Lecture notes on Hypertension


Important,  b,cose-
Secondary organ damage and
Reduced life span

Stress, Anxiety, Physical activity, etc can increase BP transiently and acutely

So, Several Estimations Needed to establish the diagnosis


In most cases, (­SBP, ­DBP, or mean BP), basic haemodynamic abnormality is Increased Vascular Resistance at Small Muscular Arteries.

This is due to

  1. Ratio of lumen to wall thickness

  1. Neural influences

Norepinephrine- vasoconstrictor
Acetylocholine- vasodialator

  1. Humeral and Locally acing substances

Angiotensin II- Vasoconstrictor

Prostaglandins and Kinins- Vasodilators
Hypoxia, Acidosis- Vasodilators

Systolic Hypertension

            Mostly in Elderly
            Due mainly to
1.Decreased Compliance of aortic wall due to Atherosclerosis
                           Is a risk factor for atherosclerosis

2. Due to ­ CO - In Thyrotoxicosis, Fever, Anemia, PDA, AV Fistula, 
   AR ctc,

                           Here there is a Wide Pulse pressure( Low Diastolic BP)

Theories of mechanism of Hypertension

            1, Hypertension as a reaction to Deficient Renal Na output

            ¯ Na excretion® ­ Blood Volume, ­ CVP, ­ CO, ­ Systemic Blood Flow
            Tissues react to this overperfusion by increasing local vascular resistance
            So, BP rises, ­ Afterload, ¯ Stroke volume and CO

            ­ Pressure ® ­ Renal flow, ­ Na excretion, ¯ Blood volume, ¯ CVP, ¯ CO

            So, end result is
                        Increased PVR
                        Increased BP
Normal B Volume, Normal CO, Normal CVP, Normal Na excretion

            2. Primary elevation in Peripheral Vascular Resistance
                        May be due to
                                    Increased Activity/Sensitivity of vasoconstrictors
                                    Reduced activity of vasodilators
                                    Change in size arterial smooth muscle

Both the above theories are equally valid and not mutually exclusive
Both may be important in any particular patient

In Hypertension due to Stress, Epinephrine may be the cause of  ­ BP

What is High BP?

            Due consideration needed for both Systolic and Diastolic BP

            150/90 in Men above 45 yrs or
130/90 in Men below 45 yrs

Sustained Hypertension- If Diastolic BP is always above these  levels

Labile Hypertension- They occasionally have BP in the hypertensive range

Malignant Hypertension- BP above 240/140, with Papilloedema

Acclerated Hypertension-
Recent increase in a hypertensive patient along with vascular damage in fundoscopy ,but without Papilloedema

Young Black Males have higher BP and increased incidence of complications


            Primary- Essential or Idiopathic- > 90%

                        Systolic and Diastolic Hypertension
1.      Renal
Ac and Ch Glomerulonephritis
Polycystic Renal Disease
Diabetic Nephropathy
                                                Renovascular stenosis and Infarction
                                                Renin producing Tumours

2.      Endocrine
Oral contraceptuives
Adrenocortical hyperfunction
            Cushings Disease/Syndrome
            Primary Hyperaldosteronism
            Con/Heriditory Adrenogenital syndromes

3.      Neurogenic
Familial Dysautonomia
Acute Porphyria,
Lead Poisoning
Increased Intracranial pressure

4.      Miscellaneous
Coarctation of aorta
Excessive transfusion,
Polyarteritis Nodosa

5.      Unknown Etiology
Toxemia of Pregnancy
Acute Intermittent Porphyria
Essential Hypertension

            Underlying mechanism not known

            Kidney probably has a central role
            Positive family history often present
            Inheritance is probably multifactorial

            Environmental factors
                        Salt intake, Obesity, Occupation, Family size, Overcrowding

            Modifying factors
                        Age- Younger the patient, greater the reduction in life expectancy

                        Females- fare better than men, But CV complications same

Serum Cholesterol, Smoking, Glucose intolerance, all increase
Atherosclerosis and effect of Hypertension

Obesity- Higher incidence of high BP, but does not affect mortality

            Untreated- Shortens life by 10-20 yrs- due to atherosclerosis and its effects

            Mild disease  with no end organ involvement- Untreated , compli in 7-10 yrs

                        30% will have atherosclerosis
            50% will have end organ damage due to Hypertension-
         Cardiomegaly, CCF, CVA, Renal insufficiency, Retinopathy etc

            Factors indicating Bad prognosis

1.      Young patient
2.      Male
3.      Persistent Diastolic BP above 115
4.      Smoking
5.      DM
6.      Dyslipidemia
7.      Obesity
8.      Evidence of End organ damage
1.      Cardiac
ECG – Ischemia or LV strain
2.      Eyes
Retinal Exudates, Haemorrhage
3.      Renal
Impaired Renal function
4.      Nervous system- CVA

Secondary Hypertension

            Cause can be identified only in a small group of patients
            But important b,cose Correction of cause cures Hypertension

■ Renal Hypertension
            Due to either
1.      Deranged renal handling of Na and Fluids® Volume expansion
2.      Altered renal secretion of vasoactive substances® change in arteriolar tone

Subdivisions of Renal Hypertension
1.      Renovascular ( Including pre-eclampsia and Eclampsia)
2.      Renal parenchymal Hypertension


There is decreased perfusion of Renal tissue due to Stenosis or Occlusion
Renin- angiotensin system is activated
Angiotensin raises BP by direct vasoconstriction and stimulates adrenergic system
It stimulates Aldosterone which causes Na retention

Angiotensin antagonist Saralasin reduces BP in such patients

Usual causes are Renal artery Stenosis due to Atherosclerosis- More in males, Occurs in advancing age

♦Fibromuscular Dysplasia-

Fibromuscular thickening of Intima, Media and Sub adventitial region

            More in
10 times more in Females,
Often B/L,
Usually in 3rd decade
Involves Distal part of RA and branches
Does not usually affect Asians and Africans
PTA S is very successful


1.      IVP

Small kidney
♦ Delayed appearance of contrast in affected kidney
♦ Hyperconcentration in affected kidney in late films
♦ Filling defects in Pelvis and Ureter due to dilated collateral

2.      Ultrasound

3.      Doppler

4.      CT Angiography

5.      MR Angiography

6.      Radionuclide Renogram

7.      Arteriography

8.      Renal vein and Aortic Renin sampling- Atleast 50% increase on affected side

9.      Fall in BP following Saralasin ( atleast by 10 mm Hg)

Renal Parenchymal Hypertension

There is Decreased perfusion of Renal parenchyma due to Inflammatory and Fibrotic changes in multiple small intra renal vessels.
This leads to stimulation of Renin- Angiotensin mechanism

May be other factors are also involved

1.      Damaged tissue produce some vasoconstrictor – other than Renin
2.      They fail to produce vasodilators
3.      They fail to inactivate circulating vasopressors
4.      They are ineffective in disposing Na → Na retention results
This is probably the best explanation

            Renin secreting Tumours

Juxtaglomerular cell tumours and Nephroblastomas may secrete excess Renin
They present like Primary Hyperaldosteronism
But peripheral Renin activity is increased instead of Subnormal

■ Endocrine Hypertension

1.      Adrenal Hypertension
            Primary Hyperaldosteronism

                        Leads to Na retention and Hypertension
                        Hypokalemia is a prominent feature(K exchanged for Na)
                        Serum K is a screening test
                        There is Suppression of Renin activity and Aldosterone levels are high

                        May be due to Adrenal tumour or B/L Hyperplasia
                        B/L Hyperplasia is not surgically treatable

            Cushing Syndrome

                        Glucocorticoids Increase Na retention
                        This is Due to production of Renin substrate- Angiotensin

                        Mineralocorticoids may also be increased in Cushings

            Adrenogenital Syndromes

                        C-11 or C-17 Hydroxylase deficiency causes Na retention
                        Renin is suppressed


                        Increased Epi and Norepinephrine
                        Peripheral vasoconstriction and Cardiac stimulation

                        Rare tumour- But curable, 0.1% of all hypertensives

                        ♦May be Adrenal or Extra adrenal
( Coeliac plexus, SM ganglia or IMGanglia)

♦May be associated with
-MEN II(Pheochromocytoma, MTC & Parathyroid hyperplasia)
-MEN III(MTC, Pheo & Mucosal neuromas)and
-Von R Disease,

80% Unilteral, 10% B/L 10% Extra adrenal
Right side is favoured

Usually Young Adults affected- Slight Female preponderance
Sustained Hypertension-in 60%.

Half of them have paroxysms of Hypertention and associated signs
40% have High BP only during attacks
Precipitated by any abdominal movement
Paroxysmal attacks-
            Sudden onset, Lasts minutes to hours
            Headache, Profuse sweating, Palpitation, anxiety
            Feeling of Impending death
            Chest or abdominal pain with Nausea and Vomiting
            Pallor and flushing
            High BP and Tachycardia
            Urinary Catecholamines (Normal 100-150 µg per 24 hrs)
            VMA- ( Normal-7 mg/24 hrs )
            Urinary Metanephrines( Normal- 1.3 mg/24 hrs)


                        High BP due to Nephrocalcinosis and Nephrolithiasis
                        Ca may have  a direct Vasoconstrictive effect

            Oral Contraceptives

                        From Oestrogen containing pills

                        Oestrogen stimulates production of Angiotensinogen from liver
                        Thus Angiotensin II and Aldosterone are produced

                        Not all on OC develop High BP, Why?
                                    ? Increased sensitivity to AngiotensinII
                                    ? Family H/O High BP
                                    ? Mild Renal disease present
                                    ? Obesity

                        May regress after 6 months of stopping OC

            Pre-Eclampsia and Eclampsia

                        Pre eclampsia-
Usually 3rd trimester
                                    High BP, Oedema, Proteinuria

                        Thickened Glomerular Basement Membrane
                        Due to Increase in cytoplasm of endothelial cells
                        So, Lumen narrowed(Glomerular Endotheliosis)
                        Sub endothelial fibrinoid deposition also may occur


                        Narrowing of Intralobular arteries

                        Due to deposition of Fibrin and Mucopolysacchrides

                        Distal occlusion leads to Ischemia and infarction

                        Haemorrhages and wedge shaped cortical infarcts are seen

            Polyarteritis Nodosa

                        Progressive, Recurrent Necrotizing Inflammatory disease of Medium
small sized muscular arteries

Occur at Sites of Branching

Subendothelial and Medial oedema, Fibrinoid necrosis, Infiltration with inflammatory cells, Proliferation of Fibroblasts

During healing, vessel wall replaced by fibrous tissue and lumen narrowed
Renal Insufficiency and Hypertension develops

Approach to patients with High BP

            Symptoms and Signs
            Clinical Evaluation
                                    Family History
                                    Age- below 35 and above 55, think of Sec.Hypertension
                                    Use of steroids
                                    Repeated UTI
                                    Weight gain
                                    Look for risk factors

                        Physical Exam
                                    Obesity, esp truncal

                                    BP- Rise in Diastoilc on standing Essential Hypertension
                                    Fall In Diastolic- ? Secondary

                                                Keith- Wagner- Barker grading
                                                4 grades-
                                    Chest exam- For cardiac disease

                                    Abdominal Bruits
                                    BF Delay, Collaterals on Chest wall
                        Lab Tests

1.      Basic Investigations

Always should be done
            Urine- Protein, Blood, Glucose
            Serum K
            Serum Creatinine, Urea

Done if cost allows
            Urine microscopy
            WBC Count
            Serum Glucose, Cholesterol, Tg
            Serum Ca, Po4, Uric acid
            Chest X-Ray

2.      Special studies

A.     Renovascular
IVP, Renogram, Arteriogram, Saralasin test

                             B.   Pheochromocytoma
                                    Urine VMA, Metanephrines, Catecholamines

                           C.  Cushing
                                    Overnight Deaxamethasone Suppression test



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