1. Pathogenesis and clinical features of Hypertension
Prof KR Sethuraman. MD
Thanks to:
Dr. Suresh, for the PPT set

2. Learning objectives Definition and classification of hypertension
Pathogenesis of hypertension
Regulation of blood pressure & recording of BP
Pathogenesis of essential hypertension and secondary hypertension and their causes
Pathophysiology of complications due to hypertension
Clinical features and diagnosis of hypertension

3. Hypertension - Introduction
Silent Killer – painless & complication is first hint
Complications bring to diagnosis but late…
Chronic, vascular & end organ damage.
It is the leading risk factor – Myocardial Infarction, Heart failure and Stroke
Responsible for the majority of hospital visits,
20 to 25% of population is affected, 70 to 80% of them are aware and out of them only 20% have BP under control ..! (“rule of halves”)

4. Definition of Hypertension
Classification of blood pressure (in mm Hg) for adults aged 18 years or older in the 7th Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the is as follows:
Normal†
Systolic <120, diastolic <80
Pre hypertension
Systolic , diastolic 80-99
Stage 1
Systolic , diastolic 90-99
Stage 2
Systolic >= 160, diastolic >= 100

5. Pathogenesis of Hypertension
It is multifactorial
Humoral mediators
Vascular reactivity – especially the arterioles
Blood volume
Vascular caliber
Blood viscosity
Cardiac output (= Heart rate x Stroke volume)
Blood vessel elasticity
Neural stimulation

7. Regulation of BP: BP = Cardiac Output x Peripheral Resistance
(Cardiac output= heart rate x stroke volume)
Endocrine Factors
Renin, Angiotensin, ANP, ADH, Aldosterone.
Neural Factors
Sympathetic & Parasympathetic
Blood Volume
Sodium, Mineralocorticoids, ANP
Cardiac Factors
Heart rate & Contractility.

8. Control of Blood Pressure:
Humoral Factors
Vasoconstrictors
Angiotensin II
Catecholamines
Vasodilators
Pg & Kinins
Blood Volume
Na+, Aldosterone BP
Cardiac
Output
Peripheral
Resistance
Cardiac Factors
Rate & Contract..
Local Factors
pH, Hypoxia
Neural Factors
Adrenergic – Cons
ß Adrenergic - Dil

9. Etiologic Classification:
Primary or Essential Hypertension(95%)
rule out “white coat hypertension”
Artifact: BP cuff too small
Secondary Hypertension (5-10%)
Renal – Chronic kidney disease, Acute and chronic glomerulonephritis, Polycystic kidney disease, Rennin secreting tumors
Endocrine – Cushing’s syndrome, Thyroid disorders, Pheochromocytoma, Acromegaly.

11. Secondary Hypertension: causes
Renovascular hypertension
Vascular: coarctation of aorta, polyarteritis nodosa,
Neurogenic: raised intracranial pressure, psychogenic, etc.
Drugs and toxins: oral contraceptives, alcohol, NSAIDs, cocaine, cyclosporin, etc.
Pregnancy induced hypertension
Hypercalcemia and hyperparathyroidism
Obstructive sleep apnoea

12. Pathogenesis of Hypertension:
Pathogenesis in Essential hypertension - Multifactorial
Increased blood volume - Sodium retention ADH, Aldosterone.
Increased sympathetic tone - Adrenal tumours, sympathetic stimulation.
Increased vasoactive hormones - Cushings, Pheochromocytoma,

13. Pathogenesis of Essential HT
It is also multifactorial
Genetic predisposition
Excess dietary salt intake
Increased adrenergic tone
Stress
Obesity
Endothelium derived factors

14. Pathogenesis of Renovascular HTN:
GFR
Renin by JGA
Aldosterone
Angiotensin II
Sodium Retention
Blood Volume
Vasoconstriction
 P. Resistance
Hypertension

15. Pathophysiology of target organ damage due to hypertension
Cardiovascular system:
Left ventricular hypertrophy
Aortic root dilatation
Congestive cardiac failure
Ischemic heart disease

16. Left ventricular hypertrophy
Myocardium undergoes structural changes in response to increased afterload
Cardiac myocytes respond by hypertrophy, allowing the heart to pump more strongly against the elevated pressure
However the contractile function of LV remains normal until late stages
Eventually LVH lessens the chamber lumen, limiting diastolic filling and stroke volume
LV diastolic function is markedly compromised in long standing hypertension

17. Left Ventricular Hypertrophy:

18. Hypertension and CNS
Long-standing hypertension may manifest as hemorrhagic and athero embolic stroke or encephalopathy.
High systolic pressure (> 160 mm Hg) and a diastolic pressure (>100 mm Hg) have led to a significant incidence of strokes.
Others - dementia.

19. Cerebral Infarction (Stroke) :
Haemorrhagic
Necrosis

20. Subarachnoid Haemorrhage:
Cerebral Blood vessels
Special features:
Thin walled*
End arteries*
Cong. Aneurisms
May present as “Thunder clap Headache”

21. Lacunar Infarcts: Single or multiple cavitary infarcts – lacunes.
Arteriolosclerosis of deep penetrating arterioles of brain stem.
Lenticular nucleus, thalamus
Slit Haemorrhages.

22. Hypertension and kidney disease
Nephrosclerosis is one of the possible complications of long-standing hypertension.
The renin-angiotensin system activity influences the progression of renal disease. Angiotensin II acts more on the efferent arteriole, which leads to an increase of the intraglomerular pressure.
Volume expansion is the main cause of hypertension in patients with glomerular disease (nephrotic and nephritic syndrome).

23. Benign Nephrosclerosis:
Leathery Granularity
due to minute scarring

25. Hypertension and kidney disease
Hypertension in patients with vascular disease is the result of the activation of the renin-angiotensin system, which is often secondary to ischemia.
The combination of volume expansion and the activation of the renin-angiotensin system is believed to be the main factor behind hypertension in patients with chronic renal failure

26. Consequences of Hypertension:
Blood Vessels
Atherosclerosis and its complications like aortic aneurysm, aortic dissection, Rupture, necrosis.
Heart
Left Ventricular Hypertrophy, Cardiac failure, IHD, MI.
Kidney
Benign/Malignant nephrosclerosis. Infarction
Eyes:
Hypertensive retinopathy
Brain:
Haemorrhage, infarction, dementia, etc.

27. Hyperplastic Arteriolosclerosis:
Narrow Lumen
Onion Skin Thickening
Of arterioles.

28. Normal Retina - Fundoscopy

29. Hypertensive Retinopathy:
Grade I – Thickening of arterioles.
Grade II – Focal Arteriolar spasms. Vein constriction.
Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool and hard waxy exudates.
Grade IV - Papilloedema

30. Malignant Hypertension:
Defined as High BP >220mmHg over 110mmHg associated with evidence of target organ damage. May lead to
Intravascular thrombosis.
Renal failure
Hypertensive encephalopathy.
Left ventricular failure.

31. Clinical features of Hypertension
Part 2
Clinical features of Hypertension

32. Common Presentation of HT
Usually asymptomatic
Occipital headaches characteristic but uncommon
Blurring of vision (retinal involvement)
Breathlessness and chest pain (cardiopulmonary involvement)
Irritability, confusion and somnolence are signs of encephalopathy

33. Diagnostic clues of Hypertension
Following the presentation of patients with suspected symptoms, Hypertension which is confirmed after properly measuring BP on atleast 3 separate occasions (based on the average of 2 or more readings taken at each of 2 or more visits after initial screening)
A history of cardiovascular risk factors includes hypercholesterolemia, diabetes mellitus, and tobacco use (including chewing tobacco).

34. Diagnostic clues of Hypertension
History of over-the-counter medication use, ethanol intake.
The historical and physical findings that suggest the possibility of secondary hypertension are a history of known renal disease, abdominal masses, anemia,
A history of sweating, labile hypertension, and palpitations suggests the diagnosis of pheochromocytoma.

35. Diagnostic clues of Hypertension
A history of cold or heat tolerance, sweating, lack of energy, and bradycardia or tachycardia may indicate hypothyroidism or hyperthyroidism.
A history of weakness suggests hyperaldosteronism.
Abdominal bruit suggests the possibility of renal artery stenosis.
Absence of femoral pulses suggests coarctation of aorta.
Kidney stones raise the possibility of hyperparathyroidism.

36. Methodology of recording BP
An accurate measurement of blood pressure is the key to diagnosis. Several determinations should be made over a period of several weeks.
At any given visit, an average of 3 blood pressure readings taken 2 minutes apart using a mercury manometer is preferable. Blood pressure should be measured in both the supine and sitting positions, auscultating with the bell of the stethoscope..

37. Methodology of recording BP
As the improper cuff size may influence blood pressure measurement, a wider cuff is preferable, particularly if the patient's arm circumference exceeds 30 cm.
The patient should rest quietly for at least 5 minutes before the measurement.
Although somewhat controversial, the common practice is to document phase V (a disappearance of all sounds) of Korotkoff sounds as the diastolic pressure.

38. Physical signs of Hypertension
A fundoscopic evaluation of the eyes should be performed to detect any evidence of hypertensive retinopathy. These are flame-shaped hemorrhages and cotton wool exudates.
Palpation of all peripheral pulses should be performed.

39. Physical signs of Hypertension
Look for renal artery bruit over the upper abdomen; the presence of a unilateral bruit suggests renal artery stenosis.
A careful cardiac examination is performed to evaluate signs of LVH. These include displacement of apex, a sustained and enlarged apical impulse, and the presence of an S4.

40. Conclusion: Persistent increased blood pressure (140/90)
95% Essential, 5% secondary - Renovascular
Benign and Malignant types (>120Diastolic)
Vessel damage & Arteriolosclerosis
Complicates - Atherosclerosis, Diabetes, IHD
Ischemia or Infarction in end organs.
Kidney, Brain, Heart & Eyes.
Nephrosclerosis, renal damage, IHD, MI, Stroke & Retinopathy.

41. “Do what you love, love what you do, and deliver more than you promise”
– Harvey Mackay

42. Thank you
Any questions??