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HYPERTENSION
By
DR MBADIWE NKEIRUKA C.
OUTLINE
• Introduction
• Definitions
• Classification
• Pathophysiology
• Management
-symptoms and signs of HTN
-Investigations
- treatment
• complication
Introduction
Epidemiology
• World wide, HBP is estimated to cause about 7.5
million deaths, and about 12.8 % of all total
deaths.
• Globally, as at year 2022,an estimated 26% of the
world’s population (972 million people) has HTN.,
and the prevalence is expected to increase to
29% by the year 2025.
• Across the WHO regions, the prevalence of HBP
was highest in Africa, 46% for males and females
combined.
Epidemiology contd.
• HTN is a major modifiable risk factor for
stroke, MI, HF, ESRD, PVD, dementia,
progressive atherosclerosis
• Uncontrolled hypertension is associated with
serious end organ damage including heart
disease, stroke, blindness and renal disease.
4
Definition of Hypertension
• HYPERTENSION is currently defined as
persistent elevation of BP of ≥140 &/or
/90 mmHg for adults ≥ 18 years who are
not taking antihypertensive medication.
• BLOOD PRESSURE is the measurement
of the force exerted against the wall of
your arteries as your heart pumps blood
around your body.
Types of hypertension
• Primary (essential) hypertension- no particular
or specific cause is found.
• Secondary hypertension- due to a specific
medical conditions with potential for cure. Also
occur in children.
Risk factors for Essential Hypertension
Modifiable and non modifiable
Non modifiable risk factors:
Male gender
Increasing age
Ethnicity (African/afro American), Genetics, etc.
Fetal factors -low birth weight
Risk factors for Essential Hypertension
Modifiable risk factors:
Diet: high Na salts, low k
0besity ,
Chronic stress,
anxiety
Alcohol,
 Smoking
Sedentary life
Diabetes Mellitus
Causes of secondary HBP
RENAL:
• Glomerulonephritis, diabethic nephropathy
• Atherosclerosis, Renovascular disease, adult
polycystic kidneys dx, chronic tubulointerstitial
dx
Endocrine:
• Hormone related dxs e.g. Hyperthyriodism,
hypothyroidism, acromegaly,Cushing's
syndrome, Pheochromocytoma,
hyperparathyroidism etc.
Causes of secondary HBP
Adrenal:
-e.g. Pheochromocythoma, conn’s syndrome,
adrenal hyperplasia
Pregnancy (pre-eclampsia)
Drugs/Medications e.g. NSAIDS, Steroids, diet pills,
migraine pills, oral contraceptive pills,
sympathomimetics, vasopressin, monoamine
oxidase inhibitors, etc .
Cardiovascular:
-e.g. Aortic coarctation
Classification of Hypertension?
WHO Classification of Hypertension
Category Systolic BP
(mmHg)
Diastolic BP
(mmHg)
Optimal BP
Normal
High-Normal BP
Hypertension:
Grade 1 HT (mild)
Grade 2 HT (moderate)
Grade 3 HT (severe)
Isolated Systolic HT
<120
<130
130 – 139
140 - 159 and/or
160 – 179 and/or
≥180 and/or
≥140
<80
<85
85 – 89
90 – 99
100 – 109
≥110
<90
The Nigerian Hypertension Society Classification
Category Systolic BP
(mmHg)
Diastolic BP
(mmHg)
Optimal BP
Normal
High-Normal BP
Grade 1 HT (mild)
Grade 2 HT (moderate)
Grade 3 HT (severe)
Isolated Systolic HT
<120
<130
130 – 139
140 - 159 and/or
160 – 179 and/or
≥180 and/or
≥140
<80
<85
85 – 89
90 – 99
100 – 109
≥110
<90
TABLE 1. JOINT NATIONAL COMMITTEE – 7 (JNC-7) 2003 GUIDELINES
Category Systolic BP (mmHg) Diastolic BP (mmHg)
Normal
Prehypertension
Stage 1 Hypertension
Stage 2 Hypertension
<120 and
120 - 139 or
140 – 159 or
≥160 or
<80
80 – 89
90 – 99
≥100
Source: Arch Int. Med. 2006; 157:2413
Pathophysiology of HTN
• The actual pathogenesis of essential
Hypertension is not very clear. However,
certain pathophysiological mechanisms have
been postulated:
• It is believed that in some young persons who
become hypertensive, an early increase in
cardiac output, together with an increased
pulse rate leads to changes in the sensitivity of
the baroreceptor, which cause it to operate at
a higher level of blood pressure.
1. Cardiac changes:
• Resistance vessels, i.e the small arteries and
arterioles show structural changes in
hypertension, with increase in wall thickness
and reduction in the diameter of the lumen
of the vessels. This increases the peripheral
vascular resistance which maintains the
blood pressure at an elevated level.
• Also the vessels undergo rarefaction
(reduction in density) and the entire mechs
give rise to increase in overall total
peripheral resistance.
2. Large vessel changes:
• Thickening of the media occurs with increase in
collagen and secondary deposition of calcium.
These changes result in loss of arterial
compliance, which in turn leads to more
pronounced arterial pressure wave.
3. Pulse wave velocity:
• This is a measure of arterial stiffness, and is
inversely related to its distensibility.
• Usually, with each systolic contraction, a
pulse wave travels down the arterial wall
before the flow of blood. The more rigid the
vessel, the faster the pulse wave travels.
• The interaction of these mechanical stresses
and low growth factors leads to
development of Atheroma in the large
arteries.
• There is also endothelial dysfunction with
alterations in certain agents like Nitric Oxide,
and endothelins.
4. Left Ventricular Hypertrophy:
• Results from increased peripheral vascular
resistance and ↑ left ventricular load.
5. Renal Changes:
• Changed renal vasculature eventually leads
to ↓ renal perfusion, ↓ glomerular filtration
& sodium and water excretion. Decreased
renal perfusion may → activation of the
renin-angiotensin system with increased
secretion of aldosterone and further salt and
water retention.
6. Cerebral Changes:
• Changes in small vessels cause lacunae
(lacunar or small infarcts) and reversible
neurological deficits which will not show
abnormalities in imaging such as CT Scan or
MRI. These however may eventually lead to
dementia or stroke.
Management of Hypertension:
Hx (syptoms)
Physical examination (signs)
Lab investigations
treatment
Symptoms of High BP
• No symptoms, incidental finding, silent killer.
• Headaches,
• Insomnia
• visual blurring,
• dizziness,
• nausea. Vomiting,
• confusion etc.
Signs of High BP
• For acute stage of HTN, i.e. for new onset HTN,
there may be no signs.
• But for long standing HTN, signs include:
- Thickened radial arterial wall
- locomotor brachialis
- displaced, heaving apex beat.
- Xray evidence of aortic unfolding and
cardiomegaly
- Retinopathy -seen on fundoscopy.
Lab investigations
• Chest X-Ray
• Electrocardiogram,
• Echocardiogram
• Fundoscopy
• FBC
• Urinalysis
• FBG, (Glucose tolerance test if FBG is >5.6mmol/L
or 100 mg/dl).
• SEUC
• Fasting Lipids profile
Aim of Treatment of hypertension:
• Control BP down to target
• Prevent target organ damage
• Stop further organ damage
• Reverse organ damage where possible
Treatment modalities
1. Non pharmacological-
-Life style change:
• Exercise, Weight reduction
• Stop smoking, reduce alcohol consumption
• Diet modification- low Na salt, ↑K, low
cholesterol
2. Pharmacological- use of antihypertensive
drugs
Classes of drugs used in Rx of HTN
• Alpha-blockers: E.g. Doxazosin, Indoramin,
Phenoxybenzamine, Phentolamine.
• Aldosterone antagonists: E.g. Spironolactone,
Eplerenone.
• Angiotensin-converting enzyme inhibitors:
E.g. Enalapril, Lisinopril, Perindopril, Ramipril.
• Angiotensin II receptor blockers: E.g.
Losartan, Candesartan, Valsartan, Olmesartan,
Telmisartan.
• Beta-blockers: E.g. Atenolol, Bisoprolol,
Nebivolol, Carvedilol, Labetalol.
Classes of drugs in Rx of HTN contd.
• Calcium channel blockers: E.g. Amlodipine,
Nifedipine (long acting), Diltiazem (long acting),
Verapamil.
• Centrally acting: E.g. Methldopa, Moxonidine.
• Diuretics: E.g. Hydrochlorthiazide,
Bendroflumethiazide, Chlortalidone,
Furosemide.
• Renin inhibitors: E.g. Aliskiren.
• Vasodilators: E.g. Hydralazine, Minoxidil, Sodium
Nitroprusside.
Complications of Hypertension
• Brain - Strokes, dementia.
• Eyes - Hypertensive retinopathy, blindness.
• Heart –Long standing HTN can lead to the
following Hypertensive heart Diseases(HHDs): 1.
Left ventricular hypertrophy, 2. Ischaemic heart
disease/coronary artery disease, 3. heart failure,
4. conduction defects(heat blocks), 5. arrhythmias
• Kidney - Hypertensive nephrosclerosis, CKD.
• Peripheral vessels/ Vascular - peripheral vascular
disease, aortic aneurysm etc.
Acute Complications of Hypertension
• Hypertensive Emergencies
• Acute Strokes, Subarachnoid haemorrhage
etc.
• Acute Myocardial infarction etc.
• Aortic aneurysm dissection
Acute Complications of Hypertension
Hypertensive Emergencies:
• Refer to a spectrum of clinical presentations in
which uncontrolled blood pressure leads to
progressive or impending end-organ damage,
and requires aggressive lowering of blood
pressure, over minutes to hours. This usually
entails the use of parenteral route of
antihypertensive drug administration.
Acute Complications of Hypertension
Hypertensive Emergencies include:
• Hypertensive encephalopathy,
• Malignant Hypertension,
• Acute left ventricular failure,
• Eclampsia
• Pheochromocytoma, etc.
Thank you !
ANY QUESTIONS?

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HYPERTENSION/high blood pressure- a lecture-1.pptx

  • 2. OUTLINE • Introduction • Definitions • Classification • Pathophysiology • Management -symptoms and signs of HTN -Investigations - treatment • complication
  • 3. Introduction Epidemiology • World wide, HBP is estimated to cause about 7.5 million deaths, and about 12.8 % of all total deaths. • Globally, as at year 2022,an estimated 26% of the world’s population (972 million people) has HTN., and the prevalence is expected to increase to 29% by the year 2025. • Across the WHO regions, the prevalence of HBP was highest in Africa, 46% for males and females combined.
  • 4. Epidemiology contd. • HTN is a major modifiable risk factor for stroke, MI, HF, ESRD, PVD, dementia, progressive atherosclerosis • Uncontrolled hypertension is associated with serious end organ damage including heart disease, stroke, blindness and renal disease. 4
  • 5. Definition of Hypertension • HYPERTENSION is currently defined as persistent elevation of BP of ≥140 &/or /90 mmHg for adults ≥ 18 years who are not taking antihypertensive medication. • BLOOD PRESSURE is the measurement of the force exerted against the wall of your arteries as your heart pumps blood around your body.
  • 6. Types of hypertension • Primary (essential) hypertension- no particular or specific cause is found. • Secondary hypertension- due to a specific medical conditions with potential for cure. Also occur in children.
  • 7. Risk factors for Essential Hypertension Modifiable and non modifiable Non modifiable risk factors: Male gender Increasing age Ethnicity (African/afro American), Genetics, etc. Fetal factors -low birth weight
  • 8. Risk factors for Essential Hypertension Modifiable risk factors: Diet: high Na salts, low k 0besity , Chronic stress, anxiety Alcohol,  Smoking Sedentary life Diabetes Mellitus
  • 9. Causes of secondary HBP RENAL: • Glomerulonephritis, diabethic nephropathy • Atherosclerosis, Renovascular disease, adult polycystic kidneys dx, chronic tubulointerstitial dx Endocrine: • Hormone related dxs e.g. Hyperthyriodism, hypothyroidism, acromegaly,Cushing's syndrome, Pheochromocytoma, hyperparathyroidism etc.
  • 10. Causes of secondary HBP Adrenal: -e.g. Pheochromocythoma, conn’s syndrome, adrenal hyperplasia Pregnancy (pre-eclampsia) Drugs/Medications e.g. NSAIDS, Steroids, diet pills, migraine pills, oral contraceptive pills, sympathomimetics, vasopressin, monoamine oxidase inhibitors, etc . Cardiovascular: -e.g. Aortic coarctation
  • 12. WHO Classification of Hypertension Category Systolic BP (mmHg) Diastolic BP (mmHg) Optimal BP Normal High-Normal BP Hypertension: Grade 1 HT (mild) Grade 2 HT (moderate) Grade 3 HT (severe) Isolated Systolic HT <120 <130 130 – 139 140 - 159 and/or 160 – 179 and/or ≥180 and/or ≥140 <80 <85 85 – 89 90 – 99 100 – 109 ≥110 <90
  • 13. The Nigerian Hypertension Society Classification Category Systolic BP (mmHg) Diastolic BP (mmHg) Optimal BP Normal High-Normal BP Grade 1 HT (mild) Grade 2 HT (moderate) Grade 3 HT (severe) Isolated Systolic HT <120 <130 130 – 139 140 - 159 and/or 160 – 179 and/or ≥180 and/or ≥140 <80 <85 85 – 89 90 – 99 100 – 109 ≥110 <90
  • 14. TABLE 1. JOINT NATIONAL COMMITTEE – 7 (JNC-7) 2003 GUIDELINES Category Systolic BP (mmHg) Diastolic BP (mmHg) Normal Prehypertension Stage 1 Hypertension Stage 2 Hypertension <120 and 120 - 139 or 140 – 159 or ≥160 or <80 80 – 89 90 – 99 ≥100 Source: Arch Int. Med. 2006; 157:2413
  • 15. Pathophysiology of HTN • The actual pathogenesis of essential Hypertension is not very clear. However, certain pathophysiological mechanisms have been postulated: • It is believed that in some young persons who become hypertensive, an early increase in cardiac output, together with an increased pulse rate leads to changes in the sensitivity of the baroreceptor, which cause it to operate at a higher level of blood pressure.
  • 16. 1. Cardiac changes: • Resistance vessels, i.e the small arteries and arterioles show structural changes in hypertension, with increase in wall thickness and reduction in the diameter of the lumen of the vessels. This increases the peripheral vascular resistance which maintains the blood pressure at an elevated level. • Also the vessels undergo rarefaction (reduction in density) and the entire mechs give rise to increase in overall total peripheral resistance.
  • 17. 2. Large vessel changes: • Thickening of the media occurs with increase in collagen and secondary deposition of calcium. These changes result in loss of arterial compliance, which in turn leads to more pronounced arterial pressure wave. 3. Pulse wave velocity: • This is a measure of arterial stiffness, and is inversely related to its distensibility.
  • 18. • Usually, with each systolic contraction, a pulse wave travels down the arterial wall before the flow of blood. The more rigid the vessel, the faster the pulse wave travels. • The interaction of these mechanical stresses and low growth factors leads to development of Atheroma in the large arteries. • There is also endothelial dysfunction with alterations in certain agents like Nitric Oxide, and endothelins.
  • 19. 4. Left Ventricular Hypertrophy: • Results from increased peripheral vascular resistance and ↑ left ventricular load. 5. Renal Changes: • Changed renal vasculature eventually leads to ↓ renal perfusion, ↓ glomerular filtration & sodium and water excretion. Decreased renal perfusion may → activation of the renin-angiotensin system with increased secretion of aldosterone and further salt and water retention.
  • 20. 6. Cerebral Changes: • Changes in small vessels cause lacunae (lacunar or small infarcts) and reversible neurological deficits which will not show abnormalities in imaging such as CT Scan or MRI. These however may eventually lead to dementia or stroke.
  • 21. Management of Hypertension: Hx (syptoms) Physical examination (signs) Lab investigations treatment
  • 22. Symptoms of High BP • No symptoms, incidental finding, silent killer. • Headaches, • Insomnia • visual blurring, • dizziness, • nausea. Vomiting, • confusion etc.
  • 23. Signs of High BP • For acute stage of HTN, i.e. for new onset HTN, there may be no signs. • But for long standing HTN, signs include: - Thickened radial arterial wall - locomotor brachialis - displaced, heaving apex beat. - Xray evidence of aortic unfolding and cardiomegaly - Retinopathy -seen on fundoscopy.
  • 24. Lab investigations • Chest X-Ray • Electrocardiogram, • Echocardiogram • Fundoscopy • FBC • Urinalysis • FBG, (Glucose tolerance test if FBG is >5.6mmol/L or 100 mg/dl). • SEUC • Fasting Lipids profile
  • 25. Aim of Treatment of hypertension: • Control BP down to target • Prevent target organ damage • Stop further organ damage • Reverse organ damage where possible
  • 26. Treatment modalities 1. Non pharmacological- -Life style change: • Exercise, Weight reduction • Stop smoking, reduce alcohol consumption • Diet modification- low Na salt, ↑K, low cholesterol 2. Pharmacological- use of antihypertensive drugs
  • 27. Classes of drugs used in Rx of HTN • Alpha-blockers: E.g. Doxazosin, Indoramin, Phenoxybenzamine, Phentolamine. • Aldosterone antagonists: E.g. Spironolactone, Eplerenone. • Angiotensin-converting enzyme inhibitors: E.g. Enalapril, Lisinopril, Perindopril, Ramipril. • Angiotensin II receptor blockers: E.g. Losartan, Candesartan, Valsartan, Olmesartan, Telmisartan. • Beta-blockers: E.g. Atenolol, Bisoprolol, Nebivolol, Carvedilol, Labetalol.
  • 28. Classes of drugs in Rx of HTN contd. • Calcium channel blockers: E.g. Amlodipine, Nifedipine (long acting), Diltiazem (long acting), Verapamil. • Centrally acting: E.g. Methldopa, Moxonidine. • Diuretics: E.g. Hydrochlorthiazide, Bendroflumethiazide, Chlortalidone, Furosemide. • Renin inhibitors: E.g. Aliskiren. • Vasodilators: E.g. Hydralazine, Minoxidil, Sodium Nitroprusside.
  • 29. Complications of Hypertension • Brain - Strokes, dementia. • Eyes - Hypertensive retinopathy, blindness. • Heart –Long standing HTN can lead to the following Hypertensive heart Diseases(HHDs): 1. Left ventricular hypertrophy, 2. Ischaemic heart disease/coronary artery disease, 3. heart failure, 4. conduction defects(heat blocks), 5. arrhythmias • Kidney - Hypertensive nephrosclerosis, CKD. • Peripheral vessels/ Vascular - peripheral vascular disease, aortic aneurysm etc.
  • 30. Acute Complications of Hypertension • Hypertensive Emergencies • Acute Strokes, Subarachnoid haemorrhage etc. • Acute Myocardial infarction etc. • Aortic aneurysm dissection
  • 31. Acute Complications of Hypertension Hypertensive Emergencies: • Refer to a spectrum of clinical presentations in which uncontrolled blood pressure leads to progressive or impending end-organ damage, and requires aggressive lowering of blood pressure, over minutes to hours. This usually entails the use of parenteral route of antihypertensive drug administration.
  • 32. Acute Complications of Hypertension Hypertensive Emergencies include: • Hypertensive encephalopathy, • Malignant Hypertension, • Acute left ventricular failure, • Eclampsia • Pheochromocytoma, etc.
  • 33. Thank you ! ANY QUESTIONS?
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