Ayur Health: Ayurveda Medicine

The Ayur Health Ayurveda Clinic Adelaide blog is your go-to resource for authentic Ayurvedic insights and holistic wellness advice. Dedicated to promoting natural healing, this blog offers a wealth of information on ancient Ayurvedic practices tailored to modern lifestyles. Whether you're seeking remedies for specific ailments, tips on maintaining balance through diet and lifestyle, or deeper understanding of Ayurvedic principles, blog provides expert guidance from experienced practitioners.

Showing posts with label HYPERTENSION. Show all posts

Treatment formulation for reducing hypertension

Haritaki

Vaca

Saindhava

Amalaki

Pippali

Vidanga

Sunthi

Haridra

This is a combination of single drugs to reduce hypertension.
Try this and live long...

Raktamoksha in Hypertension

Importance of Raktamoksana (blood letting) is quoted by Susruta by stating that it is Ardhacikitsa in Salya Tanrtra. not only Susruta, but Caraka and Vagbhata also accepted and indicated this. For ex. in Visarpa cikista

Rakta is equated to life, due to vitiation at Rakta, life is also get disturbed, diseased produced by vitiated Rakta are in abundance having range from skin diseases upto life threatening diseases hypertension. delirium and coma etc. So, the treatment Raktamosana indicated field of action and efficacy.

Bloodletting is also one of the treatment in modern science also and it's importance illustrated in Cambridge history of medicine as

(1) Getting rid of poisons

(2) Isabella Beeten - In case of great emergency self blood letting.

(3) Samual Gross : Blood letting annual spring tonic

(4) To be a surgeon or medical man before 1870 meant blood letting.

Savill's also advised, blood letting in following disorders as a part of treatment which are Acute pericarditis, acute pulmonary oedema, Acute lobar, Uraemia.

complications of hypertension

Cardiac : There includes coronary artery disease, left ventricular failure and congestive heart failure.

Renal : Renal Failure

Vascular : Dissection of aorta and atherosclearosis are the main vascular complication.

Optic : Hypertensive retinopathy, which has been, graded into 4 grades by Keith wagener and Barber is common.

Effect of HT on organs involved

The pathological changes occurring in these organs are :

Heart :

Sustained HT leads to increased work load and left ventricular hypertrophy. The weight of heart is closely related to the degree of HT not only do the cardiac cell size but there is also an increase in the number of cells.

Progressive changes on other hand increase the muscle mass between the capillaries thus reducing blood supply to the heart. Because of left ventricular wall thickness there is an increase in the pressure gradient from the epicrdium to endocardium , reducing blood supply to the inner portion of the heart muscle Atheromatus changes on the coronary arteries further reduce blood supply causing fibrotic changes and even infarction of heart muscle leading to hypertension heart failure.

Brain :

Medial and initimal hypertrophy is also seen in arteries supplying the brain. There may be degenerative lesions of large vessels e.g. middle cerebral and carotid vessels, which cause thrombotic stroke. In older people tiny aneurysm (Charcot Bouchard aneurysm) have also been seen which cause cerebral hemorrhage. Thus cerebral infarction is secondary to the increased atherosclerosis but cerebral hemorrhage is the result of both, elevated BP and microaneuryzms.

Cerebral Encephalopathy consist of the following symptom complex. Severe HT, disordered consciousness, increase intracranial pressure, retinopathy with Papilloedema and seizures.

Kidneys :

Arteriosclerotic lesions of the afferent and efferent arterioles and the glomerular capillary tufts are the most common renal vascular lesions in HT and results in a decreased glomerular filtration rate and tabular dysfunction. Proteinuria and microscopic haematuria occur because of glomerular lesion and approximately 10% death caused by HT result from renal failure.

Arteries :

Initially there is thickening of the muscular coat, which can add to the increase in peripheral resistance following different stimulas later, there is intimal hypertrophy and generalized degenerative arterial lesions. Although the exact mechanism is not understood there is retention of certain lipoproteins which along with damage to the endothelium from shear forces and several other mechanisms leads to degenerative lesions. The overall lesions are a combination of medial hypertrophy, elastic proliferation, intimal proliferation, lipid deposition, degeneration and thrombotic events.

Retina :

The initial lesion is the irregular caliber of arterioles with localized constriction and dilatation. Due to constriction of arteries the ratio of veins to artery is increased. Micro infarcts may cause cotton wool exudates said to be due to increased axonal fluid transport in normal neurons near the site of the infarct. Rupture of capillaries can cause flame shaped hemorrhages. Swelling of the optic disc (Papilloedema) which is seen in malignant hypertension may not always be associated with hemorrhages and exudates and is due to generalized brain edema.

Features of Hypertension

CLINICAL FEATURES

*Sr. No.*	*Symptoms*	*Asymptomatic*	*Organ involment*
(1)	Headache		Heart
(2)	Giddiness		Brain
(3)	Irritability		Retina
(4)	Fatigue		Kidney
(5)	Insomnia
(6)	Vertigo positional
(7)	Palpitation
(8)	Polyuria

Symptoms showing organ involvement or symptoms related with complications

(I) Heart

(1) Angina

(2) Dyspnoea -Nocturnal

(3) Orthopnea

(II) Brain

(2) Visual Disturbances

(2) Severe Headache

(3) Stroke

(4) Encephalopathy

(III) Kidney

(1) Polyuria

(2) Nocturia

(3) Fatigue

(4) Anemia

(5) Vomiting

(6) Edema

(7) Features of Uremia

(IV) Retina

(1) Visual disturbance

(2) Retinal hemorrhage

(3) Retinal detachment

Asymptomatic :

A large number of patient in the early stages have no symptoms \. That is why it is called the silent killer.

Symptoms :

(1) Headache

(i) Present on waking in the morning.

(ii) Usually in occipital region, radiating to frontal.

(iii) Throbbing

(iv) Most headaches are tension headaches.

(v) Paroxysmal.

(2) Epistaxis

It is not particularly associated with mild hypertension where patients present with epistaxis and high blood pressure. It is important to dissociate HT as a cause of epistaxis from a pressure response to the episode.

(3) Nocturia

This is one of the most frequent consequences of blood pressure elevation resulting from reduction in urine concentrating capacity.

Signs :

(1) Elevated blood pressure i.e. blood pressure above 139 mm of Hg systolic and above 89 mm Hg diastolic on several occasions qualifies as hypertension irrespective of age

In the established cases, the blood pressure is persistently 180 mm systolic and 100 mm diastolic or over. It may be much higher reaching 260 mm systolic and 120 mm diastolic.

(2) There is left ventricular hypertrophy recognized by

(a) Cardiac impulse which is forceful and sustained

(b) An increase ,in the area of cardiac dullness.

(d) Increase is size of the heart in radiography

(e) Left axis deviation in ECG

(3) The 2nd aortic sound is accentuated.

(4) The radial pulse is hard and resists compression. The artery is generally felt to be thickened and it may be tortuous.

(5) The changes in Retina :

These have been divided in 4 grades (Keith &Wagenar)

(a) Grade-I : Changes consist of narrowing tortuosity and irregularity of the renal A.

(b) Grade-II : The changes are more marked and there is nipping of veins where the arteries cross in front of them.

(d) Grade-IV : Papilloedema

HYPERTENSION

HYPERTENSION

Blood pressure like height and weight is a biological characteristic of an individual and shows interindividual variability. Hypertension is a condition in which the patient has high blood pressure than judged to be normal.

Classification :

The raised blood pressure can be found in various conditions.

(1) Temperary : Symptamatic hypertension occures during exercise emotional, disturbances. Also can be seen in acute attacks of gout.

(2) Paroxysmal : It is due to tumor of suprarenal medula (Phacochromocytoma)

(3) Persistent hypertension : It is a clinical entity.

It can be divided in 2 according to aetiology.

(a) Primary (2) Secondary

SECONDARY HYPERTENSION

The hypertension secondary to renal, vascular, endocrine lesion

(1) Renal Cause of Secondary HT

(a) Chronic Diffuse glomerulonephritis

(b) Pyelonephritis

(c) Polycystic kidnees

(d) Diabetic nephropathy

(e) Renovascular disease

(2) Endocrine Cause

(a) Cushings syndrome

(b) Pheochromocytoma

(c) Primary hyper aldesternism

(3) Vascular Causes

(a) Renal artery disease

(b) Coarcation of aorta

(4) Other

(a) alcohol

(b) Drugs

(c) Pregnancy.

But the for the present study essential hypertension is only taken in account

ESSENTIAL HYPERTENSION

In 90% of patient with hypertension although some mechanisms may be operating it is not possible to define a specific underlying cause and they are said to have essential hypertension.

Synonyms : (1) Primary hypertention

(2) Idiopathic hypertension

(3) Hyperpeisia (Sir clifford Albutt)

Definition :

Essential hypertension is defined as sustained high blood pressure not attributable to a single cause but reflecting the interaction of multiple genetic and environmental influence.

Prevalence :

The prevalence rate of HT increases with age and higher in blacks than in whites.

HT is more common in men than in women upto the age 50 yrs. after which in is more common in women.

E.H.T. is especially frequent in some race particularly American blacks and Japanese and commoner in carries where there is high salt intake.

Thus the causes can be divided as :

(1) Genetic

(2) Environmental

(3) Other Disease Related

The Etiological Factors

Genetic :

(1) The influence of genetic factors contribute about 30% blood pressure variation.

(2) The inheritance is multifactorial and of heterogeneous nature.

(3) The genes that contribute to human essential HT have not been identified, but both monogenic defects (e.g. glucocorticoid remediable aldesternism and Liddles syndrome) and susceptibility genes (e.g. angeotensinogengene) have been now reported which have as one of their consequences an increased acture pressure.

Environmental Factors :

(1) Nutrition :

Several component of diet may change blood pressure. Some important facts are related with this:-

(a) The maternal malnutrition may be an important cause of HT Some studies have shown that the subject with the lower birth weightt and higher placental weight, have higher blood pressure in middle age.

(b) Vegetarians have lower blood pressure at all ages than omnivorous one possibility is that unsaturated vegetable fat lowers blood pressure.

(c) A number of studies have shown a positive association between Na intake and BP and a negative association between potassium intake and BP, but on current evidence the contribution of excessive sodium intake or inadequate potassium intake on HT in western society is small.

(2) Habits - HT

(1) Alcohol intake :

High alcohol intake (more than 6 units a day) have been shown to be associated with elevated BP in large number of studies.

(2) Smoking :

Nicotine and carbon monoxide the two major products of tobacco combustion are both potent vasoconstrictors. Nicotine also stimulates increase secretion of catecholamines, Tobacco smoking is well known to cause an acute rise in BP but whether prolonged smoking leads to sustained HT has not been so well established.

Stress :

D Exposure to a prolonged emotional stress and type-A personality are said to cause or aggravate high BP.

D Acute pain, tension, mental stress produces significant rise in BP.

D Chronic job strains leads to progressive increase in blood pressure.

D Modern City life, worry, anxiety and prolonged mental strain especially when combined with sleeplessness and lack of regular exercise are the general causes of HT.

Other Diseases And H T Relation

(1) Obesity :

High BP is associated with a high body mass index. Mainly central, obesity correlates well with BP than overall body mass the association with BP may reflect humoral factors and perhaps genetic linkage.

(2) Diabetes Mellitus:

Diabetics tend to have higher prevalence of atherosclesosis and HT. Insulin resistance or insulinemia have been suggested as being responsible for the increased Arterial pressure. Insulin resistance is common in patients with non insulin dependant. DM (NIDDM).

(3) Gout and Osteoarthritis:

These are also, often associated with HT.

(4) At the climacteric or after removal of both ovaries HT is seen, the associated rapid gain in weight is an important causal factor.

(5) Chronic lead poisoning is exogenous ... raised serum lipids HT. associated with raised and lipid ........... much higher risk of C.V.S. complication.