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
Mechanism
In most cases, (SBP, DBP, or mean BP), basic haemodynamic abnormality is Increased Vascular Resistance at Small Muscular Arteries.
This is due to
- Ratio of lumen to wall thickness
- Neural influences
Norepinephrine- vasoconstrictor
Acetylocholine- vasodialator
- 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
Etiology
Primary- Essential or Idiopathic- > 90%
Secondary-
Systolic and Diastolic Hypertension
1. Renal
Ch.Pyelonephritis
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
Pheochromocytoma
Acromegaly
3. Neurogenic
Psychogenioc
Familial Dysautonomia
Acute Porphyria,
Lead Poisoning
Increased Intracranial pressure
4. Miscellaneous
Coarctation of aorta
Excessive transfusion,
Polycythemia
Scleroderma
Polyarteritis Nodosa
Hypercalcemia
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
Cardiomegaly
ECG – Ischemia or LV
MI
CCF
2. Eyes
Retinal Exudates, Haemorrhage
Papilloedema
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
♦Renovascular
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
Investigations
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
vessels
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
Pheochromocytoma
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
Diagnosis
Urinary Catecholamines (Normal 100-150 µg per 24 hrs)
VMA- ( Normal-7 mg/24 hrs )
Urinary Metanephrines( Normal-
Acromegaly
Hypercalcemia
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
Scleroderma
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
History
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
Fundus
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
Haematocrit
Serum K
Serum Creatinine, Urea
ECG
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
