophic
vascular remodeling results in decreased lumen
size and, hence, increased peripheral resistance
Immune mechanism, inflammation & oxidative
stress
 Inflammation, vascular stretch, angiotensin II, and
salt have all been shown to result in the generation
of reactive oxygen species (ROS), which modify T
cell function and further enhance inflammation.
 ROS also attenuate the effects of endogenous
small-molecule vasodilators.

11. ESSENTIAL HYPERTENSION
Primary hypertension tends to be familial and is likely
to be the consequence of an interaction between
environmental and genetic factors.
Etiology-
 Environmental factors
 Genetic factors
 Fetal factors
 Humoral mechanisms
 Insulin resistance - Metabolic syndrome

12. CONT.
Environmental factors
 –Obesity
 Fat people have higher blood pressures than thin people.
 Sleep disordered breathing often seen with obesity may be an
additional risk factor
 Alcohol intake
 Close relationship between the consumption of alcohol and
blood pressure level.
 But small amounts of alcohol seem to be beneficial
 Sodium intake
 Directly proportional
 Some evidence that a high potassium diet can protect
against the effects of a high sodium intake
 Stress
 Chronic stress – uncertain
 Acute pain or stress can raise blood pressure

13. CONT.
Genetic factors
 Tends to run in families, by shared environmental
influences.
 Still largely unidentified genetic component.
Fetal factors
Low birth weight: May be due to fetal adaptation to
intrauterine undernutrition with
 long-term changes in blood vessel structure
 Or the function of crucial hormonal systems.

14. CONT.
Humoral mechanisms
 Autonomic nervous system, renin angiotensin system,
natriuretic peptide and kallikrein-kinin system - short-
term changes in blood pressure
 But no convincing evidence - directly involved in the
maintenance of hypertension
Insulin resistance - Metabolic syndrome
 Hyperinsulinaemia, glucose intolerance, reduced levels
of HDL cholesterol, hypertriglyceridaemia and central
obesity with with hypertension
 Association between diabetes and hypertension has
long been recognized

15. SECONDARY HYPERTENSION

16. HIGH INDEX OF SUSPICION OF
SECONDARY HYPERTENSION

17. BLOOD PRESSURE MEASUREMENT
 Blood pressure should be measured after the
patient has emptied their bladder and has been
seated for five minutes with back supported and
legs resting on the ground (not crossed).
 Arm used for measurement should rest on a table,
at heart level.
 Use a sphygmomanometer/stethoscope or
automated electronic device (preferred) with the
correct size arm cuff.
 Take two readings one to two minutes apart, and
average the readings (preferred).
 Measure blood pressure in both arms at initial
evaluation. Use the higher reading for
measurements thereafter.

18. COMPLICATIONS OF HYPERTENSION
The primary target organs of HTN include-
 Heart.
 Vascular system.
 Brain.
 Kidney.
 Retina.

19. COMPLICATIONS: HEART
 Left ventricular
hypertrophy,
dysfunction and failure.
 Arrhythmias
 Coronary artery
disease, Acute MI
 Arterial aneurysm,
dissection, and rupture.

20. COMPLICATIONS: BLOOD VESSELS
 Atherosclerosis
(frequently involving
large & medium sized
arteries).
 Hyaline arteiosclerosis.
 Hyperplastic
arteriosclerosis.

21. COMPLICATIONS: BRAIN
 Cerebro-vascular
accidents:
 TIA
 Stroke (Ishchaemic or
Haemorrhagic)
 Sub-arachnoid
haemorrhage.
 Hypertensive
Encephalopathy
 Multi-infarct Dementia

22. COMPLICATIONS: KIDNEYS
 Primarily affect preglomerular arterioles, resulting in ischemic
changes in the glomeruli and postglomerular structures.
 Glomerular injury also may be a consequence of direct damage to
the glomerular capillaries due to glomerular hyperperfusion.
 Loss of autoregulation of renal blood flow at the afferent arteriole
results in transmission of elevated pressures to an unprotected
glomerulus with ensuing hyperfiltration, hypertrophy, and eventual
focal segmental glomerular sclerosis.
 The renal lesion associated with malignant hypertension consists of
fibrinoid necrosis of the afferent arterioles, sometimes extending into
the glomerulus, and may result in focal necrosis of the glomerular
tuft.
 Clinically, macroalbuminuria (a random urine albumin/creatinine
ratio >300 mg/g) or microalbuminuria (a random urine albumin/
creatinine ratio 30–300 mg/g) are early markers of renal injury.

23. COMPLICATIONS: RETINA
 Retinopathy, retinal hemorrhages and impaired
vision.
 Vitreous hemorrhage, retinal detachment
 Neuropathy of the nerves leading to extraoccular
muscle paralysis and dysfunction

24. NORMAL RETINA AND HYPERTENSIVE
RETINOPATHY
Normal Retina Hypertensive RetinopathyA: Hemorrhages
B: Exudates (Fatty
Deposits)
C: Cotton Wool Spots
(Micro Strokes)
A B
C

25. STAGE I- ARTERIOLAR NARROWING
Arteriolar Narrowing

26. STAGE II- AV NIPPING
AV Nicking
AV Nicking
AV Nicking

27. STAGE III- HEMORRHAGES (H), COTTON
WOOL SPOTS AND EXUDATS (E)
H
E

28. STAGE IV- STAGE III+PAPILLOEDEMA

29. INVESTIGATION OF PATIENTS WITH
HYPERTENSION
All Patients:

30. CONT.
Special Conditions:

31. TARGET BP IN ADULTS
According to JNC 8-

32. CONT.
According to ACC

33. CONT.
According to NICE

34. MANGEMENT: NON PHARMACOLOGICAL
INTERVANTIONS

36. ADDITIONAL LIFESTYLE MEASURES TO
DECREASE CARDIOVASCULAR RISK
 Stop smoking. Does not decrease BP but will
improve overall CV risk. Quitting before middle age
returns life expectancy to near that of lifelong non-
smokers.
 Reduce total fat intake.
 Replace dietary saturated fats with
monounsaturated fats.
 Increase consumption of oily fish.

37. INDICATIONS TO START
PHARMACOTHERAPY

38. ORAL ANTI HYPERTENSIVE DRUGS

40. HYPERTENSION MANAGEMENT ALGORITHM
NICE guideline

41. JNC
8

42. JNC 8

43. ACC GUIDELINE

44. ACC IN SPECIAL SITUATIONS

48. HYPERTENSIVE CRISIS
Hypertensive crises are classified as emergencies or
urgencies , based on the presence or absence of
progressive target organ dysfunction.
 Emergencies: severe increase in BP complicated
by evidence of acute or progressive organ
dysfunction.
 Urgencies: severe increase in BP without evidence
of acute or progressive target organ dysfunction.

49. ACUTE TARGET ORGAN DAMAGE
 Neurological symptoms: at risk for haemorrhagic or
thrombotic stroke, encephalopathy (altered
consciousness, fits, focal signs).
 LVF.
 Acute kidney injury failure (send U&E, dipstick
urine).
 Chest pain. Acute coronary syndrome  MI or
aortic dissection. Perform ECG, and check pulses.
If in doubt: CT aorta.
 Visual symptoms +/- either grade III or IV
hypertensive retinopathy.
 Pancreatitis due to haemorrhagic infarction (rare).

50. DRUGS USED IN HYPERTENSIVE
CRISIS

52. REFERENCE
 Harrison's principles of internal medicine (20th
edition)
 Davidson’s Principles and Practice of Medicine
(23rd edition)
 Oxford handbook of nephrology & Hypertension
(2nd edition)
 JNC 8
 NICE 2011
 ACC 2017